Current Psychiatry

I commend Dr. Henry A. Nasrallah on his editorial, “Integrating psychiatry with other medical specialties” (From the Editor, Current Psychiatry, September 2010, p. 14-15). I could not agree more with the importance of fully integrating psychiatry into mainstream medical practice, and can attest that this can be accomplished. For the past year I have been part of a family practice where I work closely with the primary care physicians, nurse practitioners, and physician assistants. This practice has electronic medical records, and I have complete access to patients’ entire medical records, allowing other practitioners to read my psychiatric evaluations and progress notes. Being in the same location facilitates easy and frequent clinical exchange. The benefits to our patients are real and substantial.

Ralph G. Walton, MD
Family Health Medical Services
Mayville, NY

I commend Dr. Henry A. Nasrallah on his editorial, “Integrating psychiatry with other medical specialties” (From the Editor, Current Psychiatry, September 2010, p. 14-15). I could not agree more with the importance of fully integrating psychiatry into mainstream medical practice, and can attest that this can be accomplished. For the past year I have been part of a family practice where I work closely with the primary care physicians, nurse practitioners, and physician assistants. This practice has electronic medical records, and I have complete access to patients’ entire medical records, allowing other practitioners to read my psychiatric evaluations and progress notes. Being in the same location facilitates easy and frequent clinical exchange. The benefits to our patients are real and substantial.

Ralph G. Walton, MD
Family Health Medical Services
Mayville, NY

I commend Dr. Henry A. Nasrallah on his editorial, “Integrating psychiatry with other medical specialties” (From the Editor, Current Psychiatry, September 2010, p. 14-15). I could not agree more with the importance of fully integrating psychiatry into mainstream medical practice, and can attest that this can be accomplished. For the past year I have been part of a family practice where I work closely with the primary care physicians, nurse practitioners, and physician assistants. This practice has electronic medical records, and I have complete access to patients’ entire medical records, allowing other practitioners to read my psychiatric evaluations and progress notes. Being in the same location facilitates easy and frequent clinical exchange. The benefits to our patients are real and substantial.

Ralph G. Walton, MD
Family Health Medical Services
Mayville, NY

We read with distress “Successfully navigating the 15-minute ‘med check,’” (Malpractice Rx, Current Psychiatry, June 2010, p. 40-43). Even if 15-minute med checks have become “standard care,” they should not be. Unless a patient is stably medicated, 15 minutes is insufficient to evaluate the situation and make treatment decisions. Psychiatric diagnoses cannot be made by drawing blood or doing physical exams, so information beyond superficial questions must be elicited.

Does it make sense, as Table 2 suggests, that a psychiatrist should “have a psychotherapist or case manager present to facilitate communication?” Clearly not. Although theoretically possible, these therapists—apart from the question of their level of competency and training—are overworked and lack time to join psychiatric sessions.

Again, in Table 2, is apologizing sufficient “when a patient truly needs more time”? Clearly not. Although the author notes that intakes should warrant extra time, there is little awareness of the “real-life” difficulty involved in seeing patients who are not new to the clinic but new to a particular psychiatrist. Patients often arrive with as many as a dozen medications and multiple conflicting diagnoses. Charts are voluminous. To become thoroughly familiar with what has transpired takes a competent psychiatrist a minimum of 30 minutes to review. Rapid staff turnover and disconnected care exacerbate this problem.

Having worked in academic settings and in the field, we can state with certainty that dangerous shortcuts are now the norm. Who, if not the psychiatrist, will be addressing the fact that many of these patients have no teeth, out-of-control diabetes, no primary care physician, etc.? This raises more than malpractice issues, this raises quality-of-care issues.

Some days there are “no-shows” and some days every patient comes. In practice, the need for more than 15 minutes per patient exceeds the time gained when a patient does not keep an appointment.

Psychiatrists should serve as purveyors of quality care, not merely signers of prescriptions.

Elizabeth H. Levin, MD
Former director of residency training
Trenton Psychiatric Hospital
Former clinical associate professor
Robert Wood Johnson Medical School
Camden, NJ

Arthur H. Schwartz, MD
Retired professor of psychiatry
Robert Wood Johnson Medical School
Piscataway, NJ

Dr. Mossman responds

Unlike Drs. Levin and Schwartz, I am unwilling to declare that colleagues who conduct 15-minute med checks are, by that fact itself, doing something psychiatrists should not do. That does not mean 15-minute med checks are ideal. But several psychiatrists feel that despite severe time constraints, they can do many patients much good in 15 minutes—certainly more good than if those patients had no time with a psychiatrist at all. No scientific evidence that I know of contradicts this position.

Drs. Levin and Schwartz and I agree that certain types of patient visits require more than 15 minutes, which is why my column contained suggestions about negotiating for “seeing no more than 3 patients an hour, scheduling longer appointments for new patients, and having some built-in time to return phone calls, do paperwork, review charts, and complete progress notes.” The “strategies” listed in Table 2 are ideas about improving care and efficiency that come from psychiatrists with a lot of med check experience. Like most clinical suggestions, the strategies may make sense in some settings, but certainly not all.

Douglas Mossman, MD
Director
Glenn M. Weaver Institute of Law and Psychiatry
University of Cincinnati College of Medicine
Adjunct professor of clinical psychiatry
University of Cincinnati College of Medicine
Cincinnati, OH

We read with distress “Successfully navigating the 15-minute ‘med check,’” (Malpractice Rx, Current Psychiatry, June 2010, p. 40-43). Even if 15-minute med checks have become “standard care,” they should not be. Unless a patient is stably medicated, 15 minutes is insufficient to evaluate the situation and make treatment decisions. Psychiatric diagnoses cannot be made by drawing blood or doing physical exams, so information beyond superficial questions must be elicited.

