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Reducing suicide risk in psychiatric disorders
Which psychotropics reduce the risk of suicide in patients with psychiatric disorders? Although no drugs eliminate the risk, new evidence is clarifying that some therapeutic choices can make a difference:
- Long-term lithium treatment apparently reduces suicide risk in patients with affective disorders; mood-altering anticonvulsants are less well studied but show less benefit than lithium.
- Effects of antidepressants remain inconclusive without adequate long-term studies.
- At least one atypical antipsychotic—clozapine—probably lowers suicide risk, although direct comparisons of antipsychotic agents are rare.
- Surprisingly little evidence is available on nondrug interventions, including rapid hospitalization, psychotherapy, and electroconvulsive therapy.1
Suicide is the leading cause of malpractice liability in psychiatry and of the heightened risk of death in persons with major affective and psychotic disorders (Box).1-4 Here are the latest findings to help you choose medications for at-risk patients with bipolar disorder, major depression, or chronic psychoses.
Suicide is by far the most common cause of premature death among patients with major mood and psychotic disorders.2,3 A major affective or psychotic disorder increases risk of suicide 8- to 22-fold (Table 1). A history of attempted suicide increases a person’s suicide risk 38-fold, so that the likelihood of dying by suicide becomes greater than one in four (28%).
Attempted suicide is less well-documented but may be 10 to 20 times more common than completed suicide in the general population. Persons with major affective and psychotic disorders complete suicide at an estimated rate of once in five attempts. This high rate suggests that their suicidal intent and methods are particularly lethal.4
BIPOLAR DISORDER AND MOOD STABILIZERS
Bipolar disorder is associated with the highest suicide rate among all major psychiatric illnesses, with an international incidence averaging 0.31% of patients per year.4 This rate may slightly exceed the suicide rate of patients with major depression, which averages 0.29%/year.
Risk of suicidal behavior is similar among patients with bipolar type II (depression with hypomania) and type I disorder (depression with mania), supporting the view that type II is not a milder form of bipolar illness.4-6 Indeed, one study of suicide attempts found a higher risk among bipolar II patients (24%) than in bipolar I patients (17%) as well as a higher risk in both bipolar types than in persons diagnosed with unipolar major depression (12%).4
Suicidal behavior in bipolar disorder is associated almost entirely with ongoing depression or dysphoria and is especially likely to follow severe and highly recurrent depressive episodes.5,6 Combinations of depressive-dysphoric and irritable, agitated, anxious features in “mixed states” may be particularly dangerous and can be hard to diagnose with confidence. Moreover, DSM-IV criteria for mixed states are far too narrow in requiring symptoms to simultaneously fulfill criteria for both mania and major depression. More broadly defined mixed states are very common. Underdiagnosis risks underestimation of suicidal potential, and misdiagnosis as “agitated depression” encourages potentially dangerous overuse of antidepressants.5,7
Depression or dysphoria is the most prevalent morbidity in patients with bipolar disorder. Major and minor depressive states and mixed-dysphoric phases account for nearly one-third of time in follow-up care, exceeding time in mania or hypomania by more than 4-fold.8 Ironically, however, bipolar depression is one of the least-studied forms of major depression. Suicidal bipolar patients are typically excluded from antidepressant studies because of the risks of inducing greater instability, agitation, or mania while treating them with an antidepressant but without a mood stabilizer.7
LITHIUM’S PROTECTIVE EFFECT
Decades of research and clinical use demonstrate substantially lower risks of suicide and serious suicide attempts when patients with bipolar disorder are treated long-term with lithium salts in standard clinical doses (serum concentrations typically 0.6 to 0.8 mEq/L). Lithium is highly effective in treating all phases of bipolar disorder. A recent meta-analysis of 26 long-term trials of lithium reported between 1967 and 2001 found an average 3.2-fold sparing of morbidity or relapse risk.9
Benefits in types I and II. A large European sample10 compared percent-time-ill in bipolar patients before and after they received lithium as maintenance treatment. Unexpectedly, lithium therapy reduced percent-time-ill to a greater extent among patients with type II than type I bipolar disorder. Time in mania and time in depression were reduced 2.5-fold and 2.0-fold, respectively, in type I patients, compared with nearly 5-fold for time in hypomania and 2.5-fold for time in depression among type II patients.
Because depression is associated with the highest rates of suicidal behavior in all phases of bipolar disorders, lithium’s effects in preventing depressive recurrence are especially important for reducing suicide risk.6
In a review of 22 studies11 —some including patients with bipolar or recurrent unipolar major depression—risk of death by suicide was reduced at least 5-fold, based on an informal comparison of pooled rates in treated versus untreated samples. Based on quantitative meta-analysis, the pooled risk of death by suicide was reduced nearly 9-fold (or by 89%) in patients who received lithium maintenance treatment compared with those who did not. The risk for suicide attempts fell nearly 10-fold in a compilation of 33 studies (Table 2).12 Available studies do not permit separate analysis of lithium’s effects on suicidal behavior among patients with bipolar disorder and recurrent unipolar depression, leaving the relative benefit by diagnosis uncertain.
Table 1
Suicide risks in selected psychiatric disorders*
| Condition | Relative risk | Incidence (%/year) | Lifetime risk (%) |
|---|---|---|---|
| Prior suicide attempt | 38.4 | 0.549 | 27.5 |
| Bipolar disorder | 21.7 | 0.310 | 15.5 |
| Major depression | 20.4 | 0.292 | 14.6 |
| Mixed drug abuse | 19.2 | 0.275 | 14.7 |
| Dysthymia | 12.1 | 0.173 | 8.65 |
| Obsessive-compulsive disorder | 11.5 | 0.143 | 8.15 |
| Panic disorder | 10.0 | 0.160 | 7.15 |
| Schizophrenia | 8.45 | 0.121 | 6.05 |
| Personality disorders | 7.08 | 0.101 | 5.05 |
| Alcohol abuse | 5.86 | 0.084 | 4.20 |
| Cancer | 1.80 | 0.026 | 1.30 |
| General population | 1.00 | 0.014 | 0.72 |
| * Estimated relative risks compared with the general population,2 with recently updated information about bipolar disorders.6 Annual rates are based on international general population average (14.3/100,000/year) × standardized mortality ratio; lifetime estimates are based on annual rates × 50 years as an estimate of lifetime exposure for years at major risk. | |||
Dangers of stopping lithium. In our study5 of more than 200 patients with DSM-IV bipolar I or II disorder, prophylactic lithium treatment for an average of 4 years reduced the risk of completed and attempted suicide by 6.5-fold. A subgroup of more than 100 patients discontinued lithium, usually after prolonged stability, and we excluded from analysis any cases of suspected emerging illness associated with discontinuation. Within 6 to 12 months after stopping treatment, this subgroup’s rates of suicidal behavior increased markedly—by 20-fold above treated rates.5 Thereafter, their rates returned to prelithium treatment levels.
Of particular clinical importance:
- discontinuing lithium gradually—over at least 2 weeks—was associated with a 2-fold lower suicide risk than more-abrupt discontinuation
- suicidal behavior after lithium discontinuation was almost always associated with emerging depression, which can provide an early warning of impending suicidal risk.
Table 2
Effect of lithium treatment on risk of completed and attempted suicide in patients with bipolar and recurrent depressive disorders*
| Treatment or sample | Suicides | Attempts | All acts | A/S ratio |
|---|---|---|---|---|
| With lithium | 0.16 | 0.41 | 0.57 | 2.6 |
| Without lithium | 0.88 | 4.02 | 4.90 | 4.6 |
| Off/on lithium ratio | 5.5 | 9.8 | 8.6 | — |
| General population | 0.014 | 0.21 | 0.22 | 15.3 |
| Off lithium/general population ratio | 56.4 | 19.1 | 22.3 | — |
| On lithium/general population ratio | 11.4 | 2.0 | 2.6 | — |
| A/S ratio: Attempts versus completed suicides | ||||
| * Rates (acts/year/100 persons, or %/year), based on previously reported averages derived from analyses of data from 33 studies with 55 treatment-arms,12 from a more selected analysis of 22 studies of completed suicides,11 and updated estimates for general population rates.6 | ||||
This is not the first time we have found evidence of a dramatic—but time-limited—increase in risk of recurrent bipolar illness when lithium treatment was discontinued.13 Bipolar disorder patients who discontinue long-term lithium treatment abruptly are at high risk of recurrent depression and mania.13
Incomplete protection. Lithium’s protection against suicidal risk is incomplete, as one can see by comparing lithium-treated versus untreated bipolar patients’ suicide rates with those of the general population (Table 2).6
With lithium:
- suicides plus attempts declined 8.6-fold to levels 2.6 times greater than those of the general population
- suicide attempts fell 10-fold to levels that are about twice that of the general population
- risk of completed suicides declined 5.5-fold with lithium treatment but remained 11 times higher than that of the general population.
Without lithium:
- risk of suicide in bipolar patients is approximately 22 times greater than that of the general population
- ratio of attempts to suicides among bipolar disorder patients averages 4.6, suggesting that suicide attempts by patients with bipolar disorder are relatively lethal.6
Effect of delayed lithium therapy. Many patients with bipolar disorder do not receive sustained prophylactic treatment early in the illness.
Studies typically show an average 5- to 10-year gap between illness onset and the start of sustained lithium maintenance treatment. This delay averages more than 3 years longer among women with bipolar II disorder than men with bipolar I disorder, evidently reflecting major clinical dissimilarities between these groups.6,14 In contrast, we found that nearly one-quarter of long-term risk of suicidal behavior emerges within the first year of bipolar illness.5 Clearly, patients with recurrent major affective illness require earlier intervention and more consistent clinical care.
We have also found that delayed maintenance treatment or the number of prior episodes of bipolar illness do not seem to limit therapeutic response to lithium.14,15 These findings support the conclusion that prophylactic lithium treatment can be worthwhile, even after years of illness and many recurrences. Moreover, our recent meta-analysis of treatment options for rapid-cycling bipolar illness indicates that—even though all treatments have yielded inferior results compared with nonrapidly-cycling patients—no alternative has outperformed lithium.16
Anticonvulsants. Evidence regarding the effects of other mood stabilizers on suicide risk in bipolar disorder remains limited:
- In a European collaborative study, several hundred patients with bipolar or schizoaffective disorder were randomly assigned to receive lithium or carbamazepine for nearly 2 years. Rates of suicidal acts were 2.5%/year with the anticonvulsant, but there were no suicides or attempts in patients receiving lithium.17 Direct comparisons are rare, but this difference was both striking and statistically significant.
- Computerized records of approximately 20,000 patients diagnosed with bipolar disorder at two large American HMOs were analyzed to compare suicidal behaviors associated with specific treatments. Lithium yielded 2.7-fold greater protection against suicidal behavior (mainly attempts because suicides were rare) compared with anticonvulsants (mainly divalproex).18
Treatment recommendation. These observations support lithium’s value in long-term maintenance of patients with bipolar disorder. Lithium’s apparent reduction of suicide risk is striking and may be superior to that of other mood-stabilizers. Alternate treatments and lithium’s potential value for reducing suicide risk in patients with unipolar depression require further study.
It is important to emphasize that lithium can be toxic or even fatal in acute overdose. This risk is integral to the equation when you assess risks and benefits for individual patients.
MAJOR DEPRESSION AND ANTIDEPRESSANTS
Major depression and depressive components of other disorders are major risk factors for suicide.1,2,6 Depression continues to be surprisingly underrecognized and undertreated, even though relatively safe and tolerable antidepressants are readily available.1,6,19,20 Patients with recurrent unipolar major depression often remain inconsistently or inadequately treated, even after they attempt suicide.19
Recent reviews of suicide risk during research on antidepressant treatment in major depression suggest that:
- antidepressants of various kinds may tend to reduce the risk of suicidal behavior, but any such effect is small and statistically nonsignificant (Baldessarini et al, 2003, unpublished)
- tricyclic antidepressants may yield lower rates of suicidal behavior than selective serotonin reuptake inhibitors (SSRIs). Similarly, however, such trends reflect highly variable research methods and inconsistent findings and do not hold up to quantitative analysis (Baldessarini et al, 2003, unpublished).
The suicidal events encountered during research mainly involve attempts because suicides are rare, particularly in relatively brief treatment trials that exclude acutely suicidal subjects. Analyses are further complicated by trends toward paradoxically lower suicidal risks among depressed patients randomized to a placebo in controlled antidepressant trials. This paradox is paralleled by often earlier removal of patients treated with a placebo than with an active antidepressant, perhaps in association with emerging suicidality.21
Table 3
Preventing suicide: How effective are specific treatments?
| Treatments compared | Disorder treated | Benefit/risk ratio |
|---|---|---|
| Mood stabilizers | ||
| Lithium vs. none or placebo* | Bipolar disorder | |
| Suicides | 8.8 (4.1 to 19.1)a | |
| Attempts | 9.9 (5.0 to 14.8)b | |
| Lithium vs. carbamazepine* | Bipolar disorder | ≥2.5c |
| Lithium vs. divalproex* | Bipolar disorder | 2.7 (1.2 to 6.2)d |
| Antidepressants | ||
| Antidepressants (any) vs. placebo/none | Major depressive disorder | 1.1 (0.7 to 1.6)e |
| Tricyclics vs. SSRIs | Major depressive disorder | 1.2 (0.7 to 2.1)e |
| Antipsychotics | ||
| Clozapine vs. any antipsychotic* | Schizophrenia | |
| Suicides + attempts | 3.3 (1.7 to 6.3)f | |
| Attempts | 2.9 (1.5 to 5.7)f | |
| Clozapine vs. olanzapine* | Schizophrenia | |
| Suicides + attempts | 1.3 (1.0 to 1.7)g | |
| a. Tondo et al, 200111 | ||
| b. Baldessarini et al, 20035 | ||
| c. Thies-Flechtner et al, 199517 | ||
| d. Goodwin et al, 200218 | ||
| e. Baldessarini et al, 20035 | ||
| f. Baldessarini & Hennen, 200322 | ||
| g. Meltzer et al, 200324 | ||
| * First agent is statistically more effective, based on benefit/risk ratio (95% CI). | ||
These trends toward lower suicide risk among patients receiving a placebo are somewhat reassuring, given concern that placebo randomization for scientific purposes may endanger study subjects. However, these artifacts confound interpretation of results and make it difficult to measure the effects of antidepressant treatment.
Treatment recommendation. Clinical prudence requires us to treat potentially lethal major depressive illness aggressively, even though one cannot state with confidence that any antidepressant class lowers suicide risk or that one class is significantly more effective than others (Table 3).
SCHIZOPHRENIA AND ANTIPSYCHOTICS
For schizophrenia and other primary psychotic disorders, little research exists to indicate that atypical antipsychotics reduce suicide risk. Evidence is emerging, however, that clozapine may offer this benefit,22 in addition to its well-substantiated clinical superiority in treatment-resistant psychotic illness.23
Pooled evidence from controlled trials comparing clozapine with other antipsychotics indicates a 2-fold lower risk of mortality from all causes.23 This finding was highly suggestive but not statistically significant, and the specific contribution of suicide to this risk is unknown.23 Our recent meta-analysis of the few available studies found that clozapine was associated with a statistically significant, 3.3-fold lower overall suicidal risk compared with other antipsychotic treatments.22
A well-designed, 2-year study randomly assigned 980 patients with schizophrenia or schizoaffective disorder who were at high risk for suicide to clozapine (mean 274 mg/d) or olanzapine (mean 16.6 mg/d). Clozapine showed moderately greater benefit in reducing suicide attempts and need for urgent intervention for perceived emerging suicide risk, although it did not lower suicide risk per se.24 Another study associated olanzapine with a 2.3-fold lower risk of suicidal behavior, compared with haloperidol.25
Comparing two potentially effective agents may have limited the observed difference between clozapine and olanzapine.24 Nevertheless, previous (largely uncontrolled) comparisons with other treatment options indicate substantially lower risks of both suicides and attempts with clozapine.22 In December 2002, the FDA approved a unique indication for clozapine: to reduce the risk of recurrent suicidal behavior in patients with schizophrenia or schizoaffective disorder.
Treatment recommendation. Risks of suicide and other causes of premature death are high in patients with chronic psychotic disorders, underlining the importance of appropriate longterm care. Clozapine has shown benefit in reducing risk of suicidal behaviors. When clozapine is otherwise a plausible option, this additional potential benefit can be considered when selecting therapy for individual patients.
Related resources
- American Psychiatric Association. Suicide-prevention practice guidelines. Washington, DC: American Psychiatric Press, 2003 (in press).
- American Foundation for Suicide Prevention. http://www.afsp.org
- American Association of Suicidology. www.suicidology.org
- National Institute of Mental Health (NIMH)/Suicide.
Drug brand names
- Clozapine • Clozaril
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Haloperidol • Haldol
- Lithium carbonate • Eskalith, Lithobid, others
- Olanzapine • Zyprexa
Disclosure
Dr. Baldessarini has received research grants from Molecular Insight Pharmaceuticals, Eli Lilly and Co., Janssen Pharmaceutica, Protarga Inc., and Solvay Pharmaceuticals, and is a consultant to Auritec Laboratories, Molecular Insight Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, Janssen Pharmaceutica, and Protarga Inc.
1. Goldsmith SK, Pellmar TC, Kleinman AM. Bunney WE, Jr (eds). Reducing suicide: A national imperative. Washington DC: National Academies Press, 2002.
2. Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J Psychiatry 1997;170:205-28.
3. Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord 2002;68:167-81.
4. Rihmer Z, Pestality P. Bipolar II disorder and suicidal behavior. Psychiatr Clin North Am 1999;22:667-73.
5. Baldessarini RJ, Tondo L, Hennen J. Lithium treatment and suicide risk in major affective disorders: update and new findings. J Clin Psychiatry 2003;64(suppl 5):44-52.
6. Tondo L, Isacsson G, Baldessarini RJ. Suicide in bipolar disorder: risk and prevention. CNS Drugs 2003;17:491-511.
7. Ghaemi SN, Lenox MS, Baldessarini RJ. Effectiveness and safety of long-term antidepressant treatment in bipolar disorder. J Clin Psychiatry 2001;62:565-9.
8. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry 2002;59:530-7.
9. Baldessarini RJ, Tondo L, Hennen J, Viguera AC. Is lithium still worth using? An update of selected recent research. Harvard Rev Psychiatry 2002;10:59-75.
10. Tondo L, Baldessarini RJ, Floris G. Long-term clinical effectiveness of lithium maintenance treatment in types I and II bipolar disorders. Br J Psychiatry 2001;178(suppl 41):S184-90.
11. Tondo L, Hennen J, Baldessarini RJ. Lower suicide risk with longterm lithium treatment in major affective illness: a meta-analysis. Acta Psychiatr Scand 2001;104:163-72.
12. Baldessarini RJ, Tondo L, Hennen J. Treating the suicidal patient with bipolar disorder: reducing suicide risk with lithium. Ann NY Acad Sci 2001;932:24-43.
13. Baldessarini RJ, Tondo L, Viguera AC. Discontinuing lithium maintenance treatment in bipolar disorder: risks and implications. Bipolar Disord 1999;1:17-24.
14. Baldessarini RJ, Tondo L, Hennen J. Treatment latency and previous episodes: relationships to pretreatment morbidity and response to maintenance treatment in bipolar I and II disorders. Bipolar Disord 2003;5:169-79.
15. Bratti IM, Baldessarini RJ, Baethge C, Tondo L. Pretreatment episode count and response to lithium treatment in manic-depressive illness. Harvard Rev Psychiatry (in press).
16. Tondo L, Hennen J, Baldessarini RJ. Rapid-cycling bipolar disorder: effects of long-term treatments. Acta Psychiatr Scand 2003;108:4-14.
17. Thies-Flechtner K, Miller-Oerlinghausen B, Seibert W, et al. Effect of prophylactic treatment on suicide risk in patients with major affective disorders: data from a randomized prospective trial. Pharmacopsychiatry 1996;29:103-7.
18. Goodwin FK, Fireman B, Simon G, et al. Suicide attempts in bipolar patients on lithium vs. divalproex (abstract 45; cited with permission of Dr. Goodwin). San Juan, PR: American College of Neuropsychopharmacology annual meeting, 2002.
19. Suominen KH, Isometsa ET, Henriksson MM, et al. Inadequate treatment for major depression both before and after attempted suicide. Am J Psychiatry 1998;155:1778-880.
20. Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA 2003;289:3095-105.
21. Khan A, Khan S, Kolts R, Brown WA. Suicide rates in clinical trials of SSRIs, other antidepressants, and placebo: analysis of FDA reports. Am J Psychiatry 2003;160:790-2.
22. Baldessarini RJ, Hennen J. Reduced suicidal risk during treatment with clozapine: A meta-analysis. Manuscript in review, 2003.
23. Wahlbeck K, Cheine M, Essali A, Adams C. Evidence of clozapine’s effectiveness in schizophrenia: a systematic review and meta-analysis of randomized trials. Am J Psychiatry 1999;156:990-9.
24. Meltzer HY, Alphs L, Green AI, et al. Clozapine treatment for suicidality in schizophrenia: International Suicide Prevention Trial (InterSePT). Arch Gen Psychiatry 2003;60:82-91.
25. Glazer WM. Formulary decisions and health economics. J Clin Psychiatry 1998;59(suppl 19):23-9.
Which psychotropics reduce the risk of suicide in patients with psychiatric disorders? Although no drugs eliminate the risk, new evidence is clarifying that some therapeutic choices can make a difference:
- Long-term lithium treatment apparently reduces suicide risk in patients with affective disorders; mood-altering anticonvulsants are less well studied but show less benefit than lithium.
- Effects of antidepressants remain inconclusive without adequate long-term studies.
- At least one atypical antipsychotic—clozapine—probably lowers suicide risk, although direct comparisons of antipsychotic agents are rare.
- Surprisingly little evidence is available on nondrug interventions, including rapid hospitalization, psychotherapy, and electroconvulsive therapy.1
Suicide is the leading cause of malpractice liability in psychiatry and of the heightened risk of death in persons with major affective and psychotic disorders (Box).1-4 Here are the latest findings to help you choose medications for at-risk patients with bipolar disorder, major depression, or chronic psychoses.
Suicide is by far the most common cause of premature death among patients with major mood and psychotic disorders.2,3 A major affective or psychotic disorder increases risk of suicide 8- to 22-fold (Table 1). A history of attempted suicide increases a person’s suicide risk 38-fold, so that the likelihood of dying by suicide becomes greater than one in four (28%).
Attempted suicide is less well-documented but may be 10 to 20 times more common than completed suicide in the general population. Persons with major affective and psychotic disorders complete suicide at an estimated rate of once in five attempts. This high rate suggests that their suicidal intent and methods are particularly lethal.4
BIPOLAR DISORDER AND MOOD STABILIZERS
Bipolar disorder is associated with the highest suicide rate among all major psychiatric illnesses, with an international incidence averaging 0.31% of patients per year.4 This rate may slightly exceed the suicide rate of patients with major depression, which averages 0.29%/year.
Risk of suicidal behavior is similar among patients with bipolar type II (depression with hypomania) and type I disorder (depression with mania), supporting the view that type II is not a milder form of bipolar illness.4-6 Indeed, one study of suicide attempts found a higher risk among bipolar II patients (24%) than in bipolar I patients (17%) as well as a higher risk in both bipolar types than in persons diagnosed with unipolar major depression (12%).4
Suicidal behavior in bipolar disorder is associated almost entirely with ongoing depression or dysphoria and is especially likely to follow severe and highly recurrent depressive episodes.5,6 Combinations of depressive-dysphoric and irritable, agitated, anxious features in “mixed states” may be particularly dangerous and can be hard to diagnose with confidence. Moreover, DSM-IV criteria for mixed states are far too narrow in requiring symptoms to simultaneously fulfill criteria for both mania and major depression. More broadly defined mixed states are very common. Underdiagnosis risks underestimation of suicidal potential, and misdiagnosis as “agitated depression” encourages potentially dangerous overuse of antidepressants.5,7
Depression or dysphoria is the most prevalent morbidity in patients with bipolar disorder. Major and minor depressive states and mixed-dysphoric phases account for nearly one-third of time in follow-up care, exceeding time in mania or hypomania by more than 4-fold.8 Ironically, however, bipolar depression is one of the least-studied forms of major depression. Suicidal bipolar patients are typically excluded from antidepressant studies because of the risks of inducing greater instability, agitation, or mania while treating them with an antidepressant but without a mood stabilizer.7
LITHIUM’S PROTECTIVE EFFECT
Decades of research and clinical use demonstrate substantially lower risks of suicide and serious suicide attempts when patients with bipolar disorder are treated long-term with lithium salts in standard clinical doses (serum concentrations typically 0.6 to 0.8 mEq/L). Lithium is highly effective in treating all phases of bipolar disorder. A recent meta-analysis of 26 long-term trials of lithium reported between 1967 and 2001 found an average 3.2-fold sparing of morbidity or relapse risk.9
Benefits in types I and II. A large European sample10 compared percent-time-ill in bipolar patients before and after they received lithium as maintenance treatment. Unexpectedly, lithium therapy reduced percent-time-ill to a greater extent among patients with type II than type I bipolar disorder. Time in mania and time in depression were reduced 2.5-fold and 2.0-fold, respectively, in type I patients, compared with nearly 5-fold for time in hypomania and 2.5-fold for time in depression among type II patients.
Because depression is associated with the highest rates of suicidal behavior in all phases of bipolar disorders, lithium’s effects in preventing depressive recurrence are especially important for reducing suicide risk.6
In a review of 22 studies11 —some including patients with bipolar or recurrent unipolar major depression—risk of death by suicide was reduced at least 5-fold, based on an informal comparison of pooled rates in treated versus untreated samples. Based on quantitative meta-analysis, the pooled risk of death by suicide was reduced nearly 9-fold (or by 89%) in patients who received lithium maintenance treatment compared with those who did not. The risk for suicide attempts fell nearly 10-fold in a compilation of 33 studies (Table 2).12 Available studies do not permit separate analysis of lithium’s effects on suicidal behavior among patients with bipolar disorder and recurrent unipolar depression, leaving the relative benefit by diagnosis uncertain.
Table 1
Suicide risks in selected psychiatric disorders*
| Condition | Relative risk | Incidence (%/year) | Lifetime risk (%) |
|---|---|---|---|
| Prior suicide attempt | 38.4 | 0.549 | 27.5 |
| Bipolar disorder | 21.7 | 0.310 | 15.5 |
| Major depression | 20.4 | 0.292 | 14.6 |
| Mixed drug abuse | 19.2 | 0.275 | 14.7 |
| Dysthymia | 12.1 | 0.173 | 8.65 |
| Obsessive-compulsive disorder | 11.5 | 0.143 | 8.15 |
| Panic disorder | 10.0 | 0.160 | 7.15 |
| Schizophrenia | 8.45 | 0.121 | 6.05 |
| Personality disorders | 7.08 | 0.101 | 5.05 |
| Alcohol abuse | 5.86 | 0.084 | 4.20 |
| Cancer | 1.80 | 0.026 | 1.30 |
| General population | 1.00 | 0.014 | 0.72 |
| * Estimated relative risks compared with the general population,2 with recently updated information about bipolar disorders.6 Annual rates are based on international general population average (14.3/100,000/year) × standardized mortality ratio; lifetime estimates are based on annual rates × 50 years as an estimate of lifetime exposure for years at major risk. | |||
Dangers of stopping lithium. In our study5 of more than 200 patients with DSM-IV bipolar I or II disorder, prophylactic lithium treatment for an average of 4 years reduced the risk of completed and attempted suicide by 6.5-fold. A subgroup of more than 100 patients discontinued lithium, usually after prolonged stability, and we excluded from analysis any cases of suspected emerging illness associated with discontinuation. Within 6 to 12 months after stopping treatment, this subgroup’s rates of suicidal behavior increased markedly—by 20-fold above treated rates.5 Thereafter, their rates returned to prelithium treatment levels.
Of particular clinical importance:
- discontinuing lithium gradually—over at least 2 weeks—was associated with a 2-fold lower suicide risk than more-abrupt discontinuation
- suicidal behavior after lithium discontinuation was almost always associated with emerging depression, which can provide an early warning of impending suicidal risk.
Table 2
Effect of lithium treatment on risk of completed and attempted suicide in patients with bipolar and recurrent depressive disorders*
| Treatment or sample | Suicides | Attempts | All acts | A/S ratio |
|---|---|---|---|---|
| With lithium | 0.16 | 0.41 | 0.57 | 2.6 |
| Without lithium | 0.88 | 4.02 | 4.90 | 4.6 |
| Off/on lithium ratio | 5.5 | 9.8 | 8.6 | — |
| General population | 0.014 | 0.21 | 0.22 | 15.3 |
| Off lithium/general population ratio | 56.4 | 19.1 | 22.3 | — |
| On lithium/general population ratio | 11.4 | 2.0 | 2.6 | — |
| A/S ratio: Attempts versus completed suicides | ||||
| * Rates (acts/year/100 persons, or %/year), based on previously reported averages derived from analyses of data from 33 studies with 55 treatment-arms,12 from a more selected analysis of 22 studies of completed suicides,11 and updated estimates for general population rates.6 | ||||
This is not the first time we have found evidence of a dramatic—but time-limited—increase in risk of recurrent bipolar illness when lithium treatment was discontinued.13 Bipolar disorder patients who discontinue long-term lithium treatment abruptly are at high risk of recurrent depression and mania.13
Incomplete protection. Lithium’s protection against suicidal risk is incomplete, as one can see by comparing lithium-treated versus untreated bipolar patients’ suicide rates with those of the general population (Table 2).6
With lithium:
- suicides plus attempts declined 8.6-fold to levels 2.6 times greater than those of the general population
- suicide attempts fell 10-fold to levels that are about twice that of the general population
- risk of completed suicides declined 5.5-fold with lithium treatment but remained 11 times higher than that of the general population.
Without lithium:
- risk of suicide in bipolar patients is approximately 22 times greater than that of the general population
- ratio of attempts to suicides among bipolar disorder patients averages 4.6, suggesting that suicide attempts by patients with bipolar disorder are relatively lethal.6
Effect of delayed lithium therapy. Many patients with bipolar disorder do not receive sustained prophylactic treatment early in the illness.
Studies typically show an average 5- to 10-year gap between illness onset and the start of sustained lithium maintenance treatment. This delay averages more than 3 years longer among women with bipolar II disorder than men with bipolar I disorder, evidently reflecting major clinical dissimilarities between these groups.6,14 In contrast, we found that nearly one-quarter of long-term risk of suicidal behavior emerges within the first year of bipolar illness.5 Clearly, patients with recurrent major affective illness require earlier intervention and more consistent clinical care.
We have also found that delayed maintenance treatment or the number of prior episodes of bipolar illness do not seem to limit therapeutic response to lithium.14,15 These findings support the conclusion that prophylactic lithium treatment can be worthwhile, even after years of illness and many recurrences. Moreover, our recent meta-analysis of treatment options for rapid-cycling bipolar illness indicates that—even though all treatments have yielded inferior results compared with nonrapidly-cycling patients—no alternative has outperformed lithium.16
Anticonvulsants. Evidence regarding the effects of other mood stabilizers on suicide risk in bipolar disorder remains limited:
- In a European collaborative study, several hundred patients with bipolar or schizoaffective disorder were randomly assigned to receive lithium or carbamazepine for nearly 2 years. Rates of suicidal acts were 2.5%/year with the anticonvulsant, but there were no suicides or attempts in patients receiving lithium.17 Direct comparisons are rare, but this difference was both striking and statistically significant.
- Computerized records of approximately 20,000 patients diagnosed with bipolar disorder at two large American HMOs were analyzed to compare suicidal behaviors associated with specific treatments. Lithium yielded 2.7-fold greater protection against suicidal behavior (mainly attempts because suicides were rare) compared with anticonvulsants (mainly divalproex).18
Treatment recommendation. These observations support lithium’s value in long-term maintenance of patients with bipolar disorder. Lithium’s apparent reduction of suicide risk is striking and may be superior to that of other mood-stabilizers. Alternate treatments and lithium’s potential value for reducing suicide risk in patients with unipolar depression require further study.
It is important to emphasize that lithium can be toxic or even fatal in acute overdose. This risk is integral to the equation when you assess risks and benefits for individual patients.
MAJOR DEPRESSION AND ANTIDEPRESSANTS
Major depression and depressive components of other disorders are major risk factors for suicide.1,2,6 Depression continues to be surprisingly underrecognized and undertreated, even though relatively safe and tolerable antidepressants are readily available.1,6,19,20 Patients with recurrent unipolar major depression often remain inconsistently or inadequately treated, even after they attempt suicide.19
Recent reviews of suicide risk during research on antidepressant treatment in major depression suggest that:
- antidepressants of various kinds may tend to reduce the risk of suicidal behavior, but any such effect is small and statistically nonsignificant (Baldessarini et al, 2003, unpublished)
- tricyclic antidepressants may yield lower rates of suicidal behavior than selective serotonin reuptake inhibitors (SSRIs). Similarly, however, such trends reflect highly variable research methods and inconsistent findings and do not hold up to quantitative analysis (Baldessarini et al, 2003, unpublished).
The suicidal events encountered during research mainly involve attempts because suicides are rare, particularly in relatively brief treatment trials that exclude acutely suicidal subjects. Analyses are further complicated by trends toward paradoxically lower suicidal risks among depressed patients randomized to a placebo in controlled antidepressant trials. This paradox is paralleled by often earlier removal of patients treated with a placebo than with an active antidepressant, perhaps in association with emerging suicidality.21
Table 3
Preventing suicide: How effective are specific treatments?
| Treatments compared | Disorder treated | Benefit/risk ratio |
|---|---|---|
| Mood stabilizers | ||
| Lithium vs. none or placebo* | Bipolar disorder | |
| Suicides | 8.8 (4.1 to 19.1)a | |
| Attempts | 9.9 (5.0 to 14.8)b | |
| Lithium vs. carbamazepine* | Bipolar disorder | ≥2.5c |
| Lithium vs. divalproex* | Bipolar disorder | 2.7 (1.2 to 6.2)d |
| Antidepressants | ||
| Antidepressants (any) vs. placebo/none | Major depressive disorder | 1.1 (0.7 to 1.6)e |
| Tricyclics vs. SSRIs | Major depressive disorder | 1.2 (0.7 to 2.1)e |
| Antipsychotics | ||
| Clozapine vs. any antipsychotic* | Schizophrenia | |
| Suicides + attempts | 3.3 (1.7 to 6.3)f | |
| Attempts | 2.9 (1.5 to 5.7)f | |
| Clozapine vs. olanzapine* | Schizophrenia | |
| Suicides + attempts | 1.3 (1.0 to 1.7)g | |
| a. Tondo et al, 200111 | ||
| b. Baldessarini et al, 20035 | ||
| c. Thies-Flechtner et al, 199517 | ||
| d. Goodwin et al, 200218 | ||
| e. Baldessarini et al, 20035 | ||
| f. Baldessarini & Hennen, 200322 | ||
| g. Meltzer et al, 200324 | ||
| * First agent is statistically more effective, based on benefit/risk ratio (95% CI). | ||
These trends toward lower suicide risk among patients receiving a placebo are somewhat reassuring, given concern that placebo randomization for scientific purposes may endanger study subjects. However, these artifacts confound interpretation of results and make it difficult to measure the effects of antidepressant treatment.
