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What is your liability for involuntary commitment based on faulty information?
Dear Dr. Mossman,
Last week, I hospitalized a patient against her will, based in part on what her family members told me she had threatened to do. The patient threatened to sue me and said I should have known that her relatives were lying. What if my patient is right? Could I face liability if I involuntarily hospitalized her based on bad collateral information?
Submitted by “Dr. R”
In all U.S. states, laws permit psychiatrists to involuntarily hospitalize persons who pose a danger to themselves or others because of mental illness.1 But taking this step can be tough. Deciding to hospitalize a patient against her will involves weighing her wants and freedom against your duty to look out for her long-term welfare and the community’s safety.2,3 Often, psychiatrists make these decisions under pressure because the family wants something done immediately, other patients also need attention, the clinical picture is incomplete, or potential dispositions (eg, crisis care and inpatient beds) are limited.3 Given such constraints, you can’t always make perfect decisions.
Dr. R’s question has 2 parts:
- What liabilities can a clinician face if a patient is wrongfully committed?
- What liabilities could arise from relying on inaccurate information or making a false petition in order to hospitalize a patient?
We hope that as you and Dr. R read our answers, you’ll have a clearer understanding of:
- the rationale for civil commitment
- how patients, doctors, and courts view civil commitment
- the role of collateral information in decision-making
- relevant legal concepts and case law.
Rationale for civil commitment
For centuries, society has used civil commitment as one of its legal methods for intervening when persons pose a danger to themselves or others because of their mental illness.4 Because incapacitation or death could result from a “false-negative” decision to release a dangerous patient, psychiatrists err on the side of caution and tolerate many “false-positive” hospitalizations of persons who wouldn’t have hurt anyone.5
We can never know if a patient would have done harm had she not been hospitalized. Measures of suicidality and hostility tend to subside during involuntary hospital treatment.6 After hospitalization, many patients cite protection from harm as a reason they are thankful for their treatment.7-9 Some involuntary inpatients want to be hospitalized but hide this for conscious or unconscious reasons,10,11 and involuntary treatment sometimes is the only way to help persons whose illness-induced anosognosia12 prevents them from understanding why they need treatment.13 Involuntary inpatient care leads to modest symptom reduction14,15 and produces treatment outcomes no worse than those of non-coerced patients.10
Patients’ views
Patients often view commitment as unjustified.16 They and their advocates object to what some view as the ultimate infringement on civil liberty.7,17 By its nature, involuntary commitment eliminates patients’ involvement in a major treatment decision,8 disempowers them,18 and influences their relationship with the treatment team.15
Some involuntary patients feel disrespected by staff members8 or experience inadvertent psychological harm, including “loss of self-esteem, identity, self-control, and self-efficacy, as well as diminished hope in the possibility of recovery.”15 Involuntary hospitalization also can have serious practical consequences. Commitment can lead to social stigma, loss of gun rights, increased risks of losing child custody, housing problems, and possible disqualification from some professions.19
Having seen many involuntary patients undergo a change of heart after treatment, psychiatrist Alan Stone proposed the “Thank You Theory” of civil commitment: involuntary hospitalization can be justified by showing that the patient is grateful after recovering.20 Studies show, however, that gratitude is far from universal.1
How coercion is experienced often depends on how it is communicated. The less coercion patients perceive, the better they feel about the treatment they received.21 Satisfaction is important because it leads to less compulsory readmission,22 and dissatisfaction makes malpractice lawsuits more likely.23
Commitment decision-making
States’ laws, judges’ attitudes, and court decisions establish each jurisdiction’s legal methods for instituting emergency holds and willingness to tolerate “false-positive” involuntary hospitalization,4,24 all of which create variation between and within states in how civil commitment laws are applied. As a result, clinicians’ decisions are influenced “by a range of social, political, and economic factors,”25 including patients’ sex, race, age, homelessness, employment status, living situation, diagnoses, previous involuntary treatment, and dissatisfaction with mental health treatment.22,26-32 Furthermore, the potential for coercion often blurs the line between an offer of voluntary admission and an involuntary hospitalization.18
Collateral information
Psychiatrists owe each patient a sound clinical assessment before deciding to initiate involuntarily hospitalization. During a psychiatric crisis, a patient might not be forthcoming or could have impaired memory or judgment. Information from friends or family can help fill in gaps in a patient’s self-report.33 As Dr. R’s question illustrates, adequate assessment often includes seeking information from persons familiar with the patient.1 A report on the Virginia Tech shootings by the Virginia Office of the Inspector General describes how collateral sources can provide otherwise missing evidence of dangerousness,34 and it often leads clinicians toward favoring admission.35
Yet clinicians should regard third-party reports with caution.36 As one attorney warns, “Psychiatrists should be cautious of the underlying motives of well-meaning family members and relatives.”37 If you make a decision to hospitalize a patient involuntarily based on collateral information that turns out to be flawed, are you at fault and potentially liable for harm to the patient?
False petitions and liability
If you’re in a situation similar to the one Dr. R describes, you can take solace in knowing that courts generally provide immunity to a psychiatrist who makes a reasonable, well-intentioned decision to commit someone. The degree of immunity offered varies by jurisdiction. Table 1 provides examples of immunity language from several states’ statutes.
Many states’ statutes also lay out the potential consequences if a psychiatrist takes action to involuntarily hospitalize someone in bad faith or with malicious intent. In some jurisdictions, such actions can lead to criminal sanctions against the doctor or against the party who made a false petition (eg, a devious family member) (Table 2). Commenting on Texas’s statute, attorney Jeffrey Anderson explains, “The touchstone for causes of action based upon a wrongful civil commitment require that the psychiatrist[’s] conduct be found to be unreasonable and negligent. [Immunity…] still requires that a psychiatrist[’s] diagnosis of a patient[’s] threat to harm himself or others be a reasonable and prudent one.”37
The immunity extended through such statutes usually is limited to claims arising directly from the detention. For example, in the California case of Jacobs v Grossmont Hospital, a patient under a 72-hour hold fell and fractured her leg, and she sought damages. The trial court dismissed the suit under the immunity statute applicable to commitment decisions, but the appellate court held that “the immunity did not extend to other negligent acts.… The trial court erred in assuming that … the hospital was exempt from all liability for any negligence that occurred during the lawful hold.”38
Bingham v Cedars-Sinai Health Systems illustrates how physicians can lose immunity.39 A nurse contacted her supervisor to report a colleague who had stolen narcotics from work and compromised patient care. In response, the supervisor, hospital, and several physicians agreed to have her involuntarily committed. Later, it was confirmed that the colleague had taken the narcotics. She later sued the hospital system, claiming—in addition to malpractice—retaliation, invasion of privacy, assault and battery, false imprisonment, defamation, intentional infliction of emotional distress, disability-based harassment, and violation of her civil rights. Citing California’s immunity statute, the trial court granted summary judgment to the clinicians and hospital system. On appeal, however, the appellate court reversed the judgment, holding that the defendants had not shown that “the decision to detain Bingham was based on probable cause, a prerequisite to the exemption from liability,” and that Bingham had some legitimate grounds for her lawsuit.
A key point for Dr. R to consider is that, although some states provide immunity if the psychiatrist’s admitting decision was based on an evaluation “performed in good faith,”40 other states’ immunity provisions apply only if the psychiatrist had probable cause to make a decision to detain.41
Ways to reduce liability risk
Although an involuntary hospitalization could have an uncertain basis, psychiatrists can reduce the risk of legal liability for their decisions. Good documentation is important. Admitting psychiatrists usually make sound decisions, but the corresponding documentation frequently lacks clinical justification.42-44 As the rate of appropriate documentation of admission decision-making improves, the rate of commitment falls,44 and patients’ legal rights enjoy greater protection.43 Poor communication can decrease the quality of care and increase the risk of a malpractice lawsuit.45 This is just one of many reasons why you should explain your reasons for involuntary hospitalization and inform patients of the procedures for judicial review.8,9 Table 3 summarizes other steps to reduce liability risk when committing patients to the hospital.1,8,15,21,33,35-37,42,45-47
1. Pinals DA, Mossman D. Evaluation for civil commitment: best practices for forensic mental health assessments. New York, NY: Oxford University Press; 2011.
2. Testa M, West SG. Civil commitment in the United States. Psychiatry (Edgemont). 2010;7(10):30-40.
3. Hedman LC, Petrila J, Fisher WH, et al. State laws on emergency holds for mental health stabilization. Psychiatr Serv. 2016;67(5):529-535.
4. Groendyk Z. “It takes a lot to get into Bellevue”: a pro-rights critique of New York’s involuntary commitment law. Fordham Urban Law J. 2013;40(1):548-585.
5. Brooks RA. U.S. psychiatrists’ beliefs and wants about involuntary civil commitment grounds. Int J Law Psychiatry. 2006;29(1):13-21.
6. Giacco D, Priebe S. Suicidality and hostility following involuntary hospital treatment. PLoS One. 2016;11(5):e0154458. doi: 10.1371/journal.pone.0154458.
