Evidence-Based Reviews

Self-mutilation has the power to confuse, frustrate, and frighten patients and their families. Psychiatrists, too, are not immune to the intense emotional responses that pathologic self-mutilation can provoke.

One definition of self-mutilation is any self-directed, repetitive behavior that causes physical injury.¹ Examples vary widely and include skin cutting, burning, or picking as well as head banging and extreme injuries such as auto enucleation. Most acts of self-mutilation are not suicide attempts but behaviors meant to express or release emotional turmoil.

As difficult as self-mutilation may be to understand, managing this condition may be even more complex. A multidisciplinary approach may be required, but evidence for the effectiveness of psycho- and pharmacotherapies is limited. This article reviews some theories of pathologic self-mutilation and describes emerging clinical strategies to treat it.

Four types of self-mutilation

DSM-IV does not recognize self-mutilation as a separate disorder but sees it as a symptom of other psychiatric conditions.^2,3 It is briefly mentioned as one criterion for diagnosing borderline personality disorder (“recurrent suicidal behaviors, gestures or threats or self-mutilating behaviors”), and it also appears in the catch-all diagnosis of impulse control disorders, not otherwise specified (NOS). Other self-injurious behaviors such as substance use disorders, trichotillomania, and, in some respects, pathologic gambling have found their way into DSM-IV as addiction or impulse control disorders. Self-mutilation appears to fall between these diagnostic categories, as it contains elements of many psychiatric disorders, such as:

• loss of behavioral control
• repetitive actions despite negative consequences
• and clear dysregulation of thought and emotions.⁴

Self-mutilation presents in a variety of forms and encompasses many behaviors, from the socially acceptable to the bizarre and grotesque (Table 1). Favazza and Rosenthal described three main forms of pathologic self-mutilation.^2,5 A fourth form (such as ear piercing) is socially accepted and not considered pathologic.

Table 1

FOUR TYPES OF SELF-MUTILATION

• Severe self-mutilation manifests as extensive (and often irreversible) body damage. Examples include eye enucleation, castration, or amputation. Intense psychotic states and intoxication from illicit substances—usually amphetamines—are the main causes of this relatively rare type, which fortunately is not frequently repeated.
• Stereotyped self-mutilation is self-directed physical injury (head banging, biting oneself) seen in mental retardation and developmental disorders. This type has a stereotyped and repetitive rhythm and presents in the clear context of a neurobiological insult.
• Superficial or moderate self-mutilation—seen most commonly in general psychiatric practice—includes skin cutting, burning, or picking by nonpsychotic, nonmentally retarded patients. The behavior tends to be repetitive. Patients with this type usually present with comorbid conditions, particularly personality disorders.
• Socially accepted self-mutilation includes ear piercing, tattoos, or culturally based behaviors, such as lip piercing or ear stretching seen in some African cultures.

An impulse control disorder?

Over the last 15 years, increasing evidence has suggested that pathologic self-mutilation may be an impulse control disorder.⁶ Many clinical case reports demonstrate that self-mutilation shares two characteristics of impulse control disorders that involve such behaviors as gambling, sex, or stealing:

• failure to resist impulses/urges to participate in a particular behavior
• increasing tension or physical arousal before the act and release of pleasure or gratification after the act.

In the case report, “Pain from cutting makes me feel alive” (box), the patient describes being unable to resist thoughts of cutting herself or to stop the behavior, despite knowing that she should. Self-mutilators also have been shown to have biological measures of impulsivity—namely decreased serotonin levels—similar to those seen with other impulse control disorders.^7,8 Finally, evidence is emerging that acts of self-mutilation are socially triggered expressions of impulsive psychological traits.^5-7

Risk factors

Accurate estimates of self-mutilation’s incidence and prevalence are lacking, mainly because the behavior is difficult to define. In the U.S. population, Favazza estimated the prevalence as 0.75% and the incidence between 14 and 600 per 100,000 persons annually.⁵ Known risk factors are:

• female gender
• adolescence and college age
• substance abuse and/or personality disorders
• history of self-mutilation^3,9,10 (Table 2).

Comorbidities such as depression, bipolar disorder, substance abuse, and schizophrenia are common. Axis II phenomena are common, especially the cluster B traits of histrionic, narcissistic, and borderline personalities.

Finally, little is known about the course of self-mutilation, but it tends to begin in adolescence and follows an episodic, recurrent pattern.¹¹ Reports are scant of self-mutilation in the elderly, although clinical experience tells us that it does occur in this age group.

Causes

Several theories addressing the causes of self-mutilation have been championed. A few, with particular attention to impulse-control dysfunction, are described here.

Biological contributions. Support for a biological mechanism is beginning to emerge. Dysregulation in neurotransmission or neurobiological function may predispose a person to self-mutilate through the expression of impulsive traits such as motor disinhibition and a tendency to physical aggression.⁶ Decreased serotonergic functioning or a central deficit in serotonergic functioning—as measured by platelet imipramine binding levels and serotonin metabolites in the CSF—are seen in self-mutilators and persons with other impulsive behaviors, such as completed suicide, physical aggression, and pathologic gambling.^11,12

Box

CASE REPORT ‘PAIN FROM CUTTING MAKES ME FEEL ALIVE’

Mrs. K, age 39, is being treated for depression. She reports an onset of cutting behavior in college after she broke up with a boyfriend. She recalls being so agitated at the time that she instinctively grabbed a knife and began scraping her forearm. Since then, she has been cutting about three to four times a year and always in the context of an overwhelming stressful situation. So far, no serious medical consequences have resulted; she usually draws blood, then cleans and bandages the wound.

She is facing a divorce and is in a tumultuous battle with her estranged husband over custody of their children. As a result, her cutting behavior has increased in frequency to once or twice a week. These behaviors bother her, but she also reports that cutting allows her to “feel pain that makes me feel alive.” She denies suicidal intent. She wishes she could use another way to deal with emotional pain but finds herself yielding to cutting behaviors. Mrs. K has tried alcohol on some occasions and thought about using illicit drugs but did not know how to get them.

One of the reasons she sought treatment was to reduce her cutting behaviors. She feels that she can’t control her behavior and wants to understand why she repetitively chooses to engage in it.

Self-mutilators also respond abnormally to infusions of the adrenergic agent fenfluramine—they show decreased release of prolactin, which signals reduced serotonergic function.^11,12 Reports of a blunted serotonergic response in patients who attempt suicide and in those who complete a self-mutilation act strengthen this theory of a biological contribution.¹²

Finally, in examining the relationship of impulsivity and serotonergic function, Herpertz found a link between trait impulsivity—as measured by a deficit in problem-solving ability and affective hyperreactivity—and low serotonergic function.⁶ What remains unclear, however, is cause and effect: do impulsivity traits cause serotonergic dysfunction, or do serotonin function deficits manifest as impulsivity?

Table 2

PROFILE OF PATHOLOGIC SELF-MUTILATORS

In one fascinating study, self-mutilators whose primary diagnosis was borderline personality disorder tolerated more physical pain than did healthy controls.⁷ When they were tested during a distressed state of mind, self-mutilators’ pain thresholds were even more elevated. This finding suggests alterations in the opiate systems and stress-response pathways.

Further work—including genetic studies and functional neuroimaging—is needed to better understand the neurobiological locus of pathologic self-mutilation.

Psychological contributions. Self-mutilation may represent a compromise between choosing life or death. Some analysts have viewed self-mutilation as a coping mechanism to avoid suicide.^1,13 In other words, self-mutilation is the expression of psychic pain turned outward but without the intent to end life. Self-mutilation may then be viewed as a way to concretely demonstrate negative affective states to the self and to the world. It also may serve as a tool to regulate and cope with these negative affective states.

Unfortunately, this coping behavior can become irresistible and psychologically tempting. One self-mutilator writes, “It’s like a relief; I do it [cutting on her wrists] every couple of weeks, just to get relief…from pressure that builds up inside…you feel like you’re going to explode if you don’t cut.”¹ The described rise in tension is reminiscent of other impulse control disorders.

Hyperreactivity of decision-making also is correlated with self-mutilation, as it is with impulse-control disorders. Impulsive people tend to respond very quickly to environmental stimuli, rather than suppressing physical and emotional responses.⁶ One behavioral definition of impulsivity is the tendency to choose smaller, more immediate rewards instead of larger, delayed rewards. In the case report presented earlier, Mrs. K chose to cut her wrists instead of waiting for the negative affective state to pass. Waiting—which would have taken more time—would have offered the obvious benefit of avoiding physical harm.

Social contributions. The act of self-mutilation typically grabs the attention of a therapist, friends, or spouses. Operant conditioning—where the positive rewards of help, empathy, and attention follow self-mutilation—may reinforce and perpetuate the behavior.¹ Other social contributions may include:

• dysfunctional family systems
• lack of social support
• poor communication skills
• role expectations, such as school/work performance, sexuality, or career obligations.¹³

When social pressures demand immediate decisions, impulsive self-mutilators may feel an urgency to act instead of using other coping mechanisms. Leibenluft et al published what may be the only empiric study that addresses this “inner experience” of the self-mutilator with borderline personality disorder.¹⁴ In our case example, the pressures of an imminent divorce trial triggered Mrs. K’s most recent cutting behavior. She did not have a strong support system and—in her desperation to control something—she resorted to cutting.

Pharmacologic treatment

Just as the cause of self-mutilation is multidimensional, so is its treatment. Research has focused on medications, individual therapy, and social therapy. Not surprisingly, these approaches resemble the treatment of other impulse control disorders.

Most of the evidence for drug treatment of self-mutilation comes from case reports and small openlabel studies. A variety of medication classes have been tried.

Antidepressants. In theory, if reduced serotonin neurotransmission helps drive pathologic self-mutilation, then using selective serotonin reuptake inhibitors (SSRIs) to increase serotonin availability may reduce impulsivity. For example, Velazquez described the case of an 11-year-old boy whose finger-chewing behavior diminished with fluoxetine therapy.¹⁵

Most of the SSRI studies have examined self-mutilation in the context of treating personality disorders, especially borderline personality disorder. SSRIs have been shown to modestly reduce anger and negative affective states, but the studies do not refer specifically to their effect on the frequency of self-mutilation. Given the present evidence, SSRIs appear to be an appropriate first-line treatment for self-mutilation because of their:

• overall safety profile
• effectiveness in treating mood lability and reactivity
• documented deficits in serotonergic neurotransmission.

Still, little empiric data exists regarding their use in treating self-mutilation, and prescribers should watch for possible side effects. No SSRI appears to be best suited to treat this disorder. Base initial selection on prior medication trials and on whether a drug’s side effects could work in the patient’s favor. For example, paroxetine’s more sedating properties may benefit a patient with difficulty sleeping, whereas sertraline’s more activating properties may help the lethargic patient with psychomotor retardation.

Atypical antipsychotics are often used in patients with borderline personality disorders or mental retardation to reduce impulsive physical aggression and mood lability. Their wide range of pharmacologic effects—including serotonin and dopamine blockade—suggests why they may have thymoleptic properties related to mood, anxiety, impulsiveness, and overall behavioral control. Small trials have demonstrated that olanzapine and clozapine may help control self-mutilation,^16,17 but controlled trials are lacking.

