Current Psychiatry

What makes a first-class psychiatrist? What are the traits that characterize the “ideal” psychiatrist? How does a good psychiatrist become great? There are many possible answers depending on who is asked.

In my view, after observing countless fellow psychiatrists over 3 decades in various settings, I have concluded there are 7 domains that determine the caliber of psychiatrists that we all aspire to be. It may be difficult to possess all the traits across all 7 domains but I propose it as an idealized model and a road map for the journey toward peak performance in our profession.

Domain I: Personal attributes

• The ability to listen “actively” and observe “comprehensively”
• Psychological mindedness and curiosity
• Skillfully engages and develops therapeutic alliance with patients from the first encounter
• Compassion and empathy, but pragmatic firmness about boundaries
• Nonjudgmental stance and cognizance of one’s own limitations
• Impeccable integrity and ethical conduct.

Domain II: Clinical mastery

• Thorough familiarity with the principles of psychiatry and models of behavior and psychopathology
• Rigor in applying a diagnostic label by employing the skills of a physician to check patients’ medical status to rule out general medical etiologies; monitors patients’ physical and mental health and refers as needed
• Establishes a skillful biopsychosocial treatment plan requiring extensive knowledge of psychopharmacology and psychotherapy
• Applies evidence-based interventions wherever available
• Always checks and deals with countertransference issues.

Domain III: Professionalism and leadership

• Always well dressed and groomed with a professional appearance; projects the identity of being a physician; leadership of mental health teams
• Involved in local, state, national, and international professional societies
• Raises the profile of psychiatry within the medical field by networking with other physician organizations and participating in medical initiatives.

Domain IV: Organizational effectiveness

• Leads balanced and well organized professional and personal lives
• Smooth working relationship with individuals or agencies relevant to the patient’s treatment, including family members, medical and mental health professionals, hospital administrators, clinics, insurance companies, advocacy groups, and the legal system
• Maintains an organized and complete medical record with measurement-based ratings of illness severity and side effects.

Domain V: Societal role

• Establishes one’s self as a role model for those seeking advice and guidance not only for psychiatric disorders, but for various societal dilemmas and is an effective communicator
• Feels comfortable in being a public figure in one’s community whose opinions are valued by laymen as well as other professionals
• Serves as an ambassador for the profession by educating the public via various media outlets to erase misperceptions about mental illness or psychiatry, and to rebut and neutralize the occasional venomous assaults recklessly hurled by antipsychiatry cults.

Domain VI: Lifelong learning

• Convinced of the need for continuous learning in an era of logarithmic growth of medical knowledge
• Reads several articles a week from key journals about recent clinical and scientific advances and applies them to patients when appropriate
• Attends or presents at continuing medical education meetings and asks questions or makes comments (active, not passive attendance).

Domain VII: Contribution to new knowledge

• Recognizes the vast unmet needs in psychiatry, supports research, and understands that the research of today is the better treatment of tomorrow
• Refers patients to clinical research protocols at the local academic institution and offers to collaborate as a rater or data collector
• Takes the time to write up unusual clinical cases as a letter to the editor or case report and generate new clinical ideas
• If not a full-time academic, volunteers to teach or supervise medical students or residents at the local medical school or teaching hospital.

Very few psychiatrists can excel at all 7 domains, but most meet the criteria for several of them. Every psychiatrist can move from good to great with a modicum of effort and motivation. If most of us do that, the caliber and standing of our psychiatric profession will continue to escalate.

What makes a first-class psychiatrist? What are the traits that characterize the “ideal” psychiatrist? How does a good psychiatrist become great? There are many possible answers depending on who is asked.

In my view, after observing countless fellow psychiatrists over 3 decades in various settings, I have concluded there are 7 domains that determine the caliber of psychiatrists that we all aspire to be. It may be difficult to possess all the traits across all 7 domains but I propose it as an idealized model and a road map for the journey toward peak performance in our profession.

Domain I: Personal attributes

• The ability to listen “actively” and observe “comprehensively”
• Psychological mindedness and curiosity
• Skillfully engages and develops therapeutic alliance with patients from the first encounter
• Compassion and empathy, but pragmatic firmness about boundaries
• Nonjudgmental stance and cognizance of one’s own limitations
• Impeccable integrity and ethical conduct.

Domain II: Clinical mastery

• Thorough familiarity with the principles of psychiatry and models of behavior and psychopathology
• Rigor in applying a diagnostic label by employing the skills of a physician to check patients’ medical status to rule out general medical etiologies; monitors patients’ physical and mental health and refers as needed
• Establishes a skillful biopsychosocial treatment plan requiring extensive knowledge of psychopharmacology and psychotherapy
• Applies evidence-based interventions wherever available
• Always checks and deals with countertransference issues.

Domain III: Professionalism and leadership

• Always well dressed and groomed with a professional appearance; projects the identity of being a physician; leadership of mental health teams
• Involved in local, state, national, and international professional societies
• Raises the profile of psychiatry within the medical field by networking with other physician organizations and participating in medical initiatives.

Domain IV: Organizational effectiveness

• Leads balanced and well organized professional and personal lives
• Smooth working relationship with individuals or agencies relevant to the patient’s treatment, including family members, medical and mental health professionals, hospital administrators, clinics, insurance companies, advocacy groups, and the legal system
• Maintains an organized and complete medical record with measurement-based ratings of illness severity and side effects.

Domain V: Societal role

• Establishes one’s self as a role model for those seeking advice and guidance not only for psychiatric disorders, but for various societal dilemmas and is an effective communicator
• Feels comfortable in being a public figure in one’s community whose opinions are valued by laymen as well as other professionals
• Serves as an ambassador for the profession by educating the public via various media outlets to erase misperceptions about mental illness or psychiatry, and to rebut and neutralize the occasional venomous assaults recklessly hurled by antipsychiatry cults.

Domain VI: Lifelong learning

• Convinced of the need for continuous learning in an era of logarithmic growth of medical knowledge
• Reads several articles a week from key journals about recent clinical and scientific advances and applies them to patients when appropriate
• Attends or presents at continuing medical education meetings and asks questions or makes comments (active, not passive attendance).

Domain VII: Contribution to new knowledge

• Recognizes the vast unmet needs in psychiatry, supports research, and understands that the research of today is the better treatment of tomorrow
• Refers patients to clinical research protocols at the local academic institution and offers to collaborate as a rater or data collector
• Takes the time to write up unusual clinical cases as a letter to the editor or case report and generate new clinical ideas
• If not a full-time academic, volunteers to teach or supervise medical students or residents at the local medical school or teaching hospital.

Very few psychiatrists can excel at all 7 domains, but most meet the criteria for several of them. Every psychiatrist can move from good to great with a modicum of effort and motivation. If most of us do that, the caliber and standing of our psychiatric profession will continue to escalate.

What makes a first-class psychiatrist? What are the traits that characterize the “ideal” psychiatrist? How does a good psychiatrist become great? There are many possible answers depending on who is asked.

In my view, after observing countless fellow psychiatrists over 3 decades in various settings, I have concluded there are 7 domains that determine the caliber of psychiatrists that we all aspire to be. It may be difficult to possess all the traits across all 7 domains but I propose it as an idealized model and a road map for the journey toward peak performance in our profession.

Domain I: Personal attributes

• The ability to listen “actively” and observe “comprehensively”
• Psychological mindedness and curiosity
• Skillfully engages and develops therapeutic alliance with patients from the first encounter
• Compassion and empathy, but pragmatic firmness about boundaries
• Nonjudgmental stance and cognizance of one’s own limitations
• Impeccable integrity and ethical conduct.

Domain II: Clinical mastery

• Thorough familiarity with the principles of psychiatry and models of behavior and psychopathology
• Rigor in applying a diagnostic label by employing the skills of a physician to check patients’ medical status to rule out general medical etiologies; monitors patients’ physical and mental health and refers as needed
• Establishes a skillful biopsychosocial treatment plan requiring extensive knowledge of psychopharmacology and psychotherapy
• Applies evidence-based interventions wherever available
• Always checks and deals with countertransference issues.

Domain III: Professionalism and leadership

• Always well dressed and groomed with a professional appearance; projects the identity of being a physician; leadership of mental health teams
• Involved in local, state, national, and international professional societies
• Raises the profile of psychiatry within the medical field by networking with other physician organizations and participating in medical initiatives.

Domain IV: Organizational effectiveness

• Leads balanced and well organized professional and personal lives
• Smooth working relationship with individuals or agencies relevant to the patient’s treatment, including family members, medical and mental health professionals, hospital administrators, clinics, insurance companies, advocacy groups, and the legal system
• Maintains an organized and complete medical record with measurement-based ratings of illness severity and side effects.

Domain V: Societal role

• Establishes one’s self as a role model for those seeking advice and guidance not only for psychiatric disorders, but for various societal dilemmas and is an effective communicator
• Feels comfortable in being a public figure in one’s community whose opinions are valued by laymen as well as other professionals
• Serves as an ambassador for the profession by educating the public via various media outlets to erase misperceptions about mental illness or psychiatry, and to rebut and neutralize the occasional venomous assaults recklessly hurled by antipsychiatry cults.

Domain VI: Lifelong learning

• Convinced of the need for continuous learning in an era of logarithmic growth of medical knowledge
• Reads several articles a week from key journals about recent clinical and scientific advances and applies them to patients when appropriate
• Attends or presents at continuing medical education meetings and asks questions or makes comments (active, not passive attendance).

Domain VII: Contribution to new knowledge

• Recognizes the vast unmet needs in psychiatry, supports research, and understands that the research of today is the better treatment of tomorrow
• Refers patients to clinical research protocols at the local academic institution and offers to collaborate as a rater or data collector
• Takes the time to write up unusual clinical cases as a letter to the editor or case report and generate new clinical ideas
• If not a full-time academic, volunteers to teach or supervise medical students or residents at the local medical school or teaching hospital.

Very few psychiatrists can excel at all 7 domains, but most meet the criteria for several of them. Every psychiatrist can move from good to great with a modicum of effort and motivation. If most of us do that, the caliber and standing of our psychiatric profession will continue to escalate.

Not all patients who experience hallucinations have a psychotic disorder. Many physical and psychiatric disorders can manifest with hallucinations, and some patients have >1 disorder that could cause different types of hallucinations. To avoid providing unnecessary or ineffective treatments—and to ensure that patients receive proper care for nonpsychiatric conditions—it is important to accurately diagnose the disorder causing a patient’s hallucinations.

In this article we describe common features and psychiatric and nonpsychiatric causes of auditory, visual, olfactory, gustatory, tactile, and somatic hallucinations. Awareness of typical presentations of hallucinations associated with specific disorders can help narrow the diagnosis and provide appropriate treatment.

Auditory hallucinations

Also known as paracusia, auditory hallucinations are perceptions of sounds without identifiable external stimuli. This type of hallucination has various causes (Table 1).¹ A frequent symptom of schizophrenia, auditory hallucinations can cause substantial distress and functional disability.² Approximately 60% to 90% of patients with schizophrenia and up to 80% of those with affective psychoses experience auditory hallucinations.¹

Auditory hallucinations in psychosis usually are formed and complex.³ A common manifestation is hearing ≥1 voices. A patient might experience 2 voices talking about him in the third person. The voices may be perceived as coming from inside or outside the patient’s head. Some might hear their own thoughts spoken aloud. According to DSM-IV-TR, “hearing voices” is sufficient to diagnose schizophrenia if the hallucinations consist of a voice keeping up a running commentary on the person’s behavior or ≥2 voices conversing with each other.⁴ Auditory hallucinations also are seen in mood disorders but tend to be milder than their psychosis-induced counterparts.

Simple (unformed) auditory hallucinations—referred to as tinnitus—can be caused by disease of the middle ear (otosclerosis) or inner ear. These unformed hallucinations consist of buzzing or tones of varying pitch and timbre.¹

Partial seizures may cause auditory hallucinations. Perceptions of music have been associated with partial seizures.⁵ Curie and colleagues found that 17% of 514 patients with temporal lobe epilepsy had auditory hallucinations as a component of their seizures.⁶ These hallucinations typically are brief, stereotyped sensory impressions and, if formed, may be trivial sentences, previously heard phrases, or commands.

Alcoholic hallucinosis is a hallucinatory syndrome caused by alcohol withdrawal. These hallucinations usually are vocal and typically consist of accusatory, threatening, and/or critical voices directed at the patient.¹ Patients with alcohol hallucinosis also may experience musical auditory hallucinations.^7,8

CNS neoplasms can produce auditory hallucinations in 3% to 10% of patients.⁹ Hemorrhages and arteriovenous malformations in the pontine tegmentum and lower midbrain have been associated with acute onset of auditory hallucinations. The sounds typically are unformed mechanical or seashell-like noises or music.¹⁰

Patients with migraines rarely report auditory hallucinations. When they occur, they typically consist of perceived unilateral tinnitus, phonophobia, or hearing loss.