7. Wyder M, Bland R, Herriot A, et al. The experiences of the legal processes of involuntary treatment orders: tension between the legal and medical frameworks. Int J Law Psychiatry. 2015;38:44-50.
8. Valenti E, Giacco D, Katasakou C, et al. Which values are important for patients during involuntary treatment? A qualitative study with psychiatric inpatients. J Med Ethics. 2014;40(12):832-836.
9. Katsakou C, Rose D, Amos T, et al. Psychiatric patients’ views on why their involuntary hospitalisation was right or wrong: a qualitative study. Soc Psychiatry Psychiatr Epidemiol. 2012;42(7):1169-1179.
10. Kaltiala-Heino R, Laippala P, Salokangas RK. Impact of coercion on treatment outcome. Int J Law Psychiatry. 1997;20(3):311-322.
11. Hoge SK, Lidz CW, Eisenberg M, et al. Perceptions of coercion in the admission of voluntary and involuntary psychiatric patients. Int J Law Psychiatry. 1997;20(2):167-181.
12. Lehrer DS, Lorenz J. Anosognosia in schizophrenia: hidden in plain sight. Innov Clin Neurosci. 2014;11(5-6):10-17. 13. Gordon S. The danger zone: how the dangerousness standard in civil commitment proceedings harms people with serious mental illness. Case Western Reserve Law Review. 2016;66(3):657-700.
14. Kallert TW, Katsakou C, Adamowski T, et al. Coerced hospital admission and symptom change—a prospective observational multi-centre study. PLoS One. 2011;6(11):e28191. doi: 10.1371/journal.pone.0028191.
15. Danzer G, Wilkus-Stone A. The give and take of freedom: the role of involuntary hospitalization and treatment in recovery from mental illness. Bull Menninger Clin. 2015;79(3):255-280.
16. Roe D, Weishut DJ, Jaglom M, et al. Patients’ and staff members’ attitudes about the rights of hospitalized psychiatric patients. Psychiatr Serv. 2002;53(1):87-91.
17. Amidov T. Involuntary commitment is unnecessary and discriminatory. In: Berlatsky N, ed. Mental illness. Farmington Hills, MI: Greenhaven Press; 2016;140-145.
18. Monahan J, Hoge SK, Lidz C, et al. Coercion and commitment: understanding involuntary mental hospital admission. Int J Law Psychiatry. 1995;18(3):249-263.
19. Guest Pryal KR. Heller’s scapegoats. North Carolina Law Review. 2015;93(5):1439-1473.
20. Stone AA. Mental health and law: a system in transition. Washington, DC: U.S. Government Printing Office; 1975:75-176.
21. Katsakou C, Bowers L, Amos T, et al. Coercion and treatment satisfaction among involuntary patients. Psychiatr Serv. 2010;61(3):286-292.
22. Setkowski K, van der Post LF, Peen J, et al. Changing patient perspectives after compulsory admission and the risk of re-admission during 5 years of follow-up: the Amsterdam study of acute psychiatry IX. Int J Soc Psychiatry. 2016;62(6):578-588.
23. Stelfox HT, Gandhi TK, Orav EJ, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133.
24. Goldman A. Continued overreliance on involuntary commitment: the need for a less restrictive alternative. J Leg Med. 2015;36(2):233-251.
25. Fisher WH, Grisso T. Commentary: civil commitment statutes—40 years of circumvention. J Am Acad Psychiatry Law. 2010;38(3):365-368.
26. Curley A, Agada E, Emechebe A, et al. Exploring and explaining involuntary care: the relationship between psychiatric admission status, gender and other demographic and clinical variables. Int J Law Psychiatry. 2016;47:53-59.
27. Muroff JR, Jackson JS, Mowbray CT, et al. The influence of gender, patient volume and time on clinical diagnostic decision making in psychiatric emergency services. Gen Hosp Psychiatry. 2007;29(6):481-488.
28. Muroff JR, Edelsohn GA, Joe S, et al. The role of race in diagnostic and disposition decision making in a pediatric psychiatric emergency service. Gen Hosp Psychiatry. 2008;30(3):269-276.
29. Unick GJ, Kessell E, Woodard EK, et al. Factors affecting psychiatric inpatient hospitalization from a psychiatric emergency service. Gen Hosp Psychiatry. 2011;33(6):618-625.
30. Ng XT, Kelly BD. Voluntary and involuntary care: three-year study of demographic and diagnostic admission statistics at an inner-city adult psychiatry unit. Int J Law Psychiatry. 2012;35(4):317-326.
31. Lo TT, Woo BK. The impact of unemployment on utilization of psychiatric emergency services. Gen Hosp Psychiatry. 2011;33(3):e7-e8. doi: 10.1016/j.genhosppsych.2010.10.010.
32. van der Post LFM, Peen J, Dekker JJ. A prediction model for the incidence of civil detention for crisis patients with psychiatric illnesses; the Amsterdam study of acute psychiatry VII. Soc Psychiatry Psychiatr Epidemiol. 2014;49(2):283-290.
33. Heilbrun K, NeMoyer A, King C, et al. Using third-party information in forensic mental health assessment: a critical review. Court Review. 2015;51(1):16-35.
34. Mass shootings at Virginia Tech, April 16, 2007 report of the Virginia Tech Review Panel presented to Timothy M. Kaine, Governor, Commonwealth of Virginia. http://cdm16064.contentdm.oclc.org/cdm/ref/collection/p266901coll4/id/904. Accessed February 2, 2017.
35. Segal SP, Laurie TA, Segal MJ. Factors in the use of coercive retention in civil commitment evaluations in psychiatric emergency services. Psychiatr Serv. 2001;52(4):514-520.
36. Lincoln A, Allen MH. The influence of collateral information on access to inpatient psychiatric services. International Journal of Psychosocial Rehabilitation. 2002;6:99-108.
37. Anderson JC. How I decided to sue you: misadventures in psychiatry. Reprinted in part from: Moody CE, Smith MT, Maedgen BJ. Litigation of psychiatric malpractice claims. Presented at: Medical Malpractice Conference; April 15, 1993; San Antonio, TX. http://www.texaslawfirm.com/Articles/How_I_Decided_to_Sue_You__Misadventrues_in_Psychiatry.pdf. Accessed December 27, 2016.
38. Jacobs v Grossmont Hospital, 108 Cal App 4th 69, 133 Cal Rptr 2d9 (2003).
39. Bingham v Cedars Sinai Health Systems, WL 2137442, Cal App 2 Dist (2004).
40. Ohio Revised Code §5122.34.
41. California Welfare & Institutions Code §5150(E).
42. Hashmi A, Shad M, Rhoades HM, et al. Involuntary detention: do psychiatrists clinically justify continuing involuntary hospitalization? Psychiatr Q. 2014;85(3):285-293.
43. Brayley J, Alston A, Rogers K. Legal criteria for involuntary mental health admission: clinician performance in recording grounds for decision. Med J Aust. 2015;203(8):334.
44. Perrigo TL, Williams KA. Implementation of an evidence based guideline for assessment and documentation of the civil commitment process. Community Ment Health J. 2016;52(8):1033-1036.
45. Mor S, Rabinovich-Einy O. Relational malpractice. Seton Hall Law Rev. 2012;42(2):601-642.
46. Tate v Kaiser Foundation Hospitals, WL 176625, U.S. Dist. LEXIS 5891 (CD Cal 2014).
47. Ranieri V, Madigan K, Roche E, et al. Caregivers’ perceptions of coercion in psychiatric hospital admission. Psychiatry Res. 2015;22(3)8:380-385.
Dear Dr. Mossman,
Last week, I hospitalized a patient against her will, based in part on what her family members told me she had threatened to do. The patient threatened to sue me and said I should have known that her relatives were lying. What if my patient is right? Could I face liability if I involuntarily hospitalized her based on bad collateral information?
Submitted by “Dr. R”
In all U.S. states, laws permit psychiatrists to involuntarily hospitalize persons who pose a danger to themselves or others because of mental illness.1 But taking this step can be tough. Deciding to hospitalize a patient against her will involves weighing her wants and freedom against your duty to look out for her long-term welfare and the community’s safety.2,3 Often, psychiatrists make these decisions under pressure because the family wants something done immediately, other patients also need attention, the clinical picture is incomplete, or potential dispositions (eg, crisis care and inpatient beds) are limited.3 Given such constraints, you can’t always make perfect decisions.
Dr. R’s question has 2 parts:
- What liabilities can a clinician face if a patient is wrongfully committed?
- What liabilities could arise from relying on inaccurate information or making a false petition in order to hospitalize a patient?
We hope that as you and Dr. R read our answers, you’ll have a clearer understanding of:
- the rationale for civil commitment
- how patients, doctors, and courts view civil commitment
- the role of collateral information in decision-making
- relevant legal concepts and case law.