Treatment recommendation. Clinical prudence requires us to treat potentially lethal major depressive illness aggressively, even though one cannot state with confidence that any antidepressant class lowers suicide risk or that one class is significantly more effective than others (Table 3).
SCHIZOPHRENIA AND ANTIPSYCHOTICS
For schizophrenia and other primary psychotic disorders, little research exists to indicate that atypical antipsychotics reduce suicide risk. Evidence is emerging, however, that clozapine may offer this benefit,22 in addition to its well-substantiated clinical superiority in treatment-resistant psychotic illness.23
Pooled evidence from controlled trials comparing clozapine with other antipsychotics indicates a 2-fold lower risk of mortality from all causes.23 This finding was highly suggestive but not statistically significant, and the specific contribution of suicide to this risk is unknown.23 Our recent meta-analysis of the few available studies found that clozapine was associated with a statistically significant, 3.3-fold lower overall suicidal risk compared with other antipsychotic treatments.22
A well-designed, 2-year study randomly assigned 980 patients with schizophrenia or schizoaffective disorder who were at high risk for suicide to clozapine (mean 274 mg/d) or olanzapine (mean 16.6 mg/d). Clozapine showed moderately greater benefit in reducing suicide attempts and need for urgent intervention for perceived emerging suicide risk, although it did not lower suicide risk per se.24 Another study associated olanzapine with a 2.3-fold lower risk of suicidal behavior, compared with haloperidol.25
Comparing two potentially effective agents may have limited the observed difference between clozapine and olanzapine.24 Nevertheless, previous (largely uncontrolled) comparisons with other treatment options indicate substantially lower risks of both suicides and attempts with clozapine.22 In December 2002, the FDA approved a unique indication for clozapine: to reduce the risk of recurrent suicidal behavior in patients with schizophrenia or schizoaffective disorder.
Treatment recommendation. Risks of suicide and other causes of premature death are high in patients with chronic psychotic disorders, underlining the importance of appropriate longterm care. Clozapine has shown benefit in reducing risk of suicidal behaviors. When clozapine is otherwise a plausible option, this additional potential benefit can be considered when selecting therapy for individual patients.
Related resources
- American Psychiatric Association. Suicide-prevention practice guidelines. Washington, DC: American Psychiatric Press, 2003 (in press).
- American Foundation for Suicide Prevention. http://www.afsp.org
- American Association of Suicidology. www.suicidology.org
- National Institute of Mental Health (NIMH)/Suicide.
Drug brand names
- Clozapine • Clozaril
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Haloperidol • Haldol
- Lithium carbonate • Eskalith, Lithobid, others
- Olanzapine • Zyprexa
Disclosure
Dr. Baldessarini has received research grants from Molecular Insight Pharmaceuticals, Eli Lilly and Co., Janssen Pharmaceutica, Protarga Inc., and Solvay Pharmaceuticals, and is a consultant to Auritec Laboratories, Molecular Insight Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, Janssen Pharmaceutica, and Protarga Inc.
Which psychotropics reduce the risk of suicide in patients with psychiatric disorders? Although no drugs eliminate the risk, new evidence is clarifying that some therapeutic choices can make a difference:
- Long-term lithium treatment apparently reduces suicide risk in patients with affective disorders; mood-altering anticonvulsants are less well studied but show less benefit than lithium.
- Effects of antidepressants remain inconclusive without adequate long-term studies.
- At least one atypical antipsychotic—clozapine—probably lowers suicide risk, although direct comparisons of antipsychotic agents are rare.
- Surprisingly little evidence is available on nondrug interventions, including rapid hospitalization, psychotherapy, and electroconvulsive therapy.1
Suicide is the leading cause of malpractice liability in psychiatry and of the heightened risk of death in persons with major affective and psychotic disorders (Box).1-4 Here are the latest findings to help you choose medications for at-risk patients with bipolar disorder, major depression, or chronic psychoses.
Suicide is by far the most common cause of premature death among patients with major mood and psychotic disorders.2,3 A major affective or psychotic disorder increases risk of suicide 8- to 22-fold (Table 1). A history of attempted suicide increases a person’s suicide risk 38-fold, so that the likelihood of dying by suicide becomes greater than one in four (28%).
Attempted suicide is less well-documented but may be 10 to 20 times more common than completed suicide in the general population. Persons with major affective and psychotic disorders complete suicide at an estimated rate of once in five attempts. This high rate suggests that their suicidal intent and methods are particularly lethal.4
BIPOLAR DISORDER AND MOOD STABILIZERS
Bipolar disorder is associated with the highest suicide rate among all major psychiatric illnesses, with an international incidence averaging 0.31% of patients per year.4 This rate may slightly exceed the suicide rate of patients with major depression, which averages 0.29%/year.
Risk of suicidal behavior is similar among patients with bipolar type II (depression with hypomania) and type I disorder (depression with mania), supporting the view that type II is not a milder form of bipolar illness.4-6 Indeed, one study of suicide attempts found a higher risk among bipolar II patients (24%) than in bipolar I patients (17%) as well as a higher risk in both bipolar types than in persons diagnosed with unipolar major depression (12%).4
Suicidal behavior in bipolar disorder is associated almost entirely with ongoing depression or dysphoria and is especially likely to follow severe and highly recurrent depressive episodes.5,6 Combinations of depressive-dysphoric and irritable, agitated, anxious features in “mixed states” may be particularly dangerous and can be hard to diagnose with confidence. Moreover, DSM-IV criteria for mixed states are far too narrow in requiring symptoms to simultaneously fulfill criteria for both mania and major depression. More broadly defined mixed states are very common. Underdiagnosis risks underestimation of suicidal potential, and misdiagnosis as “agitated depression” encourages potentially dangerous overuse of antidepressants.5,7
Depression or dysphoria is the most prevalent morbidity in patients with bipolar disorder. Major and minor depressive states and mixed-dysphoric phases account for nearly one-third of time in follow-up care, exceeding time in mania or hypomania by more than 4-fold.8 Ironically, however, bipolar depression is one of the least-studied forms of major depression. Suicidal bipolar patients are typically excluded from antidepressant studies because of the risks of inducing greater instability, agitation, or mania while treating them with an antidepressant but without a mood stabilizer.7
LITHIUM’S PROTECTIVE EFFECT
Decades of research and clinical use demonstrate substantially lower risks of suicide and serious suicide attempts when patients with bipolar disorder are treated long-term with lithium salts in standard clinical doses (serum concentrations typically 0.6 to 0.8 mEq/L). Lithium is highly effective in treating all phases of bipolar disorder. A recent meta-analysis of 26 long-term trials of lithium reported between 1967 and 2001 found an average 3.2-fold sparing of morbidity or relapse risk.9
Benefits in types I and II. A large European sample10 compared percent-time-ill in bipolar patients before and after they received lithium as maintenance treatment. Unexpectedly, lithium therapy reduced percent-time-ill to a greater extent among patients with type II than type I bipolar disorder. Time in mania and time in depression were reduced 2.5-fold and 2.0-fold, respectively, in type I patients, compared with nearly 5-fold for time in hypomania and 2.5-fold for time in depression among type II patients.
Because depression is associated with the highest rates of suicidal behavior in all phases of bipolar disorders, lithium’s effects in preventing depressive recurrence are especially important for reducing suicide risk.6
In a review of 22 studies11 —some including patients with bipolar or recurrent unipolar major depression—risk of death by suicide was reduced at least 5-fold, based on an informal comparison of pooled rates in treated versus untreated samples. Based on quantitative meta-analysis, the pooled risk of death by suicide was reduced nearly 9-fold (or by 89%) in patients who received lithium maintenance treatment compared with those who did not. The risk for suicide attempts fell nearly 10-fold in a compilation of 33 studies (Table 2).12 Available studies do not permit separate analysis of lithium’s effects on suicidal behavior among patients with bipolar disorder and recurrent unipolar depression, leaving the relative benefit by diagnosis uncertain.
Table 1
Suicide risks in selected psychiatric disorders*
| Condition | Relative risk | Incidence (%/year) | Lifetime risk (%) |
|---|---|---|---|
| Prior suicide attempt | 38.4 | 0.549 | 27.5 |
| Bipolar disorder | 21.7 | 0.310 | 15.5 |
| Major depression | 20.4 | 0.292 | 14.6 |
| Mixed drug abuse | 19.2 | 0.275 | 14.7 |
| Dysthymia | 12.1 | 0.173 | 8.65 |
| Obsessive-compulsive disorder | 11.5 | 0.143 | 8.15 |
| Panic disorder | 10.0 | 0.160 | 7.15 |
| Schizophrenia | 8.45 | 0.121 | 6.05 |
| Personality disorders | 7.08 | 0.101 | 5.05 |
| Alcohol abuse | 5.86 | 0.084 | 4.20 |
| Cancer | 1.80 | 0.026 | 1.30 |
| General population | 1.00 | 0.014 | 0.72 |
| * Estimated relative risks compared with the general population,2 with recently updated information about bipolar disorders.6 Annual rates are based on international general population average (14.3/100,000/year) × standardized mortality ratio; lifetime estimates are based on annual rates × 50 years as an estimate of lifetime exposure for years at major risk. | |||
Dangers of stopping lithium. In our study5 of more than 200 patients with DSM-IV bipolar I or II disorder, prophylactic lithium treatment for an average of 4 years reduced the risk of completed and attempted suicide by 6.5-fold. A subgroup of more than 100 patients discontinued lithium, usually after prolonged stability, and we excluded from analysis any cases of suspected emerging illness associated with discontinuation. Within 6 to 12 months after stopping treatment, this subgroup’s rates of suicidal behavior increased markedly—by 20-fold above treated rates.5 Thereafter, their rates returned to prelithium treatment levels.
Of particular clinical importance:
- discontinuing lithium gradually—over at least 2 weeks—was associated with a 2-fold lower suicide risk than more-abrupt discontinuation
- suicidal behavior after lithium discontinuation was almost always associated with emerging depression, which can provide an early warning of impending suicidal risk.
Table 2
Effect of lithium treatment on risk of completed and attempted suicide in patients with bipolar and recurrent depressive disorders*
| Treatment or sample | Suicides | Attempts | All acts | A/S ratio |
|---|---|---|---|---|
| With lithium | 0.16 | 0.41 | 0.57 | 2.6 |
| Without lithium | 0.88 | 4.02 | 4.90 | 4.6 |
| Off/on lithium ratio | 5.5 | 9.8 | 8.6 | — |
| General population | 0.014 | 0.21 | 0.22 | 15.3 |
| Off lithium/general population ratio | 56.4 | 19.1 | 22.3 | — |
| On lithium/general population ratio | 11.4 | 2.0 | 2.6 | — |
| A/S ratio: Attempts versus completed suicides | ||||
| * Rates (acts/year/100 persons, or %/year), based on previously reported averages derived from analyses of data from 33 studies with 55 treatment-arms,12 from a more selected analysis of 22 studies of completed suicides,11 and updated estimates for general population rates.6 | ||||
This is not the first time we have found evidence of a dramatic—but time-limited—increase in risk of recurrent bipolar illness when lithium treatment was discontinued.13 Bipolar disorder patients who discontinue long-term lithium treatment abruptly are at high risk of recurrent depression and mania.13
Incomplete protection. Lithium’s protection against suicidal risk is incomplete, as one can see by comparing lithium-treated versus untreated bipolar patients’ suicide rates with those of the general population (Table 2).6
With lithium:
- suicides plus attempts declined 8.6-fold to levels 2.6 times greater than those of the general population
- suicide attempts fell 10-fold to levels that are about twice that of the general population
- risk of completed suicides declined 5.5-fold with lithium treatment but remained 11 times higher than that of the general population.
Without lithium:
- risk of suicide in bipolar patients is approximately 22 times greater than that of the general population
- ratio of attempts to suicides among bipolar disorder patients averages 4.6, suggesting that suicide attempts by patients with bipolar disorder are relatively lethal.6
Effect of delayed lithium therapy. Many patients with bipolar disorder do not receive sustained prophylactic treatment early in the illness.
Studies typically show an average 5- to 10-year gap between illness onset and the start of sustained lithium maintenance treatment. This delay averages more than 3 years longer among women with bipolar II disorder than men with bipolar I disorder, evidently reflecting major clinical dissimilarities between these groups.6,14 In contrast, we found that nearly one-quarter of long-term risk of suicidal behavior emerges within the first year of bipolar illness.5 Clearly, patients with recurrent major affective illness require earlier intervention and more consistent clinical care.
We have also found that delayed maintenance treatment or the number of prior episodes of bipolar illness do not seem to limit therapeutic response to lithium.14,15 These findings support the conclusion that prophylactic lithium treatment can be worthwhile, even after years of illness and many recurrences. Moreover, our recent meta-analysis of treatment options for rapid-cycling bipolar illness indicates that—even though all treatments have yielded inferior results compared with nonrapidly-cycling patients—no alternative has outperformed lithium.16
Anticonvulsants. Evidence regarding the effects of other mood stabilizers on suicide risk in bipolar disorder remains limited:
- In a European collaborative study, several hundred patients with bipolar or schizoaffective disorder were randomly assigned to receive lithium or carbamazepine for nearly 2 years. Rates of suicidal acts were 2.5%/year with the anticonvulsant, but there were no suicides or attempts in patients receiving lithium.17 Direct comparisons are rare, but this difference was both striking and statistically significant.
- Computerized records of approximately 20,000 patients diagnosed with bipolar disorder at two large American HMOs were analyzed to compare suicidal behaviors associated with specific treatments. Lithium yielded 2.7-fold greater protection against suicidal behavior (mainly attempts because suicides were rare) compared with anticonvulsants (mainly divalproex).18
Treatment recommendation. These observations support lithium’s value in long-term maintenance of patients with bipolar disorder. Lithium’s apparent reduction of suicide risk is striking and may be superior to that of other mood-stabilizers. Alternate treatments and lithium’s potential value for reducing suicide risk in patients with unipolar depression require further study.
It is important to emphasize that lithium can be toxic or even fatal in acute overdose. This risk is integral to the equation when you assess risks and benefits for individual patients.
MAJOR DEPRESSION AND ANTIDEPRESSANTS
Major depression and depressive components of other disorders are major risk factors for suicide.1,2,6 Depression continues to be surprisingly underrecognized and undertreated, even though relatively safe and tolerable antidepressants are readily available.1,6,19,20 Patients with recurrent unipolar major depression often remain inconsistently or inadequately treated, even after they attempt suicide.19
Recent reviews of suicide risk during research on antidepressant treatment in major depression suggest that:
- antidepressants of various kinds may tend to reduce the risk of suicidal behavior, but any such effect is small and statistically nonsignificant (Baldessarini et al, 2003, unpublished)
- tricyclic antidepressants may yield lower rates of suicidal behavior than selective serotonin reuptake inhibitors (SSRIs). Similarly, however, such trends reflect highly variable research methods and inconsistent findings and do not hold up to quantitative analysis (Baldessarini et al, 2003, unpublished).
The suicidal events encountered during research mainly involve attempts because suicides are rare, particularly in relatively brief treatment trials that exclude acutely suicidal subjects. Analyses are further complicated by trends toward paradoxically lower suicidal risks among depressed patients randomized to a placebo in controlled antidepressant trials. This paradox is paralleled by often earlier removal of patients treated with a placebo than with an active antidepressant, perhaps in association with emerging suicidality.21
Table 3
Preventing suicide: How effective are specific treatments?
| Treatments compared | Disorder treated | Benefit/risk ratio |
|---|---|---|
| Mood stabilizers | ||
| Lithium vs. none or placebo* | Bipolar disorder | |
| Suicides | 8.8 (4.1 to 19.1)a | |
| Attempts | 9.9 (5.0 to 14.8)b | |
| Lithium vs. carbamazepine* | Bipolar disorder | ≥2.5c |
| Lithium vs. divalproex* | Bipolar disorder | 2.7 (1.2 to 6.2)d |
| Antidepressants | ||
| Antidepressants (any) vs. placebo/none | Major depressive disorder | 1.1 (0.7 to 1.6)e |
| Tricyclics vs. SSRIs | Major depressive disorder | 1.2 (0.7 to 2.1)e |
| Antipsychotics | ||
| Clozapine vs. any antipsychotic* | Schizophrenia | |
| Suicides + attempts | 3.3 (1.7 to 6.3)f | |
| Attempts | 2.9 (1.5 to 5.7)f | |
| Clozapine vs. olanzapine* | Schizophrenia | |
| Suicides + attempts | 1.3 (1.0 to 1.7)g | |
| a. Tondo et al, 200111 | ||
| b. Baldessarini et al, 20035 | ||
| c. Thies-Flechtner et al, 199517 | ||
| d. Goodwin et al, 200218 | ||
| e. Baldessarini et al, 20035 | ||
| f. Baldessarini & Hennen, 200322 | ||
| g. Meltzer et al, 200324 | ||
| * First agent is statistically more effective, based on benefit/risk ratio (95% CI). | ||
These trends toward lower suicide risk among patients receiving a placebo are somewhat reassuring, given concern that placebo randomization for scientific purposes may endanger study subjects. However, these artifacts confound interpretation of results and make it difficult to measure the effects of antidepressant treatment.
Treatment recommendation. Clinical prudence requires us to treat potentially lethal major depressive illness aggressively, even though one cannot state with confidence that any antidepressant class lowers suicide risk or that one class is significantly more effective than others (Table 3).
SCHIZOPHRENIA AND ANTIPSYCHOTICS
For schizophrenia and other primary psychotic disorders, little research exists to indicate that atypical antipsychotics reduce suicide risk. Evidence is emerging, however, that clozapine may offer this benefit,22 in addition to its well-substantiated clinical superiority in treatment-resistant psychotic illness.23
Pooled evidence from controlled trials comparing clozapine with other antipsychotics indicates a 2-fold lower risk of mortality from all causes.23 This finding was highly suggestive but not statistically significant, and the specific contribution of suicide to this risk is unknown.23 Our recent meta-analysis of the few available studies found that clozapine was associated with a statistically significant, 3.3-fold lower overall suicidal risk compared with other antipsychotic treatments.22
A well-designed, 2-year study randomly assigned 980 patients with schizophrenia or schizoaffective disorder who were at high risk for suicide to clozapine (mean 274 mg/d) or olanzapine (mean 16.6 mg/d). Clozapine showed moderately greater benefit in reducing suicide attempts and need for urgent intervention for perceived emerging suicide risk, although it did not lower suicide risk per se.24 Another study associated olanzapine with a 2.3-fold lower risk of suicidal behavior, compared with haloperidol.25
Comparing two potentially effective agents may have limited the observed difference between clozapine and olanzapine.24 Nevertheless, previous (largely uncontrolled) comparisons with other treatment options indicate substantially lower risks of both suicides and attempts with clozapine.22 In December 2002, the FDA approved a unique indication for clozapine: to reduce the risk of recurrent suicidal behavior in patients with schizophrenia or schizoaffective disorder.
Treatment recommendation. Risks of suicide and other causes of premature death are high in patients with chronic psychotic disorders, underlining the importance of appropriate longterm care. Clozapine has shown benefit in reducing risk of suicidal behaviors. When clozapine is otherwise a plausible option, this additional potential benefit can be considered when selecting therapy for individual patients.
Related resources
- American Psychiatric Association. Suicide-prevention practice guidelines. Washington, DC: American Psychiatric Press, 2003 (in press).
- American Foundation for Suicide Prevention. http://www.afsp.org
- American Association of Suicidology. www.suicidology.org
- National Institute of Mental Health (NIMH)/Suicide.
Drug brand names
- Clozapine • Clozaril
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Haloperidol • Haldol
- Lithium carbonate • Eskalith, Lithobid, others
- Olanzapine • Zyprexa
Disclosure
Dr. Baldessarini has received research grants from Molecular Insight Pharmaceuticals, Eli Lilly and Co., Janssen Pharmaceutica, Protarga Inc., and Solvay Pharmaceuticals, and is a consultant to Auritec Laboratories, Molecular Insight Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, Janssen Pharmaceutica, and Protarga Inc.
1. Goldsmith SK, Pellmar TC, Kleinman AM. Bunney WE, Jr (eds). Reducing suicide: A national imperative. Washington DC: National Academies Press, 2002.
2. Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J Psychiatry 1997;170:205-28.
3. Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord 2002;68:167-81.
4. Rihmer Z, Pestality P. Bipolar II disorder and suicidal behavior. Psychiatr Clin North Am 1999;22:667-73.
5. Baldessarini RJ, Tondo L, Hennen J. Lithium treatment and suicide risk in major affective disorders: update and new findings. J Clin Psychiatry 2003;64(suppl 5):44-52.
6. Tondo L, Isacsson G, Baldessarini RJ. Suicide in bipolar disorder: risk and prevention. CNS Drugs 2003;17:491-511.
7. Ghaemi SN, Lenox MS, Baldessarini RJ. Effectiveness and safety of long-term antidepressant treatment in bipolar disorder. J Clin Psychiatry 2001;62:565-9.
8. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry 2002;59:530-7.
9. Baldessarini RJ, Tondo L, Hennen J, Viguera AC. Is lithium still worth using? An update of selected recent research. Harvard Rev Psychiatry 2002;10:59-75.
10. Tondo L, Baldessarini RJ, Floris G. Long-term clinical effectiveness of lithium maintenance treatment in types I and II bipolar disorders. Br J Psychiatry 2001;178(suppl 41):S184-90.
11. Tondo L, Hennen J, Baldessarini RJ. Lower suicide risk with longterm lithium treatment in major affective illness: a meta-analysis. Acta Psychiatr Scand 2001;104:163-72.
12. Baldessarini RJ, Tondo L, Hennen J. Treating the suicidal patient with bipolar disorder: reducing suicide risk with lithium. Ann NY Acad Sci 2001;932:24-43.
13. Baldessarini RJ, Tondo L, Viguera AC. Discontinuing lithium maintenance treatment in bipolar disorder: risks and implications. Bipolar Disord 1999;1:17-24.
14. Baldessarini RJ, Tondo L, Hennen J. Treatment latency and previous episodes: relationships to pretreatment morbidity and response to maintenance treatment in bipolar I and II disorders. Bipolar Disord 2003;5:169-79.
15. Bratti IM, Baldessarini RJ, Baethge C, Tondo L. Pretreatment episode count and response to lithium treatment in manic-depressive illness. Harvard Rev Psychiatry (in press).
16. Tondo L, Hennen J, Baldessarini RJ. Rapid-cycling bipolar disorder: effects of long-term treatments. Acta Psychiatr Scand 2003;108:4-14.
17. Thies-Flechtner K, Miller-Oerlinghausen B, Seibert W, et al. Effect of prophylactic treatment on suicide risk in patients with major affective disorders: data from a randomized prospective trial. Pharmacopsychiatry 1996;29:103-7.
18. Goodwin FK, Fireman B, Simon G, et al. Suicide attempts in bipolar patients on lithium vs. divalproex (abstract 45; cited with permission of Dr. Goodwin). San Juan, PR: American College of Neuropsychopharmacology annual meeting, 2002.
19. Suominen KH, Isometsa ET, Henriksson MM, et al. Inadequate treatment for major depression both before and after attempted suicide. Am J Psychiatry 1998;155:1778-880.
20. Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA 2003;289:3095-105.
21. Khan A, Khan S, Kolts R, Brown WA. Suicide rates in clinical trials of SSRIs, other antidepressants, and placebo: analysis of FDA reports. Am J Psychiatry 2003;160:790-2.
22. Baldessarini RJ, Hennen J. Reduced suicidal risk during treatment with clozapine: A meta-analysis. Manuscript in review, 2003.
23. Wahlbeck K, Cheine M, Essali A, Adams C. Evidence of clozapine’s effectiveness in schizophrenia: a systematic review and meta-analysis of randomized trials. Am J Psychiatry 1999;156:990-9.
24. Meltzer HY, Alphs L, Green AI, et al. Clozapine treatment for suicidality in schizophrenia: International Suicide Prevention Trial (InterSePT). Arch Gen Psychiatry 2003;60:82-91.
25. Glazer WM. Formulary decisions and health economics. J Clin Psychiatry 1998;59(suppl 19):23-9.
1. Goldsmith SK, Pellmar TC, Kleinman AM. Bunney WE, Jr (eds). Reducing suicide: A national imperative. Washington DC: National Academies Press, 2002.
2. Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J Psychiatry 1997;170:205-28.
3. Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord 2002;68:167-81.
4. Rihmer Z, Pestality P. Bipolar II disorder and suicidal behavior. Psychiatr Clin North Am 1999;22:667-73.
5. Baldessarini RJ, Tondo L, Hennen J. Lithium treatment and suicide risk in major affective disorders: update and new findings. J Clin Psychiatry 2003;64(suppl 5):44-52.
6. Tondo L, Isacsson G, Baldessarini RJ. Suicide in bipolar disorder: risk and prevention. CNS Drugs 2003;17:491-511.
7. Ghaemi SN, Lenox MS, Baldessarini RJ. Effectiveness and safety of long-term antidepressant treatment in bipolar disorder. J Clin Psychiatry 2001;62:565-9.
8. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry 2002;59:530-7.
9. Baldessarini RJ, Tondo L, Hennen J, Viguera AC. Is lithium still worth using? An update of selected recent research. Harvard Rev Psychiatry 2002;10:59-75.
10. Tondo L, Baldessarini RJ, Floris G. Long-term clinical effectiveness of lithium maintenance treatment in types I and II bipolar disorders. Br J Psychiatry 2001;178(suppl 41):S184-90.
11. Tondo L, Hennen J, Baldessarini RJ. Lower suicide risk with longterm lithium treatment in major affective illness: a meta-analysis. Acta Psychiatr Scand 2001;104:163-72.
12. Baldessarini RJ, Tondo L, Hennen J. Treating the suicidal patient with bipolar disorder: reducing suicide risk with lithium. Ann NY Acad Sci 2001;932:24-43.
13. Baldessarini RJ, Tondo L, Viguera AC. Discontinuing lithium maintenance treatment in bipolar disorder: risks and implications. Bipolar Disord 1999;1:17-24.
14. Baldessarini RJ, Tondo L, Hennen J. Treatment latency and previous episodes: relationships to pretreatment morbidity and response to maintenance treatment in bipolar I and II disorders. Bipolar Disord 2003;5:169-79.
15. Bratti IM, Baldessarini RJ, Baethge C, Tondo L. Pretreatment episode count and response to lithium treatment in manic-depressive illness. Harvard Rev Psychiatry (in press).
16. Tondo L, Hennen J, Baldessarini RJ. Rapid-cycling bipolar disorder: effects of long-term treatments. Acta Psychiatr Scand 2003;108:4-14.
17. Thies-Flechtner K, Miller-Oerlinghausen B, Seibert W, et al. Effect of prophylactic treatment on suicide risk in patients with major affective disorders: data from a randomized prospective trial. Pharmacopsychiatry 1996;29:103-7.
18. Goodwin FK, Fireman B, Simon G, et al. Suicide attempts in bipolar patients on lithium vs. divalproex (abstract 45; cited with permission of Dr. Goodwin). San Juan, PR: American College of Neuropsychopharmacology annual meeting, 2002.
19. Suominen KH, Isometsa ET, Henriksson MM, et al. Inadequate treatment for major depression both before and after attempted suicide. Am J Psychiatry 1998;155:1778-880.
20. Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA 2003;289:3095-105.
21. Khan A, Khan S, Kolts R, Brown WA. Suicide rates in clinical trials of SSRIs, other antidepressants, and placebo: analysis of FDA reports. Am J Psychiatry 2003;160:790-2.
22. Baldessarini RJ, Hennen J. Reduced suicidal risk during treatment with clozapine: A meta-analysis. Manuscript in review, 2003.
23. Wahlbeck K, Cheine M, Essali A, Adams C. Evidence of clozapine’s effectiveness in schizophrenia: a systematic review and meta-analysis of randomized trials. Am J Psychiatry 1999;156:990-9.
24. Meltzer HY, Alphs L, Green AI, et al. Clozapine treatment for suicidality in schizophrenia: International Suicide Prevention Trial (InterSePT). Arch Gen Psychiatry 2003;60:82-91.
25. Glazer WM. Formulary decisions and health economics. J Clin Psychiatry 1998;59(suppl 19):23-9.
5 keys to improve counseling for dual-diagnosis patients
Psychiatrists frequently encounter dual-diagnosis patients (Box) and may often wonder which to treat first—the substance abuse or the psychiatric comorbidity. Five principles can help you counsel dual-diagnosis patients more effectively. Briefly, they are to:
- appreciate this population’s heterogeneity
- adopt a longitudinal treatment approach, reassessing patients’ progress and adjusting interventions as needed over time
- be empathic rather than confrontational
- realize that treatment often proceeds in stages—not on a smooth, linear path
- recognize the importance of medication compliance.
ASSESSMENT
Different patients, different problems. All counseling of dual-diagnosis patients begins with a thorough assessment aimed at making an accurate diagnosis and understanding the relationship between the co-existing disorders. Although some people refer to “dual-diagnosis patients” as a single entity, these patients differ according to:
The National Institute of Mental Health’s Epidemiologic Catchment Area study documented high rates of substance use disorders in patients with psychiatric disorders.1 Lifetime prevalence of co-occurrence was 61% for bipolar disorder (the highest of any Axis I disorder),47% for schizophrenia, and 36% for panic disorder.
Dual-diagnosis patients face a more bleak prognosis than those with a single disorder, including higher rates of relapse, hospitalization, violence, incarceration, homelessness, and serious infections such as hepatitis and HIV.2 Unfortunately, these findings have not always led to effective treatments.
These patients represent a heterogeneous group and require individualized treatment. For example, abstinence from alcohol or drugs may worsen psychiatric symptoms in a patient with posttraumatic stress disorder and substance abuse. On the other hand, abstinence would be expected to improve the symptoms of a patient with comorbid major depressive disorder and substance abuse.
- diagnosis, with a myriad of potential combinations of substance use and psychiatric disorders
- severity of disorder, with some having a predominant psychiatric or substance use problem and others experiencing severe courses of both problems
- causes of their substance abuse and psychiatric disorders, based in part on which problem is primary and which is secondary
- level of motivation for treatment and their treatment goals.
Primary versus secondary disorders. How to distinguish “primary” from “secondary” disorders in dually diagnosed patients has prompted much research and debate.
A psychiatric disorder is typically called primary when it can be viewed as independent from the substance use disorder. The term “secondary psychiatric disorder” connotes that the substance use disorder is causing the psychiatric symptoms. For example, alcohol-dependent patients in detoxification programs often have depressive symptoms, some of which abate with abstinence. They are frequently diagnosed as having “secondary depression,” or—in DSM-IV diagnostic terms—substance-induced mood disorder.
Unfortunately, distinguishing primary from secondary disorders is sometimes difficult because of patients’ poor memory, recall bias, and inadequate periods of sobriety (“I’ve been drinking for a long time and have been depressed for a long time, so I don’t remember what I was like when I was sober”). Thus, the diagnostic assessment is generally accomplished over time, rather than in a single interview.
Our research3 and clinical experience have taught us that patients’ recall about the relationship between their substance use and psychiatric symptoms often changes over time. Determining the “primary” disorder may also have limited validity in predicting treatment response.4
Stages of Change model. The Stages of Change model5,6 is useful for assessing a dually diagnosed patient’s motivation to change, although its use in addictive disorders has been challenged.7,8 According to the transtheoretical model developed by Prochaska et al (Table 1),5 people generally make behavioral changes in stages defined by their level of willingness to make these changes.
When counseling the dually diagnosed patient, it is useful to assess readiness to change and to suggest behavioral steps the patient is able and willing to make. Thus, it would not be appropriate to discuss drug refusal methods with a patient who does not see his substance use as a problem. Rather, addressing this patient’s ambivalence would be more useful.
Table 1
5 stages of change: The transtheoretical model of behavior change
| Stage of change | Patient behavior |
|---|---|
| Precontemplation | No intention to change behavior in the foreseeable future; little or no awareness of problems |
| Contemplation | Aware that a problem exists; seriously thinking about overcoming it but no commitment to take action |
| Preparation | Intends to take action within the next month; has tried unsuccessfully to take action in the past year |
| Action | Modifies behavior, experiences, or environment to overcome problems |
| Maintenance | Works to prevent relapse and consolidate gains attained during action stage; for addictive behaviors, maintenance extends indefinitely from 6 months after the initial action |
| Source: Prochaska JO. Transtheoretical model: Stages of Change. Cancer Prevention Research Center, University of Rhode Island. http://www.uri.edu/research/cprc/TTM/StagesOfChange.htm | |
It is important to note that many patients move back and forth between stages of readiness to change. For example, a patient in the action stage (entering treatment and pursuing a goal of abstinence) may revert to contemplation and again question whether he or she has a serious substance abuse problem. We recommend that clinicians reassess patients regularly and continue to match interventions with the current level of motivation.
WHICH DISORDER IS TREATED FIRST?
Three approaches are used for treating the coexisting problems of dual-diagnosis patients—sequential, parallel, and integrated.
Sequential treatment addresses the more acute disorder first; the other disorder receives greater attention later. This model is commonly used with hospital treatment, in which comparatively little attention would be paid to substance use in a patient who is acutely psychotic.
Parallel treatment addresses each disorder contemporaneously but in different settings (such as at a substance abuse program on Monday and a mental health center on Thursday).