Table 1

Common causes of auditory hallucinations

Visual hallucinations

Visual hallucinations manifest as visual sensory perceptions in the absence of external stimuli.¹¹ These false perceptions may consist of formed images (eg, people) or unformed images (eg, flashes of light).¹² Visual hallucinations occur in numerous ophthalmologic, neurologic, medical, and psychiatric disorders (Table 2).¹³

DSM-IV-TR lists visual hallucinations as a primary diagnostic criterion for several psychotic disorders, including schizophrenia and schizoaffective disorder,⁴ and they occur in 16% to 72% of patients with these conditions.^14,15 Patients with major depressive disorder or bipolar disorder also may experience visual hallucinations. Visual hallucinations in those with schizophrenia tend to involve vivid scenes with family members, religious figures, and/or animals.¹⁶

Delirium is a transient, reversible cause of cerebral dysfunction that often presents with hallucinations. Several studies have shown that visual hallucinations are the most common type among patients with delirium. Webster and Holroyd found visual hallucinations in 27% of 227 delirium patients.¹⁷

Delirium tremens typically is accompanied by visual hallucinations. Visions of small animals and crawling insects are common.¹⁸ Hallucinations due to drug intoxication or withdrawal generally vary in duration from brief to continuous; such experiences often contribute to agitation.¹⁹

Migraines are a well-recognized cause of visual hallucinations. Up to 31% of those with migraines experience an aura, and nearly 99% of those with aura have visual symptoms.^20,21 The classic visual aura starts as an irregular colored crescent of light with multi-colored edges in the center of the visual field that gradually progresses toward the periphery, lasting <60 minutes. These simple visual hallucinations are most common; more complex hallucinations are seen more frequently in migraine coma and familial hemiplegic migraine.

Approximately 5% of patients with epilepsy have occipital seizures, which almost always have visual manifestations. Epileptic visual hallucinations often are simple, brief, stereotyped, and fragmentary. They usually consist of small, brightly colored spots or shapes that flash.²² Complex visual hallucinations in epilepsy are similar to hypnagogic hallucinations but are rare. Intracranial electroencephalography recordings have shown that pathological excitation of visual cortical areas may be responsible for complex visual hallucinations in epilepsy.¹⁹

Dementia with Lewy bodies (DLB) is associated with visual hallucinations.²³ Visual hallucinations occur in >20% of patients with DLB.²⁴ Patients with DLB may see complex scenarios of people and items that are not present. Visual hallucinations have an 83% positive predictive value for distinguishing DLB from dementia of the Alzheimer’s type.²⁵ There is a strong correlation between Lewy bodies located in the amygdala and parahippocampus and well-formed visual hallucinations.²⁶

Visual hallucinations are common in Parkinson’s disease and may occur in up to one-half of patients.²⁷ Patients with Parkinson’s disease may experience hallucinations similar to those observed in DLB, which can range from seeing a person or animal to more complex, formed, and mobile people, animals, or objects.

Table 2

Common causes of visual hallucinations

Olfactory hallucinations

Also known as phantosmia, olfactory hallucinations involve smelling odors that are not derived from any physical stimulus. They can occur with several psychiatric conditions, including schizophrenia, depression, bipolar disorder, eating disorders, and substance abuse.²⁸ Olfactory hallucinations caused by epileptic activity are rare. They constitute approximately 0.9% of all auras and typically are described as unpleasant. Tumors that affect the medial temporal lobe and mesial temporal sclerosis are associated with olfactory hallucinations.²⁹ Olfactory hallucinations also have been reported in patients with multi-infarct dementia, Alzheimer’s disease, and alcoholic psychosyndromes. In patients with schizophrenia, the smell may be perceived as coming from an external source, whereas patients with depression may perceive the source as internal.³⁰ Patients who perceive that they are the source of an offensive odor—a condition known as olfactory reference syndrome—may wash excessively, overuse deodorants and perfumes, or become socially withdrawn.³⁰

Gustatory hallucinations

Patients with gustatory hallucinations may experience salivation, sensation of thirst, or taste alterations. These hallucinations can be observed when the sylvian fissure that extends to the insula is stimulated electrically.³¹ Similar to olfactory hallucinations, gustatory hallucinations are associated with temporal lobe disease and parietal operculum lesions.^31,32 Sinus diseases have been associated with olfactory and gustatory hallucinations.³³ Brief gustatory hallucinations can be elicited with stimulation of the right rolandic operculum, parietal operculum, amygdala, hippocampus, medial temporal gyrus, and anterior part of right temporal gyrus.³⁴

Tactile hallucinations

These hallucinations may include perceptions of insects crawling over or under the skin (formication) or simulation of pressure on skin.³⁵ They have been associated with substance abuse, toxicity, or withdrawal.²⁸ Tactile hallucinations are characteristic of cocaine or amphetamine intoxication.³⁵

Tactile hallucinations are a rare symptom of schizophrenia. Heveling and colleagues reported a case of a woman, age 68, with chronic schizophrenia who experienced touching and being touched by a “shadow man” several times a day in addition to auditory and visual hallucinations.³⁶ Her symptoms disappeared after 4 weeks of antipsychotic and mood stabilizer therapy.

Tactile hallucinations have been associated with obsessive-compulsive disorder (OCD).³⁷ Fontenelle and colleagues suggested that OCD and psychotic disorders may share dysfunctional dopaminergic circuits.³⁷

Somatic hallucinations

Patients who have somatic hallucinations report perceptions of abnormal body sensations or physical experiences. For example, a patient may have sense of not having a stomach while eating.³⁵

This type of hallucination has been associated with activation of postcentral gyrus, parietal operculum, insula, and inferior parietal lobule on stereoelectroencephalography.³⁴ In a study of cerebral blood flow in 20 geriatric patients with delusional disorder, somatic type who were experiencing somatic hallucinations, positron emission testing scan demonstrated increased perfusion in somatic sensory processing regions, particularly the left postcentral gyrus and the right paracentral lobule.³⁸ Other researchers have linked somatic hallucinations with activation in the primary somatosensory and posterior parietal cortex, areas that normally mediate tactile perception.³⁹

Related Resource

• Teeple RC, Caplan JP, Stern TA. Visual hallucinations: differential diagnosis and treatment. Prim Care Companion J Clin Psychiatry. 2009;11(1):26-32.

Disclosures

Drs. Ali, Patel, Avenido, Bailey, and Jabeen report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Riley is on the board of directors for Vertex Pharmaceuticals.

Acknowledgment

The authors would like to thank Marwah Shahid, Research Associate, Vanderbilt University, Nashville, TN.

Not all patients who experience hallucinations have a psychotic disorder. Many physical and psychiatric disorders can manifest with hallucinations, and some patients have >1 disorder that could cause different types of hallucinations. To avoid providing unnecessary or ineffective treatments—and to ensure that patients receive proper care for nonpsychiatric conditions—it is important to accurately diagnose the disorder causing a patient’s hallucinations.

In this article we describe common features and psychiatric and nonpsychiatric causes of auditory, visual, olfactory, gustatory, tactile, and somatic hallucinations. Awareness of typical presentations of hallucinations associated with specific disorders can help narrow the diagnosis and provide appropriate treatment.

Auditory hallucinations

Also known as paracusia, auditory hallucinations are perceptions of sounds without identifiable external stimuli. This type of hallucination has various causes (Table 1).¹ A frequent symptom of schizophrenia, auditory hallucinations can cause substantial distress and functional disability.² Approximately 60% to 90% of patients with schizophrenia and up to 80% of those with affective psychoses experience auditory hallucinations.¹

Auditory hallucinations in psychosis usually are formed and complex.³ A common manifestation is hearing ≥1 voices. A patient might experience 2 voices talking about him in the third person. The voices may be perceived as coming from inside or outside the patient’s head. Some might hear their own thoughts spoken aloud. According to DSM-IV-TR, “hearing voices” is sufficient to diagnose schizophrenia if the hallucinations consist of a voice keeping up a running commentary on the person’s behavior or ≥2 voices conversing with each other.⁴ Auditory hallucinations also are seen in mood disorders but tend to be milder than their psychosis-induced counterparts.

Simple (unformed) auditory hallucinations—referred to as tinnitus—can be caused by disease of the middle ear (otosclerosis) or inner ear. These unformed hallucinations consist of buzzing or tones of varying pitch and timbre.¹

Partial seizures may cause auditory hallucinations. Perceptions of music have been associated with partial seizures.⁵ Curie and colleagues found that 17% of 514 patients with temporal lobe epilepsy had auditory hallucinations as a component of their seizures.⁶ These hallucinations typically are brief, stereotyped sensory impressions and, if formed, may be trivial sentences, previously heard phrases, or commands.

Alcoholic hallucinosis is a hallucinatory syndrome caused by alcohol withdrawal. These hallucinations usually are vocal and typically consist of accusatory, threatening, and/or critical voices directed at the patient.¹ Patients with alcohol hallucinosis also may experience musical auditory hallucinations.^7,8

CNS neoplasms can produce auditory hallucinations in 3% to 10% of patients.⁹ Hemorrhages and arteriovenous malformations in the pontine tegmentum and lower midbrain have been associated with acute onset of auditory hallucinations. The sounds typically are unformed mechanical or seashell-like noises or music.¹⁰

Patients with migraines rarely report auditory hallucinations. When they occur, they typically consist of perceived unilateral tinnitus, phonophobia, or hearing loss.

Table 1

Common causes of auditory hallucinations

Visual hallucinations

Visual hallucinations manifest as visual sensory perceptions in the absence of external stimuli.¹¹ These false perceptions may consist of formed images (eg, people) or unformed images (eg, flashes of light).¹² Visual hallucinations occur in numerous ophthalmologic, neurologic, medical, and psychiatric disorders (Table 2).¹³

DSM-IV-TR lists visual hallucinations as a primary diagnostic criterion for several psychotic disorders, including schizophrenia and schizoaffective disorder,⁴ and they occur in 16% to 72% of patients with these conditions.^14,15 Patients with major depressive disorder or bipolar disorder also may experience visual hallucinations. Visual hallucinations in those with schizophrenia tend to involve vivid scenes with family members, religious figures, and/or animals.¹⁶

Delirium is a transient, reversible cause of cerebral dysfunction that often presents with hallucinations. Several studies have shown that visual hallucinations are the most common type among patients with delirium. Webster and Holroyd found visual hallucinations in 27% of 227 delirium patients.¹⁷

Delirium tremens typically is accompanied by visual hallucinations. Visions of small animals and crawling insects are common.¹⁸ Hallucinations due to drug intoxication or withdrawal generally vary in duration from brief to continuous; such experiences often contribute to agitation.¹⁹

Migraines are a well-recognized cause of visual hallucinations. Up to 31% of those with migraines experience an aura, and nearly 99% of those with aura have visual symptoms.^20,21 The classic visual aura starts as an irregular colored crescent of light with multi-colored edges in the center of the visual field that gradually progresses toward the periphery, lasting <60 minutes. These simple visual hallucinations are most common; more complex hallucinations are seen more frequently in migraine coma and familial hemiplegic migraine.

Approximately 5% of patients with epilepsy have occipital seizures, which almost always have visual manifestations. Epileptic visual hallucinations often are simple, brief, stereotyped, and fragmentary. They usually consist of small, brightly colored spots or shapes that flash.²² Complex visual hallucinations in epilepsy are similar to hypnagogic hallucinations but are rare. Intracranial electroencephalography recordings have shown that pathological excitation of visual cortical areas may be responsible for complex visual hallucinations in epilepsy.¹⁹

Dementia with Lewy bodies (DLB) is associated with visual hallucinations.²³ Visual hallucinations occur in >20% of patients with DLB.²⁴ Patients with DLB may see complex scenarios of people and items that are not present. Visual hallucinations have an 83% positive predictive value for distinguishing DLB from dementia of the Alzheimer’s type.²⁵ There is a strong correlation between Lewy bodies located in the amygdala and parahippocampus and well-formed visual hallucinations.²⁶

Visual hallucinations are common in Parkinson’s disease and may occur in up to one-half of patients.²⁷ Patients with Parkinson’s disease may experience hallucinations similar to those observed in DLB, which can range from seeing a person or animal to more complex, formed, and mobile people, animals, or objects.