Rationale for civil commitment
For centuries, society has used civil commitment as one of its legal methods for intervening when persons pose a danger to themselves or others because of their mental illness.4 Because incapacitation or death could result from a “false-negative” decision to release a dangerous patient, psychiatrists err on the side of caution and tolerate many “false-positive” hospitalizations of persons who wouldn’t have hurt anyone.5
We can never know if a patient would have done harm had she not been hospitalized. Measures of suicidality and hostility tend to subside during involuntary hospital treatment.6 After hospitalization, many patients cite protection from harm as a reason they are thankful for their treatment.7-9 Some involuntary inpatients want to be hospitalized but hide this for conscious or unconscious reasons,10,11 and involuntary treatment sometimes is the only way to help persons whose illness-induced anosognosia12 prevents them from understanding why they need treatment.13 Involuntary inpatient care leads to modest symptom reduction14,15 and produces treatment outcomes no worse than those of non-coerced patients.10
Patients’ views
Patients often view commitment as unjustified.16 They and their advocates object to what some view as the ultimate infringement on civil liberty.7,17 By its nature, involuntary commitment eliminates patients’ involvement in a major treatment decision,8 disempowers them,18 and influences their relationship with the treatment team.15
Some involuntary patients feel disrespected by staff members8 or experience inadvertent psychological harm, including “loss of self-esteem, identity, self-control, and self-efficacy, as well as diminished hope in the possibility of recovery.”15 Involuntary hospitalization also can have serious practical consequences. Commitment can lead to social stigma, loss of gun rights, increased risks of losing child custody, housing problems, and possible disqualification from some professions.19
Having seen many involuntary patients undergo a change of heart after treatment, psychiatrist Alan Stone proposed the “Thank You Theory” of civil commitment: involuntary hospitalization can be justified by showing that the patient is grateful after recovering.20 Studies show, however, that gratitude is far from universal.1
How coercion is experienced often depends on how it is communicated. The less coercion patients perceive, the better they feel about the treatment they received.21 Satisfaction is important because it leads to less compulsory readmission,22 and dissatisfaction makes malpractice lawsuits more likely.23
Commitment decision-making
States’ laws, judges’ attitudes, and court decisions establish each jurisdiction’s legal methods for instituting emergency holds and willingness to tolerate “false-positive” involuntary hospitalization,4,24 all of which create variation between and within states in how civil commitment laws are applied. As a result, clinicians’ decisions are influenced “by a range of social, political, and economic factors,”25 including patients’ sex, race, age, homelessness, employment status, living situation, diagnoses, previous involuntary treatment, and dissatisfaction with mental health treatment.22,26-32 Furthermore, the potential for coercion often blurs the line between an offer of voluntary admission and an involuntary hospitalization.18
Collateral information
Psychiatrists owe each patient a sound clinical assessment before deciding to initiate involuntarily hospitalization. During a psychiatric crisis, a patient might not be forthcoming or could have impaired memory or judgment. Information from friends or family can help fill in gaps in a patient’s self-report.33 As Dr. R’s question illustrates, adequate assessment often includes seeking information from persons familiar with the patient.1 A report on the Virginia Tech shootings by the Virginia Office of the Inspector General describes how collateral sources can provide otherwise missing evidence of dangerousness,34 and it often leads clinicians toward favoring admission.35
Yet clinicians should regard third-party reports with caution.36 As one attorney warns, “Psychiatrists should be cautious of the underlying motives of well-meaning family members and relatives.”37 If you make a decision to hospitalize a patient involuntarily based on collateral information that turns out to be flawed, are you at fault and potentially liable for harm to the patient?
False petitions and liability
If you’re in a situation similar to the one Dr. R describes, you can take solace in knowing that courts generally provide immunity to a psychiatrist who makes a reasonable, well-intentioned decision to commit someone. The degree of immunity offered varies by jurisdiction. Table 1 provides examples of immunity language from several states’ statutes.
Many states’ statutes also lay out the potential consequences if a psychiatrist takes action to involuntarily hospitalize someone in bad faith or with malicious intent. In some jurisdictions, such actions can lead to criminal sanctions against the doctor or against the party who made a false petition (eg, a devious family member) (Table 2). Commenting on Texas’s statute, attorney Jeffrey Anderson explains, “The touchstone for causes of action based upon a wrongful civil commitment require that the psychiatrist[’s] conduct be found to be unreasonable and negligent. [Immunity…] still requires that a psychiatrist[’s] diagnosis of a patient[’s] threat to harm himself or others be a reasonable and prudent one.”37
The immunity extended through such statutes usually is limited to claims arising directly from the detention. For example, in the California case of Jacobs v Grossmont Hospital, a patient under a 72-hour hold fell and fractured her leg, and she sought damages. The trial court dismissed the suit under the immunity statute applicable to commitment decisions, but the appellate court held that “the immunity did not extend to other negligent acts.… The trial court erred in assuming that … the hospital was exempt from all liability for any negligence that occurred during the lawful hold.”38
Bingham v Cedars-Sinai Health Systems illustrates how physicians can lose immunity.39 A nurse contacted her supervisor to report a colleague who had stolen narcotics from work and compromised patient care. In response, the supervisor, hospital, and several physicians agreed to have her involuntarily committed. Later, it was confirmed that the colleague had taken the narcotics. She later sued the hospital system, claiming—in addition to malpractice—retaliation, invasion of privacy, assault and battery, false imprisonment, defamation, intentional infliction of emotional distress, disability-based harassment, and violation of her civil rights. Citing California’s immunity statute, the trial court granted summary judgment to the clinicians and hospital system. On appeal, however, the appellate court reversed the judgment, holding that the defendants had not shown that “the decision to detain Bingham was based on probable cause, a prerequisite to the exemption from liability,” and that Bingham had some legitimate grounds for her lawsuit.
A key point for Dr. R to consider is that, although some states provide immunity if the psychiatrist’s admitting decision was based on an evaluation “performed in good faith,”40 other states’ immunity provisions apply only if the psychiatrist had probable cause to make a decision to detain.41
Ways to reduce liability risk
Although an involuntary hospitalization could have an uncertain basis, psychiatrists can reduce the risk of legal liability for their decisions. Good documentation is important. Admitting psychiatrists usually make sound decisions, but the corresponding documentation frequently lacks clinical justification.42-44 As the rate of appropriate documentation of admission decision-making improves, the rate of commitment falls,44 and patients’ legal rights enjoy greater protection.43 Poor communication can decrease the quality of care and increase the risk of a malpractice lawsuit.45 This is just one of many reasons why you should explain your reasons for involuntary hospitalization and inform patients of the procedures for judicial review.8,9 Table 3 summarizes other steps to reduce liability risk when committing patients to the hospital.1,8,15,21,33,35-37,42,45-47
Dear Dr. Mossman,
Last week, I hospitalized a patient against her will, based in part on what her family members told me she had threatened to do. The patient threatened to sue me and said I should have known that her relatives were lying. What if my patient is right? Could I face liability if I involuntarily hospitalized her based on bad collateral information?
Submitted by “Dr. R”
In all U.S. states, laws permit psychiatrists to involuntarily hospitalize persons who pose a danger to themselves or others because of mental illness.1 But taking this step can be tough. Deciding to hospitalize a patient against her will involves weighing her wants and freedom against your duty to look out for her long-term welfare and the community’s safety.2,3 Often, psychiatrists make these decisions under pressure because the family wants something done immediately, other patients also need attention, the clinical picture is incomplete, or potential dispositions (eg, crisis care and inpatient beds) are limited.3 Given such constraints, you can’t always make perfect decisions.
Dr. R’s question has 2 parts:
- What liabilities can a clinician face if a patient is wrongfully committed?
- What liabilities could arise from relying on inaccurate information or making a false petition in order to hospitalize a patient?
We hope that as you and Dr. R read our answers, you’ll have a clearer understanding of:
- the rationale for civil commitment
- how patients, doctors, and courts view civil commitment
- the role of collateral information in decision-making
- relevant legal concepts and case law.
