Case-Based Review

CASE: ’I’m not crazy’

Ms. S, age 55, presents for treatment because she is feeling depressed and anxious. Her symptoms include decreased concentration, intermittent irritability, hoarding, and difficulty starting and completing tasks. She also has chronic sleep difficulties that often keep her awake until dawn.

Fatigue, lack of focus, and poor comprehension and motivation have left her unemployed. She and her teenage daughter live with Ms. S’s elderly mother. Ms. S feels tremendous guilt because she cannot be the mother and daughter she wants to be.

Initially, I (PK) diagnose Ms. S with major depressive disorder and prescribe sertraline, 100 mg/d, which improves her mood and energy. However, her inability to stay organized results in her being “let go” from job training.

Ms. S reports similar difficulties in school as a child. I determine that she meets DSM-IV-TR criteria for attention-deficit/hyperactivity disorder (ADHD). Adding methylphenidate, 10 mg bid, improves her concentration and ability to complete tasks. It also reduces the impulsivity that has disrupted her relationships.

Despite a strong desire to normalize her sleep schedule, Ms. S continues to have difficulty falling asleep, so I add melatonin, 3 to 6 mg at bedtime. Her sleeping pattern is improved, but still variable. She also tries quetiapine, 25 mg at bedtime, but soon discontinues it due to intolerance.

As our rapport strengthens, Ms. S reveals that she has had multiple encounters with aliens beginning at age 3. Although she has not had an “alien experience” for about 5 years, she does not feel safe sleeping at night and instead sleeps during the day. Her efforts to stay awake at night strain her relationship with her mother.

The authors’ observations

Approximately 1% of the U.S. population report alien abduction experiences (AAE)—an umbrella term that includes alleged contact with aliens ranging from sightings to abductions.¹ Patients rarely report AAE to mental health professionals. In our society, claiming to be an “abductee” implies that one might be insane. A survey of 398 Canadian students that assessed attitudes, beliefs, and experiences regarding alien abductions found that 79% of respondents believed they would have mostly negative consequences—such as being laughed at or socially isolated—if they claimed to have encountered aliens.¹

Persons who have AAE may attend support groups of fellow “abductees” to accumulate behavior-consonant information (hearing other people’s abduction stories) and reduce dissonance by being surrounded by others who share a questionable belief.² A survey of “abductees” found that 88% report at least some positive aspects of the experience, such as a sense of importance or feeling as though they were chosen to bridge communication between extraterrestrials and humans.³

Data collected over 17 years from Minnesota Multiphasic Personality Inventory (MMPI) scores of 225 persons who reported AAE reveal common personality traits, including:

• high levels of psychic energy
  
• self-sufficiency
  
• resourcefulness
  
• a tendency to question authority and to be exposed to situational conflicts.¹
  

Other common characteristics include above-average intelligence, assertiveness, a tendency to be reserved and absorbed in thought, and a tendency toward defensiveness, but no overt psychopathology.¹

After Ms. S reveals her alien experiences, I reassure her in a nonjudgmental manner that we will explore her experiences and determine ways to help her cope with them.

HISTORY: Terrifying experiences

Ms. S elaborates on her alien experiences, relating a particularly terrifying example from her teen years. She was lying awake in bed, looking at the ceiling, where she saw a jeweled spider with a drill. As the spider descended from the ceiling and spread its legs, she recalled a noise like a dentist’s drill. As the spider neared her face, it grew larger and larger. Terrified, Ms. S was unable to scream for help or move anything except her eyes as the spider clamped its legs around her head and bored into her skull. She reported that although she could feel the drill go in, it wasn’t painful.

Other experiences included giving birth, undergoing examinations or probes, and communicating with aliens. Although she is very distressed by most memories, she feels she benefited from others. For example, as a child, Ms. S’s math skills improved dramatically after an AAE episode; she believes this was a gift from the aliens. Ms. S’s AAE memories are as vivid to her as memories of her college graduation. She had been reluctant to discuss these events with anyone outside her family out of fear of being perceived as “crazy.”

Ms. S says she was a shy child who had difficulty making friends. She was plagued with fatigue and worry about family members. She believed that aliens might attack her sisters and felt obligated to stay awake at night to protect them. Aside from alien experiences, Ms. S reports a happy childhood.

 

She has always been an avid reader. At age 8 or 9, after reading a book on alien abduction, she concluded that she had been abducted. Later, she joined a group of professed alien abductees. She feels accepted and validated by this group and has a forum for discussing her experiences without fear of ridicule or rejection.

Ms. S remains frightened by things that remind her of aliens. Although she wrote a summary of her alien experiences, she cannot draw a picture of an alien, and thoughts or images of the prototypical “grey” alien trigger panic. She also feels somewhat “different,” nervous, and distant from others.

The authors’ observations

Reviewing AAE literature led me to consider several diagnoses, including:

• psychosis
  
• seizures
  
• false memory (sexual abuse, trauma)
  
• narcolepsy
  
• sleep paralysis.
  

A medical workup ruled out common organic causes of psychosis. Results were normal for brain MRI, ECG, comprehensive metabolic panel, thyroid function tests, complete blood count with differential, serum alcohol, urinalysis, and urine drug screen.

Electroencephalography (during drowsiness) revealed abnormal activity (occurrences of widely scattered bursts of nonspecific, round, sharply contoured slow waves in the left frontal region) only in the F7 electrode. In the absence of clinical symptoms and when found in a single lead, this is considered a normal variant.

Psychological testing—including MMPI, Myers-Briggs Type Indicator (MBTI), and Wechsler Adult Intelligence Scale (WAIS III)—revealed no evidence of psychosis or personality disorder, and intelligence was within the average range. Mental status exam was normal. Aside from the alien experiences, Ms. S denied any memory of childhood trauma. Interviews did not reveal symptoms compatible with narcolepsy.

Diagnostic testing ruled out hallucinosis related to seizures. I also ruled out false memory related to sexual abuse or trauma, which is commonly found in patients who present with AAE.

Collaborative information from relatives did not uncover a history of psychosis. She and family members reported, however, that Ms. S’s father and 1 sister had periodic sleep disturbances with associated hallucinations. I began to suspect sleep paralysis.

The authors’ observations

Full-body paralysis normally accompanies rapid eye movement (REM) sleep, which occurs several times a night.⁴ Sleep paralysis is a transient state that occurs when an individual becomes conscious of this immobility, typically while falling asleep or awakening.⁵ These experiences can be accompanied by hypnagogic (while falling asleep) or hypnopompic (while awakening) hallucinations. An estimated 30% of the population has had at least one sleep paralysis episode.⁶ In one study, 5% of sleep paralysis patients had episodes that were accompanied by hallucinations.⁷

Although individuals cannot make gross body movements during sleep paralysis, they can open their eyes and are able to report events that occurred around them during the episode.⁸ Patients interpret sleep paralysis experiences in subjective terms. Common descriptions include intense fear, breathing difficulties, feeling of bodily pressure—especially on the chest—and sensations of floating, flying, or falling (Table 1).^7,9

During sleep paralysis episodes, individuals typically sense a threatening presence.⁶ Patients have reported beastly and demonic figures of doom: devils, demons, witches, aliens, and even cinematic villains such as Darth Vader and Freddy Kruger.⁶ Others have described this presence in terms of alien visitations or abductions.

Table 1

4 types of sleep paralysis-related hallucinations

Intruder	Vague sense of a threatening presence accompanied by visual, auditory, and tactile hallucinations—noises, footsteps, gibbering voices, humanoid apparitions, and sensation of being touched or grabbed
Incubus	Breathing difficulties, feelings of suffocation, bodily pressure (particularly on the chest, as if someone were sitting or standing on it), pain, and thoughts of impending death
Vestibular-motor	Sensations of floating (levitation), flying, and falling
Other	Out-of-body experiences, autoscopy (seeing oneself from an external point), and fictive motor movements, ranging from simple arm movements to sitting up to apparent locomotion through the environment
Source: References 7,9

Internationally, most alien experience reports come from countries dominated by Western culture and values. This suggests that a belief in aliens serves as a template against which people share ambiguous information, diffuse physical sensations, and vivid hallucinations of alien encounters that they experience as real events.¹⁰

A Harvard University study of 11 individuals who reported alien abductions found that all participants experienced a similar sequence of events:

• They suspected abduction after sleep episodes characterized by awakening, full-body paralysis, intense fear, and a feeling of a presence. Several reported tactile or visual sensations strikingly similar to descriptions of sleep paralysis, such as levitating, being touched, and seeing shadowy figures.
  
• They sought explanations for what they perceived as anomalous experiences.
  
• They “recovered” abduction memories in therapy (with the help of techniques such as hypnosis) or spontaneously (after reading books or seeing movies or television shows depicting similar episodes).⁴
  

 

Ms. S reported no daytime sleep attacks, cataplexy, or rapid onset of dreaming. Because her reported AAEs were spread out and the last occurred approximately 5 years ago, I decided against conducting a sleep study because it likely would be low yield and costly. I reached a diagnosis of sleep paralysis-familial type, chronic based on:

• an absence of organic or psychiatric dysfunction
  
• a familial pattern of sleep disturbances
  
• the temporal pattern and description of her symptoms (Table 2).¹¹
  

All of Ms. S’s episodes occurred at night or times of quiet restfulness. She usually slept on her back, which may be a risk factor for sleep paralysis.¹²

Table 2

Diagnostic criteria for sleep paralysis

A. Patient complains of inability to move the trunk or limbs at sleep onset or upon awakening
B. Brief episodes of partial or complete skeletal muscle paralysis
C. Episodes can be associated with hypnagogic (preceding sleep) hallucinations or dreamlike mentation
D. Polysomnographic monitoring demonstrates at least 1 of the following: Suppression of skeletal muscle tone A sleep-onset REM period Dissociated REM sleep
E. Symptoms are not associated with other medical or mental disorders, such as hysteria or hypokalemic paralysis
Minimal criteria are A plus B plus E
Note: If symptoms are associated with a familial history, the diagnosis is sleep paralysis-familial type. If symptoms are not associated with a familial history, the diagnosis is sleep paralysis-isolated type
Severity criteria Mild: Moderate: >1 episode per month but Severe: ≥1 episode per week
Duration criteria Acute: ≤1 month Subacute: >1 month but Chronic: ≥6 months
REM: rapid eye movement
Source: Reference 11

TREATMENT: Reassurance, therapy

Effective treatment for Ms. S required helping her to understand that an organic condition was the foundation of her experiences. I began by conveying the sleep paralysis diagnosis and my understanding of the occupational and personal consequences that this condition had had for her. I explained the physiology of sleep paralysis and that memories or hallucinations (dreamlike mentation) are preserved in an extremely vivid fashion because her eyes are open. I acknowledged the realistic character of her experiences and the resulting symptoms of posttraumatic stress disorder (PTSD).

I refer Ms. S to a therapist for psychotherapy. The therapist begins by using trauma informed techniques to address Ms. S’s PTSD. As she improves, her therapy evolves into a combination of narrative and supportive psychotherapy, and then family systems therapy to address issues with her daughter and mother.

In a follow-up visit 1 year after beginning treatment, Ms. S cites multiple improvements, with no recurrence of sleep paralysis episodes. She continues to take sertraline, which relieves her depression and anxiety, and methylphenidate to improve her attention and concentration. She has taken on more responsibility at home, cleaning, preparing meals, helping her daughter choose a college, and attending to her mother’s health issues. Ms. S still has difficulties with her sleep patterns, and her new psychiatrist is exploring the possibility of a bipolar component to her mood disorder.

The authors’ observations

Like other traumas, AAE can induce symptoms of acute or chronic PTSD. The various psychoses, personality disorders, and dissociative disorders that could account for abduction experiences are characterized by delusions, so conduct ongoing assessment for these conditions in patients who report AAE. However, evidence suggests that serious psychopathology is no more common among “abductees” than among the general population.¹²

Persons reporting AAE exhibit physiologic reactivity as profound as that of survivors of combat or sexual assault.¹³ This reactivity confirms that the emotional power of the memory is as evocative and problematic as the physiologic reactions attributable to genuine (documented) traumatic events. Because patients have difficulty differentiating these hallucinations from actual events, they experience emotional pain and suffering. Fifty-seven percent of sleep paralysis patients who report AAE attempt suicide.¹⁴

Offer patients with AAE psychotherapy to deal with long-term effects of trauma and problems with mood, sleep, daily functioning, and/or relationships.

There are no FDA-approved medications for treating sleep paralysis. Pharmacotherapy can be used to address psychiatric symptoms such as the depression and anxiety Ms. S exhibited.

Related resources

• American Academy of Sleep Medicine. International classification of sleep disorders, revised: diagnostic and coding manual. Chicago, IL: American Academy of Sleep Medicine; 2001:166-9.
  
• Cheyne JA. Sleep paralysis and associated hypnagogic and hypnopompic experiences. http://watarts.uwaterloo.ca/~acheyne/S_P.html.
  

Drug brand names

• Methylphenidate • Ritalin
  
• Quetiapine • Seroquel
  
• Sertraline • Zoloft
  

 

Disclosure

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

CASE: ’I’m not crazy’

Ms. S, age 55, presents for treatment because she is feeling depressed and anxious. Her symptoms include decreased concentration, intermittent irritability, hoarding, and difficulty starting and completing tasks. She also has chronic sleep difficulties that often keep her awake until dawn.

Fatigue, lack of focus, and poor comprehension and motivation have left her unemployed. She and her teenage daughter live with Ms. S’s elderly mother. Ms. S feels tremendous guilt because she cannot be the mother and daughter she wants to be.

Initially, I (PK) diagnose Ms. S with major depressive disorder and prescribe sertraline, 100 mg/d, which improves her mood and energy. However, her inability to stay organized results in her being “let go” from job training.

Ms. S reports similar difficulties in school as a child. I determine that she meets DSM-IV-TR criteria for attention-deficit/hyperactivity disorder (ADHD). Adding methylphenidate, 10 mg bid, improves her concentration and ability to complete tasks. It also reduces the impulsivity that has disrupted her relationships.

Despite a strong desire to normalize her sleep schedule, Ms. S continues to have difficulty falling asleep, so I add melatonin, 3 to 6 mg at bedtime. Her sleeping pattern is improved, but still variable. She also tries quetiapine, 25 mg at bedtime, but soon discontinues it due to intolerance.

As our rapport strengthens, Ms. S reveals that she has had multiple encounters with aliens beginning at age 3. Although she has not had an “alien experience” for about 5 years, she does not feel safe sleeping at night and instead sleeps during the day. Her efforts to stay awake at night strain her relationship with her mother.

The authors’ observations

Approximately 1% of the U.S. population report alien abduction experiences (AAE)—an umbrella term that includes alleged contact with aliens ranging from sightings to abductions.¹ Patients rarely report AAE to mental health professionals. In our society, claiming to be an “abductee” implies that one might be insane. A survey of 398 Canadian students that assessed attitudes, beliefs, and experiences regarding alien abductions found that 79% of respondents believed they would have mostly negative consequences—such as being laughed at or socially isolated—if they claimed to have encountered aliens.¹

Persons who have AAE may attend support groups of fellow “abductees” to accumulate behavior-consonant information (hearing other people’s abduction stories) and reduce dissonance by being surrounded by others who share a questionable belief.² A survey of “abductees” found that 88% report at least some positive aspects of the experience, such as a sense of importance or feeling as though they were chosen to bridge communication between extraterrestrials and humans.³

Data collected over 17 years from Minnesota Multiphasic Personality Inventory (MMPI) scores of 225 persons who reported AAE reveal common personality traits, including:

• high levels of psychic energy
  
• self-sufficiency
  
• resourcefulness
  
• a tendency to question authority and to be exposed to situational conflicts.¹
  

Other common characteristics include above-average intelligence, assertiveness, a tendency to be reserved and absorbed in thought, and a tendency toward defensiveness, but no overt psychopathology.¹

After Ms. S reveals her alien experiences, I reassure her in a nonjudgmental manner that we will explore her experiences and determine ways to help her cope with them.

HISTORY: Terrifying experiences

Ms. S elaborates on her alien experiences, relating a particularly terrifying example from her teen years. She was lying awake in bed, looking at the ceiling, where she saw a jeweled spider with a drill. As the spider descended from the ceiling and spread its legs, she recalled a noise like a dentist’s drill. As the spider neared her face, it grew larger and larger. Terrified, Ms. S was unable to scream for help or move anything except her eyes as the spider clamped its legs around her head and bored into her skull. She reported that although she could feel the drill go in, it wasn’t painful.

Other experiences included giving birth, undergoing examinations or probes, and communicating with aliens. Although she is very distressed by most memories, she feels she benefited from others. For example, as a child, Ms. S’s math skills improved dramatically after an AAE episode; she believes this was a gift from the aliens. Ms. S’s AAE memories are as vivid to her as memories of her college graduation. She had been reluctant to discuss these events with anyone outside her family out of fear of being perceived as “crazy.”

Ms. S says she was a shy child who had difficulty making friends. She was plagued with fatigue and worry about family members. She believed that aliens might attack her sisters and felt obligated to stay awake at night to protect them. Aside from alien experiences, Ms. S reports a happy childhood.

 

She has always been an avid reader. At age 8 or 9, after reading a book on alien abduction, she concluded that she had been abducted. Later, she joined a group of professed alien abductees. She feels accepted and validated by this group and has a forum for discussing her experiences without fear of ridicule or rejection.

Ms. S remains frightened by things that remind her of aliens. Although she wrote a summary of her alien experiences, she cannot draw a picture of an alien, and thoughts or images of the prototypical “grey” alien trigger panic. She also feels somewhat “different,” nervous, and distant from others.

The authors’ observations

Reviewing AAE literature led me to consider several diagnoses, including:

• psychosis
  
• seizures
  
• false memory (sexual abuse, trauma)
  
• narcolepsy
  
• sleep paralysis.
  

A medical workup ruled out common organic causes of psychosis. Results were normal for brain MRI, ECG, comprehensive metabolic panel, thyroid function tests, complete blood count with differential, serum alcohol, urinalysis, and urine drug screen.

Electroencephalography (during drowsiness) revealed abnormal activity (occurrences of widely scattered bursts of nonspecific, round, sharply contoured slow waves in the left frontal region) only in the F7 electrode. In the absence of clinical symptoms and when found in a single lead, this is considered a normal variant.

Psychological testing—including MMPI, Myers-Briggs Type Indicator (MBTI), and Wechsler Adult Intelligence Scale (WAIS III)—revealed no evidence of psychosis or personality disorder, and intelligence was within the average range. Mental status exam was normal. Aside from the alien experiences, Ms. S denied any memory of childhood trauma. Interviews did not reveal symptoms compatible with narcolepsy.

Diagnostic testing ruled out hallucinosis related to seizures. I also ruled out false memory related to sexual abuse or trauma, which is commonly found in patients who present with AAE.

Collaborative information from relatives did not uncover a history of psychosis. She and family members reported, however, that Ms. S’s father and 1 sister had periodic sleep disturbances with associated hallucinations. I began to suspect sleep paralysis.

The authors’ observations

Full-body paralysis normally accompanies rapid eye movement (REM) sleep, which occurs several times a night.⁴ Sleep paralysis is a transient state that occurs when an individual becomes conscious of this immobility, typically while falling asleep or awakening.⁵ These experiences can be accompanied by hypnagogic (while falling asleep) or hypnopompic (while awakening) hallucinations. An estimated 30% of the population has had at least one sleep paralysis episode.⁶ In one study, 5% of sleep paralysis patients had episodes that were accompanied by hallucinations.⁷

Although individuals cannot make gross body movements during sleep paralysis, they can open their eyes and are able to report events that occurred around them during the episode.⁸ Patients interpret sleep paralysis experiences in subjective terms. Common descriptions include intense fear, breathing difficulties, feeling of bodily pressure—especially on the chest—and sensations of floating, flying, or falling (Table 1).^7,9

During sleep paralysis episodes, individuals typically sense a threatening presence.⁶ Patients have reported beastly and demonic figures of doom: devils, demons, witches, aliens, and even cinematic villains such as Darth Vader and Freddy Kruger.⁶ Others have described this presence in terms of alien visitations or abductions.

Table 1

4 types of sleep paralysis-related hallucinations

Intruder	Vague sense of a threatening presence accompanied by visual, auditory, and tactile hallucinations—noises, footsteps, gibbering voices, humanoid apparitions, and sensation of being touched or grabbed
Incubus	Breathing difficulties, feelings of suffocation, bodily pressure (particularly on the chest, as if someone were sitting or standing on it), pain, and thoughts of impending death
Vestibular-motor	Sensations of floating (levitation), flying, and falling
Other	Out-of-body experiences, autoscopy (seeing oneself from an external point), and fictive motor movements, ranging from simple arm movements to sitting up to apparent locomotion through the environment
Source: References 7,9

Internationally, most alien experience reports come from countries dominated by Western culture and values. This suggests that a belief in aliens serves as a template against which people share ambiguous information, diffuse physical sensations, and vivid hallucinations of alien encounters that they experience as real events.¹⁰

A Harvard University study of 11 individuals who reported alien abductions found that all participants experienced a similar sequence of events:

• They suspected abduction after sleep episodes characterized by awakening, full-body paralysis, intense fear, and a feeling of a presence. Several reported tactile or visual sensations strikingly similar to descriptions of sleep paralysis, such as levitating, being touched, and seeing shadowy figures.
  
• They sought explanations for what they perceived as anomalous experiences.
  
• They “recovered” abduction memories in therapy (with the help of techniques such as hypnosis) or spontaneously (after reading books or seeing movies or television shows depicting similar episodes).⁴
  

 

Ms. S reported no daytime sleep attacks, cataplexy, or rapid onset of dreaming. Because her reported AAEs were spread out and the last occurred approximately 5 years ago, I decided against conducting a sleep study because it likely would be low yield and costly. I reached a diagnosis of sleep paralysis-familial type, chronic based on:

• an absence of organic or psychiatric dysfunction
  
• a familial pattern of sleep disturbances
  
• the temporal pattern and description of her symptoms (Table 2).¹¹
  

All of Ms. S’s episodes occurred at night or times of quiet restfulness. She usually slept on her back, which may be a risk factor for sleep paralysis.¹²

Table 2

Diagnostic criteria for sleep paralysis

A. Patient complains of inability to move the trunk or limbs at sleep onset or upon awakening
B. Brief episodes of partial or complete skeletal muscle paralysis
C. Episodes can be associated with hypnagogic (preceding sleep) hallucinations or dreamlike mentation
D. Polysomnographic monitoring demonstrates at least 1 of the following: Suppression of skeletal muscle tone A sleep-onset REM period Dissociated REM sleep
E. Symptoms are not associated with other medical or mental disorders, such as hysteria or hypokalemic paralysis
Minimal criteria are A plus B plus E
Note: If symptoms are associated with a familial history, the diagnosis is sleep paralysis-familial type. If symptoms are not associated with a familial history, the diagnosis is sleep paralysis-isolated type
Severity criteria Mild: Moderate: >1 episode per month but Severe: ≥1 episode per week
Duration criteria Acute: ≤1 month Subacute: >1 month but Chronic: ≥6 months
REM: rapid eye movement
Source: Reference 11

TREATMENT: Reassurance, therapy

Effective treatment for Ms. S required helping her to understand that an organic condition was the foundation of her experiences. I began by conveying the sleep paralysis diagnosis and my understanding of the occupational and personal consequences that this condition had had for her. I explained the physiology of sleep paralysis and that memories or hallucinations (dreamlike mentation) are preserved in an extremely vivid fashion because her eyes are open. I acknowledged the realistic character of her experiences and the resulting symptoms of posttraumatic stress disorder (PTSD).

I refer Ms. S to a therapist for psychotherapy. The therapist begins by using trauma informed techniques to address Ms. S’s PTSD. As she improves, her therapy evolves into a combination of narrative and supportive psychotherapy, and then family systems therapy to address issues with her daughter and mother.

In a follow-up visit 1 year after beginning treatment, Ms. S cites multiple improvements, with no recurrence of sleep paralysis episodes. She continues to take sertraline, which relieves her depression and anxiety, and methylphenidate to improve her attention and concentration. She has taken on more responsibility at home, cleaning, preparing meals, helping her daughter choose a college, and attending to her mother’s health issues. Ms. S still has difficulties with her sleep patterns, and her new psychiatrist is exploring the possibility of a bipolar component to her mood disorder.