Does it make sense, as Table 2 suggests, that a psychiatrist should “have a psychotherapist or case manager present to facilitate communication?” Clearly not. Although theoretically possible, these therapists—apart from the question of their level of competency and training—are overworked and lack time to join psychiatric sessions.

Again, in Table 2, is apologizing sufficient “when a patient truly needs more time”? Clearly not. Although the author notes that intakes should warrant extra time, there is little awareness of the “real-life” difficulty involved in seeing patients who are not new to the clinic but new to a particular psychiatrist. Patients often arrive with as many as a dozen medications and multiple conflicting diagnoses. Charts are voluminous. To become thoroughly familiar with what has transpired takes a competent psychiatrist a minimum of 30 minutes to review. Rapid staff turnover and disconnected care exacerbate this problem.

Having worked in academic settings and in the field, we can state with certainty that dangerous shortcuts are now the norm. Who, if not the psychiatrist, will be addressing the fact that many of these patients have no teeth, out-of-control diabetes, no primary care physician, etc.? This raises more than malpractice issues, this raises quality-of-care issues.

Some days there are “no-shows” and some days every patient comes. In practice, the need for more than 15 minutes per patient exceeds the time gained when a patient does not keep an appointment.

Psychiatrists should serve as purveyors of quality care, not merely signers of prescriptions.

Elizabeth H. Levin, MD
Former director of residency training
Trenton Psychiatric Hospital
Former clinical associate professor
Robert Wood Johnson Medical School
Camden, NJ

Arthur H. Schwartz, MD
Retired professor of psychiatry
Robert Wood Johnson Medical School
Piscataway, NJ

Dr. Mossman responds

Unlike Drs. Levin and Schwartz, I am unwilling to declare that colleagues who conduct 15-minute med checks are, by that fact itself, doing something psychiatrists should not do. That does not mean 15-minute med checks are ideal. But several psychiatrists feel that despite severe time constraints, they can do many patients much good in 15 minutes—certainly more good than if those patients had no time with a psychiatrist at all. No scientific evidence that I know of contradicts this position.

Drs. Levin and Schwartz and I agree that certain types of patient visits require more than 15 minutes, which is why my column contained suggestions about negotiating for “seeing no more than 3 patients an hour, scheduling longer appointments for new patients, and having some built-in time to return phone calls, do paperwork, review charts, and complete progress notes.” The “strategies” listed in Table 2 are ideas about improving care and efficiency that come from psychiatrists with a lot of med check experience. Like most clinical suggestions, the strategies may make sense in some settings, but certainly not all.

Douglas Mossman, MD
Director
Glenn M. Weaver Institute of Law and Psychiatry
University of Cincinnati College of Medicine
Adjunct professor of clinical psychiatry
University of Cincinnati College of Medicine
Cincinnati, OH

We read with distress “Successfully navigating the 15-minute ‘med check,’” (Malpractice Rx, Current Psychiatry, June 2010, p. 40-43). Even if 15-minute med checks have become “standard care,” they should not be. Unless a patient is stably medicated, 15 minutes is insufficient to evaluate the situation and make treatment decisions. Psychiatric diagnoses cannot be made by drawing blood or doing physical exams, so information beyond superficial questions must be elicited.

Does it make sense, as Table 2 suggests, that a psychiatrist should “have a psychotherapist or case manager present to facilitate communication?” Clearly not. Although theoretically possible, these therapists—apart from the question of their level of competency and training—are overworked and lack time to join psychiatric sessions.

Again, in Table 2, is apologizing sufficient “when a patient truly needs more time”? Clearly not. Although the author notes that intakes should warrant extra time, there is little awareness of the “real-life” difficulty involved in seeing patients who are not new to the clinic but new to a particular psychiatrist. Patients often arrive with as many as a dozen medications and multiple conflicting diagnoses. Charts are voluminous. To become thoroughly familiar with what has transpired takes a competent psychiatrist a minimum of 30 minutes to review. Rapid staff turnover and disconnected care exacerbate this problem.

Having worked in academic settings and in the field, we can state with certainty that dangerous shortcuts are now the norm. Who, if not the psychiatrist, will be addressing the fact that many of these patients have no teeth, out-of-control diabetes, no primary care physician, etc.? This raises more than malpractice issues, this raises quality-of-care issues.

Some days there are “no-shows” and some days every patient comes. In practice, the need for more than 15 minutes per patient exceeds the time gained when a patient does not keep an appointment.

Psychiatrists should serve as purveyors of quality care, not merely signers of prescriptions.

Elizabeth H. Levin, MD
Former director of residency training
Trenton Psychiatric Hospital
Former clinical associate professor
Robert Wood Johnson Medical School
Camden, NJ

Arthur H. Schwartz, MD
Retired professor of psychiatry
Robert Wood Johnson Medical School
Piscataway, NJ

Dr. Mossman responds

Unlike Drs. Levin and Schwartz, I am unwilling to declare that colleagues who conduct 15-minute med checks are, by that fact itself, doing something psychiatrists should not do. That does not mean 15-minute med checks are ideal. But several psychiatrists feel that despite severe time constraints, they can do many patients much good in 15 minutes—certainly more good than if those patients had no time with a psychiatrist at all. No scientific evidence that I know of contradicts this position.

Drs. Levin and Schwartz and I agree that certain types of patient visits require more than 15 minutes, which is why my column contained suggestions about negotiating for “seeing no more than 3 patients an hour, scheduling longer appointments for new patients, and having some built-in time to return phone calls, do paperwork, review charts, and complete progress notes.” The “strategies” listed in Table 2 are ideas about improving care and efficiency that come from psychiatrists with a lot of med check experience. Like most clinical suggestions, the strategies may make sense in some settings, but certainly not all.