One limitation of the sequential and parallel models is that psychiatric and substance abuse programs typically have different orientations. A lack of comprehensive assessment may leave the substance abuse or psychiatric disorder underdiagnosed, depending on the setting. Staff members may also project negative attitudes toward patients with psychiatric or substance use disorders if they know comparatively little about the diagnosis and treatment of the other type of disorder. Treatment in two settings also can lead to communication problems and differences of opinion among the treating clinicians.
Integrated treatment, in which both disorders are treated simultaneously in the same setting, has shown favorable outcomes in several initial studies.9 11 Different integrated treatment models have been described, which vary according to the psychiatric disorders’ nature and the treatment’s theoretical orientation. Integrated treatment strategies include:
- focusing on psychiatric and substance abuse issues simultaneously or in alternating sessions
- providing intense case management
- stressing the importance of medication compliance.12
COUNSELING PRINCIPLES
As mentioned, a careful history and thorough assessment are the keys to effectively treating the dually diagnosed patient.
Assess how the patient perceives the relationship between his substance use disorder and psychiatric symptoms. For example, ask, “What do you see as the relationship between your drinking and your depression, if any?”
As part of this process, explore both the immediate and long-term relationships between the two phenomena. For example, some patients will say that drinking offers them immediate relief from their depressive symptoms but exacerbates their depression the following day. Encouraging patients to look beyond the immediate—often positive—effects of their substance use may help them understand the negative consequences of continued use.
Review previous periods of recovery and relapse. For patients who have had substantial periods of recovery, it is important to acknowledge these successes and to ask in an upbeat and admiring way, “How did you do it?” This approach may remind patients of past successes and counterbalance their frequent feelings of discouragement and hopelessness.
Table 2
4 phases in treating the dually diagnosed patient
| Phase | Therapeutic goals |
|---|---|
| Engagement | Build an alliance Attract patient to treatment program |
| Persuasion | Convince engaged patient to accept longer-term, abstinence-based treatment |
| Active treatment | Help patient develop attitudes and techniques essential to maintain sobriety |
| Relapse prevention | Help patient maintain gains made in active treatment and cope with lapses/relapses should they occur |
To help clarify the relationship between coexisting disorders, ask patients about psychiatric symptoms they have experienced during periods of substance use and recovery. Taking a relapse history can help you and the patient identify decisions and behaviors he or she must avoid (such as stopping medication, failing to attend treatment, or engaging in high-risk activities as in going to bars).
PHASES OF TREATMENT
Four phases of dual-diagnosis treatment—engagement, persuasion, active treatment, and relapse prevention—have been described, along with their therapeutic goals (Table 2).13 Consider these phases when treating this population, even though most patients do not proceed through them in an orderly, linear fashion.
Engagement. At the onset, the therapist tries to build an alliance and begins to establish trust and credibility.
Persuasion involves helping the patient comprehend the need to seriously address his or her substance use. It is important during engagement and persuasion stages to be empathic, using reflective listening and validating techniques.
Helping the patient see the discrepancy between his or her long-term goals and current behavior can create the impetus for change. Linking the substance use and psychiatric symptoms and exploring their impact on each other may help the patient understand the problem.
Ambivalence and resistance are normal reactions to this process of change, so avoid arguing with the patient. Confrontation—long a common strategy in substance abuse treatment—is losing favor and is being supplanted in many cases by a more supportive, empathic approach.14 Indeed, patients with co-occurring psychiatric illness generally respond particularly poorly to confrontation.
Active treatment focuses on techniques to achieve abstinence, including alcohol and drug refusal skills, methods to deal with craving, and ways to recognize and avoid situations that present a high risk for relapse.
Relapse prevention reinforces gains made in previous stages. Here, the patient learns how to identify and deal with risky situations and how to handle a “slip” if it occurs.
ADJUNCTIVE TREATMENTS
Self-help groups. Ask whether the patient has attended self-help groups for addiction or psychiatric illness. If so, then ask, “What did you think of the meetings? What did you like and dislike?”
Self-help groups such as Alcoholics Anonymous (AA) or the Manic-Depressive and Depressive Association (MDDA) can help enormously in the recovery process. These groups are free, readily available, and can offer patients a support network. Although many dual-diagnosis patients are reluctant to attend self-help groups, they may benefit from the support, role modeling, practical advice, and structure that these meetings offer.
Drug therapy for the dual-diagnosis patient focuses on the psychiatric disorder and is usually combined with psychosocial approaches. There is little evidence that one medication is more effective than others for these patients.
Because medication compliance is key to their effective treatment, be sure to ask patients at each visit, “Have you been taking your medication as prescribed?” Because dual-diagnosis patients have been shown to take more or less medication than prescribed,15 asking how much medication they are taking can be revealing.
Related resources
- American Academy of Addiction Psychiatry www.aaap.org
- National Institute on Drug Abuse www.nida.nih.gov
- National Institute on Alcohol Abuse and Alcoholism www.niaaa.nih.gov
Disclosure
Dr. Manwani receives research support from Abbott Laboratories.
Dr. Weiss is a speaker for Abbott Laboratories and Eli Lilly and Co.
Acknowledgment
Supported by grants K0200326, DA09400, and DA15968 from the National Institute on Drug Abuse and a grant from the Dr. Ralph and Marian C. Falk Medical Research Trust.
1. Reigier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-18.
2. Drake RE, Essock SM, Shaner A, et al. Implementing dual diagnosis services for clients with severe mental illness. Psychiatr Serv 2001;52:469-76.
3. Griffin ML, Weiss RD, Mirin SM, et al. The use of the Diagnostic Interview Schedule in drug-dependent patients. Am. J Drug Alcohol Abuse 1987;13(3):281-91.
4. Mason BJ, Kocsis JH, Ritvo EC, et al. A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified on the presence or absence of major depression. JAMA 1996;275(10):761-7.
5. Prochaska JO, DiClemente CC, Norcross JC. In search of how people change: applications to addictive behaviors. Am Psychol 1992;47:1102-14.
6. Connors GJ, Donovan DM, DiClemente CC. Substance abuse treatment and the stages of change. New York: Guilford Press, 2001.
7. Carey KB, Purnine DM, Maisto SA, et al. Assessing readiness to change substance abuse: a critical review of instruments. Clinical Psychol 1999;6:245-66.
8. Sutton S. Back to the drawing board? A review of applications of the transtheoretical model to substance use. Addiction 2001;96:175-86.
9. Drake RE, McHugo GJ, Noordsy DL. Treatment of alcoholism among schizophrenic outpatients: 4-year outcomes. Am J Psychiatry 1993;150:328-9.
10. Hellerstein DJ, Rosenthal RN, Miner CR. A prospective study of integrated outpatient treatment for substance-abusing schizophrenic patients. Am J Addict 1995;4:33-42.
11. Drake RE, Yovetich NA, Bebout RR, et al. Integrated treatment for dually diagnosed homeless adults. J Nerv Ment Dis 1997;185:298-305.
12. Weiss RD, Najavits LM, Hennessy G. Overview of treatment modalities for dual diagnosis patients: pharmacotherapy, psychotherapy, and twelve-step programs. In: Kranzler HR, Tinsley J (eds). Dual diagnosis: substance abuse and comorbid disorders. (2nd ed). New York: Marcel Dekker. In press.
13. Osher FC, Kofoed LL. Treatment of patients with psychiatric and psychoactive substance abuse disorders. Hosp Community Psychiatry 1989;40(10):1025-30.
14. Miller WR, Rollnick S. Motivational interviewing: preparing for change (2nd ed). New York: Guilford Press, 2002.
15. Weiss RD, Greenfield SF, Najavits LM, et al. Medication compliance among patients with bipolar disorder and substance use disorder. J Clin Psychiatry 1998;59(4):172-4.
Psychiatrists frequently encounter dual-diagnosis patients (Box) and may often wonder which to treat first—the substance abuse or the psychiatric comorbidity. Five principles can help you counsel dual-diagnosis patients more effectively. Briefly, they are to:
- appreciate this population’s heterogeneity
- adopt a longitudinal treatment approach, reassessing patients’ progress and adjusting interventions as needed over time
- be empathic rather than confrontational
- realize that treatment often proceeds in stages—not on a smooth, linear path
- recognize the importance of medication compliance.
ASSESSMENT
Different patients, different problems. All counseling of dual-diagnosis patients begins with a thorough assessment aimed at making an accurate diagnosis and understanding the relationship between the co-existing disorders. Although some people refer to “dual-diagnosis patients” as a single entity, these patients differ according to:
The National Institute of Mental Health’s Epidemiologic Catchment Area study documented high rates of substance use disorders in patients with psychiatric disorders.1 Lifetime prevalence of co-occurrence was 61% for bipolar disorder (the highest of any Axis I disorder),47% for schizophrenia, and 36% for panic disorder.
Dual-diagnosis patients face a more bleak prognosis than those with a single disorder, including higher rates of relapse, hospitalization, violence, incarceration, homelessness, and serious infections such as hepatitis and HIV.2 Unfortunately, these findings have not always led to effective treatments.
These patients represent a heterogeneous group and require individualized treatment. For example, abstinence from alcohol or drugs may worsen psychiatric symptoms in a patient with posttraumatic stress disorder and substance abuse. On the other hand, abstinence would be expected to improve the symptoms of a patient with comorbid major depressive disorder and substance abuse.
- diagnosis, with a myriad of potential combinations of substance use and psychiatric disorders
- severity of disorder, with some having a predominant psychiatric or substance use problem and others experiencing severe courses of both problems
- causes of their substance abuse and psychiatric disorders, based in part on which problem is primary and which is secondary
- level of motivation for treatment and their treatment goals.
Primary versus secondary disorders. How to distinguish “primary” from “secondary” disorders in dually diagnosed patients has prompted much research and debate.
A psychiatric disorder is typically called primary when it can be viewed as independent from the substance use disorder. The term “secondary psychiatric disorder” connotes that the substance use disorder is causing the psychiatric symptoms. For example, alcohol-dependent patients in detoxification programs often have depressive symptoms, some of which abate with abstinence. They are frequently diagnosed as having “secondary depression,” or—in DSM-IV diagnostic terms—substance-induced mood disorder.
Unfortunately, distinguishing primary from secondary disorders is sometimes difficult because of patients’ poor memory, recall bias, and inadequate periods of sobriety (“I’ve been drinking for a long time and have been depressed for a long time, so I don’t remember what I was like when I was sober”). Thus, the diagnostic assessment is generally accomplished over time, rather than in a single interview.
Our research3 and clinical experience have taught us that patients’ recall about the relationship between their substance use and psychiatric symptoms often changes over time. Determining the “primary” disorder may also have limited validity in predicting treatment response.4
Stages of Change model. The Stages of Change model5,6 is useful for assessing a dually diagnosed patient’s motivation to change, although its use in addictive disorders has been challenged.7,8 According to the transtheoretical model developed by Prochaska et al (Table 1),5 people generally make behavioral changes in stages defined by their level of willingness to make these changes.
When counseling the dually diagnosed patient, it is useful to assess readiness to change and to suggest behavioral steps the patient is able and willing to make. Thus, it would not be appropriate to discuss drug refusal methods with a patient who does not see his substance use as a problem. Rather, addressing this patient’s ambivalence would be more useful.
Table 1
5 stages of change: The transtheoretical model of behavior change
| Stage of change | Patient behavior |
|---|---|
| Precontemplation | No intention to change behavior in the foreseeable future; little or no awareness of problems |
| Contemplation | Aware that a problem exists; seriously thinking about overcoming it but no commitment to take action |
| Preparation | Intends to take action within the next month; has tried unsuccessfully to take action in the past year |
| Action | Modifies behavior, experiences, or environment to overcome problems |
| Maintenance | Works to prevent relapse and consolidate gains attained during action stage; for addictive behaviors, maintenance extends indefinitely from 6 months after the initial action |
| Source: Prochaska JO. Transtheoretical model: Stages of Change. Cancer Prevention Research Center, University of Rhode Island. http://www.uri.edu/research/cprc/TTM/StagesOfChange.htm | |
It is important to note that many patients move back and forth between stages of readiness to change. For example, a patient in the action stage (entering treatment and pursuing a goal of abstinence) may revert to contemplation and again question whether he or she has a serious substance abuse problem. We recommend that clinicians reassess patients regularly and continue to match interventions with the current level of motivation.
WHICH DISORDER IS TREATED FIRST?
Three approaches are used for treating the coexisting problems of dual-diagnosis patients—sequential, parallel, and integrated.
Sequential treatment addresses the more acute disorder first; the other disorder receives greater attention later. This model is commonly used with hospital treatment, in which comparatively little attention would be paid to substance use in a patient who is acutely psychotic.
Parallel treatment addresses each disorder contemporaneously but in different settings (such as at a substance abuse program on Monday and a mental health center on Thursday).
One limitation of the sequential and parallel models is that psychiatric and substance abuse programs typically have different orientations. A lack of comprehensive assessment may leave the substance abuse or psychiatric disorder underdiagnosed, depending on the setting. Staff members may also project negative attitudes toward patients with psychiatric or substance use disorders if they know comparatively little about the diagnosis and treatment of the other type of disorder. Treatment in two settings also can lead to communication problems and differences of opinion among the treating clinicians.
Integrated treatment, in which both disorders are treated simultaneously in the same setting, has shown favorable outcomes in several initial studies.9 11 Different integrated treatment models have been described, which vary according to the psychiatric disorders’ nature and the treatment’s theoretical orientation. Integrated treatment strategies include:
- focusing on psychiatric and substance abuse issues simultaneously or in alternating sessions
- providing intense case management
- stressing the importance of medication compliance.12
COUNSELING PRINCIPLES
As mentioned, a careful history and thorough assessment are the keys to effectively treating the dually diagnosed patient.
Assess how the patient perceives the relationship between his substance use disorder and psychiatric symptoms. For example, ask, “What do you see as the relationship between your drinking and your depression, if any?”
As part of this process, explore both the immediate and long-term relationships between the two phenomena. For example, some patients will say that drinking offers them immediate relief from their depressive symptoms but exacerbates their depression the following day. Encouraging patients to look beyond the immediate—often positive—effects of their substance use may help them understand the negative consequences of continued use.
Review previous periods of recovery and relapse. For patients who have had substantial periods of recovery, it is important to acknowledge these successes and to ask in an upbeat and admiring way, “How did you do it?” This approach may remind patients of past successes and counterbalance their frequent feelings of discouragement and hopelessness.
Table 2
4 phases in treating the dually diagnosed patient
| Phase | Therapeutic goals |
|---|---|
| Engagement | Build an alliance Attract patient to treatment program |
| Persuasion | Convince engaged patient to accept longer-term, abstinence-based treatment |
| Active treatment | Help patient develop attitudes and techniques essential to maintain sobriety |
| Relapse prevention | Help patient maintain gains made in active treatment and cope with lapses/relapses should they occur |
To help clarify the relationship between coexisting disorders, ask patients about psychiatric symptoms they have experienced during periods of substance use and recovery. Taking a relapse history can help you and the patient identify decisions and behaviors he or she must avoid (such as stopping medication, failing to attend treatment, or engaging in high-risk activities as in going to bars).
PHASES OF TREATMENT
Four phases of dual-diagnosis treatment—engagement, persuasion, active treatment, and relapse prevention—have been described, along with their therapeutic goals (Table 2).13 Consider these phases when treating this population, even though most patients do not proceed through them in an orderly, linear fashion.
Engagement. At the onset, the therapist tries to build an alliance and begins to establish trust and credibility.
Persuasion involves helping the patient comprehend the need to seriously address his or her substance use. It is important during engagement and persuasion stages to be empathic, using reflective listening and validating techniques.
Helping the patient see the discrepancy between his or her long-term goals and current behavior can create the impetus for change. Linking the substance use and psychiatric symptoms and exploring their impact on each other may help the patient understand the problem.
Ambivalence and resistance are normal reactions to this process of change, so avoid arguing with the patient. Confrontation—long a common strategy in substance abuse treatment—is losing favor and is being supplanted in many cases by a more supportive, empathic approach.14 Indeed, patients with co-occurring psychiatric illness generally respond particularly poorly to confrontation.
Active treatment focuses on techniques to achieve abstinence, including alcohol and drug refusal skills, methods to deal with craving, and ways to recognize and avoid situations that present a high risk for relapse.
Relapse prevention reinforces gains made in previous stages. Here, the patient learns how to identify and deal with risky situations and how to handle a “slip” if it occurs.
ADJUNCTIVE TREATMENTS
Self-help groups. Ask whether the patient has attended self-help groups for addiction or psychiatric illness. If so, then ask, “What did you think of the meetings? What did you like and dislike?”
Self-help groups such as Alcoholics Anonymous (AA) or the Manic-Depressive and Depressive Association (MDDA) can help enormously in the recovery process. These groups are free, readily available, and can offer patients a support network. Although many dual-diagnosis patients are reluctant to attend self-help groups, they may benefit from the support, role modeling, practical advice, and structure that these meetings offer.
Drug therapy for the dual-diagnosis patient focuses on the psychiatric disorder and is usually combined with psychosocial approaches. There is little evidence that one medication is more effective than others for these patients.
Because medication compliance is key to their effective treatment, be sure to ask patients at each visit, “Have you been taking your medication as prescribed?” Because dual-diagnosis patients have been shown to take more or less medication than prescribed,15 asking how much medication they are taking can be revealing.
Related resources
- American Academy of Addiction Psychiatry www.aaap.org
- National Institute on Drug Abuse www.nida.nih.gov
- National Institute on Alcohol Abuse and Alcoholism www.niaaa.nih.gov
Disclosure
Dr. Manwani receives research support from Abbott Laboratories.
Dr. Weiss is a speaker for Abbott Laboratories and Eli Lilly and Co.
Acknowledgment
Supported by grants K0200326, DA09400, and DA15968 from the National Institute on Drug Abuse and a grant from the Dr. Ralph and Marian C. Falk Medical Research Trust.
Psychiatrists frequently encounter dual-diagnosis patients (Box) and may often wonder which to treat first—the substance abuse or the psychiatric comorbidity. Five principles can help you counsel dual-diagnosis patients more effectively. Briefly, they are to:
- appreciate this population’s heterogeneity
- adopt a longitudinal treatment approach, reassessing patients’ progress and adjusting interventions as needed over time
- be empathic rather than confrontational
- realize that treatment often proceeds in stages—not on a smooth, linear path
- recognize the importance of medication compliance.
ASSESSMENT
Different patients, different problems. All counseling of dual-diagnosis patients begins with a thorough assessment aimed at making an accurate diagnosis and understanding the relationship between the co-existing disorders. Although some people refer to “dual-diagnosis patients” as a single entity, these patients differ according to:
The National Institute of Mental Health’s Epidemiologic Catchment Area study documented high rates of substance use disorders in patients with psychiatric disorders.1 Lifetime prevalence of co-occurrence was 61% for bipolar disorder (the highest of any Axis I disorder),47% for schizophrenia, and 36% for panic disorder.
Dual-diagnosis patients face a more bleak prognosis than those with a single disorder, including higher rates of relapse, hospitalization, violence, incarceration, homelessness, and serious infections such as hepatitis and HIV.2 Unfortunately, these findings have not always led to effective treatments.
These patients represent a heterogeneous group and require individualized treatment. For example, abstinence from alcohol or drugs may worsen psychiatric symptoms in a patient with posttraumatic stress disorder and substance abuse. On the other hand, abstinence would be expected to improve the symptoms of a patient with comorbid major depressive disorder and substance abuse.
- diagnosis, with a myriad of potential combinations of substance use and psychiatric disorders
- severity of disorder, with some having a predominant psychiatric or substance use problem and others experiencing severe courses of both problems
- causes of their substance abuse and psychiatric disorders, based in part on which problem is primary and which is secondary
- level of motivation for treatment and their treatment goals.
Primary versus secondary disorders. How to distinguish “primary” from “secondary” disorders in dually diagnosed patients has prompted much research and debate.
A psychiatric disorder is typically called primary when it can be viewed as independent from the substance use disorder. The term “secondary psychiatric disorder” connotes that the substance use disorder is causing the psychiatric symptoms. For example, alcohol-dependent patients in detoxification programs often have depressive symptoms, some of which abate with abstinence. They are frequently diagnosed as having “secondary depression,” or—in DSM-IV diagnostic terms—substance-induced mood disorder.
Unfortunately, distinguishing primary from secondary disorders is sometimes difficult because of patients’ poor memory, recall bias, and inadequate periods of sobriety (“I’ve been drinking for a long time and have been depressed for a long time, so I don’t remember what I was like when I was sober”). Thus, the diagnostic assessment is generally accomplished over time, rather than in a single interview.
Our research3 and clinical experience have taught us that patients’ recall about the relationship between their substance use and psychiatric symptoms often changes over time. Determining the “primary” disorder may also have limited validity in predicting treatment response.4
Stages of Change model. The Stages of Change model5,6 is useful for assessing a dually diagnosed patient’s motivation to change, although its use in addictive disorders has been challenged.7,8 According to the transtheoretical model developed by Prochaska et al (Table 1),5 people generally make behavioral changes in stages defined by their level of willingness to make these changes.
When counseling the dually diagnosed patient, it is useful to assess readiness to change and to suggest behavioral steps the patient is able and willing to make. Thus, it would not be appropriate to discuss drug refusal methods with a patient who does not see his substance use as a problem. Rather, addressing this patient’s ambivalence would be more useful.
Table 1
5 stages of change: The transtheoretical model of behavior change
| Stage of change | Patient behavior |
|---|---|
| Precontemplation | No intention to change behavior in the foreseeable future; little or no awareness of problems |
| Contemplation | Aware that a problem exists; seriously thinking about overcoming it but no commitment to take action |
| Preparation | Intends to take action within the next month; has tried unsuccessfully to take action in the past year |
| Action | Modifies behavior, experiences, or environment to overcome problems |
| Maintenance | Works to prevent relapse and consolidate gains attained during action stage; for addictive behaviors, maintenance extends indefinitely from 6 months after the initial action |
| Source: Prochaska JO. Transtheoretical model: Stages of Change. Cancer Prevention Research Center, University of Rhode Island. http://www.uri.edu/research/cprc/TTM/StagesOfChange.htm | |
It is important to note that many patients move back and forth between stages of readiness to change. For example, a patient in the action stage (entering treatment and pursuing a goal of abstinence) may revert to contemplation and again question whether he or she has a serious substance abuse problem. We recommend that clinicians reassess patients regularly and continue to match interventions with the current level of motivation.
WHICH DISORDER IS TREATED FIRST?
Three approaches are used for treating the coexisting problems of dual-diagnosis patients—sequential, parallel, and integrated.
Sequential treatment addresses the more acute disorder first; the other disorder receives greater attention later. This model is commonly used with hospital treatment, in which comparatively little attention would be paid to substance use in a patient who is acutely psychotic.
Parallel treatment addresses each disorder contemporaneously but in different settings (such as at a substance abuse program on Monday and a mental health center on Thursday).
One limitation of the sequential and parallel models is that psychiatric and substance abuse programs typically have different orientations. A lack of comprehensive assessment may leave the substance abuse or psychiatric disorder underdiagnosed, depending on the setting. Staff members may also project negative attitudes toward patients with psychiatric or substance use disorders if they know comparatively little about the diagnosis and treatment of the other type of disorder. Treatment in two settings also can lead to communication problems and differences of opinion among the treating clinicians.
Integrated treatment, in which both disorders are treated simultaneously in the same setting, has shown favorable outcomes in several initial studies.9 11 Different integrated treatment models have been described, which vary according to the psychiatric disorders’ nature and the treatment’s theoretical orientation. Integrated treatment strategies include:
- focusing on psychiatric and substance abuse issues simultaneously or in alternating sessions
- providing intense case management
- stressing the importance of medication compliance.12
COUNSELING PRINCIPLES
As mentioned, a careful history and thorough assessment are the keys to effectively treating the dually diagnosed patient.
Assess how the patient perceives the relationship between his substance use disorder and psychiatric symptoms. For example, ask, “What do you see as the relationship between your drinking and your depression, if any?”
As part of this process, explore both the immediate and long-term relationships between the two phenomena. For example, some patients will say that drinking offers them immediate relief from their depressive symptoms but exacerbates their depression the following day. Encouraging patients to look beyond the immediate—often positive—effects of their substance use may help them understand the negative consequences of continued use.
Review previous periods of recovery and relapse. For patients who have had substantial periods of recovery, it is important to acknowledge these successes and to ask in an upbeat and admiring way, “How did you do it?” This approach may remind patients of past successes and counterbalance their frequent feelings of discouragement and hopelessness.
Table 2
4 phases in treating the dually diagnosed patient
| Phase | Therapeutic goals |
|---|---|
| Engagement | Build an alliance Attract patient to treatment program |
| Persuasion | Convince engaged patient to accept longer-term, abstinence-based treatment |
| Active treatment | Help patient develop attitudes and techniques essential to maintain sobriety |
| Relapse prevention | Help patient maintain gains made in active treatment and cope with lapses/relapses should they occur |
To help clarify the relationship between coexisting disorders, ask patients about psychiatric symptoms they have experienced during periods of substance use and recovery. Taking a relapse history can help you and the patient identify decisions and behaviors he or she must avoid (such as stopping medication, failing to attend treatment, or engaging in high-risk activities as in going to bars).
PHASES OF TREATMENT
Four phases of dual-diagnosis treatment—engagement, persuasion, active treatment, and relapse prevention—have been described, along with their therapeutic goals (Table 2).13 Consider these phases when treating this population, even though most patients do not proceed through them in an orderly, linear fashion.
Engagement. At the onset, the therapist tries to build an alliance and begins to establish trust and credibility.
Persuasion involves helping the patient comprehend the need to seriously address his or her substance use. It is important during engagement and persuasion stages to be empathic, using reflective listening and validating techniques.
Helping the patient see the discrepancy between his or her long-term goals and current behavior can create the impetus for change. Linking the substance use and psychiatric symptoms and exploring their impact on each other may help the patient understand the problem.
Ambivalence and resistance are normal reactions to this process of change, so avoid arguing with the patient. Confrontation—long a common strategy in substance abuse treatment—is losing favor and is being supplanted in many cases by a more supportive, empathic approach.14 Indeed, patients with co-occurring psychiatric illness generally respond particularly poorly to confrontation.
Active treatment focuses on techniques to achieve abstinence, including alcohol and drug refusal skills, methods to deal with craving, and ways to recognize and avoid situations that present a high risk for relapse.
Relapse prevention reinforces gains made in previous stages. Here, the patient learns how to identify and deal with risky situations and how to handle a “slip” if it occurs.
ADJUNCTIVE TREATMENTS
Self-help groups. Ask whether the patient has attended self-help groups for addiction or psychiatric illness. If so, then ask, “What did you think of the meetings? What did you like and dislike?”
Self-help groups such as Alcoholics Anonymous (AA) or the Manic-Depressive and Depressive Association (MDDA) can help enormously in the recovery process. These groups are free, readily available, and can offer patients a support network. Although many dual-diagnosis patients are reluctant to attend self-help groups, they may benefit from the support, role modeling, practical advice, and structure that these meetings offer.
Drug therapy for the dual-diagnosis patient focuses on the psychiatric disorder and is usually combined with psychosocial approaches. There is little evidence that one medication is more effective than others for these patients.
Because medication compliance is key to their effective treatment, be sure to ask patients at each visit, “Have you been taking your medication as prescribed?” Because dual-diagnosis patients have been shown to take more or less medication than prescribed,15 asking how much medication they are taking can be revealing.
Related resources
- American Academy of Addiction Psychiatry www.aaap.org
- National Institute on Drug Abuse www.nida.nih.gov
- National Institute on Alcohol Abuse and Alcoholism www.niaaa.nih.gov
Disclosure
Dr. Manwani receives research support from Abbott Laboratories.
Dr. Weiss is a speaker for Abbott Laboratories and Eli Lilly and Co.
Acknowledgment
Supported by grants K0200326, DA09400, and DA15968 from the National Institute on Drug Abuse and a grant from the Dr. Ralph and Marian C. Falk Medical Research Trust.
1. Reigier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-18.
2. Drake RE, Essock SM, Shaner A, et al. Implementing dual diagnosis services for clients with severe mental illness. Psychiatr Serv 2001;52:469-76.
3. Griffin ML, Weiss RD, Mirin SM, et al. The use of the Diagnostic Interview Schedule in drug-dependent patients. Am. J Drug Alcohol Abuse 1987;13(3):281-91.
4. Mason BJ, Kocsis JH, Ritvo EC, et al. A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified on the presence or absence of major depression. JAMA 1996;275(10):761-7.
5. Prochaska JO, DiClemente CC, Norcross JC. In search of how people change: applications to addictive behaviors. Am Psychol 1992;47:1102-14.
6. Connors GJ, Donovan DM, DiClemente CC. Substance abuse treatment and the stages of change. New York: Guilford Press, 2001.
7. Carey KB, Purnine DM, Maisto SA, et al. Assessing readiness to change substance abuse: a critical review of instruments. Clinical Psychol 1999;6:245-66.
8. Sutton S. Back to the drawing board? A review of applications of the transtheoretical model to substance use. Addiction 2001;96:175-86.
9. Drake RE, McHugo GJ, Noordsy DL. Treatment of alcoholism among schizophrenic outpatients: 4-year outcomes. Am J Psychiatry 1993;150:328-9.
10. Hellerstein DJ, Rosenthal RN, Miner CR. A prospective study of integrated outpatient treatment for substance-abusing schizophrenic patients. Am J Addict 1995;4:33-42.
11. Drake RE, Yovetich NA, Bebout RR, et al. Integrated treatment for dually diagnosed homeless adults. J Nerv Ment Dis 1997;185:298-305.
12. Weiss RD, Najavits LM, Hennessy G. Overview of treatment modalities for dual diagnosis patients: pharmacotherapy, psychotherapy, and twelve-step programs. In: Kranzler HR, Tinsley J (eds). Dual diagnosis: substance abuse and comorbid disorders. (2nd ed). New York: Marcel Dekker. In press.
13. Osher FC, Kofoed LL. Treatment of patients with psychiatric and psychoactive substance abuse disorders. Hosp Community Psychiatry 1989;40(10):1025-30.
14. Miller WR, Rollnick S. Motivational interviewing: preparing for change (2nd ed). New York: Guilford Press, 2002.
15. Weiss RD, Greenfield SF, Najavits LM, et al. Medication compliance among patients with bipolar disorder and substance use disorder. J Clin Psychiatry 1998;59(4):172-4.
1. Reigier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-18.
2. Drake RE, Essock SM, Shaner A, et al. Implementing dual diagnosis services for clients with severe mental illness. Psychiatr Serv 2001;52:469-76.
3. Griffin ML, Weiss RD, Mirin SM, et al. The use of the Diagnostic Interview Schedule in drug-dependent patients. Am. J Drug Alcohol Abuse 1987;13(3):281-91.
4. Mason BJ, Kocsis JH, Ritvo EC, et al. A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified on the presence or absence of major depression. JAMA 1996;275(10):761-7.
5. Prochaska JO, DiClemente CC, Norcross JC. In search of how people change: applications to addictive behaviors. Am Psychol 1992;47:1102-14.
6. Connors GJ, Donovan DM, DiClemente CC. Substance abuse treatment and the stages of change. New York: Guilford Press, 2001.
7. Carey KB, Purnine DM, Maisto SA, et al. Assessing readiness to change substance abuse: a critical review of instruments. Clinical Psychol 1999;6:245-66.
8. Sutton S. Back to the drawing board? A review of applications of the transtheoretical model to substance use. Addiction 2001;96:175-86.
9. Drake RE, McHugo GJ, Noordsy DL. Treatment of alcoholism among schizophrenic outpatients: 4-year outcomes. Am J Psychiatry 1993;150:328-9.
10. Hellerstein DJ, Rosenthal RN, Miner CR. A prospective study of integrated outpatient treatment for substance-abusing schizophrenic patients. Am J Addict 1995;4:33-42.
11. Drake RE, Yovetich NA, Bebout RR, et al. Integrated treatment for dually diagnosed homeless adults. J Nerv Ment Dis 1997;185:298-305.
12. Weiss RD, Najavits LM, Hennessy G. Overview of treatment modalities for dual diagnosis patients: pharmacotherapy, psychotherapy, and twelve-step programs. In: Kranzler HR, Tinsley J (eds). Dual diagnosis: substance abuse and comorbid disorders. (2nd ed). New York: Marcel Dekker. In press.
13. Osher FC, Kofoed LL. Treatment of patients with psychiatric and psychoactive substance abuse disorders. Hosp Community Psychiatry 1989;40(10):1025-30.
14. Miller WR, Rollnick S. Motivational interviewing: preparing for change (2nd ed). New York: Guilford Press, 2002.
15. Weiss RD, Greenfield SF, Najavits LM, et al. Medication compliance among patients with bipolar disorder and substance use disorder. J Clin Psychiatry 1998;59(4):172-4.
Spam: Lower your intake
You’re anxiously awaiting an important e-mail from a patient or colleague. You click into your in box, only to find a string of solicitations urging you to refinance your mortgage, buy cheap Viagra, or get rich quick.
Meanwhile, that important message may have been bounced back to the sender and lost.
This is just one way electronic junk mail, or spam, wreaks havoc on millions of e-mail users. If you’re tired of ‘spammers’ feeding you unwanted messages, read on.
Why spam is a problem
Mailing printed advertisements to 20 million people can cost tens of thousands of dollars in postage, mailing lists, and printing. By contrast, a spammer can reach that same audience for a fraction of the cost. Anyone with an Internet service provider (ISP) and a mass-mailing program can flood cyberspace with junk messages.
As a result, users waste precious time and money deleting junk messages by the score. Spam is especially costly to users who pay by the hour for dial-up Internet access.
What’s more, ISPs need to purchase additional processing servers to handle the increase in e-mail volume caused by excessive junk messages. This often leads to rate increases for subscribers with DSL, cable-modem, or other broadband connections.
Fighting back
Federal lawmakers have begun taking aim at unwanted e-mails. The Can Spam Act of 2003, which awaits a Senate vote, would outlaw misleading advertising and mandate a range of requirements on e-solicitors, from inclusion of unsubscribe options on messages to use of functional return e-mail addresses. Violators would face fines of as much as $1 million and/or 1 year in prison.1 Several states, such as Minnesota, also have been considering fines for junk e-mail.2
In the meantime, users can take measures—common-sense and technological—against spam.