The authors’ observations

Like other traumas, AAE can induce symptoms of acute or chronic PTSD. The various psychoses, personality disorders, and dissociative disorders that could account for abduction experiences are characterized by delusions, so conduct ongoing assessment for these conditions in patients who report AAE. However, evidence suggests that serious psychopathology is no more common among “abductees” than among the general population.¹²

Persons reporting AAE exhibit physiologic reactivity as profound as that of survivors of combat or sexual assault.¹³ This reactivity confirms that the emotional power of the memory is as evocative and problematic as the physiologic reactions attributable to genuine (documented) traumatic events. Because patients have difficulty differentiating these hallucinations from actual events, they experience emotional pain and suffering. Fifty-seven percent of sleep paralysis patients who report AAE attempt suicide.¹⁴

Offer patients with AAE psychotherapy to deal with long-term effects of trauma and problems with mood, sleep, daily functioning, and/or relationships.

There are no FDA-approved medications for treating sleep paralysis. Pharmacotherapy can be used to address psychiatric symptoms such as the depression and anxiety Ms. S exhibited.

Related resources

• American Academy of Sleep Medicine. International classification of sleep disorders, revised: diagnostic and coding manual. Chicago, IL: American Academy of Sleep Medicine; 2001:166-9.
  
• Cheyne JA. Sleep paralysis and associated hypnagogic and hypnopompic experiences. http://watarts.uwaterloo.ca/~acheyne/S_P.html.
  

Drug brand names

• Methylphenidate • Ritalin
  
• Quetiapine • Seroquel
  
• Sertraline • Zoloft
  

 

Disclosure

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

CASE: ’I’m not crazy’

Ms. S, age 55, presents for treatment because she is feeling depressed and anxious. Her symptoms include decreased concentration, intermittent irritability, hoarding, and difficulty starting and completing tasks. She also has chronic sleep difficulties that often keep her awake until dawn.

Fatigue, lack of focus, and poor comprehension and motivation have left her unemployed. She and her teenage daughter live with Ms. S’s elderly mother. Ms. S feels tremendous guilt because she cannot be the mother and daughter she wants to be.

Initially, I (PK) diagnose Ms. S with major depressive disorder and prescribe sertraline, 100 mg/d, which improves her mood and energy. However, her inability to stay organized results in her being “let go” from job training.

Ms. S reports similar difficulties in school as a child. I determine that she meets DSM-IV-TR criteria for attention-deficit/hyperactivity disorder (ADHD). Adding methylphenidate, 10 mg bid, improves her concentration and ability to complete tasks. It also reduces the impulsivity that has disrupted her relationships.

Despite a strong desire to normalize her sleep schedule, Ms. S continues to have difficulty falling asleep, so I add melatonin, 3 to 6 mg at bedtime. Her sleeping pattern is improved, but still variable. She also tries quetiapine, 25 mg at bedtime, but soon discontinues it due to intolerance.

As our rapport strengthens, Ms. S reveals that she has had multiple encounters with aliens beginning at age 3. Although she has not had an “alien experience” for about 5 years, she does not feel safe sleeping at night and instead sleeps during the day. Her efforts to stay awake at night strain her relationship with her mother.

The authors’ observations

Approximately 1% of the U.S. population report alien abduction experiences (AAE)—an umbrella term that includes alleged contact with aliens ranging from sightings to abductions.¹ Patients rarely report AAE to mental health professionals. In our society, claiming to be an “abductee” implies that one might be insane. A survey of 398 Canadian students that assessed attitudes, beliefs, and experiences regarding alien abductions found that 79% of respondents believed they would have mostly negative consequences—such as being laughed at or socially isolated—if they claimed to have encountered aliens.¹

Persons who have AAE may attend support groups of fellow “abductees” to accumulate behavior-consonant information (hearing other people’s abduction stories) and reduce dissonance by being surrounded by others who share a questionable belief.² A survey of “abductees” found that 88% report at least some positive aspects of the experience, such as a sense of importance or feeling as though they were chosen to bridge communication between extraterrestrials and humans.³

Data collected over 17 years from Minnesota Multiphasic Personality Inventory (MMPI) scores of 225 persons who reported AAE reveal common personality traits, including:

• high levels of psychic energy
  
• self-sufficiency
  
• resourcefulness
  
• a tendency to question authority and to be exposed to situational conflicts.¹
  

Other common characteristics include above-average intelligence, assertiveness, a tendency to be reserved and absorbed in thought, and a tendency toward defensiveness, but no overt psychopathology.¹

After Ms. S reveals her alien experiences, I reassure her in a nonjudgmental manner that we will explore her experiences and determine ways to help her cope with them.

HISTORY: Terrifying experiences

Ms. S elaborates on her alien experiences, relating a particularly terrifying example from her teen years. She was lying awake in bed, looking at the ceiling, where she saw a jeweled spider with a drill. As the spider descended from the ceiling and spread its legs, she recalled a noise like a dentist’s drill. As the spider neared her face, it grew larger and larger. Terrified, Ms. S was unable to scream for help or move anything except her eyes as the spider clamped its legs around her head and bored into her skull. She reported that although she could feel the drill go in, it wasn’t painful.

Other experiences included giving birth, undergoing examinations or probes, and communicating with aliens. Although she is very distressed by most memories, she feels she benefited from others. For example, as a child, Ms. S’s math skills improved dramatically after an AAE episode; she believes this was a gift from the aliens. Ms. S’s AAE memories are as vivid to her as memories of her college graduation. She had been reluctant to discuss these events with anyone outside her family out of fear of being perceived as “crazy.”

Ms. S says she was a shy child who had difficulty making friends. She was plagued with fatigue and worry about family members. She believed that aliens might attack her sisters and felt obligated to stay awake at night to protect them. Aside from alien experiences, Ms. S reports a happy childhood.

 

She has always been an avid reader. At age 8 or 9, after reading a book on alien abduction, she concluded that she had been abducted. Later, she joined a group of professed alien abductees. She feels accepted and validated by this group and has a forum for discussing her experiences without fear of ridicule or rejection.

Ms. S remains frightened by things that remind her of aliens. Although she wrote a summary of her alien experiences, she cannot draw a picture of an alien, and thoughts or images of the prototypical “grey” alien trigger panic. She also feels somewhat “different,” nervous, and distant from others.

The authors’ observations

Reviewing AAE literature led me to consider several diagnoses, including:

• psychosis
  
• seizures
  
• false memory (sexual abuse, trauma)
  
• narcolepsy
  
• sleep paralysis.
  

A medical workup ruled out common organic causes of psychosis. Results were normal for brain MRI, ECG, comprehensive metabolic panel, thyroid function tests, complete blood count with differential, serum alcohol, urinalysis, and urine drug screen.

Electroencephalography (during drowsiness) revealed abnormal activity (occurrences of widely scattered bursts of nonspecific, round, sharply contoured slow waves in the left frontal region) only in the F7 electrode. In the absence of clinical symptoms and when found in a single lead, this is considered a normal variant.

Psychological testing—including MMPI, Myers-Briggs Type Indicator (MBTI), and Wechsler Adult Intelligence Scale (WAIS III)—revealed no evidence of psychosis or personality disorder, and intelligence was within the average range. Mental status exam was normal. Aside from the alien experiences, Ms. S denied any memory of childhood trauma. Interviews did not reveal symptoms compatible with narcolepsy.

Diagnostic testing ruled out hallucinosis related to seizures. I also ruled out false memory related to sexual abuse or trauma, which is commonly found in patients who present with AAE.

Collaborative information from relatives did not uncover a history of psychosis. She and family members reported, however, that Ms. S’s father and 1 sister had periodic sleep disturbances with associated hallucinations. I began to suspect sleep paralysis.

The authors’ observations

Full-body paralysis normally accompanies rapid eye movement (REM) sleep, which occurs several times a night.⁴ Sleep paralysis is a transient state that occurs when an individual becomes conscious of this immobility, typically while falling asleep or awakening.⁵ These experiences can be accompanied by hypnagogic (while falling asleep) or hypnopompic (while awakening) hallucinations. An estimated 30% of the population has had at least one sleep paralysis episode.⁶ In one study, 5% of sleep paralysis patients had episodes that were accompanied by hallucinations.⁷

Although individuals cannot make gross body movements during sleep paralysis, they can open their eyes and are able to report events that occurred around them during the episode.⁸ Patients interpret sleep paralysis experiences in subjective terms. Common descriptions include intense fear, breathing difficulties, feeling of bodily pressure—especially on the chest—and sensations of floating, flying, or falling (Table 1).^7,9

During sleep paralysis episodes, individuals typically sense a threatening presence.⁶ Patients have reported beastly and demonic figures of doom: devils, demons, witches, aliens, and even cinematic villains such as Darth Vader and Freddy Kruger.⁶ Others have described this presence in terms of alien visitations or abductions.

Table 1

4 types of sleep paralysis-related hallucinations

Intruder	Vague sense of a threatening presence accompanied by visual, auditory, and tactile hallucinations—noises, footsteps, gibbering voices, humanoid apparitions, and sensation of being touched or grabbed
Incubus	Breathing difficulties, feelings of suffocation, bodily pressure (particularly on the chest, as if someone were sitting or standing on it), pain, and thoughts of impending death
Vestibular-motor	Sensations of floating (levitation), flying, and falling
Other	Out-of-body experiences, autoscopy (seeing oneself from an external point), and fictive motor movements, ranging from simple arm movements to sitting up to apparent locomotion through the environment
Source: References 7,9

Internationally, most alien experience reports come from countries dominated by Western culture and values. This suggests that a belief in aliens serves as a template against which people share ambiguous information, diffuse physical sensations, and vivid hallucinations of alien encounters that they experience as real events.¹⁰

A Harvard University study of 11 individuals who reported alien abductions found that all participants experienced a similar sequence of events:

• They suspected abduction after sleep episodes characterized by awakening, full-body paralysis, intense fear, and a feeling of a presence. Several reported tactile or visual sensations strikingly similar to descriptions of sleep paralysis, such as levitating, being touched, and seeing shadowy figures.
  
• They sought explanations for what they perceived as anomalous experiences.
  
• They “recovered” abduction memories in therapy (with the help of techniques such as hypnosis) or spontaneously (after reading books or seeing movies or television shows depicting similar episodes).⁴
  

 

Ms. S reported no daytime sleep attacks, cataplexy, or rapid onset of dreaming. Because her reported AAEs were spread out and the last occurred approximately 5 years ago, I decided against conducting a sleep study because it likely would be low yield and costly. I reached a diagnosis of sleep paralysis-familial type, chronic based on:

• an absence of organic or psychiatric dysfunction
  
• a familial pattern of sleep disturbances
  
• the temporal pattern and description of her symptoms (Table 2).¹¹
  

All of Ms. S’s episodes occurred at night or times of quiet restfulness. She usually slept on her back, which may be a risk factor for sleep paralysis.¹²

Table 2

Diagnostic criteria for sleep paralysis

A. Patient complains of inability to move the trunk or limbs at sleep onset or upon awakening
B. Brief episodes of partial or complete skeletal muscle paralysis
C. Episodes can be associated with hypnagogic (preceding sleep) hallucinations or dreamlike mentation
D. Polysomnographic monitoring demonstrates at least 1 of the following: Suppression of skeletal muscle tone A sleep-onset REM period Dissociated REM sleep
E. Symptoms are not associated with other medical or mental disorders, such as hysteria or hypokalemic paralysis
Minimal criteria are A plus B plus E
Note: If symptoms are associated with a familial history, the diagnosis is sleep paralysis-familial type. If symptoms are not associated with a familial history, the diagnosis is sleep paralysis-isolated type
Severity criteria Mild: Moderate: >1 episode per month but Severe: ≥1 episode per week
Duration criteria Acute: ≤1 month Subacute: >1 month but Chronic: ≥6 months
REM: rapid eye movement
Source: Reference 11

TREATMENT: Reassurance, therapy

Effective treatment for Ms. S required helping her to understand that an organic condition was the foundation of her experiences. I began by conveying the sleep paralysis diagnosis and my understanding of the occupational and personal consequences that this condition had had for her. I explained the physiology of sleep paralysis and that memories or hallucinations (dreamlike mentation) are preserved in an extremely vivid fashion because her eyes are open. I acknowledged the realistic character of her experiences and the resulting symptoms of posttraumatic stress disorder (PTSD).

I refer Ms. S to a therapist for psychotherapy. The therapist begins by using trauma informed techniques to address Ms. S’s PTSD. As she improves, her therapy evolves into a combination of narrative and supportive psychotherapy, and then family systems therapy to address issues with her daughter and mother.

In a follow-up visit 1 year after beginning treatment, Ms. S cites multiple improvements, with no recurrence of sleep paralysis episodes. She continues to take sertraline, which relieves her depression and anxiety, and methylphenidate to improve her attention and concentration. She has taken on more responsibility at home, cleaning, preparing meals, helping her daughter choose a college, and attending to her mother’s health issues. Ms. S still has difficulties with her sleep patterns, and her new psychiatrist is exploring the possibility of a bipolar component to her mood disorder.

The authors’ observations

Like other traumas, AAE can induce symptoms of acute or chronic PTSD. The various psychoses, personality disorders, and dissociative disorders that could account for abduction experiences are characterized by delusions, so conduct ongoing assessment for these conditions in patients who report AAE. However, evidence suggests that serious psychopathology is no more common among “abductees” than among the general population.¹²

Persons reporting AAE exhibit physiologic reactivity as profound as that of survivors of combat or sexual assault.¹³ This reactivity confirms that the emotional power of the memory is as evocative and problematic as the physiologic reactions attributable to genuine (documented) traumatic events. Because patients have difficulty differentiating these hallucinations from actual events, they experience emotional pain and suffering. Fifty-seven percent of sleep paralysis patients who report AAE attempt suicide.¹⁴

Offer patients with AAE psychotherapy to deal with long-term effects of trauma and problems with mood, sleep, daily functioning, and/or relationships.

There are no FDA-approved medications for treating sleep paralysis. Pharmacotherapy can be used to address psychiatric symptoms such as the depression and anxiety Ms. S exhibited.

Related resources

• American Academy of Sleep Medicine. International classification of sleep disorders, revised: diagnostic and coding manual. Chicago, IL: American Academy of Sleep Medicine; 2001:166-9.
  
• Cheyne JA. Sleep paralysis and associated hypnagogic and hypnopompic experiences. http://watarts.uwaterloo.ca/~acheyne/S_P.html.
  

Drug brand names

• Methylphenidate • Ritalin
  
• Quetiapine • Seroquel
  
• Sertraline • Zoloft
  

 

Disclosure

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

HISTORY: ‘They’re out to get me’

Mrs. V, age 64, tells her primary care physician she has felt “bad” for 2 weeks. She complains of depressed mood, middle insomnia, diminished appetite, poor concentration, and poor energy. She denies suicidal thoughts but reports feeling alone, overwhelmed, and unable to manage her daily life.

Mrs. V is very concerned about losing her job because she cannot function at work. She believes her coworkers may be plotting to get her fired. The primary care physician refers Mrs. V to us to evaluate her mood.

According to her daughter, Mrs. V has had multiple psychiatric hospitalizations; the most recent occurred 2 years ago when she was admitted for paranoia and disorganized behavior. The daughter also mentions that her mother has a remote history of daily alcohol use, drinking until she was intoxicated. Mrs. V says she occasionally drinks beer and she scores 2 out of 4 on the CAGE questionnaire, which may indicate alcohol dependence.

During mental status examination, Mrs. V is alert and oriented to person, place, and date. She is pleasant and cooperative but shows apparent thought blocking and some tangentiality. She has substantial difficulty answering questions and articulating symptoms. Speech is slow in rate and rhythm. Mrs. V’s mood is severely depressed and her affect constricted.

She denies suicidal or homicidal ideations or visual or auditory hallucinations. Cognitive testing reveals mild deficits in recall memory and poor concentration. Her insight is limited and her judgment fair.

Her medical history includes hypertension, hyperlipidemia, coronary artery disease, cardiac catheterization, and hyponatremia. Her medication regimen consists of aripiprazole, 15 mg/d; diltiazem, 180 mg/d; atenolol, 25 mg/d; aspirin, 325 mg/d; atorvastatin, 10 mg/d; sertraline, 50 mg/d; and ibuprofen, 600 mg as needed for hip pain. She also reports taking diuretics in the past.

Vital signs include blood pressure, 125/95 mm Hg; respirations, 16/min; temperature, 98.2° F; and pulse rate, 72/min. Serum investigations reveal sodium, 119 mEq/L (normal range: 135 to 145 mEq/L) and random blood sugar, 160 mg/dL (normal range: 60 to 114 mg/dL).

The authors’ observations

The combination of major depression with psychosis and hyponatremia makes Mrs. V’s case challenging. Hyponatremia in psychiatric inpatients can prompt medical consultation, thus possibly halting or delaying psychiatric treatment.

Hyponatremia has been associated with the use of:

• diuretics
  
• selective serotonin reuptake inhibitors (SSRIs)
  
• serotonin-norepinephrine reuptake inhibitors (SNRIs)
  
• tricyclic antidepressants
  
• calcium antagonists.
  

Elevated creatinine levels, chronic obstructive pulmonary disease, hypertension, systolic blood pressure, and diabetes also can lead to hyponatremia.

Among psychiatric inpatients, the risk of hyponatremia is doubled in women.¹ It is unclear, however, if female gender is an independent risk factor for hyponatremia. Sharabi et al² reported that patients of both sexes age >65 have a 9-fold greater risk of developing hyponatremia than younger counterparts.

In addition, hyponatremia risk during any antidepressant treatment is highest:

• in the summer
  
• during the first weeks of treatment
  
• with concomitant drug use, especially with diuretics.³
  

The authors’ observations

To identify the cause of Mrs. V’s hyponatremia, we determine her volume status and measure serum osmolality.⁴ Next, we mea-sure urinary sodium and osmolality and assess her extracellular fluid status. We also evaluate her renal and adrenal function, which were within normal limits. Although Mrs. V reports fatigue and weakness, there is no evidence of dehydration.

Based on Mrs. V’s initial lab results (Table 1), we classify her hyponatremia as euvolemic, with high urine osmolarity (≥100 mOsm/L). That helps narrow our differential diagnosis to glucocorticoid deficiency, hypothyroidism, and SIADH (Table 2).⁵ We exclude psychogenic polydipsia, “tea and toast” syndrome, or beer potomania because they usually present as euvolemic hyponatremia with low urinary osmolality.

SSRI use in elderly persons has been associated with hyponatremia, which in some cases may be consistent with SIADH. Unfortunately, few psychiatrists are aware of this potentially fatal side effect.

SIADH occurs in association with reduced serum osmolality. It is characterized by:

• hypotonic hyponatremia (serum sodium
• inappropriately elevated urine osmolarity (>200 mOsm/L) relative to plasma osmolarity
  
• elevated urine sodium (typically >20 mEq/L).⁴
  

We diagnose Mrs. V with SIADH because she has these lab findings in the absence of diuretic therapy; in the presence of euvolemia without edema; and in the setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function.

The key to the pathophysiology, signs, symptoms, and treatment of SIADH is understanding that the hyponatremia is a result of excess water and not a sodium deficiency. Hyponatremia’s signs and symptoms primarily are related to CNS dysfunction and correlate with how rapidly and severely the condition develops.

 

We monitor Mrs. V for anorexia, nausea, and malaise because they would be the earliest findings, followed by headache, irritability, confusion, muscle cramps, weakness, obtundation, seizures, and coma. These occur as osmotic fluid shifts and results in cerebral edema and increased intracranial pressure. When sodium concentration drops below 105 mEq/L, life-threatening complications are likely.

Table 1

Mrs. V’s laboratory results

		Mrs. V’s results
	Normal range	Before Tx	After Tx
Serum sodium (mEq/L)	135 to 145	119	127
Serum potassium (mEq/L)	3.5 to 5.0	3.6	3.8
Creatinine (mg/dL)	0.5 to 1.7	0.74	0.84
Glucose (mg/dL)	60 to 114	160	150
Osmolarity
Serum (measured; mOsm/L)	275 to 300	258	242
Urine (mOsm/L)		257	180
Urine sodium (mEq/L)	20 to 40	48	42

Table 2

Mrs. V’s laboratory results

Hypovolemic hyponatremia	Euvolemic hyponatremia	Hypervolemic hyponatremia
Vomiting Diarrhea Laxative abuse Renal disease Nasogastric suction Salt-wasting nephropathy Addison’s disease	Normal urinary sodium   Glucocorticoid deficiency   Hypothyroidism   Certain drugs   SIADH	Congestive heart failure Nephrotic syndrome Cirrhosis
	Low urinary osmolality   Psychogenic polydipsia   ‘Tea and toast’ syndrome   Beer potomania
SIADH: syndrome of inappropriate antidiuretic hormone
Source: Reference 5

SSRIs and SIADH

Bouman et al⁶ estimated that the incidence of SSRI-induced SIADH in elderly patients is 12%. Liu et al⁷ described 706 cases of hyponatremia associated with SSRI use in unpublished reports. Fluoxetine was most commonly the cause (75.3% cases), followed by paroxetine (12.4%), sertraline (11.7%), and fluvoxamine (1.5%). Resuming the same drug resulted in hyponatremia in 16 of 24 of these cases (66.7%).

Kirby et al,⁸ however, found no clear advantages in different SSRIs’ propensity to cause hyponatremia. Seventy-one percent of patients treated with the SNRI venlafaxine developed hyponatremia, compared with 32% taking paroxetine and 29% receiving sertraline. It is unclear whether a specific SSRI or venlafaxine has a stronger association with hyponatremia than any other antidepressant.

Hyponatremia’s nonspecific symptoms and wide range of time to detection (1 to 253 days) suggest clinicians usually detect the condition by chance rather than specifically assessing for it.⁹

TREATMENT: Medication change?

Coordinating Mrs. V’s depression and hyponatremia treatment is critical. We propose discontinuing sertraline and treating Mrs. V’s symptoms with electroconvulsive therapy (ECT). She refuses ECT, stating “I don’t feel that bad. My father was treated with ECT and I am scared of it.”

We decide to switch to mirtazapine, a tetracyclic antidepressant. In a case report mirtazapine was successfully used in a similar patient.¹⁰ We continue to monitor Mrs. V’s serum sodium concentrations and emphasize the importance of complying with fluid restrictions, instructing her to limit her fluid intake to 250 to 500 mL (1 to 2 glasses) per day.

The authors’ observations

SSRI-induced hyponatremia can be transient or persistent and recurrent. The usual approach is to discontinue the SSRI and try a different antidepressant. Because hyponatremia has been associated with all SSRIs and SNRIs, it would be prudent to choose an alternate antidepressant agent outside these classes. If patients must continue taking an antidepressant that causes hyponatremia, avoid concurrent use of drugs that cause hyponatremia, restrict fluid intake, and consider adding a medication that prevents hyponatremia, such as demeclocycline or fludrocortisone.

SSRI-induced hyponatremia may resolve:

• with SSRI discontinuation alone¹¹
  
• with fluid restriction and without discontinuation of the SSRI¹¹
  
• with drug discontinuation, fluid restriction, and sodium chloride and potassium supplementation.¹²
  

FOLLOW-UP: Analysis error?

Despite modifications to Mrs. V’s diet, her fasting serum glucose level remains >100. She is diagnosed with diabetes mellitus type 2 and treated with metformin. We continue mirtazapine, which has successfully controlled Mrs. V’s depressive symptoms. Her serum sodium levels start normalizing.

The authors’ observations

In patients with serum hyperglycemia— such as Mrs. V—correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypo-osmotic state. Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. For each 100 mg/dL increase above normal serum glucose concentration, serum sodium concentration is diluted by a factor of 1.6 mEq/L. Systemic osmolarity is normal or increased, but not decreased as would be the case in true (hypo-osmotic) hyponatremia.

Related resources

• Siegel AJ. Hyponatremia in psychiatric patients: update on evaluation and management. Harv Rev Psychiatry 2008;16(1):13-24.
  
• Atalay A, Turhan N, Aki OE. A challenging case of syndrome of inappropriate secretion of antidiuretic hormone in an elderly patient secondary to quetiapine. South Med J 2007;100(8):832-3.
  