Table 2

Common causes of visual hallucinations

Olfactory hallucinations

Also known as phantosmia, olfactory hallucinations involve smelling odors that are not derived from any physical stimulus. They can occur with several psychiatric conditions, including schizophrenia, depression, bipolar disorder, eating disorders, and substance abuse.²⁸ Olfactory hallucinations caused by epileptic activity are rare. They constitute approximately 0.9% of all auras and typically are described as unpleasant. Tumors that affect the medial temporal lobe and mesial temporal sclerosis are associated with olfactory hallucinations.²⁹ Olfactory hallucinations also have been reported in patients with multi-infarct dementia, Alzheimer’s disease, and alcoholic psychosyndromes. In patients with schizophrenia, the smell may be perceived as coming from an external source, whereas patients with depression may perceive the source as internal.³⁰ Patients who perceive that they are the source of an offensive odor—a condition known as olfactory reference syndrome—may wash excessively, overuse deodorants and perfumes, or become socially withdrawn.³⁰

Gustatory hallucinations

Patients with gustatory hallucinations may experience salivation, sensation of thirst, or taste alterations. These hallucinations can be observed when the sylvian fissure that extends to the insula is stimulated electrically.³¹ Similar to olfactory hallucinations, gustatory hallucinations are associated with temporal lobe disease and parietal operculum lesions.^31,32 Sinus diseases have been associated with olfactory and gustatory hallucinations.³³ Brief gustatory hallucinations can be elicited with stimulation of the right rolandic operculum, parietal operculum, amygdala, hippocampus, medial temporal gyrus, and anterior part of right temporal gyrus.³⁴

Tactile hallucinations

These hallucinations may include perceptions of insects crawling over or under the skin (formication) or simulation of pressure on skin.³⁵ They have been associated with substance abuse, toxicity, or withdrawal.²⁸ Tactile hallucinations are characteristic of cocaine or amphetamine intoxication.³⁵

Tactile hallucinations are a rare symptom of schizophrenia. Heveling and colleagues reported a case of a woman, age 68, with chronic schizophrenia who experienced touching and being touched by a “shadow man” several times a day in addition to auditory and visual hallucinations.³⁶ Her symptoms disappeared after 4 weeks of antipsychotic and mood stabilizer therapy.

Tactile hallucinations have been associated with obsessive-compulsive disorder (OCD).³⁷ Fontenelle and colleagues suggested that OCD and psychotic disorders may share dysfunctional dopaminergic circuits.³⁷

Somatic hallucinations

Patients who have somatic hallucinations report perceptions of abnormal body sensations or physical experiences. For example, a patient may have sense of not having a stomach while eating.³⁵

This type of hallucination has been associated with activation of postcentral gyrus, parietal operculum, insula, and inferior parietal lobule on stereoelectroencephalography.³⁴ In a study of cerebral blood flow in 20 geriatric patients with delusional disorder, somatic type who were experiencing somatic hallucinations, positron emission testing scan demonstrated increased perfusion in somatic sensory processing regions, particularly the left postcentral gyrus and the right paracentral lobule.³⁸ Other researchers have linked somatic hallucinations with activation in the primary somatosensory and posterior parietal cortex, areas that normally mediate tactile perception.³⁹

Related Resource

• Teeple RC, Caplan JP, Stern TA. Visual hallucinations: differential diagnosis and treatment. Prim Care Companion J Clin Psychiatry. 2009;11(1):26-32.

Disclosures

Drs. Ali, Patel, Avenido, Bailey, and Jabeen report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Riley is on the board of directors for Vertex Pharmaceuticals.

Acknowledgment

The authors would like to thank Marwah Shahid, Research Associate, Vanderbilt University, Nashville, TN.

Not all patients who experience hallucinations have a psychotic disorder. Many physical and psychiatric disorders can manifest with hallucinations, and some patients have >1 disorder that could cause different types of hallucinations. To avoid providing unnecessary or ineffective treatments—and to ensure that patients receive proper care for nonpsychiatric conditions—it is important to accurately diagnose the disorder causing a patient’s hallucinations.

In this article we describe common features and psychiatric and nonpsychiatric causes of auditory, visual, olfactory, gustatory, tactile, and somatic hallucinations. Awareness of typical presentations of hallucinations associated with specific disorders can help narrow the diagnosis and provide appropriate treatment.

Auditory hallucinations

Also known as paracusia, auditory hallucinations are perceptions of sounds without identifiable external stimuli. This type of hallucination has various causes (Table 1).¹ A frequent symptom of schizophrenia, auditory hallucinations can cause substantial distress and functional disability.² Approximately 60% to 90% of patients with schizophrenia and up to 80% of those with affective psychoses experience auditory hallucinations.¹

Auditory hallucinations in psychosis usually are formed and complex.³ A common manifestation is hearing ≥1 voices. A patient might experience 2 voices talking about him in the third person. The voices may be perceived as coming from inside or outside the patient’s head. Some might hear their own thoughts spoken aloud. According to DSM-IV-TR, “hearing voices” is sufficient to diagnose schizophrenia if the hallucinations consist of a voice keeping up a running commentary on the person’s behavior or ≥2 voices conversing with each other.⁴ Auditory hallucinations also are seen in mood disorders but tend to be milder than their psychosis-induced counterparts.

Simple (unformed) auditory hallucinations—referred to as tinnitus—can be caused by disease of the middle ear (otosclerosis) or inner ear. These unformed hallucinations consist of buzzing or tones of varying pitch and timbre.¹

Partial seizures may cause auditory hallucinations. Perceptions of music have been associated with partial seizures.⁵ Curie and colleagues found that 17% of 514 patients with temporal lobe epilepsy had auditory hallucinations as a component of their seizures.⁶ These hallucinations typically are brief, stereotyped sensory impressions and, if formed, may be trivial sentences, previously heard phrases, or commands.

Alcoholic hallucinosis is a hallucinatory syndrome caused by alcohol withdrawal. These hallucinations usually are vocal and typically consist of accusatory, threatening, and/or critical voices directed at the patient.¹ Patients with alcohol hallucinosis also may experience musical auditory hallucinations.^7,8

CNS neoplasms can produce auditory hallucinations in 3% to 10% of patients.⁹ Hemorrhages and arteriovenous malformations in the pontine tegmentum and lower midbrain have been associated with acute onset of auditory hallucinations. The sounds typically are unformed mechanical or seashell-like noises or music.¹⁰

Patients with migraines rarely report auditory hallucinations. When they occur, they typically consist of perceived unilateral tinnitus, phonophobia, or hearing loss.

Table 1

Common causes of auditory hallucinations

Visual hallucinations

Visual hallucinations manifest as visual sensory perceptions in the absence of external stimuli.¹¹ These false perceptions may consist of formed images (eg, people) or unformed images (eg, flashes of light).¹² Visual hallucinations occur in numerous ophthalmologic, neurologic, medical, and psychiatric disorders (Table 2).¹³

DSM-IV-TR lists visual hallucinations as a primary diagnostic criterion for several psychotic disorders, including schizophrenia and schizoaffective disorder,⁴ and they occur in 16% to 72% of patients with these conditions.^14,15 Patients with major depressive disorder or bipolar disorder also may experience visual hallucinations. Visual hallucinations in those with schizophrenia tend to involve vivid scenes with family members, religious figures, and/or animals.¹⁶

Delirium is a transient, reversible cause of cerebral dysfunction that often presents with hallucinations. Several studies have shown that visual hallucinations are the most common type among patients with delirium. Webster and Holroyd found visual hallucinations in 27% of 227 delirium patients.¹⁷

Delirium tremens typically is accompanied by visual hallucinations. Visions of small animals and crawling insects are common.¹⁸ Hallucinations due to drug intoxication or withdrawal generally vary in duration from brief to continuous; such experiences often contribute to agitation.¹⁹

Migraines are a well-recognized cause of visual hallucinations. Up to 31% of those with migraines experience an aura, and nearly 99% of those with aura have visual symptoms.^20,21 The classic visual aura starts as an irregular colored crescent of light with multi-colored edges in the center of the visual field that gradually progresses toward the periphery, lasting <60 minutes. These simple visual hallucinations are most common; more complex hallucinations are seen more frequently in migraine coma and familial hemiplegic migraine.

Approximately 5% of patients with epilepsy have occipital seizures, which almost always have visual manifestations. Epileptic visual hallucinations often are simple, brief, stereotyped, and fragmentary. They usually consist of small, brightly colored spots or shapes that flash.²² Complex visual hallucinations in epilepsy are similar to hypnagogic hallucinations but are rare. Intracranial electroencephalography recordings have shown that pathological excitation of visual cortical areas may be responsible for complex visual hallucinations in epilepsy.¹⁹

Dementia with Lewy bodies (DLB) is associated with visual hallucinations.²³ Visual hallucinations occur in >20% of patients with DLB.²⁴ Patients with DLB may see complex scenarios of people and items that are not present. Visual hallucinations have an 83% positive predictive value for distinguishing DLB from dementia of the Alzheimer’s type.²⁵ There is a strong correlation between Lewy bodies located in the amygdala and parahippocampus and well-formed visual hallucinations.²⁶

Visual hallucinations are common in Parkinson’s disease and may occur in up to one-half of patients.²⁷ Patients with Parkinson’s disease may experience hallucinations similar to those observed in DLB, which can range from seeing a person or animal to more complex, formed, and mobile people, animals, or objects.

Table 2

Common causes of visual hallucinations

Olfactory hallucinations

Also known as phantosmia, olfactory hallucinations involve smelling odors that are not derived from any physical stimulus. They can occur with several psychiatric conditions, including schizophrenia, depression, bipolar disorder, eating disorders, and substance abuse.²⁸ Olfactory hallucinations caused by epileptic activity are rare. They constitute approximately 0.9% of all auras and typically are described as unpleasant. Tumors that affect the medial temporal lobe and mesial temporal sclerosis are associated with olfactory hallucinations.²⁹ Olfactory hallucinations also have been reported in patients with multi-infarct dementia, Alzheimer’s disease, and alcoholic psychosyndromes. In patients with schizophrenia, the smell may be perceived as coming from an external source, whereas patients with depression may perceive the source as internal.³⁰ Patients who perceive that they are the source of an offensive odor—a condition known as olfactory reference syndrome—may wash excessively, overuse deodorants and perfumes, or become socially withdrawn.³⁰

Gustatory hallucinations

Patients with gustatory hallucinations may experience salivation, sensation of thirst, or taste alterations. These hallucinations can be observed when the sylvian fissure that extends to the insula is stimulated electrically.³¹ Similar to olfactory hallucinations, gustatory hallucinations are associated with temporal lobe disease and parietal operculum lesions.^31,32 Sinus diseases have been associated with olfactory and gustatory hallucinations.³³ Brief gustatory hallucinations can be elicited with stimulation of the right rolandic operculum, parietal operculum, amygdala, hippocampus, medial temporal gyrus, and anterior part of right temporal gyrus.³⁴

Tactile hallucinations

These hallucinations may include perceptions of insects crawling over or under the skin (formication) or simulation of pressure on skin.³⁵ They have been associated with substance abuse, toxicity, or withdrawal.²⁸ Tactile hallucinations are characteristic of cocaine or amphetamine intoxication.³⁵

Tactile hallucinations are a rare symptom of schizophrenia. Heveling and colleagues reported a case of a woman, age 68, with chronic schizophrenia who experienced touching and being touched by a “shadow man” several times a day in addition to auditory and visual hallucinations.³⁶ Her symptoms disappeared after 4 weeks of antipsychotic and mood stabilizer therapy.

Tactile hallucinations have been associated with obsessive-compulsive disorder (OCD).³⁷ Fontenelle and colleagues suggested that OCD and psychotic disorders may share dysfunctional dopaminergic circuits.³⁷

Somatic hallucinations

Patients who have somatic hallucinations report perceptions of abnormal body sensations or physical experiences. For example, a patient may have sense of not having a stomach while eating.³⁵

This type of hallucination has been associated with activation of postcentral gyrus, parietal operculum, insula, and inferior parietal lobule on stereoelectroencephalography.³⁴ In a study of cerebral blood flow in 20 geriatric patients with delusional disorder, somatic type who were experiencing somatic hallucinations, positron emission testing scan demonstrated increased perfusion in somatic sensory processing regions, particularly the left postcentral gyrus and the right paracentral lobule.³⁸ Other researchers have linked somatic hallucinations with activation in the primary somatosensory and posterior parietal cortex, areas that normally mediate tactile perception.³⁹

Related Resource

• Teeple RC, Caplan JP, Stern TA. Visual hallucinations: differential diagnosis and treatment. Prim Care Companion J Clin Psychiatry. 2009;11(1):26-32.

Disclosures

Drs. Ali, Patel, Avenido, Bailey, and Jabeen report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Riley is on the board of directors for Vertex Pharmaceuticals.

Acknowledgment

The authors would like to thank Marwah Shahid, Research Associate, Vanderbilt University, Nashville, TN.

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. Z, age 61, is referred by his primary care clinician to the hospital’s medical service with increasing depressive symptoms and non-pruritic rash. He has a history of bipolar I disorder for >30 years. When the primary care physician evaluated Mr. Z, his vitals were normal, but blood work revealed mild anemia and thrombocytopenia of 34 x10³/μL, which prompted referral to the hospital. During admission, the psychiatric consultation service is called to evaluate Mr. Z’s depressive symptoms.

Mr. Z reports having chronic sleep problems and feeling cold and tired, shivering at times, but has no pain. He says he’s worried because he feels severely depressed, worthless, and hopeless, but denies suicidal ideation and psychosis. Mr. Z says he started experiencing increasingly depressed mood, anhedonia, insomnia, fatigue, poor appetite, and concentration 2 months ago. At that time his outpatient psychiatrist started Mr. Z on risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime because of emerging mood symptoms, after he was off medication for 7 months. Mr. Z attributed his worsened mood symptoms to being overwhelmed by several psychosocial stressors, including going through a complicated divorce, financial problems, and homelessness after being evicted from his apartment.