Follow these 4 steps
To keep your e-mail address out of spammers’ hands, do not:
- Open spam messages. Just as traditional junk mail is immediately discarded, spam should be deleted without opening. By clicking anywhere in the body of the junk e-mail, the sender receives a return message that e-mail access is valid, subjecting you to more spam.
- Click on the ‘unsubscribe’ link. “Spammers” will not honor this request but will instead store your e-mail address for future reference. For similar reasons, do not reply to the e-mail.
- Post your e-mail address on a Web page. Many spammers use programs that “harvest” e-mail addresses. These programs are particularly attracted to Web pages with hyperlinked e-mail addresses.
- Use an obvious address. Some spammers use “dictionary spamming” by combining common last names and initials to find new e-mail targets. Try to include unusual numeral and character combinations in your address.
Also, use “jsluo|at|email.com” instead of [email protected]. Replacing @ with |at| prevents mass-mailing programs from automatically harvesting and using that address. However, some novice users may not realize they need to type |at| instead of @ to contact you.
Finally, use an alternate e-mail address for contests and newsletters if you suspect these will open the floodgates for spam.
Fighting spam with technology
Many free Web-based e-mail accounts such as Hotmail or Yahoo allow users to receive and delete e-mail in bulk by checking one box. Most providers also employ proprietary anti-spam software to protect their subscribers and servers.
E-mail clients such as Microsoft Outlook or Outlook Express allow you to set up rules to organize mail. Mail from certain users or with particular subjects can be automatically moved from the in box to designated folders. Messages containing terms such as ‘mortgage’ or ‘improve your sex life’ can be automatically deleted. Certain senders can be sent directly to the trash. Consult the “Help” section of these clients for directions.
Check your “deleted items” box to ensure that your rules are not sending important mail to the trash. Once you know that the rules work, you can automatically delete the files.
An anti-spam program can be added to your mail client (Table). These programs work via a combination of methods:
- The program checks a message’s subject content and source to see if the address matches with a list of known spammers. Most spam has a characteristic style, format and phrasing that programs can spot.
- Users can “teach” the program which e-mails to block by verifying wanted and unwanted messages. Some programs send an e-mail to the sender requesting verification. Once the sender replies, mail will go through automatically.
But be careful. If you set your filter to get rid of any subject with ‘urgent,’ the filter may block a patient’s urgent message.
Blowing the whistle
You can also report a spammer to his or her ISP, which in turn may rescind the spammer’s account or assess “cleanup fees.”
Programs such as SpamCop and the Network Abuse Clearinghouse offer reporting/filtering programs that electronically forward spam complaints to ISPs and, in some cases, get a spammer’s address blacklisted, meaning that the user can be denied Internet access through that ISP.
Senders who advertise fraudulent products can also be reported to the Federal Trade Commission. Those who advertise unapproved medical products can be reported to the Food and Drug Administration at (800) 532-4440.
Selected anti-spam programs
| Program | URL | Clients | Cost |
|---|---|---|---|
| SpamBayes | http://spambayes.sourceforge.net/index.html | Microsoft Outlook 2000/XP | Free |
| spamassassin | http://www.spamassasin.org | Any POP clients | Free |
| SpamCop | http://www.spamcop.net | Reporting | Free |
| Network Abuse Clearinghouse | http://www.abuse.net | Reporting | Free |
| MailFrontier Matador | http://www.mailfrontier.com | Microsoft Outlook, Outlook Express | $29.95 |
| Ella | http://www.openfieldsoftware.com/ | Microsoft Outlook 2000/02, Outlook Express 5/6 | $29.95 |
| InBoxer | http://www.inboxer.com | Microsoft Outlook 2000/02/XP | $29.95 |
| EmailProtect | http://www.contentwatch.com/email_protect/index.php | Any POP or IMAP e-mail client | $39.95 |
| (STEVEN) | http://www.softwaredevelopment.net.au/pge_steven.htm | Any POP client, Microsoft Outlook and Outlook Express | Free and $29 registered versions |
| Vipul’s Razor | http://razor.sourceforge.net/ | Requires PERL, software agents | Free |
| SpamEater Pro | http://www.hms.com/spameater.asp | Any POP client | $24.95 |
Related Resources
Spam safety tips. http://www.spamfilterreview.com/spam-saftey-tips.html
Spam Tips and Help. http://spam.abuse.net/userhelp/
Mark R. Senate panel overwhelmingly passes anti-spam bill. dc.internet.com June 19, 2003. Available at: http://dc.internet.com/news/article.php/2224681. Accessed Sept. 5, 2003
Sturdevant C. Can-Spam Act can’t. eWeek June 9, 2003. Available at: http://www.eweek.com/print_article/0,3668,a=43121,00.asp. Accessed Sept. 5, 2003
If you have any questions about these products or comments about Psyber Psychiatry, click here to contact Dr. Luo or send an e-mail to [email protected].
Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.
You’re anxiously awaiting an important e-mail from a patient or colleague. You click into your in box, only to find a string of solicitations urging you to refinance your mortgage, buy cheap Viagra, or get rich quick.
Meanwhile, that important message may have been bounced back to the sender and lost.
This is just one way electronic junk mail, or spam, wreaks havoc on millions of e-mail users. If you’re tired of ‘spammers’ feeding you unwanted messages, read on.
Why spam is a problem
Mailing printed advertisements to 20 million people can cost tens of thousands of dollars in postage, mailing lists, and printing. By contrast, a spammer can reach that same audience for a fraction of the cost. Anyone with an Internet service provider (ISP) and a mass-mailing program can flood cyberspace with junk messages.
As a result, users waste precious time and money deleting junk messages by the score. Spam is especially costly to users who pay by the hour for dial-up Internet access.
What’s more, ISPs need to purchase additional processing servers to handle the increase in e-mail volume caused by excessive junk messages. This often leads to rate increases for subscribers with DSL, cable-modem, or other broadband connections.
Fighting back
Federal lawmakers have begun taking aim at unwanted e-mails. The Can Spam Act of 2003, which awaits a Senate vote, would outlaw misleading advertising and mandate a range of requirements on e-solicitors, from inclusion of unsubscribe options on messages to use of functional return e-mail addresses. Violators would face fines of as much as $1 million and/or 1 year in prison.1 Several states, such as Minnesota, also have been considering fines for junk e-mail.2
In the meantime, users can take measures—common-sense and technological—against spam.
Follow these 4 steps
To keep your e-mail address out of spammers’ hands, do not:
- Open spam messages. Just as traditional junk mail is immediately discarded, spam should be deleted without opening. By clicking anywhere in the body of the junk e-mail, the sender receives a return message that e-mail access is valid, subjecting you to more spam.
- Click on the ‘unsubscribe’ link. “Spammers” will not honor this request but will instead store your e-mail address for future reference. For similar reasons, do not reply to the e-mail.
- Post your e-mail address on a Web page. Many spammers use programs that “harvest” e-mail addresses. These programs are particularly attracted to Web pages with hyperlinked e-mail addresses.
- Use an obvious address. Some spammers use “dictionary spamming” by combining common last names and initials to find new e-mail targets. Try to include unusual numeral and character combinations in your address.
Also, use “jsluo|at|email.com” instead of [email protected]. Replacing @ with |at| prevents mass-mailing programs from automatically harvesting and using that address. However, some novice users may not realize they need to type |at| instead of @ to contact you.
Finally, use an alternate e-mail address for contests and newsletters if you suspect these will open the floodgates for spam.
Fighting spam with technology
Many free Web-based e-mail accounts such as Hotmail or Yahoo allow users to receive and delete e-mail in bulk by checking one box. Most providers also employ proprietary anti-spam software to protect their subscribers and servers.
E-mail clients such as Microsoft Outlook or Outlook Express allow you to set up rules to organize mail. Mail from certain users or with particular subjects can be automatically moved from the in box to designated folders. Messages containing terms such as ‘mortgage’ or ‘improve your sex life’ can be automatically deleted. Certain senders can be sent directly to the trash. Consult the “Help” section of these clients for directions.
Check your “deleted items” box to ensure that your rules are not sending important mail to the trash. Once you know that the rules work, you can automatically delete the files.
An anti-spam program can be added to your mail client (Table). These programs work via a combination of methods:
- The program checks a message’s subject content and source to see if the address matches with a list of known spammers. Most spam has a characteristic style, format and phrasing that programs can spot.
- Users can “teach” the program which e-mails to block by verifying wanted and unwanted messages. Some programs send an e-mail to the sender requesting verification. Once the sender replies, mail will go through automatically.
But be careful. If you set your filter to get rid of any subject with ‘urgent,’ the filter may block a patient’s urgent message.
Blowing the whistle
You can also report a spammer to his or her ISP, which in turn may rescind the spammer’s account or assess “cleanup fees.”
Programs such as SpamCop and the Network Abuse Clearinghouse offer reporting/filtering programs that electronically forward spam complaints to ISPs and, in some cases, get a spammer’s address blacklisted, meaning that the user can be denied Internet access through that ISP.
Senders who advertise fraudulent products can also be reported to the Federal Trade Commission. Those who advertise unapproved medical products can be reported to the Food and Drug Administration at (800) 532-4440.
Selected anti-spam programs
| Program | URL | Clients | Cost |
|---|---|---|---|
| SpamBayes | http://spambayes.sourceforge.net/index.html | Microsoft Outlook 2000/XP | Free |
| spamassassin | http://www.spamassasin.org | Any POP clients | Free |
| SpamCop | http://www.spamcop.net | Reporting | Free |
| Network Abuse Clearinghouse | http://www.abuse.net | Reporting | Free |
| MailFrontier Matador | http://www.mailfrontier.com | Microsoft Outlook, Outlook Express | $29.95 |
| Ella | http://www.openfieldsoftware.com/ | Microsoft Outlook 2000/02, Outlook Express 5/6 | $29.95 |
| InBoxer | http://www.inboxer.com | Microsoft Outlook 2000/02/XP | $29.95 |
| EmailProtect | http://www.contentwatch.com/email_protect/index.php | Any POP or IMAP e-mail client | $39.95 |
| (STEVEN) | http://www.softwaredevelopment.net.au/pge_steven.htm | Any POP client, Microsoft Outlook and Outlook Express | Free and $29 registered versions |
| Vipul’s Razor | http://razor.sourceforge.net/ | Requires PERL, software agents | Free |
| SpamEater Pro | http://www.hms.com/spameater.asp | Any POP client | $24.95 |
Related Resources
Spam safety tips. http://www.spamfilterreview.com/spam-saftey-tips.html
Spam Tips and Help. http://spam.abuse.net/userhelp/
Mark R. Senate panel overwhelmingly passes anti-spam bill. dc.internet.com June 19, 2003. Available at: http://dc.internet.com/news/article.php/2224681. Accessed Sept. 5, 2003
Sturdevant C. Can-Spam Act can’t. eWeek June 9, 2003. Available at: http://www.eweek.com/print_article/0,3668,a=43121,00.asp. Accessed Sept. 5, 2003
If you have any questions about these products or comments about Psyber Psychiatry, click here to contact Dr. Luo or send an e-mail to [email protected].
Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.
You’re anxiously awaiting an important e-mail from a patient or colleague. You click into your in box, only to find a string of solicitations urging you to refinance your mortgage, buy cheap Viagra, or get rich quick.
Meanwhile, that important message may have been bounced back to the sender and lost.
This is just one way electronic junk mail, or spam, wreaks havoc on millions of e-mail users. If you’re tired of ‘spammers’ feeding you unwanted messages, read on.
Why spam is a problem
Mailing printed advertisements to 20 million people can cost tens of thousands of dollars in postage, mailing lists, and printing. By contrast, a spammer can reach that same audience for a fraction of the cost. Anyone with an Internet service provider (ISP) and a mass-mailing program can flood cyberspace with junk messages.
As a result, users waste precious time and money deleting junk messages by the score. Spam is especially costly to users who pay by the hour for dial-up Internet access.
What’s more, ISPs need to purchase additional processing servers to handle the increase in e-mail volume caused by excessive junk messages. This often leads to rate increases for subscribers with DSL, cable-modem, or other broadband connections.
Fighting back
Federal lawmakers have begun taking aim at unwanted e-mails. The Can Spam Act of 2003, which awaits a Senate vote, would outlaw misleading advertising and mandate a range of requirements on e-solicitors, from inclusion of unsubscribe options on messages to use of functional return e-mail addresses. Violators would face fines of as much as $1 million and/or 1 year in prison.1 Several states, such as Minnesota, also have been considering fines for junk e-mail.2
In the meantime, users can take measures—common-sense and technological—against spam.
Follow these 4 steps
To keep your e-mail address out of spammers’ hands, do not:
- Open spam messages. Just as traditional junk mail is immediately discarded, spam should be deleted without opening. By clicking anywhere in the body of the junk e-mail, the sender receives a return message that e-mail access is valid, subjecting you to more spam.
- Click on the ‘unsubscribe’ link. “Spammers” will not honor this request but will instead store your e-mail address for future reference. For similar reasons, do not reply to the e-mail.
- Post your e-mail address on a Web page. Many spammers use programs that “harvest” e-mail addresses. These programs are particularly attracted to Web pages with hyperlinked e-mail addresses.
- Use an obvious address. Some spammers use “dictionary spamming” by combining common last names and initials to find new e-mail targets. Try to include unusual numeral and character combinations in your address.
Also, use “jsluo|at|email.com” instead of [email protected]. Replacing @ with |at| prevents mass-mailing programs from automatically harvesting and using that address. However, some novice users may not realize they need to type |at| instead of @ to contact you.
Finally, use an alternate e-mail address for contests and newsletters if you suspect these will open the floodgates for spam.
Fighting spam with technology
Many free Web-based e-mail accounts such as Hotmail or Yahoo allow users to receive and delete e-mail in bulk by checking one box. Most providers also employ proprietary anti-spam software to protect their subscribers and servers.
E-mail clients such as Microsoft Outlook or Outlook Express allow you to set up rules to organize mail. Mail from certain users or with particular subjects can be automatically moved from the in box to designated folders. Messages containing terms such as ‘mortgage’ or ‘improve your sex life’ can be automatically deleted. Certain senders can be sent directly to the trash. Consult the “Help” section of these clients for directions.
Check your “deleted items” box to ensure that your rules are not sending important mail to the trash. Once you know that the rules work, you can automatically delete the files.
An anti-spam program can be added to your mail client (Table). These programs work via a combination of methods:
- The program checks a message’s subject content and source to see if the address matches with a list of known spammers. Most spam has a characteristic style, format and phrasing that programs can spot.
- Users can “teach” the program which e-mails to block by verifying wanted and unwanted messages. Some programs send an e-mail to the sender requesting verification. Once the sender replies, mail will go through automatically.
But be careful. If you set your filter to get rid of any subject with ‘urgent,’ the filter may block a patient’s urgent message.
Blowing the whistle
You can also report a spammer to his or her ISP, which in turn may rescind the spammer’s account or assess “cleanup fees.”
Programs such as SpamCop and the Network Abuse Clearinghouse offer reporting/filtering programs that electronically forward spam complaints to ISPs and, in some cases, get a spammer’s address blacklisted, meaning that the user can be denied Internet access through that ISP.
Senders who advertise fraudulent products can also be reported to the Federal Trade Commission. Those who advertise unapproved medical products can be reported to the Food and Drug Administration at (800) 532-4440.
Selected anti-spam programs
| Program | URL | Clients | Cost |
|---|---|---|---|
| SpamBayes | http://spambayes.sourceforge.net/index.html | Microsoft Outlook 2000/XP | Free |
| spamassassin | http://www.spamassasin.org | Any POP clients | Free |
| SpamCop | http://www.spamcop.net | Reporting | Free |
| Network Abuse Clearinghouse | http://www.abuse.net | Reporting | Free |
| MailFrontier Matador | http://www.mailfrontier.com | Microsoft Outlook, Outlook Express | $29.95 |
| Ella | http://www.openfieldsoftware.com/ | Microsoft Outlook 2000/02, Outlook Express 5/6 | $29.95 |
| InBoxer | http://www.inboxer.com | Microsoft Outlook 2000/02/XP | $29.95 |
| EmailProtect | http://www.contentwatch.com/email_protect/index.php | Any POP or IMAP e-mail client | $39.95 |
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Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.
Tips for using lithium in bipolar disorder
Despite numerous drug treatment innovations, just about all patients with bipolar disorder that I have treated reported improvement after starting a lithium regimen.
In the 1970s, the clinical literature began highlighting numerous drug therapies for different bipolar symptoms. Before then, I had been taught to treat all “manic-depressive” patients with lithium—regardless of whether mood swings, bouts of anger, depression, or mania were the dominant symptoms.
So I experimented. I prescribed lithium to any potential bipolar patient who did not meet DSM criteria for another mental illness. I discovered the following:
- A family history of any mental illness, especially alcohol abuse and depression, is a strong indicator of bipolar disorder and of potential positive response to lithium.
- The existence of mood swings, especially without cause, confirms the diagnosis of bipolar disorder when paired with family history.
- Lithium, 900 mg/d, works fine as acute or maintenance therapy. I would decrease the dosage for smaller people (eg, 600 mg/d for a patient weighing approximately 125 lbs). I would only increase the dosage—to 1,200 mg/d—for patients with severe mania.
- Gauging lithium blood levels is a waste of time, assuming you have checked for kidney disease. Across 3 decades in practice, the only patient I have ever seen with an abnormally high lithium blood count also suffered renal failure.
- Side effects I have seen most commonly with lithium are:
- weight gain in women, in which case another medication should be prescribed
- tremor, which should warrant a check of the patient’s caffeine intake.
Other side effects (such as diarrhea and GI upset) are usually mild and easy to control by adding other medications.
Dr. Magnon practices general psychiatry in Bradenton, FL.
Despite numerous drug treatment innovations, just about all patients with bipolar disorder that I have treated reported improvement after starting a lithium regimen.
In the 1970s, the clinical literature began highlighting numerous drug therapies for different bipolar symptoms. Before then, I had been taught to treat all “manic-depressive” patients with lithium—regardless of whether mood swings, bouts of anger, depression, or mania were the dominant symptoms.
So I experimented. I prescribed lithium to any potential bipolar patient who did not meet DSM criteria for another mental illness. I discovered the following:
- A family history of any mental illness, especially alcohol abuse and depression, is a strong indicator of bipolar disorder and of potential positive response to lithium.
- The existence of mood swings, especially without cause, confirms the diagnosis of bipolar disorder when paired with family history.
- Lithium, 900 mg/d, works fine as acute or maintenance therapy. I would decrease the dosage for smaller people (eg, 600 mg/d for a patient weighing approximately 125 lbs). I would only increase the dosage—to 1,200 mg/d—for patients with severe mania.
- Gauging lithium blood levels is a waste of time, assuming you have checked for kidney disease. Across 3 decades in practice, the only patient I have ever seen with an abnormally high lithium blood count also suffered renal failure.
- Side effects I have seen most commonly with lithium are:
- weight gain in women, in which case another medication should be prescribed
- tremor, which should warrant a check of the patient’s caffeine intake.
Other side effects (such as diarrhea and GI upset) are usually mild and easy to control by adding other medications.
Despite numerous drug treatment innovations, just about all patients with bipolar disorder that I have treated reported improvement after starting a lithium regimen.
In the 1970s, the clinical literature began highlighting numerous drug therapies for different bipolar symptoms. Before then, I had been taught to treat all “manic-depressive” patients with lithium—regardless of whether mood swings, bouts of anger, depression, or mania were the dominant symptoms.
So I experimented. I prescribed lithium to any potential bipolar patient who did not meet DSM criteria for another mental illness. I discovered the following:
- A family history of any mental illness, especially alcohol abuse and depression, is a strong indicator of bipolar disorder and of potential positive response to lithium.
- The existence of mood swings, especially without cause, confirms the diagnosis of bipolar disorder when paired with family history.
- Lithium, 900 mg/d, works fine as acute or maintenance therapy. I would decrease the dosage for smaller people (eg, 600 mg/d for a patient weighing approximately 125 lbs). I would only increase the dosage—to 1,200 mg/d—for patients with severe mania.
- Gauging lithium blood levels is a waste of time, assuming you have checked for kidney disease. Across 3 decades in practice, the only patient I have ever seen with an abnormally high lithium blood count also suffered renal failure.
- Side effects I have seen most commonly with lithium are:
- weight gain in women, in which case another medication should be prescribed
- tremor, which should warrant a check of the patient’s caffeine intake.
Other side effects (such as diarrhea and GI upset) are usually mild and easy to control by adding other medications.
Dr. Magnon practices general psychiatry in Bradenton, FL.
Dr. Magnon practices general psychiatry in Bradenton, FL.
Is it adolescent psychosis? Consider these 6 issues
Psychotic disorders are difficult to detect in children and adolescents. Such disorders often masquerade as a general medical condition or as a substance abuse, anxiety, mood, or pervasive developmental disorder. On the other hand, some youths whose presentations meet no psychiatric syndrome criteria may complain of psychotic symptoms.1
Consider these six issues when a youth presents with symptoms that may indicate psychosis.
- Mood disorders. Psychotic symptoms in the young:
- Cluster of symptoms. Psychosis is characterized by positive and negative symptoms and by symptoms of disorganization such as thought disorder. Youths with schizophrenia present with a cluster of psychotic symptoms.3,4
- Age. Childhood-onset schizophrenia is rare; adolescent-onset schizophrenia is not.5 The younger the patient, the less likely he or she is psychotic.
- Course. A careful retrospective assessment may confirm schizophrenia by uncovering premorbid difficulties with function and a prodrome that preceded more-extensive symptom expression.4
- Family history. Genetics are an important risk factor for schizophrenia.6 A thorough family history may help assess for schizophrenia and schizophrenia-spectrum disorders (including cluster A personality disorders).
- Multidimensionally impaired syndrome (MIS). Patients with MIS do not have schizophrenia per se. Their symptoms include mild hallucinations, mood instability, social skills deficits, neuropsychological impairments, or excessive preoccupations with fantasy or magical thinking that are developmentally inappropriate but not clearly delusional.7
1. Findling RL, Schulz SC, Kashani JH, Harlan E. Psychotic disorders in children and adolescents. Thousand Oaks, CA: Sage Publications, 2001.
2. Findling RL, Kowatch RA, Post RM. Pediatric bipolar disorder. A handbook for clinicians. London: Martin Dunitz, 2002.
3. Russell AT. The clinical presentation of childhood-onset schizophrenia. Schizophr Bull 1994;20:631-46.
4. American Academy of Child and Adolescent Psychiatry Practice parameter for the assessment and treatment of children and adolescents with schizophrenia. J Am Acad Child Adolesc Psychiatry 2001;40:4S-23S.
5. Häfner H, Maurer K, Löffler W, Riecher-Rössler A. The influence of age and sex on the onset and early course of schizophrenia. Br J Psychiatry 1993;162:80-6.
6. Nicolson R, Brookner FB, Lenane M, et al. Parental schizophrenia spectrum disorders in childhood-onset and adult-onset schizophrenia. Am J Psychiatry 2003;160:490-5.
7. McKenna K, Gordon CT, Lenane M, et al. Looking for childhood-onset schizophrenia: the first 71 cases screened. J Am Acad Child Adolesc Psychiatry 1994;33:636-44.
Dr. Findling is director of child and adolescent psychiatry, University Hospitals of Cleveland, Cleveland, OH.
Psychotic disorders are difficult to detect in children and adolescents. Such disorders often masquerade as a general medical condition or as a substance abuse, anxiety, mood, or pervasive developmental disorder. On the other hand, some youths whose presentations meet no psychiatric syndrome criteria may complain of psychotic symptoms.1
Consider these six issues when a youth presents with symptoms that may indicate psychosis.
- Mood disorders. Psychotic symptoms in the young:
- Cluster of symptoms. Psychosis is characterized by positive and negative symptoms and by symptoms of disorganization such as thought disorder. Youths with schizophrenia present with a cluster of psychotic symptoms.3,4
- Age. Childhood-onset schizophrenia is rare; adolescent-onset schizophrenia is not.5 The younger the patient, the less likely he or she is psychotic.
- Course. A careful retrospective assessment may confirm schizophrenia by uncovering premorbid difficulties with function and a prodrome that preceded more-extensive symptom expression.4
- Family history. Genetics are an important risk factor for schizophrenia.6 A thorough family history may help assess for schizophrenia and schizophrenia-spectrum disorders (including cluster A personality disorders).
- Multidimensionally impaired syndrome (MIS). Patients with MIS do not have schizophrenia per se. Their symptoms include mild hallucinations, mood instability, social skills deficits, neuropsychological impairments, or excessive preoccupations with fantasy or magical thinking that are developmentally inappropriate but not clearly delusional.7
Psychotic disorders are difficult to detect in children and adolescents. Such disorders often masquerade as a general medical condition or as a substance abuse, anxiety, mood, or pervasive developmental disorder. On the other hand, some youths whose presentations meet no psychiatric syndrome criteria may complain of psychotic symptoms.1
Consider these six issues when a youth presents with symptoms that may indicate psychosis.
- Mood disorders. Psychotic symptoms in the young:
- Cluster of symptoms. Psychosis is characterized by positive and negative symptoms and by symptoms of disorganization such as thought disorder. Youths with schizophrenia present with a cluster of psychotic symptoms.3,4
- Age. Childhood-onset schizophrenia is rare; adolescent-onset schizophrenia is not.5 The younger the patient, the less likely he or she is psychotic.
- Course. A careful retrospective assessment may confirm schizophrenia by uncovering premorbid difficulties with function and a prodrome that preceded more-extensive symptom expression.4
- Family history. Genetics are an important risk factor for schizophrenia.6 A thorough family history may help assess for schizophrenia and schizophrenia-spectrum disorders (including cluster A personality disorders).
- Multidimensionally impaired syndrome (MIS). Patients with MIS do not have schizophrenia per se. Their symptoms include mild hallucinations, mood instability, social skills deficits, neuropsychological impairments, or excessive preoccupations with fantasy or magical thinking that are developmentally inappropriate but not clearly delusional.7
1. Findling RL, Schulz SC, Kashani JH, Harlan E. Psychotic disorders in children and adolescents. Thousand Oaks, CA: Sage Publications, 2001.
2. Findling RL, Kowatch RA, Post RM. Pediatric bipolar disorder. A handbook for clinicians. London: Martin Dunitz, 2002.
3. Russell AT. The clinical presentation of childhood-onset schizophrenia. Schizophr Bull 1994;20:631-46.
4. American Academy of Child and Adolescent Psychiatry Practice parameter for the assessment and treatment of children and adolescents with schizophrenia. J Am Acad Child Adolesc Psychiatry 2001;40:4S-23S.
5. Häfner H, Maurer K, Löffler W, Riecher-Rössler A. The influence of age and sex on the onset and early course of schizophrenia. Br J Psychiatry 1993;162:80-6.
6. Nicolson R, Brookner FB, Lenane M, et al. Parental schizophrenia spectrum disorders in childhood-onset and adult-onset schizophrenia. Am J Psychiatry 2003;160:490-5.
7. McKenna K, Gordon CT, Lenane M, et al. Looking for childhood-onset schizophrenia: the first 71 cases screened. J Am Acad Child Adolesc Psychiatry 1994;33:636-44.
Dr. Findling is director of child and adolescent psychiatry, University Hospitals of Cleveland, Cleveland, OH.
1. Findling RL, Schulz SC, Kashani JH, Harlan E. Psychotic disorders in children and adolescents. Thousand Oaks, CA: Sage Publications, 2001.
2. Findling RL, Kowatch RA, Post RM. Pediatric bipolar disorder. A handbook for clinicians. London: Martin Dunitz, 2002.
3. Russell AT. The clinical presentation of childhood-onset schizophrenia. Schizophr Bull 1994;20:631-46.
4. American Academy of Child and Adolescent Psychiatry Practice parameter for the assessment and treatment of children and adolescents with schizophrenia. J Am Acad Child Adolesc Psychiatry 2001;40:4S-23S.
5. Häfner H, Maurer K, Löffler W, Riecher-Rössler A. The influence of age and sex on the onset and early course of schizophrenia. Br J Psychiatry 1993;162:80-6.
6. Nicolson R, Brookner FB, Lenane M, et al. Parental schizophrenia spectrum disorders in childhood-onset and adult-onset schizophrenia. Am J Psychiatry 2003;160:490-5.
7. McKenna K, Gordon CT, Lenane M, et al. Looking for childhood-onset schizophrenia: the first 71 cases screened. J Am Acad Child Adolesc Psychiatry 1994;33:636-44.
Dr. Findling is director of child and adolescent psychiatry, University Hospitals of Cleveland, Cleveland, OH.
Domestic violence: How to detect abuse in psychiatric patients
Victims of domestic abuse/violence often present with medical and psychiatric disorders (Box 1, Table 1). Identifying abuse—and encouraging the frightened or ashamed patient to seek help—is critical to evaluating presenting complaints, improving out-come,7 and possibly saving the patient’s life.
This article will discuss ways to:
- detect signs of abuse
- determine whether a victim is in danger
- share information about crisis resources
- help those who are considering leaving an abusive partner to make a safety plan.
Domestic violence/abuse affects 1 of 4 women in the United States. Men also are victims, but the prevalence (1 of 14) and degree of injury is much lower.1 Domestic violence/abuse occurs among all socioeconomic and ethnic groups.1,2
Domestic violence/abuse impairs victims’ physical and mental health.2 Injuries and ailments more prevalent among domestic abuse victims than among the general population include:2,3
- digestive problems (diarrhea, nausea, appetite loss, spastic colon, constipation, eating disorders,
- urinary problems and infections
- vaginal infections, sexually transmitted diseases, pelvic pain, menstrual problems
- sexual dysfunction
- hypertension
- fainting
- chronic pain (headaches, pelvic, abdominal, back and neck)
- pregnancy problems (preterm labor, poor weight gain)
CASE REPORT: TWO YEARS OF HURT
Ms. W, age 26, is referred to a psychiatrist for treatment-resistant depression. Courses of fluoxetine, 20 mg/d titrated to 80 mg/d, and venlafaxine, 150 mg bid, failed to improve her symptoms. Her Beck Depression Inventory score at baseline is 18, suggesting borderline clinical depression.
Table 1
Psychiatric disorders in victims of domestic abuse/violence
| Disorder | Weighted mean prevalence among abuse victims | Lifetime prevalence among general population |
|---|---|---|
| Alcohol abuse/dependence 4 | 19% | 5 to 8% |
| Depression 4 | 48% | 10% to 21% |
| Drug abuse disorder 4 | 9% | 5% to 6% |
| Posttraumatic stress disorder 4 | 64% | 1% to 12% |
| Suicidality 4 | 18% (ideation and attempts) | Ideation 1-16% Attempts <1-4% |
| % of abused sample | % of non-abused sample | |
| Anxiety symptoms 5 | 26% | 8% |
| Generalized anxiety Disorder 6 | 10% | 4% |
| Panic disorder 6 | 13% | <1% |
She has two children—ages 2 and 4—with her husband, a habitual crack cocaine user. She does not use drugs or alcohol.
When asked about her life at home, Ms. W laments that her husband is not helpful. When asked if her husband hurts her, she replies tearfully that he constantly yells at her and insults her, calling her “ugly” and “a lousy mom.” Upon further questioning, she reveals that her husband, when high on crack, sometimes hits her.
Ms. W does not work outside the home and did not finish high school. She is afraid to leave her husband because his mother helps care for the children and provides money, housing, and food. She constantly feels tearful and trapped.
The psychiatrist increases the venlafaxine to 375 mg/d and suggests that Ms. W call a domestic violence crisis center. She does not call the center, but agrees to see the psychiatrist monthly. Across 3 months her Beck score improves to 14.
SCREENING FOR ABUSE
The American Medical Association, American College of Physicians, and other physician and nursing organizations recommend routinely screening women for domestic abuse/violence.8-10 Some patients will not disclose abuse to their physicians when asked, but most patients say they want doctors to ask them about domestic violence/abuse and to offer crisis phone numbers, pamphlets, and other resources.11
Anyone who presents with complaints of fatigue, depression, anxiety, insomnia, hypervigilance, a treatment-resistant psychiatric disorder, or a visible physical injury (such as a black eye or bruises) should be screened for domestic abuse.
Prevention and treatment guidelines for physicians9,12,13 recommend interviewing the patient—without the partner or children—in a nonjudgmental and empathic fashion.11
Written questionnaires—such as the Woman Abuse Screening Tool (WAST), WAST-short, and HITS—are another screening option.
WAST-Short has demonstrated 92% sensitivity in identifying emotional or physical abuse (Table 2).14
WAST. The longer version of WAST has demonstrated 96% sensitivity in detecting physical or emotional abuse.14 It includes the two WAST-short questions, plus five questions about whether:
- arguments with an intimate partner ever diminish the patient’s self-esteem
- such arguments ever result in kicking or hitting
- the patient ever feels frightened by the partner’s words or actions
- the patient has ever been physically or emotionally abused by his or her partner.
Because the additional questions are not scored, the longer WAST is not well suited to clinical practice. However, a patient who scores a 1 on the WAST-Short exam can provide more in-depth information on her troubled relationship by answering the extra questions.
HITS can be self-administered and its title is easy to remember, but the scoring system is cumbersome. The patient is asked: “How often does your partner:
- Hurt you physically?
- Insult you or talk down to you?
- Threaten you with harm?
- Scream or curse at you?”
Each answer is scored on a 1-to-5 scale—never, rarely, sometimes, fairly often, or frequently. A score ≥ 10.5 has demonstrated 96% sensitivity in identifying physical and verbal abuse.15
Encouraging disclosure. Ask patients about domestic abuse when inquiring about smoking, alcohol use, or household makeup as part of the patient history. Your line of questioning might proceed as follows:
- “Do you live alone?”
- “Do you have a significant other?”
- “How is your relationship going?”
- “Is your partner supportive?”
- “What happens when you and your partner disagree?”