Rationale for civil commitment
For centuries, society has used civil commitment as one of its legal methods for intervening when persons pose a danger to themselves or others because of their mental illness.4 Because incapacitation or death could result from a “false-negative” decision to release a dangerous patient, psychiatrists err on the side of caution and tolerate many “false-positive” hospitalizations of persons who wouldn’t have hurt anyone.5
We can never know if a patient would have done harm had she not been hospitalized. Measures of suicidality and hostility tend to subside during involuntary hospital treatment.6 After hospitalization, many patients cite protection from harm as a reason they are thankful for their treatment.7-9 Some involuntary inpatients want to be hospitalized but hide this for conscious or unconscious reasons,10,11 and involuntary treatment sometimes is the only way to help persons whose illness-induced anosognosia12 prevents them from understanding why they need treatment.13 Involuntary inpatient care leads to modest symptom reduction14,15 and produces treatment outcomes no worse than those of non-coerced patients.10
Patients’ views
Patients often view commitment as unjustified.16 They and their advocates object to what some view as the ultimate infringement on civil liberty.7,17 By its nature, involuntary commitment eliminates patients’ involvement in a major treatment decision,8 disempowers them,18 and influences their relationship with the treatment team.15
Some involuntary patients feel disrespected by staff members8 or experience inadvertent psychological harm, including “loss of self-esteem, identity, self-control, and self-efficacy, as well as diminished hope in the possibility of recovery.”15 Involuntary hospitalization also can have serious practical consequences. Commitment can lead to social stigma, loss of gun rights, increased risks of losing child custody, housing problems, and possible disqualification from some professions.19
Having seen many involuntary patients undergo a change of heart after treatment, psychiatrist Alan Stone proposed the “Thank You Theory” of civil commitment: involuntary hospitalization can be justified by showing that the patient is grateful after recovering.20 Studies show, however, that gratitude is far from universal.1
How coercion is experienced often depends on how it is communicated. The less coercion patients perceive, the better they feel about the treatment they received.21 Satisfaction is important because it leads to less compulsory readmission,22 and dissatisfaction makes malpractice lawsuits more likely.23
Commitment decision-making
States’ laws, judges’ attitudes, and court decisions establish each jurisdiction’s legal methods for instituting emergency holds and willingness to tolerate “false-positive” involuntary hospitalization,4,24 all of which create variation between and within states in how civil commitment laws are applied. As a result, clinicians’ decisions are influenced “by a range of social, political, and economic factors,”25 including patients’ sex, race, age, homelessness, employment status, living situation, diagnoses, previous involuntary treatment, and dissatisfaction with mental health treatment.22,26-32 Furthermore, the potential for coercion often blurs the line between an offer of voluntary admission and an involuntary hospitalization.18
Collateral information
Psychiatrists owe each patient a sound clinical assessment before deciding to initiate involuntarily hospitalization. During a psychiatric crisis, a patient might not be forthcoming or could have impaired memory or judgment. Information from friends or family can help fill in gaps in a patient’s self-report.33 As Dr. R’s question illustrates, adequate assessment often includes seeking information from persons familiar with the patient.1 A report on the Virginia Tech shootings by the Virginia Office of the Inspector General describes how collateral sources can provide otherwise missing evidence of dangerousness,34 and it often leads clinicians toward favoring admission.35
Yet clinicians should regard third-party reports with caution.36 As one attorney warns, “Psychiatrists should be cautious of the underlying motives of well-meaning family members and relatives.”37 If you make a decision to hospitalize a patient involuntarily based on collateral information that turns out to be flawed, are you at fault and potentially liable for harm to the patient?
False petitions and liability
If you’re in a situation similar to the one Dr. R describes, you can take solace in knowing that courts generally provide immunity to a psychiatrist who makes a reasonable, well-intentioned decision to commit someone. The degree of immunity offered varies by jurisdiction. Table 1 provides examples of immunity language from several states’ statutes.
Many states’ statutes also lay out the potential consequences if a psychiatrist takes action to involuntarily hospitalize someone in bad faith or with malicious intent. In some jurisdictions, such actions can lead to criminal sanctions against the doctor or against the party who made a false petition (eg, a devious family member) (Table 2). Commenting on Texas’s statute, attorney Jeffrey Anderson explains, “The touchstone for causes of action based upon a wrongful civil commitment require that the psychiatrist[’s] conduct be found to be unreasonable and negligent. [Immunity…] still requires that a psychiatrist[’s] diagnosis of a patient[’s] threat to harm himself or others be a reasonable and prudent one.”37
The immunity extended through such statutes usually is limited to claims arising directly from the detention. For example, in the California case of Jacobs v Grossmont Hospital, a patient under a 72-hour hold fell and fractured her leg, and she sought damages. The trial court dismissed the suit under the immunity statute applicable to commitment decisions, but the appellate court held that “the immunity did not extend to other negligent acts.… The trial court erred in assuming that … the hospital was exempt from all liability for any negligence that occurred during the lawful hold.”38
Bingham v Cedars-Sinai Health Systems illustrates how physicians can lose immunity.39 A nurse contacted her supervisor to report a colleague who had stolen narcotics from work and compromised patient care. In response, the supervisor, hospital, and several physicians agreed to have her involuntarily committed. Later, it was confirmed that the colleague had taken the narcotics. She later sued the hospital system, claiming—in addition to malpractice—retaliation, invasion of privacy, assault and battery, false imprisonment, defamation, intentional infliction of emotional distress, disability-based harassment, and violation of her civil rights. Citing California’s immunity statute, the trial court granted summary judgment to the clinicians and hospital system. On appeal, however, the appellate court reversed the judgment, holding that the defendants had not shown that “the decision to detain Bingham was based on probable cause, a prerequisite to the exemption from liability,” and that Bingham had some legitimate grounds for her lawsuit.
A key point for Dr. R to consider is that, although some states provide immunity if the psychiatrist’s admitting decision was based on an evaluation “performed in good faith,”40 other states’ immunity provisions apply only if the psychiatrist had probable cause to make a decision to detain.41
Ways to reduce liability risk
Although an involuntary hospitalization could have an uncertain basis, psychiatrists can reduce the risk of legal liability for their decisions. Good documentation is important. Admitting psychiatrists usually make sound decisions, but the corresponding documentation frequently lacks clinical justification.42-44 As the rate of appropriate documentation of admission decision-making improves, the rate of commitment falls,44 and patients’ legal rights enjoy greater protection.43 Poor communication can decrease the quality of care and increase the risk of a malpractice lawsuit.45 This is just one of many reasons why you should explain your reasons for involuntary hospitalization and inform patients of the procedures for judicial review.8,9 Table 3 summarizes other steps to reduce liability risk when committing patients to the hospital.1,8,15,21,33,35-37,42,45-47
1. Pinals DA, Mossman D. Evaluation for civil commitment: best practices for forensic mental health assessments. New York, NY: Oxford University Press; 2011.
2. Testa M, West SG. Civil commitment in the United States. Psychiatry (Edgemont). 2010;7(10):30-40.
3. Hedman LC, Petrila J, Fisher WH, et al. State laws on emergency holds for mental health stabilization. Psychiatr Serv. 2016;67(5):529-535.
4. Groendyk Z. “It takes a lot to get into Bellevue”: a pro-rights critique of New York’s involuntary commitment law. Fordham Urban Law J. 2013;40(1):548-585.
5. Brooks RA. U.S. psychiatrists’ beliefs and wants about involuntary civil commitment grounds. Int J Law Psychiatry. 2006;29(1):13-21.
6. Giacco D, Priebe S. Suicidality and hostility following involuntary hospital treatment. PLoS One. 2016;11(5):e0154458. doi: 10.1371/journal.pone.0154458.
7. Wyder M, Bland R, Herriot A, et al. The experiences of the legal processes of involuntary treatment orders: tension between the legal and medical frameworks. Int J Law Psychiatry. 2015;38:44-50.
8. Valenti E, Giacco D, Katasakou C, et al. Which values are important for patients during involuntary treatment? A qualitative study with psychiatric inpatients. J Med Ethics. 2014;40(12):832-836.
9. Katsakou C, Rose D, Amos T, et al. Psychiatric patients’ views on why their involuntary hospitalisation was right or wrong: a qualitative study. Soc Psychiatry Psychiatr Epidemiol. 2012;42(7):1169-1179.
10. Kaltiala-Heino R, Laippala P, Salokangas RK. Impact of coercion on treatment outcome. Int J Law Psychiatry. 1997;20(3):311-322.
11. Hoge SK, Lidz CW, Eisenberg M, et al. Perceptions of coercion in the admission of voluntary and involuntary psychiatric patients. Int J Law Psychiatry. 1997;20(2):167-181.
12. Lehrer DS, Lorenz J. Anosognosia in schizophrenia: hidden in plain sight. Innov Clin Neurosci. 2014;11(5-6):10-17. 13. Gordon S. The danger zone: how the dangerousness standard in civil commitment proceedings harms people with serious mental illness. Case Western Reserve Law Review. 2016;66(3):657-700.
14. Kallert TW, Katsakou C, Adamowski T, et al. Coerced hospital admission and symptom change—a prospective observational multi-centre study. PLoS One. 2011;6(11):e28191. doi: 10.1371/journal.pone.0028191.
15. Danzer G, Wilkus-Stone A. The give and take of freedom: the role of involuntary hospitalization and treatment in recovery from mental illness. Bull Menninger Clin. 2015;79(3):255-280.
16. Roe D, Weishut DJ, Jaglom M, et al. Patients’ and staff members’ attitudes about the rights of hospitalized psychiatric patients. Psychiatr Serv. 2002;53(1):87-91.
17. Amidov T. Involuntary commitment is unnecessary and discriminatory. In: Berlatsky N, ed. Mental illness. Farmington Hills, MI: Greenhaven Press; 2016;140-145.
18. Monahan J, Hoge SK, Lidz C, et al. Coercion and commitment: understanding involuntary mental hospital admission. Int J Law Psychiatry. 1995;18(3):249-263.
19. Guest Pryal KR. Heller’s scapegoats. North Carolina Law Review. 2015;93(5):1439-1473.
20. Stone AA. Mental health and law: a system in transition. Washington, DC: U.S. Government Printing Office; 1975:75-176.