Douglas Mossman, MD
Director
Glenn M. Weaver Institute of Law and Psychiatry
University of Cincinnati College of Medicine
Adjunct professor of clinical psychiatry
University of Cincinnati College of Medicine
Cincinnati, OH

As a National Institutes of Health-trained psychopharmacologist who also received substantial psychotherapy training during residency, I value both as pillars of psychiatric practice.

However, often I think about the evidence-based conduct of psychotherapy, which I regard as a neurobiologic treatment similar to drug therapy, and then I ask research questions that remain unanswered, such as:

• What is the therapeutic “dose” of psychotherapy? Does it differ by type of therapy or the patient’s diagnosis?
• Is the dose measured in the number of sessions or the time the patient is in a therapy session? Is there a loading dose? What is the maintenance dose?
• What is the optimal schedule for psychotherapy? By what established criteria does a therapist determine how often to administer psychotherapy? Why weekly and not daily? Why not 2 or 3 times a day intensive psychotherapy for acutely ill patients? Is the scheduling based on the cost to the patient, the therapist’s availability, or insurance coverage rather than the patient’s needs?
• How long should a session be? How was the weekly 50-minute session determined? Why not 10, 20, 30, or 40 minutes? Is 15 minutes 3 times a week more or less effective than 50 minutes once a week?
• What is the primary indication for a given psychotherapy? Why do therapists use the same psychotherapy for many different psychiatric disorders? Isn’t that like giving the same drug to everyone with any psychiatric illness? Is there such a thing as using a psychotherapeutic technique “off-label”? Why don’t therapy techniques come with a label like drug therapy?
• What is the best time of day to conduct psychotherapy to achieve maximum benefit? Patients are assigned a slot almost randomly between 8 am and 5 pm, but is early morning psychotherapy more effective than, say, mid-afternoon? Could going to sleep immediately after a session help consolidate memories, insights, learning, and emotional processing more than returning to one’s work setting or home, where many distractions may disrupt or erase the salutary neurobiologic effects of psychotherapy? If this could be proven with controlled studies then perhaps patients could schedule a nap right after a session in a dark cubicle adjacent to the therapist’s suite? This could result in a boom of “psychotherapy motels!”
• What effect does food have on psychotherapy efficacy? Is an empty stomach and hunger better or worse for patients? Would the borborygmi be distracting to some therapists? Is there a possible benefit for a postprandial session when serum glucose levels are higher? Could cognition be sharper for assimilating psychotherapy after eating vs before?
• Does ambient light intensity impact psychotherapy? Could ultra-bright light that is used for seasonal depression (10,000 lux vs the usual 100 lux fluorescent bulbs) placed in a patient’s field of vision during a session accentuate psychotherapy’s beneficial effects?
• What are the side effects of psychotherapy? Why is it assumed that psychotherapy exerts efficacy without any tolerability or safety problems? Can certain types of psychotherapy cause somatic adverse effects—such as headache, nausea, dizziness, or appetite and sleep changes—that are unwittingly attributed to the psychiatric illness rather than the treatment?
• Is there such a thing as psychotherapy overdose? What is it and what are its symptoms? Is it initiated by the patient, the therapist, or both?
• Could co-administration of modest doses of neurogenesis-enhancing drugs such as a selective serotonin reuptake inhibitor or lithium potentiate the effects of psychotherapy, because learning and memory are improved with neurogenesis-associated hippocampal growth?
• Does psychotherapy work differently in different age groups (adolescent vs adult vs middle age vs elderly) because of ongoing brain circuitry and neuroplastic changes throughout the life cycle?
• Are there “me too” psychotherapies similar to “me too” drugs?
• Can a combination of 2 or 3 different psychotherapies work better than a single psychotherapy? Could cognitive-behavioral therapy combined with psychodynamic psychotherapy exert higher efficacy then either alone?
• Assuming that ongoing psychotherapy costs about $100 per session and a patient receives 40 to 50 sessions a year for a total of $4,000 to $5,000 a year, why the outcry about medications that cost a similar amount?
• Is the adherence rate to psychotherapy similar to that of pharmacotherapy? Do some patients “intellectually cheek” an occasional psychotherapeutic dose?
• Is there a generic psychotherapy? Is it cheaper? Is it as good as “brand-name” psychotherapy?

I am sure readers realize that some of my questions are serious while others are tongue-in-cheek, but I hope my musings prompt you to join me in thinking outside the box about psychotherapy and the many gaps of knowledge that persist. Rigorous research is needed to substantiate or negate some current assumptions about the use of psychotherapy.

As a National Institutes of Health-trained psychopharmacologist who also received substantial psychotherapy training during residency, I value both as pillars of psychiatric practice.

However, often I think about the evidence-based conduct of psychotherapy, which I regard as a neurobiologic treatment similar to drug therapy, and then I ask research questions that remain unanswered, such as:

• What is the therapeutic “dose” of psychotherapy? Does it differ by type of therapy or the patient’s diagnosis?
• Is the dose measured in the number of sessions or the time the patient is in a therapy session? Is there a loading dose? What is the maintenance dose?
• What is the optimal schedule for psychotherapy? By what established criteria does a therapist determine how often to administer psychotherapy? Why weekly and not daily? Why not 2 or 3 times a day intensive psychotherapy for acutely ill patients? Is the scheduling based on the cost to the patient, the therapist’s availability, or insurance coverage rather than the patient’s needs?
• How long should a session be? How was the weekly 50-minute session determined? Why not 10, 20, 30, or 40 minutes? Is 15 minutes 3 times a week more or less effective than 50 minutes once a week?
• What is the primary indication for a given psychotherapy? Why do therapists use the same psychotherapy for many different psychiatric disorders? Isn’t that like giving the same drug to everyone with any psychiatric illness? Is there such a thing as using a psychotherapeutic technique “off-label”? Why don’t therapy techniques come with a label like drug therapy?
• What is the best time of day to conduct psychotherapy to achieve maximum benefit? Patients are assigned a slot almost randomly between 8 am and 5 pm, but is early morning psychotherapy more effective than, say, mid-afternoon? Could going to sleep immediately after a session help consolidate memories, insights, learning, and emotional processing more than returning to one’s work setting or home, where many distractions may disrupt or erase the salutary neurobiologic effects of psychotherapy? If this could be proven with controlled studies then perhaps patients could schedule a nap right after a session in a dark cubicle adjacent to the therapist’s suite? This could result in a boom of “psychotherapy motels!”
• What effect does food have on psychotherapy efficacy? Is an empty stomach and hunger better or worse for patients? Would the borborygmi be distracting to some therapists? Is there a possible benefit for a postprandial session when serum glucose levels are higher? Could cognition be sharper for assimilating psychotherapy after eating vs before?
• Does ambient light intensity impact psychotherapy? Could ultra-bright light that is used for seasonal depression (10,000 lux vs the usual 100 lux fluorescent bulbs) placed in a patient’s field of vision during a session accentuate psychotherapy’s beneficial effects?
• What are the side effects of psychotherapy? Why is it assumed that psychotherapy exerts efficacy without any tolerability or safety problems? Can certain types of psychotherapy cause somatic adverse effects—such as headache, nausea, dizziness, or appetite and sleep changes—that are unwittingly attributed to the psychiatric illness rather than the treatment?
• Is there such a thing as psychotherapy overdose? What is it and what are its symptoms? Is it initiated by the patient, the therapist, or both?
• Could co-administration of modest doses of neurogenesis-enhancing drugs such as a selective serotonin reuptake inhibitor or lithium potentiate the effects of psychotherapy, because learning and memory are improved with neurogenesis-associated hippocampal growth?
• Does psychotherapy work differently in different age groups (adolescent vs adult vs middle age vs elderly) because of ongoing brain circuitry and neuroplastic changes throughout the life cycle?
• Are there “me too” psychotherapies similar to “me too” drugs?
• Can a combination of 2 or 3 different psychotherapies work better than a single psychotherapy? Could cognitive-behavioral therapy combined with psychodynamic psychotherapy exert higher efficacy then either alone?
• Assuming that ongoing psychotherapy costs about $100 per session and a patient receives 40 to 50 sessions a year for a total of $4,000 to $5,000 a year, why the outcry about medications that cost a similar amount?
• Is the adherence rate to psychotherapy similar to that of pharmacotherapy? Do some patients “intellectually cheek” an occasional psychotherapeutic dose?
• Is there a generic psychotherapy? Is it cheaper? Is it as good as “brand-name” psychotherapy?

I am sure readers realize that some of my questions are serious while others are tongue-in-cheek, but I hope my musings prompt you to join me in thinking outside the box about psychotherapy and the many gaps of knowledge that persist. Rigorous research is needed to substantiate or negate some current assumptions about the use of psychotherapy.

As a National Institutes of Health-trained psychopharmacologist who also received substantial psychotherapy training during residency, I value both as pillars of psychiatric practice.

However, often I think about the evidence-based conduct of psychotherapy, which I regard as a neurobiologic treatment similar to drug therapy, and then I ask research questions that remain unanswered, such as:

• What is the therapeutic “dose” of psychotherapy? Does it differ by type of therapy or the patient’s diagnosis?
• Is the dose measured in the number of sessions or the time the patient is in a therapy session? Is there a loading dose? What is the maintenance dose?
• What is the optimal schedule for psychotherapy? By what established criteria does a therapist determine how often to administer psychotherapy? Why weekly and not daily? Why not 2 or 3 times a day intensive psychotherapy for acutely ill patients? Is the scheduling based on the cost to the patient, the therapist’s availability, or insurance coverage rather than the patient’s needs?
• How long should a session be? How was the weekly 50-minute session determined? Why not 10, 20, 30, or 40 minutes? Is 15 minutes 3 times a week more or less effective than 50 minutes once a week?
• What is the primary indication for a given psychotherapy? Why do therapists use the same psychotherapy for many different psychiatric disorders? Isn’t that like giving the same drug to everyone with any psychiatric illness? Is there such a thing as using a psychotherapeutic technique “off-label”? Why don’t therapy techniques come with a label like drug therapy?
• What is the best time of day to conduct psychotherapy to achieve maximum benefit? Patients are assigned a slot almost randomly between 8 am and 5 pm, but is early morning psychotherapy more effective than, say, mid-afternoon? Could going to sleep immediately after a session help consolidate memories, insights, learning, and emotional processing more than returning to one’s work setting or home, where many distractions may disrupt or erase the salutary neurobiologic effects of psychotherapy? If this could be proven with controlled studies then perhaps patients could schedule a nap right after a session in a dark cubicle adjacent to the therapist’s suite? This could result in a boom of “psychotherapy motels!”
• What effect does food have on psychotherapy efficacy? Is an empty stomach and hunger better or worse for patients? Would the borborygmi be distracting to some therapists? Is there a possible benefit for a postprandial session when serum glucose levels are higher? Could cognition be sharper for assimilating psychotherapy after eating vs before?
• Does ambient light intensity impact psychotherapy? Could ultra-bright light that is used for seasonal depression (10,000 lux vs the usual 100 lux fluorescent bulbs) placed in a patient’s field of vision during a session accentuate psychotherapy’s beneficial effects?
• What are the side effects of psychotherapy? Why is it assumed that psychotherapy exerts efficacy without any tolerability or safety problems? Can certain types of psychotherapy cause somatic adverse effects—such as headache, nausea, dizziness, or appetite and sleep changes—that are unwittingly attributed to the psychiatric illness rather than the treatment?
• Is there such a thing as psychotherapy overdose? What is it and what are its symptoms? Is it initiated by the patient, the therapist, or both?
• Could co-administration of modest doses of neurogenesis-enhancing drugs such as a selective serotonin reuptake inhibitor or lithium potentiate the effects of psychotherapy, because learning and memory are improved with neurogenesis-associated hippocampal growth?
• Does psychotherapy work differently in different age groups (adolescent vs adult vs middle age vs elderly) because of ongoing brain circuitry and neuroplastic changes throughout the life cycle?
• Are there “me too” psychotherapies similar to “me too” drugs?
• Can a combination of 2 or 3 different psychotherapies work better than a single psychotherapy? Could cognitive-behavioral therapy combined with psychodynamic psychotherapy exert higher efficacy then either alone?
• Assuming that ongoing psychotherapy costs about $100 per session and a patient receives 40 to 50 sessions a year for a total of $4,000 to $5,000 a year, why the outcry about medications that cost a similar amount?
• Is the adherence rate to psychotherapy similar to that of pharmacotherapy? Do some patients “intellectually cheek” an occasional psychotherapeutic dose?
• Is there a generic psychotherapy? Is it cheaper? Is it as good as “brand-name” psychotherapy?