A review of Mr. Z’s psychiatric history reveals several remote hospitalizations—the last was 7 years ago—for escalated manic symptoms after he stopped taking his medication. He denies past suicide attempts. Mr. Z says he is compliant with his current medication regimen—risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime. He denies illicit drug use and says he drinks “a couple of beers, mostly on weekends.” Family history is positive for depression and bipolar II disorder.

His medical history is significant for hypothyroidism after goiter removal 6 years ago, for which he takes levothyroxine, 150 mcg/d, and a sports injury-related splenectomy in childhood. He reports no allergies. Vital signs at the time of admission are temperature, 99.1°F; pulse, 98 beats per minute; respiration, 16 breaths per minute; blood pressure, 123/73 mm/Hg; and oxygen saturation, 97%.

During the interview, Mr. Z presents with tired facies and exhibits psychomotor retardation. He has to force himself to stay engaged in the evaluation and maintain eye contact. His speech is clear, regular, and soft. Mr. Z says he is “very depressed”; his affect is constricted, almost flat, stable, and consistent with depressed mood. His thought process is linear and somewhat concrete and his thought content is notable for hopelessness, although Mr. Z continues to deny suicidal or homicidal ideations. No hallucinations or apparent delusions are noted. Insight and judgment are fair. Mr. Z understands his current mental state; however, he displays some lack of knowledge regarding his current hospitalization. Cognition is intact.

The authors’ observations

The differential diagnosis in patients presenting with mood changes is extensive (Table 1)¹ and in Mr. Z’s case includes several precipitating and perpetuating factors. Mr. Z presents with severe depressive symptoms and meets DSM-IV-TR criteria for a major depressive episode (MDE). This presentation is not typical of his bipolar I disorder because Mr. Z has never experienced an MDE and usually presents with escalating hypomanic/manic symptoms in the context of medication nonadherence. Nevertheless, Mr. Z has several risk factors for severe depression, including a family psychiatric history, multiple enduring social stressors and life crises, and medical conditions.

In the general population, the lifetime risk for developing depression is 8% to 17%.² The risk of developing a mood disorder increases significantly if a first-degree relative is diagnosed with a mood disorder; the relative risk is 10.3 for bipolar disorder and 3.2 for depression.³ Additionally, Mr. Z is going through a complicated divorce, has financial problems, and is homeless, all of which could trigger an MDE. Furthermore, hypothyroidism shares many symptoms of depression, including fatigue, lethargy, anhedonia, cold intolerance, and low mood; mental status changes frequently are the initial presentation of thyroid problems.⁴ Physicians started Mr. Z on a new medication regimen (risperidone and divalproex) to control mood instability, which coincided with symptom onset. Atypical antipsychotics have been reported to precipitate depressive symptoms; their side effect profile includes extrapyramidal effects, such as flat affect, which can be mistaken for depression.⁵ Rapid valproate titration can mimic neurovegetative symptoms of depression and cause dose-dependent thrombocytopenia and rash, which could explain his initial presentation.⁶ Finally, Mr. Z’s history of traumatic splenectomy, change in mental status, and thrombocytopenia suggest an infectious etiology.

Table 1

Differential diagnosis in patients presenting with mood changes

Possible infectious causes

The increased prevalence of immune suppression due to human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) or from therapeutic modalities such as cancer therapy or splenectomy has led to an increased number of chronic CNS infections, manifesting with an array of neuropsychiatric symptoms and nonspecific physiological reactions.^1,7 Mr. Z complains of a 2-month period of worsening depression that could suggest an infectious process with an insidious onset. Some infectious agents that can cause chronic CNS infection and encephalopathy are presented in Table 2.⁸ HIV, tuberculosis, syphilis, Lyme disease, and herpes simplex virus are becoming more prevalent and can present with neuropsychiatric symptoms.¹ For example, in addition to thrombocytopenia and low-grade fever, patients with HIV may exhibit a broad range of neuropsychiatric symptoms such as cognitive problems, impaired executive and motor functioning, sleep disturbance, and anxiety. These patients frequently present with low mood and neurovegetative symptoms of depression.⁷ Similarly, the same tick responsible for Lyme disease infection can transmit other infectious agents that can cause thrombocytopenia, including Babesia, Ehrlichia chaffeensis, Anaplasma phagocytophilum, and human Ewingii ehrlichiosis.

The authors’ observations

Diagnosis of a mood change, particularly an MDE, is clinical, based on careful psychiatric evaluation using standardized criteria rather than a specific lab test. However, some laboratory studies (Table 3)¹ are useful in differentiating medical illnesses that may present with depression. Mr. Z’s presentation warrants investigating these tests. His history of traumatic splenectomy and night sweats suggests an infection. The team’s initial recommendations include laboratory tests, discontinuing divalproex because it may be causing thrombocytopenia, and decreasing risperidone to 2 mg/d to improve his fatigue and possibly developed extrapyramidal symptoms.

Table 2

Potential infectious causes of chronic encephalopathy

Table 3

Differentiating medical illnesses that may mimic depression

TREATMENT: Cause revealed

Mr. Z develops a persistent fever of 102°F with continuous profuse sweating and a hypotensive episode. Blood work reveals mild anemia, thrombocytopenia, and increased coagulation parameters with high D-dimer and low fibrinogen, consistent with diagnosis of disseminated intravascular coagulation (DIC) secondary to infectious etiology. Thyroid and HIV tests are negative. After further evaluation, Mr. Z remembers that 4 months earlier he removed several ticks from his legs after hunting; he also remembers experiencing shivering and night sweats several weeks before he was hospitalized. His blood smear is positive for babesiosis and further testing confirms positive Lyme antibodies. Mr. Z is started on aggressive hemodynamic stabilization and a pathogen-tailored course of antibiotics for several weeks. This results in improvement and discharge home in a stable condition. His depression and fatigue improve but do not fully remit by the time he is discharged.

The authors’ observations

Lyme disease is one of the fastest-growing infectious diseases in the United States.⁹ The prevalence of positive Lyme antibodies is 30% higher in psychiatric populations than the general population.¹⁰ Lyme disease is transmitted by deer tick bite, often undetected, that is infected with spirochete Borrelia burgdorferi. To be infectious, ticks need to be attached to the skin for 24 to 48 hours,^11,12 although individual cases have reported transmission in <24 hours. The clinical manifestations of Lyme disease can be divided into 3 phases:

• early localized phase, characterized by the distinctive skin lesion erythema migrans with or without constitutional symptoms
• early disseminated phase, characterized by multiple erythema migrans lesions and neurologic and/or cardiac findings
• late or chronic disease associated with intermittent/persistent arthritis and/or neurologic problems.^11,13

The clinical features of each stage frequently overlap and some patients in a later stage of Lyme disease do not have prior signs or symptoms of the disease. Because it is a multisystem disease, Lyme disease can attack the CNS in the form of neuroborreliosis, a clinical diagnosis, without involving other systems, and its neuropsychiatric manifestations can resemble neurosyphilis because both organisms are spirochetes.^11,13,14 CNS disorders have been found in up to 40% of Lyme disease cases.¹¹ In neuroborreliosis, cognitive problems usually predominate; however, neuroborreliosis can mimic multiple brain diseases presenting with various neurologic and psychiatric symptoms (Table 4)^14,15 and can present at any time after the tick bite. Furthermore neuroborreliosis is difficult to diagnose because symptoms may remain dormant and emerge after several years.^11,13,14Borrelia burgdorferi is challenging to isolate and grow in the lab, and enzyme-linked immunosorbent assay (ELISA) testing for antibodies is highly specific but not very sensitive,¹⁶ frequently giving false negative results. Western blot confirms the diagnosis.

Table 4

Late-stage neuropsychiatric symptoms of Lyme disease

Mr. Z’s presentation also reflects co-infection with babesiosis. Babesia is malaria-like protozoa diagnosed by blood smear that can cause a fatal illness in immuno-compromised patients. The clinical picture varies from mild symptoms such as night sweats, chills, arthralgias, and anorexia with thrombocytopenia to severe and potentially fatal outcomes in immunocompromised patients, including DIC, acute renal failure, sepsis, congestive heart failure, and myocardial infarction.¹¹ Risk factors for the severest forms of babesiosis are age >50, co-infection with Lyme disease, and splenectomy,¹¹ all of which were present in Mr. Z. Co-infected patients experience fatigue, headache, anorexia, and emotional lability more frequently than those with Lyme disease alone.¹²

Treatment options

Treatment of Lyme disease/neuroborreliosis is complex. The mainstay approach is antibiotics. Despite adequate treatment, many patients experience continued impairment, including chronic pain, fatigue, and cognitive and psychiatric symptoms.^11,14 There is some evidence Borrelia burgdorferi can persist and re-emerge after adequate treatment.^14,17 The National Institute of Health sponsored several clinical trials of prolonged antibiotic treatment for chronic Lyme disease. Some results suggested improvement in fatigue and cognitive function, although these results were not sustained.¹⁸

There is a strong link between mental illness and increased prevalence of positive Lyme disease antibodies.¹⁰ Several studies report increased risk of infection during psychological stress that may be related to an altered immune system response.¹⁹ Evidence suggests that Borrelia burgdorferi can alter immune system response, making T cells more reactive not only to Borrelia burgdorferi antigens but also to host antigens,²⁰ creating autoimmune inflammatory reactions that could explain chronic neuropsychiatric symptoms. It appears Lyme disease antigens can mimic certain autoantigens (for example, in the thyroid gland).²¹ Whether there is a role for autoimmune therapy in treating chronic symptoms needs to be investigated.

Once Lyme disease is diagnosed, educating patients and families becomes an important part of treatment because many patients report feeling stigmatized by the diagnosis. Referral to a Lyme disease support group may be beneficial. Patients with neuropsychiatric symptoms that persist after antibiotic treatment should be offered symptom-based treatment, including medications and therapy.

Related Resource

• Centers for Disease Control and Prevention. Lyme disease: Resources for clinicians. www.cdc.gov/lyme/healthcare/clinicians.html.

Drug Brand Names

• Divalproex sodium • Depakote
• Levothyroxine • Levoxyl, Synthroid
• 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.

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. Z, age 61, is referred by his primary care clinician to the hospital’s medical service with increasing depressive symptoms and non-pruritic rash. He has a history of bipolar I disorder for >30 years. When the primary care physician evaluated Mr. Z, his vitals were normal, but blood work revealed mild anemia and thrombocytopenia of 34 x10³/μL, which prompted referral to the hospital. During admission, the psychiatric consultation service is called to evaluate Mr. Z’s depressive symptoms.

Mr. Z reports having chronic sleep problems and feeling cold and tired, shivering at times, but has no pain. He says he’s worried because he feels severely depressed, worthless, and hopeless, but denies suicidal ideation and psychosis. Mr. Z says he started experiencing increasingly depressed mood, anhedonia, insomnia, fatigue, poor appetite, and concentration 2 months ago. At that time his outpatient psychiatrist started Mr. Z on risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime because of emerging mood symptoms, after he was off medication for 7 months. Mr. Z attributed his worsened mood symptoms to being overwhelmed by several psychosocial stressors, including going through a complicated divorce, financial problems, and homelessness after being evicted from his apartment.

A review of Mr. Z’s psychiatric history reveals several remote hospitalizations—the last was 7 years ago—for escalated manic symptoms after he stopped taking his medication. He denies past suicide attempts. Mr. Z says he is compliant with his current medication regimen—risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime. He denies illicit drug use and says he drinks “a couple of beers, mostly on weekends.” Family history is positive for depression and bipolar II disorder.

His medical history is significant for hypothyroidism after goiter removal 6 years ago, for which he takes levothyroxine, 150 mcg/d, and a sports injury-related splenectomy in childhood. He reports no allergies. Vital signs at the time of admission are temperature, 99.1°F; pulse, 98 beats per minute; respiration, 16 breaths per minute; blood pressure, 123/73 mm/Hg; and oxygen saturation, 97%.

During the interview, Mr. Z presents with tired facies and exhibits psychomotor retardation. He has to force himself to stay engaged in the evaluation and maintain eye contact. His speech is clear, regular, and soft. Mr. Z says he is “very depressed”; his affect is constricted, almost flat, stable, and consistent with depressed mood. His thought process is linear and somewhat concrete and his thought content is notable for hopelessness, although Mr. Z continues to deny suicidal or homicidal ideations. No hallucinations or apparent delusions are noted. Insight and judgment are fair. Mr. Z understands his current mental state; however, he displays some lack of knowledge regarding his current hospitalization. Cognition is intact.