21. Katsakou C, Bowers L, Amos T, et al. Coercion and treatment satisfaction among involuntary patients. Psychiatr Serv. 2010;61(3):286-292.
22. Setkowski K, van der Post LF, Peen J, et al. Changing patient perspectives after compulsory admission and the risk of re-admission during 5 years of follow-up: the Amsterdam study of acute psychiatry IX. Int J Soc Psychiatry. 2016;62(6):578-588.
23. Stelfox HT, Gandhi TK, Orav EJ, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133.
24. Goldman A. Continued overreliance on involuntary commitment: the need for a less restrictive alternative. J Leg Med. 2015;36(2):233-251.
25. Fisher WH, Grisso T. Commentary: civil commitment statutes—40 years of circumvention. J Am Acad Psychiatry Law. 2010;38(3):365-368.
26. Curley A, Agada E, Emechebe A, et al. Exploring and explaining involuntary care: the relationship between psychiatric admission status, gender and other demographic and clinical variables. Int J Law Psychiatry. 2016;47:53-59.
27. Muroff JR, Jackson JS, Mowbray CT, et al. The influence of gender, patient volume and time on clinical diagnostic decision making in psychiatric emergency services. Gen Hosp Psychiatry. 2007;29(6):481-488.
28. Muroff JR, Edelsohn GA, Joe S, et al. The role of race in diagnostic and disposition decision making in a pediatric psychiatric emergency service. Gen Hosp Psychiatry. 2008;30(3):269-276.
29. Unick GJ, Kessell E, Woodard EK, et al. Factors affecting psychiatric inpatient hospitalization from a psychiatric emergency service. Gen Hosp Psychiatry. 2011;33(6):618-625.
30. Ng XT, Kelly BD. Voluntary and involuntary care: three-year study of demographic and diagnostic admission statistics at an inner-city adult psychiatry unit. Int J Law Psychiatry. 2012;35(4):317-326.
31. Lo TT, Woo BK. The impact of unemployment on utilization of psychiatric emergency services. Gen Hosp Psychiatry. 2011;33(3):e7-e8. doi: 10.1016/j.genhosppsych.2010.10.010.
32. van der Post LFM, Peen J, Dekker JJ. A prediction model for the incidence of civil detention for crisis patients with psychiatric illnesses; the Amsterdam study of acute psychiatry VII. Soc Psychiatry Psychiatr Epidemiol. 2014;49(2):283-290.
33. Heilbrun K, NeMoyer A, King C, et al. Using third-party information in forensic mental health assessment: a critical review. Court Review. 2015;51(1):16-35.
34. Mass shootings at Virginia Tech, April 16, 2007 report of the Virginia Tech Review Panel presented to Timothy M. Kaine, Governor, Commonwealth of Virginia. http://cdm16064.contentdm.oclc.org/cdm/ref/collection/p266901coll4/id/904. Accessed February 2, 2017.
35. Segal SP, Laurie TA, Segal MJ. Factors in the use of coercive retention in civil commitment evaluations in psychiatric emergency services. Psychiatr Serv. 2001;52(4):514-520.
36. Lincoln A, Allen MH. The influence of collateral information on access to inpatient psychiatric services. International Journal of Psychosocial Rehabilitation. 2002;6:99-108.
37. Anderson JC. How I decided to sue you: misadventures in psychiatry. Reprinted in part from: Moody CE, Smith MT, Maedgen BJ. Litigation of psychiatric malpractice claims. Presented at: Medical Malpractice Conference; April 15, 1993; San Antonio, TX. http://www.texaslawfirm.com/Articles/How_I_Decided_to_Sue_You__Misadventrues_in_Psychiatry.pdf. Accessed December 27, 2016.
38. Jacobs v Grossmont Hospital, 108 Cal App 4th 69, 133 Cal Rptr 2d9 (2003).
39. Bingham v Cedars Sinai Health Systems, WL 2137442, Cal App 2 Dist (2004).
40. Ohio Revised Code §5122.34.
41. California Welfare & Institutions Code §5150(E).
42. Hashmi A, Shad M, Rhoades HM, et al. Involuntary detention: do psychiatrists clinically justify continuing involuntary hospitalization? Psychiatr Q. 2014;85(3):285-293.
43. Brayley J, Alston A, Rogers K. Legal criteria for involuntary mental health admission: clinician performance in recording grounds for decision. Med J Aust. 2015;203(8):334.
44. Perrigo TL, Williams KA. Implementation of an evidence based guideline for assessment and documentation of the civil commitment process. Community Ment Health J. 2016;52(8):1033-1036.
45. Mor S, Rabinovich-Einy O. Relational malpractice. Seton Hall Law Rev. 2012;42(2):601-642.
46. Tate v Kaiser Foundation Hospitals, WL 176625, U.S. Dist. LEXIS 5891 (CD Cal 2014).
47. Ranieri V, Madigan K, Roche E, et al. Caregivers’ perceptions of coercion in psychiatric hospital admission. Psychiatry Res. 2015;22(3)8:380-385.
1. Pinals DA, Mossman D. Evaluation for civil commitment: best practices for forensic mental health assessments. New York, NY: Oxford University Press; 2011.
2. Testa M, West SG. Civil commitment in the United States. Psychiatry (Edgemont). 2010;7(10):30-40.
3. Hedman LC, Petrila J, Fisher WH, et al. State laws on emergency holds for mental health stabilization. Psychiatr Serv. 2016;67(5):529-535.
4. Groendyk Z. “It takes a lot to get into Bellevue”: a pro-rights critique of New York’s involuntary commitment law. Fordham Urban Law J. 2013;40(1):548-585.
5. Brooks RA. U.S. psychiatrists’ beliefs and wants about involuntary civil commitment grounds. Int J Law Psychiatry. 2006;29(1):13-21.
6. Giacco D, Priebe S. Suicidality and hostility following involuntary hospital treatment. PLoS One. 2016;11(5):e0154458. doi: 10.1371/journal.pone.0154458.
7. Wyder M, Bland R, Herriot A, et al. The experiences of the legal processes of involuntary treatment orders: tension between the legal and medical frameworks. Int J Law Psychiatry. 2015;38:44-50.
8. Valenti E, Giacco D, Katasakou C, et al. Which values are important for patients during involuntary treatment? A qualitative study with psychiatric inpatients. J Med Ethics. 2014;40(12):832-836.
9. Katsakou C, Rose D, Amos T, et al. Psychiatric patients’ views on why their involuntary hospitalisation was right or wrong: a qualitative study. Soc Psychiatry Psychiatr Epidemiol. 2012;42(7):1169-1179.
10. Kaltiala-Heino R, Laippala P, Salokangas RK. Impact of coercion on treatment outcome. Int J Law Psychiatry. 1997;20(3):311-322.
11. Hoge SK, Lidz CW, Eisenberg M, et al. Perceptions of coercion in the admission of voluntary and involuntary psychiatric patients. Int J Law Psychiatry. 1997;20(2):167-181.
12. Lehrer DS, Lorenz J. Anosognosia in schizophrenia: hidden in plain sight. Innov Clin Neurosci. 2014;11(5-6):10-17. 13. Gordon S. The danger zone: how the dangerousness standard in civil commitment proceedings harms people with serious mental illness. Case Western Reserve Law Review. 2016;66(3):657-700.
14. Kallert TW, Katsakou C, Adamowski T, et al. Coerced hospital admission and symptom change—a prospective observational multi-centre study. PLoS One. 2011;6(11):e28191. doi: 10.1371/journal.pone.0028191.
15. Danzer G, Wilkus-Stone A. The give and take of freedom: the role of involuntary hospitalization and treatment in recovery from mental illness. Bull Menninger Clin. 2015;79(3):255-280.
16. Roe D, Weishut DJ, Jaglom M, et al. Patients’ and staff members’ attitudes about the rights of hospitalized psychiatric patients. Psychiatr Serv. 2002;53(1):87-91.
17. Amidov T. Involuntary commitment is unnecessary and discriminatory. In: Berlatsky N, ed. Mental illness. Farmington Hills, MI: Greenhaven Press; 2016;140-145.
18. Monahan J, Hoge SK, Lidz C, et al. Coercion and commitment: understanding involuntary mental hospital admission. Int J Law Psychiatry. 1995;18(3):249-263.
19. Guest Pryal KR. Heller’s scapegoats. North Carolina Law Review. 2015;93(5):1439-1473.
20. Stone AA. Mental health and law: a system in transition. Washington, DC: U.S. Government Printing Office; 1975:75-176.
21. Katsakou C, Bowers L, Amos T, et al. Coercion and treatment satisfaction among involuntary patients. Psychiatr Serv. 2010;61(3):286-292.
22. Setkowski K, van der Post LF, Peen J, et al. Changing patient perspectives after compulsory admission and the risk of re-admission during 5 years of follow-up: the Amsterdam study of acute psychiatry IX. Int J Soc Psychiatry. 2016;62(6):578-588.