I am sure readers realize that some of my questions are serious while others are tongue-in-cheek, but I hope my musings prompt you to join me in thinking outside the box about psychotherapy and the many gaps of knowledge that persist. Rigorous research is needed to substantiate or negate some current assumptions about the use of psychotherapy.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/10/hallucinations-in-children-diagnostic.html#comments

Hallucinations in children are of grave concern to parents and clinicians, but aren’t necessarily a symptom of mental illness. In adults, hallucinations usually are linked to serious psychopathology; however, in children they are not uncommon and may be part of normal development (Box).

A hallucination is a false auditory, visual, gustatory, tactile, or olfactory perception not associated with real external stimuli.¹ It must be differentiated from similar phenomenon such as illusions (misperception of actual stimuli), elaborate fantasies, imaginary companions, and eidetic images (visual images stored in memory).

Box

Common, yet a cause for concern

Epidemiologic studies show 2.8% of adults report hallucinations before age 21.² Nonpsychotic children as young as age 5 have reported hallucinations.³ Hallucinatory phenomenon may be present in 8% to 21% of all 11-year-old children; two-thirds of these patients have no DSM-IV-TR diagnosis.^4,5 However, 1 evaluation of 62 nonpsychotic hallucinating children treated in a psychiatric emergency department (ED):

• 34% had depression
• 22% had attention-deficit/hyperactivity disorder (ADHD)
• 21% had disruptive behavior disorders
• 23% had other diagnoses.⁶

Studies suggest that children who have hallucinations but no other psychotic symptoms have a better long-term prognosis than those with additional psychotic symptoms.⁷ A 17-year longitudinal study of children with hallucinations and concurrent emotional and conduct problems found:

• up to 50% of patients still experience hallucinations at age 30
• hallucinations did not significantly predict clinical outcome at age 30
• childhood hallucinations did not increase the risk for psychosis, depression, organic brain disorder, or other psychiatric illnesses.⁷

In a study of children with psychosis and disruptive disorders, at 2- to 8-years follow-up 50% met criteria for major depressive disorder, bipolar disorder, or schizophreniform disorders.⁸ In a 15-year longitudinal study of 11-year-olds, self-reported psychotic symptoms—such as delusional beliefs and hallucinatory experiences—predicted a high risk of schizophreniform disorder at age 26.⁹ These studies suggest that experiencing significant disruptions in thoughts and perceptions during childhood may be related to later development of prominent mood and thought disorders.

Differential diagnosis

Table 1 lists possible causes of hallucination in children.^6,10-13 Hallucinations during childhood can occur in the context of several psychiatric disorders, including:

• schizophrenia
• schizophreniform disorders
• mood disorders with psychotic features (Table 2).¹⁴

They can also manifest as comorbid or associated symptoms of disorders not commonly associated with hallucinations, such as ADHD, disruptive disorders, anxiety disorders, and prodromal clinical states. Medications, substance use, and organic and metabolic disorders also must be considered in the differential diagnosis (Table 3).

Hallucinations may occur in low-functioning or anxious children, in the context of psychosocial adversity or abuse, and during bereavement of a deceased parent when the surviving parent is emotionally unavailable.^11-13,15-17 Rule out hypnagogic and hypnopompic hallucinations, which are predominantly visual hallucinations that occur immediately before falling asleep and during the transition from sleep to wakefulness, respectively.¹⁸ Rarely, a child who has had hallucinations for some time may learn to complain of them when he or she is not hallucinating in order to obtain a primary or secondary gain, such as getting attention from caregivers.

Little is known about psychosis and hallucinations in preschoolers (age ≤5); therefore, their language use may help assessment. Because of cognitive immaturity, children often use illogical thinking and loose association and may describe their thoughts as “voices.” This is common in children with language disorders—and sometimes in healthy patients—who may talk about voices because they cannot describe their own thoughts.

Children with ADHD and/or oppositional defiant disorder often are impulsive and show poor judgment and may blame voices for telling them to do bad things. These “hallucinations” may represent internal thoughts battling with the child’s conscience.⁶ Auditory and visual hallucinations have been reported in children with Tourette syndrome, especially when associated with ADHD or obsessive-compulsive disorder.¹⁹

Medical causes. Electrolyte disturbances, metabolic disorders, fever, and serious infections are common nonpsychiatric causes of hallucinations.²⁰ Brain neoplasm—particularly in visual association areas, the temporal lobe, or portions of the optic nerve or retina—also may produce hallucinations, which can be complex with full images.²¹

Medications such as steroids and anticholinergics may cause hallucinations. Case studies report visual and tactile hallucinations with methylphenidate therapy that resolve after discontinuing the medication.²² Illicit substances, including cannabis, lysergic acid diethylamide (LSD), cocaine, amphetamines, 3,4-methylenedioxymeth-amphetamine (ecstasy), opiates, and barbiturates, can induce hallucinations.