The authors’ observations

The differential diagnosis in patients presenting with mood changes is extensive (Table 1)¹ and in Mr. Z’s case includes several precipitating and perpetuating factors. Mr. Z presents with severe depressive symptoms and meets DSM-IV-TR criteria for a major depressive episode (MDE). This presentation is not typical of his bipolar I disorder because Mr. Z has never experienced an MDE and usually presents with escalating hypomanic/manic symptoms in the context of medication nonadherence. Nevertheless, Mr. Z has several risk factors for severe depression, including a family psychiatric history, multiple enduring social stressors and life crises, and medical conditions.

In the general population, the lifetime risk for developing depression is 8% to 17%.² The risk of developing a mood disorder increases significantly if a first-degree relative is diagnosed with a mood disorder; the relative risk is 10.3 for bipolar disorder and 3.2 for depression.³ Additionally, Mr. Z is going through a complicated divorce, has financial problems, and is homeless, all of which could trigger an MDE. Furthermore, hypothyroidism shares many symptoms of depression, including fatigue, lethargy, anhedonia, cold intolerance, and low mood; mental status changes frequently are the initial presentation of thyroid problems.⁴ Physicians started Mr. Z on a new medication regimen (risperidone and divalproex) to control mood instability, which coincided with symptom onset. Atypical antipsychotics have been reported to precipitate depressive symptoms; their side effect profile includes extrapyramidal effects, such as flat affect, which can be mistaken for depression.⁵ Rapid valproate titration can mimic neurovegetative symptoms of depression and cause dose-dependent thrombocytopenia and rash, which could explain his initial presentation.⁶ Finally, Mr. Z’s history of traumatic splenectomy, change in mental status, and thrombocytopenia suggest an infectious etiology.

Table 1

Differential diagnosis in patients presenting with mood changes

Possible infectious causes

The increased prevalence of immune suppression due to human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) or from therapeutic modalities such as cancer therapy or splenectomy has led to an increased number of chronic CNS infections, manifesting with an array of neuropsychiatric symptoms and nonspecific physiological reactions.^1,7 Mr. Z complains of a 2-month period of worsening depression that could suggest an infectious process with an insidious onset. Some infectious agents that can cause chronic CNS infection and encephalopathy are presented in Table 2.⁸ HIV, tuberculosis, syphilis, Lyme disease, and herpes simplex virus are becoming more prevalent and can present with neuropsychiatric symptoms.¹ For example, in addition to thrombocytopenia and low-grade fever, patients with HIV may exhibit a broad range of neuropsychiatric symptoms such as cognitive problems, impaired executive and motor functioning, sleep disturbance, and anxiety. These patients frequently present with low mood and neurovegetative symptoms of depression.⁷ Similarly, the same tick responsible for Lyme disease infection can transmit other infectious agents that can cause thrombocytopenia, including Babesia, Ehrlichia chaffeensis, Anaplasma phagocytophilum, and human Ewingii ehrlichiosis.

The authors’ observations

Diagnosis of a mood change, particularly an MDE, is clinical, based on careful psychiatric evaluation using standardized criteria rather than a specific lab test. However, some laboratory studies (Table 3)¹ are useful in differentiating medical illnesses that may present with depression. Mr. Z’s presentation warrants investigating these tests. His history of traumatic splenectomy and night sweats suggests an infection. The team’s initial recommendations include laboratory tests, discontinuing divalproex because it may be causing thrombocytopenia, and decreasing risperidone to 2 mg/d to improve his fatigue and possibly developed extrapyramidal symptoms.

Table 2

Potential infectious causes of chronic encephalopathy

Table 3

Differentiating medical illnesses that may mimic depression

TREATMENT: Cause revealed

Mr. Z develops a persistent fever of 102°F with continuous profuse sweating and a hypotensive episode. Blood work reveals mild anemia, thrombocytopenia, and increased coagulation parameters with high D-dimer and low fibrinogen, consistent with diagnosis of disseminated intravascular coagulation (DIC) secondary to infectious etiology. Thyroid and HIV tests are negative. After further evaluation, Mr. Z remembers that 4 months earlier he removed several ticks from his legs after hunting; he also remembers experiencing shivering and night sweats several weeks before he was hospitalized. His blood smear is positive for babesiosis and further testing confirms positive Lyme antibodies. Mr. Z is started on aggressive hemodynamic stabilization and a pathogen-tailored course of antibiotics for several weeks. This results in improvement and discharge home in a stable condition. His depression and fatigue improve but do not fully remit by the time he is discharged.

The authors’ observations

Lyme disease is one of the fastest-growing infectious diseases in the United States.⁹ The prevalence of positive Lyme antibodies is 30% higher in psychiatric populations than the general population.¹⁰ Lyme disease is transmitted by deer tick bite, often undetected, that is infected with spirochete Borrelia burgdorferi. To be infectious, ticks need to be attached to the skin for 24 to 48 hours,^11,12 although individual cases have reported transmission in <24 hours. The clinical manifestations of Lyme disease can be divided into 3 phases:

• early localized phase, characterized by the distinctive skin lesion erythema migrans with or without constitutional symptoms
• early disseminated phase, characterized by multiple erythema migrans lesions and neurologic and/or cardiac findings
• late or chronic disease associated with intermittent/persistent arthritis and/or neurologic problems.^11,13

The clinical features of each stage frequently overlap and some patients in a later stage of Lyme disease do not have prior signs or symptoms of the disease. Because it is a multisystem disease, Lyme disease can attack the CNS in the form of neuroborreliosis, a clinical diagnosis, without involving other systems, and its neuropsychiatric manifestations can resemble neurosyphilis because both organisms are spirochetes.^11,13,14 CNS disorders have been found in up to 40% of Lyme disease cases.¹¹ In neuroborreliosis, cognitive problems usually predominate; however, neuroborreliosis can mimic multiple brain diseases presenting with various neurologic and psychiatric symptoms (Table 4)^14,15 and can present at any time after the tick bite. Furthermore neuroborreliosis is difficult to diagnose because symptoms may remain dormant and emerge after several years.^11,13,14Borrelia burgdorferi is challenging to isolate and grow in the lab, and enzyme-linked immunosorbent assay (ELISA) testing for antibodies is highly specific but not very sensitive,¹⁶ frequently giving false negative results. Western blot confirms the diagnosis.

Table 4

Late-stage neuropsychiatric symptoms of Lyme disease

Mr. Z’s presentation also reflects co-infection with babesiosis. Babesia is malaria-like protozoa diagnosed by blood smear that can cause a fatal illness in immuno-compromised patients. The clinical picture varies from mild symptoms such as night sweats, chills, arthralgias, and anorexia with thrombocytopenia to severe and potentially fatal outcomes in immunocompromised patients, including DIC, acute renal failure, sepsis, congestive heart failure, and myocardial infarction.¹¹ Risk factors for the severest forms of babesiosis are age >50, co-infection with Lyme disease, and splenectomy,¹¹ all of which were present in Mr. Z. Co-infected patients experience fatigue, headache, anorexia, and emotional lability more frequently than those with Lyme disease alone.¹²

Treatment options

Treatment of Lyme disease/neuroborreliosis is complex. The mainstay approach is antibiotics. Despite adequate treatment, many patients experience continued impairment, including chronic pain, fatigue, and cognitive and psychiatric symptoms.^11,14 There is some evidence Borrelia burgdorferi can persist and re-emerge after adequate treatment.^14,17 The National Institute of Health sponsored several clinical trials of prolonged antibiotic treatment for chronic Lyme disease. Some results suggested improvement in fatigue and cognitive function, although these results were not sustained.¹⁸

There is a strong link between mental illness and increased prevalence of positive Lyme disease antibodies.¹⁰ Several studies report increased risk of infection during psychological stress that may be related to an altered immune system response.¹⁹ Evidence suggests that Borrelia burgdorferi can alter immune system response, making T cells more reactive not only to Borrelia burgdorferi antigens but also to host antigens,²⁰ creating autoimmune inflammatory reactions that could explain chronic neuropsychiatric symptoms. It appears Lyme disease antigens can mimic certain autoantigens (for example, in the thyroid gland).²¹ Whether there is a role for autoimmune therapy in treating chronic symptoms needs to be investigated.

Once Lyme disease is diagnosed, educating patients and families becomes an important part of treatment because many patients report feeling stigmatized by the diagnosis. Referral to a Lyme disease support group may be beneficial. Patients with neuropsychiatric symptoms that persist after antibiotic treatment should be offered symptom-based treatment, including medications and therapy.

Related Resource

• Centers for Disease Control and Prevention. Lyme disease: Resources for clinicians. www.cdc.gov/lyme/healthcare/clinicians.html.

Drug Brand Names

• Divalproex sodium • Depakote
• Levothyroxine • Levoxyl, Synthroid
• 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.

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. Z, age 61, is referred by his primary care clinician to the hospital’s medical service with increasing depressive symptoms and non-pruritic rash. He has a history of bipolar I disorder for >30 years. When the primary care physician evaluated Mr. Z, his vitals were normal, but blood work revealed mild anemia and thrombocytopenia of 34 x10³/μL, which prompted referral to the hospital. During admission, the psychiatric consultation service is called to evaluate Mr. Z’s depressive symptoms.

Mr. Z reports having chronic sleep problems and feeling cold and tired, shivering at times, but has no pain. He says he’s worried because he feels severely depressed, worthless, and hopeless, but denies suicidal ideation and psychosis. Mr. Z says he started experiencing increasingly depressed mood, anhedonia, insomnia, fatigue, poor appetite, and concentration 2 months ago. At that time his outpatient psychiatrist started Mr. Z on risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime because of emerging mood symptoms, after he was off medication for 7 months. Mr. Z attributed his worsened mood symptoms to being overwhelmed by several psychosocial stressors, including going through a complicated divorce, financial problems, and homelessness after being evicted from his apartment.

A review of Mr. Z’s psychiatric history reveals several remote hospitalizations—the last was 7 years ago—for escalated manic symptoms after he stopped taking his medication. He denies past suicide attempts. Mr. Z says he is compliant with his current medication regimen—risperidone, 6 mg/d, and divalproex, 1,500 mg at bedtime. He denies illicit drug use and says he drinks “a couple of beers, mostly on weekends.” Family history is positive for depression and bipolar II disorder.

His medical history is significant for hypothyroidism after goiter removal 6 years ago, for which he takes levothyroxine, 150 mcg/d, and a sports injury-related splenectomy in childhood. He reports no allergies. Vital signs at the time of admission are temperature, 99.1°F; pulse, 98 beats per minute; respiration, 16 breaths per minute; blood pressure, 123/73 mm/Hg; and oxygen saturation, 97%.

During the interview, Mr. Z presents with tired facies and exhibits psychomotor retardation. He has to force himself to stay engaged in the evaluation and maintain eye contact. His speech is clear, regular, and soft. Mr. Z says he is “very depressed”; his affect is constricted, almost flat, stable, and consistent with depressed mood. His thought process is linear and somewhat concrete and his thought content is notable for hopelessness, although Mr. Z continues to deny suicidal or homicidal ideations. No hallucinations or apparent delusions are noted. Insight and judgment are fair. Mr. Z understands his current mental state; however, he displays some lack of knowledge regarding his current hospitalization. Cognition is intact.

The authors’ observations

The differential diagnosis in patients presenting with mood changes is extensive (Table 1)¹ and in Mr. Z’s case includes several precipitating and perpetuating factors. Mr. Z presents with severe depressive symptoms and meets DSM-IV-TR criteria for a major depressive episode (MDE). This presentation is not typical of his bipolar I disorder because Mr. Z has never experienced an MDE and usually presents with escalating hypomanic/manic symptoms in the context of medication nonadherence. Nevertheless, Mr. Z has several risk factors for severe depression, including a family psychiatric history, multiple enduring social stressors and life crises, and medical conditions.

In the general population, the lifetime risk for developing depression is 8% to 17%.² The risk of developing a mood disorder increases significantly if a first-degree relative is diagnosed with a mood disorder; the relative risk is 10.3 for bipolar disorder and 3.2 for depression.³ Additionally, Mr. Z is going through a complicated divorce, has financial problems, and is homeless, all of which could trigger an MDE. Furthermore, hypothyroidism shares many symptoms of depression, including fatigue, lethargy, anhedonia, cold intolerance, and low mood; mental status changes frequently are the initial presentation of thyroid problems.⁴ Physicians started Mr. Z on a new medication regimen (risperidone and divalproex) to control mood instability, which coincided with symptom onset. Atypical antipsychotics have been reported to precipitate depressive symptoms; their side effect profile includes extrapyramidal effects, such as flat affect, which can be mistaken for depression.⁵ Rapid valproate titration can mimic neurovegetative symptoms of depression and cause dose-dependent thrombocytopenia and rash, which could explain his initial presentation.⁶ Finally, Mr. Z’s history of traumatic splenectomy, change in mental status, and thrombocytopenia suggest an infectious etiology.