Drug brand name

• Aripiprazole • Abilify
  
• Atenolol • Tenormin
  
• Atorvastatin • Lipitor
  
• Demeclocycline • Declomycin, Declostatin, others
  
• Diltiazem • Cardizem, Dilacor, others
  
• Fludrocortisone • Florinef
  
• Fluvoxamine • Luvox
  
• Ibuprofen • Advil, Motrin, others
  
• Metformin • Glucophage, Diabex, others
  
• Mirtazapine • Remeron
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

 

Disclosures

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

Dr. Ramaswamy receives research support from Bristol-Myers Squibb, Shire, and Forest Pharmaceuticals and is a consultant to Dainippon Sumitomo Pharma.

Dr. Wilson receives research support from the National Institute of Mental Health, the Veterans Administration, the State of Nebraska, Health Futures Foundation, Inc., AstraZeneca, Dainippon Sumitomo Pharma, Eli Lilly and Company, and Pfizer Inc. and serves as a consultant to the Substance Abuse and Mental Health Services Administration and the State of Nebraska.

HISTORY: ‘They’re out to get me’

Mrs. V, age 64, tells her primary care physician she has felt “bad” for 2 weeks. She complains of depressed mood, middle insomnia, diminished appetite, poor concentration, and poor energy. She denies suicidal thoughts but reports feeling alone, overwhelmed, and unable to manage her daily life.

Mrs. V is very concerned about losing her job because she cannot function at work. She believes her coworkers may be plotting to get her fired. The primary care physician refers Mrs. V to us to evaluate her mood.

According to her daughter, Mrs. V has had multiple psychiatric hospitalizations; the most recent occurred 2 years ago when she was admitted for paranoia and disorganized behavior. The daughter also mentions that her mother has a remote history of daily alcohol use, drinking until she was intoxicated. Mrs. V says she occasionally drinks beer and she scores 2 out of 4 on the CAGE questionnaire, which may indicate alcohol dependence.

During mental status examination, Mrs. V is alert and oriented to person, place, and date. She is pleasant and cooperative but shows apparent thought blocking and some tangentiality. She has substantial difficulty answering questions and articulating symptoms. Speech is slow in rate and rhythm. Mrs. V’s mood is severely depressed and her affect constricted.

She denies suicidal or homicidal ideations or visual or auditory hallucinations. Cognitive testing reveals mild deficits in recall memory and poor concentration. Her insight is limited and her judgment fair.

Her medical history includes hypertension, hyperlipidemia, coronary artery disease, cardiac catheterization, and hyponatremia. Her medication regimen consists of aripiprazole, 15 mg/d; diltiazem, 180 mg/d; atenolol, 25 mg/d; aspirin, 325 mg/d; atorvastatin, 10 mg/d; sertraline, 50 mg/d; and ibuprofen, 600 mg as needed for hip pain. She also reports taking diuretics in the past.

Vital signs include blood pressure, 125/95 mm Hg; respirations, 16/min; temperature, 98.2° F; and pulse rate, 72/min. Serum investigations reveal sodium, 119 mEq/L (normal range: 135 to 145 mEq/L) and random blood sugar, 160 mg/dL (normal range: 60 to 114 mg/dL).

The authors’ observations

The combination of major depression with psychosis and hyponatremia makes Mrs. V’s case challenging. Hyponatremia in psychiatric inpatients can prompt medical consultation, thus possibly halting or delaying psychiatric treatment.

Hyponatremia has been associated with the use of:

• diuretics
  
• selective serotonin reuptake inhibitors (SSRIs)
  
• serotonin-norepinephrine reuptake inhibitors (SNRIs)
  
• tricyclic antidepressants
  
• calcium antagonists.
  

Elevated creatinine levels, chronic obstructive pulmonary disease, hypertension, systolic blood pressure, and diabetes also can lead to hyponatremia.

Among psychiatric inpatients, the risk of hyponatremia is doubled in women.¹ It is unclear, however, if female gender is an independent risk factor for hyponatremia. Sharabi et al² reported that patients of both sexes age >65 have a 9-fold greater risk of developing hyponatremia than younger counterparts.

In addition, hyponatremia risk during any antidepressant treatment is highest:

• in the summer
  
• during the first weeks of treatment
  
• with concomitant drug use, especially with diuretics.³
  

The authors’ observations

To identify the cause of Mrs. V’s hyponatremia, we determine her volume status and measure serum osmolality.⁴ Next, we mea-sure urinary sodium and osmolality and assess her extracellular fluid status. We also evaluate her renal and adrenal function, which were within normal limits. Although Mrs. V reports fatigue and weakness, there is no evidence of dehydration.

Based on Mrs. V’s initial lab results (Table 1), we classify her hyponatremia as euvolemic, with high urine osmolarity (≥100 mOsm/L). That helps narrow our differential diagnosis to glucocorticoid deficiency, hypothyroidism, and SIADH (Table 2).⁵ We exclude psychogenic polydipsia, “tea and toast” syndrome, or beer potomania because they usually present as euvolemic hyponatremia with low urinary osmolality.

SSRI use in elderly persons has been associated with hyponatremia, which in some cases may be consistent with SIADH. Unfortunately, few psychiatrists are aware of this potentially fatal side effect.

SIADH occurs in association with reduced serum osmolality. It is characterized by:

• hypotonic hyponatremia (serum sodium
• inappropriately elevated urine osmolarity (>200 mOsm/L) relative to plasma osmolarity
  
• elevated urine sodium (typically >20 mEq/L).⁴
  

We diagnose Mrs. V with SIADH because she has these lab findings in the absence of diuretic therapy; in the presence of euvolemia without edema; and in the setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function.

The key to the pathophysiology, signs, symptoms, and treatment of SIADH is understanding that the hyponatremia is a result of excess water and not a sodium deficiency. Hyponatremia’s signs and symptoms primarily are related to CNS dysfunction and correlate with how rapidly and severely the condition develops.

 

We monitor Mrs. V for anorexia, nausea, and malaise because they would be the earliest findings, followed by headache, irritability, confusion, muscle cramps, weakness, obtundation, seizures, and coma. These occur as osmotic fluid shifts and results in cerebral edema and increased intracranial pressure. When sodium concentration drops below 105 mEq/L, life-threatening complications are likely.

Table 1

Mrs. V’s laboratory results

		Mrs. V’s results
	Normal range	Before Tx	After Tx
Serum sodium (mEq/L)	135 to 145	119	127
Serum potassium (mEq/L)	3.5 to 5.0	3.6	3.8
Creatinine (mg/dL)	0.5 to 1.7	0.74	0.84
Glucose (mg/dL)	60 to 114	160	150
Osmolarity
Serum (measured; mOsm/L)	275 to 300	258	242
Urine (mOsm/L)		257	180
Urine sodium (mEq/L)	20 to 40	48	42

Table 2

Mrs. V’s laboratory results

Hypovolemic hyponatremia	Euvolemic hyponatremia	Hypervolemic hyponatremia
Vomiting Diarrhea Laxative abuse Renal disease Nasogastric suction Salt-wasting nephropathy Addison’s disease	Normal urinary sodium   Glucocorticoid deficiency   Hypothyroidism   Certain drugs   SIADH	Congestive heart failure Nephrotic syndrome Cirrhosis
	Low urinary osmolality   Psychogenic polydipsia   ‘Tea and toast’ syndrome   Beer potomania
SIADH: syndrome of inappropriate antidiuretic hormone
Source: Reference 5

SSRIs and SIADH

Bouman et al⁶ estimated that the incidence of SSRI-induced SIADH in elderly patients is 12%. Liu et al⁷ described 706 cases of hyponatremia associated with SSRI use in unpublished reports. Fluoxetine was most commonly the cause (75.3% cases), followed by paroxetine (12.4%), sertraline (11.7%), and fluvoxamine (1.5%). Resuming the same drug resulted in hyponatremia in 16 of 24 of these cases (66.7%).

Kirby et al,⁸ however, found no clear advantages in different SSRIs’ propensity to cause hyponatremia. Seventy-one percent of patients treated with the SNRI venlafaxine developed hyponatremia, compared with 32% taking paroxetine and 29% receiving sertraline. It is unclear whether a specific SSRI or venlafaxine has a stronger association with hyponatremia than any other antidepressant.

Hyponatremia’s nonspecific symptoms and wide range of time to detection (1 to 253 days) suggest clinicians usually detect the condition by chance rather than specifically assessing for it.⁹

TREATMENT: Medication change?

Coordinating Mrs. V’s depression and hyponatremia treatment is critical. We propose discontinuing sertraline and treating Mrs. V’s symptoms with electroconvulsive therapy (ECT). She refuses ECT, stating “I don’t feel that bad. My father was treated with ECT and I am scared of it.”

We decide to switch to mirtazapine, a tetracyclic antidepressant. In a case report mirtazapine was successfully used in a similar patient.¹⁰ We continue to monitor Mrs. V’s serum sodium concentrations and emphasize the importance of complying with fluid restrictions, instructing her to limit her fluid intake to 250 to 500 mL (1 to 2 glasses) per day.

The authors’ observations

SSRI-induced hyponatremia can be transient or persistent and recurrent. The usual approach is to discontinue the SSRI and try a different antidepressant. Because hyponatremia has been associated with all SSRIs and SNRIs, it would be prudent to choose an alternate antidepressant agent outside these classes. If patients must continue taking an antidepressant that causes hyponatremia, avoid concurrent use of drugs that cause hyponatremia, restrict fluid intake, and consider adding a medication that prevents hyponatremia, such as demeclocycline or fludrocortisone.

SSRI-induced hyponatremia may resolve:

• with SSRI discontinuation alone¹¹
  
• with fluid restriction and without discontinuation of the SSRI¹¹
  
• with drug discontinuation, fluid restriction, and sodium chloride and potassium supplementation.¹²
  

FOLLOW-UP: Analysis error?

Despite modifications to Mrs. V’s diet, her fasting serum glucose level remains >100. She is diagnosed with diabetes mellitus type 2 and treated with metformin. We continue mirtazapine, which has successfully controlled Mrs. V’s depressive symptoms. Her serum sodium levels start normalizing.

The authors’ observations

In patients with serum hyperglycemia— such as Mrs. V—correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypo-osmotic state. Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. For each 100 mg/dL increase above normal serum glucose concentration, serum sodium concentration is diluted by a factor of 1.6 mEq/L. Systemic osmolarity is normal or increased, but not decreased as would be the case in true (hypo-osmotic) hyponatremia.

Related resources

• Siegel AJ. Hyponatremia in psychiatric patients: update on evaluation and management. Harv Rev Psychiatry 2008;16(1):13-24.
  
• Atalay A, Turhan N, Aki OE. A challenging case of syndrome of inappropriate secretion of antidiuretic hormone in an elderly patient secondary to quetiapine. South Med J 2007;100(8):832-3.
  

Drug brand name

• Aripiprazole • Abilify
  
• Atenolol • Tenormin
  
• Atorvastatin • Lipitor
  
• Demeclocycline • Declomycin, Declostatin, others
  
• Diltiazem • Cardizem, Dilacor, others
  
• Fludrocortisone • Florinef
  
• Fluvoxamine • Luvox
  
• Ibuprofen • Advil, Motrin, others
  
• Metformin • Glucophage, Diabex, others
  
• Mirtazapine • Remeron
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

 

Disclosures

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

Dr. Ramaswamy receives research support from Bristol-Myers Squibb, Shire, and Forest Pharmaceuticals and is a consultant to Dainippon Sumitomo Pharma.

Dr. Wilson receives research support from the National Institute of Mental Health, the Veterans Administration, the State of Nebraska, Health Futures Foundation, Inc., AstraZeneca, Dainippon Sumitomo Pharma, Eli Lilly and Company, and Pfizer Inc. and serves as a consultant to the Substance Abuse and Mental Health Services Administration and the State of Nebraska.

HISTORY: ‘They’re out to get me’

Mrs. V, age 64, tells her primary care physician she has felt “bad” for 2 weeks. She complains of depressed mood, middle insomnia, diminished appetite, poor concentration, and poor energy. She denies suicidal thoughts but reports feeling alone, overwhelmed, and unable to manage her daily life.

Mrs. V is very concerned about losing her job because she cannot function at work. She believes her coworkers may be plotting to get her fired. The primary care physician refers Mrs. V to us to evaluate her mood.

According to her daughter, Mrs. V has had multiple psychiatric hospitalizations; the most recent occurred 2 years ago when she was admitted for paranoia and disorganized behavior. The daughter also mentions that her mother has a remote history of daily alcohol use, drinking until she was intoxicated. Mrs. V says she occasionally drinks beer and she scores 2 out of 4 on the CAGE questionnaire, which may indicate alcohol dependence.

During mental status examination, Mrs. V is alert and oriented to person, place, and date. She is pleasant and cooperative but shows apparent thought blocking and some tangentiality. She has substantial difficulty answering questions and articulating symptoms. Speech is slow in rate and rhythm. Mrs. V’s mood is severely depressed and her affect constricted.

She denies suicidal or homicidal ideations or visual or auditory hallucinations. Cognitive testing reveals mild deficits in recall memory and poor concentration. Her insight is limited and her judgment fair.

Her medical history includes hypertension, hyperlipidemia, coronary artery disease, cardiac catheterization, and hyponatremia. Her medication regimen consists of aripiprazole, 15 mg/d; diltiazem, 180 mg/d; atenolol, 25 mg/d; aspirin, 325 mg/d; atorvastatin, 10 mg/d; sertraline, 50 mg/d; and ibuprofen, 600 mg as needed for hip pain. She also reports taking diuretics in the past.

Vital signs include blood pressure, 125/95 mm Hg; respirations, 16/min; temperature, 98.2° F; and pulse rate, 72/min. Serum investigations reveal sodium, 119 mEq/L (normal range: 135 to 145 mEq/L) and random blood sugar, 160 mg/dL (normal range: 60 to 114 mg/dL).

The authors’ observations

The combination of major depression with psychosis and hyponatremia makes Mrs. V’s case challenging. Hyponatremia in psychiatric inpatients can prompt medical consultation, thus possibly halting or delaying psychiatric treatment.

Hyponatremia has been associated with the use of:

• diuretics
  
• selective serotonin reuptake inhibitors (SSRIs)
  
• serotonin-norepinephrine reuptake inhibitors (SNRIs)
  
• tricyclic antidepressants
  
• calcium antagonists.
  

Elevated creatinine levels, chronic obstructive pulmonary disease, hypertension, systolic blood pressure, and diabetes also can lead to hyponatremia.

Among psychiatric inpatients, the risk of hyponatremia is doubled in women.¹ It is unclear, however, if female gender is an independent risk factor for hyponatremia. Sharabi et al² reported that patients of both sexes age >65 have a 9-fold greater risk of developing hyponatremia than younger counterparts.

In addition, hyponatremia risk during any antidepressant treatment is highest:

• in the summer
  
• during the first weeks of treatment
  
• with concomitant drug use, especially with diuretics.³
  

The authors’ observations

To identify the cause of Mrs. V’s hyponatremia, we determine her volume status and measure serum osmolality.⁴ Next, we mea-sure urinary sodium and osmolality and assess her extracellular fluid status. We also evaluate her renal and adrenal function, which were within normal limits. Although Mrs. V reports fatigue and weakness, there is no evidence of dehydration.

Based on Mrs. V’s initial lab results (Table 1), we classify her hyponatremia as euvolemic, with high urine osmolarity (≥100 mOsm/L). That helps narrow our differential diagnosis to glucocorticoid deficiency, hypothyroidism, and SIADH (Table 2).⁵ We exclude psychogenic polydipsia, “tea and toast” syndrome, or beer potomania because they usually present as euvolemic hyponatremia with low urinary osmolality.

SSRI use in elderly persons has been associated with hyponatremia, which in some cases may be consistent with SIADH. Unfortunately, few psychiatrists are aware of this potentially fatal side effect.

SIADH occurs in association with reduced serum osmolality. It is characterized by:

• hypotonic hyponatremia (serum sodium
• inappropriately elevated urine osmolarity (>200 mOsm/L) relative to plasma osmolarity
  
• elevated urine sodium (typically >20 mEq/L).⁴
  

We diagnose Mrs. V with SIADH because she has these lab findings in the absence of diuretic therapy; in the presence of euvolemia without edema; and in the setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function.

The key to the pathophysiology, signs, symptoms, and treatment of SIADH is understanding that the hyponatremia is a result of excess water and not a sodium deficiency. Hyponatremia’s signs and symptoms primarily are related to CNS dysfunction and correlate with how rapidly and severely the condition develops.

 

We monitor Mrs. V for anorexia, nausea, and malaise because they would be the earliest findings, followed by headache, irritability, confusion, muscle cramps, weakness, obtundation, seizures, and coma. These occur as osmotic fluid shifts and results in cerebral edema and increased intracranial pressure. When sodium concentration drops below 105 mEq/L, life-threatening complications are likely.

Table 1

Mrs. V’s laboratory results

		Mrs. V’s results
	Normal range	Before Tx	After Tx
Serum sodium (mEq/L)	135 to 145	119	127
Serum potassium (mEq/L)	3.5 to 5.0	3.6	3.8
Creatinine (mg/dL)	0.5 to 1.7	0.74	0.84
Glucose (mg/dL)	60 to 114	160	150
Osmolarity
Serum (measured; mOsm/L)	275 to 300	258	242
Urine (mOsm/L)		257	180
Urine sodium (mEq/L)	20 to 40	48	42

Table 2

Mrs. V’s laboratory results

Hypovolemic hyponatremia	Euvolemic hyponatremia	Hypervolemic hyponatremia
Vomiting Diarrhea Laxative abuse Renal disease Nasogastric suction Salt-wasting nephropathy Addison’s disease	Normal urinary sodium   Glucocorticoid deficiency   Hypothyroidism   Certain drugs   SIADH	Congestive heart failure Nephrotic syndrome Cirrhosis
	Low urinary osmolality   Psychogenic polydipsia   ‘Tea and toast’ syndrome   Beer potomania
SIADH: syndrome of inappropriate antidiuretic hormone
Source: Reference 5

SSRIs and SIADH

Bouman et al⁶ estimated that the incidence of SSRI-induced SIADH in elderly patients is 12%. Liu et al⁷ described 706 cases of hyponatremia associated with SSRI use in unpublished reports. Fluoxetine was most commonly the cause (75.3% cases), followed by paroxetine (12.4%), sertraline (11.7%), and fluvoxamine (1.5%). Resuming the same drug resulted in hyponatremia in 16 of 24 of these cases (66.7%).

Kirby et al,⁸ however, found no clear advantages in different SSRIs’ propensity to cause hyponatremia. Seventy-one percent of patients treated with the SNRI venlafaxine developed hyponatremia, compared with 32% taking paroxetine and 29% receiving sertraline. It is unclear whether a specific SSRI or venlafaxine has a stronger association with hyponatremia than any other antidepressant.

Hyponatremia’s nonspecific symptoms and wide range of time to detection (1 to 253 days) suggest clinicians usually detect the condition by chance rather than specifically assessing for it.⁹

TREATMENT: Medication change?

Coordinating Mrs. V’s depression and hyponatremia treatment is critical. We propose discontinuing sertraline and treating Mrs. V’s symptoms with electroconvulsive therapy (ECT). She refuses ECT, stating “I don’t feel that bad. My father was treated with ECT and I am scared of it.”

We decide to switch to mirtazapine, a tetracyclic antidepressant. In a case report mirtazapine was successfully used in a similar patient.¹⁰ We continue to monitor Mrs. V’s serum sodium concentrations and emphasize the importance of complying with fluid restrictions, instructing her to limit her fluid intake to 250 to 500 mL (1 to 2 glasses) per day.

The authors’ observations

SSRI-induced hyponatremia can be transient or persistent and recurrent. The usual approach is to discontinue the SSRI and try a different antidepressant. Because hyponatremia has been associated with all SSRIs and SNRIs, it would be prudent to choose an alternate antidepressant agent outside these classes. If patients must continue taking an antidepressant that causes hyponatremia, avoid concurrent use of drugs that cause hyponatremia, restrict fluid intake, and consider adding a medication that prevents hyponatremia, such as demeclocycline or fludrocortisone.

SSRI-induced hyponatremia may resolve:

• with SSRI discontinuation alone¹¹
  
• with fluid restriction and without discontinuation of the SSRI¹¹
  
• with drug discontinuation, fluid restriction, and sodium chloride and potassium supplementation.¹²
  

FOLLOW-UP: Analysis error?

Despite modifications to Mrs. V’s diet, her fasting serum glucose level remains >100. She is diagnosed with diabetes mellitus type 2 and treated with metformin. We continue mirtazapine, which has successfully controlled Mrs. V’s depressive symptoms. Her serum sodium levels start normalizing.

The authors’ observations

In patients with serum hyperglycemia— such as Mrs. V—correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypo-osmotic state. Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. For each 100 mg/dL increase above normal serum glucose concentration, serum sodium concentration is diluted by a factor of 1.6 mEq/L. Systemic osmolarity is normal or increased, but not decreased as would be the case in true (hypo-osmotic) hyponatremia.

Related resources

• Siegel AJ. Hyponatremia in psychiatric patients: update on evaluation and management. Harv Rev Psychiatry 2008;16(1):13-24.
  
• Atalay A, Turhan N, Aki OE. A challenging case of syndrome of inappropriate secretion of antidiuretic hormone in an elderly patient secondary to quetiapine. South Med J 2007;100(8):832-3.
  

Drug brand name

• Aripiprazole • Abilify
  
• Atenolol • Tenormin
  
• Atorvastatin • Lipitor
  
• Demeclocycline • Declomycin, Declostatin, others
  
• Diltiazem • Cardizem, Dilacor, others
  
• Fludrocortisone • Florinef
  
• Fluvoxamine • Luvox
  
• Ibuprofen • Advil, Motrin, others
  
• Metformin • Glucophage, Diabex, others
  
• Mirtazapine • Remeron
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

 

Disclosures

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

Dr. Ramaswamy receives research support from Bristol-Myers Squibb, Shire, and Forest Pharmaceuticals and is a consultant to Dainippon Sumitomo Pharma.

Dr. Wilson receives research support from the National Institute of Mental Health, the Veterans Administration, the State of Nebraska, Health Futures Foundation, Inc., AstraZeneca, Dainippon Sumitomo Pharma, Eli Lilly and Company, and Pfizer Inc. and serves as a consultant to the Substance Abuse and Mental Health Services Administration and the State of Nebraska.

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

Reverend R tells us he is ordained and was working for a church 15 years ago when a drunk driver hit him. Since then, he has lived in a nursing home. Although he can no longer work as a minister, he says the nursing home staff on occasion invites him to deliver sermons at the facility. He also serves as the nursing home’s public relations director and writes faith-based literature for the residents.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

 

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

Period	Event
Childhood	Sexually assaulted by an uncle
Young adulthood	Develops depression; 1 hospitalization in his 30s; sexually assaulted by male nurse while hospitalized
Adulthood	Motor vehicle accident results in traumatic brain injury and leads to nursing home placement in his late 40s
3 months ago	Hospitalized for abdominal pain secondary to recurring bowel obstruction; medical history includes colon cancer, cerebral palsy
Presently	Loses pregnant, 24-year-old fiancée in a traffic accident

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

He reports being upbeat since his nasogastric tube was removed, and he is able to tolerate a clear liquid diet. Reverend R says he is looking forward to returning to the nursing home but expresses trepidation. He is concerned that his conversations with us might jeopardize his return: “I hope I haven’t said anything that will get me into trouble.” He also acknowledges that he was diagnosed with a traumatic brain injury following the motor vehicle accident 15 years ago.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

 

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

In addition, we determine Reverend R has pseudologia fantastica, a rarely seen form of pathological lying characterized by telling elaborate lies that may have a kernel of truth (Table 3).² The syndrome often is associated with cognitive dysfunction, learning disabilities, factitious disorder, and childhood traumatic experiences.^3,4

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Intentional production or feigning of physical or psychological signs and symptoms
Motivation for the behavior is to assume the sick role
External incentives such as economic gain, avoiding legal responsibility, or improving physical well-being are absent
* Specifiers include with predominantly psychological signs and symptoms, with predominantly physical signs and symptoms, or a combination of both
Source: Reference 1

Table 3

Characteristics of stories told by patients with pseudologia fantastica

not entirely improbable
long-lasting, often repeated over years
self-aggrandizing
not told for personal profit
not delusions (when confronted with facts, patient can acknowledge the stories as falsehoods)
Source: Reference 2

A patient with pseudologia fantastica effectively weaves a fabric of lies in a dramatic style. When challenged, he or she improvises yet another story. Inconsistencies can be detected by spending time with the individual. The patient is consistently vague when asked to provide additional details. The reward is the attention.