Mood stabilizers. Case reports have described use of lithium, divalproex, and topiramate to reduce the frequency of self-mutilation, but—as with antipsychotics—controlled studies are lacking.¹⁸ Mood stabilizers are appropriate in self-mutilators with co-existing bipolar disorder and possibly in those whose self-mutilation has cycling or circadian properties.

Anxiolytics. The sedative effects of benzodiazepines such as lorazepam or clonazepam may help control agitation and attempts to self-mutilate in emergent inpatient settings. This drug class carries a high abuse potential and may cause behavioral disinhibition, especially with mentally retarded patients. These properties limit benzodiazepines’ usefulness in outpatient treatment of self-mutilation.

Box 2

Opiate antagonists. Naltrexone and nalmefene have been shown to be effective in other impulse control disorders, such as pathologic gambling and kleptomania.^19,20 In self-mutilation, the use of opiate antagonists has been limited to case reports in patients with autism or mental retardation.

Although unproven, it may be that self-injurious behaviors are reinforced by a release of endogenous opioids. In theory, then, blocking opiate release would reduce the behaviors, as patients would then respond more normally to pain. The behavior would extinguish without the reward.^19,20

Opiate antagonists, which purportedly reduce urges and cravings to drink or to gamble, may also block urges and cravings to self-mutilate. Problems with using these agents include the need for periodic liver function tests and side effects such as nausea and gastrointestinal disturbances.

Psychotherapeutic approaches

Psychodynamic psychotherapy is the most common form of individual therapy used in treating self-mutilation. Effective therapy enables patients to understand why they self-mutilate and teaches them more healthy ways to deal with negative internal states.^2,3

Individual therapy is the mainstay of self-mutilation treatment, although no known studies have confirmed that psychodynamic psychotherapy reduces acts of self-mutilation. Because self-mutilators tend to have poor boundaries, supervision and peer collaboration are highly recommended to maintain an effective therapeutic relationship.¹

Yet to be answered is whether healthier coping strategies alter measures of impulsivity. Patients who have improved report they are better able to cope with negative affective states and to verbalize their feelings.

Dialectical behavior therapy (DBT) is another psychotherapeutic option. Used in treating personality disorders, DBT combines cognitive, behavioral, and supportive interventions. In one study, DBT reduced the frequency of self-mutilation to 1.5 acts per year, compared with 9 acts per year in a treatment-as-usual control group.²¹

Need for ‘emergency plans’

Relaxation training, exposure therapy, and response prevention have been suggested as treatments for pathologic self-mutilation, but there is no convincing evidence to support their efficacy.¹ Contracts against self-mutilation do not appear to be effective. Instead, “emergency plans” may be needed to deal with urges to self-mutilate.

Crisis intervention strategies that may help the self-mutilator include:

• partial hospitalizations to focus on increasing coping skills and strengthening a patient’s sense of self-reliance and individual responsibility
• increased frequency of visits
• educating the patient to use medications such as atypical neuroleptics or benzodiazepines as needed (“in case of emergency, take this medication instead of cutting”).

Crisis interventions should focus on understanding and changing pathologic behaviors. Self-mutilation behavior may be reinforced if attention is given without enough emphasis on developing coping skills.

Group therapy may be another treatment option. Group support helps patients with pathologic gambling, addictive, or other impulse control disorders to prevent relapse and learn to deal with urges and impulses.

Related resources

• Self-injury Web site offering information about self-harming behavior plus coping skills, alternatives to self-injury, support groups. www.selfabuse.com
• Levenkron S. Cutting: understanding and overcoming self-mutilation. New York: WW Norton and Company Ltd, 1998.
• SAFE (Self-Abuse Finally Ends), www.selfinjury.com. Resources for patients, families, and therapists. Recording at 1-800-DON’T-CUT (800-366-8288) offers to mail information on self-injury and the SAFE Alternatives program.

Drug brand names

• Clonazepam • Klonopin
• Clozapine • Clozaril
• Fluoxetine • Prozac
• Lorazepam • Ativan
• Naltrexone • ReVia
• Nalmefene • Revex
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Sertraline • Zoloft
• Topiramate • Topamax

Disclosure

Dr. Fong reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Self-mutilation has the power to confuse, frustrate, and frighten patients and their families. Psychiatrists, too, are not immune to the intense emotional responses that pathologic self-mutilation can provoke.

One definition of self-mutilation is any self-directed, repetitive behavior that causes physical injury.¹ Examples vary widely and include skin cutting, burning, or picking as well as head banging and extreme injuries such as auto enucleation. Most acts of self-mutilation are not suicide attempts but behaviors meant to express or release emotional turmoil.

As difficult as self-mutilation may be to understand, managing this condition may be even more complex. A multidisciplinary approach may be required, but evidence for the effectiveness of psycho- and pharmacotherapies is limited. This article reviews some theories of pathologic self-mutilation and describes emerging clinical strategies to treat it.

Four types of self-mutilation

DSM-IV does not recognize self-mutilation as a separate disorder but sees it as a symptom of other psychiatric conditions.^2,3 It is briefly mentioned as one criterion for diagnosing borderline personality disorder (“recurrent suicidal behaviors, gestures or threats or self-mutilating behaviors”), and it also appears in the catch-all diagnosis of impulse control disorders, not otherwise specified (NOS). Other self-injurious behaviors such as substance use disorders, trichotillomania, and, in some respects, pathologic gambling have found their way into DSM-IV as addiction or impulse control disorders. Self-mutilation appears to fall between these diagnostic categories, as it contains elements of many psychiatric disorders, such as:

• loss of behavioral control
• repetitive actions despite negative consequences
• and clear dysregulation of thought and emotions.⁴

Self-mutilation presents in a variety of forms and encompasses many behaviors, from the socially acceptable to the bizarre and grotesque (Table 1). Favazza and Rosenthal described three main forms of pathologic self-mutilation.^2,5 A fourth form (such as ear piercing) is socially accepted and not considered pathologic.

Table 1

FOUR TYPES OF SELF-MUTILATION

• Severe self-mutilation manifests as extensive (and often irreversible) body damage. Examples include eye enucleation, castration, or amputation. Intense psychotic states and intoxication from illicit substances—usually amphetamines—are the main causes of this relatively rare type, which fortunately is not frequently repeated.
• Stereotyped self-mutilation is self-directed physical injury (head banging, biting oneself) seen in mental retardation and developmental disorders. This type has a stereotyped and repetitive rhythm and presents in the clear context of a neurobiological insult.
• Superficial or moderate self-mutilation—seen most commonly in general psychiatric practice—includes skin cutting, burning, or picking by nonpsychotic, nonmentally retarded patients. The behavior tends to be repetitive. Patients with this type usually present with comorbid conditions, particularly personality disorders.
• Socially accepted self-mutilation includes ear piercing, tattoos, or culturally based behaviors, such as lip piercing or ear stretching seen in some African cultures.

An impulse control disorder?

Over the last 15 years, increasing evidence has suggested that pathologic self-mutilation may be an impulse control disorder.⁶ Many clinical case reports demonstrate that self-mutilation shares two characteristics of impulse control disorders that involve such behaviors as gambling, sex, or stealing:

• failure to resist impulses/urges to participate in a particular behavior
• increasing tension or physical arousal before the act and release of pleasure or gratification after the act.

In the case report, “Pain from cutting makes me feel alive” (box), the patient describes being unable to resist thoughts of cutting herself or to stop the behavior, despite knowing that she should. Self-mutilators also have been shown to have biological measures of impulsivity—namely decreased serotonin levels—similar to those seen with other impulse control disorders.^7,8 Finally, evidence is emerging that acts of self-mutilation are socially triggered expressions of impulsive psychological traits.^5-7

Risk factors

Accurate estimates of self-mutilation’s incidence and prevalence are lacking, mainly because the behavior is difficult to define. In the U.S. population, Favazza estimated the prevalence as 0.75% and the incidence between 14 and 600 per 100,000 persons annually.⁵ Known risk factors are:

• female gender
• adolescence and college age
• substance abuse and/or personality disorders
• history of self-mutilation^3,9,10 (Table 2).

Comorbidities such as depression, bipolar disorder, substance abuse, and schizophrenia are common. Axis II phenomena are common, especially the cluster B traits of histrionic, narcissistic, and borderline personalities.

Finally, little is known about the course of self-mutilation, but it tends to begin in adolescence and follows an episodic, recurrent pattern.¹¹ Reports are scant of self-mutilation in the elderly, although clinical experience tells us that it does occur in this age group.

Causes

Several theories addressing the causes of self-mutilation have been championed. A few, with particular attention to impulse-control dysfunction, are described here.

Biological contributions. Support for a biological mechanism is beginning to emerge. Dysregulation in neurotransmission or neurobiological function may predispose a person to self-mutilate through the expression of impulsive traits such as motor disinhibition and a tendency to physical aggression.⁶ Decreased serotonergic functioning or a central deficit in serotonergic functioning—as measured by platelet imipramine binding levels and serotonin metabolites in the CSF—are seen in self-mutilators and persons with other impulsive behaviors, such as completed suicide, physical aggression, and pathologic gambling.^11,12

Box

CASE REPORT ‘PAIN FROM CUTTING MAKES ME FEEL ALIVE’

Mrs. K, age 39, is being treated for depression. She reports an onset of cutting behavior in college after she broke up with a boyfriend. She recalls being so agitated at the time that she instinctively grabbed a knife and began scraping her forearm. Since then, she has been cutting about three to four times a year and always in the context of an overwhelming stressful situation. So far, no serious medical consequences have resulted; she usually draws blood, then cleans and bandages the wound.

She is facing a divorce and is in a tumultuous battle with her estranged husband over custody of their children. As a result, her cutting behavior has increased in frequency to once or twice a week. These behaviors bother her, but she also reports that cutting allows her to “feel pain that makes me feel alive.” She denies suicidal intent. She wishes she could use another way to deal with emotional pain but finds herself yielding to cutting behaviors. Mrs. K has tried alcohol on some occasions and thought about using illicit drugs but did not know how to get them.

One of the reasons she sought treatment was to reduce her cutting behaviors. She feels that she can’t control her behavior and wants to understand why she repetitively chooses to engage in it.

Self-mutilators also respond abnormally to infusions of the adrenergic agent fenfluramine—they show decreased release of prolactin, which signals reduced serotonergic function.^11,12 Reports of a blunted serotonergic response in patients who attempt suicide and in those who complete a self-mutilation act strengthen this theory of a biological contribution.¹²

Finally, in examining the relationship of impulsivity and serotonergic function, Herpertz found a link between trait impulsivity—as measured by a deficit in problem-solving ability and affective hyperreactivity—and low serotonergic function.⁶ What remains unclear, however, is cause and effect: do impulsivity traits cause serotonergic dysfunction, or do serotonin function deficits manifest as impulsivity?

Table 2

PROFILE OF PATHOLOGIC SELF-MUTILATORS

In one fascinating study, self-mutilators whose primary diagnosis was borderline personality disorder tolerated more physical pain than did healthy controls.⁷ When they were tested during a distressed state of mind, self-mutilators’ pain thresholds were even more elevated. This finding suggests alterations in the opiate systems and stress-response pathways.