Table 1

Differential diagnosis in patients presenting with mood changes

Possible infectious causes

The increased prevalence of immune suppression due to human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) or from therapeutic modalities such as cancer therapy or splenectomy has led to an increased number of chronic CNS infections, manifesting with an array of neuropsychiatric symptoms and nonspecific physiological reactions.^1,7 Mr. Z complains of a 2-month period of worsening depression that could suggest an infectious process with an insidious onset. Some infectious agents that can cause chronic CNS infection and encephalopathy are presented in Table 2.⁸ HIV, tuberculosis, syphilis, Lyme disease, and herpes simplex virus are becoming more prevalent and can present with neuropsychiatric symptoms.¹ For example, in addition to thrombocytopenia and low-grade fever, patients with HIV may exhibit a broad range of neuropsychiatric symptoms such as cognitive problems, impaired executive and motor functioning, sleep disturbance, and anxiety. These patients frequently present with low mood and neurovegetative symptoms of depression.⁷ Similarly, the same tick responsible for Lyme disease infection can transmit other infectious agents that can cause thrombocytopenia, including Babesia, Ehrlichia chaffeensis, Anaplasma phagocytophilum, and human Ewingii ehrlichiosis.

The authors’ observations

Diagnosis of a mood change, particularly an MDE, is clinical, based on careful psychiatric evaluation using standardized criteria rather than a specific lab test. However, some laboratory studies (Table 3)¹ are useful in differentiating medical illnesses that may present with depression. Mr. Z’s presentation warrants investigating these tests. His history of traumatic splenectomy and night sweats suggests an infection. The team’s initial recommendations include laboratory tests, discontinuing divalproex because it may be causing thrombocytopenia, and decreasing risperidone to 2 mg/d to improve his fatigue and possibly developed extrapyramidal symptoms.

Table 2

Potential infectious causes of chronic encephalopathy

Table 3

Differentiating medical illnesses that may mimic depression

TREATMENT: Cause revealed

Mr. Z develops a persistent fever of 102°F with continuous profuse sweating and a hypotensive episode. Blood work reveals mild anemia, thrombocytopenia, and increased coagulation parameters with high D-dimer and low fibrinogen, consistent with diagnosis of disseminated intravascular coagulation (DIC) secondary to infectious etiology. Thyroid and HIV tests are negative. After further evaluation, Mr. Z remembers that 4 months earlier he removed several ticks from his legs after hunting; he also remembers experiencing shivering and night sweats several weeks before he was hospitalized. His blood smear is positive for babesiosis and further testing confirms positive Lyme antibodies. Mr. Z is started on aggressive hemodynamic stabilization and a pathogen-tailored course of antibiotics for several weeks. This results in improvement and discharge home in a stable condition. His depression and fatigue improve but do not fully remit by the time he is discharged.

The authors’ observations

Lyme disease is one of the fastest-growing infectious diseases in the United States.⁹ The prevalence of positive Lyme antibodies is 30% higher in psychiatric populations than the general population.¹⁰ Lyme disease is transmitted by deer tick bite, often undetected, that is infected with spirochete Borrelia burgdorferi. To be infectious, ticks need to be attached to the skin for 24 to 48 hours,^11,12 although individual cases have reported transmission in <24 hours. The clinical manifestations of Lyme disease can be divided into 3 phases:

• early localized phase, characterized by the distinctive skin lesion erythema migrans with or without constitutional symptoms
• early disseminated phase, characterized by multiple erythema migrans lesions and neurologic and/or cardiac findings
• late or chronic disease associated with intermittent/persistent arthritis and/or neurologic problems.^11,13

The clinical features of each stage frequently overlap and some patients in a later stage of Lyme disease do not have prior signs or symptoms of the disease. Because it is a multisystem disease, Lyme disease can attack the CNS in the form of neuroborreliosis, a clinical diagnosis, without involving other systems, and its neuropsychiatric manifestations can resemble neurosyphilis because both organisms are spirochetes.^11,13,14 CNS disorders have been found in up to 40% of Lyme disease cases.¹¹ In neuroborreliosis, cognitive problems usually predominate; however, neuroborreliosis can mimic multiple brain diseases presenting with various neurologic and psychiatric symptoms (Table 4)^14,15 and can present at any time after the tick bite. Furthermore neuroborreliosis is difficult to diagnose because symptoms may remain dormant and emerge after several years.^11,13,14Borrelia burgdorferi is challenging to isolate and grow in the lab, and enzyme-linked immunosorbent assay (ELISA) testing for antibodies is highly specific but not very sensitive,¹⁶ frequently giving false negative results. Western blot confirms the diagnosis.

Table 4

Late-stage neuropsychiatric symptoms of Lyme disease

Mr. Z’s presentation also reflects co-infection with babesiosis. Babesia is malaria-like protozoa diagnosed by blood smear that can cause a fatal illness in immuno-compromised patients. The clinical picture varies from mild symptoms such as night sweats, chills, arthralgias, and anorexia with thrombocytopenia to severe and potentially fatal outcomes in immunocompromised patients, including DIC, acute renal failure, sepsis, congestive heart failure, and myocardial infarction.¹¹ Risk factors for the severest forms of babesiosis are age >50, co-infection with Lyme disease, and splenectomy,¹¹ all of which were present in Mr. Z. Co-infected patients experience fatigue, headache, anorexia, and emotional lability more frequently than those with Lyme disease alone.¹²

Treatment options

Treatment of Lyme disease/neuroborreliosis is complex. The mainstay approach is antibiotics. Despite adequate treatment, many patients experience continued impairment, including chronic pain, fatigue, and cognitive and psychiatric symptoms.^11,14 There is some evidence Borrelia burgdorferi can persist and re-emerge after adequate treatment.^14,17 The National Institute of Health sponsored several clinical trials of prolonged antibiotic treatment for chronic Lyme disease. Some results suggested improvement in fatigue and cognitive function, although these results were not sustained.¹⁸

There is a strong link between mental illness and increased prevalence of positive Lyme disease antibodies.¹⁰ Several studies report increased risk of infection during psychological stress that may be related to an altered immune system response.¹⁹ Evidence suggests that Borrelia burgdorferi can alter immune system response, making T cells more reactive not only to Borrelia burgdorferi antigens but also to host antigens,²⁰ creating autoimmune inflammatory reactions that could explain chronic neuropsychiatric symptoms. It appears Lyme disease antigens can mimic certain autoantigens (for example, in the thyroid gland).²¹ Whether there is a role for autoimmune therapy in treating chronic symptoms needs to be investigated.

Once Lyme disease is diagnosed, educating patients and families becomes an important part of treatment because many patients report feeling stigmatized by the diagnosis. Referral to a Lyme disease support group may be beneficial. Patients with neuropsychiatric symptoms that persist after antibiotic treatment should be offered symptom-based treatment, including medications and therapy.

Related Resource

• Centers for Disease Control and Prevention. Lyme disease: Resources for clinicians. www.cdc.gov/lyme/healthcare/clinicians.html.

Drug Brand Names

• Divalproex sodium • Depakote
• Levothyroxine • Levoxyl, Synthroid
• 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.

Discuss this article at www.facebook.com/CurrentPsychiatry

Patients with bipolar disorder (BD) have a high risk for suicidal ideation, suicide attempts, and suicide.^1-3 Approximately 25% to 50% of BD patients attempt suicide at least once, and their attempts often are lethal—the ratio of attempts to completed suicides in BD patients is 3:1, compared with 30:1 in the general population.⁴ Lithium has been shown to effectively stabilize BD patients’ mood and significantly reduce the rates of suicide attempts and completed suicides,^5-9 but does not reduce BD patients’ long-term suicide risk to that of the general population.

Literature on psychotherapeutic treatments for patients with BD primarily focuses on improving patients’ adherence to pharmacotherapy and achieving faster recovery and remission.¹⁰ Nonpharmacologic treatments for patients with BD include psychoeducation, family-focused psychoeducation, cognitive therapy, and interpersonal and social rhythm therapy (Table 1).¹¹ Literature on nonpharmacologic treatments to address suicidality in BD patients is limited,^12,13 and additional psychotherapeutic interventions to reduce suicide risk in BD patients are needed.¹⁴

In this article, I describe a novel psychotherapeutic intervention I use that integrates cognitive therapy principles with ideas derived from the psychosynthesis model.^15,16 It consists of teaching patients to “disidentify” from suicidal thoughts, followed by a guided-imagery exercise in which patients experience a future positive life event with all 5 senses and internalize this experience. This creates a “hook into the future” that changes the present to match the future event and acts as an antidote to suicidal thoughts. I have used this strategy successfully in many patients as an adjunct to pharmacotherapy.

Table 1

Nonpharmacologic interventions for bipolar disorder

A theoretical model

Roberto Assagioli, who established the approach to psychology called psychosynthesis, formulated a fundamental psychological principle in controlling one’s behavior: “We are dominated by everything with which our self becomes identified. We can dominate and control everything from which we disidentify ourselves.”¹⁵ According to the psychosynthesis model, it is easier to change thoughts we identify as foreign to “the self” (ego-dystonic) than thoughts we identify as being part of “the self” (ego-syntonic).

Patients whose suicidal thoughts are ego-syntonic identify with the thoughts as representing themselves and take ownership of these thoughts. Such patients are at a greater risk of acting on suicidal thoughts.

Patients whose suicidal thoughts are ego-dystonic consider the suicidal thoughts foreign to their core self and do not believe such thoughts represent them. In essence, they “disown” the thoughts and typically want to control and eliminate them. Examples of patients’ ego-syntonic vs ego-dystonic suicidal thoughts are listed in Table 2.

This construct calls for an intervention to help patients who have ego-syntonic suicidal thoughts restructure them as a manifestation of BD, rather then the patient’s core self belief. The intervention emphasizes the patient is not “a suicidal patient” but suffers from an illness that may manifest with suicidal ideation. Many BD patients overly identify with their disease, stating, “I am bipolar” or “I am suicidal.” The “I am” statement originates from the verb “to be,” which implies the disease is part of the patient’s identity. The goal of this intervention is to help the patient learn to disidentify from the disease and decide that suicidal thoughts do not represent their core self, but are a manifestation of the underlying disease.

The psychosynthesis model of helping patients disidentify and therefore disown suicidal thoughts is compatible with interventions that use mindfulness-based cognitive therapy training to teach patients to experience their thoughts as just passing through their consciousness without taking ownership of them.¹⁷

Table 2

Examples of ego-syntonic vs ego-dystonic suicidal thoughts

The intervention

Assessment of suicidality is a fundamental skill for every mental health clinician.¹⁸ The psychotherapeutic intervention I use integrates the cognitive therapy principles of reframing, relabeling, and restructuring patients’ thoughts with disidentification from dysfunctional thoughts, feelings, and desires, based on psychosynthesis principles.

First, I conduct a comprehensive mental status examination that includes an in-depth exploration of the patient’s suicidal thoughts to determine if they are ego-syntonic or ego-dystonic. I begin by asking patients to clarify and elaborate on their statements referring to suicide, asking questions such as “Is there a part of you that objects to these thoughts?” and “Is there a part of you that wants to live?” If a patient indicates that he or she does experience inner conflict regarding such thoughts, these thoughts are classified as ego-dystonic. If a patient does not have any counter thoughts regarding the suicidal thoughts and fully identifies with them, the thoughts are classified as ego-syntonic.

I follow this with a treatment plan that helps patients change their view of their suicidal thoughts. I ask the patient to change these suicidal thoughts to ego-dystonic by focusing on the following statement: “I, (patient’s name), am a human being and like all human beings, I have thoughts; however, I am not my thoughts, I am much more than that.” I ask my patient to read this out loud and to mindfully meditate on this statement several times a day to reinforce the new understanding that these suicidal thoughts are a manifestation of the chemical imbalance of the mood disorder, and do not represent the patient as a person.

This intervention is paired with a future-focused internalized imagery experience I have described in previous articles.^19,20 In this part of the treatment, the patient and I discuss a specific expected life milestone that is positive and for which he or she would want to be present (eg, children graduating from high school or college, a wedding, birth of a child/grandchild, etc.). Using guided imagery, the patient experiences this event with all 5 senses during the session. I instruct the patient to internalize the experience and bring it back from the future to the present. This creates a “hook into the future” that is coupled with this desired milestone event in the patient’s life.

The following 3 case studies provide examples of the application of this treatment intervention.

CASE 1: Disidentifying family history

Mrs. G, a 42-year-old mother of 2, suffers from bipolar II disorder with recurrent episodes of depression associated with ego-syntonic suicidal thoughts. She states that at times she feels she is a burden to her husband and children and believes they may be better off without her. She says she believes “ending it all” must be her destiny. After further investigation, I learn Mrs. G has a family history of BD and 3 relatives have committed suicide. This family history may partially explain her belief that suicide must be “in her genes.”

I discuss with Mrs. G the strategy of changing her thoughts. I tell her to write in her journal—which she brings to her sessions—the following statements: “I am a human being. I am an adult woman and mother of 2 children. I know I have thoughts but I am not my thoughts, I am much more than that. I know I have genes but I am not my genes, I am much more than that. I know I have feelings, but I am not my feelings, I am much more than that. I know I have cousins, uncles, aunts, and other relatives but I am not my relatives. I am uniquely myself, different from the others.”