Table 2
Woman Abuse Screening Tool-Short version
| 1. In general, how would you describe your relationship? | ||
| □ a lot of tension | □ some tension | □ no tension |
| 2. Do you and your partner work out arguments with: | ||
| □ great difficulty | □ some difficulty | □ no difficulty |
| Answers are scored on a 1-to-3 scale, with 1 meaning “a lot of tension” or “great difficulty.” A score of 1 on either question indicates possible domestic abuse/violence. | ||
| Source: Reference 14 | ||
Be empathic. Explain the association between domestic abuse/violence and mental and physical disorders. Tell the patient that domestic abuse is common and help is readily available. Share information about crisis services even if the patient does not immediately disclose suspected abuse. Victims generally feel tremendous shame from living with the abuse, so disclosure takes time and trust.
Most states do not require physicians to report domestic abuse to the police unless injuries are caused by a weapon (knife or gun). However, physicians in California, Colorado, Kentucky, and New York must report any injuries resulting from domestic abuse—even if not caused by a weapon.16 In these states, clinicians should disclose their reporting obligation at the start of the patient interview.
Assess danger to any patient who reports being a victim of domestic abuse/violence. Consider danger imminent if the patient acknowledges any one of the following:
- Homicide or suicide threats from partner
- Weapons in the home
- Excessive substance use by partner or victim
- Escalating abuse or threats
- Physical/verbal abuse of children
- Harm to pets
- Fear of the partner
Source: Reference 17
Advise a patient who reports domestic abuse/violence to pack important belongings in case she needs to immediately leave an abusive partner.
The emergency bag should contain:
- Identification for self and children (birth certificates, driver’s license)
- Important documents (school and health records, insurance cards, car title, marriage license, mortgage or rental papers, protective orders, custody papers, divorce papers)
- Medications (for victim and children)
- Keys (auto, home, safe deposit box)
- Phone numbers
- Clothing (for victim and children)
- Comfort items, such as toys and blankets for children.
Source: Reference 17
WHEN A PATIENT CONFIRMS ABUSE
Affirm the difficulty of sharing this information and reassure the patient that she is not alone. Tell her, for example, “I know this is difficult to talk about. No one deserves to be treated this way.”
Reaffirm confidentiality. Victims fear harm to themselves or their children if their abusers find out they have discussed the abuse.
Assess the danger to the patient (Box 2).17
Refer the patient to a local domestic violence crisis agency or to a therapist knowledgeable about domestic abuse. A patient who reports being threatened at gunpoint or who fears for her safety should be urged to call police.
Do not refer the victim and partner to couples counseling. Such therapy is contraindicated because of the relationship’s power imbalance and the risk that the abuser will retaliate when alone with the victim.
DEVELOPING A SAFETY PLAN
Patients who have decided to leave an abusive partner need help forming a safety plan. Assistance from a domestic violence crisis agency is invaluable, but some patients prefer to work with their physicians. Safety planning involves helping the victim identify options and needs upon leaving the relationship.
Start by asking the patient:
- “If you leave home, where will you go?
- Is there an alternative if you cannot stay where you planned?
- Do you have an emergency bag?” (Box 3) 17
Remind the patient to keep her emergency bag, purse, and keys handy in case she needs to leave quickly.
Instruct the patient to:
- Tell a neighbor about the violence and ask him or her to call police if he or she hears suspicious noises from the victim’s residence.
- Teach children to dial 911 or 0 or to make a collect call to a relative, friend, minister, or other trusted person in an emergency. Also teach children addresses of close relatives and friends.
- Learn the local domestic violence hotline number.17
IF A PATIENT DENIES ABUSE
If a suspected victim denies she is being abused, schedule regular visits and let her know you are concerned. Ask how the relationship is progressing at the next monthly visit. If you fear the patient is in danger, schedule weekly or biweekly visits.
Above all, do not tell the victim what to do. Some patients are not ready to act, while others may call the local agency from your office.
Related resources
- National Domestic Violence Hotline (24-hour). 1-800-799-SAFE (7233). Translation services available.
- National Resource Center on Domestic Violence. (800) 537-2238 or www.ndvh.org
- American Medical Association Domestic Violence Resources. www.ama-assn.org/ama/pub/article/3216-6827.html
- American Medical Women’s Association online CME course educates physicians about domestic violence. Physicians can earn two CME credits at no charge. www.dvcme.org
Drug brand names
- Fluoxetine • Prozac
- Venlafaxine • Effexor
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Tjaden P, Thoennes N. Extent, nature, and consequences of intimate partner violence: findings from the National Violence Against Women Survey. Report for grant 93-IJ-CX-0012. Washington, DC: National Institute of Justice and the Centers for Disease Control, 2000.
2. Campbell JC. Health consequences of intimate partner violence. Lancet 2002;359:1331-6.
3. Gazmararian JA, Lazorick S, Spitz AM, et al. Prevalence of violence against pregnant women. JAMA 1996;275:1915-20.
4. Golding JM. Intimate partner violence as a risk factor for mental disorders: a meta-analysis. J Fam Violence 1999;14:99-132.
5. Carlson B, McNutt LA, Choi D. Intimate partner abuse and mental health: the role of social support and protective factors. Violence Against Women 2002;8:720-45.
6. Cascardi M, O’Leary K, Lawrence E, Schlee K. Characteristics of women physically abused by their spouses and who seek treatment regarding marital conflict. J Consult Clin Psychol 1995;63:616-23.
7. Rhodes KV, Levinson W. Interventions for intimate partner violence against women: clinical applications. JAMA 2003;289:601-5.
8. American College of Physicians. Domestic violence: Position paper of the American College of Physicians. Philadelphia: American College of Physicians, 1986
9. American Medical Association Diagnostic and treatment guidelines for domestic violence. Arch Fam Med 1992;1:39-47.
10. American College of Obstetricians and Gynecologists. Domestic Violence. Washington DC: ACOG Educational Bulletin, No. 257, December 1999.
11. Gerbert B, Abercrombie P, Caspers N, et al. How health care providers help battered women: the survivor’s perspective. Women Health 1999;29:115-35.
12. Warshaw C, Ganley A. Improving the health care response to domestic violence: a resource manual for health care providers (2nd ed). San Francisco: Family Violence Prevention Fund; 1996.
13. U.S. Preventive Services Task Force. Guide to clinical preventive services (2nd ed). Baltimore: Williams & Wilkins, 1996.
14. Brown J, Lent B, Schmidt G, Sas G. Application of the Woman Abuse Screening Tool (WAST) and WAST-short in the family practice setting. J Fam Pract 2000;49:896-903.
15. Sherin K, Sinacore J, Li X, et al. HITS: a short domestic violence screening tool for use in a family practice setting. Fam Med 1998;30:508-12.
16. National Advisory Committee of FVPF. National consensus guidelines: on identifying and responding to domestic violence victimization in the health care setting. San Francisco: Family Violence Prevention Fund, 2002.
17. Davies J, Lyon E, Monti-Cantania D. Safety planning with battered women: complex lives, difficult choices. Thousand Oaks, CA: SAGE Publications, 1998.
Victims of domestic abuse/violence often present with medical and psychiatric disorders (Box 1, Table 1). Identifying abuse—and encouraging the frightened or ashamed patient to seek help—is critical to evaluating presenting complaints, improving out-come,7 and possibly saving the patient’s life.
This article will discuss ways to:
- detect signs of abuse
- determine whether a victim is in danger
- share information about crisis resources
- help those who are considering leaving an abusive partner to make a safety plan.
Domestic violence/abuse affects 1 of 4 women in the United States. Men also are victims, but the prevalence (1 of 14) and degree of injury is much lower.1 Domestic violence/abuse occurs among all socioeconomic and ethnic groups.1,2
Domestic violence/abuse impairs victims’ physical and mental health.2 Injuries and ailments more prevalent among domestic abuse victims than among the general population include:2,3
- digestive problems (diarrhea, nausea, appetite loss, spastic colon, constipation, eating disorders,
- urinary problems and infections
- vaginal infections, sexually transmitted diseases, pelvic pain, menstrual problems
- sexual dysfunction
- hypertension
- fainting
- chronic pain (headaches, pelvic, abdominal, back and neck)
- pregnancy problems (preterm labor, poor weight gain)
CASE REPORT: TWO YEARS OF HURT
Ms. W, age 26, is referred to a psychiatrist for treatment-resistant depression. Courses of fluoxetine, 20 mg/d titrated to 80 mg/d, and venlafaxine, 150 mg bid, failed to improve her symptoms. Her Beck Depression Inventory score at baseline is 18, suggesting borderline clinical depression.
Table 1
Psychiatric disorders in victims of domestic abuse/violence
| Disorder | Weighted mean prevalence among abuse victims | Lifetime prevalence among general population |
|---|---|---|
| Alcohol abuse/dependence 4 | 19% | 5 to 8% |
| Depression 4 | 48% | 10% to 21% |
| Drug abuse disorder 4 | 9% | 5% to 6% |
| Posttraumatic stress disorder 4 | 64% | 1% to 12% |
| Suicidality 4 | 18% (ideation and attempts) | Ideation 1-16% Attempts <1-4% |
| % of abused sample | % of non-abused sample | |
| Anxiety symptoms 5 | 26% | 8% |
| Generalized anxiety Disorder 6 | 10% | 4% |
| Panic disorder 6 | 13% | <1% |
She has two children—ages 2 and 4—with her husband, a habitual crack cocaine user. She does not use drugs or alcohol.
When asked about her life at home, Ms. W laments that her husband is not helpful. When asked if her husband hurts her, she replies tearfully that he constantly yells at her and insults her, calling her “ugly” and “a lousy mom.” Upon further questioning, she reveals that her husband, when high on crack, sometimes hits her.
Ms. W does not work outside the home and did not finish high school. She is afraid to leave her husband because his mother helps care for the children and provides money, housing, and food. She constantly feels tearful and trapped.
The psychiatrist increases the venlafaxine to 375 mg/d and suggests that Ms. W call a domestic violence crisis center. She does not call the center, but agrees to see the psychiatrist monthly. Across 3 months her Beck score improves to 14.
SCREENING FOR ABUSE
The American Medical Association, American College of Physicians, and other physician and nursing organizations recommend routinely screening women for domestic abuse/violence.8-10 Some patients will not disclose abuse to their physicians when asked, but most patients say they want doctors to ask them about domestic violence/abuse and to offer crisis phone numbers, pamphlets, and other resources.11
Anyone who presents with complaints of fatigue, depression, anxiety, insomnia, hypervigilance, a treatment-resistant psychiatric disorder, or a visible physical injury (such as a black eye or bruises) should be screened for domestic abuse.
Prevention and treatment guidelines for physicians9,12,13 recommend interviewing the patient—without the partner or children—in a nonjudgmental and empathic fashion.11
Written questionnaires—such as the Woman Abuse Screening Tool (WAST), WAST-short, and HITS—are another screening option.
WAST-Short has demonstrated 92% sensitivity in identifying emotional or physical abuse (Table 2).14
WAST. The longer version of WAST has demonstrated 96% sensitivity in detecting physical or emotional abuse.14 It includes the two WAST-short questions, plus five questions about whether:
- arguments with an intimate partner ever diminish the patient’s self-esteem
- such arguments ever result in kicking or hitting
- the patient ever feels frightened by the partner’s words or actions
- the patient has ever been physically or emotionally abused by his or her partner.
Because the additional questions are not scored, the longer WAST is not well suited to clinical practice. However, a patient who scores a 1 on the WAST-Short exam can provide more in-depth information on her troubled relationship by answering the extra questions.
HITS can be self-administered and its title is easy to remember, but the scoring system is cumbersome. The patient is asked: “How often does your partner:
- Hurt you physically?
- Insult you or talk down to you?
- Threaten you with harm?
- Scream or curse at you?”
Each answer is scored on a 1-to-5 scale—never, rarely, sometimes, fairly often, or frequently. A score ≥ 10.5 has demonstrated 96% sensitivity in identifying physical and verbal abuse.15
Encouraging disclosure. Ask patients about domestic abuse when inquiring about smoking, alcohol use, or household makeup as part of the patient history. Your line of questioning might proceed as follows:
- “Do you live alone?”
- “Do you have a significant other?”
- “How is your relationship going?”
- “Is your partner supportive?”
- “What happens when you and your partner disagree?”
Table 2
Woman Abuse Screening Tool-Short version
| 1. In general, how would you describe your relationship? | ||
| □ a lot of tension | □ some tension | □ no tension |
| 2. Do you and your partner work out arguments with: | ||
| □ great difficulty | □ some difficulty | □ no difficulty |
| Answers are scored on a 1-to-3 scale, with 1 meaning “a lot of tension” or “great difficulty.” A score of 1 on either question indicates possible domestic abuse/violence. | ||
| Source: Reference 14 | ||
Be empathic. Explain the association between domestic abuse/violence and mental and physical disorders. Tell the patient that domestic abuse is common and help is readily available. Share information about crisis services even if the patient does not immediately disclose suspected abuse. Victims generally feel tremendous shame from living with the abuse, so disclosure takes time and trust.
Most states do not require physicians to report domestic abuse to the police unless injuries are caused by a weapon (knife or gun). However, physicians in California, Colorado, Kentucky, and New York must report any injuries resulting from domestic abuse—even if not caused by a weapon.16 In these states, clinicians should disclose their reporting obligation at the start of the patient interview.
Assess danger to any patient who reports being a victim of domestic abuse/violence. Consider danger imminent if the patient acknowledges any one of the following:
- Homicide or suicide threats from partner
- Weapons in the home
- Excessive substance use by partner or victim
- Escalating abuse or threats
- Physical/verbal abuse of children
- Harm to pets
- Fear of the partner
Source: Reference 17
Advise a patient who reports domestic abuse/violence to pack important belongings in case she needs to immediately leave an abusive partner.
The emergency bag should contain:
- Identification for self and children (birth certificates, driver’s license)
- Important documents (school and health records, insurance cards, car title, marriage license, mortgage or rental papers, protective orders, custody papers, divorce papers)
- Medications (for victim and children)
- Keys (auto, home, safe deposit box)
- Phone numbers
- Clothing (for victim and children)
- Comfort items, such as toys and blankets for children.
Source: Reference 17
WHEN A PATIENT CONFIRMS ABUSE
Affirm the difficulty of sharing this information and reassure the patient that she is not alone. Tell her, for example, “I know this is difficult to talk about. No one deserves to be treated this way.”
Reaffirm confidentiality. Victims fear harm to themselves or their children if their abusers find out they have discussed the abuse.
Assess the danger to the patient (Box 2).17
Refer the patient to a local domestic violence crisis agency or to a therapist knowledgeable about domestic abuse. A patient who reports being threatened at gunpoint or who fears for her safety should be urged to call police.
Do not refer the victim and partner to couples counseling. Such therapy is contraindicated because of the relationship’s power imbalance and the risk that the abuser will retaliate when alone with the victim.
DEVELOPING A SAFETY PLAN
Patients who have decided to leave an abusive partner need help forming a safety plan. Assistance from a domestic violence crisis agency is invaluable, but some patients prefer to work with their physicians. Safety planning involves helping the victim identify options and needs upon leaving the relationship.
Start by asking the patient:
- “If you leave home, where will you go?
- Is there an alternative if you cannot stay where you planned?
- Do you have an emergency bag?” (Box 3) 17
Remind the patient to keep her emergency bag, purse, and keys handy in case she needs to leave quickly.
Instruct the patient to:
- Tell a neighbor about the violence and ask him or her to call police if he or she hears suspicious noises from the victim’s residence.
- Teach children to dial 911 or 0 or to make a collect call to a relative, friend, minister, or other trusted person in an emergency. Also teach children addresses of close relatives and friends.
- Learn the local domestic violence hotline number.17
IF A PATIENT DENIES ABUSE
If a suspected victim denies she is being abused, schedule regular visits and let her know you are concerned. Ask how the relationship is progressing at the next monthly visit. If you fear the patient is in danger, schedule weekly or biweekly visits.
Above all, do not tell the victim what to do. Some patients are not ready to act, while others may call the local agency from your office.
Related resources
- National Domestic Violence Hotline (24-hour). 1-800-799-SAFE (7233). Translation services available.
- National Resource Center on Domestic Violence. (800) 537-2238 or www.ndvh.org
- American Medical Association Domestic Violence Resources. www.ama-assn.org/ama/pub/article/3216-6827.html
- American Medical Women’s Association online CME course educates physicians about domestic violence. Physicians can earn two CME credits at no charge. www.dvcme.org
Drug brand names
- Fluoxetine • Prozac
- Venlafaxine • Effexor
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
Victims of domestic abuse/violence often present with medical and psychiatric disorders (Box 1, Table 1). Identifying abuse—and encouraging the frightened or ashamed patient to seek help—is critical to evaluating presenting complaints, improving out-come,7 and possibly saving the patient’s life.
This article will discuss ways to:
- detect signs of abuse
- determine whether a victim is in danger
- share information about crisis resources
- help those who are considering leaving an abusive partner to make a safety plan.
Domestic violence/abuse affects 1 of 4 women in the United States. Men also are victims, but the prevalence (1 of 14) and degree of injury is much lower.1 Domestic violence/abuse occurs among all socioeconomic and ethnic groups.1,2
Domestic violence/abuse impairs victims’ physical and mental health.2 Injuries and ailments more prevalent among domestic abuse victims than among the general population include:2,3
- digestive problems (diarrhea, nausea, appetite loss, spastic colon, constipation, eating disorders,
- urinary problems and infections
- vaginal infections, sexually transmitted diseases, pelvic pain, menstrual problems
- sexual dysfunction
- hypertension
- fainting
- chronic pain (headaches, pelvic, abdominal, back and neck)
- pregnancy problems (preterm labor, poor weight gain)
CASE REPORT: TWO YEARS OF HURT
Ms. W, age 26, is referred to a psychiatrist for treatment-resistant depression. Courses of fluoxetine, 20 mg/d titrated to 80 mg/d, and venlafaxine, 150 mg bid, failed to improve her symptoms. Her Beck Depression Inventory score at baseline is 18, suggesting borderline clinical depression.
Table 1
Psychiatric disorders in victims of domestic abuse/violence
| Disorder | Weighted mean prevalence among abuse victims | Lifetime prevalence among general population |
|---|---|---|
| Alcohol abuse/dependence 4 | 19% | 5 to 8% |
| Depression 4 | 48% | 10% to 21% |
| Drug abuse disorder 4 | 9% | 5% to 6% |
| Posttraumatic stress disorder 4 | 64% | 1% to 12% |
| Suicidality 4 | 18% (ideation and attempts) | Ideation 1-16% Attempts <1-4% |
| % of abused sample | % of non-abused sample | |
| Anxiety symptoms 5 | 26% | 8% |
| Generalized anxiety Disorder 6 | 10% | 4% |
| Panic disorder 6 | 13% | <1% |
She has two children—ages 2 and 4—with her husband, a habitual crack cocaine user. She does not use drugs or alcohol.
When asked about her life at home, Ms. W laments that her husband is not helpful. When asked if her husband hurts her, she replies tearfully that he constantly yells at her and insults her, calling her “ugly” and “a lousy mom.” Upon further questioning, she reveals that her husband, when high on crack, sometimes hits her.
Ms. W does not work outside the home and did not finish high school. She is afraid to leave her husband because his mother helps care for the children and provides money, housing, and food. She constantly feels tearful and trapped.
The psychiatrist increases the venlafaxine to 375 mg/d and suggests that Ms. W call a domestic violence crisis center. She does not call the center, but agrees to see the psychiatrist monthly. Across 3 months her Beck score improves to 14.
SCREENING FOR ABUSE
The American Medical Association, American College of Physicians, and other physician and nursing organizations recommend routinely screening women for domestic abuse/violence.8-10 Some patients will not disclose abuse to their physicians when asked, but most patients say they want doctors to ask them about domestic violence/abuse and to offer crisis phone numbers, pamphlets, and other resources.11
Anyone who presents with complaints of fatigue, depression, anxiety, insomnia, hypervigilance, a treatment-resistant psychiatric disorder, or a visible physical injury (such as a black eye or bruises) should be screened for domestic abuse.
Prevention and treatment guidelines for physicians9,12,13 recommend interviewing the patient—without the partner or children—in a nonjudgmental and empathic fashion.11
Written questionnaires—such as the Woman Abuse Screening Tool (WAST), WAST-short, and HITS—are another screening option.
WAST-Short has demonstrated 92% sensitivity in identifying emotional or physical abuse (Table 2).14
WAST. The longer version of WAST has demonstrated 96% sensitivity in detecting physical or emotional abuse.14 It includes the two WAST-short questions, plus five questions about whether:
- arguments with an intimate partner ever diminish the patient’s self-esteem
- such arguments ever result in kicking or hitting
- the patient ever feels frightened by the partner’s words or actions
- the patient has ever been physically or emotionally abused by his or her partner.
Because the additional questions are not scored, the longer WAST is not well suited to clinical practice. However, a patient who scores a 1 on the WAST-Short exam can provide more in-depth information on her troubled relationship by answering the extra questions.
HITS can be self-administered and its title is easy to remember, but the scoring system is cumbersome. The patient is asked: “How often does your partner:
- Hurt you physically?
- Insult you or talk down to you?
- Threaten you with harm?
- Scream or curse at you?”
Each answer is scored on a 1-to-5 scale—never, rarely, sometimes, fairly often, or frequently. A score ≥ 10.5 has demonstrated 96% sensitivity in identifying physical and verbal abuse.15
Encouraging disclosure. Ask patients about domestic abuse when inquiring about smoking, alcohol use, or household makeup as part of the patient history. Your line of questioning might proceed as follows:
- “Do you live alone?”
- “Do you have a significant other?”
- “How is your relationship going?”
- “Is your partner supportive?”
- “What happens when you and your partner disagree?”
Table 2
Woman Abuse Screening Tool-Short version
| 1. In general, how would you describe your relationship? | ||
| □ a lot of tension | □ some tension | □ no tension |
| 2. Do you and your partner work out arguments with: | ||
| □ great difficulty | □ some difficulty | □ no difficulty |
| Answers are scored on a 1-to-3 scale, with 1 meaning “a lot of tension” or “great difficulty.” A score of 1 on either question indicates possible domestic abuse/violence. | ||
| Source: Reference 14 | ||
Be empathic. Explain the association between domestic abuse/violence and mental and physical disorders. Tell the patient that domestic abuse is common and help is readily available. Share information about crisis services even if the patient does not immediately disclose suspected abuse. Victims generally feel tremendous shame from living with the abuse, so disclosure takes time and trust.
Most states do not require physicians to report domestic abuse to the police unless injuries are caused by a weapon (knife or gun). However, physicians in California, Colorado, Kentucky, and New York must report any injuries resulting from domestic abuse—even if not caused by a weapon.16 In these states, clinicians should disclose their reporting obligation at the start of the patient interview.
Assess danger to any patient who reports being a victim of domestic abuse/violence. Consider danger imminent if the patient acknowledges any one of the following:
- Homicide or suicide threats from partner
- Weapons in the home
- Excessive substance use by partner or victim
- Escalating abuse or threats
- Physical/verbal abuse of children
- Harm to pets
- Fear of the partner
Source: Reference 17
Advise a patient who reports domestic abuse/violence to pack important belongings in case she needs to immediately leave an abusive partner.
The emergency bag should contain:
- Identification for self and children (birth certificates, driver’s license)
- Important documents (school and health records, insurance cards, car title, marriage license, mortgage or rental papers, protective orders, custody papers, divorce papers)
- Medications (for victim and children)
- Keys (auto, home, safe deposit box)
- Phone numbers
- Clothing (for victim and children)
- Comfort items, such as toys and blankets for children.
Source: Reference 17
WHEN A PATIENT CONFIRMS ABUSE
Affirm the difficulty of sharing this information and reassure the patient that she is not alone. Tell her, for example, “I know this is difficult to talk about. No one deserves to be treated this way.”
Reaffirm confidentiality. Victims fear harm to themselves or their children if their abusers find out they have discussed the abuse.
Assess the danger to the patient (Box 2).17
Refer the patient to a local domestic violence crisis agency or to a therapist knowledgeable about domestic abuse. A patient who reports being threatened at gunpoint or who fears for her safety should be urged to call police.
Do not refer the victim and partner to couples counseling. Such therapy is contraindicated because of the relationship’s power imbalance and the risk that the abuser will retaliate when alone with the victim.
DEVELOPING A SAFETY PLAN
Patients who have decided to leave an abusive partner need help forming a safety plan. Assistance from a domestic violence crisis agency is invaluable, but some patients prefer to work with their physicians. Safety planning involves helping the victim identify options and needs upon leaving the relationship.
Start by asking the patient:
- “If you leave home, where will you go?
- Is there an alternative if you cannot stay where you planned?
- Do you have an emergency bag?” (Box 3) 17
Remind the patient to keep her emergency bag, purse, and keys handy in case she needs to leave quickly.
Instruct the patient to:
- Tell a neighbor about the violence and ask him or her to call police if he or she hears suspicious noises from the victim’s residence.
- Teach children to dial 911 or 0 or to make a collect call to a relative, friend, minister, or other trusted person in an emergency. Also teach children addresses of close relatives and friends.
- Learn the local domestic violence hotline number.17
IF A PATIENT DENIES ABUSE
If a suspected victim denies she is being abused, schedule regular visits and let her know you are concerned. Ask how the relationship is progressing at the next monthly visit. If you fear the patient is in danger, schedule weekly or biweekly visits.
Above all, do not tell the victim what to do. Some patients are not ready to act, while others may call the local agency from your office.
Related resources
- National Domestic Violence Hotline (24-hour). 1-800-799-SAFE (7233). Translation services available.
- National Resource Center on Domestic Violence. (800) 537-2238 or www.ndvh.org
- American Medical Association Domestic Violence Resources. www.ama-assn.org/ama/pub/article/3216-6827.html
- American Medical Women’s Association online CME course educates physicians about domestic violence. Physicians can earn two CME credits at no charge. www.dvcme.org
Drug brand names
- Fluoxetine • Prozac
- Venlafaxine • Effexor
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Tjaden P, Thoennes N. Extent, nature, and consequences of intimate partner violence: findings from the National Violence Against Women Survey. Report for grant 93-IJ-CX-0012. Washington, DC: National Institute of Justice and the Centers for Disease Control, 2000.
2. Campbell JC. Health consequences of intimate partner violence. Lancet 2002;359:1331-6.
3. Gazmararian JA, Lazorick S, Spitz AM, et al. Prevalence of violence against pregnant women. JAMA 1996;275:1915-20.
4. Golding JM. Intimate partner violence as a risk factor for mental disorders: a meta-analysis. J Fam Violence 1999;14:99-132.
5. Carlson B, McNutt LA, Choi D. Intimate partner abuse and mental health: the role of social support and protective factors. Violence Against Women 2002;8:720-45.
6. Cascardi M, O’Leary K, Lawrence E, Schlee K. Characteristics of women physically abused by their spouses and who seek treatment regarding marital conflict. J Consult Clin Psychol 1995;63:616-23.
7. Rhodes KV, Levinson W. Interventions for intimate partner violence against women: clinical applications. JAMA 2003;289:601-5.
8. American College of Physicians. Domestic violence: Position paper of the American College of Physicians. Philadelphia: American College of Physicians, 1986
9. American Medical Association Diagnostic and treatment guidelines for domestic violence. Arch Fam Med 1992;1:39-47.
10. American College of Obstetricians and Gynecologists. Domestic Violence. Washington DC: ACOG Educational Bulletin, No. 257, December 1999.
11. Gerbert B, Abercrombie P, Caspers N, et al. How health care providers help battered women: the survivor’s perspective. Women Health 1999;29:115-35.
12. Warshaw C, Ganley A. Improving the health care response to domestic violence: a resource manual for health care providers (2nd ed). San Francisco: Family Violence Prevention Fund; 1996.
13. U.S. Preventive Services Task Force. Guide to clinical preventive services (2nd ed). Baltimore: Williams & Wilkins, 1996.
14. Brown J, Lent B, Schmidt G, Sas G. Application of the Woman Abuse Screening Tool (WAST) and WAST-short in the family practice setting. J Fam Pract 2000;49:896-903.
15. Sherin K, Sinacore J, Li X, et al. HITS: a short domestic violence screening tool for use in a family practice setting. Fam Med 1998;30:508-12.
16. National Advisory Committee of FVPF. National consensus guidelines: on identifying and responding to domestic violence victimization in the health care setting. San Francisco: Family Violence Prevention Fund, 2002.
17. Davies J, Lyon E, Monti-Cantania D. Safety planning with battered women: complex lives, difficult choices. Thousand Oaks, CA: SAGE Publications, 1998.
1. Tjaden P, Thoennes N. Extent, nature, and consequences of intimate partner violence: findings from the National Violence Against Women Survey. Report for grant 93-IJ-CX-0012. Washington, DC: National Institute of Justice and the Centers for Disease Control, 2000.
2. Campbell JC. Health consequences of intimate partner violence. Lancet 2002;359:1331-6.
3. Gazmararian JA, Lazorick S, Spitz AM, et al. Prevalence of violence against pregnant women. JAMA 1996;275:1915-20.
4. Golding JM. Intimate partner violence as a risk factor for mental disorders: a meta-analysis. J Fam Violence 1999;14:99-132.
5. Carlson B, McNutt LA, Choi D. Intimate partner abuse and mental health: the role of social support and protective factors. Violence Against Women 2002;8:720-45.
6. Cascardi M, O’Leary K, Lawrence E, Schlee K. Characteristics of women physically abused by their spouses and who seek treatment regarding marital conflict. J Consult Clin Psychol 1995;63:616-23.
7. Rhodes KV, Levinson W. Interventions for intimate partner violence against women: clinical applications. JAMA 2003;289:601-5.
8. American College of Physicians. Domestic violence: Position paper of the American College of Physicians. Philadelphia: American College of Physicians, 1986
9. American Medical Association Diagnostic and treatment guidelines for domestic violence. Arch Fam Med 1992;1:39-47.
10. American College of Obstetricians and Gynecologists. Domestic Violence. Washington DC: ACOG Educational Bulletin, No. 257, December 1999.
11. Gerbert B, Abercrombie P, Caspers N, et al. How health care providers help battered women: the survivor’s perspective. Women Health 1999;29:115-35.
12. Warshaw C, Ganley A. Improving the health care response to domestic violence: a resource manual for health care providers (2nd ed). San Francisco: Family Violence Prevention Fund; 1996.
13. U.S. Preventive Services Task Force. Guide to clinical preventive services (2nd ed). Baltimore: Williams & Wilkins, 1996.
14. Brown J, Lent B, Schmidt G, Sas G. Application of the Woman Abuse Screening Tool (WAST) and WAST-short in the family practice setting. J Fam Pract 2000;49:896-903.
15. Sherin K, Sinacore J, Li X, et al. HITS: a short domestic violence screening tool for use in a family practice setting. Fam Med 1998;30:508-12.
16. National Advisory Committee of FVPF. National consensus guidelines: on identifying and responding to domestic violence victimization in the health care setting. San Francisco: Family Violence Prevention Fund, 2002.
17. Davies J, Lyon E, Monti-Cantania D. Safety planning with battered women: complex lives, difficult choices. Thousand Oaks, CA: SAGE Publications, 1998.
Don’t be fooled by hypochondria
A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.
We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.
WORKING AS A TEAM
Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:
- offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
- set appropriate time limits and guidelines for the patient’s care
- dissuade patients from “doctor shopping”
- set limits on how often patients may visit their doctors and request reassurance.
Hypochondriasis: Persistent, unwarranted distress
Hypochondriasis is an excessive and persistent fear or belief that one has a serious illness, despite medical reassurance and lack of diagnostic findings that would warrant the health concern. If a medical disorder is present, the distress and preoccupation exceed what the patient’s physician considers reasonable. Illness preoccupation is intense enough to cause great distress or to interfere with daily functioning and may cause the person to miss work or cancel social engagements.1
DSM-IV criteria. A patient’s fear or conviction that he or she has a serious health threat must persist at least 6 months and may be accompanied by specific somatic symptoms, vague symptoms,1 or no symptoms.2 Hypochondriacal preoccupation may be stable over time, where one illness concern dominates, or it may shift—from fear of AIDS to fear of a heart attack.
A common disorder. Hypochondriasis occurs in 4 to 6% of the general medical population. In psychiatric or medical clinics, women are identified as having hypochondriasis three to four times more often than men. Average age of onset is in the early 20s.3
For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”
A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.
DIAGNOSTIC FEATURES
Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).1-4
Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).5 Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.
Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).6 Patients with hypochondriasis are three times more likely than the general population to have personality disorders;6,7 the prognosis is believed to be more promising for patients without personality disorders.
Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.
HYPOCHONDRIASIS CHECKLIST
Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.
Table 1
Three common presentations of hypochondriasis
| Predominant symptom | Characterization |
|---|---|
| Disease conviction | Patient may appear delusional in believing he or she has a disease and in persistent efforts to find a doctor who will make the “accurate” diagnosis |
| Disease fear | Patient may avoid doctors because of fear associated with confirmation of a dreaded disease |
| Bodily preoccupation | Patient may complain of multiple somatic symptoms, which mask underlying fear or belief of having a serious disease |
Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.
Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,8 although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.
Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:
- If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
- If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.
Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.
Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.
Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:
- undergoing extensive medical tests
- seeking habitual reassurance from doctors and family
- consulting medical literature
- performing repeated body checks for perceived lumps or bumps
- avoiding activities that trigger their health-related stress.9
Table 2
How to distinguish somatoform disorders
| Disorder | Patient focuses on… |
|---|---|
| Hypochondriasis | physical symptoms’ meaning (abnormal cognition) |
| Somatization disorder | multiple unexplained physical symptoms (abnormal sensation) |
| Body dysmorphic disorder | perceived abnormal bodily appearance |
| Conversion disorder | motor or sensory function abnormalities that develop soon after life stressors or conflict |
| Pain disorder | intense pain, in which psychological factors contribute to pain onset, severity, or maintenance |
OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.
Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”
Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.
Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.
Table 3
Recommended dosages for treating primary hypochondriasis
| Drug | Starting dosage | Maximum dosage |
|---|---|---|
| Fluoxetine | 10 mg/d if panic symptoms are present; 20 mg/d otherwise | 80 mg/d |
| Fluvoxamine | 50 mg at bedtime | 150 mg bid |
| Nefazodone | 100 mg bid | 300 mg bid |
| Paroxetine | 20 mg once daily | 50 mg once daily |
Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:
- Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.10 They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
- Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.
TREATING PRIMARY SYMPTOMS
Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.13 In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.10
Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).14
Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.
Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.15 CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.
Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.
Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.
Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.
Bottom line
Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.
Related resources
- Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
- Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
- Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.