Further work—including genetic studies and functional neuroimaging—is needed to better understand the neurobiological locus of pathologic self-mutilation.

Psychological contributions. Self-mutilation may represent a compromise between choosing life or death. Some analysts have viewed self-mutilation as a coping mechanism to avoid suicide.^1,13 In other words, self-mutilation is the expression of psychic pain turned outward but without the intent to end life. Self-mutilation may then be viewed as a way to concretely demonstrate negative affective states to the self and to the world. It also may serve as a tool to regulate and cope with these negative affective states.

Unfortunately, this coping behavior can become irresistible and psychologically tempting. One self-mutilator writes, “It’s like a relief; I do it [cutting on her wrists] every couple of weeks, just to get relief…from pressure that builds up inside…you feel like you’re going to explode if you don’t cut.”¹ The described rise in tension is reminiscent of other impulse control disorders.

Hyperreactivity of decision-making also is correlated with self-mutilation, as it is with impulse-control disorders. Impulsive people tend to respond very quickly to environmental stimuli, rather than suppressing physical and emotional responses.⁶ One behavioral definition of impulsivity is the tendency to choose smaller, more immediate rewards instead of larger, delayed rewards. In the case report presented earlier, Mrs. K chose to cut her wrists instead of waiting for the negative affective state to pass. Waiting—which would have taken more time—would have offered the obvious benefit of avoiding physical harm.

Social contributions. The act of self-mutilation typically grabs the attention of a therapist, friends, or spouses. Operant conditioning—where the positive rewards of help, empathy, and attention follow self-mutilation—may reinforce and perpetuate the behavior.¹ Other social contributions may include:

• dysfunctional family systems
• lack of social support
• poor communication skills
• role expectations, such as school/work performance, sexuality, or career obligations.¹³

When social pressures demand immediate decisions, impulsive self-mutilators may feel an urgency to act instead of using other coping mechanisms. Leibenluft et al published what may be the only empiric study that addresses this “inner experience” of the self-mutilator with borderline personality disorder.¹⁴ In our case example, the pressures of an imminent divorce trial triggered Mrs. K’s most recent cutting behavior. She did not have a strong support system and—in her desperation to control something—she resorted to cutting.

Pharmacologic treatment

Just as the cause of self-mutilation is multidimensional, so is its treatment. Research has focused on medications, individual therapy, and social therapy. Not surprisingly, these approaches resemble the treatment of other impulse control disorders.

Most of the evidence for drug treatment of self-mutilation comes from case reports and small openlabel studies. A variety of medication classes have been tried.

Antidepressants. In theory, if reduced serotonin neurotransmission helps drive pathologic self-mutilation, then using selective serotonin reuptake inhibitors (SSRIs) to increase serotonin availability may reduce impulsivity. For example, Velazquez described the case of an 11-year-old boy whose finger-chewing behavior diminished with fluoxetine therapy.¹⁵

Most of the SSRI studies have examined self-mutilation in the context of treating personality disorders, especially borderline personality disorder. SSRIs have been shown to modestly reduce anger and negative affective states, but the studies do not refer specifically to their effect on the frequency of self-mutilation. Given the present evidence, SSRIs appear to be an appropriate first-line treatment for self-mutilation because of their:

• overall safety profile
• effectiveness in treating mood lability and reactivity
• documented deficits in serotonergic neurotransmission.

Still, little empiric data exists regarding their use in treating self-mutilation, and prescribers should watch for possible side effects. No SSRI appears to be best suited to treat this disorder. Base initial selection on prior medication trials and on whether a drug’s side effects could work in the patient’s favor. For example, paroxetine’s more sedating properties may benefit a patient with difficulty sleeping, whereas sertraline’s more activating properties may help the lethargic patient with psychomotor retardation.

Atypical antipsychotics are often used in patients with borderline personality disorders or mental retardation to reduce impulsive physical aggression and mood lability. Their wide range of pharmacologic effects—including serotonin and dopamine blockade—suggests why they may have thymoleptic properties related to mood, anxiety, impulsiveness, and overall behavioral control. Small trials have demonstrated that olanzapine and clozapine may help control self-mutilation,^16,17 but controlled trials are lacking.

Mood stabilizers. Case reports have described use of lithium, divalproex, and topiramate to reduce the frequency of self-mutilation, but—as with antipsychotics—controlled studies are lacking.¹⁸ Mood stabilizers are appropriate in self-mutilators with co-existing bipolar disorder and possibly in those whose self-mutilation has cycling or circadian properties.

Anxiolytics. The sedative effects of benzodiazepines such as lorazepam or clonazepam may help control agitation and attempts to self-mutilate in emergent inpatient settings. This drug class carries a high abuse potential and may cause behavioral disinhibition, especially with mentally retarded patients. These properties limit benzodiazepines’ usefulness in outpatient treatment of self-mutilation.

Box 2

Opiate antagonists. Naltrexone and nalmefene have been shown to be effective in other impulse control disorders, such as pathologic gambling and kleptomania.^19,20 In self-mutilation, the use of opiate antagonists has been limited to case reports in patients with autism or mental retardation.

Although unproven, it may be that self-injurious behaviors are reinforced by a release of endogenous opioids. In theory, then, blocking opiate release would reduce the behaviors, as patients would then respond more normally to pain. The behavior would extinguish without the reward.^19,20

Opiate antagonists, which purportedly reduce urges and cravings to drink or to gamble, may also block urges and cravings to self-mutilate. Problems with using these agents include the need for periodic liver function tests and side effects such as nausea and gastrointestinal disturbances.

Psychotherapeutic approaches

Psychodynamic psychotherapy is the most common form of individual therapy used in treating self-mutilation. Effective therapy enables patients to understand why they self-mutilate and teaches them more healthy ways to deal with negative internal states.^2,3

Individual therapy is the mainstay of self-mutilation treatment, although no known studies have confirmed that psychodynamic psychotherapy reduces acts of self-mutilation. Because self-mutilators tend to have poor boundaries, supervision and peer collaboration are highly recommended to maintain an effective therapeutic relationship.¹

Yet to be answered is whether healthier coping strategies alter measures of impulsivity. Patients who have improved report they are better able to cope with negative affective states and to verbalize their feelings.

Dialectical behavior therapy (DBT) is another psychotherapeutic option. Used in treating personality disorders, DBT combines cognitive, behavioral, and supportive interventions. In one study, DBT reduced the frequency of self-mutilation to 1.5 acts per year, compared with 9 acts per year in a treatment-as-usual control group.²¹

Need for ‘emergency plans’

Relaxation training, exposure therapy, and response prevention have been suggested as treatments for pathologic self-mutilation, but there is no convincing evidence to support their efficacy.¹ Contracts against self-mutilation do not appear to be effective. Instead, “emergency plans” may be needed to deal with urges to self-mutilate.

Crisis intervention strategies that may help the self-mutilator include:

• partial hospitalizations to focus on increasing coping skills and strengthening a patient’s sense of self-reliance and individual responsibility
• increased frequency of visits
• educating the patient to use medications such as atypical neuroleptics or benzodiazepines as needed (“in case of emergency, take this medication instead of cutting”).

Crisis interventions should focus on understanding and changing pathologic behaviors. Self-mutilation behavior may be reinforced if attention is given without enough emphasis on developing coping skills.

Group therapy may be another treatment option. Group support helps patients with pathologic gambling, addictive, or other impulse control disorders to prevent relapse and learn to deal with urges and impulses.

Related resources

• Self-injury Web site offering information about self-harming behavior plus coping skills, alternatives to self-injury, support groups. www.selfabuse.com
• Levenkron S. Cutting: understanding and overcoming self-mutilation. New York: WW Norton and Company Ltd, 1998.
• SAFE (Self-Abuse Finally Ends), www.selfinjury.com. Resources for patients, families, and therapists. Recording at 1-800-DON’T-CUT (800-366-8288) offers to mail information on self-injury and the SAFE Alternatives program.

Drug brand names

• Clonazepam • Klonopin
• Clozapine • Clozaril
• Fluoxetine • Prozac
• Lorazepam • Ativan
• Naltrexone • ReVia
• Nalmefene • Revex
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Sertraline • Zoloft
• Topiramate • Topamax

Disclosure

Dr. Fong reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Self-mutilation has the power to confuse, frustrate, and frighten patients and their families. Psychiatrists, too, are not immune to the intense emotional responses that pathologic self-mutilation can provoke.

One definition of self-mutilation is any self-directed, repetitive behavior that causes physical injury.¹ Examples vary widely and include skin cutting, burning, or picking as well as head banging and extreme injuries such as auto enucleation. Most acts of self-mutilation are not suicide attempts but behaviors meant to express or release emotional turmoil.

As difficult as self-mutilation may be to understand, managing this condition may be even more complex. A multidisciplinary approach may be required, but evidence for the effectiveness of psycho- and pharmacotherapies is limited. This article reviews some theories of pathologic self-mutilation and describes emerging clinical strategies to treat it.

Four types of self-mutilation

DSM-IV does not recognize self-mutilation as a separate disorder but sees it as a symptom of other psychiatric conditions.^2,3 It is briefly mentioned as one criterion for diagnosing borderline personality disorder (“recurrent suicidal behaviors, gestures or threats or self-mutilating behaviors”), and it also appears in the catch-all diagnosis of impulse control disorders, not otherwise specified (NOS). Other self-injurious behaviors such as substance use disorders, trichotillomania, and, in some respects, pathologic gambling have found their way into DSM-IV as addiction or impulse control disorders. Self-mutilation appears to fall between these diagnostic categories, as it contains elements of many psychiatric disorders, such as:

• loss of behavioral control
• repetitive actions despite negative consequences
• and clear dysregulation of thought and emotions.⁴

Self-mutilation presents in a variety of forms and encompasses many behaviors, from the socially acceptable to the bizarre and grotesque (Table 1). Favazza and Rosenthal described three main forms of pathologic self-mutilation.^2,5 A fourth form (such as ear piercing) is socially accepted and not considered pathologic.

Table 1

FOUR TYPES OF SELF-MUTILATION

• Severe self-mutilation manifests as extensive (and often irreversible) body damage. Examples include eye enucleation, castration, or amputation. Intense psychotic states and intoxication from illicit substances—usually amphetamines—are the main causes of this relatively rare type, which fortunately is not frequently repeated.
• Stereotyped self-mutilation is self-directed physical injury (head banging, biting oneself) seen in mental retardation and developmental disorders. This type has a stereotyped and repetitive rhythm and presents in the clear context of a neurobiological insult.
• Superficial or moderate self-mutilation—seen most commonly in general psychiatric practice—includes skin cutting, burning, or picking by nonpsychotic, nonmentally retarded patients. The behavior tends to be repetitive. Patients with this type usually present with comorbid conditions, particularly personality disorders.
• Socially accepted self-mutilation includes ear piercing, tattoos, or culturally based behaviors, such as lip piercing or ear stretching seen in some African cultures.

An impulse control disorder?

Over the last 15 years, increasing evidence has suggested that pathologic self-mutilation may be an impulse control disorder.⁶ Many clinical case reports demonstrate that self-mutilation shares two characteristics of impulse control disorders that involve such behaviors as gambling, sex, or stealing:

• failure to resist impulses/urges to participate in a particular behavior
• increasing tension or physical arousal before the act and release of pleasure or gratification after the act.