Suspect substance-induced hallucinations if your patient shows:

• acute onset of hallucinations
• dilated pupils
• extreme agitation or drowsiness
• other signs of intoxication.

Hallucinations caused by seizure disorders are rare but can be somatosensory, visual (occipital lobe focus), auditory, olfactory (uncinate, complex partial), or gustatory. The hallucinations may be unformed (flashing lights or rushing noises) or formed (images, spoken words, or music) and could be part of the aura arising from the temporal lobe (dreamlike, flashbacks). Command hallucinations are rare and adult and pediatric patients usually sense they are not real.²³

Migraines occur in approximately 5% of prepubertal children and often are comorbid with affective and anxiety disorders.²⁴ Hallucinations associated with migraine commonly are visual, but gustatory, olfactory, and auditory hallucinations also can occur, with or without headaches.³ Any hallucination associated with headaches should be investigated neurologically. Other diagnostic aspects of hallucinations to consider while interviewing children are listed in Table 4.^25-28

Table 1

Possible causes of hallucinations in children and adolescents

Table 2

Content of hallucinations may point to their cause

Table 3

Hallucinations in young patients: Differential diagnoses

Table 4

Diagnostic considerations when assessing a hallucinating child

Psychotic disorder not otherwise specified

(NOS) in children often is overused and misused. One reason could be that DSM-IV-TR does not have a category for hallucinations in nonpsychotic children or for children who are at risk for psychosis. However, recommendations regarding the diagnosis of psychotic disorder NOS note it:

• may be used if uncertainty persists after ruling out all other diagnoses
• should be avoided when hallucinations occur in nonpsychotic children
• should not be used longitudinally if a clinician later determines a specific disorder accounts for the hallucinations.²⁹

Treatment

Addressing underlying medical or psychiatric illness, including substance use, is primary. Some adolescents or children may think that cannabis use is relatively benign. Discuss the risks of cannabis use in an age-appropriate manner.

In the ED. Children or adolescents who present with hallucinations in the ED should undergo a thorough evaluation that explores the differential diagnoses. Suggestions for evaluating patients in this setting appear in Table 5.²¹

Prodromal or at-risk children. There is no consensus on how early to initiate treatment for children in the prodromal stages of psychosis. Early identification and treatment is imperative because duration of untreated psychosis (DUP) is a primary predictor of treatment response in first-admission patients, and longer DUP corresponds to poorer prognosis in children.³⁰

Assessment scales for early identification of psychosis have limitations because most are not standardized for use in children age <14. To assess symptoms and predict future psychosis in children consider using:

• Scale of Prodromal Symptoms
• Structured Interview for Prodromal Symptoms
• Comprehensive Assessment of At-Risk Mental States
• Bonn Scale for the Assessment of Basic Symptoms.

A hallucinating child may be considered prodromal if he or she has:

• 30% drop in Global Assessment Functioning score in the past month
• a first-degree relative with affective or nonaffective psychotic disorder or schizotypal personality disorder.³¹

Antipsychotics. When treating children, use antipsychotics with caution and consider short- and long-term risks and benefits. Early treatment is indicated when hallucinations are among a patient’s psychotic symptoms; however, antipsychotic use for children in the prodromal phase lacks consensus. McGlashan et al³² showed that in 60 high-risk patients (mean age 16), olanzapine, 5 to 15 mg/d, reduced conversion to psychosis by 50% over 6 months. McGorry et al³³ observed that in 59 ultra-high risk patients (mean age 20), adding low-dose risperidone (1 to 2 mg/d) and cognitive-behavioral therapy (CBT) was superior to case management and supportive psychotherapy in preventing psychosis after 6 months of treatment, but this difference was not maintained at 6 months of follow-up.

CBT slows progression to psychosis in ultra-high risk patients and reduces positive symptoms more specifically than it improves emotional dysfunction.³⁴ CBT for psychosis is based on the concept that auditory hallucinations have an underlying personalized meaning or cognitive schema.³⁵ The initial goal of treatment is to engage the child and understand:

• What do the hallucinations mean to the patient?
• How did they start?
• Can the child start or stop them?
• What does the patient think they are?

The clinician then strives to help the child identify alternative explanations for these hallucinations and develop coping strategies.³⁶ “Normalizing” the voices helps the child attribute these voices to a less anxiety-provoking cause.³⁷ Consider suggesting common reasons for the hallucinations, such as:

• lack of sleep
• isolation
• dehydration
• extreme stress
• strong thoughts (obsessions)
• fever and illness
• lack of food
• drugs and alcohol.

If your patient learns that any of these reasons could explain the hallucinations, he or she may start to have a less delusional understanding of them. Suggest that the voices are “real” only if your patient believes it.

Help children develop coping strategies to control auditory hallucinations such as:

• humming
• listening to music
• reading (forwards and backwards)
• talking to others
• exercising
• singing
• medication
• ignoring the voices.

With normalization and other coping strategies, children with visual hallucinations can learn to transform in their mind the frightful image to a funnier one, which is less anxiety-provoking and gives them a sense of control.

Table 5

Suggestions for evaluating hallucinating children in the ED

Related Resources

• Bartels-Velthuis AA, Jenner JA, van de Willige G, et al. Prevalence and correlates of auditory vocal hallucinations in middle childhood. Br J Psychiatry. 2010;196(1):41-46.
• Cepeda C. Psychotic symptoms in children and adolescents: assessment, differential diagnosis, and treatment. New York, NY: Routledge; 2007.