Because of an unstable self image, the pseudologia fantastica patient constantly battles to regulate his or her sense of self. The dramatic production of symptoms due to this constant battle is thought to be a way for the patient to stabilize the self by making the experience of distress concrete and legitimate.⁵ It was fascinating to see Reverend R’s defense mechanisms work.

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

Drug brand name

• Sertraline • Zoloft
  

Disclosure

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

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

Reverend R tells us he is ordained and was working for a church 15 years ago when a drunk driver hit him. Since then, he has lived in a nursing home. Although he can no longer work as a minister, he says the nursing home staff on occasion invites him to deliver sermons at the facility. He also serves as the nursing home’s public relations director and writes faith-based literature for the residents.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

 

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

Period	Event
Childhood	Sexually assaulted by an uncle
Young adulthood	Develops depression; 1 hospitalization in his 30s; sexually assaulted by male nurse while hospitalized
Adulthood	Motor vehicle accident results in traumatic brain injury and leads to nursing home placement in his late 40s
3 months ago	Hospitalized for abdominal pain secondary to recurring bowel obstruction; medical history includes colon cancer, cerebral palsy
Presently	Loses pregnant, 24-year-old fiancée in a traffic accident

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

He reports being upbeat since his nasogastric tube was removed, and he is able to tolerate a clear liquid diet. Reverend R says he is looking forward to returning to the nursing home but expresses trepidation. He is concerned that his conversations with us might jeopardize his return: “I hope I haven’t said anything that will get me into trouble.” He also acknowledges that he was diagnosed with a traumatic brain injury following the motor vehicle accident 15 years ago.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

 

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

In addition, we determine Reverend R has pseudologia fantastica, a rarely seen form of pathological lying characterized by telling elaborate lies that may have a kernel of truth (Table 3).² The syndrome often is associated with cognitive dysfunction, learning disabilities, factitious disorder, and childhood traumatic experiences.^3,4

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Intentional production or feigning of physical or psychological signs and symptoms
Motivation for the behavior is to assume the sick role
External incentives such as economic gain, avoiding legal responsibility, or improving physical well-being are absent
* Specifiers include with predominantly psychological signs and symptoms, with predominantly physical signs and symptoms, or a combination of both
Source: Reference 1

Table 3

Characteristics of stories told by patients with pseudologia fantastica

not entirely improbable
long-lasting, often repeated over years
self-aggrandizing
not told for personal profit
not delusions (when confronted with facts, patient can acknowledge the stories as falsehoods)
Source: Reference 2

A patient with pseudologia fantastica effectively weaves a fabric of lies in a dramatic style. When challenged, he or she improvises yet another story. Inconsistencies can be detected by spending time with the individual. The patient is consistently vague when asked to provide additional details. The reward is the attention.

Because of an unstable self image, the pseudologia fantastica patient constantly battles to regulate his or her sense of self. The dramatic production of symptoms due to this constant battle is thought to be a way for the patient to stabilize the self by making the experience of distress concrete and legitimate.⁵ It was fascinating to see Reverend R’s defense mechanisms work.

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

Drug brand name

• Sertraline • Zoloft
  

Disclosure

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

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

Reverend R tells us he is ordained and was working for a church 15 years ago when a drunk driver hit him. Since then, he has lived in a nursing home. Although he can no longer work as a minister, he says the nursing home staff on occasion invites him to deliver sermons at the facility. He also serves as the nursing home’s public relations director and writes faith-based literature for the residents.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

 

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

Period	Event
Childhood	Sexually assaulted by an uncle
Young adulthood	Develops depression; 1 hospitalization in his 30s; sexually assaulted by male nurse while hospitalized
Adulthood	Motor vehicle accident results in traumatic brain injury and leads to nursing home placement in his late 40s
3 months ago	Hospitalized for abdominal pain secondary to recurring bowel obstruction; medical history includes colon cancer, cerebral palsy
Presently	Loses pregnant, 24-year-old fiancée in a traffic accident

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

He reports being upbeat since his nasogastric tube was removed, and he is able to tolerate a clear liquid diet. Reverend R says he is looking forward to returning to the nursing home but expresses trepidation. He is concerned that his conversations with us might jeopardize his return: “I hope I haven’t said anything that will get me into trouble.” He also acknowledges that he was diagnosed with a traumatic brain injury following the motor vehicle accident 15 years ago.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

 

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

In addition, we determine Reverend R has pseudologia fantastica, a rarely seen form of pathological lying characterized by telling elaborate lies that may have a kernel of truth (Table 3).² The syndrome often is associated with cognitive dysfunction, learning disabilities, factitious disorder, and childhood traumatic experiences.^3,4

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Intentional production or feigning of physical or psychological signs and symptoms
Motivation for the behavior is to assume the sick role
External incentives such as economic gain, avoiding legal responsibility, or improving physical well-being are absent
* Specifiers include with predominantly psychological signs and symptoms, with predominantly physical signs and symptoms, or a combination of both
Source: Reference 1

Table 3

Characteristics of stories told by patients with pseudologia fantastica

not entirely improbable
long-lasting, often repeated over years
self-aggrandizing
not told for personal profit
not delusions (when confronted with facts, patient can acknowledge the stories as falsehoods)
Source: Reference 2

A patient with pseudologia fantastica effectively weaves a fabric of lies in a dramatic style. When challenged, he or she improvises yet another story. Inconsistencies can be detected by spending time with the individual. The patient is consistently vague when asked to provide additional details. The reward is the attention.

Because of an unstable self image, the pseudologia fantastica patient constantly battles to regulate his or her sense of self. The dramatic production of symptoms due to this constant battle is thought to be a way for the patient to stabilize the self by making the experience of distress concrete and legitimate.⁵ It was fascinating to see Reverend R’s defense mechanisms work.

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

Drug brand name

• Sertraline • Zoloft
  

Disclosure

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

CASE: She’s not herself

Mrs. M, age 74, is brought to the ER by her husband after he finds her lying on their bedroom floor, incoherent and extremely drowsy. He reports that his wife, who suffers chronic arthritic back and joint pain, might have overdosed on pain medications.

According to her husband, Mrs. M has been taking combination oxycodone/acetaminophen and transdermal fentanyl at unknown dosages, but he is unsure when she started using these medications or if she is taking others. Serum toxicology screening shows twice the normal values for opioids and benzodiazepines; other laboratory results are normal.

Mrs. M is medically stable but her mental status is altered. She is oblivious to time, place and person, speaks to no one, and seems lost in her own world. The hospital’s medical service admits Mrs. M for stabilization and to determine whether the overdose was intentional.

Two days later, we evaluate Mrs. M’s mental status at the attending physician’s request. She appears confused and cannot answer our questions. Her husband tells us she was “doing fine” until approximately 4 months ago, when she started becoming increasingly forgetful and lethargic. He says she has been forgetting routine chores such as paying bills and grocery shopping. Recently, she has been getting lost during her evening walk; neighbors often help her find her way home.

Mrs. M has had no past psychiatric or medical problems but her husband says she has become increasingly suspicious and paranoid the past 2 months. After being happily married for 40 years, he says his wife now frequently accuses him of infidelity or stealing her possessions. Last week, she misplaced her medications and accused him of hiding them.

The authors’ observations

Two opioid medications—oxycodone/acetaminophen combination and transdermal fentanyl—are commonly used to manage moderate or severe pain from any type of chronic arthritis.

• Oxycodone, a semisynthetic opioid analgesic indicated for moderate to moderately severe pain, is used when nondrug measures and nonnarcotic medications do not control the pain.
  
• Transdermal fentanyl, a potent analgesic indicated for persistent moderate to severe chronic pain, typically is prescribed to patients who tolerate oral oxycodone, 30 mg/d; morphine, 60 mg; hydromorphone, 8 mg; or an equianalgesic dosage of another opioid for ≥1 week.
  

Mrs. M’s confusion and cloudy consciousness at admission strongly suggest delirium. Rapid opioid escalation can cause delirium,^1-3 but no preadmission laboratory work was done to affirm this.

Mrs. M also was taking a benzodiazepine, but which medication—and why she was taking it—were unclear. She had no psychiatric diagnosis, and her husband could not recall her medication history.

We also cannot explain Mrs. M’s negative cognitive and behavioral changes. Opioid overuse and onset of dementia-related cognitive decline are possibilities.

TRANSFER Why is she confused?

Based on information from the pharmacy department, doctors at the medical unit restart oxycodone/acetaminophen, 7.5/325 mg tid, and transdermal fentanyl, 25 mcg/hr every 3 days. After discussing how to treat Mrs. M, the psychiatric and medical services transfer her to the geriatric psychiatric inpatient unit 3 days after admission.

We visit Mrs. M hours after her transfer. She seems lethargic but not confused, although Mini-Mental State Examination (MMSE) score of 15 suggests moderate cognitive impairment. Vitamin B₁₂ and thyroid levels, erythrocyte sedimentation rate, and syphilis test results are normal, allowing us to rule out organic causes for her dementia. Brain MRI shows no neurologic damage. On a scale of 1 to 5 with 5 being most severe, Mrs. M scores her pain as 2 (mild) and her sedation as 3 (moderate).

Mrs. M acknowledges that on the day she collapsed, she might have forgotten she had taken oxycodone/acetaminophen and took it a second time. She then reveals she also had been taking “nerve pills” and might have taken more than usual that day. She says she has been feeling anxious about her forgetfulness and fears she is developing dementia, but she endorses no other current or past psychiatric symptoms.

With Mrs. M’s permission, we call her primary care physician for collateral information. The physician tells us Mrs. M has suffered severe joint pain for 2 years. Nonnarcotic medications and treatments—including counseling, support groups, massage, yoga, exercise, biofeedback, relaxation therapy, and physical therapy—were ineffective.

Approximately 10 months ago, the physician started oxycodone/acetaminophen at 2.5/325 mg bid and titrated it over 6 weeks to 7.5/325 mg tid for Mrs. M’s persistent joint pain. Four months ago, with her pain still severe, the physician added transdermal fentanyl, 25 mcg/hr every 3 days, after which the patient reported mild improvement.

 

One month after starting the fentanyl patch, Mrs. M complained of sudden forgetfulness, low energy, poor concentration, and increased sleep. The physician suspected depression with possible comorbid anxiety and prescribed sertraline, 50 mg/d, and alprazolam, 0.5 mg bid. Mrs. M stopped sertraline after 3 days because it was causing diarrhea but kept taking alprazolam.

Mrs. M saw her primary care physician once after starting alprazolam and sertraline but missed her most recent appointment last month. The physician says he inadvertently approved at least 1 premature request for an alprazolam refill.

Six days after admission, Mrs. M’s sedation, cognitive impairment, and lethargy persist. She reports no mood and anxiety problems, and we have not restarted alprazolam.

The authors’ observations

The fentanyl patch most likely began to diminish Mrs. M’s alertness soon after she started using it. The doctor, however, mistook cognitive slowing for new-onset depression or anxiety. Depressive symptoms can imitate dementia, but Mrs. M’s severe sedation and denial of depressive symptoms suggest a medication side effect.

The primary care physician’s reconstruction of Mrs. M’s history explained her positive benzodiazepine reading, and her use of the short-acting benzodiazepine alprazolam could account for her sudden-onset paranoia and cognitive decline (Box). Benzodiazepines can cause behavioral side effects such as disinhibition, agitation, or paranoia, and patients age ≥65 are at increased risk for these side effects.⁴ In particular, benzodiazepines with half-lives ≥6 to 8 hours such as clonazepam and oxazepam can cause short-term memory impairment, confusion, and delirium.^5-7

Box

Because alprazolam’s mean plasma half-life can be as short as 8 hours, 3 to 4 daily doses usually are necessary for day-long therapeutic effect. Multiple dosing of benzodiazepines, however, can cause withdrawal symptoms such as rebound anxiety and insomnia. To quell these symptoms, patients often take higher or additional benzodiazepine doses without a doctor’s permission, leading to potential overuse, addiction, or overdose.

When prescribing benzodiazepines (especially in older patients) watch for signs of overuse or abuse, such as early requests for refills, unkempt appearance, excessive sleepiness, or agitation (Table 1).

Table 1

Warning signs of opioid, benzodiazepine overuse

Frequent requests for early refills
Patient exceeds prescribed dosage without authorization
Patient reports lost/stolen prescription; if patient has history of substance abuse/dependence or legal problems, even 1 report should raise a red flag
Patient increasingly unkempt or impaired
Negative mood change
Agitation
Patient involved in car or other accidents
Sedation
Purposeful oversedation, particularly when patient has an apparent secondary gain from opioid use (such as qualifying for disability benefits or escaping from work)
New-onset cognitive impairment
Patient abusing alcohol or other illicit CNS depressants

The authors’ observations

Persistent chronic pain in the elderly can diminish health and quality of life, resulting in depression, social isolation, immobility, and sleep disturbance.

Managing an older patient’s pain can be challenging (Table 2). Opioids are effective painkillers, but even at relatively low dosages they can diminish function and cognition and increase risk of delirium. Also, patients’ ability to tolerate different opioids at different dosages varies widely.

Mrs. M’s opioid regimen was intolerable and numerous other treatments did not alleviate her pain. At this point, replacing fentanyl with another opioid was our best option.⁸

We decided to try methadone, which is indicated for moderate to severe pain that does not respond to nonnarcotic treatments. Methadone often is used for chronic pain associated with arthritis or malignancy.

Methadone is less sedating, more tolerable, and carries a lower risk of cognitive side effects than other opioids. Methadone also is fast- and long-acting—its analgesic effects begin within 30 minutes to 1 hour of oral administration⁹ and last approximately 12 hours, thus reducing the risk of breakthrough pain. Methadone also:

 

• has no active metabolites, which decreases the risk of hepatic side effects
  
• offers a high volume of distribution, thus allowing clinical effect with minimal dosing.
  

Oral methadone is a strong analgesic—20 mg is as potent as 100 mg of oral morphine. Start methadone at 5 to 10 mg bid or tid for chronic pain management and titrate according to clinical response and tolerability.^10-12

Beware the potential for addiction when prescribing opioids to any patient.^13,14 The U.S. Drug Enforcement Agency classifies both methadone and fentanyl as schedule II substances, which applies to highly addictive medications with FDA-approved indications. See patients at least biweekly, especially when switching or titrating pain medications, and watch closely for signs of overuse or addiction. Inform patients to:

• watch for symptoms such as oversedation, memory and concentration problems, and sudden changes in personality
  
• call you to clarify if these symptoms are methadone side effects.
  

Increase methadone by 5 mg every 3 to 4 days based on patient tolerance and response. If side effects decrease function or treatment response is lacking, consider a different opioid or another treatment. Decrease visit frequency to once monthly when the pain is under control and the patient experiences no side effects.

Watch for other potential side effects of methadone, such as constipation, sedation, breakthrough pain, sexual dysfunction, decreased immunity, respiratory depression, or prolonged corrected QT intervals.

Patients usually tolerate an immediate switch from transdermal fentanyl to methadone, but a sudden switch from high-dose fentanyl can reduce methadone’s effectiveness. Starting methadone at a high dosage to compensate for loss of effectiveness could increase side effect risk. If the fentanyl dosage exceeds 100 mcg/hr, taper by 25 mcg weekly. Simultaneously start methadone at a low dosage and titrate by 5 to 10 mg weekly as needed.

Table 2

Chronic pain management in the elderly: Dos and don’ts

DO
Use self rating scales, as patient can gauge his/her own pain most accurately
Consider nonpharmacologic treatments and nonnarcotic analgesics first
Watch closely for side effects and drug-drug/drug-disease interactions in patients receiving analgesics long-term
Monitor patients receiving opioids long-term for oversedation, changes in cognition and function
Consider switching to methadone or another opioid if patient cannot tolerate current opioid regimen
DO NOT
Prescribe propoxyphene or meperidine—which carry a higher risk of adverse effects than other opioids—to older patient
Prescribe opioids if the medical history is unclear
Increase opioid dosages without seeing the patient

TREATMENT Medication change

We stop transdermal fentanyl and start oral methadone, 5 mg bid, while continuing oxycodone/acetaminophen at the previous dosage.

Two days later, Mrs. M is much more alert. Since admission 1 week ago, her sedation rating has improved from 3 (mildly sedated) to 4 (almost fully alert). She rates her pain as mild and reports no breakthrough pain or other side effects from methadone. Her MMSE score has improved to 24—suggesting close to normal cognition—and she is much more interactive with staff and family.

Eight days after we start methadone, we stop oxycodone/acetaminophen and increase methadone to 10 mg bid to further improve cognition and alertness and to see if 1 pain medication is suffcient. Two days later, we discharge Mrs. M. She is fully alert, feels little or no joint pain, and is tolerating the methadone increase.

At outpatient follow-up 4 weeks later, Mrs. M remains pain-free and her MMSE score is 29, suggesting normal cognition. Over 8 months, we continue to see her monthly and then bi-monthly, after which we refer her to her primary care physician.

Related resources

• American Association for Geriatric Psychiatry. www.aagponline.org.
  
• American Pain Society. www.ampainsoc.org.
  

Drug brand names

• Alprazolam • Xanax
  
• Clonazepam • Klonopin
  
• Fentanyl (transdermal) • Duragesic
  
• Hydromorphone • Dilaudid
  
• Meperidine • Demerol
  
• Methadone • Dolophine
  
• Oxazepam • Serax
  
• Oxycodone • OxyContin, Roxicodone
  
• Oxycodone/acetaminophen • Percocet
  
• Propoxyphene • Darvon
  
• Sertraline • Zoloft
  

Disclosure

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

CASE: She’s not herself

Mrs. M, age 74, is brought to the ER by her husband after he finds her lying on their bedroom floor, incoherent and extremely drowsy. He reports that his wife, who suffers chronic arthritic back and joint pain, might have overdosed on pain medications.

According to her husband, Mrs. M has been taking combination oxycodone/acetaminophen and transdermal fentanyl at unknown dosages, but he is unsure when she started using these medications or if she is taking others. Serum toxicology screening shows twice the normal values for opioids and benzodiazepines; other laboratory results are normal.

Mrs. M is medically stable but her mental status is altered. She is oblivious to time, place and person, speaks to no one, and seems lost in her own world. The hospital’s medical service admits Mrs. M for stabilization and to determine whether the overdose was intentional.

Two days later, we evaluate Mrs. M’s mental status at the attending physician’s request. She appears confused and cannot answer our questions. Her husband tells us she was “doing fine” until approximately 4 months ago, when she started becoming increasingly forgetful and lethargic. He says she has been forgetting routine chores such as paying bills and grocery shopping. Recently, she has been getting lost during her evening walk; neighbors often help her find her way home.

Mrs. M has had no past psychiatric or medical problems but her husband says she has become increasingly suspicious and paranoid the past 2 months. After being happily married for 40 years, he says his wife now frequently accuses him of infidelity or stealing her possessions. Last week, she misplaced her medications and accused him of hiding them.

The authors’ observations

Two opioid medications—oxycodone/acetaminophen combination and transdermal fentanyl—are commonly used to manage moderate or severe pain from any type of chronic arthritis.

• Oxycodone, a semisynthetic opioid analgesic indicated for moderate to moderately severe pain, is used when nondrug measures and nonnarcotic medications do not control the pain.
  
• Transdermal fentanyl, a potent analgesic indicated for persistent moderate to severe chronic pain, typically is prescribed to patients who tolerate oral oxycodone, 30 mg/d; morphine, 60 mg; hydromorphone, 8 mg; or an equianalgesic dosage of another opioid for ≥1 week.
  

Mrs. M’s confusion and cloudy consciousness at admission strongly suggest delirium. Rapid opioid escalation can cause delirium,^1-3 but no preadmission laboratory work was done to affirm this.

Mrs. M also was taking a benzodiazepine, but which medication—and why she was taking it—were unclear. She had no psychiatric diagnosis, and her husband could not recall her medication history.

We also cannot explain Mrs. M’s negative cognitive and behavioral changes. Opioid overuse and onset of dementia-related cognitive decline are possibilities.

TRANSFER Why is she confused?

Based on information from the pharmacy department, doctors at the medical unit restart oxycodone/acetaminophen, 7.5/325 mg tid, and transdermal fentanyl, 25 mcg/hr every 3 days. After discussing how to treat Mrs. M, the psychiatric and medical services transfer her to the geriatric psychiatric inpatient unit 3 days after admission.

We visit Mrs. M hours after her transfer. She seems lethargic but not confused, although Mini-Mental State Examination (MMSE) score of 15 suggests moderate cognitive impairment. Vitamin B₁₂ and thyroid levels, erythrocyte sedimentation rate, and syphilis test results are normal, allowing us to rule out organic causes for her dementia. Brain MRI shows no neurologic damage. On a scale of 1 to 5 with 5 being most severe, Mrs. M scores her pain as 2 (mild) and her sedation as 3 (moderate).

Mrs. M acknowledges that on the day she collapsed, she might have forgotten she had taken oxycodone/acetaminophen and took it a second time. She then reveals she also had been taking “nerve pills” and might have taken more than usual that day. She says she has been feeling anxious about her forgetfulness and fears she is developing dementia, but she endorses no other current or past psychiatric symptoms.

With Mrs. M’s permission, we call her primary care physician for collateral information. The physician tells us Mrs. M has suffered severe joint pain for 2 years. Nonnarcotic medications and treatments—including counseling, support groups, massage, yoga, exercise, biofeedback, relaxation therapy, and physical therapy—were ineffective.

Approximately 10 months ago, the physician started oxycodone/acetaminophen at 2.5/325 mg bid and titrated it over 6 weeks to 7.5/325 mg tid for Mrs. M’s persistent joint pain. Four months ago, with her pain still severe, the physician added transdermal fentanyl, 25 mcg/hr every 3 days, after which the patient reported mild improvement.

 

One month after starting the fentanyl patch, Mrs. M complained of sudden forgetfulness, low energy, poor concentration, and increased sleep. The physician suspected depression with possible comorbid anxiety and prescribed sertraline, 50 mg/d, and alprazolam, 0.5 mg bid. Mrs. M stopped sertraline after 3 days because it was causing diarrhea but kept taking alprazolam.

Mrs. M saw her primary care physician once after starting alprazolam and sertraline but missed her most recent appointment last month. The physician says he inadvertently approved at least 1 premature request for an alprazolam refill.

Six days after admission, Mrs. M’s sedation, cognitive impairment, and lethargy persist. She reports no mood and anxiety problems, and we have not restarted alprazolam.

The authors’ observations

The fentanyl patch most likely began to diminish Mrs. M’s alertness soon after she started using it. The doctor, however, mistook cognitive slowing for new-onset depression or anxiety. Depressive symptoms can imitate dementia, but Mrs. M’s severe sedation and denial of depressive symptoms suggest a medication side effect.

The primary care physician’s reconstruction of Mrs. M’s history explained her positive benzodiazepine reading, and her use of the short-acting benzodiazepine alprazolam could account for her sudden-onset paranoia and cognitive decline (Box). Benzodiazepines can cause behavioral side effects such as disinhibition, agitation, or paranoia, and patients age ≥65 are at increased risk for these side effects.⁴ In particular, benzodiazepines with half-lives ≥6 to 8 hours such as clonazepam and oxazepam can cause short-term memory impairment, confusion, and delirium.^5-7

Box

Because alprazolam’s mean plasma half-life can be as short as 8 hours, 3 to 4 daily doses usually are necessary for day-long therapeutic effect. Multiple dosing of benzodiazepines, however, can cause withdrawal symptoms such as rebound anxiety and insomnia. To quell these symptoms, patients often take higher or additional benzodiazepine doses without a doctor’s permission, leading to potential overuse, addiction, or overdose.

When prescribing benzodiazepines (especially in older patients) watch for signs of overuse or abuse, such as early requests for refills, unkempt appearance, excessive sleepiness, or agitation (Table 1).

Table 1

Warning signs of opioid, benzodiazepine overuse

Frequent requests for early refills
Patient exceeds prescribed dosage without authorization
Patient reports lost/stolen prescription; if patient has history of substance abuse/dependence or legal problems, even 1 report should raise a red flag
Patient increasingly unkempt or impaired
Negative mood change
Agitation
Patient involved in car or other accidents
Sedation
Purposeful oversedation, particularly when patient has an apparent secondary gain from opioid use (such as qualifying for disability benefits or escaping from work)
New-onset cognitive impairment
Patient abusing alcohol or other illicit CNS depressants

The authors’ observations

Persistent chronic pain in the elderly can diminish health and quality of life, resulting in depression, social isolation, immobility, and sleep disturbance.