Drug brand names
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Nefazodone • Serzone
- Paroxetine • Paxil
1. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC: American Psychiatric Association, 2000.
2. Task Force on DSM-IV. DSM-IV options book. Washington DC: American Psychiatric Association, 1991.
3. Barsky AJ, Wyshak G, Klerman GL, Lathan KS. The prevalence of hypochondriasis in medical outpatients. Soc Psychiatry Psychiatr Epidemiol 1990;25(2):89-94.
4. Salkovskis PM, Clark DM. Panic and hypochondriasis. Adv Behav Res Ther 1993;15:23-48.
5. Pilowsky I. Dimensions of hypochondriasis. Br J Psychiatry 1967;113(494):89-93.
6. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry 1992;49(2):101-8.
7. Kellner R. The prognosis of treated hypochondriasis: a clinical study. Acta Psychiatr Scand 1983;67(2):69-79.
8. Noyes R, Jr, Kathol RG, Fisher M, Phillips BM, et al. The validity of DSM-III-R hypochondriasis. Arch Gen Psychiatry 1993;50(12):961-70.
9. Fallon BA, Qureshi AI, Laje G, Klein B. Hypochondriasis and its relationship to obsessive-compulsive disorder. Psychiatr Clin North Am 2000;23(3):605-16.
10. Fallon BA, Schneier FR, Marshall R, Campeas R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull 1996;32:607-11.
11. Kellner R, Fava GA, Lisansky J, et al. Hypochondriacal fears and beliefs in DSM-III melancholia: changes with amitriptyline. J Affect Disord 1986;10(1):21-6.
12. Noyes R, Jr, Reich J, Clancy J, O’Gorman TW. Reduction in hypochondriasis with treatment of panic disorder. Br J Psychiatry 1986;149:631-5(erratum in Br J Psychiatry 1987;150:273).
13. Kjernisted KD, Ennis MW, Lander M. An open-label clinical trial of nefazodone in hypochondriasis. Psychosomatics 2002;43:290-4.
14. Fallon BA. Pharmacologic strategies for hypochondriasis. In: Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady. New York: Oxford University Press, 2001;329-51.
15. Warwick HMC, Salkovskis PM. Hypochondriasis. In: Scott J, Williams JMG, Beck AT (eds). Cognitive therapy in clinical practice: an illustrative casebook. London; Routledge, 1989;78-102.
A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.
We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.
WORKING AS A TEAM
Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:
- offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
- set appropriate time limits and guidelines for the patient’s care
- dissuade patients from “doctor shopping”
- set limits on how often patients may visit their doctors and request reassurance.
Hypochondriasis: Persistent, unwarranted distress
Hypochondriasis is an excessive and persistent fear or belief that one has a serious illness, despite medical reassurance and lack of diagnostic findings that would warrant the health concern. If a medical disorder is present, the distress and preoccupation exceed what the patient’s physician considers reasonable. Illness preoccupation is intense enough to cause great distress or to interfere with daily functioning and may cause the person to miss work or cancel social engagements.1
DSM-IV criteria. A patient’s fear or conviction that he or she has a serious health threat must persist at least 6 months and may be accompanied by specific somatic symptoms, vague symptoms,1 or no symptoms.2 Hypochondriacal preoccupation may be stable over time, where one illness concern dominates, or it may shift—from fear of AIDS to fear of a heart attack.
A common disorder. Hypochondriasis occurs in 4 to 6% of the general medical population. In psychiatric or medical clinics, women are identified as having hypochondriasis three to four times more often than men. Average age of onset is in the early 20s.3
For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”
A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.
DIAGNOSTIC FEATURES
Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).1-4
Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).5 Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.
Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).6 Patients with hypochondriasis are three times more likely than the general population to have personality disorders;6,7 the prognosis is believed to be more promising for patients without personality disorders.
Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.
HYPOCHONDRIASIS CHECKLIST
Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.
Table 1
Three common presentations of hypochondriasis
| Predominant symptom | Characterization |
|---|---|
| Disease conviction | Patient may appear delusional in believing he or she has a disease and in persistent efforts to find a doctor who will make the “accurate” diagnosis |
| Disease fear | Patient may avoid doctors because of fear associated with confirmation of a dreaded disease |
| Bodily preoccupation | Patient may complain of multiple somatic symptoms, which mask underlying fear or belief of having a serious disease |
Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.
Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,8 although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.
Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:
- If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
- If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.
Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.
Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.
Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:
- undergoing extensive medical tests
- seeking habitual reassurance from doctors and family
- consulting medical literature
- performing repeated body checks for perceived lumps or bumps
- avoiding activities that trigger their health-related stress.9
Table 2
How to distinguish somatoform disorders
| Disorder | Patient focuses on… |
|---|---|
| Hypochondriasis | physical symptoms’ meaning (abnormal cognition) |
| Somatization disorder | multiple unexplained physical symptoms (abnormal sensation) |
| Body dysmorphic disorder | perceived abnormal bodily appearance |
| Conversion disorder | motor or sensory function abnormalities that develop soon after life stressors or conflict |
| Pain disorder | intense pain, in which psychological factors contribute to pain onset, severity, or maintenance |
OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.
Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”
Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.
Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.
Table 3
Recommended dosages for treating primary hypochondriasis
| Drug | Starting dosage | Maximum dosage |
|---|---|---|
| Fluoxetine | 10 mg/d if panic symptoms are present; 20 mg/d otherwise | 80 mg/d |
| Fluvoxamine | 50 mg at bedtime | 150 mg bid |
| Nefazodone | 100 mg bid | 300 mg bid |
| Paroxetine | 20 mg once daily | 50 mg once daily |
Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:
- Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.10 They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
- Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.
TREATING PRIMARY SYMPTOMS
Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.13 In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.10
Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).14
Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.
Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.15 CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.
Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.
Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.
Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.
Bottom line
Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.
Related resources
- Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
- Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
- Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.
Drug brand names
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Nefazodone • Serzone
- Paroxetine • Paxil
A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.
We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.
WORKING AS A TEAM
Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:
- offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
- set appropriate time limits and guidelines for the patient’s care
- dissuade patients from “doctor shopping”
- set limits on how often patients may visit their doctors and request reassurance.
Hypochondriasis: Persistent, unwarranted distress
Hypochondriasis is an excessive and persistent fear or belief that one has a serious illness, despite medical reassurance and lack of diagnostic findings that would warrant the health concern. If a medical disorder is present, the distress and preoccupation exceed what the patient’s physician considers reasonable. Illness preoccupation is intense enough to cause great distress or to interfere with daily functioning and may cause the person to miss work or cancel social engagements.1
DSM-IV criteria. A patient’s fear or conviction that he or she has a serious health threat must persist at least 6 months and may be accompanied by specific somatic symptoms, vague symptoms,1 or no symptoms.2 Hypochondriacal preoccupation may be stable over time, where one illness concern dominates, or it may shift—from fear of AIDS to fear of a heart attack.
A common disorder. Hypochondriasis occurs in 4 to 6% of the general medical population. In psychiatric or medical clinics, women are identified as having hypochondriasis three to four times more often than men. Average age of onset is in the early 20s.3
For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”
A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.
DIAGNOSTIC FEATURES
Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).1-4
Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).5 Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.
Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).6 Patients with hypochondriasis are three times more likely than the general population to have personality disorders;6,7 the prognosis is believed to be more promising for patients without personality disorders.
Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.
HYPOCHONDRIASIS CHECKLIST
Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.
Table 1
Three common presentations of hypochondriasis
| Predominant symptom | Characterization |
|---|---|
| Disease conviction | Patient may appear delusional in believing he or she has a disease and in persistent efforts to find a doctor who will make the “accurate” diagnosis |
| Disease fear | Patient may avoid doctors because of fear associated with confirmation of a dreaded disease |
| Bodily preoccupation | Patient may complain of multiple somatic symptoms, which mask underlying fear or belief of having a serious disease |
Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.
Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,8 although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.
Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:
- If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
- If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.
Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.
Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.
Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:
- undergoing extensive medical tests
- seeking habitual reassurance from doctors and family
- consulting medical literature
- performing repeated body checks for perceived lumps or bumps
- avoiding activities that trigger their health-related stress.9
Table 2
How to distinguish somatoform disorders
| Disorder | Patient focuses on… |
|---|---|
| Hypochondriasis | physical symptoms’ meaning (abnormal cognition) |
| Somatization disorder | multiple unexplained physical symptoms (abnormal sensation) |
| Body dysmorphic disorder | perceived abnormal bodily appearance |
| Conversion disorder | motor or sensory function abnormalities that develop soon after life stressors or conflict |
| Pain disorder | intense pain, in which psychological factors contribute to pain onset, severity, or maintenance |
OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.
Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”
Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.
Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.
Table 3
Recommended dosages for treating primary hypochondriasis
| Drug | Starting dosage | Maximum dosage |
|---|---|---|
| Fluoxetine | 10 mg/d if panic symptoms are present; 20 mg/d otherwise | 80 mg/d |
| Fluvoxamine | 50 mg at bedtime | 150 mg bid |
| Nefazodone | 100 mg bid | 300 mg bid |
| Paroxetine | 20 mg once daily | 50 mg once daily |
Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:
- Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.10 They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
- Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.
TREATING PRIMARY SYMPTOMS
Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.13 In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.10
Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).14
Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.
Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.15 CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.
Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.
Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.
Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.
Bottom line
Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.
Related resources
- Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
- Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
- Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.
Drug brand names
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Nefazodone • Serzone
- Paroxetine • Paxil
1. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC: American Psychiatric Association, 2000.
2. Task Force on DSM-IV. DSM-IV options book. Washington DC: American Psychiatric Association, 1991.
3. Barsky AJ, Wyshak G, Klerman GL, Lathan KS. The prevalence of hypochondriasis in medical outpatients. Soc Psychiatry Psychiatr Epidemiol 1990;25(2):89-94.
4. Salkovskis PM, Clark DM. Panic and hypochondriasis. Adv Behav Res Ther 1993;15:23-48.
5. Pilowsky I. Dimensions of hypochondriasis. Br J Psychiatry 1967;113(494):89-93.
6. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry 1992;49(2):101-8.
7. Kellner R. The prognosis of treated hypochondriasis: a clinical study. Acta Psychiatr Scand 1983;67(2):69-79.
8. Noyes R, Jr, Kathol RG, Fisher M, Phillips BM, et al. The validity of DSM-III-R hypochondriasis. Arch Gen Psychiatry 1993;50(12):961-70.
9. Fallon BA, Qureshi AI, Laje G, Klein B. Hypochondriasis and its relationship to obsessive-compulsive disorder. Psychiatr Clin North Am 2000;23(3):605-16.
10. Fallon BA, Schneier FR, Marshall R, Campeas R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull 1996;32:607-11.
11. Kellner R, Fava GA, Lisansky J, et al. Hypochondriacal fears and beliefs in DSM-III melancholia: changes with amitriptyline. J Affect Disord 1986;10(1):21-6.
12. Noyes R, Jr, Reich J, Clancy J, O’Gorman TW. Reduction in hypochondriasis with treatment of panic disorder. Br J Psychiatry 1986;149:631-5(erratum in Br J Psychiatry 1987;150:273).
13. Kjernisted KD, Ennis MW, Lander M. An open-label clinical trial of nefazodone in hypochondriasis. Psychosomatics 2002;43:290-4.
14. Fallon BA. Pharmacologic strategies for hypochondriasis. In: Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady. New York: Oxford University Press, 2001;329-51.
15. Warwick HMC, Salkovskis PM. Hypochondriasis. In: Scott J, Williams JMG, Beck AT (eds). Cognitive therapy in clinical practice: an illustrative casebook. London; Routledge, 1989;78-102.
1. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC: American Psychiatric Association, 2000.
2. Task Force on DSM-IV. DSM-IV options book. Washington DC: American Psychiatric Association, 1991.
3. Barsky AJ, Wyshak G, Klerman GL, Lathan KS. The prevalence of hypochondriasis in medical outpatients. Soc Psychiatry Psychiatr Epidemiol 1990;25(2):89-94.
4. Salkovskis PM, Clark DM. Panic and hypochondriasis. Adv Behav Res Ther 1993;15:23-48.
5. Pilowsky I. Dimensions of hypochondriasis. Br J Psychiatry 1967;113(494):89-93.
6. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry 1992;49(2):101-8.
7. Kellner R. The prognosis of treated hypochondriasis: a clinical study. Acta Psychiatr Scand 1983;67(2):69-79.
8. Noyes R, Jr, Kathol RG, Fisher M, Phillips BM, et al. The validity of DSM-III-R hypochondriasis. Arch Gen Psychiatry 1993;50(12):961-70.
9. Fallon BA, Qureshi AI, Laje G, Klein B. Hypochondriasis and its relationship to obsessive-compulsive disorder. Psychiatr Clin North Am 2000;23(3):605-16.
10. Fallon BA, Schneier FR, Marshall R, Campeas R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull 1996;32:607-11.
11. Kellner R, Fava GA, Lisansky J, et al. Hypochondriacal fears and beliefs in DSM-III melancholia: changes with amitriptyline. J Affect Disord 1986;10(1):21-6.
12. Noyes R, Jr, Reich J, Clancy J, O’Gorman TW. Reduction in hypochondriasis with treatment of panic disorder. Br J Psychiatry 1986;149:631-5(erratum in Br J Psychiatry 1987;150:273).
13. Kjernisted KD, Ennis MW, Lander M. An open-label clinical trial of nefazodone in hypochondriasis. Psychosomatics 2002;43:290-4.
14. Fallon BA. Pharmacologic strategies for hypochondriasis. In: Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady. New York: Oxford University Press, 2001;329-51.
15. Warwick HMC, Salkovskis PM. Hypochondriasis. In: Scott J, Williams JMG, Beck AT (eds). Cognitive therapy in clinical practice: an illustrative casebook. London; Routledge, 1989;78-102.
Psychosis or ‘cultural paranoia?’
Culture-related anxiety and paranoia can be difficult to treat because they are reinforced by socially normative practices and beliefs.1 As in the two cases described below, psychiatric patients with deep underlying mistrust may view a therapist from another culture—even though well-meaning—as a racist oppressor.
The clinician’s approach to therapy can help prevent cultural misunderstandings and—most important—misdiagnosis (Box).
MR. A’S CASE: ‘She’s out to get me’
Mr. A, age 38 and African-American, was admitted to the inpatient psychiatry service with neurovegetative depressive symptoms and apparent delusional thinking.
His wife of 20 years, also African-American, was concerned that he was becoming increasingly irrational. She said he accused her of conspiring with his predominantly white supervisors to “bring about my destruction.”
Mr. A consented to admission, acknowledging to the psychiatrist that he had felt depressed and at times considered suicide. He complained that he had recently experienced several unusual “happenings:”
- Pointing to recent weight loss, Mr. A feared someone was poisoning his food or that he had swallowed a “tracking” device.
- Mr. A feared that workers who were repairing flood damage in his home were sent to kill him. He remained home during the project, but the fear drove him to a panic attack.
- After more than 18 years working for the same employer with no notable interpersonal difficulties, Mr. A suddenly could not get along with his coworkers. He accused one colleague of following him to a restaurant.
Mr. A had no previous psychiatric disorder, but some distant relatives had schizophrenia. He was diagnosed as having major depressive disorder, severe with psychotic features; delusional disorder was ruled out. He was prescribed olanzapine, 10 mg at bedtime, and fluoxetine, 20 mg/d.
In the hospital, Mr. A spoke normally with no agitation, increased activity, or evidence of racing thoughts. In group therapy, he explained that he felt “confused.” He also disclosed that a recent extramarital affair left him feeling extremely guilty.
- Set treatment goals at the start. Make sure you and the patient agree on these goals.
- Make sure the patient understands he or she can cease treatment at any time. Stress that you are there simply to help achieve the patient’s stated goals.
- Avoid direct empathic statements during psychotherapy (eg, “You feel angry”); the patient may suspect you are imposing your beliefs. Indirect statements (eg, “It wouldn’t surprise me if you felt angry”) convey curiosity about the patient’s reactions and invite further discussion.
- Admit when you do not understand a culturally specific colloquialism or mannerism, and ask the patient to explain it at the next session. This usually encourages the patient to keep the follow-up appointment.
A few days later, Mr. A’s suicidal and paranoid ideations disappeared. He expressed anger only while discussing his diagnosis with the attending psychiatrist, who is white. The patient feared that being diagnosed with a psychotic illness would hurt his career. He admitted he felt depressed, but insisted that he now realized his paranoid thoughts were irrational.
Mr. A was discharged after 6 days. He remained on fluoxetine, 20 mg/d; olanzapine was discontinued due to excessive sedation.
The patient also entered insight-oriented psychotherapy to address his depression. Mr. A and the therapist, who is white, spent most of the initial sessions discussing their racial differences. At one point, Mr. A complained to the therapist that white physicians were trying to “railroad” him because of his race.
After nine sessions, Mr. A revealed that he felt isolated at an early age, thinking that others “will use what they know about me against me.” He described growing up in a predominantly black community where most of his neighbors felt oppressed by white people. As therapy progressed, Mr. A realized that this experience influenced his attitudes about race, and that his extramarital affair destroyed his sense of self-trust, which may have fueled his mistrust of others.
After 20 sessions, his marriage and work relationships were stable and his overall mood was much improved. His Outcome Questionnaire 45.2 score decreased across 12 months from 88 (moderate to severe distress) to 55 (level of distress similar to that of non-patients). Delusional behavior has not re-emerged, although his comments continue to reflect mistrust of his supervisors and of white people in general.
What would your diagnosis be? What clues would you gather from Mr. A’s pretreatment behavior and from his progress in therapy?
Dr. Benzick’s observations
Mr. A’s diagnosis upon admission reflected the psychiatrist’s belief that he suffered fixed delusions. By definition, however, a delusion is a false belief that is not “ordinarily accepted by other members of the person’s culture or subculture.”2
Growing up, Mr. A shared his neighbors’ suspicion of white people. Further, his overvalued conspiracy theory involving his wife might have projected his own guilt over his infidelity onto a pre-existing paranoid personality.
Based on his psychosocial history, rapid progress in psychotherapy, and marked improvement in Outcome Questionnaire 45.2 scores, Mr. A does not have a personality disorder. What’s more, paranoid ideation is not uncommon in African-Americans with depressive symptoms, as demonstrated by Bazargan et al. 3
Mr. A’s diagnosis was changed to major depressive disorder, moderate, in partial remission. He is still seen approximately every 6 weeks for medication maintenance; he continues taking fluoxetine, 20 mg/d.
MR. B’S CASE: ‘Singled’ out
Mr. B, age 42 and African-American, was referred from an alcohol rehabilitation program to the psychiatry unit after exhibiting depressive and paranoid symptoms.
After 17 years with his employer, he started clashing with his supervisors and coworkers—most of whom are white. He claimed his colleagues were talking behind his back, jealous that he is single and spends his evenings at nightclubs. He alleged that his bosses were singling him out after he was transferred to another department and reprimanded for arriving late to work. Resultant worry about job security brought on panic symptoms (shortness of breath, lightheadedness, dissociative feelings, and palpitations).
Upon further questioning, Mr. B said he felt depressed and isolated. He had been prescribed nortriptyline 2 years ago but discontinued it after a few weeks because of side effects.
Mr. B said that not having a steady companion contributed to his depression and alcohol use. He had been drinking heavily for about 3 years, consuming at least a six-pack daily. He acknowledged that his suspicion of his white coworkers long preceded his alcoholism. Still, he did not see this mistrust as a problem.
Mr. B was diagnosed with major depressive disorder, severe with psychotic features. Treatment consisted of:
- paroxetine, 20 mg/d
- attendance at Alcoholics Anonymous meetings (at least three meetings per week were recommended)
- and 12 sessions of interpersonal psychotherapy. During these sessions, the therapist began to uncover the roots of Mr. B’s symptoms.
School days. Mr. B described how, as a little boy, he once watched his mother being beaten by his drunken father. He told the therapist that the beatings occurred frequently.
When he was age 5, Mr. B’s parents divorced and he and his mother moved to a mostly white Midwest neighborhood so that he could attend a high school with an advanced music program (he was honored for exceptional talent on several instruments).
In his youth, Mr. B’s mother repeatedly told him that teachers and students would treat him “differently” because of his color, though she never explained what she meant. While in high school, he began to worry about his social functioning, appearance, work performance, and future accomplishments.
After four psychotherapy sessions, Mr. B revealed that while in grade school, he was sexually assaulted by an older white boy. For more than 30 years, he had told no one. He denied hyperautonomic and re-experiencing symptoms but realized that this incident may have kept him from starting a romantic relationship.
After psychotherapy, Mr. B reported reduced depression and increased social interaction. His Beck Depression Inventory score dropped from 23 (moderate depression) to 4 (normal mood), and his Beck Anxiety Inventory score improved from 33 (moderate anxiety) to 3 (very low anxiety). He has been sober for 6 months and handles stress more effectively, although his mistrust toward coworkers is still apparent.
How would you diagnose Mr. B? Do his symptoms characterize “psychotic features” or an anxiety or alcohol-related disorder?
Dr. Benzick’s observations
Mr. B’s case illustrates how deep-seated cultural perceptions and past trauma together can cause severe anxiety—and how that anxiety can be misperceived as psychosis.4 Anxiety also can manifest as paranoia in “psychotically vulnerable” individuals.5-7
Chronic anxiety seemed to cause Mr. B’s depressed mood and social withdrawal. Several anxiety disorder diagnoses were considered, including:
- panic disorder
- posttraumatic stress disorder
- social phobia
- alcohol-induced anxiety disorder
- and generalized anxiety disorder.
Mr. B, however, exhibited no evidence of repeated episodic anxiety, nor did he describe reexperiencing phenomena. His anxiety extended beyond social situations and preceded his heavy alcohol consumption. Paranoid personality disorder was also considered, but Mr. B sought relationships and lacked the angry, unforgiving qualities associated with this pathology. Finally, a battery of psychological tests did not reveal frank psychosis but suggested an avoidant personality style.
Mr. B’s diagnosis was changed to generalized anxiety disorder. He requested a trial off medications during the latter stages of therapy, but his severe anxiety returned. He was then prescribed venlafaxine, 37.5 mg/d titrated to 225 mg/d across 3 weeks. His anxiety symptoms again abated.
How could Mr A’s and Mr. B’s doctors have avoided their initial misdiagnoses?
Dr. Benzick’s observations
“Cultural paranoia” describes adaptive or healthy responses by African-Americans living in a society they perceive as racially prejudiced.8 Several researchers have studied this concept of protecting self-esteem by blaming an external source for negative events. Women who plausibly attribute unflattering feedback to prejudice exhibit higher self-esteem.9 A person who believes he or she is a target of discrimination identifies more strongly with his or her racial or ethnic group, leading to reduced depression, higher self-esteem, and improved psychological adjustment.9
Perceived discrimination, however, can also elicit feelings of hopelessness and resignation when it leads to widespread bias against the alleged oppressing racial or ethnic group. The resulting sense of social exclusion has been linked to lower self-esteem and higher rates of anxiety and depression.9 Thus, the individual’s environment and ability to develop relationships will determine whether “cultural paranoia” is “adaptive.”
Paranoia or prejudice? Distinguishing culturally sanctioned “paranoia” from “prejudice” can be difficult. “Prejudice” is defined as the negative evaluation of a group or individual based on group membership.10 “Paranoia” (using the DSM-IV definition of “paranoid ideation”) is a belief of less than delusional intensity “involving suspiciousness or the belief that one is being harassed, persecuted, or unfairly treated.”2
So while an individual may be prejudiced toward a group, cultural paranoia would exist only if other family members or acquaintances believe the other group is conspiring against them. Additionally, while prejudice tends to be ego-syntonic,11 paranoia is more distressing because it produces heightened vigilance and possibly fear.
Both cases describe how a lack of cultural understanding between African-American patients and physicians of other ethnicities or races can lead to misdiagnosis of psychosis.12 They also illustrate that while prejudice may be tightly focused (eg, hatred of anyone from a specific racial or ethnic group), paranoid ideation can be generalized. For example, Mr. A believed that his wife, an African-American, conspired with his white supervisors against him.
Mr. A’s and Mr. B’s depressive and anxiety symptoms unmasked longstanding, deeply rooted beliefs. Both patients’ neurovegetative symptoms responded to medication and brief psychotherapy, and both returned to prior levels of functioning. The underlying mistrust remained, however.
Related resources
- Lu FG. Annotated bibliography on cultural psychiatry and related topics-June 2003. Available at: http://www.admsep.org/culture.html. Accessed July 18, 2003.
- Forsell Y, Henderson S. Epidemiology of paranoid disorders in an elderly population. Br J Psychiatry 1998; 172:429-32.
Drug brand names
- Fluoxetine • Prozac
- Olanzapine • Zyprexa
- Nortriptyline • Aventyl, Pamelor
- Paroxetine • Paxil
- Venlafaxine • Effexor
Disclosure
Dr. Benzick reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Kirmayer LJ, Young A, Hayton BC. The cultural context of anxiety disorders. Psychiatr Clin North Am 1995;18:503-21.
2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC. American Psychiatric Association, 2000.
3. Bazargan M, Bazargan S, King L. Paranoid ideation among elderly African American persons. Gerontologist 2001;41:366-73.
4. Newhill CE. The role of culture in the development of paranoid symptomatology. Am J Orthopsychiatry 1990;60:176-85.
5. Bermanzohn PC, Arlow PB, Pitch RJ, Siris SG. Panic and paranoia (letter). J Clin Psychiatry 1997;58:325.-
6. Bermanzohn PC, Arlow PB, Albert C, Siris SG. Relationship of panic attacks to paranoia. Am J Psychiatry 1999;156:1469.-
7. Galynker I, Ieronimo C, Perez-Acquino A, et al. Panic attacks with psychotic features. J Clin Psychiatry 1996;57:402-6.
8. Ridley CR. Clinical treatment of the nondisclosing black client. A therapeutic paradox. Am Psychol 1984;39:1233-43.
9. Branscombe NR, Schmitt MT, Harvey RD. Perceiving pervasive discrimination among African Americans: implications for group identification and well-being. J Pers Soc Psychol 1999;77:135-49.
10. Crandall CS, Eshleman A, O’Brien L. Social norms and suppression of prejudice: the struggle for internalization. J Pers Soc Psychol 2002;82:359-78.
11. Ryan MK, Buirski P. Prejudice as a function of self-organization. Psychoanalytic Psychol 2001;18:21-36.
12. Whaley AL. Psychometric analysis of the cultural mistrust inventory with a black psychiatric inpatient sample. J Clin Psychology 2002;58:383-96.
Culture-related anxiety and paranoia can be difficult to treat because they are reinforced by socially normative practices and beliefs.1 As in the two cases described below, psychiatric patients with deep underlying mistrust may view a therapist from another culture—even though well-meaning—as a racist oppressor.
The clinician’s approach to therapy can help prevent cultural misunderstandings and—most important—misdiagnosis (Box).
MR. A’S CASE: ‘She’s out to get me’
Mr. A, age 38 and African-American, was admitted to the inpatient psychiatry service with neurovegetative depressive symptoms and apparent delusional thinking.
His wife of 20 years, also African-American, was concerned that he was becoming increasingly irrational. She said he accused her of conspiring with his predominantly white supervisors to “bring about my destruction.”
Mr. A consented to admission, acknowledging to the psychiatrist that he had felt depressed and at times considered suicide. He complained that he had recently experienced several unusual “happenings:”
- Pointing to recent weight loss, Mr. A feared someone was poisoning his food or that he had swallowed a “tracking” device.
- Mr. A feared that workers who were repairing flood damage in his home were sent to kill him. He remained home during the project, but the fear drove him to a panic attack.
- After more than 18 years working for the same employer with no notable interpersonal difficulties, Mr. A suddenly could not get along with his coworkers. He accused one colleague of following him to a restaurant.
Mr. A had no previous psychiatric disorder, but some distant relatives had schizophrenia. He was diagnosed as having major depressive disorder, severe with psychotic features; delusional disorder was ruled out. He was prescribed olanzapine, 10 mg at bedtime, and fluoxetine, 20 mg/d.
In the hospital, Mr. A spoke normally with no agitation, increased activity, or evidence of racing thoughts. In group therapy, he explained that he felt “confused.” He also disclosed that a recent extramarital affair left him feeling extremely guilty.
- Set treatment goals at the start. Make sure you and the patient agree on these goals.
- Make sure the patient understands he or she can cease treatment at any time. Stress that you are there simply to help achieve the patient’s stated goals.
- Avoid direct empathic statements during psychotherapy (eg, “You feel angry”); the patient may suspect you are imposing your beliefs. Indirect statements (eg, “It wouldn’t surprise me if you felt angry”) convey curiosity about the patient’s reactions and invite further discussion.
- Admit when you do not understand a culturally specific colloquialism or mannerism, and ask the patient to explain it at the next session. This usually encourages the patient to keep the follow-up appointment.
A few days later, Mr. A’s suicidal and paranoid ideations disappeared. He expressed anger only while discussing his diagnosis with the attending psychiatrist, who is white. The patient feared that being diagnosed with a psychotic illness would hurt his career. He admitted he felt depressed, but insisted that he now realized his paranoid thoughts were irrational.
Mr. A was discharged after 6 days. He remained on fluoxetine, 20 mg/d; olanzapine was discontinued due to excessive sedation.
The patient also entered insight-oriented psychotherapy to address his depression. Mr. A and the therapist, who is white, spent most of the initial sessions discussing their racial differences. At one point, Mr. A complained to the therapist that white physicians were trying to “railroad” him because of his race.
After nine sessions, Mr. A revealed that he felt isolated at an early age, thinking that others “will use what they know about me against me.” He described growing up in a predominantly black community where most of his neighbors felt oppressed by white people. As therapy progressed, Mr. A realized that this experience influenced his attitudes about race, and that his extramarital affair destroyed his sense of self-trust, which may have fueled his mistrust of others.
After 20 sessions, his marriage and work relationships were stable and his overall mood was much improved. His Outcome Questionnaire 45.2 score decreased across 12 months from 88 (moderate to severe distress) to 55 (level of distress similar to that of non-patients). Delusional behavior has not re-emerged, although his comments continue to reflect mistrust of his supervisors and of white people in general.
What would your diagnosis be? What clues would you gather from Mr. A’s pretreatment behavior and from his progress in therapy?
Dr. Benzick’s observations
Mr. A’s diagnosis upon admission reflected the psychiatrist’s belief that he suffered fixed delusions. By definition, however, a delusion is a false belief that is not “ordinarily accepted by other members of the person’s culture or subculture.”2
Growing up, Mr. A shared his neighbors’ suspicion of white people. Further, his overvalued conspiracy theory involving his wife might have projected his own guilt over his infidelity onto a pre-existing paranoid personality.
Based on his psychosocial history, rapid progress in psychotherapy, and marked improvement in Outcome Questionnaire 45.2 scores, Mr. A does not have a personality disorder. What’s more, paranoid ideation is not uncommon in African-Americans with depressive symptoms, as demonstrated by Bazargan et al. 3
Mr. A’s diagnosis was changed to major depressive disorder, moderate, in partial remission. He is still seen approximately every 6 weeks for medication maintenance; he continues taking fluoxetine, 20 mg/d.
MR. B’S CASE: ‘Singled’ out
Mr. B, age 42 and African-American, was referred from an alcohol rehabilitation program to the psychiatry unit after exhibiting depressive and paranoid symptoms.
After 17 years with his employer, he started clashing with his supervisors and coworkers—most of whom are white. He claimed his colleagues were talking behind his back, jealous that he is single and spends his evenings at nightclubs. He alleged that his bosses were singling him out after he was transferred to another department and reprimanded for arriving late to work. Resultant worry about job security brought on panic symptoms (shortness of breath, lightheadedness, dissociative feelings, and palpitations).
Upon further questioning, Mr. B said he felt depressed and isolated. He had been prescribed nortriptyline 2 years ago but discontinued it after a few weeks because of side effects.
Mr. B said that not having a steady companion contributed to his depression and alcohol use. He had been drinking heavily for about 3 years, consuming at least a six-pack daily. He acknowledged that his suspicion of his white coworkers long preceded his alcoholism. Still, he did not see this mistrust as a problem.
Mr. B was diagnosed with major depressive disorder, severe with psychotic features. Treatment consisted of:
- paroxetine, 20 mg/d
- attendance at Alcoholics Anonymous meetings (at least three meetings per week were recommended)
- and 12 sessions of interpersonal psychotherapy. During these sessions, the therapist began to uncover the roots of Mr. B’s symptoms.
School days. Mr. B described how, as a little boy, he once watched his mother being beaten by his drunken father. He told the therapist that the beatings occurred frequently.
When he was age 5, Mr. B’s parents divorced and he and his mother moved to a mostly white Midwest neighborhood so that he could attend a high school with an advanced music program (he was honored for exceptional talent on several instruments).
In his youth, Mr. B’s mother repeatedly told him that teachers and students would treat him “differently” because of his color, though she never explained what she meant. While in high school, he began to worry about his social functioning, appearance, work performance, and future accomplishments.
After four psychotherapy sessions, Mr. B revealed that while in grade school, he was sexually assaulted by an older white boy. For more than 30 years, he had told no one. He denied hyperautonomic and re-experiencing symptoms but realized that this incident may have kept him from starting a romantic relationship.
After psychotherapy, Mr. B reported reduced depression and increased social interaction. His Beck Depression Inventory score dropped from 23 (moderate depression) to 4 (normal mood), and his Beck Anxiety Inventory score improved from 33 (moderate anxiety) to 3 (very low anxiety). He has been sober for 6 months and handles stress more effectively, although his mistrust toward coworkers is still apparent.
How would you diagnose Mr. B? Do his symptoms characterize “psychotic features” or an anxiety or alcohol-related disorder?
Dr. Benzick’s observations
Mr. B’s case illustrates how deep-seated cultural perceptions and past trauma together can cause severe anxiety—and how that anxiety can be misperceived as psychosis.4 Anxiety also can manifest as paranoia in “psychotically vulnerable” individuals.5-7
Chronic anxiety seemed to cause Mr. B’s depressed mood and social withdrawal. Several anxiety disorder diagnoses were considered, including:
- panic disorder
- posttraumatic stress disorder
- social phobia
- alcohol-induced anxiety disorder
- and generalized anxiety disorder.