Drug Brand Names

• Methylphenidate • Ritalin
• Olanzapine • Zyprexa
• 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 http://currentpsychiatry.blogspot.com/2010/10/hallucinations-in-children-diagnostic.html#comments

Hallucinations in children are of grave concern to parents and clinicians, but aren’t necessarily a symptom of mental illness. In adults, hallucinations usually are linked to serious psychopathology; however, in children they are not uncommon and may be part of normal development (Box).

A hallucination is a false auditory, visual, gustatory, tactile, or olfactory perception not associated with real external stimuli.¹ It must be differentiated from similar phenomenon such as illusions (misperception of actual stimuli), elaborate fantasies, imaginary companions, and eidetic images (visual images stored in memory).

Box

Common, yet a cause for concern

Epidemiologic studies show 2.8% of adults report hallucinations before age 21.² Nonpsychotic children as young as age 5 have reported hallucinations.³ Hallucinatory phenomenon may be present in 8% to 21% of all 11-year-old children; two-thirds of these patients have no DSM-IV-TR diagnosis.^4,5 However, 1 evaluation of 62 nonpsychotic hallucinating children treated in a psychiatric emergency department (ED):

• 34% had depression
• 22% had attention-deficit/hyperactivity disorder (ADHD)
• 21% had disruptive behavior disorders
• 23% had other diagnoses.⁶

Studies suggest that children who have hallucinations but no other psychotic symptoms have a better long-term prognosis than those with additional psychotic symptoms.⁷ A 17-year longitudinal study of children with hallucinations and concurrent emotional and conduct problems found:

• up to 50% of patients still experience hallucinations at age 30
• hallucinations did not significantly predict clinical outcome at age 30
• childhood hallucinations did not increase the risk for psychosis, depression, organic brain disorder, or other psychiatric illnesses.⁷

In a study of children with psychosis and disruptive disorders, at 2- to 8-years follow-up 50% met criteria for major depressive disorder, bipolar disorder, or schizophreniform disorders.⁸ In a 15-year longitudinal study of 11-year-olds, self-reported psychotic symptoms—such as delusional beliefs and hallucinatory experiences—predicted a high risk of schizophreniform disorder at age 26.⁹ These studies suggest that experiencing significant disruptions in thoughts and perceptions during childhood may be related to later development of prominent mood and thought disorders.

Differential diagnosis

Table 1 lists possible causes of hallucination in children.^6,10-13 Hallucinations during childhood can occur in the context of several psychiatric disorders, including:

• schizophrenia
• schizophreniform disorders
• mood disorders with psychotic features (Table 2).¹⁴

They can also manifest as comorbid or associated symptoms of disorders not commonly associated with hallucinations, such as ADHD, disruptive disorders, anxiety disorders, and prodromal clinical states. Medications, substance use, and organic and metabolic disorders also must be considered in the differential diagnosis (Table 3).

Hallucinations may occur in low-functioning or anxious children, in the context of psychosocial adversity or abuse, and during bereavement of a deceased parent when the surviving parent is emotionally unavailable.^11-13,15-17 Rule out hypnagogic and hypnopompic hallucinations, which are predominantly visual hallucinations that occur immediately before falling asleep and during the transition from sleep to wakefulness, respectively.¹⁸ Rarely, a child who has had hallucinations for some time may learn to complain of them when he or she is not hallucinating in order to obtain a primary or secondary gain, such as getting attention from caregivers.

Little is known about psychosis and hallucinations in preschoolers (age ≤5); therefore, their language use may help assessment. Because of cognitive immaturity, children often use illogical thinking and loose association and may describe their thoughts as “voices.” This is common in children with language disorders—and sometimes in healthy patients—who may talk about voices because they cannot describe their own thoughts.

Children with ADHD and/or oppositional defiant disorder often are impulsive and show poor judgment and may blame voices for telling them to do bad things. These “hallucinations” may represent internal thoughts battling with the child’s conscience.⁶ Auditory and visual hallucinations have been reported in children with Tourette syndrome, especially when associated with ADHD or obsessive-compulsive disorder.¹⁹

Medical causes. Electrolyte disturbances, metabolic disorders, fever, and serious infections are common nonpsychiatric causes of hallucinations.²⁰ Brain neoplasm—particularly in visual association areas, the temporal lobe, or portions of the optic nerve or retina—also may produce hallucinations, which can be complex with full images.²¹

Medications such as steroids and anticholinergics may cause hallucinations. Case studies report visual and tactile hallucinations with methylphenidate therapy that resolve after discontinuing the medication.²² Illicit substances, including cannabis, lysergic acid diethylamide (LSD), cocaine, amphetamines, 3,4-methylenedioxymeth-amphetamine (ecstasy), opiates, and barbiturates, can induce hallucinations.

Suspect substance-induced hallucinations if your patient shows:

• acute onset of hallucinations
• dilated pupils
• extreme agitation or drowsiness
• other signs of intoxication.