In the case report, “Pain from cutting makes me feel alive” (box), the patient describes being unable to resist thoughts of cutting herself or to stop the behavior, despite knowing that she should. Self-mutilators also have been shown to have biological measures of impulsivity—namely decreased serotonin levels—similar to those seen with other impulse control disorders.^7,8 Finally, evidence is emerging that acts of self-mutilation are socially triggered expressions of impulsive psychological traits.^5-7

Risk factors

Accurate estimates of self-mutilation’s incidence and prevalence are lacking, mainly because the behavior is difficult to define. In the U.S. population, Favazza estimated the prevalence as 0.75% and the incidence between 14 and 600 per 100,000 persons annually.⁵ Known risk factors are:

• female gender
• adolescence and college age
• substance abuse and/or personality disorders
• history of self-mutilation^3,9,10 (Table 2).

Comorbidities such as depression, bipolar disorder, substance abuse, and schizophrenia are common. Axis II phenomena are common, especially the cluster B traits of histrionic, narcissistic, and borderline personalities.

Finally, little is known about the course of self-mutilation, but it tends to begin in adolescence and follows an episodic, recurrent pattern.¹¹ Reports are scant of self-mutilation in the elderly, although clinical experience tells us that it does occur in this age group.

Causes

Several theories addressing the causes of self-mutilation have been championed. A few, with particular attention to impulse-control dysfunction, are described here.

Biological contributions. Support for a biological mechanism is beginning to emerge. Dysregulation in neurotransmission or neurobiological function may predispose a person to self-mutilate through the expression of impulsive traits such as motor disinhibition and a tendency to physical aggression.⁶ Decreased serotonergic functioning or a central deficit in serotonergic functioning—as measured by platelet imipramine binding levels and serotonin metabolites in the CSF—are seen in self-mutilators and persons with other impulsive behaviors, such as completed suicide, physical aggression, and pathologic gambling.^11,12

Box

CASE REPORT ‘PAIN FROM CUTTING MAKES ME FEEL ALIVE’

Mrs. K, age 39, is being treated for depression. She reports an onset of cutting behavior in college after she broke up with a boyfriend. She recalls being so agitated at the time that she instinctively grabbed a knife and began scraping her forearm. Since then, she has been cutting about three to four times a year and always in the context of an overwhelming stressful situation. So far, no serious medical consequences have resulted; she usually draws blood, then cleans and bandages the wound.

She is facing a divorce and is in a tumultuous battle with her estranged husband over custody of their children. As a result, her cutting behavior has increased in frequency to once or twice a week. These behaviors bother her, but she also reports that cutting allows her to “feel pain that makes me feel alive.” She denies suicidal intent. She wishes she could use another way to deal with emotional pain but finds herself yielding to cutting behaviors. Mrs. K has tried alcohol on some occasions and thought about using illicit drugs but did not know how to get them.

One of the reasons she sought treatment was to reduce her cutting behaviors. She feels that she can’t control her behavior and wants to understand why she repetitively chooses to engage in it.

Self-mutilators also respond abnormally to infusions of the adrenergic agent fenfluramine—they show decreased release of prolactin, which signals reduced serotonergic function.^11,12 Reports of a blunted serotonergic response in patients who attempt suicide and in those who complete a self-mutilation act strengthen this theory of a biological contribution.¹²

Finally, in examining the relationship of impulsivity and serotonergic function, Herpertz found a link between trait impulsivity—as measured by a deficit in problem-solving ability and affective hyperreactivity—and low serotonergic function.⁶ What remains unclear, however, is cause and effect: do impulsivity traits cause serotonergic dysfunction, or do serotonin function deficits manifest as impulsivity?

Table 2

PROFILE OF PATHOLOGIC SELF-MUTILATORS

In one fascinating study, self-mutilators whose primary diagnosis was borderline personality disorder tolerated more physical pain than did healthy controls.⁷ When they were tested during a distressed state of mind, self-mutilators’ pain thresholds were even more elevated. This finding suggests alterations in the opiate systems and stress-response pathways.

Further work—including genetic studies and functional neuroimaging—is needed to better understand the neurobiological locus of pathologic self-mutilation.

Psychological contributions. Self-mutilation may represent a compromise between choosing life or death. Some analysts have viewed self-mutilation as a coping mechanism to avoid suicide.^1,13 In other words, self-mutilation is the expression of psychic pain turned outward but without the intent to end life. Self-mutilation may then be viewed as a way to concretely demonstrate negative affective states to the self and to the world. It also may serve as a tool to regulate and cope with these negative affective states.

Unfortunately, this coping behavior can become irresistible and psychologically tempting. One self-mutilator writes, “It’s like a relief; I do it [cutting on her wrists] every couple of weeks, just to get relief…from pressure that builds up inside…you feel like you’re going to explode if you don’t cut.”¹ The described rise in tension is reminiscent of other impulse control disorders.

Hyperreactivity of decision-making also is correlated with self-mutilation, as it is with impulse-control disorders. Impulsive people tend to respond very quickly to environmental stimuli, rather than suppressing physical and emotional responses.⁶ One behavioral definition of impulsivity is the tendency to choose smaller, more immediate rewards instead of larger, delayed rewards. In the case report presented earlier, Mrs. K chose to cut her wrists instead of waiting for the negative affective state to pass. Waiting—which would have taken more time—would have offered the obvious benefit of avoiding physical harm.

Social contributions. The act of self-mutilation typically grabs the attention of a therapist, friends, or spouses. Operant conditioning—where the positive rewards of help, empathy, and attention follow self-mutilation—may reinforce and perpetuate the behavior.¹ Other social contributions may include:

• dysfunctional family systems
• lack of social support
• poor communication skills
• role expectations, such as school/work performance, sexuality, or career obligations.¹³

When social pressures demand immediate decisions, impulsive self-mutilators may feel an urgency to act instead of using other coping mechanisms. Leibenluft et al published what may be the only empiric study that addresses this “inner experience” of the self-mutilator with borderline personality disorder.¹⁴ In our case example, the pressures of an imminent divorce trial triggered Mrs. K’s most recent cutting behavior. She did not have a strong support system and—in her desperation to control something—she resorted to cutting.

Pharmacologic treatment

Just as the cause of self-mutilation is multidimensional, so is its treatment. Research has focused on medications, individual therapy, and social therapy. Not surprisingly, these approaches resemble the treatment of other impulse control disorders.

Most of the evidence for drug treatment of self-mutilation comes from case reports and small openlabel studies. A variety of medication classes have been tried.

Antidepressants. In theory, if reduced serotonin neurotransmission helps drive pathologic self-mutilation, then using selective serotonin reuptake inhibitors (SSRIs) to increase serotonin availability may reduce impulsivity. For example, Velazquez described the case of an 11-year-old boy whose finger-chewing behavior diminished with fluoxetine therapy.¹⁵

Most of the SSRI studies have examined self-mutilation in the context of treating personality disorders, especially borderline personality disorder. SSRIs have been shown to modestly reduce anger and negative affective states, but the studies do not refer specifically to their effect on the frequency of self-mutilation. Given the present evidence, SSRIs appear to be an appropriate first-line treatment for self-mutilation because of their:

• overall safety profile
• effectiveness in treating mood lability and reactivity
• documented deficits in serotonergic neurotransmission.

Still, little empiric data exists regarding their use in treating self-mutilation, and prescribers should watch for possible side effects. No SSRI appears to be best suited to treat this disorder. Base initial selection on prior medication trials and on whether a drug’s side effects could work in the patient’s favor. For example, paroxetine’s more sedating properties may benefit a patient with difficulty sleeping, whereas sertraline’s more activating properties may help the lethargic patient with psychomotor retardation.

Atypical antipsychotics are often used in patients with borderline personality disorders or mental retardation to reduce impulsive physical aggression and mood lability. Their wide range of pharmacologic effects—including serotonin and dopamine blockade—suggests why they may have thymoleptic properties related to mood, anxiety, impulsiveness, and overall behavioral control. Small trials have demonstrated that olanzapine and clozapine may help control self-mutilation,^16,17 but controlled trials are lacking.

Mood stabilizers. Case reports have described use of lithium, divalproex, and topiramate to reduce the frequency of self-mutilation, but—as with antipsychotics—controlled studies are lacking.¹⁸ Mood stabilizers are appropriate in self-mutilators with co-existing bipolar disorder and possibly in those whose self-mutilation has cycling or circadian properties.

Anxiolytics. The sedative effects of benzodiazepines such as lorazepam or clonazepam may help control agitation and attempts to self-mutilate in emergent inpatient settings. This drug class carries a high abuse potential and may cause behavioral disinhibition, especially with mentally retarded patients. These properties limit benzodiazepines’ usefulness in outpatient treatment of self-mutilation.

Box 2

Opiate antagonists. Naltrexone and nalmefene have been shown to be effective in other impulse control disorders, such as pathologic gambling and kleptomania.^19,20 In self-mutilation, the use of opiate antagonists has been limited to case reports in patients with autism or mental retardation.

Although unproven, it may be that self-injurious behaviors are reinforced by a release of endogenous opioids. In theory, then, blocking opiate release would reduce the behaviors, as patients would then respond more normally to pain. The behavior would extinguish without the reward.^19,20

Opiate antagonists, which purportedly reduce urges and cravings to drink or to gamble, may also block urges and cravings to self-mutilate. Problems with using these agents include the need for periodic liver function tests and side effects such as nausea and gastrointestinal disturbances.

Psychotherapeutic approaches

Psychodynamic psychotherapy is the most common form of individual therapy used in treating self-mutilation. Effective therapy enables patients to understand why they self-mutilate and teaches them more healthy ways to deal with negative internal states.^2,3

Individual therapy is the mainstay of self-mutilation treatment, although no known studies have confirmed that psychodynamic psychotherapy reduces acts of self-mutilation. Because self-mutilators tend to have poor boundaries, supervision and peer collaboration are highly recommended to maintain an effective therapeutic relationship.¹

Yet to be answered is whether healthier coping strategies alter measures of impulsivity. Patients who have improved report they are better able to cope with negative affective states and to verbalize their feelings.

Dialectical behavior therapy (DBT) is another psychotherapeutic option. Used in treating personality disorders, DBT combines cognitive, behavioral, and supportive interventions. In one study, DBT reduced the frequency of self-mutilation to 1.5 acts per year, compared with 9 acts per year in a treatment-as-usual control group.²¹

Need for ‘emergency plans’

Relaxation training, exposure therapy, and response prevention have been suggested as treatments for pathologic self-mutilation, but there is no convincing evidence to support their efficacy.¹ Contracts against self-mutilation do not appear to be effective. Instead, “emergency plans” may be needed to deal with urges to self-mutilate.

Crisis intervention strategies that may help the self-mutilator include:

• partial hospitalizations to focus on increasing coping skills and strengthening a patient’s sense of self-reliance and individual responsibility
• increased frequency of visits
• educating the patient to use medications such as atypical neuroleptics or benzodiazepines as needed (“in case of emergency, take this medication instead of cutting”).