I ask Mrs. G to read these statements out loud and repeat them several times a day to reinforce this new way of perceiving the suicidal thoughts and to disidentify from the thoughts and her family history as it relates to suicide.

Mrs. G and I talk about the future and expected family milestones. When I ask if her son would want her to be present at his college graduation, she says yes. We then discuss in detail the date, time of day, and location of this event, followed by a guided imagery exercise focused on the graduation. She is guided to experience this event with all 5 senses and describes the event in detail, including the expression on the faces of her husband and children, their voices, and the scent of their aftershave lotion. She hears her son saying, “Mom, I love you. Thank you for being there with me all these years. I could not have done it without you.” I ask Mrs. G to internalize these experiences and carve them into her memory. She is instructed to come back from this future-focused guided imagery experience. When her eyes open, she looks at me and describes her experience in great detail, at times using the past tense, which confirms that the future-focused event was internalized.

In her next session, Mrs. G reports an improvement in her sleep and a change in her suicidal thoughts, which now are only fleeting.

CASE 2: Experiencing graduation

Ms. J, age 17, was diagnosed with bipolar I disorder when she was 15. She has a family history of BD in her mother, 2 maternal aunts, her grandmother, and an older sister. All these women have a history of suicidal thoughts and suicide attempts requiring hospital treatment, but no completed suicides.

Ms. J has been taking an adequate combination of mood stabilizers. She has recovered from 2 previous depressive episodes and is experiencing a third relapse with suicidal thoughts. At times, she experiences these thoughts as ego-syntonic; at other times, they are ego-dystonic.

I first educate her about the nature of BD, explaining that her suicidal thoughts are a manifestation of a chemical imbalance in her brain as a result of the depressive relapse. I teach her to use guided imagery to focus on her favorite place of peace and serenity, the beach, which produces immediate relief of the intense anxiety she felt.

After we complete the disidentification exercise, I ask her to focus on her high school graduation ceremony, which is scheduled to take place in 1 year. In a state of guided imagery, she experiences her graduation from high school with all 5 senses. As she returns to a state of full alertness with her eyes open, she describes the graduation ceremony experience in detail using the past tense, as if it had already occurred, thereby creating her own hook into the future. I instruct her to write about this experience in her journal and bring it with her to the next session.

The following session, Ms. J reports that her suicide ideations have “disappeared.” She says this was accompanied by improvements in her overall mood and sleep.

CASE 3: Internalizing the future

Mr. C, a 38-year-old married father of 4 children, has bipolar II disorder and is in a depressed state. He has been treated with optimal doses of mood stabilizers and atypical antipsychotics but continues to have suicidal thoughts. These thoughts are at times ego-syntonic; he says, “My family would be better off without me.” When Mr. C’s mood improves, however, the suicidal thoughts become more ego-dystonic; he expresses fear that he might act out on the thoughts and states that he does not want to die, he really wants to live and get better. He has no history of suicide attempts.

During our session, I ask Mr. C to focus on a new perspective to understand his thoughts by repeating the following statements: “I, JC, am a human being. I know I have a bipolar mood disorder; however, I must remember I am not bipolar. I have suicidal thoughts; however, I am not my thoughts, I am much more than that. I know I want to live, to heal, and to get better. I want to be alive and well so I can see and participate in my children’s graduation from high school and be there when they get married and when my grandchildren are born.”

I teach Mr. C to use guided imagery, during which he experiences such future positive images and milestones in his life in all 5 senses and internalizes them by using the “back from the future” technique.¹⁷ By the end of the session, he reports feeling better, more hopeful, and confident in his abilities to control his suicidal thoughts. I instruct him to write in his diary about his experiences with the future-focused positive milestones and to bring this assignment to his next appointment.

At his next appointment, Mr. C reports that his suicidal thoughts have become more fleeting, lasting for 10 to 30 seconds, and then spontaneously change to focus on issues of the “here and now.” When I ask him to read what he’s written, what stands out is the use of past tense verbs to describe future-focused experiences. For me, this confirms that Mr. C has internalized the future, creating the desirable “future hook” that acts as an antidote to the suicidal thoughts.

Related Resources

• Rouget BW, Aubry JM. Efficacy of psychoeducational approaches on bipolar disorders: a review of the literature. J Affect Disord. 2007;98:11-27.
• Weinberg I, Ronningstam E, Goldblatt MJ, et al. Strategies in treatment of suicidality: identification of common and treatment-specific interventions in empirically supported treatment manuals. J Clin Psychiatry. 2010;71:699-706.

Drug Brand Name

• Lithium • Eskalith, Lithobid

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Patients with bipolar disorder (BD) have a high risk for suicidal ideation, suicide attempts, and suicide.^1-3 Approximately 25% to 50% of BD patients attempt suicide at least once, and their attempts often are lethal—the ratio of attempts to completed suicides in BD patients is 3:1, compared with 30:1 in the general population.⁴ Lithium has been shown to effectively stabilize BD patients’ mood and significantly reduce the rates of suicide attempts and completed suicides,^5-9 but does not reduce BD patients’ long-term suicide risk to that of the general population.

Literature on psychotherapeutic treatments for patients with BD primarily focuses on improving patients’ adherence to pharmacotherapy and achieving faster recovery and remission.¹⁰ Nonpharmacologic treatments for patients with BD include psychoeducation, family-focused psychoeducation, cognitive therapy, and interpersonal and social rhythm therapy (Table 1).¹¹ Literature on nonpharmacologic treatments to address suicidality in BD patients is limited,^12,13 and additional psychotherapeutic interventions to reduce suicide risk in BD patients are needed.¹⁴

In this article, I describe a novel psychotherapeutic intervention I use that integrates cognitive therapy principles with ideas derived from the psychosynthesis model.^15,16 It consists of teaching patients to “disidentify” from suicidal thoughts, followed by a guided-imagery exercise in which patients experience a future positive life event with all 5 senses and internalize this experience. This creates a “hook into the future” that changes the present to match the future event and acts as an antidote to suicidal thoughts. I have used this strategy successfully in many patients as an adjunct to pharmacotherapy.

Table 1

Nonpharmacologic interventions for bipolar disorder

A theoretical model

Roberto Assagioli, who established the approach to psychology called psychosynthesis, formulated a fundamental psychological principle in controlling one’s behavior: “We are dominated by everything with which our self becomes identified. We can dominate and control everything from which we disidentify ourselves.”¹⁵ According to the psychosynthesis model, it is easier to change thoughts we identify as foreign to “the self” (ego-dystonic) than thoughts we identify as being part of “the self” (ego-syntonic).

Patients whose suicidal thoughts are ego-syntonic identify with the thoughts as representing themselves and take ownership of these thoughts. Such patients are at a greater risk of acting on suicidal thoughts.

Patients whose suicidal thoughts are ego-dystonic consider the suicidal thoughts foreign to their core self and do not believe such thoughts represent them. In essence, they “disown” the thoughts and typically want to control and eliminate them. Examples of patients’ ego-syntonic vs ego-dystonic suicidal thoughts are listed in Table 2.

This construct calls for an intervention to help patients who have ego-syntonic suicidal thoughts restructure them as a manifestation of BD, rather then the patient’s core self belief. The intervention emphasizes the patient is not “a suicidal patient” but suffers from an illness that may manifest with suicidal ideation. Many BD patients overly identify with their disease, stating, “I am bipolar” or “I am suicidal.” The “I am” statement originates from the verb “to be,” which implies the disease is part of the patient’s identity. The goal of this intervention is to help the patient learn to disidentify from the disease and decide that suicidal thoughts do not represent their core self, but are a manifestation of the underlying disease.

The psychosynthesis model of helping patients disidentify and therefore disown suicidal thoughts is compatible with interventions that use mindfulness-based cognitive therapy training to teach patients to experience their thoughts as just passing through their consciousness without taking ownership of them.¹⁷

Table 2

Examples of ego-syntonic vs ego-dystonic suicidal thoughts

The intervention

Assessment of suicidality is a fundamental skill for every mental health clinician.¹⁸ The psychotherapeutic intervention I use integrates the cognitive therapy principles of reframing, relabeling, and restructuring patients’ thoughts with disidentification from dysfunctional thoughts, feelings, and desires, based on psychosynthesis principles.

First, I conduct a comprehensive mental status examination that includes an in-depth exploration of the patient’s suicidal thoughts to determine if they are ego-syntonic or ego-dystonic. I begin by asking patients to clarify and elaborate on their statements referring to suicide, asking questions such as “Is there a part of you that objects to these thoughts?” and “Is there a part of you that wants to live?” If a patient indicates that he or she does experience inner conflict regarding such thoughts, these thoughts are classified as ego-dystonic. If a patient does not have any counter thoughts regarding the suicidal thoughts and fully identifies with them, the thoughts are classified as ego-syntonic.

I follow this with a treatment plan that helps patients change their view of their suicidal thoughts. I ask the patient to change these suicidal thoughts to ego-dystonic by focusing on the following statement: “I, (patient’s name), am a human being and like all human beings, I have thoughts; however, I am not my thoughts, I am much more than that.” I ask my patient to read this out loud and to mindfully meditate on this statement several times a day to reinforce the new understanding that these suicidal thoughts are a manifestation of the chemical imbalance of the mood disorder, and do not represent the patient as a person.

This intervention is paired with a future-focused internalized imagery experience I have described in previous articles.^19,20 In this part of the treatment, the patient and I discuss a specific expected life milestone that is positive and for which he or she would want to be present (eg, children graduating from high school or college, a wedding, birth of a child/grandchild, etc.). Using guided imagery, the patient experiences this event with all 5 senses during the session. I instruct the patient to internalize the experience and bring it back from the future to the present. This creates a “hook into the future” that is coupled with this desired milestone event in the patient’s life.

The following 3 case studies provide examples of the application of this treatment intervention.

CASE 1: Disidentifying family history

Mrs. G, a 42-year-old mother of 2, suffers from bipolar II disorder with recurrent episodes of depression associated with ego-syntonic suicidal thoughts. She states that at times she feels she is a burden to her husband and children and believes they may be better off without her. She says she believes “ending it all” must be her destiny. After further investigation, I learn Mrs. G has a family history of BD and 3 relatives have committed suicide. This family history may partially explain her belief that suicide must be “in her genes.”

I discuss with Mrs. G the strategy of changing her thoughts. I tell her to write in her journal—which she brings to her sessions—the following statements: “I am a human being. I am an adult woman and mother of 2 children. I know I have thoughts but I am not my thoughts, I am much more than that. I know I have genes but I am not my genes, I am much more than that. I know I have feelings, but I am not my feelings, I am much more than that. I know I have cousins, uncles, aunts, and other relatives but I am not my relatives. I am uniquely myself, different from the others.”

I ask Mrs. G to read these statements out loud and repeat them several times a day to reinforce this new way of perceiving the suicidal thoughts and to disidentify from the thoughts and her family history as it relates to suicide.

Mrs. G and I talk about the future and expected family milestones. When I ask if her son would want her to be present at his college graduation, she says yes. We then discuss in detail the date, time of day, and location of this event, followed by a guided imagery exercise focused on the graduation. She is guided to experience this event with all 5 senses and describes the event in detail, including the expression on the faces of her husband and children, their voices, and the scent of their aftershave lotion. She hears her son saying, “Mom, I love you. Thank you for being there with me all these years. I could not have done it without you.” I ask Mrs. G to internalize these experiences and carve them into her memory. She is instructed to come back from this future-focused guided imagery experience. When her eyes open, she looks at me and describes her experience in great detail, at times using the past tense, which confirms that the future-focused event was internalized.

In her next session, Mrs. G reports an improvement in her sleep and a change in her suicidal thoughts, which now are only fleeting.

CASE 2: Experiencing graduation

Ms. J, age 17, was diagnosed with bipolar I disorder when she was 15. She has a family history of BD in her mother, 2 maternal aunts, her grandmother, and an older sister. All these women have a history of suicidal thoughts and suicide attempts requiring hospital treatment, but no completed suicides.

Ms. J has been taking an adequate combination of mood stabilizers. She has recovered from 2 previous depressive episodes and is experiencing a third relapse with suicidal thoughts. At times, she experiences these thoughts as ego-syntonic; at other times, they are ego-dystonic.

I first educate her about the nature of BD, explaining that her suicidal thoughts are a manifestation of a chemical imbalance in her brain as a result of the depressive relapse. I teach her to use guided imagery to focus on her favorite place of peace and serenity, the beach, which produces immediate relief of the intense anxiety she felt.

After we complete the disidentification exercise, I ask her to focus on her high school graduation ceremony, which is scheduled to take place in 1 year. In a state of guided imagery, she experiences her graduation from high school with all 5 senses. As she returns to a state of full alertness with her eyes open, she describes the graduation ceremony experience in detail using the past tense, as if it had already occurred, thereby creating her own hook into the future. I instruct her to write about this experience in her journal and bring it with her to the next session.