Managing an older patient’s pain can be challenging (Table 2). Opioids are effective painkillers, but even at relatively low dosages they can diminish function and cognition and increase risk of delirium. Also, patients’ ability to tolerate different opioids at different dosages varies widely.

Mrs. M’s opioid regimen was intolerable and numerous other treatments did not alleviate her pain. At this point, replacing fentanyl with another opioid was our best option.⁸

We decided to try methadone, which is indicated for moderate to severe pain that does not respond to nonnarcotic treatments. Methadone often is used for chronic pain associated with arthritis or malignancy.

Methadone is less sedating, more tolerable, and carries a lower risk of cognitive side effects than other opioids. Methadone also is fast- and long-acting—its analgesic effects begin within 30 minutes to 1 hour of oral administration⁹ and last approximately 12 hours, thus reducing the risk of breakthrough pain. Methadone also:

 

• has no active metabolites, which decreases the risk of hepatic side effects
  
• offers a high volume of distribution, thus allowing clinical effect with minimal dosing.
  

Oral methadone is a strong analgesic—20 mg is as potent as 100 mg of oral morphine. Start methadone at 5 to 10 mg bid or tid for chronic pain management and titrate according to clinical response and tolerability.^10-12

Beware the potential for addiction when prescribing opioids to any patient.^13,14 The U.S. Drug Enforcement Agency classifies both methadone and fentanyl as schedule II substances, which applies to highly addictive medications with FDA-approved indications. See patients at least biweekly, especially when switching or titrating pain medications, and watch closely for signs of overuse or addiction. Inform patients to:

• watch for symptoms such as oversedation, memory and concentration problems, and sudden changes in personality
  
• call you to clarify if these symptoms are methadone side effects.
  

Increase methadone by 5 mg every 3 to 4 days based on patient tolerance and response. If side effects decrease function or treatment response is lacking, consider a different opioid or another treatment. Decrease visit frequency to once monthly when the pain is under control and the patient experiences no side effects.

Watch for other potential side effects of methadone, such as constipation, sedation, breakthrough pain, sexual dysfunction, decreased immunity, respiratory depression, or prolonged corrected QT intervals.

Patients usually tolerate an immediate switch from transdermal fentanyl to methadone, but a sudden switch from high-dose fentanyl can reduce methadone’s effectiveness. Starting methadone at a high dosage to compensate for loss of effectiveness could increase side effect risk. If the fentanyl dosage exceeds 100 mcg/hr, taper by 25 mcg weekly. Simultaneously start methadone at a low dosage and titrate by 5 to 10 mg weekly as needed.

Table 2

Chronic pain management in the elderly: Dos and don’ts

DO
Use self rating scales, as patient can gauge his/her own pain most accurately
Consider nonpharmacologic treatments and nonnarcotic analgesics first
Watch closely for side effects and drug-drug/drug-disease interactions in patients receiving analgesics long-term
Monitor patients receiving opioids long-term for oversedation, changes in cognition and function
Consider switching to methadone or another opioid if patient cannot tolerate current opioid regimen
DO NOT
Prescribe propoxyphene or meperidine—which carry a higher risk of adverse effects than other opioids—to older patient
Prescribe opioids if the medical history is unclear
Increase opioid dosages without seeing the patient

TREATMENT Medication change

We stop transdermal fentanyl and start oral methadone, 5 mg bid, while continuing oxycodone/acetaminophen at the previous dosage.

Two days later, Mrs. M is much more alert. Since admission 1 week ago, her sedation rating has improved from 3 (mildly sedated) to 4 (almost fully alert). She rates her pain as mild and reports no breakthrough pain or other side effects from methadone. Her MMSE score has improved to 24—suggesting close to normal cognition—and she is much more interactive with staff and family.

Eight days after we start methadone, we stop oxycodone/acetaminophen and increase methadone to 10 mg bid to further improve cognition and alertness and to see if 1 pain medication is suffcient. Two days later, we discharge Mrs. M. She is fully alert, feels little or no joint pain, and is tolerating the methadone increase.

At outpatient follow-up 4 weeks later, Mrs. M remains pain-free and her MMSE score is 29, suggesting normal cognition. Over 8 months, we continue to see her monthly and then bi-monthly, after which we refer her to her primary care physician.

Related resources

• American Association for Geriatric Psychiatry. www.aagponline.org.
  
• American Pain Society. www.ampainsoc.org.
  

Drug brand names

• Alprazolam • Xanax
  
• Clonazepam • Klonopin
  
• Fentanyl (transdermal) • Duragesic
  
• Hydromorphone • Dilaudid
  
• Meperidine • Demerol
  
• Methadone • Dolophine
  
• Oxazepam • Serax
  
• Oxycodone • OxyContin, Roxicodone
  
• Oxycodone/acetaminophen • Percocet
  
• Propoxyphene • Darvon
  
• Sertraline • Zoloft
  

Disclosure

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

CASE: She’s not herself

Mrs. M, age 74, is brought to the ER by her husband after he finds her lying on their bedroom floor, incoherent and extremely drowsy. He reports that his wife, who suffers chronic arthritic back and joint pain, might have overdosed on pain medications.

According to her husband, Mrs. M has been taking combination oxycodone/acetaminophen and transdermal fentanyl at unknown dosages, but he is unsure when she started using these medications or if she is taking others. Serum toxicology screening shows twice the normal values for opioids and benzodiazepines; other laboratory results are normal.

Mrs. M is medically stable but her mental status is altered. She is oblivious to time, place and person, speaks to no one, and seems lost in her own world. The hospital’s medical service admits Mrs. M for stabilization and to determine whether the overdose was intentional.

Two days later, we evaluate Mrs. M’s mental status at the attending physician’s request. She appears confused and cannot answer our questions. Her husband tells us she was “doing fine” until approximately 4 months ago, when she started becoming increasingly forgetful and lethargic. He says she has been forgetting routine chores such as paying bills and grocery shopping. Recently, she has been getting lost during her evening walk; neighbors often help her find her way home.

Mrs. M has had no past psychiatric or medical problems but her husband says she has become increasingly suspicious and paranoid the past 2 months. After being happily married for 40 years, he says his wife now frequently accuses him of infidelity or stealing her possessions. Last week, she misplaced her medications and accused him of hiding them.

The authors’ observations

Two opioid medications—oxycodone/acetaminophen combination and transdermal fentanyl—are commonly used to manage moderate or severe pain from any type of chronic arthritis.

• Oxycodone, a semisynthetic opioid analgesic indicated for moderate to moderately severe pain, is used when nondrug measures and nonnarcotic medications do not control the pain.
  
• Transdermal fentanyl, a potent analgesic indicated for persistent moderate to severe chronic pain, typically is prescribed to patients who tolerate oral oxycodone, 30 mg/d; morphine, 60 mg; hydromorphone, 8 mg; or an equianalgesic dosage of another opioid for ≥1 week.
  

Mrs. M’s confusion and cloudy consciousness at admission strongly suggest delirium. Rapid opioid escalation can cause delirium,^1-3 but no preadmission laboratory work was done to affirm this.

Mrs. M also was taking a benzodiazepine, but which medication—and why she was taking it—were unclear. She had no psychiatric diagnosis, and her husband could not recall her medication history.

We also cannot explain Mrs. M’s negative cognitive and behavioral changes. Opioid overuse and onset of dementia-related cognitive decline are possibilities.

TRANSFER Why is she confused?

Based on information from the pharmacy department, doctors at the medical unit restart oxycodone/acetaminophen, 7.5/325 mg tid, and transdermal fentanyl, 25 mcg/hr every 3 days. After discussing how to treat Mrs. M, the psychiatric and medical services transfer her to the geriatric psychiatric inpatient unit 3 days after admission.

We visit Mrs. M hours after her transfer. She seems lethargic but not confused, although Mini-Mental State Examination (MMSE) score of 15 suggests moderate cognitive impairment. Vitamin B₁₂ and thyroid levels, erythrocyte sedimentation rate, and syphilis test results are normal, allowing us to rule out organic causes for her dementia. Brain MRI shows no neurologic damage. On a scale of 1 to 5 with 5 being most severe, Mrs. M scores her pain as 2 (mild) and her sedation as 3 (moderate).

Mrs. M acknowledges that on the day she collapsed, she might have forgotten she had taken oxycodone/acetaminophen and took it a second time. She then reveals she also had been taking “nerve pills” and might have taken more than usual that day. She says she has been feeling anxious about her forgetfulness and fears she is developing dementia, but she endorses no other current or past psychiatric symptoms.

With Mrs. M’s permission, we call her primary care physician for collateral information. The physician tells us Mrs. M has suffered severe joint pain for 2 years. Nonnarcotic medications and treatments—including counseling, support groups, massage, yoga, exercise, biofeedback, relaxation therapy, and physical therapy—were ineffective.

Approximately 10 months ago, the physician started oxycodone/acetaminophen at 2.5/325 mg bid and titrated it over 6 weeks to 7.5/325 mg tid for Mrs. M’s persistent joint pain. Four months ago, with her pain still severe, the physician added transdermal fentanyl, 25 mcg/hr every 3 days, after which the patient reported mild improvement.

 

One month after starting the fentanyl patch, Mrs. M complained of sudden forgetfulness, low energy, poor concentration, and increased sleep. The physician suspected depression with possible comorbid anxiety and prescribed sertraline, 50 mg/d, and alprazolam, 0.5 mg bid. Mrs. M stopped sertraline after 3 days because it was causing diarrhea but kept taking alprazolam.

Mrs. M saw her primary care physician once after starting alprazolam and sertraline but missed her most recent appointment last month. The physician says he inadvertently approved at least 1 premature request for an alprazolam refill.

Six days after admission, Mrs. M’s sedation, cognitive impairment, and lethargy persist. She reports no mood and anxiety problems, and we have not restarted alprazolam.

The authors’ observations

The fentanyl patch most likely began to diminish Mrs. M’s alertness soon after she started using it. The doctor, however, mistook cognitive slowing for new-onset depression or anxiety. Depressive symptoms can imitate dementia, but Mrs. M’s severe sedation and denial of depressive symptoms suggest a medication side effect.

The primary care physician’s reconstruction of Mrs. M’s history explained her positive benzodiazepine reading, and her use of the short-acting benzodiazepine alprazolam could account for her sudden-onset paranoia and cognitive decline (Box). Benzodiazepines can cause behavioral side effects such as disinhibition, agitation, or paranoia, and patients age ≥65 are at increased risk for these side effects.⁴ In particular, benzodiazepines with half-lives ≥6 to 8 hours such as clonazepam and oxazepam can cause short-term memory impairment, confusion, and delirium.^5-7

Box

Because alprazolam’s mean plasma half-life can be as short as 8 hours, 3 to 4 daily doses usually are necessary for day-long therapeutic effect. Multiple dosing of benzodiazepines, however, can cause withdrawal symptoms such as rebound anxiety and insomnia. To quell these symptoms, patients often take higher or additional benzodiazepine doses without a doctor’s permission, leading to potential overuse, addiction, or overdose.

When prescribing benzodiazepines (especially in older patients) watch for signs of overuse or abuse, such as early requests for refills, unkempt appearance, excessive sleepiness, or agitation (Table 1).

Table 1

Warning signs of opioid, benzodiazepine overuse

Frequent requests for early refills
Patient exceeds prescribed dosage without authorization
Patient reports lost/stolen prescription; if patient has history of substance abuse/dependence or legal problems, even 1 report should raise a red flag
Patient increasingly unkempt or impaired
Negative mood change
Agitation
Patient involved in car or other accidents
Sedation
Purposeful oversedation, particularly when patient has an apparent secondary gain from opioid use (such as qualifying for disability benefits or escaping from work)
New-onset cognitive impairment
Patient abusing alcohol or other illicit CNS depressants

The authors’ observations

Persistent chronic pain in the elderly can diminish health and quality of life, resulting in depression, social isolation, immobility, and sleep disturbance.

Managing an older patient’s pain can be challenging (Table 2). Opioids are effective painkillers, but even at relatively low dosages they can diminish function and cognition and increase risk of delirium. Also, patients’ ability to tolerate different opioids at different dosages varies widely.

Mrs. M’s opioid regimen was intolerable and numerous other treatments did not alleviate her pain. At this point, replacing fentanyl with another opioid was our best option.⁸

We decided to try methadone, which is indicated for moderate to severe pain that does not respond to nonnarcotic treatments. Methadone often is used for chronic pain associated with arthritis or malignancy.

Methadone is less sedating, more tolerable, and carries a lower risk of cognitive side effects than other opioids. Methadone also is fast- and long-acting—its analgesic effects begin within 30 minutes to 1 hour of oral administration⁹ and last approximately 12 hours, thus reducing the risk of breakthrough pain. Methadone also:

 

• has no active metabolites, which decreases the risk of hepatic side effects
  
• offers a high volume of distribution, thus allowing clinical effect with minimal dosing.
  

Oral methadone is a strong analgesic—20 mg is as potent as 100 mg of oral morphine. Start methadone at 5 to 10 mg bid or tid for chronic pain management and titrate according to clinical response and tolerability.^10-12

Beware the potential for addiction when prescribing opioids to any patient.^13,14 The U.S. Drug Enforcement Agency classifies both methadone and fentanyl as schedule II substances, which applies to highly addictive medications with FDA-approved indications. See patients at least biweekly, especially when switching or titrating pain medications, and watch closely for signs of overuse or addiction. Inform patients to:

• watch for symptoms such as oversedation, memory and concentration problems, and sudden changes in personality
  
• call you to clarify if these symptoms are methadone side effects.
  

Increase methadone by 5 mg every 3 to 4 days based on patient tolerance and response. If side effects decrease function or treatment response is lacking, consider a different opioid or another treatment. Decrease visit frequency to once monthly when the pain is under control and the patient experiences no side effects.

Watch for other potential side effects of methadone, such as constipation, sedation, breakthrough pain, sexual dysfunction, decreased immunity, respiratory depression, or prolonged corrected QT intervals.

Patients usually tolerate an immediate switch from transdermal fentanyl to methadone, but a sudden switch from high-dose fentanyl can reduce methadone’s effectiveness. Starting methadone at a high dosage to compensate for loss of effectiveness could increase side effect risk. If the fentanyl dosage exceeds 100 mcg/hr, taper by 25 mcg weekly. Simultaneously start methadone at a low dosage and titrate by 5 to 10 mg weekly as needed.

Table 2

Chronic pain management in the elderly: Dos and don’ts

DO
Use self rating scales, as patient can gauge his/her own pain most accurately
Consider nonpharmacologic treatments and nonnarcotic analgesics first
Watch closely for side effects and drug-drug/drug-disease interactions in patients receiving analgesics long-term
Monitor patients receiving opioids long-term for oversedation, changes in cognition and function
Consider switching to methadone or another opioid if patient cannot tolerate current opioid regimen
DO NOT
Prescribe propoxyphene or meperidine—which carry a higher risk of adverse effects than other opioids—to older patient
Prescribe opioids if the medical history is unclear
Increase opioid dosages without seeing the patient

TREATMENT Medication change

We stop transdermal fentanyl and start oral methadone, 5 mg bid, while continuing oxycodone/acetaminophen at the previous dosage.

Two days later, Mrs. M is much more alert. Since admission 1 week ago, her sedation rating has improved from 3 (mildly sedated) to 4 (almost fully alert). She rates her pain as mild and reports no breakthrough pain or other side effects from methadone. Her MMSE score has improved to 24—suggesting close to normal cognition—and she is much more interactive with staff and family.

Eight days after we start methadone, we stop oxycodone/acetaminophen and increase methadone to 10 mg bid to further improve cognition and alertness and to see if 1 pain medication is suffcient. Two days later, we discharge Mrs. M. She is fully alert, feels little or no joint pain, and is tolerating the methadone increase.

At outpatient follow-up 4 weeks later, Mrs. M remains pain-free and her MMSE score is 29, suggesting normal cognition. Over 8 months, we continue to see her monthly and then bi-monthly, after which we refer her to her primary care physician.

Related resources

• American Association for Geriatric Psychiatry. www.aagponline.org.
  
• American Pain Society. www.ampainsoc.org.
  

Drug brand names

• Alprazolam • Xanax
  
• Clonazepam • Klonopin
  
• Fentanyl (transdermal) • Duragesic
  
• Hydromorphone • Dilaudid
  
• Meperidine • Demerol
  
• Methadone • Dolophine
  
• Oxazepam • Serax
  
• Oxycodone • OxyContin, Roxicodone
  
• Oxycodone/acetaminophen • Percocet
  
• Propoxyphene • Darvon
  
• Sertraline • Zoloft
  

Disclosure

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

CASE: He bares it all

Police have arrested Mr. L, age 62, 3 times in 36 hours after spotting him walking naked in public. With the county jail jammed to capacity, police bring him each time to our hospital’s emergency room.

After his first arrest, Mr. L matter-of-factly tells us, “I want to walk naked and starve myself to death.” His self-harm exhortations amplify with each visit until—at the third presentation—he reports that he has not eaten for at least 2 days.

Mr. L had been living on the streets for nearly 1 month. Before that, he had been in jail for approximately 1 month after attacking a nursing home patient. He has been hospitalized twice in 5 months for severe depression and personality disorder and has engaged in numerous disruptive behavioral episodes and feeble suicide attempts. At this latest presentation, he appears disheveled and lacks judgment and insight into his condition.

We readmit Mr. L to the psychiatric unit to re-evaluate his treatment. He had been on citalopram, 60 mg/d, and aripiprazole, 10 mg/d, but he says he stopped taking the medications because they were not improving his mood.

The authors’ observations

We readmitted Mr. L with working diagnoses of:

• major depressive disorder with psychotic features, based on his suicide threats and complaints of depression
  
• personality disorder not otherwise specified, based on his behavioral episodes, apparent desire to be cared for (Table 1), and refusal to “get better” during 2 recent hospitalizations.
  

Table 1

A troubled life: Mr. L’s history

Period	Mr. L’s difficulties
Childhood	Has no friends in school; his mother—Mr. L’s sole source of emotional support—continues to wash his laundry, buy his food and clothes into his 20s
Adult life	Keeps ‘goofing off’ at work and has trouble staying employed; depends on wife to manage his life
2 years ago	Shows depressive symptoms (amotivation, lack of concentration, increased fatigue, decreased appetite) after shoulder injury Develops irrational fear that household appliances will malfunction Becomes hostile toward his wife of 34 years
5 months ago	Hospitalized after threatening to kill wife; has depressive symptoms and is disruptive during month-long hospitalization
4 months ago	Discharged from hospital to homeless shelter because estranged wife won’t allow him back home; is readmitted after shelter staff find him banging his head on an iron gate; again behaves disruptively
3 months ago	Discharged from second month-long hospitalization to nursing home
2 months ago	Attacks patient at nursing home; police arrest and incarcerate him on disorderly conduct charge
Past month	Released from jail after 1 month and spends weeks on the streets; lands in ER after police repeatedly catch him walking naked in public

HISTORY: His best friends

As a child, Mr. L had no friends. His father was physically present but emotionally distant, so he relied on his mother for emotional support. Throughout his teens and early adulthood, his mother continued to do his laundry, buy his food and clothes, and run his life. When he married in his early 20s, his wife assumed this role.

Mr. L avoided psychiatric care for most of his life but did not socialize outside the house, lacked ambition, and seemed content to depend on his wife. He worked primarily as a janitor or housekeeper but was constantly getting fired and drifted from job to job. His wife told us that when he was supposed to be working, he spent hours staring at the walls and watching TV.

Mr. L’s recent troubles began approximately 2 years ago, when he suffered a shoulder injury. He underwent physical therapy but refused needed surgery because he lacked money and health insurance.

As the shoulder pain intensified, Mr. L quit his job. While out of work, he stopped attending physical therapy sessions when his depressive symptoms began to offset the shoulder pain. He suffered loss of concentration and motivation, increased fatigue with hypersomnia, and decreased appetite. He lost 10 to 12 lb in 1 year.

Mr. L also started having trouble “focusing on reality” and developed obsessive fears of malfunctions around the house, such as the furnace blowing up, the stove catching fire, or the toilet backing up. At one point, he began urinating and defecating in his pants to avoid using the toilet. He began to feel hopeless and several times tried to suffocate himself by placing a plastic bag over his head.

He also grew irritable, angry, and aggressive—mostly toward his wife, who increasingly feared him. He started blaming her for “everything wrong in my life” and began contemplating stabbing her to death or striking her head with a hammer.

 

Five months ago, Mr. L was involuntarily hospitalized for depressive symptoms, suicidality, and continued homicidal thoughts toward his wife. The attending psychiatrist started olanzapine, 5 mg nightly, for psychotic features, and citalopram, 10 mg/d, for depression and anxiety, and ordered one-on-one observation to prevent additional suicide attempts. Mr. L’s shoulder pain had resolved by this time.

Three days later, Mr. L began refusing to eat. The psychiatrist then increased citalopram to 20 mg/d and olanzapine to 5 mg bid and asked a hospital internist to evaluate for malnutrition and a psychologist to gauge cognitive and intellectual function.

During the psychologist’s evaluation, Mr. L showed average global intellectual functioning but delays in visual-motor speed, visual working memory, and alertness to his environment. These findings, however, did not explain the patient’s lower functioning at home or in the hospital.

We ruled out organic causes for Mr. L’s cognitive deficits after receiving normal brain MRI, urinalysis, rapid plasma reagin titer, and thyroid-stimulating hormone test results. We also ruled out malnutrition because vitamin B12 and folate levels were normal but ordered a dietary consult to help Mr. L regain weight.

Staff and family registered Mr. L for Medicare and Medicaid benefits so that he could become more independent, but his behavior soon regressed. He complained that staff and family were ignoring him and started urinating outside the bathroom, eating and smearing his feces, and bothering other patients. Staff directed Mr. L’s wife to ignore his verbal abuse over the phone and encourage him to stay motivated for treatment.

Mr. L’s disruptive behavior stopped after the psychologist tried individual therapy with behavior modification. The psychologist helped him devise a cleanliness plan and encouraged him to express his anger verbally rather than acting out. When Mr. L smeared his feces, he was to scrub the area with soap and water, take a 5-minute cold shower, put on clean clothes, and write and read an apology to hospital staff.

DISCHARGE: Nowhere to go

One month after admission, Mr. L was free of suicidal and homicidal thoughts and other symptoms. Staff prepared him for discharge, but his wife was contemplating divorce and refused to allow him back home. He also declined community outpatient treatment because he wanted his life to return to “normal” and was unaware that he was harming himself and others.

With no other disposition options, we discharged Mr. L to a homeless shelter. Later that day, shelter staff brought him back to the ER after they found him banging his head against an iron gate. We readmitted him to the psychiatric unit, at which point he endorsed suicidal thinking.

READMISSION: ‘Cold’ case

During this second hospitalization, Mr. L was again eating his feces as well as coloring himself with green markers, writing obscenities on the wall, and tearing up other patients’ papers. He repeatedly took 15-minute cold showers and told staff as they urged him out of the shower that he wanted to die by inducing hypothermia. During these episodes, he often called his estranged wife and told her what he was doing.

After the treatment team had Mr. L civilly committed, the attending psychiatrist titrated citalopram to 60 mg/d, discontinued olanzapine, and added aripiprazole to target the patient’s underlying depressive symptoms. Aripiprazole was started at 5 mg nightly and eventually titrated to 10 mg nightly. On 3 occasions during the month-long hospitalization, Mr. L refused to take his medications because he felt he did not belong in the hospital.

The attending psychiatrist diagnosed “dependent, passive-aggressive behaviors” and noted that Mr. L was “not amenable” to psychiatric hospitalization. The treatment team and outpatient community mental health department decided the patient had a personality disorder and that continued hospitalization would prevent him from attaining autonomy.

We then discharged Mr. L to a nursing home. There, he demanded a transfer back to the hospital or to jail because he feared he could not afford nursing home care and believed he could receive more attention elsewhere. His request was rejected after our ER psychiatrist found him medically and mentally fit to stay at the nursing home.

About 1 month later, Mr. L tried to smother a female patient by holding a pillow over her face but stopped when she began to struggle. After he told the nurses what he had done, staff immediately called police, who arrested Mr. L and transferred him to the county jail.

Because police and nursing home staff viewed the incident as a cry for help rather than a cold-blooded attack, police charged Mr. L with disorderly conduct. One month later, police dropped the charge and released him to the streets.