Crisis interventions should focus on understanding and changing pathologic behaviors. Self-mutilation behavior may be reinforced if attention is given without enough emphasis on developing coping skills.

Group therapy may be another treatment option. Group support helps patients with pathologic gambling, addictive, or other impulse control disorders to prevent relapse and learn to deal with urges and impulses.

Related resources

• Self-injury Web site offering information about self-harming behavior plus coping skills, alternatives to self-injury, support groups. www.selfabuse.com
• Levenkron S. Cutting: understanding and overcoming self-mutilation. New York: WW Norton and Company Ltd, 1998.
• SAFE (Self-Abuse Finally Ends), www.selfinjury.com. Resources for patients, families, and therapists. Recording at 1-800-DON’T-CUT (800-366-8288) offers to mail information on self-injury and the SAFE Alternatives program.

Drug brand names

• Clonazepam • Klonopin
• Clozapine • Clozaril
• Fluoxetine • Prozac
• Lorazepam • Ativan
• Naltrexone • ReVia
• Nalmefene • Revex
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Sertraline • Zoloft
• Topiramate • Topamax

Disclosure

Dr. Fong reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

An orthopedic surgeon treating a patient, age 29, at a tertiary medical center asks a staff psychiatrist for advice. The patient—who has chronic bilateral knee infections—lives 350 miles away; her treatment-resistant disease has stymied and frustrated her local physicians. Her infections have persisted despite multiple courses of antibiotics and numerous surgical procedures.

Because of damage to the right knee joint, she cannot bear weight or walk. A registered nurse, she has been unable to work or care for her school-aged children for 2 years. The surgeon tells the psychiatrist that the patient denies psychiatric complaints beyond sadness over her inability to fulfill her responsibilities. She expresses a wish to recover and adamantly denies that she manipulates her wound or does anything to interfere with its healing. The medical/surgical team has noticed that while she is away from home receiving orthopedic care, her husband never visits or calls.

Cases such as the one described above are rare, but psychiatrists occasionally encounter patients with these baffling characteristics. When the patient’s disease fails to respond to treatment as expected—or progresses—members of the medical/psychiatric team need to ask themselves these questions:

• Are we dealing with a drug-resistant infection?
• Is the patient adhering fully with treatment?
• Does the patient do anything to perpetuate this disease process and wish to stay ill?

Asking this last question is difficult but necessary in certain situations. Most of us cannot imagine why a person would wish to remain sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? Yet, an unknown number of people strive to appear unwell so that they can receive ongoing medical care.

What are factitious disorders?

Factitious disorders are psychiatric conditions in which patients deliberately portray themselves as ill. They may present with physical or psychological symptoms or both. Their objective is to assume the sick role—not to procure shelter, obtain financial assistance, avoid prison, etc., which would fall into other diagnoses such as malingering.

Table 1

DSM-IV DIAGNOSTIC CRITERIA FOR FACTITIOUS DISORDER

DSM-IV criteria are straightforward and inclusive (Table 1).¹ They do not specify:

• the presence of medical and/or psychiatric disorders, which do not preclude the diagnosis
• reasons why a person may wish to assume the sick role.

The medical literature on factitious disorder includes many compelling case reports. However, the secretive nature of most patients with factitious complaints has made it difficult to conduct carefully designed community-based studies, prospective studies, or controlled randomized trials. Because research is scarce, much is unknown about who gets factitious disorder, what causes it, and how to treat it.

Differential diagnosis

Factitious disorder varies in severity. Among subtypes proposed by Folks et al (Table 2),² patients in categories 3, 4, and 5—who produce physical illness—can potentially be identified by diagnostic testing.³ Patients in categories 1 and 2—who exaggerate physical symptoms and provide a false medical history—may be more difficult to detect.

In cases where patients exaggerate symptoms or fabricate histories, little objective information is typically available to the treating physicians. Medical records revealing multiple admissions or emergency room visits may be obtained from other institutions only if the patient gives permission. However, the patient often does not consent or the materials cannot be located.

Third-party payers’ pre-authorization procedures and utilization reviews may speak volumes about a patient’s search for health care. However, patients who are unemployed or estranged from spouses may lose insurance coverage over time. Government assistance programs such as Medicare and Medicaid provide care to many patients with these chronic problems and do not perform the same degree of utilization review.

Munchausen disorder—a variant of factitious disorder—is not recognized by DSM-IV. The term—while still used primarily by nonpsychiatrists—is generally viewed as outdated. The term is reserved for patients with the most severe and chronic form of factitious disorder.⁴ The few studies done of patients with this variant have not adequately examined the specificity and sensitivity of their core symptoms or other characteristics, such as production of a misleading medical condition, travel to multiple medical centers (peregrination), and the telling of tall tales (pseudologia fantastica).

Somatoform disorder. If physicians suspect that a patient’s illness is taking an unusual course, they may suspect a somatoform rather than factitious disorder. Patients with somatoform disorder do not intentionally produce their symptoms, whereas patients with factitious disorder deliberately try to appear ill. In both disorders, the underlying cause is unconscious.

Hypochondriasis. Patients with hypochondriasis are obsessed with concerns that they have an illness. Their worries may compel them to seek out examinations and diagnostic tests. Unlike patients with factitious disorder, these patients do not deliberately provide information or manufacture symptoms to create the appearance of a medical disorder.

Malingering. Patients who malinger may engage in deceitful behaviors that can include creating a misleading impression about a medical or psychiatric illness. Being a patient, however, is not their objective. They may be seeking disability payments, insurance settlements, shelter, or food.

Patient evaluation

Patients suspected of factitious disorder merit a thorough medical and psychiatric evaluation, guided by their presenting symptoms. They commonly have comorbid psychiatric disorders (Table 3), which medical/surgical team members and the psychiatrist need to identify before considering a diagnosis of factitious disorder.

Because invasive tests such as angiography, colonoscopy, biopsies, or exploratory surgery are required to exclude some underlying medical processes, the treatment team must take care not to cause harm. The expected benefits of diagnostic testing must be balanced against the risks of an iatrogenic event.

Table 2

FIVE PROPOSED SUBTYPES OF FACTITIOUS DISORDER

Relatively little is known about how to diagnose a factitious process coexisting with a genuine medical disorder. For example, a patient with well-documented chronic inflammatory disease may easily exaggerate pain and diarrhea to facilitate hospital admission.

To confront or not to confront?

Some patients may relish the patient role for a time—such as while being evaluated for a presumed opportunistic infection—but may not consent to more definitive tests—such as HIV testing. They may demand discharge while they still may be harming themselves, such as by injecting foreign material. The patient may plan to find another health care provider and continue the maladaptive behavior.

If you suspected that our case patient was playing a role in perpetuating her chronic knee infections, would you confront her with the evidence? The answer is unclear, but some experts argue against confrontation.⁵ Once a patient believes that the medical team suspects a factitious process, he or she may no longer wish to cooperate, even if the diagnostic evaluation is incomplete. Patients often become more guarded about what they reveal after they are confronted. They may become more careful to hide evidence of wound tampering (e.g., syringes) and hesitant to discuss emotional issues (e.g., estranged relationships, feeling overwhelmed by work and home duties).

Case reports suggest that patients who simulate symptoms, modify their physiology, or induce physical illness are at high risk of morbidity and mortality. For example, one report described a patient who underwent two cardiopulmonary resuscitations because of torsades de pointes triggered by hypokalemia related to covert laxative use.⁶ Physicians must manage these cases carefully to reduce patient risk. In rare cases where a patient’s behavior becomes life-threatening, admission to a psychiatric unit—even involuntarily—may be necessary.

Collaborating with the patient

A comprehensive treatment approach is optimal for patients with factitious disorder. All the patient’s objective medical disorders should be addressed in systematically and with empathy. Treating a co-existing medical disorder may help the physician gain the patient’s trust, which in turn can help keep treatment options open.

Some patients have been known to exaggerate their physical symptoms because they feel they have a serious, undiagnosed medical problem. They feel that their assessment has been cursory and that they need to compel the physician to do a more thorough evaluation in order to identify the true underlying problem. Although no research supports this observation, these patients may be reassured when their physicians carefully evaluate their medical problems.

Eisendrath⁵ recommends that the treatment team take time to get to know the patient and convey that this attention is devoted to the person, not just the medical illness. This approach may increase the likelihood of learning about psychosocial issues the person may be trying to resolve by taking the patient role. Patients also may be more willing to complete the evaluation and adhere to recommended treatment, although these outcomes are not guaranteed.

Table 3

DISORDERS KNOWN TO CO-EXIST WITH FACTITIOUS DISORDER

Case report

For the patient with chronic knee infections, the staff psychiatrist recommended that the orthopedist develop a collaborative relationship with her. Eventually the surgeon told her that she needed psychiatric care, and the patient agreed to psychiatric hospitalization.

In this setting, she was initially observed with a 24-hour monitor and received appropriate wound care. The staff encouraged her to talk about the emotional distress related to having a chronic disease. She never admitted to perpetuating the infections in her knees, although she was suspected of injecting herself with infected material. Psychiatric evaluation revealed a history of multiple strained relationships that suggested a severe personality disorder.

Her wounds slowly began to improve, and she was discharged after 2 weeks. Throughout her stay, she remained reluctant to discuss her relationship with her husband or examine other possible sources of stress in her life. Thus, factitious behavior will probably recur unless she tackles her unconscious motivations for adopting a patient role.

If patients’ emotional needs are being met, they may reveal the mechanism of their disease. Unfortunately, experience suggests that very few confess the false nature of their medical illness, fewer accept psychiatric treatment, and even fewer complete the recommended course of treatment.

Comorbid psychiatric disorders provide an opportunity to intervene with selected medications and psychotherapy to reduce patient distress. Chemical dependency treatment in particular can help stabilize a patient with a factitious disorder so that he or she no longer seeks pain medications or sedatives. Patients with an obsessive-compulsive disorder or hypochondriasis may require specifically targeted cognitive-behavioral therapy or pharmacotherapy.

Few references regarding treatment of factitious disorder exist; the only known review of cognitive-behavioral therapy’s role in treating this disorder awaits publication.

Related resources

• Sutherland AJ, Rodin GM. Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 1990;31(4):392-9.
• Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99(2):240-7.

Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

• the evolution of schizoaffective disorder as a psychiatric diagnosis
• the four main concepts that attempt to explain the disorder’s cause
• and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin¹ riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:²

• Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
• Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.³ He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.¹ Moreover, unlike patients with dementia praecox, these blended patients exhibited:

• good premorbid adjustment
• typically a sudden illness onset with marked emotional turmoil
• few symptoms of withdrawal or passivity
• and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.⁴ Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)⁵ and DSM-II (1968)⁶ and then reclassified in DSM-III (1980)⁷ as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).⁸ The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.^9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

• psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
• and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,¹¹ which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,¹² but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.¹³

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).⁴

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.¹⁵

Concept 2: Schizoaffective disorder is a variant of mood disorder. ⁹ Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).¹⁶ Family studies are unclear about links between mood and schizoaffective disorders.¹⁷

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER

Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.¹⁸ As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.¹⁹

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support²¹).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.^4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.^4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.^4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

• National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
• Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
• Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.

Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

• the evolution of schizoaffective disorder as a psychiatric diagnosis
• the four main concepts that attempt to explain the disorder’s cause
• and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin¹ riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:²

• Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
• Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.³ He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.¹ Moreover, unlike patients with dementia praecox, these blended patients exhibited:

• good premorbid adjustment
• typically a sudden illness onset with marked emotional turmoil
• few symptoms of withdrawal or passivity
• and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.⁴ Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)⁵ and DSM-II (1968)⁶ and then reclassified in DSM-III (1980)⁷ as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).⁸ The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.^9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

• psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
• and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,¹¹ which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,¹² but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.¹³

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).⁴

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.¹⁵

Concept 2: Schizoaffective disorder is a variant of mood disorder. ⁹ Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).¹⁶ Family studies are unclear about links between mood and schizoaffective disorders.¹⁷

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER

Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.¹⁸ As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.¹⁹

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support²¹).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.^4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.^4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.^4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

• National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
• Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
• Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.

Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

• the evolution of schizoaffective disorder as a psychiatric diagnosis
• the four main concepts that attempt to explain the disorder’s cause
• and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin¹ riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:²

• Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
• Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.³ He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.¹ Moreover, unlike patients with dementia praecox, these blended patients exhibited:

• good premorbid adjustment
• typically a sudden illness onset with marked emotional turmoil
• few symptoms of withdrawal or passivity
• and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.⁴ Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)⁵ and DSM-II (1968)⁶ and then reclassified in DSM-III (1980)⁷ as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).⁸ The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.^9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

• psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
• and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,¹¹ which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,¹² but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.¹³

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).⁴

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.¹⁵

Concept 2: Schizoaffective disorder is a variant of mood disorder. ⁹ Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).¹⁶ Family studies are unclear about links between mood and schizoaffective disorders.¹⁷

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER

Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.¹⁸ As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.¹⁹

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support²¹).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.^4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.^4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.^4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

• National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
• Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
• Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.

Despite its impact on individuals and public health, depression in older persons is inadequately diagnosed and treated. Even when depression is diagnosed, only one-third of persons older than 65 receive treatment.¹ Reasons for this include:

• lack of physician awareness that depression presents differently in older than in younger adults
• patient denial of depressive symptoms
• patients’ and physicians’ mistaken belief that feeling depressed is a normal part of aging.

The good news is that when geriatric depression is recognized, it usually responds favorably to treatment, although aggressive intervention may be required.² In this article, we describe our approach to diagnosis and discuss use of selective serotonin reuptake inhibitors (SSRIs) as first-line antidepressants for older patients.

Late-life depression risk factors

Depression is common in older persons, especially in those who have experienced psychosocial or medical losses, including chronic illness. Although its presentation often does not meet criteria for major depression, the more common subsyndromal depression is debilitating and can lead to suicide.

Box

CASE REPORT: DEPRESSED, AT RISK FOR SUICIDE

A 72-year-old man presents with trouble concentrating, decreased appetite, anergy, and anhedonia. He says he frequently awakes at 3 AM, and it takes him 2 hours to return to sleep. Lately, he has thought of shooting himself with his hunting rifle. The patient’s wife died of cancer 1 year ago, and he has developed several medical illnesses within the past 10 years: chronic obstructive pulmonary disease, worsening arthritis, mild ischemic heart disease, and worsening hearing loss.

The patient denies feeling depressed and instead attributes his symptoms to his medical illnesses. He has become progressively isolated in the past year, with less social contact with his friends at the local parish. His older brother, with whom he was close, died recently. Until now, he says his “pride” has made him resist his primary care physician’s recommendation that he see a psychiatrist.

Late-life depressive syndromes commonly present with somatic complaints. Typically, patients deny having a mental illness and perceive that their symptoms are organic in origin (Box).¹

Losses. Psychosocial and medical losses are major risk factors for late-life adjustment disorders, subsyndromal depressive disorders, and major depression. Medical losses may include loss of mobility or independent function, chronic pain, or sensory losses that limit one’s ability to read or hear. Psychosocial losses may include the death of a spouse, sibling, or peer or moving from one’s longtime home to a more structured environment (assisted living, nursing home, or living with relatives).

Medical causes to rule out before starting antidepressant therapy include:

• hypothyroidism
• medication side effects
• bipolar disorder, which may require the use of a mood-stabilizing agent to prevent manic symptoms.³

History. Often a history of mood disorder in the individual or a family member can help the clinician determine that mental illness accounts for the patient’s symptoms. In older patients, it is not uncommon for psychotic symptoms to accompany a primary mood disturbance.

Suicide risk is high in depressed older persons, so detection and quick treatment of depression is paramount. Older white men are at particularly high risk for completed suicide using firearms.³

Alcohol abuse may contribute to depressive symptoms in older persons. A second peak of alcoholism occurs in the eighth decade of life and can confound diagnosis of depression in patients of this age.

Making the diagnosis. In patients who present with symptoms and risk factors for late-life depression, depression rating scales can help confirm the diagnosis. Commonly used scales include the Beck Depression Inventory, the Hamilton Depression Rating Scale, and the Zung Self-Rating Depression Scale. Specialized scales for use in older patients include the Geriatric Depression Scale and the Cornell Scale; the latter scale is designed for patients with comorbid depression and dementia.^3,4

Treatment

Antidepressant treatment in combination with psychotherapy usually is warranted when treating nonpsychotic late-life depression. In patients with psychosis, electroconvulsive therapy can help achieve remission.

Cognitive-behavioral therapy and interpersonal and insight-oriented psychotherapy have been shown to be effective in late-life depression. Social interventions aimed at preventing isolation also can work. In milder cases of depression, psychotherapy alone may be sufficient.³

Starting dosages. When antidepressant therapy is indicated in an older patient, start low and go slow.⁵ Older patients generally require prolonged titration rates and a longer course of treatment than do younger patients. Physiologic changes that occur with aging include:

• altered drug metabolism rate, including slower demethylation
• increased body fat-to-water ratio, which increases the volume of distribution for lipophilic psychotropic drugs
• decreased glomerular filtration rate, which may account for higher serum concentrations of drugs and their metabolites
• increased sensitivity of the older brain to the effects of medications.⁶

Thus—with some exceptions—recommended starting dosages for older patients are usually one-half those used in younger adults. For the frail older patient, the starting dosage should probably be even lower—about one-fourth the typical starting dosage in young adults.⁶ As in younger patients, the treatment goal is to achieve the maximal therapeutic effect with the lowest effective dosage while avoiding side effects.

More time may be required to achieve a therapeutic effect in older than in younger patients. Substantial improvement may not be seen until an older patient has been taking an antidepressant for 9 weeks or longer. In younger patients, responses are seen as early as 2 weeks after starting antidepressant therapy, and remission occurs within 6 to 8 weeks.²

SSRIs versus tricyclics

SSRIs—citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline (Table 1)⁷ —are considered first-line antidepressants for late-life depression. Although SSRIs and tricyclic antidepressants (TCAs) demonstrate equivalent efficacy in older adults, SSRIs are associated with lesstroublesome side effects.²

SSRIs are less sedating than tricyclics and are not associated with adverse effects on cognition; both qualities make these agents appropriate for older patients. Risk of overdose with SSRIs also is much lower than with TCAs.²

Both types of agent have been reported to cause movement disorders such as extrapyramidal symptoms and even tardive dyskinesia, but these side effects are much more rare with SSRIs than with TCAs.² Also—unlike the TCAs— SSRIs do not significantly effect cardiac conduction, which is an important quality in the older population with its relatively high incidence of heart disease.

Table 1

USING SSRIs TO TREAT LATE-LIFE DEPRESSION

Meta-analyses suggest that patients are more likely to discontinue taking tricyclics than SSRIs.⁸ Adherence to antidepressant medications by older patients has been associated with lower perceived stigma of mental illness, higher self-rated severity of illness, age over 60, and absence of a personality disorder.⁹

SSRI side effects

The most common side effect of SSRIs is nausea, which is usually mild and occurs in the first weeks of treatment.² Dry mouth is related to noradrenergic influences on the salivary gland. Anxiety is usually transient.

Sedation can be a problem in older patients who use SSRIs. Among the six SSRIs indicated for depression, paroxetine appears to be the most sedating.¹⁰ Paroxetine exhibits the most muscarinic blockade in vitro, with a binding affinity less than that of imipramine but greater than nortriptyline.¹¹ Studies in older patients have suggested, however, that cognitive function is not compromised with paroxetine, as is observed with other antidepressants with anticholinergic action.⁶

Table 2

CYTOCHROME P450 ISOZYMES INHIBITED BY SSRI ANTIDEPRESSANTS (IN VITRO)

Sexual function can be diminished by SSRIs; the most common sexual side effects are anorgasmia and delayed orgasm.¹² Preserving sexual function is important to many older men and women who retain their interest in sexual activity well into later life.

Withdrawal syndrome. Abrupt discontinuation of some SSRIs can lead to withdrawal side effects, such as dizziness, fatigue, and nausea. In a study of young and older adults, withdrawal syndrome followed abrupt discontinuation at rates of 14% with fluoxetine and 60% with sertraline or paroxetine.¹³

Elimination half-life. Medication half-lives tend to be prolonged in older patients because of age-related pharmacokinetic changes. SSRIs with relatively shorter half-lives—such as citalopram, sertraline, paroxetine, and fluvoxamine—could be eliminated fairly rapidly should adverse events arise.

On the other hand, use of a longer-acting agent, such as fluoxetine, may be an advantage if compliance is a problem. In this case, fluoxetine’s prolonged washout rate could help protect a patient from relapse, even when doses are missed.

Potential drug-drug interactions

Individual SSRIs have different effects on the cytochrome P450 system (Table 2).^14,15 For example, fluoxetine, sertraline, and paroxetine—but not fluvoxamine—are in vitro inhibitors of the 2D6 isoenzyme system,¹⁶ which metabolizes TCAs, type Ic antiarrhythmics, alpha-adrenergic blockers, dextromethorphan, chemotherapeutic agents, and some antipsychotics. Citalopram has minimal inhibitory activity and escitalopram has virtually no inhibitory action on CYP 2D6.¹⁷

Cytochrome P450 3A4 metabolizes numerous drugs, including alprazolam, triazolam, carbamazepine, calcium channel blockers, and others. The 3A4 enzymes are inhibited by fluoxetine, sertraline, and fluvoxamine.¹⁸

Cytochrome P450 1A2 is the liver isoenzyme responsible for dealkylating theophylline, caffeine, and phenacetin. This enzyme system also metabolizes tacrine and clozapine. Of the SSRIs, fluvoxamine is the most potent inhibitor of the 1A2 enzyme, while escitalopram is a negligible inhibitor.¹⁷

Cytochrome P450 2C is a subfamily of isoenzymes that includes 2C9, 2C10, 2C19, and others. This system metabolizes some antidepressants as well as warfarin, phenytoin, and diazepam. Inhibitors of this system include fluvoxamine, fluoxetine, sertraline, and paroxetine.¹⁸

MAO inhibitors. Concomitant use of serotonin-acting drugs and monoamine oxidase inhibitors should be avoided. When used in combination, SSRIs and MAO inhibitors can cause a serotonin syndrome, with potential hyperpyretic crises, seizures, coma, and death. When switching medications, it is important to eliminate any serotonin-acting drug before starting an MAO inhibitor.²

In young adults, a 7-day washout is needed when switching from fluvoxamine and 14 days when switching from sertraline, citalopram, or paroxetine. With fluoxetine, the washout period is 35 days in young adults. Because medication half-lives in older patients may be prolonged two- to three-fold, it is advisable to proceed conservatively and extend these washout periods accordingly.