23. Stelfox HT, Gandhi TK, Orav EJ, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133.
24. Goldman A. Continued overreliance on involuntary commitment: the need for a less restrictive alternative. J Leg Med. 2015;36(2):233-251.
25. Fisher WH, Grisso T. Commentary: civil commitment statutes—40 years of circumvention. J Am Acad Psychiatry Law. 2010;38(3):365-368.
26. Curley A, Agada E, Emechebe A, et al. Exploring and explaining involuntary care: the relationship between psychiatric admission status, gender and other demographic and clinical variables. Int J Law Psychiatry. 2016;47:53-59.
27. Muroff JR, Jackson JS, Mowbray CT, et al. The influence of gender, patient volume and time on clinical diagnostic decision making in psychiatric emergency services. Gen Hosp Psychiatry. 2007;29(6):481-488.
28. Muroff JR, Edelsohn GA, Joe S, et al. The role of race in diagnostic and disposition decision making in a pediatric psychiatric emergency service. Gen Hosp Psychiatry. 2008;30(3):269-276.
29. Unick GJ, Kessell E, Woodard EK, et al. Factors affecting psychiatric inpatient hospitalization from a psychiatric emergency service. Gen Hosp Psychiatry. 2011;33(6):618-625.
30. Ng XT, Kelly BD. Voluntary and involuntary care: three-year study of demographic and diagnostic admission statistics at an inner-city adult psychiatry unit. Int J Law Psychiatry. 2012;35(4):317-326.
31. Lo TT, Woo BK. The impact of unemployment on utilization of psychiatric emergency services. Gen Hosp Psychiatry. 2011;33(3):e7-e8. doi: 10.1016/j.genhosppsych.2010.10.010.
32. van der Post LFM, Peen J, Dekker JJ. A prediction model for the incidence of civil detention for crisis patients with psychiatric illnesses; the Amsterdam study of acute psychiatry VII. Soc Psychiatry Psychiatr Epidemiol. 2014;49(2):283-290.
33. Heilbrun K, NeMoyer A, King C, et al. Using third-party information in forensic mental health assessment: a critical review. Court Review. 2015;51(1):16-35.
34. Mass shootings at Virginia Tech, April 16, 2007 report of the Virginia Tech Review Panel presented to Timothy M. Kaine, Governor, Commonwealth of Virginia. http://cdm16064.contentdm.oclc.org/cdm/ref/collection/p266901coll4/id/904. Accessed February 2, 2017.
35. Segal SP, Laurie TA, Segal MJ. Factors in the use of coercive retention in civil commitment evaluations in psychiatric emergency services. Psychiatr Serv. 2001;52(4):514-520.
36. Lincoln A, Allen MH. The influence of collateral information on access to inpatient psychiatric services. International Journal of Psychosocial Rehabilitation. 2002;6:99-108.
37. Anderson JC. How I decided to sue you: misadventures in psychiatry. Reprinted in part from: Moody CE, Smith MT, Maedgen BJ. Litigation of psychiatric malpractice claims. Presented at: Medical Malpractice Conference; April 15, 1993; San Antonio, TX. http://www.texaslawfirm.com/Articles/How_I_Decided_to_Sue_You__Misadventrues_in_Psychiatry.pdf. Accessed December 27, 2016.
38. Jacobs v Grossmont Hospital, 108 Cal App 4th 69, 133 Cal Rptr 2d9 (2003).
39. Bingham v Cedars Sinai Health Systems, WL 2137442, Cal App 2 Dist (2004).
40. Ohio Revised Code §5122.34.
41. California Welfare & Institutions Code §5150(E).
42. Hashmi A, Shad M, Rhoades HM, et al. Involuntary detention: do psychiatrists clinically justify continuing involuntary hospitalization? Psychiatr Q. 2014;85(3):285-293.
43. Brayley J, Alston A, Rogers K. Legal criteria for involuntary mental health admission: clinician performance in recording grounds for decision. Med J Aust. 2015;203(8):334.
44. Perrigo TL, Williams KA. Implementation of an evidence based guideline for assessment and documentation of the civil commitment process. Community Ment Health J. 2016;52(8):1033-1036.
45. Mor S, Rabinovich-Einy O. Relational malpractice. Seton Hall Law Rev. 2012;42(2):601-642.
46. Tate v Kaiser Foundation Hospitals, WL 176625, U.S. Dist. LEXIS 5891 (CD Cal 2014).
47. Ranieri V, Madigan K, Roche E, et al. Caregivers’ perceptions of coercion in psychiatric hospital admission. Psychiatry Res. 2015;22(3)8:380-385.
Prazosin and doxazosin for PTSD are underutilized and underdosed
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
What I wish I knew when I started my internship
In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.
Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.
Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.
Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.
During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.
If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.
Medicine is different in the United States. As an international medica
People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.
Keep your support system. It was 3
If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.
Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.
In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.
Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.
Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.
Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.
During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.
If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.
Medicine is different in the United States. As an international medica
People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.
Keep your support system. It was 3
If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.
Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.
In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.
Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.
Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.
Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.
During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.
If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.
Medicine is different in the United States. As an international medica
People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.
Keep your support system. It was 3
If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.
Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.
Strategies for preventing and detecting false-negatives in urine drug screens
Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.1
There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.
EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.4 However, there are limitations to EIAs used in most hospital laboratories.
Limitations of EIAs
Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).5
Sensitivity. The immunoassay methods used vary in their ability to detect substances and depend on the test’s sensitivity; however, most of these versions have high sensitivity for detecting many illicit substances.4
Specificity and cross-reactivity. Unfortunately, many drugs, such as opioids, amphetamines, and commonly prescribed medications, exhibit cross-reactivity that can produce false-positive results (Table 2).5,6
Synthetic cannabinoids, such as “spice” and cathinones, also known as “bath salts,” cannot be detected with standard UDS. However, some newer EIA kits can detect synthetic cannabinoids but do not detect newer designer drugs.7 Detection of specific cathinones by EIA is not yet available.7
Preventing false-negatives
Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:
- In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.8
- In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).9
- Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.
You can spot and prevent false-negatives by:
Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.
Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.
On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.9 Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.10
Considerations
The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.3 Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.
Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.
1. Substance Abuse and Mental Health Services Administration. Results from the National Survey on Drug Use and Health: detailed tables. Prevalence estimates, standard errors, P values, and sample sizes. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015.pdf. Published September 8, 2016. Accessed February 7, 2017.
2. Schweitzer BN. An assessment of lateral flow immunoassay testing and gas chromatography mass spectrometry as methods for the detection of five drugs of abuse in forensic bloodstains. https://open.bu.edu/bitstream/handle/2144/19477/Schweitzer_bu_0017N_12357.pdf?sequence=1. Published 2016. Accessed February 7, 2017.
3. Pawlowski J, Ellingrod VL. Urine drug screens: when might a test result be false-positive? Current Psychiatry. 2015;14(10):17,22-24.
4. Tenore PL. Advanced urine toxicology testing. J Addict Dis. 2010;29(4):436-448.
5. AIT Laboratories. Physician’s reference for urine and blood drug testing and interpretation. http://web.archive.org/web/20160312195526/http://aitlabs.com/uploadedfiles/services/pocket_guide_smr086.pdf. Published 2011. Accessed February 7, 2017.
6. Saitman A, Park HD, Fitzgerald RL. False-positive interferences of common urine drug screen immunoassays: a review. J Anal Toxicol. 2014;38(7):387-396.
7. Namera A, Kawamura M, Nakamoto A, et al. Comprehensive review of the detection methods for synthetic cannabinoids and cathinones. Forensic Toxicol. 2015;33(2):175-194.
8. Cone EJ, Lange R, Darwin WD. In vivo adulteration: excess fluid ingestion causes false-negative marijuana and cocaine urine test results. J Anal Toxicol. 1998;22(6):460-473.
9. Jaffee WB, Trucco E, Levy S, et al. Is this urine really negative? A systematic review of tampering methods in urine drug screening and testing. J Subst Abuse Treat. 2007;33(1):33-42.
10. Substance Abuse and Mental Health Services Administration. Mandatory guidelines for federal workplace drug testing programs. Federal Register. 2004;69:19644-19673.
Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.1
There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.
EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.4 However, there are limitations to EIAs used in most hospital laboratories.
Limitations of EIAs
Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).5
Sensitivity. The immunoassay methods used vary in their ability to detect substances and depend on the test’s sensitivity; however, most of these versions have high sensitivity for detecting many illicit substances.4
Specificity and cross-reactivity. Unfortunately, many drugs, such as opioids, amphetamines, and commonly prescribed medications, exhibit cross-reactivity that can produce false-positive results (Table 2).5,6
Synthetic cannabinoids, such as “spice” and cathinones, also known as “bath salts,” cannot be detected with standard UDS. However, some newer EIA kits can detect synthetic cannabinoids but do not detect newer designer drugs.7 Detection of specific cathinones by EIA is not yet available.7
Preventing false-negatives
Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:
- In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.8
- In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).9
- Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.
You can spot and prevent false-negatives by:
Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.
Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.
On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.9 Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.10
Considerations
The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.3 Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.
Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.
Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.1
There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.
EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.4 However, there are limitations to EIAs used in most hospital laboratories.
Limitations of EIAs
Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).5
Sensitivity. The immunoassay methods used vary in their ability to detect substances and depend on the test’s sensitivity; however, most of these versions have high sensitivity for detecting many illicit substances.4
Specificity and cross-reactivity. Unfortunately, many drugs, such as opioids, amphetamines, and commonly prescribed medications, exhibit cross-reactivity that can produce false-positive results (Table 2).5,6
Synthetic cannabinoids, such as “spice” and cathinones, also known as “bath salts,” cannot be detected with standard UDS. However, some newer EIA kits can detect synthetic cannabinoids but do not detect newer designer drugs.7 Detection of specific cathinones by EIA is not yet available.7
Preventing false-negatives
Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:
- In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.8
- In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).9
- Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.
You can spot and prevent false-negatives by:
Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.
Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.
On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.9 Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.10
Considerations
The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.3 Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.
Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.
1. Substance Abuse and Mental Health Services Administration. Results from the National Survey on Drug Use and Health: detailed tables. Prevalence estimates, standard errors, P values, and sample sizes. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015.pdf. Published September 8, 2016. Accessed February 7, 2017.
2. Schweitzer BN. An assessment of lateral flow immunoassay testing and gas chromatography mass spectrometry as methods for the detection of five drugs of abuse in forensic bloodstains. https://open.bu.edu/bitstream/handle/2144/19477/Schweitzer_bu_0017N_12357.pdf?sequence=1. Published 2016. Accessed February 7, 2017.
3. Pawlowski J, Ellingrod VL. Urine drug screens: when might a test result be false-positive? Current Psychiatry. 2015;14(10):17,22-24.
4. Tenore PL. Advanced urine toxicology testing. J Addict Dis. 2010;29(4):436-448.
5. AIT Laboratories. Physician’s reference for urine and blood drug testing and interpretation. http://web.archive.org/web/20160312195526/http://aitlabs.com/uploadedfiles/services/pocket_guide_smr086.pdf. Published 2011. Accessed February 7, 2017.
6. Saitman A, Park HD, Fitzgerald RL. False-positive interferences of common urine drug screen immunoassays: a review. J Anal Toxicol. 2014;38(7):387-396.
7. Namera A, Kawamura M, Nakamoto A, et al. Comprehensive review of the detection methods for synthetic cannabinoids and cathinones. Forensic Toxicol. 2015;33(2):175-194.
8. Cone EJ, Lange R, Darwin WD. In vivo adulteration: excess fluid ingestion causes false-negative marijuana and cocaine urine test results. J Anal Toxicol. 1998;22(6):460-473.
9. Jaffee WB, Trucco E, Levy S, et al. Is this urine really negative? A systematic review of tampering methods in urine drug screening and testing. J Subst Abuse Treat. 2007;33(1):33-42.
10. Substance Abuse and Mental Health Services Administration. Mandatory guidelines for federal workplace drug testing programs. Federal Register. 2004;69:19644-19673.
1. Substance Abuse and Mental Health Services Administration. Results from the National Survey on Drug Use and Health: detailed tables. Prevalence estimates, standard errors, P values, and sample sizes. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015/NSDUH-DetTabs-2015.pdf. Published September 8, 2016. Accessed February 7, 2017.
2. Schweitzer BN. An assessment of lateral flow immunoassay testing and gas chromatography mass spectrometry as methods for the detection of five drugs of abuse in forensic bloodstains. https://open.bu.edu/bitstream/handle/2144/19477/Schweitzer_bu_0017N_12357.pdf?sequence=1. Published 2016. Accessed February 7, 2017.
3. Pawlowski J, Ellingrod VL. Urine drug screens: when might a test result be false-positive? Current Psychiatry. 2015;14(10):17,22-24.
4. Tenore PL. Advanced urine toxicology testing. J Addict Dis. 2010;29(4):436-448.
5. AIT Laboratories. Physician’s reference for urine and blood drug testing and interpretation. http://web.archive.org/web/20160312195526/http://aitlabs.com/uploadedfiles/services/pocket_guide_smr086.pdf. Published 2011. Accessed February 7, 2017.
6. Saitman A, Park HD, Fitzgerald RL. False-positive interferences of common urine drug screen immunoassays: a review. J Anal Toxicol. 2014;38(7):387-396.
7. Namera A, Kawamura M, Nakamoto A, et al. Comprehensive review of the detection methods for synthetic cannabinoids and cathinones. Forensic Toxicol. 2015;33(2):175-194.
8. Cone EJ, Lange R, Darwin WD. In vivo adulteration: excess fluid ingestion causes false-negative marijuana and cocaine urine test results. J Anal Toxicol. 1998;22(6):460-473.
9. Jaffee WB, Trucco E, Levy S, et al. Is this urine really negative? A systematic review of tampering methods in urine drug screening and testing. J Subst Abuse Treat. 2007;33(1):33-42.
10. Substance Abuse and Mental Health Services Administration. Mandatory guidelines for federal workplace drug testing programs. Federal Register. 2004;69:19644-19673.
Clinical rating scales
Expanding APRN practice and more
Medical psychiatry: The skill of integrating medical and psychiatric care
Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.
However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.
My years training in internal medicine were full of patients with neuropsychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.
The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.1 At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.
What is medical psychiatry, and why is it relevant now?
There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.
Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.
Whether due to infectious, autoimmune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.
An illustrative case
I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.2
Medicine is our calling
Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-
Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.
At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 19771—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”
2. Summergrad P. Depression in Binswanger’s encephalopathy responsive to tranylcypromine: case report. J Clin Psychiatry. 1985;46(2):69-70.
Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.
However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.
My years training in internal medicine were full of patients with neuropsychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.
The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.1 At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.
What is medical psychiatry, and why is it relevant now?
There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.
Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.
Whether due to infectious, autoimmune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.
An illustrative case
I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.2
Medicine is our calling
Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-
Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.
At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 19771—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”
Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.
However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.
My years training in internal medicine were full of patients with neuropsychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.
The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.1 At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.
What is medical psychiatry, and why is it relevant now?
There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.
Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.
Whether due to infectious, autoimmune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.
An illustrative case
I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.2
Medicine is our calling
Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-
Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.
At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 19771—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”
2. Summergrad P. Depression in Binswanger’s encephalopathy responsive to tranylcypromine: case report. J Clin Psychiatry. 1985;46(2):69-70.
2. Summergrad P. Depression in Binswanger’s encephalopathy responsive to tranylcypromine: case report. J Clin Psychiatry. 1985;46(2):69-70.
Don’t balk at using medical therapy to manage alcohol use disorder
There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).
Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.
Diverse presentations
Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?
Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.
As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.1 Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.2 Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.
Pharmacotherapy is underutilized
Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is underutilized: only 3% of patients have received an FDA-approved treatment.2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.3 Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.
Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.
Neuroscience supports the brain disease model of addiction, with neuroplasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.6
Why hesitate to use pharmacotherapeutics?
There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?
Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:
- lack of familiarity with available agents
- absence of guidelines for use
- disbelief that the condition is treatable.
Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.
Therapeutic options
Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.
There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.
With regard to off-label medications, topiramate has the highest evidence for efficacy. Gabapentin can augment naltrexone and also helps with sleep, anxiety, withdrawal, and cravings.4,5
Psychosocial interventions
Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.
The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.
In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.
1. Johnson L, O’Malley P, Miech RA, et al. Monitoring the Future national survey results on drug use, 1975-2015: overview, key findings on adolescent drug use. http://www.monitoringthefuture.org/pubs/monographs/mtf-overview2015.pdf. Published February 2016. Accessed January 20, 2016.
2. Substance Abuse and Mental Health Services Administration. Results from the 2013 national survey on drug use and health: mental health findings, NSDUH Series H-49, HHS Publication No. (SMA) 14-4887. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2014.
3. Grant BF, Goldstein RB, Saha TD, et al. Epidemiology of DSM-5 alcohol use disorder: results from the National Epidemiological Survey on Alcohol and Related Conditions III. JAMA Psychiatry. 2015;72(8):757-766.
4. Robinson S, Meeks TW, Geniza C. Medication for alcohol use disorder: which agents work best. Current Psychiatry. 2014;13(1):22-29.
5. Substance Abuse and Mental Health Services Administration and National Institute on Alcohol Abuse and Alcoholism. Medication for the treatment of alcohol use disorder: a brief guide. HHS Publication No. (SMA) 15-4907. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2015.
6. Volkow ND, Koob GF, McLellan AT. Neurobiological advances from the brain disease model of addiction. N Engl J Med. 2016;374(4):363-371.
There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).
Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.
Diverse presentations
Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?
Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.
As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.1 Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.2 Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.
Pharmacotherapy is underutilized
Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is underutilized: only 3% of patients have received an FDA-approved treatment.2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.3 Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.
Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.
Neuroscience supports the brain disease model of addiction, with neuroplasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.6
Why hesitate to use pharmacotherapeutics?
There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?
Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:
- lack of familiarity with available agents
- absence of guidelines for use
- disbelief that the condition is treatable.
Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.
Therapeutic options
Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.
There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.
With regard to off-label medications, topiramate has the highest evidence for efficacy. Gabapentin can augment naltrexone and also helps with sleep, anxiety, withdrawal, and cravings.4,5
Psychosocial interventions
Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.
The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.
In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.
There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).
Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.
Diverse presentations
Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?
Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.
As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.1 Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.2 Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.
Pharmacotherapy is underutilized
Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is underutilized: only 3% of patients have received an FDA-approved treatment.2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.3 Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.
Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.
Neuroscience supports the brain disease model of addiction, with neuroplasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.6
Why hesitate to use pharmacotherapeutics?
There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?
Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:
- lack of familiarity with available agents
- absence of guidelines for use
- disbelief that the condition is treatable.
Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.
Therapeutic options
Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.
There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.
With regard to off-label medications, topiramate has the highest evidence for efficacy. Gabapentin can augment naltrexone and also helps with sleep, anxiety, withdrawal, and cravings.4,5
Psychosocial interventions
Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.
The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.
In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.
1. Johnson L, O’Malley P, Miech RA, et al. Monitoring the Future national survey results on drug use, 1975-2015: overview, key findings on adolescent drug use. http://www.monitoringthefuture.org/pubs/monographs/mtf-overview2015.pdf. Published February 2016. Accessed January 20, 2016.
2. Substance Abuse and Mental Health Services Administration. Results from the 2013 national survey on drug use and health: mental health findings, NSDUH Series H-49, HHS Publication No. (SMA) 14-4887. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2014.
3. Grant BF, Goldstein RB, Saha TD, et al. Epidemiology of DSM-5 alcohol use disorder: results from the National Epidemiological Survey on Alcohol and Related Conditions III. JAMA Psychiatry. 2015;72(8):757-766.
4. Robinson S, Meeks TW, Geniza C. Medication for alcohol use disorder: which agents work best. Current Psychiatry. 2014;13(1):22-29.
5. Substance Abuse and Mental Health Services Administration and National Institute on Alcohol Abuse and Alcoholism. Medication for the treatment of alcohol use disorder: a brief guide. HHS Publication No. (SMA) 15-4907. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2015.
6. Volkow ND, Koob GF, McLellan AT. Neurobiological advances from the brain disease model of addiction. N Engl J Med. 2016;374(4):363-371.
1. Johnson L, O’Malley P, Miech RA, et al. Monitoring the Future national survey results on drug use, 1975-2015: overview, key findings on adolescent drug use. http://www.monitoringthefuture.org/pubs/monographs/mtf-overview2015.pdf. Published February 2016. Accessed January 20, 2016.
2. Substance Abuse and Mental Health Services Administration. Results from the 2013 national survey on drug use and health: mental health findings, NSDUH Series H-49, HHS Publication No. (SMA) 14-4887. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2014.
3. Grant BF, Goldstein RB, Saha TD, et al. Epidemiology of DSM-5 alcohol use disorder: results from the National Epidemiological Survey on Alcohol and Related Conditions III. JAMA Psychiatry. 2015;72(8):757-766.
4. Robinson S, Meeks TW, Geniza C. Medication for alcohol use disorder: which agents work best. Current Psychiatry. 2014;13(1):22-29.
5. Substance Abuse and Mental Health Services Administration and National Institute on Alcohol Abuse and Alcoholism. Medication for the treatment of alcohol use disorder: a brief guide. HHS Publication No. (SMA) 15-4907. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2015.
6. Volkow ND, Koob GF, McLellan AT. Neurobiological advances from the brain disease model of addiction. N Engl J Med. 2016;374(4):363-371.
When to consider cranial electrotherapy stimulation for patients with PTSD
Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).
As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.1 In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.
How CES works
After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.1 The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.3
There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.1
Evidence of efficacy
There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.
- In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.4
- In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.5 Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.5
- In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.6
Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.5
Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.7 Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.
1. Kirsch DL, Nichols F. Cranial electrotherapy stimulation for treatment of anxiety, depression, and insomnia. Psychiatr Clin North Am. 2013;36(1):169-176.
2. Feusner JD, Madsen S, Moody TD, et al. Effects of cranial electrotherapy stimulation on resting state brain activity. Brain Behav. 2012;2(3):211-220.
3. Shealy CN, Cady RK, Culver-Veehoff D, et al. Cerebrospinal fluid and plasma neurochemicals: response to cranial electrical stimulation. J Neuro Orthop Med Surg. 1998;18(2):94-97.
4. Bracciano AG, Chang WP, Kokesh S, et al. Cranial electrotherapy stimulation in the treatment of posttraumatic stress disorder: a pilot study of two military veterans. J Neurother. 2012;16(1):60-69.
5. Kirsch DL, Price LR, Nichols F, et al. Military service member and veteran self reports of efficacy of cranial electrotherapy stimulation for anxiety, posttraumatic stress disorder, insomnia, and depression. US Army Med Dep J. 2014:46-54.
6. Xenakis SN. The rise of cranial electrotherapy. Psychiatric Times. http://www.psychiatrictimes.com/electroconvulsive-therapy/rise-cranial-electrotherapy. Published July 24, 2014. Accessed December 20, 2016.
7. Mischoulon D, De Jong MF, Vitolo OV, et al. Efficacy and safety of a form of cranial electrical stimulation (CES) as an add-on intervention for treatment-resistant major depressive disorder: a three week double blind pilot study. J Psychiatr Res. 2015;70:98-105.
Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).
As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.1 In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.
How CES works
After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.1 The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.3
There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.1
Evidence of efficacy
There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.
- In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.4
- In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.5 Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.5
- In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.6
Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.5
Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.7 Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.
Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).
As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.1 In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.
How CES works
After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.1 The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.3
There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.1
Evidence of efficacy
There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.
- In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.4
- In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.5 Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.5
- In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.6
Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.5
Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.7 Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.
1. Kirsch DL, Nichols F. Cranial electrotherapy stimulation for treatment of anxiety, depression, and insomnia. Psychiatr Clin North Am. 2013;36(1):169-176.
2. Feusner JD, Madsen S, Moody TD, et al. Effects of cranial electrotherapy stimulation on resting state brain activity. Brain Behav. 2012;2(3):211-220.
3. Shealy CN, Cady RK, Culver-Veehoff D, et al. Cerebrospinal fluid and plasma neurochemicals: response to cranial electrical stimulation. J Neuro Orthop Med Surg. 1998;18(2):94-97.
4. Bracciano AG, Chang WP, Kokesh S, et al. Cranial electrotherapy stimulation in the treatment of posttraumatic stress disorder: a pilot study of two military veterans. J Neurother. 2012;16(1):60-69.
5. Kirsch DL, Price LR, Nichols F, et al. Military service member and veteran self reports of efficacy of cranial electrotherapy stimulation for anxiety, posttraumatic stress disorder, insomnia, and depression. US Army Med Dep J. 2014:46-54.
6. Xenakis SN. The rise of cranial electrotherapy. Psychiatric Times. http://www.psychiatrictimes.com/electroconvulsive-therapy/rise-cranial-electrotherapy. Published July 24, 2014. Accessed December 20, 2016.
7. Mischoulon D, De Jong MF, Vitolo OV, et al. Efficacy and safety of a form of cranial electrical stimulation (CES) as an add-on intervention for treatment-resistant major depressive disorder: a three week double blind pilot study. J Psychiatr Res. 2015;70:98-105.
1. Kirsch DL, Nichols F. Cranial electrotherapy stimulation for treatment of anxiety, depression, and insomnia. Psychiatr Clin North Am. 2013;36(1):169-176.
2. Feusner JD, Madsen S, Moody TD, et al. Effects of cranial electrotherapy stimulation on resting state brain activity. Brain Behav. 2012;2(3):211-220.
3. Shealy CN, Cady RK, Culver-Veehoff D, et al. Cerebrospinal fluid and plasma neurochemicals: response to cranial electrical stimulation. J Neuro Orthop Med Surg. 1998;18(2):94-97.
4. Bracciano AG, Chang WP, Kokesh S, et al. Cranial electrotherapy stimulation in the treatment of posttraumatic stress disorder: a pilot study of two military veterans. J Neurother. 2012;16(1):60-69.
5. Kirsch DL, Price LR, Nichols F, et al. Military service member and veteran self reports of efficacy of cranial electrotherapy stimulation for anxiety, posttraumatic stress disorder, insomnia, and depression. US Army Med Dep J. 2014:46-54.
6. Xenakis SN. The rise of cranial electrotherapy. Psychiatric Times. http://www.psychiatrictimes.com/electroconvulsive-therapy/rise-cranial-electrotherapy. Published July 24, 2014. Accessed December 20, 2016.
7. Mischoulon D, De Jong MF, Vitolo OV, et al. Efficacy and safety of a form of cranial electrical stimulation (CES) as an add-on intervention for treatment-resistant major depressive disorder: a three week double blind pilot study. J Psychiatr Res. 2015;70:98-105.