Mr. B, however, exhibited no evidence of repeated episodic anxiety, nor did he describe reexperiencing phenomena. His anxiety extended beyond social situations and preceded his heavy alcohol consumption. Paranoid personality disorder was also considered, but Mr. B sought relationships and lacked the angry, unforgiving qualities associated with this pathology. Finally, a battery of psychological tests did not reveal frank psychosis but suggested an avoidant personality style.
Mr. B’s diagnosis was changed to generalized anxiety disorder. He requested a trial off medications during the latter stages of therapy, but his severe anxiety returned. He was then prescribed venlafaxine, 37.5 mg/d titrated to 225 mg/d across 3 weeks. His anxiety symptoms again abated.
How could Mr A’s and Mr. B’s doctors have avoided their initial misdiagnoses?
Dr. Benzick’s observations
“Cultural paranoia” describes adaptive or healthy responses by African-Americans living in a society they perceive as racially prejudiced.8 Several researchers have studied this concept of protecting self-esteem by blaming an external source for negative events. Women who plausibly attribute unflattering feedback to prejudice exhibit higher self-esteem.9 A person who believes he or she is a target of discrimination identifies more strongly with his or her racial or ethnic group, leading to reduced depression, higher self-esteem, and improved psychological adjustment.9
Perceived discrimination, however, can also elicit feelings of hopelessness and resignation when it leads to widespread bias against the alleged oppressing racial or ethnic group. The resulting sense of social exclusion has been linked to lower self-esteem and higher rates of anxiety and depression.9 Thus, the individual’s environment and ability to develop relationships will determine whether “cultural paranoia” is “adaptive.”
Paranoia or prejudice? Distinguishing culturally sanctioned “paranoia” from “prejudice” can be difficult. “Prejudice” is defined as the negative evaluation of a group or individual based on group membership.10 “Paranoia” (using the DSM-IV definition of “paranoid ideation”) is a belief of less than delusional intensity “involving suspiciousness or the belief that one is being harassed, persecuted, or unfairly treated.”2
So while an individual may be prejudiced toward a group, cultural paranoia would exist only if other family members or acquaintances believe the other group is conspiring against them. Additionally, while prejudice tends to be ego-syntonic,11 paranoia is more distressing because it produces heightened vigilance and possibly fear.
Both cases describe how a lack of cultural understanding between African-American patients and physicians of other ethnicities or races can lead to misdiagnosis of psychosis.12 They also illustrate that while prejudice may be tightly focused (eg, hatred of anyone from a specific racial or ethnic group), paranoid ideation can be generalized. For example, Mr. A believed that his wife, an African-American, conspired with his white supervisors against him.
Mr. A’s and Mr. B’s depressive and anxiety symptoms unmasked longstanding, deeply rooted beliefs. Both patients’ neurovegetative symptoms responded to medication and brief psychotherapy, and both returned to prior levels of functioning. The underlying mistrust remained, however.
Related resources
- Lu FG. Annotated bibliography on cultural psychiatry and related topics-June 2003. Available at: http://www.admsep.org/culture.html. Accessed July 18, 2003.
- Forsell Y, Henderson S. Epidemiology of paranoid disorders in an elderly population. Br J Psychiatry 1998; 172:429-32.
Drug brand names
- Fluoxetine • Prozac
- Olanzapine • Zyprexa
- Nortriptyline • Aventyl, Pamelor
- Paroxetine • Paxil
- Venlafaxine • Effexor
Disclosure
Dr. Benzick reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
Culture-related anxiety and paranoia can be difficult to treat because they are reinforced by socially normative practices and beliefs.1 As in the two cases described below, psychiatric patients with deep underlying mistrust may view a therapist from another culture—even though well-meaning—as a racist oppressor.
The clinician’s approach to therapy can help prevent cultural misunderstandings and—most important—misdiagnosis (Box).
MR. A’S CASE: ‘She’s out to get me’
Mr. A, age 38 and African-American, was admitted to the inpatient psychiatry service with neurovegetative depressive symptoms and apparent delusional thinking.
His wife of 20 years, also African-American, was concerned that he was becoming increasingly irrational. She said he accused her of conspiring with his predominantly white supervisors to “bring about my destruction.”
Mr. A consented to admission, acknowledging to the psychiatrist that he had felt depressed and at times considered suicide. He complained that he had recently experienced several unusual “happenings:”
- Pointing to recent weight loss, Mr. A feared someone was poisoning his food or that he had swallowed a “tracking” device.
- Mr. A feared that workers who were repairing flood damage in his home were sent to kill him. He remained home during the project, but the fear drove him to a panic attack.
- After more than 18 years working for the same employer with no notable interpersonal difficulties, Mr. A suddenly could not get along with his coworkers. He accused one colleague of following him to a restaurant.
Mr. A had no previous psychiatric disorder, but some distant relatives had schizophrenia. He was diagnosed as having major depressive disorder, severe with psychotic features; delusional disorder was ruled out. He was prescribed olanzapine, 10 mg at bedtime, and fluoxetine, 20 mg/d.
In the hospital, Mr. A spoke normally with no agitation, increased activity, or evidence of racing thoughts. In group therapy, he explained that he felt “confused.” He also disclosed that a recent extramarital affair left him feeling extremely guilty.
- Set treatment goals at the start. Make sure you and the patient agree on these goals.
- Make sure the patient understands he or she can cease treatment at any time. Stress that you are there simply to help achieve the patient’s stated goals.
- Avoid direct empathic statements during psychotherapy (eg, “You feel angry”); the patient may suspect you are imposing your beliefs. Indirect statements (eg, “It wouldn’t surprise me if you felt angry”) convey curiosity about the patient’s reactions and invite further discussion.
- Admit when you do not understand a culturally specific colloquialism or mannerism, and ask the patient to explain it at the next session. This usually encourages the patient to keep the follow-up appointment.
A few days later, Mr. A’s suicidal and paranoid ideations disappeared. He expressed anger only while discussing his diagnosis with the attending psychiatrist, who is white. The patient feared that being diagnosed with a psychotic illness would hurt his career. He admitted he felt depressed, but insisted that he now realized his paranoid thoughts were irrational.
Mr. A was discharged after 6 days. He remained on fluoxetine, 20 mg/d; olanzapine was discontinued due to excessive sedation.
The patient also entered insight-oriented psychotherapy to address his depression. Mr. A and the therapist, who is white, spent most of the initial sessions discussing their racial differences. At one point, Mr. A complained to the therapist that white physicians were trying to “railroad” him because of his race.
After nine sessions, Mr. A revealed that he felt isolated at an early age, thinking that others “will use what they know about me against me.” He described growing up in a predominantly black community where most of his neighbors felt oppressed by white people. As therapy progressed, Mr. A realized that this experience influenced his attitudes about race, and that his extramarital affair destroyed his sense of self-trust, which may have fueled his mistrust of others.
After 20 sessions, his marriage and work relationships were stable and his overall mood was much improved. His Outcome Questionnaire 45.2 score decreased across 12 months from 88 (moderate to severe distress) to 55 (level of distress similar to that of non-patients). Delusional behavior has not re-emerged, although his comments continue to reflect mistrust of his supervisors and of white people in general.
What would your diagnosis be? What clues would you gather from Mr. A’s pretreatment behavior and from his progress in therapy?
Dr. Benzick’s observations
Mr. A’s diagnosis upon admission reflected the psychiatrist’s belief that he suffered fixed delusions. By definition, however, a delusion is a false belief that is not “ordinarily accepted by other members of the person’s culture or subculture.”2
Growing up, Mr. A shared his neighbors’ suspicion of white people. Further, his overvalued conspiracy theory involving his wife might have projected his own guilt over his infidelity onto a pre-existing paranoid personality.
Based on his psychosocial history, rapid progress in psychotherapy, and marked improvement in Outcome Questionnaire 45.2 scores, Mr. A does not have a personality disorder. What’s more, paranoid ideation is not uncommon in African-Americans with depressive symptoms, as demonstrated by Bazargan et al. 3
Mr. A’s diagnosis was changed to major depressive disorder, moderate, in partial remission. He is still seen approximately every 6 weeks for medication maintenance; he continues taking fluoxetine, 20 mg/d.
MR. B’S CASE: ‘Singled’ out
Mr. B, age 42 and African-American, was referred from an alcohol rehabilitation program to the psychiatry unit after exhibiting depressive and paranoid symptoms.
After 17 years with his employer, he started clashing with his supervisors and coworkers—most of whom are white. He claimed his colleagues were talking behind his back, jealous that he is single and spends his evenings at nightclubs. He alleged that his bosses were singling him out after he was transferred to another department and reprimanded for arriving late to work. Resultant worry about job security brought on panic symptoms (shortness of breath, lightheadedness, dissociative feelings, and palpitations).
Upon further questioning, Mr. B said he felt depressed and isolated. He had been prescribed nortriptyline 2 years ago but discontinued it after a few weeks because of side effects.
Mr. B said that not having a steady companion contributed to his depression and alcohol use. He had been drinking heavily for about 3 years, consuming at least a six-pack daily. He acknowledged that his suspicion of his white coworkers long preceded his alcoholism. Still, he did not see this mistrust as a problem.
Mr. B was diagnosed with major depressive disorder, severe with psychotic features. Treatment consisted of:
- paroxetine, 20 mg/d
- attendance at Alcoholics Anonymous meetings (at least three meetings per week were recommended)
- and 12 sessions of interpersonal psychotherapy. During these sessions, the therapist began to uncover the roots of Mr. B’s symptoms.
School days. Mr. B described how, as a little boy, he once watched his mother being beaten by his drunken father. He told the therapist that the beatings occurred frequently.
When he was age 5, Mr. B’s parents divorced and he and his mother moved to a mostly white Midwest neighborhood so that he could attend a high school with an advanced music program (he was honored for exceptional talent on several instruments).
In his youth, Mr. B’s mother repeatedly told him that teachers and students would treat him “differently” because of his color, though she never explained what she meant. While in high school, he began to worry about his social functioning, appearance, work performance, and future accomplishments.
After four psychotherapy sessions, Mr. B revealed that while in grade school, he was sexually assaulted by an older white boy. For more than 30 years, he had told no one. He denied hyperautonomic and re-experiencing symptoms but realized that this incident may have kept him from starting a romantic relationship.
After psychotherapy, Mr. B reported reduced depression and increased social interaction. His Beck Depression Inventory score dropped from 23 (moderate depression) to 4 (normal mood), and his Beck Anxiety Inventory score improved from 33 (moderate anxiety) to 3 (very low anxiety). He has been sober for 6 months and handles stress more effectively, although his mistrust toward coworkers is still apparent.
How would you diagnose Mr. B? Do his symptoms characterize “psychotic features” or an anxiety or alcohol-related disorder?
Dr. Benzick’s observations
Mr. B’s case illustrates how deep-seated cultural perceptions and past trauma together can cause severe anxiety—and how that anxiety can be misperceived as psychosis.4 Anxiety also can manifest as paranoia in “psychotically vulnerable” individuals.5-7
Chronic anxiety seemed to cause Mr. B’s depressed mood and social withdrawal. Several anxiety disorder diagnoses were considered, including:
- panic disorder
- posttraumatic stress disorder
- social phobia
- alcohol-induced anxiety disorder
- and generalized anxiety disorder.
Mr. B, however, exhibited no evidence of repeated episodic anxiety, nor did he describe reexperiencing phenomena. His anxiety extended beyond social situations and preceded his heavy alcohol consumption. Paranoid personality disorder was also considered, but Mr. B sought relationships and lacked the angry, unforgiving qualities associated with this pathology. Finally, a battery of psychological tests did not reveal frank psychosis but suggested an avoidant personality style.
Mr. B’s diagnosis was changed to generalized anxiety disorder. He requested a trial off medications during the latter stages of therapy, but his severe anxiety returned. He was then prescribed venlafaxine, 37.5 mg/d titrated to 225 mg/d across 3 weeks. His anxiety symptoms again abated.
How could Mr A’s and Mr. B’s doctors have avoided their initial misdiagnoses?
Dr. Benzick’s observations
“Cultural paranoia” describes adaptive or healthy responses by African-Americans living in a society they perceive as racially prejudiced.8 Several researchers have studied this concept of protecting self-esteem by blaming an external source for negative events. Women who plausibly attribute unflattering feedback to prejudice exhibit higher self-esteem.9 A person who believes he or she is a target of discrimination identifies more strongly with his or her racial or ethnic group, leading to reduced depression, higher self-esteem, and improved psychological adjustment.9
Perceived discrimination, however, can also elicit feelings of hopelessness and resignation when it leads to widespread bias against the alleged oppressing racial or ethnic group. The resulting sense of social exclusion has been linked to lower self-esteem and higher rates of anxiety and depression.9 Thus, the individual’s environment and ability to develop relationships will determine whether “cultural paranoia” is “adaptive.”
Paranoia or prejudice? Distinguishing culturally sanctioned “paranoia” from “prejudice” can be difficult. “Prejudice” is defined as the negative evaluation of a group or individual based on group membership.10 “Paranoia” (using the DSM-IV definition of “paranoid ideation”) is a belief of less than delusional intensity “involving suspiciousness or the belief that one is being harassed, persecuted, or unfairly treated.”2
So while an individual may be prejudiced toward a group, cultural paranoia would exist only if other family members or acquaintances believe the other group is conspiring against them. Additionally, while prejudice tends to be ego-syntonic,11 paranoia is more distressing because it produces heightened vigilance and possibly fear.
Both cases describe how a lack of cultural understanding between African-American patients and physicians of other ethnicities or races can lead to misdiagnosis of psychosis.12 They also illustrate that while prejudice may be tightly focused (eg, hatred of anyone from a specific racial or ethnic group), paranoid ideation can be generalized. For example, Mr. A believed that his wife, an African-American, conspired with his white supervisors against him.
Mr. A’s and Mr. B’s depressive and anxiety symptoms unmasked longstanding, deeply rooted beliefs. Both patients’ neurovegetative symptoms responded to medication and brief psychotherapy, and both returned to prior levels of functioning. The underlying mistrust remained, however.
Related resources
- Lu FG. Annotated bibliography on cultural psychiatry and related topics-June 2003. Available at: http://www.admsep.org/culture.html. Accessed July 18, 2003.
- Forsell Y, Henderson S. Epidemiology of paranoid disorders in an elderly population. Br J Psychiatry 1998; 172:429-32.
Drug brand names
- Fluoxetine • Prozac
- Olanzapine • Zyprexa
- Nortriptyline • Aventyl, Pamelor
- Paroxetine • Paxil
- Venlafaxine • Effexor
Disclosure
Dr. Benzick reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Kirmayer LJ, Young A, Hayton BC. The cultural context of anxiety disorders. Psychiatr Clin North Am 1995;18:503-21.
2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC. American Psychiatric Association, 2000.
3. Bazargan M, Bazargan S, King L. Paranoid ideation among elderly African American persons. Gerontologist 2001;41:366-73.
4. Newhill CE. The role of culture in the development of paranoid symptomatology. Am J Orthopsychiatry 1990;60:176-85.
5. Bermanzohn PC, Arlow PB, Pitch RJ, Siris SG. Panic and paranoia (letter). J Clin Psychiatry 1997;58:325.-
6. Bermanzohn PC, Arlow PB, Albert C, Siris SG. Relationship of panic attacks to paranoia. Am J Psychiatry 1999;156:1469.-
7. Galynker I, Ieronimo C, Perez-Acquino A, et al. Panic attacks with psychotic features. J Clin Psychiatry 1996;57:402-6.
8. Ridley CR. Clinical treatment of the nondisclosing black client. A therapeutic paradox. Am Psychol 1984;39:1233-43.
9. Branscombe NR, Schmitt MT, Harvey RD. Perceiving pervasive discrimination among African Americans: implications for group identification and well-being. J Pers Soc Psychol 1999;77:135-49.
10. Crandall CS, Eshleman A, O’Brien L. Social norms and suppression of prejudice: the struggle for internalization. J Pers Soc Psychol 2002;82:359-78.
11. Ryan MK, Buirski P. Prejudice as a function of self-organization. Psychoanalytic Psychol 2001;18:21-36.
12. Whaley AL. Psychometric analysis of the cultural mistrust inventory with a black psychiatric inpatient sample. J Clin Psychology 2002;58:383-96.
1. Kirmayer LJ, Young A, Hayton BC. The cultural context of anxiety disorders. Psychiatr Clin North Am 1995;18:503-21.
2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed-text revision). Washington, DC. American Psychiatric Association, 2000.
3. Bazargan M, Bazargan S, King L. Paranoid ideation among elderly African American persons. Gerontologist 2001;41:366-73.
4. Newhill CE. The role of culture in the development of paranoid symptomatology. Am J Orthopsychiatry 1990;60:176-85.
5. Bermanzohn PC, Arlow PB, Pitch RJ, Siris SG. Panic and paranoia (letter). J Clin Psychiatry 1997;58:325.-
6. Bermanzohn PC, Arlow PB, Albert C, Siris SG. Relationship of panic attacks to paranoia. Am J Psychiatry 1999;156:1469.-
7. Galynker I, Ieronimo C, Perez-Acquino A, et al. Panic attacks with psychotic features. J Clin Psychiatry 1996;57:402-6.
8. Ridley CR. Clinical treatment of the nondisclosing black client. A therapeutic paradox. Am Psychol 1984;39:1233-43.
9. Branscombe NR, Schmitt MT, Harvey RD. Perceiving pervasive discrimination among African Americans: implications for group identification and well-being. J Pers Soc Psychol 1999;77:135-49.
10. Crandall CS, Eshleman A, O’Brien L. Social norms and suppression of prejudice: the struggle for internalization. J Pers Soc Psychol 2002;82:359-78.
11. Ryan MK, Buirski P. Prejudice as a function of self-organization. Psychoanalytic Psychol 2001;18:21-36.
12. Whaley AL. Psychometric analysis of the cultural mistrust inventory with a black psychiatric inpatient sample. J Clin Psychology 2002;58:383-96.
Wanted: ‘Digitalis for the mind’
I’m suffering from congestive work failure. I’m sure you understand, as many of you probably are suffering from it, too, as you struggle to keep up with your work.
When I studied cardiovascular physiology in medical school, I learned about the Starling curve. Increasing work increases cardiac muscle efficiency up to a point, after which adding more work decreases cardiac output and leads to congestive heart failure. Miraculously, it seems, digitalis helps the failing heart regain its efficiency.
Congestive work failure also follows a Starling curve. I work more efficiently as my workload increases up to a point, after which more work makes me lessefficient. As I fall behind and miss deadlines, I become anxious and unhappy just thinking about all the work I have to do. So I go into work avoidance—going out for coffee, surfing the Internet, or even reading journals—to escape from thinking about how far behind I am. Of course, avoiding my work puts me even further behind.
Someday I hope the pharmaceutical industry invents a “digitalis for the mind” to treat my condition. Meanwhile, reading Current Psychiatry is the best treatment I know. It helps me to efficiently keep up with new developments in clinical practice—and sometimes provides a medium to productively channel my work avoidance.
I’m suffering from congestive work failure. I’m sure you understand, as many of you probably are suffering from it, too, as you struggle to keep up with your work.
When I studied cardiovascular physiology in medical school, I learned about the Starling curve. Increasing work increases cardiac muscle efficiency up to a point, after which adding more work decreases cardiac output and leads to congestive heart failure. Miraculously, it seems, digitalis helps the failing heart regain its efficiency.
Congestive work failure also follows a Starling curve. I work more efficiently as my workload increases up to a point, after which more work makes me lessefficient. As I fall behind and miss deadlines, I become anxious and unhappy just thinking about all the work I have to do. So I go into work avoidance—going out for coffee, surfing the Internet, or even reading journals—to escape from thinking about how far behind I am. Of course, avoiding my work puts me even further behind.
Someday I hope the pharmaceutical industry invents a “digitalis for the mind” to treat my condition. Meanwhile, reading Current Psychiatry is the best treatment I know. It helps me to efficiently keep up with new developments in clinical practice—and sometimes provides a medium to productively channel my work avoidance.
I’m suffering from congestive work failure. I’m sure you understand, as many of you probably are suffering from it, too, as you struggle to keep up with your work.
When I studied cardiovascular physiology in medical school, I learned about the Starling curve. Increasing work increases cardiac muscle efficiency up to a point, after which adding more work decreases cardiac output and leads to congestive heart failure. Miraculously, it seems, digitalis helps the failing heart regain its efficiency.
Congestive work failure also follows a Starling curve. I work more efficiently as my workload increases up to a point, after which more work makes me lessefficient. As I fall behind and miss deadlines, I become anxious and unhappy just thinking about all the work I have to do. So I go into work avoidance—going out for coffee, surfing the Internet, or even reading journals—to escape from thinking about how far behind I am. Of course, avoiding my work puts me even further behind.
Someday I hope the pharmaceutical industry invents a “digitalis for the mind” to treat my condition. Meanwhile, reading Current Psychiatry is the best treatment I know. It helps me to efficiently keep up with new developments in clinical practice—and sometimes provides a medium to productively channel my work avoidance.
Preventing late-life suicide: 6 steps to detect the warning signs
CASE REPORT: I have a gun
Mr. V, age 77, appears depressed and anxious during his appointment at a mental hygiene clinic. He reports insomnia, concentration trouble, and anhedonia. He tells the psychiatrist he keeps a loaded gun at home and is not sure he can control his suicidal impulses.
The patient is Caucasian and has a history of heart failure, pulmonary disease, and type 2 diabetes. His wife died 18 months ago. He lives alone, but his sister lives nearby. He recently received a right hip replacement, which required 3 months of rehabilitation in a nursing home to recover from surgical complications. He still has trouble walking.
As in Mr. V’s case, treating older patients referred for psychiatric care often involves evaluating suicide risk. His age, race, gender, depressed mood, recent bereavement, and medical ailments place him in the population at highest risk of suicide (Box, Table 1).1-8
Approximately 20% of all suicides in the United States are committed by persons age 65 or older,1 who account for 13% of the total population. The suicide rate among persons older than 75 is three times higher than it is for the young.2 Older Caucasian men have the highest per-capita rate of completed suicide, compared with any other group of Americans.3
Psychiatric disorders. The rates of Axis I disorders among older persons who commit suicide fall within the average range for all age groups (70 to 90%). However, the types of disorders seen in the older population differ from those of younger suicides (Table 1).4-8
Affective illness has been termed “the predominant psychopathology associated with suicide in later life.”4 Among older persons who commit suicide, three-fourths (76%) have diagnosable mood disorders4 and nearly two-thirds (63%) have depression.6 Contributing risk factors include alcoholism and substance abuse,4,6,7 Axis II disorders, and dementia.6
Losses and medical illness. In later life, bereavement, loss of independence, or financial reversals may lead to depression. Older persons who take their own lives also tend to have greater physical health burdens and more functional disabilities than those who do not commit suicide.6,8
This article describes an age-based psychiatric workup of the suicidal older patient, including factors to consider when screening for depressive symptoms, prescribing drug therapy, and determining the need for hospitalization.
AGE-BASED CLINICAL WORKUP
For older patients who report suicidal ideation, an age-appropriate workup—using clinical interviews and screening instruments—is essential. The clinical interview can build rapport and gather information about the patient’s suicidal plan or intent. Based on our experience, we recommend the following 6-step screening interview, summarized in Table 2.
- Ask about a specific plan. Does the patient have the means readily available to carry out this plan? What is the timeline (imminent versus vaguely futuristic)? Does the patient report having control over this plan?
- Gather a suicide history. Has the patient attempted suicide before? By what means? Is there a family history of suicide? If yes, by what means did this family member commit suicide, and how was the patient affected?
- Assess social status. How isolated is the patient? Have there been recent changes in his or her social circle, such as loss of a spouse? Can the patient identify at least one person who would be negatively affected by the suicide?
- Assess medical health. Does the patient suffer from chronic pain? Does the patient have a recently diagnosed medical condition? Has a longstanding medical condition become more debilitating? Does the patient report feeling hopeless about impending medical difficulties? Has he or she been keeping regularly scheduled medical appointments with outpatient clinicians?
- Assess mental health. Does the patient meet DSM-IV criteria for depression or schizophrenia, which are associated with high suicide risk? Does he or she report being hopeless or helpless? Is the suicidal ideation ego dystonic?
- Ascertain clinical signs of suicidal intent. Has the patient:
Table 1
Suicide risk with mental and physical illness, by patient age
| Risk factors | Young (21 to 34 yrs) | Middle-aged (35 to 54 yrs) | Young-old (55 to 74 yrs) | Elderly (77+ yrs) |
|---|---|---|---|---|
| Psychiatric disorders | • | • | • | • |
| Mood disorders | ○ | • | • | |
| Alcohol abuse | ○ | • | ○ | |
| Primary psychoses | • | ○ | ||
| Personality disorders | ○ | |||
| Physical ailments | • | • | ||
| • Significant risk factor ○ Potential risk factor | ||||
| Source: Compiled from information in references 4-8. | ||||
CASE REPORT continued: Some telling signs
Mr. V’s laboratory screening reveals slightly elevated serum glucose and mild anemia. An ECG reveals a type I heart block, but all other lab results are unremarkable. His sister reports he recently gave away his dog, which he and his wife had owned for many years. He has also mentioned a desire to revise his will when speaking to other family members. Hospital records indicate he has missed numerous medical appointments over the past 4 months.
SCREENING INSTRUMENTS
Psychological assessments can often buttress the clinical interview findings. Several measurements are well-suited for detecting suicidal risk and concomitant depression (Table 3).
Beck SSI-C. The Beck Scale for Suicide Ideation – Current (SSI-C) assesses a patient’s preparation and motivation to commit suicide.9 This short (19-item) self-report measure asks patients to rate their wish to die, desire to attempt suicide, duration (and frequency) of suicidal thoughts, sense of control over suicide, and deterrents they face. The SSI-C helps to measure or monitor suicidality and is reliable and valid for psychiatric outpatients.9
BDI-II. The Beck Depression Inventory—recently revised in a second edition (BDI-II)10—can be useful because depression is one of the strongest risk factors for elder suicide. The 21-item BDI-II—a psychometrically sound, self-report instrument—asks about general symptoms of depression and gauges their severity. It can be applied to diverse patient populations and ages11 and is appropriate for older patients who are also being treated medically.
Beck Hopelessness Scale. Hopelessness has been recognized as a possible harbinger of suicide.12 One study showed that depression became a clinically meaningful suicide predictor only when accompanied by hopelessness.13
A score of 10 or more on the Beck Hopelessness Scale identified 91% of patients in one study who eventually committed suicide. The hopelessness patients expressed on this scale more strongly differentiated between those who did or did not commit suicide than did their scores on the BDI or SSI-C.14
Table 2
6-step clinical interview with an older suicidal patient
|
|
| Source: Adapted from the Cincinnati Veterans Affairs Medical Center general psychological suicide assessment |
HRSD-R. The revised Hamilton Rating Scale for Depression (HRSD-R) documents patients’ levels of mood disturbance and suicidality. One item in this 21-item, clinician-administered instrument specifically asks about the patient’s level of suicidality in the past week. The scale has well-documented reliability and validity and is appropriate for psychiatric populations.15
CASE REPORT continued: Alarming findings
Along with the clinical interview, Mr. V. is screened with the Beck Hopelessness Scale and Beck Depression Inventory-II. These instruments are chosen because they are easy to administer, and patients can readily comprehend the questions—even when under duress. Mr. V’s results reveal moderate depression and severe hopelessness.
INPATIENT VS. OUTPATIENT CARE
Older patients are often referred to a psychiatrist because of vague suicidal ideation, but they may also present in an acute crisis—with immediate plans for suicide and readily accessible means. The first concern for their safety is to ensure they are not left alone.
Patient interview. First, listen empathetically and ask detailed questions, especially ones that remind patients of their daily connections and responsibilities. For instance, ask, “Do you have children who would be affected by your decision?” Address patients’ immediate needs, such as hunger, thirst, or pain.16 Work on building a therapeutic alliance before asking questions that may appear trivial to agitated patients (such as tasks assessing cognitive abilities).
Avoid arguing with patients, and refrain from offering advice or sermonizing. Allow them to describe their emotions, and communicate that you understand their concerns. Discuss how they can expect to receive treatment to ease their discomfort. Inform them that mental health specialists can treat them and monitor their progress.
Hospitalization. Begin discussing treatment options and broach the notion of hospital admission if necessary. One way to foster an alliance is to frame inpatient care as a way of helping them recover from their crisis in a safe environment.
To ensure patient safety, it is best to err on the side of admission. Admitting the suicidal patient not only guarantees strict supervision but also allows time for necessary psychological assessment. Hospitalization may also allow family members to remove any weapons or hazardous conditions from the patient’s home.
Including the family in problem-solving is especially important when managing older suicidal patients. For patients who are isolated from family or friends, recovery may depend on improving their support network.
Table 3
Comparing screening instruments for suicide risk
| Measure | Description | Time (minutes) |
|---|---|---|
| Beck Depression Inventory (BDI) | 21-item, self-administered; identifies depressive symptoms in past week | 10 |
| Beck Hopelessness Scale (BHS) | 20-item, self-administered; measures hopelessness, fatalism, and pessimism in past week | 5 |
| Beck Scale for Suicide Ideation-Current (SSI-C) | 19-item, self-administered; gauges suicidal intention | 10 |
| Hamilton Rating Scale for Depression-revised (HRSD-R) | 21-item, clinician-administered; rates depressive symptoms in past week | 25 |
Outpatient care. Not all acutely suicidal older patients require hospital admission. They may be safely managed as outpatients if they:
- have strong social support
- are not isolated
- have no access to firearms or other dangerous weapons.
Safety can be enhanced by having family members take responsibility for the senior’s well-being and by asking the patient to contract for safety. A safety contract may include:
- verbal confirmation—and ideally a written statement—that the patient will not commit suicide within a specified period
- a list of people the patient will contact when feeling suicidal
- steps being taken to monitor the patient’s welfare.
Finally, schedule follow-up appointments soon after discharge to certify patients are being closely monitored. To encourage outpatient medication adherence, build strong alliances with family members and ask patients to bring in their pill bottles during follow-up appointments.
CASE REPORT continued: Observation begins
The staff is clearly concerned about Mr. V’s suicide risk and requests that he voluntarily admit himself to the VA hospital. This decision is based on his level of isolation, the lethality of his suicide plan, access to a weapon, and the depression and hopelessness revealed by his screening tests. He reluctantly agrees and is admitted to the inpatient psychiatric unit for observation and treatment by a geriatric internist and a geriatric psychiatrist.
DRUG THERAPY FOR SUICIDALITY
For patients with mild depressive symptoms, psychotherapy may be sufficient to manage depression associated with suicidality. However, those with moderate-to-severe depression require both drug treatment and psychotherapy.
Drug selection depends upon the underlying psychiatric illness. If the older patient is experiencing a depressive disorder, a selective serotonin reuptake inhibitor (SSRI) or another antidepressant could serve as first-line treatment (Table 4). These medications are safe for suicidal patients because they are not fatal in overdose.
Administration. Because age-related changes in pharmacokinetics and spharmacodynamics can slow medication clearance, reduced dosages usually achieve a therapeutic effect and minimize the risk of side effects in geriatric patients.
Antidepressants commonly used for older patients are shown in Table 4. Excepting citalopram and escitalopram, these dosages are lower than usual. We start healthy older patients on one-half the usual dosage and those who are medically ill or have neurodegenerative disorders on one-third to one-fourth the usual dosage. We also titrate more slowly to reduce the risk of side effects.
Table 4
Antidepressants commonly used to treat geriatric depression
| Medication | Recommended dosage (mg/d) |
|---|---|
| SSRIs | |
| Citalopram | 20 to 40 |
| Escitalopram | 10 to 20 |
| Fluoxetine | 10 to 40 |
| Paroxetine | 10 to 40 |
| Sertraline | 25 to 150 |
| Others | |
| Bupropion | 100 to 400 |
| Mirtazapine | 15 to 45 |
| Venlafaxine | 75 to 225 |
As in younger patients, the most common side effects of SSRIs in older patients include GI difficulties, overactivation, and sexual dysfunction. Paroxetine’s potential for anticholinergic effects may be a concern for some older patients.
Drug-drug interactions are of great concern when treating older patients, who take an average of six to nine medications per day.17 Compared with other SSRIs, fluoxetine and paroxetine, are more likely to inhibit cytochrome P-450 enzymes 2D6 and 3A4. They could thus increase blood levels of drugs taken concomitantly that are substrates of 2D6 or 3A4.
Antidepressant side effects can sometimes be used to advantage. For example, mirtazapine’s sedating property at lower dosages could help older patients with insomnia.
CASE REPORT concluded: Finding support
Mr. V is started on an SSRI antidepressant. He also receives supportive and milieu therapy and coping skills training. During his hospitalization, Mr. V contracts for safety and allows his sister to remove the handgun from his home.
Upon discharge, Mr. V is referred to a day treatment program that operates 3 to 5 days a week and offers case management, group therapy, and individual psychotherapy. The program helps him meet other older patients and allows him to discuss his life’s accomplishments and losses with others his age. His sister is an integral part of the program, and he maintains close contact with her.
Mr. V reports vague and occasional suicidal ideation, with no specific plan or intent. He and his sister note that his medical condition improved soon after his psychiatric condition stabilized.
Related resources
- Surgeon General’s Call to Action to Prevent Suicide. www.mental-health.org/suicideprevention/calltoaction.pdf
- Centers for Disease Control and Prevention. National Center for Injury Prevention and Control.
Drug brand names
- Bupropion • Wellbutrin
- Citalopram • Celexa
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Venlafaxine • Effexor
Disclosure
Drs. Montross reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Mohamed is a speaker and consultant to Forest Laboratories and Eli Lilly and Co.
Dr. Kasckow receives research support from, is a consultant to, and is a speaker for Forest Laboratories, Eli Lilly and Co., Pfizer Inc., and Janssen Pharmaceutica.
Dr. Zisook is a consultant to GlaxoSmithKline and a speaker for GlaxoSmithKline, Wyeth Pharmaceuticals, Pfizer Inc., Forest Laboratories, and Bristol-Myers Squibb Co.
1. Centers for Disease Control and Prevention. Surveillance for Injuries and Violence Among Older Adults (CDC Surveillance Summary, December 17, 1999, Chap. 3:27-50). www.cdc.gov/mmwr/PDF/SS/SS4808.pdf
2. Kaplan HI, Sadock BJ. Synopsis of psychiatry (6th ed). Baltimore: Williams & Wilkins, 1991.
3. Lyon DE, Chase LS, Farrell SP. Using an interview guide to assess suicidal ideation. Nurse Practitioner 2002;27:26-31.