Related resources

• National Institute of Mental Health. Older adults: Depression and suicide facts. www.nimh.nih.gov/publicat/elderlydepsuicide.cfm
• WebMD Health/depression. http://my.webmd.com/condition_center/dep
• Salzman C, Wong E, Wright BC. Drug and ECT treatment of depression in the elderly, 1996-2001: a literature review. Biol Psychiatry 2002;52(3):265-84.

Drug brand names

• Alprazolam • Xanax
• Citalopram • Celexa
• Clozapine • Clozaril
• Diazepam • Valium
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Paroxetine • Paxil
• Sertraline • Zoloft
• Tacrine • Cognex
• Triazolam • Halcion

Disclosure

Dr. Kasckow reports that he receives grant/research support from, serves as a consultant to, or is on the speakers bureau of Eli Lilly and Co., Forest Laboratories, Pharmacia Corp., Solvay Pharmaceuticals, AstraZeneca Pharmaceuticals, Organon, Janssen Pharmaceutica, and Pfizer Inc.

Dr. Mohamed reports that she receives grant/research support from Forest Laboratories and serves on the speakers bureau of Eli Lilly and Co.

Dr. Herman reports that he serves as a consultant to Eli Lilly and Co.

Other co-authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Despite its impact on individuals and public health, depression in older persons is inadequately diagnosed and treated. Even when depression is diagnosed, only one-third of persons older than 65 receive treatment.¹ Reasons for this include:

• lack of physician awareness that depression presents differently in older than in younger adults
• patient denial of depressive symptoms
• patients’ and physicians’ mistaken belief that feeling depressed is a normal part of aging.

The good news is that when geriatric depression is recognized, it usually responds favorably to treatment, although aggressive intervention may be required.² In this article, we describe our approach to diagnosis and discuss use of selective serotonin reuptake inhibitors (SSRIs) as first-line antidepressants for older patients.

Late-life depression risk factors

Depression is common in older persons, especially in those who have experienced psychosocial or medical losses, including chronic illness. Although its presentation often does not meet criteria for major depression, the more common subsyndromal depression is debilitating and can lead to suicide.

Box

CASE REPORT: DEPRESSED, AT RISK FOR SUICIDE

A 72-year-old man presents with trouble concentrating, decreased appetite, anergy, and anhedonia. He says he frequently awakes at 3 AM, and it takes him 2 hours to return to sleep. Lately, he has thought of shooting himself with his hunting rifle. The patient’s wife died of cancer 1 year ago, and he has developed several medical illnesses within the past 10 years: chronic obstructive pulmonary disease, worsening arthritis, mild ischemic heart disease, and worsening hearing loss.

The patient denies feeling depressed and instead attributes his symptoms to his medical illnesses. He has become progressively isolated in the past year, with less social contact with his friends at the local parish. His older brother, with whom he was close, died recently. Until now, he says his “pride” has made him resist his primary care physician’s recommendation that he see a psychiatrist.

Late-life depressive syndromes commonly present with somatic complaints. Typically, patients deny having a mental illness and perceive that their symptoms are organic in origin (Box).¹

Losses. Psychosocial and medical losses are major risk factors for late-life adjustment disorders, subsyndromal depressive disorders, and major depression. Medical losses may include loss of mobility or independent function, chronic pain, or sensory losses that limit one’s ability to read or hear. Psychosocial losses may include the death of a spouse, sibling, or peer or moving from one’s longtime home to a more structured environment (assisted living, nursing home, or living with relatives).

Medical causes to rule out before starting antidepressant therapy include:

• hypothyroidism
• medication side effects
• bipolar disorder, which may require the use of a mood-stabilizing agent to prevent manic symptoms.³

History. Often a history of mood disorder in the individual or a family member can help the clinician determine that mental illness accounts for the patient’s symptoms. In older patients, it is not uncommon for psychotic symptoms to accompany a primary mood disturbance.

Suicide risk is high in depressed older persons, so detection and quick treatment of depression is paramount. Older white men are at particularly high risk for completed suicide using firearms.³

Alcohol abuse may contribute to depressive symptoms in older persons. A second peak of alcoholism occurs in the eighth decade of life and can confound diagnosis of depression in patients of this age.

Making the diagnosis. In patients who present with symptoms and risk factors for late-life depression, depression rating scales can help confirm the diagnosis. Commonly used scales include the Beck Depression Inventory, the Hamilton Depression Rating Scale, and the Zung Self-Rating Depression Scale. Specialized scales for use in older patients include the Geriatric Depression Scale and the Cornell Scale; the latter scale is designed for patients with comorbid depression and dementia.^3,4

Treatment

Antidepressant treatment in combination with psychotherapy usually is warranted when treating nonpsychotic late-life depression. In patients with psychosis, electroconvulsive therapy can help achieve remission.

Cognitive-behavioral therapy and interpersonal and insight-oriented psychotherapy have been shown to be effective in late-life depression. Social interventions aimed at preventing isolation also can work. In milder cases of depression, psychotherapy alone may be sufficient.³

Starting dosages. When antidepressant therapy is indicated in an older patient, start low and go slow.⁵ Older patients generally require prolonged titration rates and a longer course of treatment than do younger patients. Physiologic changes that occur with aging include:

• altered drug metabolism rate, including slower demethylation
• increased body fat-to-water ratio, which increases the volume of distribution for lipophilic psychotropic drugs
• decreased glomerular filtration rate, which may account for higher serum concentrations of drugs and their metabolites
• increased sensitivity of the older brain to the effects of medications.⁶

Thus—with some exceptions—recommended starting dosages for older patients are usually one-half those used in younger adults. For the frail older patient, the starting dosage should probably be even lower—about one-fourth the typical starting dosage in young adults.⁶ As in younger patients, the treatment goal is to achieve the maximal therapeutic effect with the lowest effective dosage while avoiding side effects.

More time may be required to achieve a therapeutic effect in older than in younger patients. Substantial improvement may not be seen until an older patient has been taking an antidepressant for 9 weeks or longer. In younger patients, responses are seen as early as 2 weeks after starting antidepressant therapy, and remission occurs within 6 to 8 weeks.²

SSRIs versus tricyclics

SSRIs—citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline (Table 1)⁷ —are considered first-line antidepressants for late-life depression. Although SSRIs and tricyclic antidepressants (TCAs) demonstrate equivalent efficacy in older adults, SSRIs are associated with lesstroublesome side effects.²

SSRIs are less sedating than tricyclics and are not associated with adverse effects on cognition; both qualities make these agents appropriate for older patients. Risk of overdose with SSRIs also is much lower than with TCAs.²

Both types of agent have been reported to cause movement disorders such as extrapyramidal symptoms and even tardive dyskinesia, but these side effects are much more rare with SSRIs than with TCAs.² Also—unlike the TCAs— SSRIs do not significantly effect cardiac conduction, which is an important quality in the older population with its relatively high incidence of heart disease.

Table 1

USING SSRIs TO TREAT LATE-LIFE DEPRESSION

Meta-analyses suggest that patients are more likely to discontinue taking tricyclics than SSRIs.⁸ Adherence to antidepressant medications by older patients has been associated with lower perceived stigma of mental illness, higher self-rated severity of illness, age over 60, and absence of a personality disorder.⁹

SSRI side effects

The most common side effect of SSRIs is nausea, which is usually mild and occurs in the first weeks of treatment.² Dry mouth is related to noradrenergic influences on the salivary gland. Anxiety is usually transient.

Sedation can be a problem in older patients who use SSRIs. Among the six SSRIs indicated for depression, paroxetine appears to be the most sedating.¹⁰ Paroxetine exhibits the most muscarinic blockade in vitro, with a binding affinity less than that of imipramine but greater than nortriptyline.¹¹ Studies in older patients have suggested, however, that cognitive function is not compromised with paroxetine, as is observed with other antidepressants with anticholinergic action.⁶

Table 2

CYTOCHROME P450 ISOZYMES INHIBITED BY SSRI ANTIDEPRESSANTS (IN VITRO)

Sexual function can be diminished by SSRIs; the most common sexual side effects are anorgasmia and delayed orgasm.¹² Preserving sexual function is important to many older men and women who retain their interest in sexual activity well into later life.

Withdrawal syndrome. Abrupt discontinuation of some SSRIs can lead to withdrawal side effects, such as dizziness, fatigue, and nausea. In a study of young and older adults, withdrawal syndrome followed abrupt discontinuation at rates of 14% with fluoxetine and 60% with sertraline or paroxetine.¹³

Elimination half-life. Medication half-lives tend to be prolonged in older patients because of age-related pharmacokinetic changes. SSRIs with relatively shorter half-lives—such as citalopram, sertraline, paroxetine, and fluvoxamine—could be eliminated fairly rapidly should adverse events arise.

On the other hand, use of a longer-acting agent, such as fluoxetine, may be an advantage if compliance is a problem. In this case, fluoxetine’s prolonged washout rate could help protect a patient from relapse, even when doses are missed.

Potential drug-drug interactions

Individual SSRIs have different effects on the cytochrome P450 system (Table 2).^14,15 For example, fluoxetine, sertraline, and paroxetine—but not fluvoxamine—are in vitro inhibitors of the 2D6 isoenzyme system,¹⁶ which metabolizes TCAs, type Ic antiarrhythmics, alpha-adrenergic blockers, dextromethorphan, chemotherapeutic agents, and some antipsychotics. Citalopram has minimal inhibitory activity and escitalopram has virtually no inhibitory action on CYP 2D6.¹⁷

Cytochrome P450 3A4 metabolizes numerous drugs, including alprazolam, triazolam, carbamazepine, calcium channel blockers, and others. The 3A4 enzymes are inhibited by fluoxetine, sertraline, and fluvoxamine.¹⁸

Cytochrome P450 1A2 is the liver isoenzyme responsible for dealkylating theophylline, caffeine, and phenacetin. This enzyme system also metabolizes tacrine and clozapine. Of the SSRIs, fluvoxamine is the most potent inhibitor of the 1A2 enzyme, while escitalopram is a negligible inhibitor.¹⁷

Cytochrome P450 2C is a subfamily of isoenzymes that includes 2C9, 2C10, 2C19, and others. This system metabolizes some antidepressants as well as warfarin, phenytoin, and diazepam. Inhibitors of this system include fluvoxamine, fluoxetine, sertraline, and paroxetine.¹⁸

MAO inhibitors. Concomitant use of serotonin-acting drugs and monoamine oxidase inhibitors should be avoided. When used in combination, SSRIs and MAO inhibitors can cause a serotonin syndrome, with potential hyperpyretic crises, seizures, coma, and death. When switching medications, it is important to eliminate any serotonin-acting drug before starting an MAO inhibitor.²

In young adults, a 7-day washout is needed when switching from fluvoxamine and 14 days when switching from sertraline, citalopram, or paroxetine. With fluoxetine, the washout period is 35 days in young adults. Because medication half-lives in older patients may be prolonged two- to three-fold, it is advisable to proceed conservatively and extend these washout periods accordingly.