 

The authors’ observations

Mr. L triggered hateful reactions among several treatment team members, many of whom felt vindicated by his arrest. Clinicians might react this way if they feel a patient is wasting their time, manipulating them, not recognizing their narcissistic need for the patient to change, or ignoring their treatment plans.¹

Acknowledging the staff’s—and your own—reaction to a difficult patient is critical. Not doing so can lead to treatment decisions based on emotions rather than evidence. In a busy clinical setting, it’s easy to lose sight of this.

The following strategies can help you manage hateful countertransference, cope with a patient’s offensive behaviors, and make appropriate decisions:

• Allow staff members to discuss their feelings. Encourage them to acknowledge and discuss their feelings during team meetings or daily treatment discussions. This helped members of our team recognize that their identification with Mr. L’s self-rejection fueled their desire to “reject” him by discharging him to police or the homeless shelter.
  
• Joke about the patient’s behavior when appropriate. Humor is a mature and potentially healing defense mechanism. When not treating Mr. L, for example, we joked among ourselves about publishing a case report titled, “The case of the poop-eater.” Never joke about the patient in the therapeutic milieu, where it can be disruptive.
  
• See the behavior as a defense mechanism. Viewing patients’ reactions as defense mechanisms—rather than effects of a psychiatric disorder—can help you better understand the patient’s underlying pathophysiology.
  

READMISSION: More bad behavior

After his 3 arrests for public nudity, we readmit Mr. L, restart citalopram at 20 mg/d, and titrate it back to 60 mg/d to target his depression. We also switch back to olanzapine, 10 mg nightly, because the patient has seen little clinical benefit from aripiprazole and feels that olanzapine had improved his sleep.

In the psychiatric ward, Mr. L is once again disturbing patients, smearing and eating feces, and making half-hearted suicide attempts. Upset that staff is “ignoring” him, he enters other patients’ rooms without invitation and urinates in places other than the bathroom.

The authors’ observations

After 3 hospital admissions, Mr. L’s diagnosis remained unclear (Table 2). At his first admission, his symptoms suggested major depression with psychotic features. With his subsequent behaviors in the inpatient psychiatric unit—including primitive suicide attempts and smearing and eating feces—Mr. L showed a strong desire to be cared for. This and his past dependence on his wife and mother suggested a severe dependent personality disorder.

At his first discharge, Mr. L was diagnosed with a personality disorder with significant passive-aggressive traits. His lifelong dysphoria and lack of ambition also suggested dysthymia.

With discharge from this latest hospitalization pending, we searched for options. We considered Mr. L’s ongoing suicidality, persistent acting out, and aggression. Treatment team members discussed his use of “primitive defenses”² stemming from his limited coping skills in the face of severe depression.

Table 2

Mr. L’s differential diagnosis

Possible diagnosis	Mr. L’s symptoms
Major depression	Diminished motivation, concentration, and appetite Increased fatigue, hypersomnia Suicidal thinking
Personality disorder	Primitive, dependent behaviors Abnormal dependence on wife, mother
Depression with psychotic features	Depressive symptoms with obsessive suicidal/homicidal thoughts, fears of household malfunctions

TREATMENT: A different course

One week after admission, Mr. L’s inpatient psychiatrist recommends electroconvulsive therapy (ECT) to target the patient’s presumed severe depressive episodes and disruptive behaviors. The psychiatrist is experienced in performing ECT, which in clinical trials³ has shown efficacy in treatment-refractory major depression.

After giving informed consent, Mr. L receives 8 bilateral ECT treatments in 3 weeks. Also, the hospital psychologist performs behavioral modification similar to the previous cleanliness plan and again encourages Mr. L to express his anger and anxiety verbally.

By the second week of ECT, Mr. L’s disruptive behaviors have ceased. By the end of week 3, his mood and motivation have improved to the point where he shows interest in becoming independent. He says he wants to show his estranged wife he can care for himself and eventually reunite with her.

As Mr. L continues to improve, we discharge him to outpatient community mental health services and continue citalopram, 60 mg/d, and olanzapine, 5 mg nightly.

Nearly 2 years later, Mr. L is living independently. He has been regularly seeing his psychiatrist at the community mental health center and is maintained on citalopram and olanzapine. He continues trying to make amends with his wife but is still out of work and receives Social Security disability benefits.

The authors’ observations

Mr. L was fortunate that his inpatient psychiatrist could re-evaluate the diagnosis after identifying the staff’s significantly hateful countertransference. This allowed staff to offer ECT, which—despite its documented efficacy for major depression—is not widely available in the United States.

 

If no ECT providers were available, we would have considered medication change and long-term treatment in a state mental hospital until Mr. L showed he could care for himself.

Related resources

• Nagera H. Countertransference (PowerPoint presentation). Tampa, FL: The Carter Jenkins Center; 2003. www.thecjc.org/ppoint/ppoint/ct.ppt.
  
• MayoClinic.com video: Electroconvulsive therapy (ECT): One woman’s journey. Click on “Video” at top, then scroll to title.
  

Drug brand names

• Aripiprazole • Abilify
  
• Olanzapine • Zyprexa
  
• Citalopram • Celexa
  

Disclosure

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

CASE: He bares it all

Police have arrested Mr. L, age 62, 3 times in 36 hours after spotting him walking naked in public. With the county jail jammed to capacity, police bring him each time to our hospital’s emergency room.

After his first arrest, Mr. L matter-of-factly tells us, “I want to walk naked and starve myself to death.” His self-harm exhortations amplify with each visit until—at the third presentation—he reports that he has not eaten for at least 2 days.

Mr. L had been living on the streets for nearly 1 month. Before that, he had been in jail for approximately 1 month after attacking a nursing home patient. He has been hospitalized twice in 5 months for severe depression and personality disorder and has engaged in numerous disruptive behavioral episodes and feeble suicide attempts. At this latest presentation, he appears disheveled and lacks judgment and insight into his condition.

We readmit Mr. L to the psychiatric unit to re-evaluate his treatment. He had been on citalopram, 60 mg/d, and aripiprazole, 10 mg/d, but he says he stopped taking the medications because they were not improving his mood.

The authors’ observations

We readmitted Mr. L with working diagnoses of:

• major depressive disorder with psychotic features, based on his suicide threats and complaints of depression
  
• personality disorder not otherwise specified, based on his behavioral episodes, apparent desire to be cared for (Table 1), and refusal to “get better” during 2 recent hospitalizations.
  

Table 1

A troubled life: Mr. L’s history

Period	Mr. L’s difficulties
Childhood	Has no friends in school; his mother—Mr. L’s sole source of emotional support—continues to wash his laundry, buy his food and clothes into his 20s
Adult life	Keeps ‘goofing off’ at work and has trouble staying employed; depends on wife to manage his life
2 years ago	Shows depressive symptoms (amotivation, lack of concentration, increased fatigue, decreased appetite) after shoulder injury Develops irrational fear that household appliances will malfunction Becomes hostile toward his wife of 34 years
5 months ago	Hospitalized after threatening to kill wife; has depressive symptoms and is disruptive during month-long hospitalization
4 months ago	Discharged from hospital to homeless shelter because estranged wife won’t allow him back home; is readmitted after shelter staff find him banging his head on an iron gate; again behaves disruptively
3 months ago	Discharged from second month-long hospitalization to nursing home
2 months ago	Attacks patient at nursing home; police arrest and incarcerate him on disorderly conduct charge
Past month	Released from jail after 1 month and spends weeks on the streets; lands in ER after police repeatedly catch him walking naked in public

HISTORY: His best friends

As a child, Mr. L had no friends. His father was physically present but emotionally distant, so he relied on his mother for emotional support. Throughout his teens and early adulthood, his mother continued to do his laundry, buy his food and clothes, and run his life. When he married in his early 20s, his wife assumed this role.

Mr. L avoided psychiatric care for most of his life but did not socialize outside the house, lacked ambition, and seemed content to depend on his wife. He worked primarily as a janitor or housekeeper but was constantly getting fired and drifted from job to job. His wife told us that when he was supposed to be working, he spent hours staring at the walls and watching TV.

Mr. L’s recent troubles began approximately 2 years ago, when he suffered a shoulder injury. He underwent physical therapy but refused needed surgery because he lacked money and health insurance.

As the shoulder pain intensified, Mr. L quit his job. While out of work, he stopped attending physical therapy sessions when his depressive symptoms began to offset the shoulder pain. He suffered loss of concentration and motivation, increased fatigue with hypersomnia, and decreased appetite. He lost 10 to 12 lb in 1 year.

Mr. L also started having trouble “focusing on reality” and developed obsessive fears of malfunctions around the house, such as the furnace blowing up, the stove catching fire, or the toilet backing up. At one point, he began urinating and defecating in his pants to avoid using the toilet. He began to feel hopeless and several times tried to suffocate himself by placing a plastic bag over his head.

He also grew irritable, angry, and aggressive—mostly toward his wife, who increasingly feared him. He started blaming her for “everything wrong in my life” and began contemplating stabbing her to death or striking her head with a hammer.

 

Five months ago, Mr. L was involuntarily hospitalized for depressive symptoms, suicidality, and continued homicidal thoughts toward his wife. The attending psychiatrist started olanzapine, 5 mg nightly, for psychotic features, and citalopram, 10 mg/d, for depression and anxiety, and ordered one-on-one observation to prevent additional suicide attempts. Mr. L’s shoulder pain had resolved by this time.

Three days later, Mr. L began refusing to eat. The psychiatrist then increased citalopram to 20 mg/d and olanzapine to 5 mg bid and asked a hospital internist to evaluate for malnutrition and a psychologist to gauge cognitive and intellectual function.

During the psychologist’s evaluation, Mr. L showed average global intellectual functioning but delays in visual-motor speed, visual working memory, and alertness to his environment. These findings, however, did not explain the patient’s lower functioning at home or in the hospital.

We ruled out organic causes for Mr. L’s cognitive deficits after receiving normal brain MRI, urinalysis, rapid plasma reagin titer, and thyroid-stimulating hormone test results. We also ruled out malnutrition because vitamin B12 and folate levels were normal but ordered a dietary consult to help Mr. L regain weight.

Staff and family registered Mr. L for Medicare and Medicaid benefits so that he could become more independent, but his behavior soon regressed. He complained that staff and family were ignoring him and started urinating outside the bathroom, eating and smearing his feces, and bothering other patients. Staff directed Mr. L’s wife to ignore his verbal abuse over the phone and encourage him to stay motivated for treatment.

Mr. L’s disruptive behavior stopped after the psychologist tried individual therapy with behavior modification. The psychologist helped him devise a cleanliness plan and encouraged him to express his anger verbally rather than acting out. When Mr. L smeared his feces, he was to scrub the area with soap and water, take a 5-minute cold shower, put on clean clothes, and write and read an apology to hospital staff.

DISCHARGE: Nowhere to go

One month after admission, Mr. L was free of suicidal and homicidal thoughts and other symptoms. Staff prepared him for discharge, but his wife was contemplating divorce and refused to allow him back home. He also declined community outpatient treatment because he wanted his life to return to “normal” and was unaware that he was harming himself and others.

With no other disposition options, we discharged Mr. L to a homeless shelter. Later that day, shelter staff brought him back to the ER after they found him banging his head against an iron gate. We readmitted him to the psychiatric unit, at which point he endorsed suicidal thinking.

READMISSION: ‘Cold’ case

During this second hospitalization, Mr. L was again eating his feces as well as coloring himself with green markers, writing obscenities on the wall, and tearing up other patients’ papers. He repeatedly took 15-minute cold showers and told staff as they urged him out of the shower that he wanted to die by inducing hypothermia. During these episodes, he often called his estranged wife and told her what he was doing.

After the treatment team had Mr. L civilly committed, the attending psychiatrist titrated citalopram to 60 mg/d, discontinued olanzapine, and added aripiprazole to target the patient’s underlying depressive symptoms. Aripiprazole was started at 5 mg nightly and eventually titrated to 10 mg nightly. On 3 occasions during the month-long hospitalization, Mr. L refused to take his medications because he felt he did not belong in the hospital.

The attending psychiatrist diagnosed “dependent, passive-aggressive behaviors” and noted that Mr. L was “not amenable” to psychiatric hospitalization. The treatment team and outpatient community mental health department decided the patient had a personality disorder and that continued hospitalization would prevent him from attaining autonomy.

We then discharged Mr. L to a nursing home. There, he demanded a transfer back to the hospital or to jail because he feared he could not afford nursing home care and believed he could receive more attention elsewhere. His request was rejected after our ER psychiatrist found him medically and mentally fit to stay at the nursing home.

About 1 month later, Mr. L tried to smother a female patient by holding a pillow over her face but stopped when she began to struggle. After he told the nurses what he had done, staff immediately called police, who arrested Mr. L and transferred him to the county jail.

Because police and nursing home staff viewed the incident as a cry for help rather than a cold-blooded attack, police charged Mr. L with disorderly conduct. One month later, police dropped the charge and released him to the streets.

 

The authors’ observations

Mr. L triggered hateful reactions among several treatment team members, many of whom felt vindicated by his arrest. Clinicians might react this way if they feel a patient is wasting their time, manipulating them, not recognizing their narcissistic need for the patient to change, or ignoring their treatment plans.¹

Acknowledging the staff’s—and your own—reaction to a difficult patient is critical. Not doing so can lead to treatment decisions based on emotions rather than evidence. In a busy clinical setting, it’s easy to lose sight of this.

The following strategies can help you manage hateful countertransference, cope with a patient’s offensive behaviors, and make appropriate decisions:

• Allow staff members to discuss their feelings. Encourage them to acknowledge and discuss their feelings during team meetings or daily treatment discussions. This helped members of our team recognize that their identification with Mr. L’s self-rejection fueled their desire to “reject” him by discharging him to police or the homeless shelter.
  
• Joke about the patient’s behavior when appropriate. Humor is a mature and potentially healing defense mechanism. When not treating Mr. L, for example, we joked among ourselves about publishing a case report titled, “The case of the poop-eater.” Never joke about the patient in the therapeutic milieu, where it can be disruptive.
  
• See the behavior as a defense mechanism. Viewing patients’ reactions as defense mechanisms—rather than effects of a psychiatric disorder—can help you better understand the patient’s underlying pathophysiology.
  

READMISSION: More bad behavior

After his 3 arrests for public nudity, we readmit Mr. L, restart citalopram at 20 mg/d, and titrate it back to 60 mg/d to target his depression. We also switch back to olanzapine, 10 mg nightly, because the patient has seen little clinical benefit from aripiprazole and feels that olanzapine had improved his sleep.

In the psychiatric ward, Mr. L is once again disturbing patients, smearing and eating feces, and making half-hearted suicide attempts. Upset that staff is “ignoring” him, he enters other patients’ rooms without invitation and urinates in places other than the bathroom.

The authors’ observations

After 3 hospital admissions, Mr. L’s diagnosis remained unclear (Table 2). At his first admission, his symptoms suggested major depression with psychotic features. With his subsequent behaviors in the inpatient psychiatric unit—including primitive suicide attempts and smearing and eating feces—Mr. L showed a strong desire to be cared for. This and his past dependence on his wife and mother suggested a severe dependent personality disorder.

At his first discharge, Mr. L was diagnosed with a personality disorder with significant passive-aggressive traits. His lifelong dysphoria and lack of ambition also suggested dysthymia.

With discharge from this latest hospitalization pending, we searched for options. We considered Mr. L’s ongoing suicidality, persistent acting out, and aggression. Treatment team members discussed his use of “primitive defenses”² stemming from his limited coping skills in the face of severe depression.

Table 2

Mr. L’s differential diagnosis

Possible diagnosis	Mr. L’s symptoms
Major depression	Diminished motivation, concentration, and appetite Increased fatigue, hypersomnia Suicidal thinking
Personality disorder	Primitive, dependent behaviors Abnormal dependence on wife, mother
Depression with psychotic features	Depressive symptoms with obsessive suicidal/homicidal thoughts, fears of household malfunctions

TREATMENT: A different course

One week after admission, Mr. L’s inpatient psychiatrist recommends electroconvulsive therapy (ECT) to target the patient’s presumed severe depressive episodes and disruptive behaviors. The psychiatrist is experienced in performing ECT, which in clinical trials³ has shown efficacy in treatment-refractory major depression.

After giving informed consent, Mr. L receives 8 bilateral ECT treatments in 3 weeks. Also, the hospital psychologist performs behavioral modification similar to the previous cleanliness plan and again encourages Mr. L to express his anger and anxiety verbally.

By the second week of ECT, Mr. L’s disruptive behaviors have ceased. By the end of week 3, his mood and motivation have improved to the point where he shows interest in becoming independent. He says he wants to show his estranged wife he can care for himself and eventually reunite with her.

As Mr. L continues to improve, we discharge him to outpatient community mental health services and continue citalopram, 60 mg/d, and olanzapine, 5 mg nightly.

Nearly 2 years later, Mr. L is living independently. He has been regularly seeing his psychiatrist at the community mental health center and is maintained on citalopram and olanzapine. He continues trying to make amends with his wife but is still out of work and receives Social Security disability benefits.

The authors’ observations

Mr. L was fortunate that his inpatient psychiatrist could re-evaluate the diagnosis after identifying the staff’s significantly hateful countertransference. This allowed staff to offer ECT, which—despite its documented efficacy for major depression—is not widely available in the United States.

 

If no ECT providers were available, we would have considered medication change and long-term treatment in a state mental hospital until Mr. L showed he could care for himself.

Related resources

• Nagera H. Countertransference (PowerPoint presentation). Tampa, FL: The Carter Jenkins Center; 2003. www.thecjc.org/ppoint/ppoint/ct.ppt.
  
• MayoClinic.com video: Electroconvulsive therapy (ECT): One woman’s journey. Click on “Video” at top, then scroll to title.
  

Drug brand names

• Aripiprazole • Abilify
  
• Olanzapine • Zyprexa
  
• Citalopram • Celexa
  

Disclosure

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

CASE: He bares it all

Police have arrested Mr. L, age 62, 3 times in 36 hours after spotting him walking naked in public. With the county jail jammed to capacity, police bring him each time to our hospital’s emergency room.

After his first arrest, Mr. L matter-of-factly tells us, “I want to walk naked and starve myself to death.” His self-harm exhortations amplify with each visit until—at the third presentation—he reports that he has not eaten for at least 2 days.

Mr. L had been living on the streets for nearly 1 month. Before that, he had been in jail for approximately 1 month after attacking a nursing home patient. He has been hospitalized twice in 5 months for severe depression and personality disorder and has engaged in numerous disruptive behavioral episodes and feeble suicide attempts. At this latest presentation, he appears disheveled and lacks judgment and insight into his condition.

We readmit Mr. L to the psychiatric unit to re-evaluate his treatment. He had been on citalopram, 60 mg/d, and aripiprazole, 10 mg/d, but he says he stopped taking the medications because they were not improving his mood.

The authors’ observations

We readmitted Mr. L with working diagnoses of:

• major depressive disorder with psychotic features, based on his suicide threats and complaints of depression
  
• personality disorder not otherwise specified, based on his behavioral episodes, apparent desire to be cared for (Table 1), and refusal to “get better” during 2 recent hospitalizations.
  

Table 1

A troubled life: Mr. L’s history

Period	Mr. L’s difficulties
Childhood	Has no friends in school; his mother—Mr. L’s sole source of emotional support—continues to wash his laundry, buy his food and clothes into his 20s
Adult life	Keeps ‘goofing off’ at work and has trouble staying employed; depends on wife to manage his life
2 years ago	Shows depressive symptoms (amotivation, lack of concentration, increased fatigue, decreased appetite) after shoulder injury Develops irrational fear that household appliances will malfunction Becomes hostile toward his wife of 34 years
5 months ago	Hospitalized after threatening to kill wife; has depressive symptoms and is disruptive during month-long hospitalization
4 months ago	Discharged from hospital to homeless shelter because estranged wife won’t allow him back home; is readmitted after shelter staff find him banging his head on an iron gate; again behaves disruptively
3 months ago	Discharged from second month-long hospitalization to nursing home
2 months ago	Attacks patient at nursing home; police arrest and incarcerate him on disorderly conduct charge
Past month	Released from jail after 1 month and spends weeks on the streets; lands in ER after police repeatedly catch him walking naked in public

HISTORY: His best friends

As a child, Mr. L had no friends. His father was physically present but emotionally distant, so he relied on his mother for emotional support. Throughout his teens and early adulthood, his mother continued to do his laundry, buy his food and clothes, and run his life. When he married in his early 20s, his wife assumed this role.

Mr. L avoided psychiatric care for most of his life but did not socialize outside the house, lacked ambition, and seemed content to depend on his wife. He worked primarily as a janitor or housekeeper but was constantly getting fired and drifted from job to job. His wife told us that when he was supposed to be working, he spent hours staring at the walls and watching TV.

Mr. L’s recent troubles began approximately 2 years ago, when he suffered a shoulder injury. He underwent physical therapy but refused needed surgery because he lacked money and health insurance.

As the shoulder pain intensified, Mr. L quit his job. While out of work, he stopped attending physical therapy sessions when his depressive symptoms began to offset the shoulder pain. He suffered loss of concentration and motivation, increased fatigue with hypersomnia, and decreased appetite. He lost 10 to 12 lb in 1 year.

Mr. L also started having trouble “focusing on reality” and developed obsessive fears of malfunctions around the house, such as the furnace blowing up, the stove catching fire, or the toilet backing up. At one point, he began urinating and defecating in his pants to avoid using the toilet. He began to feel hopeless and several times tried to suffocate himself by placing a plastic bag over his head.

He also grew irritable, angry, and aggressive—mostly toward his wife, who increasingly feared him. He started blaming her for “everything wrong in my life” and began contemplating stabbing her to death or striking her head with a hammer.

 

Five months ago, Mr. L was involuntarily hospitalized for depressive symptoms, suicidality, and continued homicidal thoughts toward his wife. The attending psychiatrist started olanzapine, 5 mg nightly, for psychotic features, and citalopram, 10 mg/d, for depression and anxiety, and ordered one-on-one observation to prevent additional suicide attempts. Mr. L’s shoulder pain had resolved by this time.

Three days later, Mr. L began refusing to eat. The psychiatrist then increased citalopram to 20 mg/d and olanzapine to 5 mg bid and asked a hospital internist to evaluate for malnutrition and a psychologist to gauge cognitive and intellectual function.

During the psychologist’s evaluation, Mr. L showed average global intellectual functioning but delays in visual-motor speed, visual working memory, and alertness to his environment. These findings, however, did not explain the patient’s lower functioning at home or in the hospital.

We ruled out organic causes for Mr. L’s cognitive deficits after receiving normal brain MRI, urinalysis, rapid plasma reagin titer, and thyroid-stimulating hormone test results. We also ruled out malnutrition because vitamin B12 and folate levels were normal but ordered a dietary consult to help Mr. L regain weight.

Staff and family registered Mr. L for Medicare and Medicaid benefits so that he could become more independent, but his behavior soon regressed. He complained that staff and family were ignoring him and started urinating outside the bathroom, eating and smearing his feces, and bothering other patients. Staff directed Mr. L’s wife to ignore his verbal abuse over the phone and encourage him to stay motivated for treatment.

Mr. L’s disruptive behavior stopped after the psychologist tried individual therapy with behavior modification. The psychologist helped him devise a cleanliness plan and encouraged him to express his anger verbally rather than acting out. When Mr. L smeared his feces, he was to scrub the area with soap and water, take a 5-minute cold shower, put on clean clothes, and write and read an apology to hospital staff.

DISCHARGE: Nowhere to go

One month after admission, Mr. L was free of suicidal and homicidal thoughts and other symptoms. Staff prepared him for discharge, but his wife was contemplating divorce and refused to allow him back home. He also declined community outpatient treatment because he wanted his life to return to “normal” and was unaware that he was harming himself and others.

With no other disposition options, we discharged Mr. L to a homeless shelter. Later that day, shelter staff brought him back to the ER after they found him banging his head against an iron gate. We readmitted him to the psychiatric unit, at which point he endorsed suicidal thinking.

READMISSION: ‘Cold’ case

During this second hospitalization, Mr. L was again eating his feces as well as coloring himself with green markers, writing obscenities on the wall, and tearing up other patients’ papers. He repeatedly took 15-minute cold showers and told staff as they urged him out of the shower that he wanted to die by inducing hypothermia. During these episodes, he often called his estranged wife and told her what he was doing.