4. Conwell Y, Lyness JM, Duberstein P, et al. Completed suicide among older patients in primary care practices: A controlled study. J Am Geriatr Soc 2000;48:23-9.
5. Conwell Y, Duberstein PR, Cox C, et al. Relationships of age and Axis I diagnoses in victims of completed suicide: A psychological autopsy study. Am J Psychiatry 1996;153:1001-8.
6. Harwood D, Hawton K, Hope T, Jacoby R. Psychiatric disorder and personality factors associated with suicide in older people: A descriptive and case-control study. Int J Geriatr Psychiatry 2001;16:155-65.
7. Henriksson MM, Marttunen MJ, Isometsa ET, et al. Mental disorders in elderly suicide. Int Psychogeriatr 1995;7:275-86.
8. Conwell Y, Duberstein PR, Caine ED. Risk factors for suicide in later life. Biol Psychiatry 2002;52:193-204.
9. Beck AT, Brown GK, Steer RA. Psychometric characteristics of the Scale for Suicide Ideation with psychiatric outpatients. Behav Res Ther 1997;35:1039-46.
10. Beck AT, Steer RA. Manual for the Beck Depression Inventory. San Antonio, TX: The Psychological Corporation, 1987.
11. Beck AT, Steer RA, Garbin MG. Psychometric properties of the Beck Depression Inventory: Twenty-five years later. Clin Psychol Rev 1988;8:77-100.
12. Beck AT, Weissman A, Lester D, Trexler L. The measurement of pessimism: The hopelessness scale. J Consult Clin Psychol 1974;42:861-5.
13. Drake RE, Cotton PG. Depression, hopelessness and suicide in chronic schizophrenia. Br J Psychiatry 1986;148:554-9.
14. Beck AT, Steer RA, Kovacs M, Garrison B. Hopelessness and eventual suicide: A 10-year perspective study of patients hospitalized with suicidal ideation. Am J Psychiatry 1985;142:559-63.
15. Riskind JH, Beck AT, Brown G, Steer RA. Taking the measure of anxiety and depression: Validity of the reconstructed Hamilton Scales. J Nerv Ment Dis 1987;175:474-9.
16. Lamberg L. Psychiatric emergencies call for comprehensive assessment and treatment. JAMA 2002;288:686-7.
17. Sadavoy J, Lazarus LW, Jarvik LF. Grossberg GT (eds). Comprehensive review of geriatric psychiatry (2nd ed). Washington, DC: American Psychiatric Press, 1996.
CASE REPORT: I have a gun
Mr. V, age 77, appears depressed and anxious during his appointment at a mental hygiene clinic. He reports insomnia, concentration trouble, and anhedonia. He tells the psychiatrist he keeps a loaded gun at home and is not sure he can control his suicidal impulses.
The patient is Caucasian and has a history of heart failure, pulmonary disease, and type 2 diabetes. His wife died 18 months ago. He lives alone, but his sister lives nearby. He recently received a right hip replacement, which required 3 months of rehabilitation in a nursing home to recover from surgical complications. He still has trouble walking.
As in Mr. V’s case, treating older patients referred for psychiatric care often involves evaluating suicide risk. His age, race, gender, depressed mood, recent bereavement, and medical ailments place him in the population at highest risk of suicide (Box, Table 1).1-8
Approximately 20% of all suicides in the United States are committed by persons age 65 or older,1 who account for 13% of the total population. The suicide rate among persons older than 75 is three times higher than it is for the young.2 Older Caucasian men have the highest per-capita rate of completed suicide, compared with any other group of Americans.3
Psychiatric disorders. The rates of Axis I disorders among older persons who commit suicide fall within the average range for all age groups (70 to 90%). However, the types of disorders seen in the older population differ from those of younger suicides (Table 1).4-8
Affective illness has been termed “the predominant psychopathology associated with suicide in later life.”4 Among older persons who commit suicide, three-fourths (76%) have diagnosable mood disorders4 and nearly two-thirds (63%) have depression.6 Contributing risk factors include alcoholism and substance abuse,4,6,7 Axis II disorders, and dementia.6
Losses and medical illness. In later life, bereavement, loss of independence, or financial reversals may lead to depression. Older persons who take their own lives also tend to have greater physical health burdens and more functional disabilities than those who do not commit suicide.6,8
This article describes an age-based psychiatric workup of the suicidal older patient, including factors to consider when screening for depressive symptoms, prescribing drug therapy, and determining the need for hospitalization.
AGE-BASED CLINICAL WORKUP
For older patients who report suicidal ideation, an age-appropriate workup—using clinical interviews and screening instruments—is essential. The clinical interview can build rapport and gather information about the patient’s suicidal plan or intent. Based on our experience, we recommend the following 6-step screening interview, summarized in Table 2.
- Ask about a specific plan. Does the patient have the means readily available to carry out this plan? What is the timeline (imminent versus vaguely futuristic)? Does the patient report having control over this plan?
- Gather a suicide history. Has the patient attempted suicide before? By what means? Is there a family history of suicide? If yes, by what means did this family member commit suicide, and how was the patient affected?
- Assess social status. How isolated is the patient? Have there been recent changes in his or her social circle, such as loss of a spouse? Can the patient identify at least one person who would be negatively affected by the suicide?
- Assess medical health. Does the patient suffer from chronic pain? Does the patient have a recently diagnosed medical condition? Has a longstanding medical condition become more debilitating? Does the patient report feeling hopeless about impending medical difficulties? Has he or she been keeping regularly scheduled medical appointments with outpatient clinicians?
- Assess mental health. Does the patient meet DSM-IV criteria for depression or schizophrenia, which are associated with high suicide risk? Does he or she report being hopeless or helpless? Is the suicidal ideation ego dystonic?
- Ascertain clinical signs of suicidal intent. Has the patient:
Table 1
Suicide risk with mental and physical illness, by patient age
| Risk factors | Young (21 to 34 yrs) | Middle-aged (35 to 54 yrs) | Young-old (55 to 74 yrs) | Elderly (77+ yrs) |
|---|---|---|---|---|
| Psychiatric disorders | • | • | • | • |
| Mood disorders | ○ | • | • | |
| Alcohol abuse | ○ | • | ○ | |
| Primary psychoses | • | ○ | ||
| Personality disorders | ○ | |||
| Physical ailments | • | • | ||
| • Significant risk factor ○ Potential risk factor | ||||
| Source: Compiled from information in references 4-8. | ||||
CASE REPORT continued: Some telling signs
Mr. V’s laboratory screening reveals slightly elevated serum glucose and mild anemia. An ECG reveals a type I heart block, but all other lab results are unremarkable. His sister reports he recently gave away his dog, which he and his wife had owned for many years. He has also mentioned a desire to revise his will when speaking to other family members. Hospital records indicate he has missed numerous medical appointments over the past 4 months.
SCREENING INSTRUMENTS
Psychological assessments can often buttress the clinical interview findings. Several measurements are well-suited for detecting suicidal risk and concomitant depression (Table 3).
Beck SSI-C. The Beck Scale for Suicide Ideation – Current (SSI-C) assesses a patient’s preparation and motivation to commit suicide.9 This short (19-item) self-report measure asks patients to rate their wish to die, desire to attempt suicide, duration (and frequency) of suicidal thoughts, sense of control over suicide, and deterrents they face. The SSI-C helps to measure or monitor suicidality and is reliable and valid for psychiatric outpatients.9
BDI-II. The Beck Depression Inventory—recently revised in a second edition (BDI-II)10—can be useful because depression is one of the strongest risk factors for elder suicide. The 21-item BDI-II—a psychometrically sound, self-report instrument—asks about general symptoms of depression and gauges their severity. It can be applied to diverse patient populations and ages11 and is appropriate for older patients who are also being treated medically.
Beck Hopelessness Scale. Hopelessness has been recognized as a possible harbinger of suicide.12 One study showed that depression became a clinically meaningful suicide predictor only when accompanied by hopelessness.13
A score of 10 or more on the Beck Hopelessness Scale identified 91% of patients in one study who eventually committed suicide. The hopelessness patients expressed on this scale more strongly differentiated between those who did or did not commit suicide than did their scores on the BDI or SSI-C.14
Table 2
6-step clinical interview with an older suicidal patient
|
|
| Source: Adapted from the Cincinnati Veterans Affairs Medical Center general psychological suicide assessment |
HRSD-R. The revised Hamilton Rating Scale for Depression (HRSD-R) documents patients’ levels of mood disturbance and suicidality. One item in this 21-item, clinician-administered instrument specifically asks about the patient’s level of suicidality in the past week. The scale has well-documented reliability and validity and is appropriate for psychiatric populations.15
CASE REPORT continued: Alarming findings
Along with the clinical interview, Mr. V. is screened with the Beck Hopelessness Scale and Beck Depression Inventory-II. These instruments are chosen because they are easy to administer, and patients can readily comprehend the questions—even when under duress. Mr. V’s results reveal moderate depression and severe hopelessness.
INPATIENT VS. OUTPATIENT CARE
Older patients are often referred to a psychiatrist because of vague suicidal ideation, but they may also present in an acute crisis—with immediate plans for suicide and readily accessible means. The first concern for their safety is to ensure they are not left alone.
Patient interview. First, listen empathetically and ask detailed questions, especially ones that remind patients of their daily connections and responsibilities. For instance, ask, “Do you have children who would be affected by your decision?” Address patients’ immediate needs, such as hunger, thirst, or pain.16 Work on building a therapeutic alliance before asking questions that may appear trivial to agitated patients (such as tasks assessing cognitive abilities).
Avoid arguing with patients, and refrain from offering advice or sermonizing. Allow them to describe their emotions, and communicate that you understand their concerns. Discuss how they can expect to receive treatment to ease their discomfort. Inform them that mental health specialists can treat them and monitor their progress.
Hospitalization. Begin discussing treatment options and broach the notion of hospital admission if necessary. One way to foster an alliance is to frame inpatient care as a way of helping them recover from their crisis in a safe environment.
To ensure patient safety, it is best to err on the side of admission. Admitting the suicidal patient not only guarantees strict supervision but also allows time for necessary psychological assessment. Hospitalization may also allow family members to remove any weapons or hazardous conditions from the patient’s home.
Including the family in problem-solving is especially important when managing older suicidal patients. For patients who are isolated from family or friends, recovery may depend on improving their support network.
Table 3
Comparing screening instruments for suicide risk
| Measure | Description | Time (minutes) |
|---|---|---|
| Beck Depression Inventory (BDI) | 21-item, self-administered; identifies depressive symptoms in past week | 10 |
| Beck Hopelessness Scale (BHS) | 20-item, self-administered; measures hopelessness, fatalism, and pessimism in past week | 5 |
| Beck Scale for Suicide Ideation-Current (SSI-C) | 19-item, self-administered; gauges suicidal intention | 10 |
| Hamilton Rating Scale for Depression-revised (HRSD-R) | 21-item, clinician-administered; rates depressive symptoms in past week | 25 |
Outpatient care. Not all acutely suicidal older patients require hospital admission. They may be safely managed as outpatients if they:
- have strong social support
- are not isolated
- have no access to firearms or other dangerous weapons.
Safety can be enhanced by having family members take responsibility for the senior’s well-being and by asking the patient to contract for safety. A safety contract may include:
- verbal confirmation—and ideally a written statement—that the patient will not commit suicide within a specified period
- a list of people the patient will contact when feeling suicidal
- steps being taken to monitor the patient’s welfare.
Finally, schedule follow-up appointments soon after discharge to certify patients are being closely monitored. To encourage outpatient medication adherence, build strong alliances with family members and ask patients to bring in their pill bottles during follow-up appointments.
CASE REPORT continued: Observation begins
The staff is clearly concerned about Mr. V’s suicide risk and requests that he voluntarily admit himself to the VA hospital. This decision is based on his level of isolation, the lethality of his suicide plan, access to a weapon, and the depression and hopelessness revealed by his screening tests. He reluctantly agrees and is admitted to the inpatient psychiatric unit for observation and treatment by a geriatric internist and a geriatric psychiatrist.
DRUG THERAPY FOR SUICIDALITY
For patients with mild depressive symptoms, psychotherapy may be sufficient to manage depression associated with suicidality. However, those with moderate-to-severe depression require both drug treatment and psychotherapy.
Drug selection depends upon the underlying psychiatric illness. If the older patient is experiencing a depressive disorder, a selective serotonin reuptake inhibitor (SSRI) or another antidepressant could serve as first-line treatment (Table 4). These medications are safe for suicidal patients because they are not fatal in overdose.
Administration. Because age-related changes in pharmacokinetics and spharmacodynamics can slow medication clearance, reduced dosages usually achieve a therapeutic effect and minimize the risk of side effects in geriatric patients.
Antidepressants commonly used for older patients are shown in Table 4. Excepting citalopram and escitalopram, these dosages are lower than usual. We start healthy older patients on one-half the usual dosage and those who are medically ill or have neurodegenerative disorders on one-third to one-fourth the usual dosage. We also titrate more slowly to reduce the risk of side effects.
Table 4
Antidepressants commonly used to treat geriatric depression
| Medication | Recommended dosage (mg/d) |
|---|---|
| SSRIs | |
| Citalopram | 20 to 40 |
| Escitalopram | 10 to 20 |
| Fluoxetine | 10 to 40 |
| Paroxetine | 10 to 40 |
| Sertraline | 25 to 150 |
| Others | |
| Bupropion | 100 to 400 |
| Mirtazapine | 15 to 45 |
| Venlafaxine | 75 to 225 |
As in younger patients, the most common side effects of SSRIs in older patients include GI difficulties, overactivation, and sexual dysfunction. Paroxetine’s potential for anticholinergic effects may be a concern for some older patients.
Drug-drug interactions are of great concern when treating older patients, who take an average of six to nine medications per day.17 Compared with other SSRIs, fluoxetine and paroxetine, are more likely to inhibit cytochrome P-450 enzymes 2D6 and 3A4. They could thus increase blood levels of drugs taken concomitantly that are substrates of 2D6 or 3A4.
Antidepressant side effects can sometimes be used to advantage. For example, mirtazapine’s sedating property at lower dosages could help older patients with insomnia.
CASE REPORT concluded: Finding support
Mr. V is started on an SSRI antidepressant. He also receives supportive and milieu therapy and coping skills training. During his hospitalization, Mr. V contracts for safety and allows his sister to remove the handgun from his home.
Upon discharge, Mr. V is referred to a day treatment program that operates 3 to 5 days a week and offers case management, group therapy, and individual psychotherapy. The program helps him meet other older patients and allows him to discuss his life’s accomplishments and losses with others his age. His sister is an integral part of the program, and he maintains close contact with her.
Mr. V reports vague and occasional suicidal ideation, with no specific plan or intent. He and his sister note that his medical condition improved soon after his psychiatric condition stabilized.
Related resources
- Surgeon General’s Call to Action to Prevent Suicide. www.mental-health.org/suicideprevention/calltoaction.pdf
- Centers for Disease Control and Prevention. National Center for Injury Prevention and Control.
Drug brand names
- Bupropion • Wellbutrin
- Citalopram • Celexa
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Venlafaxine • Effexor
Disclosure
Drs. Montross reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Mohamed is a speaker and consultant to Forest Laboratories and Eli Lilly and Co.
Dr. Kasckow receives research support from, is a consultant to, and is a speaker for Forest Laboratories, Eli Lilly and Co., Pfizer Inc., and Janssen Pharmaceutica.
Dr. Zisook is a consultant to GlaxoSmithKline and a speaker for GlaxoSmithKline, Wyeth Pharmaceuticals, Pfizer Inc., Forest Laboratories, and Bristol-Myers Squibb Co.
CASE REPORT: I have a gun
Mr. V, age 77, appears depressed and anxious during his appointment at a mental hygiene clinic. He reports insomnia, concentration trouble, and anhedonia. He tells the psychiatrist he keeps a loaded gun at home and is not sure he can control his suicidal impulses.
The patient is Caucasian and has a history of heart failure, pulmonary disease, and type 2 diabetes. His wife died 18 months ago. He lives alone, but his sister lives nearby. He recently received a right hip replacement, which required 3 months of rehabilitation in a nursing home to recover from surgical complications. He still has trouble walking.
As in Mr. V’s case, treating older patients referred for psychiatric care often involves evaluating suicide risk. His age, race, gender, depressed mood, recent bereavement, and medical ailments place him in the population at highest risk of suicide (Box, Table 1).1-8
Approximately 20% of all suicides in the United States are committed by persons age 65 or older,1 who account for 13% of the total population. The suicide rate among persons older than 75 is three times higher than it is for the young.2 Older Caucasian men have the highest per-capita rate of completed suicide, compared with any other group of Americans.3
Psychiatric disorders. The rates of Axis I disorders among older persons who commit suicide fall within the average range for all age groups (70 to 90%). However, the types of disorders seen in the older population differ from those of younger suicides (Table 1).4-8
Affective illness has been termed “the predominant psychopathology associated with suicide in later life.”4 Among older persons who commit suicide, three-fourths (76%) have diagnosable mood disorders4 and nearly two-thirds (63%) have depression.6 Contributing risk factors include alcoholism and substance abuse,4,6,7 Axis II disorders, and dementia.6
Losses and medical illness. In later life, bereavement, loss of independence, or financial reversals may lead to depression. Older persons who take their own lives also tend to have greater physical health burdens and more functional disabilities than those who do not commit suicide.6,8
This article describes an age-based psychiatric workup of the suicidal older patient, including factors to consider when screening for depressive symptoms, prescribing drug therapy, and determining the need for hospitalization.
AGE-BASED CLINICAL WORKUP
For older patients who report suicidal ideation, an age-appropriate workup—using clinical interviews and screening instruments—is essential. The clinical interview can build rapport and gather information about the patient’s suicidal plan or intent. Based on our experience, we recommend the following 6-step screening interview, summarized in Table 2.
- Ask about a specific plan. Does the patient have the means readily available to carry out this plan? What is the timeline (imminent versus vaguely futuristic)? Does the patient report having control over this plan?
- Gather a suicide history. Has the patient attempted suicide before? By what means? Is there a family history of suicide? If yes, by what means did this family member commit suicide, and how was the patient affected?
- Assess social status. How isolated is the patient? Have there been recent changes in his or her social circle, such as loss of a spouse? Can the patient identify at least one person who would be negatively affected by the suicide?
- Assess medical health. Does the patient suffer from chronic pain? Does the patient have a recently diagnosed medical condition? Has a longstanding medical condition become more debilitating? Does the patient report feeling hopeless about impending medical difficulties? Has he or she been keeping regularly scheduled medical appointments with outpatient clinicians?
- Assess mental health. Does the patient meet DSM-IV criteria for depression or schizophrenia, which are associated with high suicide risk? Does he or she report being hopeless or helpless? Is the suicidal ideation ego dystonic?
- Ascertain clinical signs of suicidal intent. Has the patient:
Table 1
Suicide risk with mental and physical illness, by patient age
| Risk factors | Young (21 to 34 yrs) | Middle-aged (35 to 54 yrs) | Young-old (55 to 74 yrs) | Elderly (77+ yrs) |
|---|---|---|---|---|
| Psychiatric disorders | • | • | • | • |
| Mood disorders | ○ | • | • | |
| Alcohol abuse | ○ | • | ○ | |
| Primary psychoses | • | ○ | ||
| Personality disorders | ○ | |||
| Physical ailments | • | • | ||
| • Significant risk factor ○ Potential risk factor | ||||
| Source: Compiled from information in references 4-8. | ||||
CASE REPORT continued: Some telling signs
Mr. V’s laboratory screening reveals slightly elevated serum glucose and mild anemia. An ECG reveals a type I heart block, but all other lab results are unremarkable. His sister reports he recently gave away his dog, which he and his wife had owned for many years. He has also mentioned a desire to revise his will when speaking to other family members. Hospital records indicate he has missed numerous medical appointments over the past 4 months.
SCREENING INSTRUMENTS
Psychological assessments can often buttress the clinical interview findings. Several measurements are well-suited for detecting suicidal risk and concomitant depression (Table 3).
Beck SSI-C. The Beck Scale for Suicide Ideation – Current (SSI-C) assesses a patient’s preparation and motivation to commit suicide.9 This short (19-item) self-report measure asks patients to rate their wish to die, desire to attempt suicide, duration (and frequency) of suicidal thoughts, sense of control over suicide, and deterrents they face. The SSI-C helps to measure or monitor suicidality and is reliable and valid for psychiatric outpatients.9
BDI-II. The Beck Depression Inventory—recently revised in a second edition (BDI-II)10—can be useful because depression is one of the strongest risk factors for elder suicide. The 21-item BDI-II—a psychometrically sound, self-report instrument—asks about general symptoms of depression and gauges their severity. It can be applied to diverse patient populations and ages11 and is appropriate for older patients who are also being treated medically.
Beck Hopelessness Scale. Hopelessness has been recognized as a possible harbinger of suicide.12 One study showed that depression became a clinically meaningful suicide predictor only when accompanied by hopelessness.13
A score of 10 or more on the Beck Hopelessness Scale identified 91% of patients in one study who eventually committed suicide. The hopelessness patients expressed on this scale more strongly differentiated between those who did or did not commit suicide than did their scores on the BDI or SSI-C.14
Table 2
6-step clinical interview with an older suicidal patient
|
|
| Source: Adapted from the Cincinnati Veterans Affairs Medical Center general psychological suicide assessment |
HRSD-R. The revised Hamilton Rating Scale for Depression (HRSD-R) documents patients’ levels of mood disturbance and suicidality. One item in this 21-item, clinician-administered instrument specifically asks about the patient’s level of suicidality in the past week. The scale has well-documented reliability and validity and is appropriate for psychiatric populations.15
CASE REPORT continued: Alarming findings
Along with the clinical interview, Mr. V. is screened with the Beck Hopelessness Scale and Beck Depression Inventory-II. These instruments are chosen because they are easy to administer, and patients can readily comprehend the questions—even when under duress. Mr. V’s results reveal moderate depression and severe hopelessness.
INPATIENT VS. OUTPATIENT CARE
Older patients are often referred to a psychiatrist because of vague suicidal ideation, but they may also present in an acute crisis—with immediate plans for suicide and readily accessible means. The first concern for their safety is to ensure they are not left alone.
Patient interview. First, listen empathetically and ask detailed questions, especially ones that remind patients of their daily connections and responsibilities. For instance, ask, “Do you have children who would be affected by your decision?” Address patients’ immediate needs, such as hunger, thirst, or pain.16 Work on building a therapeutic alliance before asking questions that may appear trivial to agitated patients (such as tasks assessing cognitive abilities).
Avoid arguing with patients, and refrain from offering advice or sermonizing. Allow them to describe their emotions, and communicate that you understand their concerns. Discuss how they can expect to receive treatment to ease their discomfort. Inform them that mental health specialists can treat them and monitor their progress.
Hospitalization. Begin discussing treatment options and broach the notion of hospital admission if necessary. One way to foster an alliance is to frame inpatient care as a way of helping them recover from their crisis in a safe environment.
To ensure patient safety, it is best to err on the side of admission. Admitting the suicidal patient not only guarantees strict supervision but also allows time for necessary psychological assessment. Hospitalization may also allow family members to remove any weapons or hazardous conditions from the patient’s home.
Including the family in problem-solving is especially important when managing older suicidal patients. For patients who are isolated from family or friends, recovery may depend on improving their support network.
Table 3
Comparing screening instruments for suicide risk
| Measure | Description | Time (minutes) |
|---|---|---|
| Beck Depression Inventory (BDI) | 21-item, self-administered; identifies depressive symptoms in past week | 10 |
| Beck Hopelessness Scale (BHS) | 20-item, self-administered; measures hopelessness, fatalism, and pessimism in past week | 5 |
| Beck Scale for Suicide Ideation-Current (SSI-C) | 19-item, self-administered; gauges suicidal intention | 10 |
| Hamilton Rating Scale for Depression-revised (HRSD-R) | 21-item, clinician-administered; rates depressive symptoms in past week | 25 |
Outpatient care. Not all acutely suicidal older patients require hospital admission. They may be safely managed as outpatients if they:
- have strong social support
- are not isolated
- have no access to firearms or other dangerous weapons.
Safety can be enhanced by having family members take responsibility for the senior’s well-being and by asking the patient to contract for safety. A safety contract may include:
- verbal confirmation—and ideally a written statement—that the patient will not commit suicide within a specified period
- a list of people the patient will contact when feeling suicidal
- steps being taken to monitor the patient’s welfare.
Finally, schedule follow-up appointments soon after discharge to certify patients are being closely monitored. To encourage outpatient medication adherence, build strong alliances with family members and ask patients to bring in their pill bottles during follow-up appointments.
CASE REPORT continued: Observation begins
The staff is clearly concerned about Mr. V’s suicide risk and requests that he voluntarily admit himself to the VA hospital. This decision is based on his level of isolation, the lethality of his suicide plan, access to a weapon, and the depression and hopelessness revealed by his screening tests. He reluctantly agrees and is admitted to the inpatient psychiatric unit for observation and treatment by a geriatric internist and a geriatric psychiatrist.
DRUG THERAPY FOR SUICIDALITY
For patients with mild depressive symptoms, psychotherapy may be sufficient to manage depression associated with suicidality. However, those with moderate-to-severe depression require both drug treatment and psychotherapy.
Drug selection depends upon the underlying psychiatric illness. If the older patient is experiencing a depressive disorder, a selective serotonin reuptake inhibitor (SSRI) or another antidepressant could serve as first-line treatment (Table 4). These medications are safe for suicidal patients because they are not fatal in overdose.
Administration. Because age-related changes in pharmacokinetics and spharmacodynamics can slow medication clearance, reduced dosages usually achieve a therapeutic effect and minimize the risk of side effects in geriatric patients.
Antidepressants commonly used for older patients are shown in Table 4. Excepting citalopram and escitalopram, these dosages are lower than usual. We start healthy older patients on one-half the usual dosage and those who are medically ill or have neurodegenerative disorders on one-third to one-fourth the usual dosage. We also titrate more slowly to reduce the risk of side effects.
Table 4
Antidepressants commonly used to treat geriatric depression
| Medication | Recommended dosage (mg/d) |
|---|---|
| SSRIs | |
| Citalopram | 20 to 40 |
| Escitalopram | 10 to 20 |
| Fluoxetine | 10 to 40 |
| Paroxetine | 10 to 40 |
| Sertraline | 25 to 150 |
| Others | |
| Bupropion | 100 to 400 |
| Mirtazapine | 15 to 45 |
| Venlafaxine | 75 to 225 |
As in younger patients, the most common side effects of SSRIs in older patients include GI difficulties, overactivation, and sexual dysfunction. Paroxetine’s potential for anticholinergic effects may be a concern for some older patients.
Drug-drug interactions are of great concern when treating older patients, who take an average of six to nine medications per day.17 Compared with other SSRIs, fluoxetine and paroxetine, are more likely to inhibit cytochrome P-450 enzymes 2D6 and 3A4. They could thus increase blood levels of drugs taken concomitantly that are substrates of 2D6 or 3A4.
Antidepressant side effects can sometimes be used to advantage. For example, mirtazapine’s sedating property at lower dosages could help older patients with insomnia.
CASE REPORT concluded: Finding support
Mr. V is started on an SSRI antidepressant. He also receives supportive and milieu therapy and coping skills training. During his hospitalization, Mr. V contracts for safety and allows his sister to remove the handgun from his home.
Upon discharge, Mr. V is referred to a day treatment program that operates 3 to 5 days a week and offers case management, group therapy, and individual psychotherapy. The program helps him meet other older patients and allows him to discuss his life’s accomplishments and losses with others his age. His sister is an integral part of the program, and he maintains close contact with her.
Mr. V reports vague and occasional suicidal ideation, with no specific plan or intent. He and his sister note that his medical condition improved soon after his psychiatric condition stabilized.
Related resources
- Surgeon General’s Call to Action to Prevent Suicide. www.mental-health.org/suicideprevention/calltoaction.pdf
- Centers for Disease Control and Prevention. National Center for Injury Prevention and Control.
Drug brand names
- Bupropion • Wellbutrin
- Citalopram • Celexa
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Venlafaxine • Effexor
Disclosure
Drs. Montross reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Mohamed is a speaker and consultant to Forest Laboratories and Eli Lilly and Co.
Dr. Kasckow receives research support from, is a consultant to, and is a speaker for Forest Laboratories, Eli Lilly and Co., Pfizer Inc., and Janssen Pharmaceutica.
Dr. Zisook is a consultant to GlaxoSmithKline and a speaker for GlaxoSmithKline, Wyeth Pharmaceuticals, Pfizer Inc., Forest Laboratories, and Bristol-Myers Squibb Co.
1. Centers for Disease Control and Prevention. Surveillance for Injuries and Violence Among Older Adults (CDC Surveillance Summary, December 17, 1999, Chap. 3:27-50). www.cdc.gov/mmwr/PDF/SS/SS4808.pdf
2. Kaplan HI, Sadock BJ. Synopsis of psychiatry (6th ed). Baltimore: Williams & Wilkins, 1991.
3. Lyon DE, Chase LS, Farrell SP. Using an interview guide to assess suicidal ideation. Nurse Practitioner 2002;27:26-31.
4. Conwell Y, Lyness JM, Duberstein P, et al. Completed suicide among older patients in primary care practices: A controlled study. J Am Geriatr Soc 2000;48:23-9.
5. Conwell Y, Duberstein PR, Cox C, et al. Relationships of age and Axis I diagnoses in victims of completed suicide: A psychological autopsy study. Am J Psychiatry 1996;153:1001-8.
6. Harwood D, Hawton K, Hope T, Jacoby R. Psychiatric disorder and personality factors associated with suicide in older people: A descriptive and case-control study. Int J Geriatr Psychiatry 2001;16:155-65.
7. Henriksson MM, Marttunen MJ, Isometsa ET, et al. Mental disorders in elderly suicide. Int Psychogeriatr 1995;7:275-86.
8. Conwell Y, Duberstein PR, Caine ED. Risk factors for suicide in later life. Biol Psychiatry 2002;52:193-204.
9. Beck AT, Brown GK, Steer RA. Psychometric characteristics of the Scale for Suicide Ideation with psychiatric outpatients. Behav Res Ther 1997;35:1039-46.
10. Beck AT, Steer RA. Manual for the Beck Depression Inventory. San Antonio, TX: The Psychological Corporation, 1987.
11. Beck AT, Steer RA, Garbin MG. Psychometric properties of the Beck Depression Inventory: Twenty-five years later. Clin Psychol Rev 1988;8:77-100.
12. Beck AT, Weissman A, Lester D, Trexler L. The measurement of pessimism: The hopelessness scale. J Consult Clin Psychol 1974;42:861-5.
13. Drake RE, Cotton PG. Depression, hopelessness and suicide in chronic schizophrenia. Br J Psychiatry 1986;148:554-9.
14. Beck AT, Steer RA, Kovacs M, Garrison B. Hopelessness and eventual suicide: A 10-year perspective study of patients hospitalized with suicidal ideation. Am J Psychiatry 1985;142:559-63.
15. Riskind JH, Beck AT, Brown G, Steer RA. Taking the measure of anxiety and depression: Validity of the reconstructed Hamilton Scales. J Nerv Ment Dis 1987;175:474-9.
16. Lamberg L. Psychiatric emergencies call for comprehensive assessment and treatment. JAMA 2002;288:686-7.
17. Sadavoy J, Lazarus LW, Jarvik LF. Grossberg GT (eds). Comprehensive review of geriatric psychiatry (2nd ed). Washington, DC: American Psychiatric Press, 1996.
1. Centers for Disease Control and Prevention. Surveillance for Injuries and Violence Among Older Adults (CDC Surveillance Summary, December 17, 1999, Chap. 3:27-50). www.cdc.gov/mmwr/PDF/SS/SS4808.pdf
2. Kaplan HI, Sadock BJ. Synopsis of psychiatry (6th ed). Baltimore: Williams & Wilkins, 1991.
3. Lyon DE, Chase LS, Farrell SP. Using an interview guide to assess suicidal ideation. Nurse Practitioner 2002;27:26-31.
4. Conwell Y, Lyness JM, Duberstein P, et al. Completed suicide among older patients in primary care practices: A controlled study. J Am Geriatr Soc 2000;48:23-9.
5. Conwell Y, Duberstein PR, Cox C, et al. Relationships of age and Axis I diagnoses in victims of completed suicide: A psychological autopsy study. Am J Psychiatry 1996;153:1001-8.
6. Harwood D, Hawton K, Hope T, Jacoby R. Psychiatric disorder and personality factors associated with suicide in older people: A descriptive and case-control study. Int J Geriatr Psychiatry 2001;16:155-65.
7. Henriksson MM, Marttunen MJ, Isometsa ET, et al. Mental disorders in elderly suicide. Int Psychogeriatr 1995;7:275-86.
8. Conwell Y, Duberstein PR, Caine ED. Risk factors for suicide in later life. Biol Psychiatry 2002;52:193-204.
9. Beck AT, Brown GK, Steer RA. Psychometric characteristics of the Scale for Suicide Ideation with psychiatric outpatients. Behav Res Ther 1997;35:1039-46.
10. Beck AT, Steer RA. Manual for the Beck Depression Inventory. San Antonio, TX: The Psychological Corporation, 1987.
11. Beck AT, Steer RA, Garbin MG. Psychometric properties of the Beck Depression Inventory: Twenty-five years later. Clin Psychol Rev 1988;8:77-100.
12. Beck AT, Weissman A, Lester D, Trexler L. The measurement of pessimism: The hopelessness scale. J Consult Clin Psychol 1974;42:861-5.
13. Drake RE, Cotton PG. Depression, hopelessness and suicide in chronic schizophrenia. Br J Psychiatry 1986;148:554-9.
14. Beck AT, Steer RA, Kovacs M, Garrison B. Hopelessness and eventual suicide: A 10-year perspective study of patients hospitalized with suicidal ideation. Am J Psychiatry 1985;142:559-63.
15. Riskind JH, Beck AT, Brown G, Steer RA. Taking the measure of anxiety and depression: Validity of the reconstructed Hamilton Scales. J Nerv Ment Dis 1987;175:474-9.
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