Related resources

• National Institute of Mental Health. Older adults: Depression and suicide facts. www.nimh.nih.gov/publicat/elderlydepsuicide.cfm
• WebMD Health/depression. http://my.webmd.com/condition_center/dep
• Salzman C, Wong E, Wright BC. Drug and ECT treatment of depression in the elderly, 1996-2001: a literature review. Biol Psychiatry 2002;52(3):265-84.

Drug brand names

• Alprazolam • Xanax
• Citalopram • Celexa
• Clozapine • Clozaril
• Diazepam • Valium
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Paroxetine • Paxil
• Sertraline • Zoloft
• Tacrine • Cognex
• Triazolam • Halcion

Disclosure

Dr. Kasckow reports that he receives grant/research support from, serves as a consultant to, or is on the speakers bureau of Eli Lilly and Co., Forest Laboratories, Pharmacia Corp., Solvay Pharmaceuticals, AstraZeneca Pharmaceuticals, Organon, Janssen Pharmaceutica, and Pfizer Inc.

Dr. Mohamed reports that she receives grant/research support from Forest Laboratories and serves on the speakers bureau of Eli Lilly and Co.

Dr. Herman reports that he serves as a consultant to Eli Lilly and Co.

Other co-authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Despite its impact on individuals and public health, depression in older persons is inadequately diagnosed and treated. Even when depression is diagnosed, only one-third of persons older than 65 receive treatment.¹ Reasons for this include:

• lack of physician awareness that depression presents differently in older than in younger adults
• patient denial of depressive symptoms
• patients’ and physicians’ mistaken belief that feeling depressed is a normal part of aging.

The good news is that when geriatric depression is recognized, it usually responds favorably to treatment, although aggressive intervention may be required.² In this article, we describe our approach to diagnosis and discuss use of selective serotonin reuptake inhibitors (SSRIs) as first-line antidepressants for older patients.

Late-life depression risk factors

Depression is common in older persons, especially in those who have experienced psychosocial or medical losses, including chronic illness. Although its presentation often does not meet criteria for major depression, the more common subsyndromal depression is debilitating and can lead to suicide.

Box

CASE REPORT: DEPRESSED, AT RISK FOR SUICIDE

A 72-year-old man presents with trouble concentrating, decreased appetite, anergy, and anhedonia. He says he frequently awakes at 3 AM, and it takes him 2 hours to return to sleep. Lately, he has thought of shooting himself with his hunting rifle. The patient’s wife died of cancer 1 year ago, and he has developed several medical illnesses within the past 10 years: chronic obstructive pulmonary disease, worsening arthritis, mild ischemic heart disease, and worsening hearing loss.

The patient denies feeling depressed and instead attributes his symptoms to his medical illnesses. He has become progressively isolated in the past year, with less social contact with his friends at the local parish. His older brother, with whom he was close, died recently. Until now, he says his “pride” has made him resist his primary care physician’s recommendation that he see a psychiatrist.

Late-life depressive syndromes commonly present with somatic complaints. Typically, patients deny having a mental illness and perceive that their symptoms are organic in origin (Box).¹

Losses. Psychosocial and medical losses are major risk factors for late-life adjustment disorders, subsyndromal depressive disorders, and major depression. Medical losses may include loss of mobility or independent function, chronic pain, or sensory losses that limit one’s ability to read or hear. Psychosocial losses may include the death of a spouse, sibling, or peer or moving from one’s longtime home to a more structured environment (assisted living, nursing home, or living with relatives).

Medical causes to rule out before starting antidepressant therapy include:

• hypothyroidism
• medication side effects
• bipolar disorder, which may require the use of a mood-stabilizing agent to prevent manic symptoms.³

History. Often a history of mood disorder in the individual or a family member can help the clinician determine that mental illness accounts for the patient’s symptoms. In older patients, it is not uncommon for psychotic symptoms to accompany a primary mood disturbance.

Suicide risk is high in depressed older persons, so detection and quick treatment of depression is paramount. Older white men are at particularly high risk for completed suicide using firearms.³

Alcohol abuse may contribute to depressive symptoms in older persons. A second peak of alcoholism occurs in the eighth decade of life and can confound diagnosis of depression in patients of this age.

Making the diagnosis. In patients who present with symptoms and risk factors for late-life depression, depression rating scales can help confirm the diagnosis. Commonly used scales include the Beck Depression Inventory, the Hamilton Depression Rating Scale, and the Zung Self-Rating Depression Scale. Specialized scales for use in older patients include the Geriatric Depression Scale and the Cornell Scale; the latter scale is designed for patients with comorbid depression and dementia.^3,4

Treatment

Antidepressant treatment in combination with psychotherapy usually is warranted when treating nonpsychotic late-life depression. In patients with psychosis, electroconvulsive therapy can help achieve remission.

Cognitive-behavioral therapy and interpersonal and insight-oriented psychotherapy have been shown to be effective in late-life depression. Social interventions aimed at preventing isolation also can work. In milder cases of depression, psychotherapy alone may be sufficient.³

Starting dosages. When antidepressant therapy is indicated in an older patient, start low and go slow.⁵ Older patients generally require prolonged titration rates and a longer course of treatment than do younger patients. Physiologic changes that occur with aging include:

• altered drug metabolism rate, including slower demethylation
• increased body fat-to-water ratio, which increases the volume of distribution for lipophilic psychotropic drugs
• decreased glomerular filtration rate, which may account for higher serum concentrations of drugs and their metabolites
• increased sensitivity of the older brain to the effects of medications.⁶

Thus—with some exceptions—recommended starting dosages for older patients are usually one-half those used in younger adults. For the frail older patient, the starting dosage should probably be even lower—about one-fourth the typical starting dosage in young adults.⁶ As in younger patients, the treatment goal is to achieve the maximal therapeutic effect with the lowest effective dosage while avoiding side effects.

More time may be required to achieve a therapeutic effect in older than in younger patients. Substantial improvement may not be seen until an older patient has been taking an antidepressant for 9 weeks or longer. In younger patients, responses are seen as early as 2 weeks after starting antidepressant therapy, and remission occurs within 6 to 8 weeks.²

SSRIs versus tricyclics

SSRIs—citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline (Table 1)⁷ —are considered first-line antidepressants for late-life depression. Although SSRIs and tricyclic antidepressants (TCAs) demonstrate equivalent efficacy in older adults, SSRIs are associated with lesstroublesome side effects.²

SSRIs are less sedating than tricyclics and are not associated with adverse effects on cognition; both qualities make these agents appropriate for older patients. Risk of overdose with SSRIs also is much lower than with TCAs.²

Both types of agent have been reported to cause movement disorders such as extrapyramidal symptoms and even tardive dyskinesia, but these side effects are much more rare with SSRIs than with TCAs.² Also—unlike the TCAs— SSRIs do not significantly effect cardiac conduction, which is an important quality in the older population with its relatively high incidence of heart disease.

Table 1

USING SSRIs TO TREAT LATE-LIFE DEPRESSION

Meta-analyses suggest that patients are more likely to discontinue taking tricyclics than SSRIs.⁸ Adherence to antidepressant medications by older patients has been associated with lower perceived stigma of mental illness, higher self-rated severity of illness, age over 60, and absence of a personality disorder.⁹

SSRI side effects

The most common side effect of SSRIs is nausea, which is usually mild and occurs in the first weeks of treatment.² Dry mouth is related to noradrenergic influences on the salivary gland. Anxiety is usually transient.

Sedation can be a problem in older patients who use SSRIs. Among the six SSRIs indicated for depression, paroxetine appears to be the most sedating.¹⁰ Paroxetine exhibits the most muscarinic blockade in vitro, with a binding affinity less than that of imipramine but greater than nortriptyline.¹¹ Studies in older patients have suggested, however, that cognitive function is not compromised with paroxetine, as is observed with other antidepressants with anticholinergic action.⁶

Table 2

CYTOCHROME P450 ISOZYMES INHIBITED BY SSRI ANTIDEPRESSANTS (IN VITRO)

Sexual function can be diminished by SSRIs; the most common sexual side effects are anorgasmia and delayed orgasm.¹² Preserving sexual function is important to many older men and women who retain their interest in sexual activity well into later life.

Withdrawal syndrome. Abrupt discontinuation of some SSRIs can lead to withdrawal side effects, such as dizziness, fatigue, and nausea. In a study of young and older adults, withdrawal syndrome followed abrupt discontinuation at rates of 14% with fluoxetine and 60% with sertraline or paroxetine.¹³

Elimination half-life. Medication half-lives tend to be prolonged in older patients because of age-related pharmacokinetic changes. SSRIs with relatively shorter half-lives—such as citalopram, sertraline, paroxetine, and fluvoxamine—could be eliminated fairly rapidly should adverse events arise.

On the other hand, use of a longer-acting agent, such as fluoxetine, may be an advantage if compliance is a problem. In this case, fluoxetine’s prolonged washout rate could help protect a patient from relapse, even when doses are missed.

Potential drug-drug interactions

Individual SSRIs have different effects on the cytochrome P450 system (Table 2).^14,15 For example, fluoxetine, sertraline, and paroxetine—but not fluvoxamine—are in vitro inhibitors of the 2D6 isoenzyme system,¹⁶ which metabolizes TCAs, type Ic antiarrhythmics, alpha-adrenergic blockers, dextromethorphan, chemotherapeutic agents, and some antipsychotics. Citalopram has minimal inhibitory activity and escitalopram has virtually no inhibitory action on CYP 2D6.¹⁷

Cytochrome P450 3A4 metabolizes numerous drugs, including alprazolam, triazolam, carbamazepine, calcium channel blockers, and others. The 3A4 enzymes are inhibited by fluoxetine, sertraline, and fluvoxamine.¹⁸

Cytochrome P450 1A2 is the liver isoenzyme responsible for dealkylating theophylline, caffeine, and phenacetin. This enzyme system also metabolizes tacrine and clozapine. Of the SSRIs, fluvoxamine is the most potent inhibitor of the 1A2 enzyme, while escitalopram is a negligible inhibitor.¹⁷

Cytochrome P450 2C is a subfamily of isoenzymes that includes 2C9, 2C10, 2C19, and others. This system metabolizes some antidepressants as well as warfarin, phenytoin, and diazepam. Inhibitors of this system include fluvoxamine, fluoxetine, sertraline, and paroxetine.¹⁸

MAO inhibitors. Concomitant use of serotonin-acting drugs and monoamine oxidase inhibitors should be avoided. When used in combination, SSRIs and MAO inhibitors can cause a serotonin syndrome, with potential hyperpyretic crises, seizures, coma, and death. When switching medications, it is important to eliminate any serotonin-acting drug before starting an MAO inhibitor.²

In young adults, a 7-day washout is needed when switching from fluvoxamine and 14 days when switching from sertraline, citalopram, or paroxetine. With fluoxetine, the washout period is 35 days in young adults. Because medication half-lives in older patients may be prolonged two- to three-fold, it is advisable to proceed conservatively and extend these washout periods accordingly.

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