After the treatment team had Mr. L civilly committed, the attending psychiatrist titrated citalopram to 60 mg/d, discontinued olanzapine, and added aripiprazole to target the patient’s underlying depressive symptoms. Aripiprazole was started at 5 mg nightly and eventually titrated to 10 mg nightly. On 3 occasions during the month-long hospitalization, Mr. L refused to take his medications because he felt he did not belong in the hospital.

The attending psychiatrist diagnosed “dependent, passive-aggressive behaviors” and noted that Mr. L was “not amenable” to psychiatric hospitalization. The treatment team and outpatient community mental health department decided the patient had a personality disorder and that continued hospitalization would prevent him from attaining autonomy.

We then discharged Mr. L to a nursing home. There, he demanded a transfer back to the hospital or to jail because he feared he could not afford nursing home care and believed he could receive more attention elsewhere. His request was rejected after our ER psychiatrist found him medically and mentally fit to stay at the nursing home.

About 1 month later, Mr. L tried to smother a female patient by holding a pillow over her face but stopped when she began to struggle. After he told the nurses what he had done, staff immediately called police, who arrested Mr. L and transferred him to the county jail.

Because police and nursing home staff viewed the incident as a cry for help rather than a cold-blooded attack, police charged Mr. L with disorderly conduct. One month later, police dropped the charge and released him to the streets.

 

The authors’ observations

Mr. L triggered hateful reactions among several treatment team members, many of whom felt vindicated by his arrest. Clinicians might react this way if they feel a patient is wasting their time, manipulating them, not recognizing their narcissistic need for the patient to change, or ignoring their treatment plans.¹

Acknowledging the staff’s—and your own—reaction to a difficult patient is critical. Not doing so can lead to treatment decisions based on emotions rather than evidence. In a busy clinical setting, it’s easy to lose sight of this.

The following strategies can help you manage hateful countertransference, cope with a patient’s offensive behaviors, and make appropriate decisions:

• Allow staff members to discuss their feelings. Encourage them to acknowledge and discuss their feelings during team meetings or daily treatment discussions. This helped members of our team recognize that their identification with Mr. L’s self-rejection fueled their desire to “reject” him by discharging him to police or the homeless shelter.
  
• Joke about the patient’s behavior when appropriate. Humor is a mature and potentially healing defense mechanism. When not treating Mr. L, for example, we joked among ourselves about publishing a case report titled, “The case of the poop-eater.” Never joke about the patient in the therapeutic milieu, where it can be disruptive.
  
• See the behavior as a defense mechanism. Viewing patients’ reactions as defense mechanisms—rather than effects of a psychiatric disorder—can help you better understand the patient’s underlying pathophysiology.
  

READMISSION: More bad behavior

After his 3 arrests for public nudity, we readmit Mr. L, restart citalopram at 20 mg/d, and titrate it back to 60 mg/d to target his depression. We also switch back to olanzapine, 10 mg nightly, because the patient has seen little clinical benefit from aripiprazole and feels that olanzapine had improved his sleep.

In the psychiatric ward, Mr. L is once again disturbing patients, smearing and eating feces, and making half-hearted suicide attempts. Upset that staff is “ignoring” him, he enters other patients’ rooms without invitation and urinates in places other than the bathroom.

The authors’ observations

After 3 hospital admissions, Mr. L’s diagnosis remained unclear (Table 2). At his first admission, his symptoms suggested major depression with psychotic features. With his subsequent behaviors in the inpatient psychiatric unit—including primitive suicide attempts and smearing and eating feces—Mr. L showed a strong desire to be cared for. This and his past dependence on his wife and mother suggested a severe dependent personality disorder.

At his first discharge, Mr. L was diagnosed with a personality disorder with significant passive-aggressive traits. His lifelong dysphoria and lack of ambition also suggested dysthymia.

With discharge from this latest hospitalization pending, we searched for options. We considered Mr. L’s ongoing suicidality, persistent acting out, and aggression. Treatment team members discussed his use of “primitive defenses”² stemming from his limited coping skills in the face of severe depression.

Table 2

Mr. L’s differential diagnosis

Possible diagnosis	Mr. L’s symptoms
Major depression	Diminished motivation, concentration, and appetite Increased fatigue, hypersomnia Suicidal thinking
Personality disorder	Primitive, dependent behaviors Abnormal dependence on wife, mother
Depression with psychotic features	Depressive symptoms with obsessive suicidal/homicidal thoughts, fears of household malfunctions

TREATMENT: A different course

One week after admission, Mr. L’s inpatient psychiatrist recommends electroconvulsive therapy (ECT) to target the patient’s presumed severe depressive episodes and disruptive behaviors. The psychiatrist is experienced in performing ECT, which in clinical trials³ has shown efficacy in treatment-refractory major depression.

After giving informed consent, Mr. L receives 8 bilateral ECT treatments in 3 weeks. Also, the hospital psychologist performs behavioral modification similar to the previous cleanliness plan and again encourages Mr. L to express his anger and anxiety verbally.

By the second week of ECT, Mr. L’s disruptive behaviors have ceased. By the end of week 3, his mood and motivation have improved to the point where he shows interest in becoming independent. He says he wants to show his estranged wife he can care for himself and eventually reunite with her.

As Mr. L continues to improve, we discharge him to outpatient community mental health services and continue citalopram, 60 mg/d, and olanzapine, 5 mg nightly.

Nearly 2 years later, Mr. L is living independently. He has been regularly seeing his psychiatrist at the community mental health center and is maintained on citalopram and olanzapine. He continues trying to make amends with his wife but is still out of work and receives Social Security disability benefits.

The authors’ observations

Mr. L was fortunate that his inpatient psychiatrist could re-evaluate the diagnosis after identifying the staff’s significantly hateful countertransference. This allowed staff to offer ECT, which—despite its documented efficacy for major depression—is not widely available in the United States.

 

If no ECT providers were available, we would have considered medication change and long-term treatment in a state mental hospital until Mr. L showed he could care for himself.

Related resources

• Nagera H. Countertransference (PowerPoint presentation). Tampa, FL: The Carter Jenkins Center; 2003. www.thecjc.org/ppoint/ppoint/ct.ppt.
  
• MayoClinic.com video: Electroconvulsive therapy (ECT): One woman’s journey. Click on “Video” at top, then scroll to title.
  

Drug brand names

• Aripiprazole • Abilify
  
• Olanzapine • Zyprexa
  
• Citalopram • Celexa
  

Disclosure

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

CASE: A ‘purification’

Mr. B, age 61, is in the ICU after shooting himself in the abdomen. The trauma team asks our psychiatry consultation/liaison service to determine if he needs special observation to prevent further self-harm.

Two days ago, Mr. B stood in the parking lot of a nearby hospital, aimed his rifle toward the left upper part of his abdomen, and fired. Bleeding profusely, he dragged himself to the hospital’s emergency room. ER staff stabilized him hemodynamically, then transferred him to our hospital’s regional trauma center, where surgeons performed an emergency laparotomy and found 2 sigmoid colon perforations, with feces floating outside the bowel.

After a partial colectomy and colostomy, Mr. B received broad-spectrum antibiotics, narcotic pain medication, and bowel rest in the ICU. When the trauma team called us, the patient’s condition was stable and he had awakened enough to communicate, although he still needed frequent monitoring.

We visit Mr. B in the ICU and ask him why he shot himself. He denies he was attempting suicide but adds that for months he has been feeling depressed, stressed, and guilty about “all the bad things I’ve done in my life.” Shooting himself helped him forget these negative thoughts.

A devout Roman Catholic, Mr. B has been researching flagellation and other forms of physical penance and considers the shooting a purification. He says he shot himself in the abdomen 2 previous times and felt better for months or years after each shooting.

Four years ago, Mr. B donated his left kidney to an unknown recipient. He does not equate the kidney donation with the shootings but says he felt happy while recuperating. He was later disappointed, however, because the procedure did not help him attract the “attention” he had hoped for.

Mr. B says he had been considering the latest shooting for at least 8 months and had carefully planned it. After studying anatomy textbooks, he figured he could fire into the left upper portion of his abdomen without striking a vital organ.

For several evenings, Mr. B aimed his rifle toward his abdomen but could not bring himself to pull the trigger. On the night of the shooting, he said, he “accidentally” fired at a more damaging angle than he had planned.

Cognitive examination results are mostly normal, although Mr. B has trouble interpreting similarities and proverbs. He appears pale but well-nourished, well-groomed, and serene. He speaks softly, often closing his eyes or staring into the distance. He says he feels “relieved” and “happy” after the shooting but did not anticipate such a severe injury. He denies suicidal thoughts and—because of his current euphoric mood—he hopes he never “needs” to shoot himself again.

The authors’ observations

We first considered delusional disorder and major depressive disorder with psychotic features. Mr. B’s belief that shooting himself would solve his problems seemed delusional, although he did not appear psychotic otherwise. Confusingly, Mr. B’s pre-admission symptoms seemed to suggest major depressive disorder, but he was happy in the ICU.

We explored other diagnoses, such as an odd form of OCD and a personality disorder (especially cluster A, given his strange beliefs), though at this point we had too little information for either diagnosis.

We also wondered if Mr. B’s behavior was normal given his strong belief in Catholic penance. Although some sects of the Catholic Church practice self-flagellation and other forms of self-punishment,^1-3 we found no evidence that the church condones or encourages self-shooting. Moreover, Mr. B admitted during questioning that a Catholic clergy member told him shooting oneself is not an appropriate penance.

The authors’ observations

Mr. B was recovering from major abdominal surgery, was taking nothing orally, and claimed to feel fine psychologically. Because he was not grossly psychotic and did not endorse anxiety or depression, we decided against medication but recommended a chaplain consult and planned to visit Mr. B daily to gather more history.

We considered Mr. B a low suicide risk—especially while hospitalized—after he said his “need” to shoot himself had dissipated. He also endorsed no suicidal thoughts or other depressive symptoms, and the nursing staff viewed him as pleasant and compliant. We noted this evidence in the chart and continued to reassess him daily.

HISTORY: Dreams, nightmares

Over the next week, Mr. B shares his life story. He says his parents divorced when he was age 5, and around that time he spent approximately 2 weeks in the hospital after being hit by a truck. He considers those 2 weeks a bright spot in an otherwise turbulent childhood because his parents did not fight and he was showered with gifts and attention.

 

Soon after, Mr. B lived with his mother. When he was 9, he heard his divorced parents arguing during a family gathering and prayed for his own death.

Throughout his childhood, Mr. B dreamed of becoming a priest and a war hero. In his early teens, he attended a church youth program where he and other youths were taught that masturbation is a mortal sin. Through high school, Mr. B’s inability to stop masturbating shook his faith and discouraged him from pursuing the priesthood.

In high school, Mr. B did not use alcohol or drugs and excelled academically but had few friends. After graduating, he enlisted in the U.S. Army and hoped to serve in Vietnam, but basic training became too stressful. The relentless harangues from drill instructors reminded him of his parents’ frequent shouting matches during his childhood.

Approximately 2 weeks into basic training, Mr. B shot himself in the abdomen and injured his liver. He underwent laparotomy and cholecystectomy and was discharged from the military. His anxiety dissipated as he recovered, though he later regretted not serving in Vietnam.

Mr. B married at age 44 and was divorced 13 years later. Throughout the marriage, he says, he verbally abused his wife and was emotionally unsupportive. After the divorce, he felt remorse over having mistreated her. His guilt disappeared after he donated his left kidney to an unknown recipient, but the guilt soon returned and drove him to shoot himself a second time in 2005.

Mr. B worked as a special education teacher for 20 years before retiring 4 years ago and has since been pursuing a similar position because he misses going to work. His inability to find a permanent job has led to anxiety, insomnia, increased guilt, and decreased appetite. He says these feelings fueled his desire to shoot himself a third time.

Since his divorce, Mr. B has lived alone and has no family or friends nearby. He feels isolated and is hurt that his family has not acknowledged the cards and notes he sent to them but adds that he did not include his return address on the mailings.

FOLLOW-UP: No relief

After 1 week in the ICU, Mr. B is transferred to the surgical ward. His condition is fair and he continues to receive IV antibiotics; analgesics as needed; omeprazole, 20 mg/d, to prevent a stress ulcer; bowel care medications; and ostomy care and education. We continue to visit him in the surgical ward almost daily. He seems to enjoy our visits, during which he openly discusses his past.

Eleven days after admission, Mr. B says shooting himself has not relieved his negative feelings, and his impending discharge makes him feel anxious with some suicidal thoughts. The surgical team delays discharge after Mr. B develops ileus with nausea and vomiting. The trauma team’s attending physician prescribes an antiemetic, and ileus resolves after 4 days. Mr. B then is discharged in stable condition after he denies intention to harm himself.

Box 1

The authors’ observations

At first we viewed Mr. B’s idea of shooting himself to solve his problems as a delusion (Box 1), but less than 2 weeks later he denied that his self-injury offered any benefit. Because his original belief was transient, we ruled out delusional disorder and major depression with psychotic features.

Some of Mr. B’s symptoms suggested OCD, including thought-related anxiety that is relieved after performing an action—in his case shooting himself. Whereas obsessions and/or compulsions occur daily in OCD, Mr. B would perform the action and then feel fine for months to years before his anxiety resurfaced. Also, he did not consider his thoughts wrong or obtrusive.

 

Box 2

Although Mr. B experienced some depressive symptoms and anxiety just before discharge, we were hesitant to diagnose major depression because his symptoms appeared tied to situational factors. He also did not fit a particular personality disorder, although he showed characteristics of:

• cluster A (odd ideas, solitary lifestyle)
  
• cluster B (self-harm, narcissistic tendencies)
  
• and cluster C (avoiding his relatives, dependence on others to meet his needs).
  

We could have diagnosed personality disorder, not otherwise specified, but we were unsure whether personality explained his pathology or if his personality characteristics warranted diagnosis.

Mr. B’s intentional production of physical symptoms strongly suggested malingering, but we instead diagnosed factitious disorder because he was clearly motivated to play the sick role despite lack of a secondary gain (Box 2). The patient admitted causing the gunshot wound and clearly connected his subsequent emotional relief with both his positive childhood experience in the hospital and his satisfaction after donating a kidney.

Researchers have tried to distinguish between factitious disorder and other types of self-harm. Claes and Vandereycken⁴ would consider Mr. B’s behavior “self-mutilation” rather than factitious. Turner calls DSM-IV-TR criteria for factitious disorder nebulous and says that lying about symptoms or their origin should be a necessary criterion.⁵ If so, then Mr. B’s condition might fit no DSM diagnosis.⁶

The authors’ observations

Although Mr. B’s diagnosis remained elusive, he needed a treatment plan before discharge to prevent another shooting and save his life.

We first considered psychotropics. Because Mr. B’s beliefs did not appear delusional, an antipsychotic would not be a useful first-line treatment. Nor would a benzodiazepine help Mr. B at this point, especially since we did not diagnose primary anxiety.

Although we did not diagnose a major depressive or anxiety-spectrum disorder, we felt an SSRI such as citalopram could help. According to some investigators, SSRIs might benefit patients with over-valued ideas that are not as persistent as delusions.^7,8

Additionally, we felt supportive therapy could help Mr. B establish a therapeutic relationship with a provider to whom he could turn during future crises. Should Mr. B contemplate self-harm, the therapist could suggest medications, hospitalization, or other interventions. We also recommended pastoral counseling to increase his support within his faith.

OUTCOME Another shot?

Before discharge, we start citalopram, 10 mg/d, and schedule a follow-up appointment within 2 weeks. We also suggest that Mr. B:

• move into an apartment near his outpatient doctors
  
• get involved with the local Catholic community to build his support network.
  

When we contact Mr. B 2 months later, he says he discontinued citalopram because he felt no benefit from it. At his initial appointment with a psychiatrist, he denied depressive symptoms and was not scheduled for ongoing therapy. He has not spoken with clergy or other local church members because “I know they would say God has forgiven me.”

Mr. B calls his recent hospitalization upsetting because “I did not get the attention I wanted.” He endorses no immediate plan to shoot himself but voices concern that when his physical problems resolve, he might shoot Himself in the liver—as he had done 40 years ago—to bring himself full circle. “There’s still something attractive about this,” he says.

The authors’ observations

Patients with factitious illness commonly refuse mental health treatment.⁹

We feel Mr. B needs frequent ongoing appointments in a medical clinic where doctors can provide sufficient attention to counter his persistent self-harm urges. Regular appointments with a primary care physician—regardless of whether Mr. B is medically ill—could help him feel supported.

Related resources

• Feldman MD, Eisendrath SJ, eds. The spectrum of factitious disorders. Washington, DC: American Psychiatric Press; 1996.
  
• Sutton J, Martinson D. Self-injury Web site: What self-injury is.www.palace.net/~llama/psych/fwhat.html.
  

Drug brand names

• Citalopram • Celexa
  
• Omeprazole • Prilosec
  

Disclosure

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

CASE: A ‘purification’

Mr. B, age 61, is in the ICU after shooting himself in the abdomen. The trauma team asks our psychiatry consultation/liaison service to determine if he needs special observation to prevent further self-harm.

Two days ago, Mr. B stood in the parking lot of a nearby hospital, aimed his rifle toward the left upper part of his abdomen, and fired. Bleeding profusely, he dragged himself to the hospital’s emergency room. ER staff stabilized him hemodynamically, then transferred him to our hospital’s regional trauma center, where surgeons performed an emergency laparotomy and found 2 sigmoid colon perforations, with feces floating outside the bowel.

After a partial colectomy and colostomy, Mr. B received broad-spectrum antibiotics, narcotic pain medication, and bowel rest in the ICU. When the trauma team called us, the patient’s condition was stable and he had awakened enough to communicate, although he still needed frequent monitoring.

We visit Mr. B in the ICU and ask him why he shot himself. He denies he was attempting suicide but adds that for months he has been feeling depressed, stressed, and guilty about “all the bad things I’ve done in my life.” Shooting himself helped him forget these negative thoughts.

A devout Roman Catholic, Mr. B has been researching flagellation and other forms of physical penance and considers the shooting a purification. He says he shot himself in the abdomen 2 previous times and felt better for months or years after each shooting.

Four years ago, Mr. B donated his left kidney to an unknown recipient. He does not equate the kidney donation with the shootings but says he felt happy while recuperating. He was later disappointed, however, because the procedure did not help him attract the “attention” he had hoped for.

Mr. B says he had been considering the latest shooting for at least 8 months and had carefully planned it. After studying anatomy textbooks, he figured he could fire into the left upper portion of his abdomen without striking a vital organ.

For several evenings, Mr. B aimed his rifle toward his abdomen but could not bring himself to pull the trigger. On the night of the shooting, he said, he “accidentally” fired at a more damaging angle than he had planned.

Cognitive examination results are mostly normal, although Mr. B has trouble interpreting similarities and proverbs. He appears pale but well-nourished, well-groomed, and serene. He speaks softly, often closing his eyes or staring into the distance. He says he feels “relieved” and “happy” after the shooting but did not anticipate such a severe injury. He denies suicidal thoughts and—because of his current euphoric mood—he hopes he never “needs” to shoot himself again.

The authors’ observations

We first considered delusional disorder and major depressive disorder with psychotic features. Mr. B’s belief that shooting himself would solve his problems seemed delusional, although he did not appear psychotic otherwise. Confusingly, Mr. B’s pre-admission symptoms seemed to suggest major depressive disorder, but he was happy in the ICU.

We explored other diagnoses, such as an odd form of OCD and a personality disorder (especially cluster A, given his strange beliefs), though at this point we had too little information for either diagnosis.

We also wondered if Mr. B’s behavior was normal given his strong belief in Catholic penance. Although some sects of the Catholic Church practice self-flagellation and other forms of self-punishment,^1-3 we found no evidence that the church condones or encourages self-shooting. Moreover, Mr. B admitted during questioning that a Catholic clergy member told him shooting oneself is not an appropriate penance.

The authors’ observations

Mr. B was recovering from major abdominal surgery, was taking nothing orally, and claimed to feel fine psychologically. Because he was not grossly psychotic and did not endorse anxiety or depression, we decided against medication but recommended a chaplain consult and planned to visit Mr. B daily to gather more history.

We considered Mr. B a low suicide risk—especially while hospitalized—after he said his “need” to shoot himself had dissipated. He also endorsed no suicidal thoughts or other depressive symptoms, and the nursing staff viewed him as pleasant and compliant. We noted this evidence in the chart and continued to reassess him daily.

HISTORY: Dreams, nightmares

Over the next week, Mr. B shares his life story. He says his parents divorced when he was age 5, and around that time he spent approximately 2 weeks in the hospital after being hit by a truck. He considers those 2 weeks a bright spot in an otherwise turbulent childhood because his parents did not fight and he was showered with gifts and attention.

 

Soon after, Mr. B lived with his mother. When he was 9, he heard his divorced parents arguing during a family gathering and prayed for his own death.

Throughout his childhood, Mr. B dreamed of becoming a priest and a war hero. In his early teens, he attended a church youth program where he and other youths were taught that masturbation is a mortal sin. Through high school, Mr. B’s inability to stop masturbating shook his faith and discouraged him from pursuing the priesthood.

In high school, Mr. B did not use alcohol or drugs and excelled academically but had few friends. After graduating, he enlisted in the U.S. Army and hoped to serve in Vietnam, but basic training became too stressful. The relentless harangues from drill instructors reminded him of his parents’ frequent shouting matches during his childhood.

Approximately 2 weeks into basic training, Mr. B shot himself in the abdomen and injured his liver. He underwent laparotomy and cholecystectomy and was discharged from the military. His anxiety dissipated as he recovered, though he later regretted not serving in Vietnam.

Mr. B married at age 44 and was divorced 13 years later. Throughout the marriage, he says, he verbally abused his wife and was emotionally unsupportive. After the divorce, he felt remorse over having mistreated her. His guilt disappeared after he donated his left kidney to an unknown recipient, but the guilt soon returned and drove him to shoot himself a second time in 2005.

Mr. B worked as a special education teacher for 20 years before retiring 4 years ago and has since been pursuing a similar position because he misses going to work. His inability to find a permanent job has led to anxiety, insomnia, increased guilt, and decreased appetite. He says these feelings fueled his desire to shoot himself a third time.

Since his divorce, Mr. B has lived alone and has no family or friends nearby. He feels isolated and is hurt that his family has not acknowledged the cards and notes he sent to them but adds that he did not include his return address on the mailings.

FOLLOW-UP: No relief

After 1 week in the ICU, Mr. B is transferred to the surgical ward. His condition is fair and he continues to receive IV antibiotics; analgesics as needed; omeprazole, 20 mg/d, to prevent a stress ulcer; bowel care medications; and ostomy care and education. We continue to visit him in the surgical ward almost daily. He seems to enjoy our visits, during which he openly discusses his past.

Eleven days after admission, Mr. B says shooting himself has not relieved his negative feelings, and his impending discharge makes him feel anxious with some suicidal thoughts. The surgical team delays discharge after Mr. B develops ileus with nausea and vomiting. The trauma team’s attending physician prescribes an antiemetic, and ileus resolves after 4 days. Mr. B then is discharged in stable condition after he denies intention to harm himself.

Box 1

The authors’ observations

At first we viewed Mr. B’s idea of shooting himself to solve his problems as a delusion (Box 1), but less than 2 weeks later he denied that his self-injury offered any benefit. Because his original belief was transient, we ruled out delusional disorder and major depression with psychotic features.

Some of Mr. B’s symptoms suggested OCD, including thought-related anxiety that is relieved after performing an action—in his case shooting himself. Whereas obsessions and/or compulsions occur daily in OCD, Mr. B would perform the action and then feel fine for months to years before his anxiety resurfaced. Also, he did not consider his thoughts wrong or obtrusive.

 

Box 2

Although Mr. B experienced some depressive symptoms and anxiety just before discharge, we were hesitant to diagnose major depression because his symptoms appeared tied to situational factors. He also did not fit a particular personality disorder, although he showed characteristics of:

• cluster A (odd ideas, solitary lifestyle)
  
• cluster B (self-harm, narcissistic tendencies)
  
• and cluster C (avoiding his relatives, dependence on others to meet his needs).
  

We could have diagnosed personality disorder, not otherwise specified, but we were unsure whether personality explained his pathology or if his personality characteristics warranted diagnosis.