The following session, Ms. J reports that her suicide ideations have “disappeared.” She says this was accompanied by improvements in her overall mood and sleep.

CASE 3: Internalizing the future

Mr. C, a 38-year-old married father of 4 children, has bipolar II disorder and is in a depressed state. He has been treated with optimal doses of mood stabilizers and atypical antipsychotics but continues to have suicidal thoughts. These thoughts are at times ego-syntonic; he says, “My family would be better off without me.” When Mr. C’s mood improves, however, the suicidal thoughts become more ego-dystonic; he expresses fear that he might act out on the thoughts and states that he does not want to die, he really wants to live and get better. He has no history of suicide attempts.

During our session, I ask Mr. C to focus on a new perspective to understand his thoughts by repeating the following statements: “I, JC, am a human being. I know I have a bipolar mood disorder; however, I must remember I am not bipolar. I have suicidal thoughts; however, I am not my thoughts, I am much more than that. I know I want to live, to heal, and to get better. I want to be alive and well so I can see and participate in my children’s graduation from high school and be there when they get married and when my grandchildren are born.”

I teach Mr. C to use guided imagery, during which he experiences such future positive images and milestones in his life in all 5 senses and internalizes them by using the “back from the future” technique.¹⁷ By the end of the session, he reports feeling better, more hopeful, and confident in his abilities to control his suicidal thoughts. I instruct him to write in his diary about his experiences with the future-focused positive milestones and to bring this assignment to his next appointment.

At his next appointment, Mr. C reports that his suicidal thoughts have become more fleeting, lasting for 10 to 30 seconds, and then spontaneously change to focus on issues of the “here and now.” When I ask him to read what he’s written, what stands out is the use of past tense verbs to describe future-focused experiences. For me, this confirms that Mr. C has internalized the future, creating the desirable “future hook” that acts as an antidote to the suicidal thoughts.

Related Resources

• Rouget BW, Aubry JM. Efficacy of psychoeducational approaches on bipolar disorders: a review of the literature. J Affect Disord. 2007;98:11-27.
• Weinberg I, Ronningstam E, Goldblatt MJ, et al. Strategies in treatment of suicidality: identification of common and treatment-specific interventions in empirically supported treatment manuals. J Clin Psychiatry. 2010;71:699-706.

Drug Brand Name

• Lithium • Eskalith, Lithobid

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Patients with bipolar disorder (BD) have a high risk for suicidal ideation, suicide attempts, and suicide.^1-3 Approximately 25% to 50% of BD patients attempt suicide at least once, and their attempts often are lethal—the ratio of attempts to completed suicides in BD patients is 3:1, compared with 30:1 in the general population.⁴ Lithium has been shown to effectively stabilize BD patients’ mood and significantly reduce the rates of suicide attempts and completed suicides,^5-9 but does not reduce BD patients’ long-term suicide risk to that of the general population.

Literature on psychotherapeutic treatments for patients with BD primarily focuses on improving patients’ adherence to pharmacotherapy and achieving faster recovery and remission.¹⁰ Nonpharmacologic treatments for patients with BD include psychoeducation, family-focused psychoeducation, cognitive therapy, and interpersonal and social rhythm therapy (Table 1).¹¹ Literature on nonpharmacologic treatments to address suicidality in BD patients is limited,^12,13 and additional psychotherapeutic interventions to reduce suicide risk in BD patients are needed.¹⁴

In this article, I describe a novel psychotherapeutic intervention I use that integrates cognitive therapy principles with ideas derived from the psychosynthesis model.^15,16 It consists of teaching patients to “disidentify” from suicidal thoughts, followed by a guided-imagery exercise in which patients experience a future positive life event with all 5 senses and internalize this experience. This creates a “hook into the future” that changes the present to match the future event and acts as an antidote to suicidal thoughts. I have used this strategy successfully in many patients as an adjunct to pharmacotherapy.

Table 1

Nonpharmacologic interventions for bipolar disorder

A theoretical model

Roberto Assagioli, who established the approach to psychology called psychosynthesis, formulated a fundamental psychological principle in controlling one’s behavior: “We are dominated by everything with which our self becomes identified. We can dominate and control everything from which we disidentify ourselves.”¹⁵ According to the psychosynthesis model, it is easier to change thoughts we identify as foreign to “the self” (ego-dystonic) than thoughts we identify as being part of “the self” (ego-syntonic).

Patients whose suicidal thoughts are ego-syntonic identify with the thoughts as representing themselves and take ownership of these thoughts. Such patients are at a greater risk of acting on suicidal thoughts.

Patients whose suicidal thoughts are ego-dystonic consider the suicidal thoughts foreign to their core self and do not believe such thoughts represent them. In essence, they “disown” the thoughts and typically want to control and eliminate them. Examples of patients’ ego-syntonic vs ego-dystonic suicidal thoughts are listed in Table 2.

This construct calls for an intervention to help patients who have ego-syntonic suicidal thoughts restructure them as a manifestation of BD, rather then the patient’s core self belief. The intervention emphasizes the patient is not “a suicidal patient” but suffers from an illness that may manifest with suicidal ideation. Many BD patients overly identify with their disease, stating, “I am bipolar” or “I am suicidal.” The “I am” statement originates from the verb “to be,” which implies the disease is part of the patient’s identity. The goal of this intervention is to help the patient learn to disidentify from the disease and decide that suicidal thoughts do not represent their core self, but are a manifestation of the underlying disease.

The psychosynthesis model of helping patients disidentify and therefore disown suicidal thoughts is compatible with interventions that use mindfulness-based cognitive therapy training to teach patients to experience their thoughts as just passing through their consciousness without taking ownership of them.¹⁷

Table 2

Examples of ego-syntonic vs ego-dystonic suicidal thoughts

The intervention

Assessment of suicidality is a fundamental skill for every mental health clinician.¹⁸ The psychotherapeutic intervention I use integrates the cognitive therapy principles of reframing, relabeling, and restructuring patients’ thoughts with disidentification from dysfunctional thoughts, feelings, and desires, based on psychosynthesis principles.

First, I conduct a comprehensive mental status examination that includes an in-depth exploration of the patient’s suicidal thoughts to determine if they are ego-syntonic or ego-dystonic. I begin by asking patients to clarify and elaborate on their statements referring to suicide, asking questions such as “Is there a part of you that objects to these thoughts?” and “Is there a part of you that wants to live?” If a patient indicates that he or she does experience inner conflict regarding such thoughts, these thoughts are classified as ego-dystonic. If a patient does not have any counter thoughts regarding the suicidal thoughts and fully identifies with them, the thoughts are classified as ego-syntonic.

I follow this with a treatment plan that helps patients change their view of their suicidal thoughts. I ask the patient to change these suicidal thoughts to ego-dystonic by focusing on the following statement: “I, (patient’s name), am a human being and like all human beings, I have thoughts; however, I am not my thoughts, I am much more than that.” I ask my patient to read this out loud and to mindfully meditate on this statement several times a day to reinforce the new understanding that these suicidal thoughts are a manifestation of the chemical imbalance of the mood disorder, and do not represent the patient as a person.

This intervention is paired with a future-focused internalized imagery experience I have described in previous articles.^19,20 In this part of the treatment, the patient and I discuss a specific expected life milestone that is positive and for which he or she would want to be present (eg, children graduating from high school or college, a wedding, birth of a child/grandchild, etc.). Using guided imagery, the patient experiences this event with all 5 senses during the session. I instruct the patient to internalize the experience and bring it back from the future to the present. This creates a “hook into the future” that is coupled with this desired milestone event in the patient’s life.

The following 3 case studies provide examples of the application of this treatment intervention.

CASE 1: Disidentifying family history

Mrs. G, a 42-year-old mother of 2, suffers from bipolar II disorder with recurrent episodes of depression associated with ego-syntonic suicidal thoughts. She states that at times she feels she is a burden to her husband and children and believes they may be better off without her. She says she believes “ending it all” must be her destiny. After further investigation, I learn Mrs. G has a family history of BD and 3 relatives have committed suicide. This family history may partially explain her belief that suicide must be “in her genes.”

I discuss with Mrs. G the strategy of changing her thoughts. I tell her to write in her journal—which she brings to her sessions—the following statements: “I am a human being. I am an adult woman and mother of 2 children. I know I have thoughts but I am not my thoughts, I am much more than that. I know I have genes but I am not my genes, I am much more than that. I know I have feelings, but I am not my feelings, I am much more than that. I know I have cousins, uncles, aunts, and other relatives but I am not my relatives. I am uniquely myself, different from the others.”

I ask Mrs. G to read these statements out loud and repeat them several times a day to reinforce this new way of perceiving the suicidal thoughts and to disidentify from the thoughts and her family history as it relates to suicide.

Mrs. G and I talk about the future and expected family milestones. When I ask if her son would want her to be present at his college graduation, she says yes. We then discuss in detail the date, time of day, and location of this event, followed by a guided imagery exercise focused on the graduation. She is guided to experience this event with all 5 senses and describes the event in detail, including the expression on the faces of her husband and children, their voices, and the scent of their aftershave lotion. She hears her son saying, “Mom, I love you. Thank you for being there with me all these years. I could not have done it without you.” I ask Mrs. G to internalize these experiences and carve them into her memory. She is instructed to come back from this future-focused guided imagery experience. When her eyes open, she looks at me and describes her experience in great detail, at times using the past tense, which confirms that the future-focused event was internalized.

In her next session, Mrs. G reports an improvement in her sleep and a change in her suicidal thoughts, which now are only fleeting.

CASE 2: Experiencing graduation

Ms. J, age 17, was diagnosed with bipolar I disorder when she was 15. She has a family history of BD in her mother, 2 maternal aunts, her grandmother, and an older sister. All these women have a history of suicidal thoughts and suicide attempts requiring hospital treatment, but no completed suicides.

Ms. J has been taking an adequate combination of mood stabilizers. She has recovered from 2 previous depressive episodes and is experiencing a third relapse with suicidal thoughts. At times, she experiences these thoughts as ego-syntonic; at other times, they are ego-dystonic.

I first educate her about the nature of BD, explaining that her suicidal thoughts are a manifestation of a chemical imbalance in her brain as a result of the depressive relapse. I teach her to use guided imagery to focus on her favorite place of peace and serenity, the beach, which produces immediate relief of the intense anxiety she felt.

After we complete the disidentification exercise, I ask her to focus on her high school graduation ceremony, which is scheduled to take place in 1 year. In a state of guided imagery, she experiences her graduation from high school with all 5 senses. As she returns to a state of full alertness with her eyes open, she describes the graduation ceremony experience in detail using the past tense, as if it had already occurred, thereby creating her own hook into the future. I instruct her to write about this experience in her journal and bring it with her to the next session.

The following session, Ms. J reports that her suicide ideations have “disappeared.” She says this was accompanied by improvements in her overall mood and sleep.

CASE 3: Internalizing the future

Mr. C, a 38-year-old married father of 4 children, has bipolar II disorder and is in a depressed state. He has been treated with optimal doses of mood stabilizers and atypical antipsychotics but continues to have suicidal thoughts. These thoughts are at times ego-syntonic; he says, “My family would be better off without me.” When Mr. C’s mood improves, however, the suicidal thoughts become more ego-dystonic; he expresses fear that he might act out on the thoughts and states that he does not want to die, he really wants to live and get better. He has no history of suicide attempts.

During our session, I ask Mr. C to focus on a new perspective to understand his thoughts by repeating the following statements: “I, JC, am a human being. I know I have a bipolar mood disorder; however, I must remember I am not bipolar. I have suicidal thoughts; however, I am not my thoughts, I am much more than that. I know I want to live, to heal, and to get better. I want to be alive and well so I can see and participate in my children’s graduation from high school and be there when they get married and when my grandchildren are born.”

I teach Mr. C to use guided imagery, during which he experiences such future positive images and milestones in his life in all 5 senses and internalizes them by using the “back from the future” technique.¹⁷ By the end of the session, he reports feeling better, more hopeful, and confident in his abilities to control his suicidal thoughts. I instruct him to write in his diary about his experiences with the future-focused positive milestones and to bring this assignment to his next appointment.

At his next appointment, Mr. C reports that his suicidal thoughts have become more fleeting, lasting for 10 to 30 seconds, and then spontaneously change to focus on issues of the “here and now.” When I ask him to read what he’s written, what stands out is the use of past tense verbs to describe future-focused experiences. For me, this confirms that Mr. C has internalized the future, creating the desirable “future hook” that acts as an antidote to the suicidal thoughts.

Related Resources

• Rouget BW, Aubry JM. Efficacy of psychoeducational approaches on bipolar disorders: a review of the literature. J Affect Disord. 2007;98:11-27.
• Weinberg I, Ronningstam E, Goldblatt MJ, et al. Strategies in treatment of suicidality: identification of common and treatment-specific interventions in empirically supported treatment manuals. J Clin Psychiatry. 2010;71:699-706.

Drug Brand Name

• Lithium • Eskalith, Lithobid

Disclosure

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