Mr. B’s intentional production of physical symptoms strongly suggested malingering, but we instead diagnosed factitious disorder because he was clearly motivated to play the sick role despite lack of a secondary gain (Box 2). The patient admitted causing the gunshot wound and clearly connected his subsequent emotional relief with both his positive childhood experience in the hospital and his satisfaction after donating a kidney.

Researchers have tried to distinguish between factitious disorder and other types of self-harm. Claes and Vandereycken⁴ would consider Mr. B’s behavior “self-mutilation” rather than factitious. Turner calls DSM-IV-TR criteria for factitious disorder nebulous and says that lying about symptoms or their origin should be a necessary criterion.⁵ If so, then Mr. B’s condition might fit no DSM diagnosis.⁶

The authors’ observations

Although Mr. B’s diagnosis remained elusive, he needed a treatment plan before discharge to prevent another shooting and save his life.

We first considered psychotropics. Because Mr. B’s beliefs did not appear delusional, an antipsychotic would not be a useful first-line treatment. Nor would a benzodiazepine help Mr. B at this point, especially since we did not diagnose primary anxiety.

Although we did not diagnose a major depressive or anxiety-spectrum disorder, we felt an SSRI such as citalopram could help. According to some investigators, SSRIs might benefit patients with over-valued ideas that are not as persistent as delusions.^7,8

Additionally, we felt supportive therapy could help Mr. B establish a therapeutic relationship with a provider to whom he could turn during future crises. Should Mr. B contemplate self-harm, the therapist could suggest medications, hospitalization, or other interventions. We also recommended pastoral counseling to increase his support within his faith.

OUTCOME Another shot?

Before discharge, we start citalopram, 10 mg/d, and schedule a follow-up appointment within 2 weeks. We also suggest that Mr. B:

• move into an apartment near his outpatient doctors
  
• get involved with the local Catholic community to build his support network.
  

When we contact Mr. B 2 months later, he says he discontinued citalopram because he felt no benefit from it. At his initial appointment with a psychiatrist, he denied depressive symptoms and was not scheduled for ongoing therapy. He has not spoken with clergy or other local church members because “I know they would say God has forgiven me.”

Mr. B calls his recent hospitalization upsetting because “I did not get the attention I wanted.” He endorses no immediate plan to shoot himself but voices concern that when his physical problems resolve, he might shoot Himself in the liver—as he had done 40 years ago—to bring himself full circle. “There’s still something attractive about this,” he says.

The authors’ observations

Patients with factitious illness commonly refuse mental health treatment.⁹

We feel Mr. B needs frequent ongoing appointments in a medical clinic where doctors can provide sufficient attention to counter his persistent self-harm urges. Regular appointments with a primary care physician—regardless of whether Mr. B is medically ill—could help him feel supported.

Related resources

• Feldman MD, Eisendrath SJ, eds. The spectrum of factitious disorders. Washington, DC: American Psychiatric Press; 1996.
  
• Sutton J, Martinson D. Self-injury Web site: What self-injury is.www.palace.net/~llama/psych/fwhat.html.
  

Drug brand names

• Citalopram • Celexa
  
• Omeprazole • Prilosec
  

Disclosure

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

CASE: A ‘purification’

Mr. B, age 61, is in the ICU after shooting himself in the abdomen. The trauma team asks our psychiatry consultation/liaison service to determine if he needs special observation to prevent further self-harm.

Two days ago, Mr. B stood in the parking lot of a nearby hospital, aimed his rifle toward the left upper part of his abdomen, and fired. Bleeding profusely, he dragged himself to the hospital’s emergency room. ER staff stabilized him hemodynamically, then transferred him to our hospital’s regional trauma center, where surgeons performed an emergency laparotomy and found 2 sigmoid colon perforations, with feces floating outside the bowel.

After a partial colectomy and colostomy, Mr. B received broad-spectrum antibiotics, narcotic pain medication, and bowel rest in the ICU. When the trauma team called us, the patient’s condition was stable and he had awakened enough to communicate, although he still needed frequent monitoring.

We visit Mr. B in the ICU and ask him why he shot himself. He denies he was attempting suicide but adds that for months he has been feeling depressed, stressed, and guilty about “all the bad things I’ve done in my life.” Shooting himself helped him forget these negative thoughts.

A devout Roman Catholic, Mr. B has been researching flagellation and other forms of physical penance and considers the shooting a purification. He says he shot himself in the abdomen 2 previous times and felt better for months or years after each shooting.

Four years ago, Mr. B donated his left kidney to an unknown recipient. He does not equate the kidney donation with the shootings but says he felt happy while recuperating. He was later disappointed, however, because the procedure did not help him attract the “attention” he had hoped for.

Mr. B says he had been considering the latest shooting for at least 8 months and had carefully planned it. After studying anatomy textbooks, he figured he could fire into the left upper portion of his abdomen without striking a vital organ.

For several evenings, Mr. B aimed his rifle toward his abdomen but could not bring himself to pull the trigger. On the night of the shooting, he said, he “accidentally” fired at a more damaging angle than he had planned.

Cognitive examination results are mostly normal, although Mr. B has trouble interpreting similarities and proverbs. He appears pale but well-nourished, well-groomed, and serene. He speaks softly, often closing his eyes or staring into the distance. He says he feels “relieved” and “happy” after the shooting but did not anticipate such a severe injury. He denies suicidal thoughts and—because of his current euphoric mood—he hopes he never “needs” to shoot himself again.

The authors’ observations

We first considered delusional disorder and major depressive disorder with psychotic features. Mr. B’s belief that shooting himself would solve his problems seemed delusional, although he did not appear psychotic otherwise. Confusingly, Mr. B’s pre-admission symptoms seemed to suggest major depressive disorder, but he was happy in the ICU.

We explored other diagnoses, such as an odd form of OCD and a personality disorder (especially cluster A, given his strange beliefs), though at this point we had too little information for either diagnosis.

We also wondered if Mr. B’s behavior was normal given his strong belief in Catholic penance. Although some sects of the Catholic Church practice self-flagellation and other forms of self-punishment,^1-3 we found no evidence that the church condones or encourages self-shooting. Moreover, Mr. B admitted during questioning that a Catholic clergy member told him shooting oneself is not an appropriate penance.

The authors’ observations

Mr. B was recovering from major abdominal surgery, was taking nothing orally, and claimed to feel fine psychologically. Because he was not grossly psychotic and did not endorse anxiety or depression, we decided against medication but recommended a chaplain consult and planned to visit Mr. B daily to gather more history.

We considered Mr. B a low suicide risk—especially while hospitalized—after he said his “need” to shoot himself had dissipated. He also endorsed no suicidal thoughts or other depressive symptoms, and the nursing staff viewed him as pleasant and compliant. We noted this evidence in the chart and continued to reassess him daily.

HISTORY: Dreams, nightmares

Over the next week, Mr. B shares his life story. He says his parents divorced when he was age 5, and around that time he spent approximately 2 weeks in the hospital after being hit by a truck. He considers those 2 weeks a bright spot in an otherwise turbulent childhood because his parents did not fight and he was showered with gifts and attention.

 

Soon after, Mr. B lived with his mother. When he was 9, he heard his divorced parents arguing during a family gathering and prayed for his own death.

Throughout his childhood, Mr. B dreamed of becoming a priest and a war hero. In his early teens, he attended a church youth program where he and other youths were taught that masturbation is a mortal sin. Through high school, Mr. B’s inability to stop masturbating shook his faith and discouraged him from pursuing the priesthood.

In high school, Mr. B did not use alcohol or drugs and excelled academically but had few friends. After graduating, he enlisted in the U.S. Army and hoped to serve in Vietnam, but basic training became too stressful. The relentless harangues from drill instructors reminded him of his parents’ frequent shouting matches during his childhood.

Approximately 2 weeks into basic training, Mr. B shot himself in the abdomen and injured his liver. He underwent laparotomy and cholecystectomy and was discharged from the military. His anxiety dissipated as he recovered, though he later regretted not serving in Vietnam.

Mr. B married at age 44 and was divorced 13 years later. Throughout the marriage, he says, he verbally abused his wife and was emotionally unsupportive. After the divorce, he felt remorse over having mistreated her. His guilt disappeared after he donated his left kidney to an unknown recipient, but the guilt soon returned and drove him to shoot himself a second time in 2005.

Mr. B worked as a special education teacher for 20 years before retiring 4 years ago and has since been pursuing a similar position because he misses going to work. His inability to find a permanent job has led to anxiety, insomnia, increased guilt, and decreased appetite. He says these feelings fueled his desire to shoot himself a third time.

Since his divorce, Mr. B has lived alone and has no family or friends nearby. He feels isolated and is hurt that his family has not acknowledged the cards and notes he sent to them but adds that he did not include his return address on the mailings.

FOLLOW-UP: No relief

After 1 week in the ICU, Mr. B is transferred to the surgical ward. His condition is fair and he continues to receive IV antibiotics; analgesics as needed; omeprazole, 20 mg/d, to prevent a stress ulcer; bowel care medications; and ostomy care and education. We continue to visit him in the surgical ward almost daily. He seems to enjoy our visits, during which he openly discusses his past.

Eleven days after admission, Mr. B says shooting himself has not relieved his negative feelings, and his impending discharge makes him feel anxious with some suicidal thoughts. The surgical team delays discharge after Mr. B develops ileus with nausea and vomiting. The trauma team’s attending physician prescribes an antiemetic, and ileus resolves after 4 days. Mr. B then is discharged in stable condition after he denies intention to harm himself.

Box 1

The authors’ observations

At first we viewed Mr. B’s idea of shooting himself to solve his problems as a delusion (Box 1), but less than 2 weeks later he denied that his self-injury offered any benefit. Because his original belief was transient, we ruled out delusional disorder and major depression with psychotic features.

Some of Mr. B’s symptoms suggested OCD, including thought-related anxiety that is relieved after performing an action—in his case shooting himself. Whereas obsessions and/or compulsions occur daily in OCD, Mr. B would perform the action and then feel fine for months to years before his anxiety resurfaced. Also, he did not consider his thoughts wrong or obtrusive.

 

Box 2

Although Mr. B experienced some depressive symptoms and anxiety just before discharge, we were hesitant to diagnose major depression because his symptoms appeared tied to situational factors. He also did not fit a particular personality disorder, although he showed characteristics of:

• cluster A (odd ideas, solitary lifestyle)
  
• cluster B (self-harm, narcissistic tendencies)
  
• and cluster C (avoiding his relatives, dependence on others to meet his needs).
  

We could have diagnosed personality disorder, not otherwise specified, but we were unsure whether personality explained his pathology or if his personality characteristics warranted diagnosis.

Mr. B’s intentional production of physical symptoms strongly suggested malingering, but we instead diagnosed factitious disorder because he was clearly motivated to play the sick role despite lack of a secondary gain (Box 2). The patient admitted causing the gunshot wound and clearly connected his subsequent emotional relief with both his positive childhood experience in the hospital and his satisfaction after donating a kidney.

Researchers have tried to distinguish between factitious disorder and other types of self-harm. Claes and Vandereycken⁴ would consider Mr. B’s behavior “self-mutilation” rather than factitious. Turner calls DSM-IV-TR criteria for factitious disorder nebulous and says that lying about symptoms or their origin should be a necessary criterion.⁵ If so, then Mr. B’s condition might fit no DSM diagnosis.⁶

The authors’ observations

Although Mr. B’s diagnosis remained elusive, he needed a treatment plan before discharge to prevent another shooting and save his life.

We first considered psychotropics. Because Mr. B’s beliefs did not appear delusional, an antipsychotic would not be a useful first-line treatment. Nor would a benzodiazepine help Mr. B at this point, especially since we did not diagnose primary anxiety.

Although we did not diagnose a major depressive or anxiety-spectrum disorder, we felt an SSRI such as citalopram could help. According to some investigators, SSRIs might benefit patients with over-valued ideas that are not as persistent as delusions.^7,8

Additionally, we felt supportive therapy could help Mr. B establish a therapeutic relationship with a provider to whom he could turn during future crises. Should Mr. B contemplate self-harm, the therapist could suggest medications, hospitalization, or other interventions. We also recommended pastoral counseling to increase his support within his faith.

OUTCOME Another shot?

Before discharge, we start citalopram, 10 mg/d, and schedule a follow-up appointment within 2 weeks. We also suggest that Mr. B:

• move into an apartment near his outpatient doctors
  
• get involved with the local Catholic community to build his support network.
  

When we contact Mr. B 2 months later, he says he discontinued citalopram because he felt no benefit from it. At his initial appointment with a psychiatrist, he denied depressive symptoms and was not scheduled for ongoing therapy. He has not spoken with clergy or other local church members because “I know they would say God has forgiven me.”

Mr. B calls his recent hospitalization upsetting because “I did not get the attention I wanted.” He endorses no immediate plan to shoot himself but voices concern that when his physical problems resolve, he might shoot Himself in the liver—as he had done 40 years ago—to bring himself full circle. “There’s still something attractive about this,” he says.

The authors’ observations

Patients with factitious illness commonly refuse mental health treatment.⁹

We feel Mr. B needs frequent ongoing appointments in a medical clinic where doctors can provide sufficient attention to counter his persistent self-harm urges. Regular appointments with a primary care physician—regardless of whether Mr. B is medically ill—could help him feel supported.

Related resources

• Feldman MD, Eisendrath SJ, eds. The spectrum of factitious disorders. Washington, DC: American Psychiatric Press; 1996.
  
• Sutton J, Martinson D. Self-injury Web site: What self-injury is.www.palace.net/~llama/psych/fwhat.html.
  

Drug brand names

• Citalopram • Celexa
  
• Omeprazole • Prilosec
  

Disclosure

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

CASE: The man from Betelgeuse

Mr. F, age 33, has been hospitalized repeatedly for psychotic episodes after abuse of dextromethorphan in cold medications.

Approximately 1 week before presenting to us, Mr. F stormed out of his house after his father, with whom he lived, confronted him about spending his allowance on cold medications. He spent the week living on the streets, abusing dextromethorphan whenever he could get it.

One night, Mr. F approached a police officer at an accident scene and exclaimed, “Dude, I’m from the planet Betelgeuse.” He appeared disorganized as police questioned him, and officers transported him to the county hospital’s psychiatric emergency service.

At presentation, Mr. F is at times silly, irritable, and sleepy, and chants incantations during the intake interview. Alternately, he hears Jesus Christ and aliens from Betelgeuse telling him “everything is going to be cool” and voices of aliens threatening to abduct him.

We admit Mr. F to the inpatient psychiatric unit, start risperidone at 2 mg nightly, and titrate it to 6 mg nightly over 3 days, after which he is significantly more organized with reduced auditory hallucinations. At discharge 6 days later, he still occasionally hears Jesus but has partial insight into his obsession with aliens and no paranoid delusions. We continue risperidone, 6 mg nightly, and refer him to an outpatient mental health program. He visits the clinic once but avoids the attending psychiatrist.

Five days later, Mr. F begins hallucinating at home and his father brings him back to the emergency psychiatry unit. At presentation, the patient claims to be an agent of Satan and waves his arms wildly while performing “black magic.” He believes he is damned and that previous messages he thought came from Jesus and extraterrestrials were instead from the devil.

Mr. F’s father reports that over the weekend his son ingested 6 boxes of cold medicine—each with 16 tablets containing 30 mg of dextromethorphan. Peeling skin on the lower part of Mr. F’s forehead, the bridge of his nose, and under his eyes suggests chronic cold tablet abuse. We re-admit the patient after extended urine drug screen shows traces of chlorpheniramine.

The authors’ observations

Routine urine drug screens based on radio-immunoassay detect many substances, but an extended or comprehensive urine drug screen based on gas chromatography-mass spectrometry is needed to detect dextromethorphan.¹ Tertiary hospitals and reference laboratories usually offer these tests.

An extended urine screen will not detect dextromethorphan 24 hours after use because the agent has a 3- to 11-hour half-life. The test can, however, detect other active cold preparation compounds with longer half-lives, such as chlorpheniramine.

If extended urine screening is not available, clinical findings discussed later in this article can confirm recent cold medication abuse. Blood testing can reveal dextromethorphan levels, but a 3- to 6-mL sample may be needed.

HISTORY: ‘Sick’ at 16

Mr. F began abusing dextromethorphan at age 16, when friends would “turn him on” to 8-ounce bottles of cough syrup every other week. He later tried marijuana, cocaine, phencyclidine, methamphetamine, morphine, and LSD. Soon after graduating from high school, he stopped using substances and remained clean for several years.

At age 25, Mr. F suffered his first psychotic break, after which a psychiatrist diagnosed schizophrenia. Initial symptom control with antipsychotics helped him finish college.

Mr. F worked as a restaurant manager for about 4 months but found the job stressful and constantly argued with staff. He resumed abusing cough syrup to relieve his stress but soon became hooked on its dissociative and hallucinogenic effects. One night he ingested enough cough syrup to remain “high” until the next morning. He was hallucinating when he reported to work that day and was fired.

Since then, Mr. F’s cold medication abuse has escalated from biweekly to almost daily at presentation. He switched to tablets because the syrup induced cold symptoms and he finds the “buzz” from the tablets easier to control.

He typically dresses in black (in keeping with his satanic obsessions) and wears a long black overcoat with several pockets, that allows him to carry boxes of cold capsules, books, and other items.

Mr. F’s father has repeatedly tried to stop his son’s cold tablet abuse by cutting off his allowance. Dextromethorphan-containing cold medications are inexpensive, however—a box of 16 30-mg tablets costs as little as $1.50. Also, Mr. F often would get money for cold capsules by going to malls and participating in market research surveys.

 

In the past year, Mr. F was hospitalized 6 times after dextromethorphan-induced psychotic decompensations. He has been unemployed for more than 5 years, has not been in a serious romantic relationship since college, and depends on his father for financial support. He is not abusing other substances.

The authors’ observations

As many as 80% of patients with schizophrenia also have a substance abuse disorder.² Access to psychoactive substances, kindling associated with schizophrenia, and attempts to stop hallucinations with alcohol or illicit drugs may explain this high prevalence.² Also, genetic or phenotypic vulnerability in schizophrenia might alter the mesolimbic dopamine system that moderates reward.

Compared with patients with schizophrenia who are substance-free, comorbid substance abuse in schizophrenia increases:

• severity of psychotic symptoms
  
• likelihood of emergency service use
  
• risk of suicide, illness, injury, hospitalization, or incarceration.³
  

Box 1

Whereas alcohol, marijuana, and cocaine abuse are common in schizophrenia,² to our knowledge only 2 other cases of comorbid dextromethorphan dependence and schizophrenia have been reported.^4,5

Mr. F responded well to risperidone when he wasn’t abusing cold tablets. After his last hospitalization, we referred him to a comprehensive outpatient program that could have addressed his cold medicine abuse and reintegrated him into the workplace. He avoided seeing the clinic psychiatrist, however, after promising his case manager that he would stop abusing dextromethorphan.

TREATMENT: Back to Betelgeuse

Upon re-admission, we restart risperidone, 6 mg nightly. Mr. F shows extreme somnolence caused by massive cold capsule use and is minimally cooperative with the psychiatrist’s follow-up interview. Over 36 hours, he awakens only for meals and medication and to use the bathroom. Once the somnolence passes, he cannot fall asleep at night.

Six days after admission, Mr. F is organized and hears voices mostly from Jesus with some demonic delusions. Extended urine drug screen taken 3 days after admission shows traces of chlorpheniramine but no dextromethorphan.

By day 7, Mr. F is nearly free of delusions and is discharged the next day. We continue risperidone, 6 mg nightly, to prevent the “voices,” and add diphenhydramine, 50 mg nightly, to regulate his sleep. We arrange follow-up care at an outpatient clinic, but Mr. F again avoids the clinic psychiatrist.

The authors’ observations

Mr. F’s “robo” binge triggered a profound and prolonged psychotic decompensation.

Dextrorphan—a pharmacologically active metabolite of dextromethorphan— might have disrupted cortical and sub-cortical glutamatergic neurotransmission,⁶ leading to florid psychosis and delayed recovery. Induction of the cytochrome P-450 2D6 isoenzyme, which metabolizes dextromethorphan, also could have prolonged Mr. F’s psychosis (Box 1).^7-11

RELAPSE: Return visits

Three weeks after discharge, Mr. F fights with police officers after they find him hallucinating in the streets. Police charge him with disorderly conduct and resisting arrest and bring him back to the psychiatric ER. We again resolve his auditory hallucinations with risperidone, 6 mg nightly. After 8 days we discharge him to police, who then transport him to jail and later release him on bail.

Six months later, Mr. F is hospitalized twice in 2 months after dextromethorphan-induced decompensations. He recovers quickly both times but lacks insight into his mental illness and his “robo” problem.

The authors’ observations

Dextromethorphan, known by many street names (Box 2), is contained in more than 100 OTC preparations, and is sold on the Internet in powder form.

Abuse of dextromethorphan-containing preparations is rising among teenagers and young adults. Nonmedical “robo” use led to 5,581 ER visits in the United States in 2004,¹² and California reported a 10-fold rise in dextromethorphan abuse among teenagers from 1999 to 2004.

 

¹³ Numerous factors explain this increase:

• Most people do not know that dextromethorphan-laced medications are dangerous if misused.
  
• These preparations can be purchased at many stores or snatched from the medicine chest.
  
• Several Web sites describe how to “safely” abuse dextromethorphan.¹³
  

Further, some pediatricians, family physicians, emergency physicians, and psychiatrists do not suspect “robo” abuse, in part because ordinary urine drug screens do not detect dextromethorphan.

medical consequences

Many dextromethorphan-laced preparations contain other active compounds—such as pseudoephedrine, acetaminophen, chlorpheniramine, guaifenesin, or bromide—that can cause serious adverse effects at above-normal doses. Abuse of medications containing both chlorpheniramine and dextromethorphan leads to hallucinogenic euphoria and dissociation, followed by hours of intense somnolence.

Dextromethorphan can cause serotonin syndrome when taken with serotonergic drugs such as amphetamines, cocaine, monoamine oxidase inhibitors, or selective serotonin reuptake inhibitors. Symptoms include tachycardia, hypertension, diaphoresis, mydriasis, myoclonus, agitation, and seizures.

Box 2

The authors’ observations

Physical and psychiatric symptoms, patient history, and collateral information together can confirm dextromethorphan abuse in patients who present with mainly visual and tactile hallucinations. The signs are easy to miss in patients with schizophrenia because schizophrenia is believed to be causing the psychosis.

Psychiatric/physical symptoms. Psychiatric symptoms of “robo” intoxication include euphoria, altered time perception, disorientation, and tactile, visual and auditory hallucinations.⁷ Physical symptoms include excitation, nystagmus, tachycardia, hypertension, hyperthermia, vomiting, urinary retention, drowsiness, and rash. Extreme dextromethorphan withdrawal can cause dysphoria, insomnia, vomiting, diaphoresis, abdominal pain, and diarrhea.⁷

Psychiatric symptoms of intoxication with dextromethorphan or phencyclidine are similar, but phencyclidine-intoxicated patients typically present with fluctuating behavior and motor symptoms including tremor, dystonic reactions, and catalepsy.

Also watch for dermatitis on the forehead, nose, or cheeks, which can result from chronic abuse of preparations containing dextromethorphan plus bromide or chlorpheniramine.

Patient history. Has the patient abused dextromethorphan before? If so, how often? When was he last treated for decompensation after cold medication abuse?

Also check for abuse of other substances, and ask teenage patients if their friends use cold preparations recreationally.

Collateral information. Ask family members to search the patient’s room for supplies of cold medicine and for empty boxes and capsule cards, check the medicine chest regularly to see if cold medications are missing, and check the patient’s jacket or coat pockets for cold tablets or cough syrup.

Treating ‘robo’ abuse

Convincing the patient and family that dextromethorphan abuse can cause severe harm is critical to promoting a positive outcome. Referral to a substance abuse rehabilitation program or 12-step group can help.

Related resources

• U.S. Department of Justice, National Drug Intelligence Center. Intelligence bulletin: DXM (dextromethorphan). www.usdoj.gov/ndic/pubs11/11563/index.htm.
  
• Partnership for a Drug-Free America. Resource for parents. www.drugfree.org/Parent. Click on “Cough Medicine Abuse” under “Special Drug Reports.”
  
• U.S. Food and Drug Administraton. FDA warns against abuse of dextromethorphan (DXM). www.fda.gov, enter “dextromethorphan” in search field.
  

Drug brand names

• Risperidone • Risperdal
  

Disclosure

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