Hallucinations caused by seizure disorders are rare but can be somatosensory, visual (occipital lobe focus), auditory, olfactory (uncinate, complex partial), or gustatory. The hallucinations may be unformed (flashing lights or rushing noises) or formed (images, spoken words, or music) and could be part of the aura arising from the temporal lobe (dreamlike, flashbacks). Command hallucinations are rare and adult and pediatric patients usually sense they are not real.²³

Migraines occur in approximately 5% of prepubertal children and often are comorbid with affective and anxiety disorders.²⁴ Hallucinations associated with migraine commonly are visual, but gustatory, olfactory, and auditory hallucinations also can occur, with or without headaches.³ Any hallucination associated with headaches should be investigated neurologically. Other diagnostic aspects of hallucinations to consider while interviewing children are listed in Table 4.^25-28

Table 1

Possible causes of hallucinations in children and adolescents

Table 2

Content of hallucinations may point to their cause

Table 3

Hallucinations in young patients: Differential diagnoses

Table 4

Diagnostic considerations when assessing a hallucinating child

Psychotic disorder not otherwise specified

(NOS) in children often is overused and misused. One reason could be that DSM-IV-TR does not have a category for hallucinations in nonpsychotic children or for children who are at risk for psychosis. However, recommendations regarding the diagnosis of psychotic disorder NOS note it:

• may be used if uncertainty persists after ruling out all other diagnoses
• should be avoided when hallucinations occur in nonpsychotic children
• should not be used longitudinally if a clinician later determines a specific disorder accounts for the hallucinations.²⁹

Treatment

Addressing underlying medical or psychiatric illness, including substance use, is primary. Some adolescents or children may think that cannabis use is relatively benign. Discuss the risks of cannabis use in an age-appropriate manner.

In the ED. Children or adolescents who present with hallucinations in the ED should undergo a thorough evaluation that explores the differential diagnoses. Suggestions for evaluating patients in this setting appear in Table 5.²¹

Prodromal or at-risk children. There is no consensus on how early to initiate treatment for children in the prodromal stages of psychosis. Early identification and treatment is imperative because duration of untreated psychosis (DUP) is a primary predictor of treatment response in first-admission patients, and longer DUP corresponds to poorer prognosis in children.³⁰

Assessment scales for early identification of psychosis have limitations because most are not standardized for use in children age <14. To assess symptoms and predict future psychosis in children consider using:

• Scale of Prodromal Symptoms
• Structured Interview for Prodromal Symptoms
• Comprehensive Assessment of At-Risk Mental States
• Bonn Scale for the Assessment of Basic Symptoms.

A hallucinating child may be considered prodromal if he or she has:

• 30% drop in Global Assessment Functioning score in the past month
• a first-degree relative with affective or nonaffective psychotic disorder or schizotypal personality disorder.³¹

Antipsychotics. When treating children, use antipsychotics with caution and consider short- and long-term risks and benefits. Early treatment is indicated when hallucinations are among a patient’s psychotic symptoms; however, antipsychotic use for children in the prodromal phase lacks consensus. McGlashan et al³² showed that in 60 high-risk patients (mean age 16), olanzapine, 5 to 15 mg/d, reduced conversion to psychosis by 50% over 6 months. McGorry et al³³ observed that in 59 ultra-high risk patients (mean age 20), adding low-dose risperidone (1 to 2 mg/d) and cognitive-behavioral therapy (CBT) was superior to case management and supportive psychotherapy in preventing psychosis after 6 months of treatment, but this difference was not maintained at 6 months of follow-up.

CBT slows progression to psychosis in ultra-high risk patients and reduces positive symptoms more specifically than it improves emotional dysfunction.³⁴ CBT for psychosis is based on the concept that auditory hallucinations have an underlying personalized meaning or cognitive schema.³⁵ The initial goal of treatment is to engage the child and understand:

• What do the hallucinations mean to the patient?
• How did they start?
• Can the child start or stop them?
• What does the patient think they are?

The clinician then strives to help the child identify alternative explanations for these hallucinations and develop coping strategies.³⁶ “Normalizing” the voices helps the child attribute these voices to a less anxiety-provoking cause.³⁷ Consider suggesting common reasons for the hallucinations, such as:

• lack of sleep
• isolation
• dehydration
• extreme stress
• strong thoughts (obsessions)
• fever and illness
• lack of food
• drugs and alcohol.

If your patient learns that any of these reasons could explain the hallucinations, he or she may start to have a less delusional understanding of them. Suggest that the voices are “real” only if your patient believes it.

Help children develop coping strategies to control auditory hallucinations such as:

• humming
• listening to music
• reading (forwards and backwards)
• talking to others
• exercising
• singing
• medication
• ignoring the voices.

With normalization and other coping strategies, children with visual hallucinations can learn to transform in their mind the frightful image to a funnier one, which is less anxiety-provoking and gives them a sense of control.

Table 5

Suggestions for evaluating hallucinating children in the ED

Related Resources

• Bartels-Velthuis AA, Jenner JA, van de Willige G, et al. Prevalence and correlates of auditory vocal hallucinations in middle childhood. Br J Psychiatry. 2010;196(1):41-46.
• Cepeda C. Psychotic symptoms in children and adolescents: assessment, differential diagnosis, and treatment. New York, NY: Routledge; 2007.

Drug Brand Names

• Methylphenidate • Ritalin
• Olanzapine • Zyprexa
• 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 http://currentpsychiatry.blogspot.com/2010/10/hallucinations-in-children-diagnostic.html#comments

Hallucinations in children are of grave concern to parents and clinicians, but aren’t necessarily a symptom of mental illness. In adults, hallucinations usually are linked to serious psychopathology; however, in children they are not uncommon and may be part of normal development (Box).

A hallucination is a false auditory, visual, gustatory, tactile, or olfactory perception not associated with real external stimuli.¹ It must be differentiated from similar phenomenon such as illusions (misperception of actual stimuli), elaborate fantasies, imaginary companions, and eidetic images (visual images stored in memory).

Box

Common, yet a cause for concern

Epidemiologic studies show 2.8% of adults report hallucinations before age 21.² Nonpsychotic children as young as age 5 have reported hallucinations.³ Hallucinatory phenomenon may be present in 8% to 21% of all 11-year-old children; two-thirds of these patients have no DSM-IV-TR diagnosis.^4,5 However, 1 evaluation of 62 nonpsychotic hallucinating children treated in a psychiatric emergency department (ED):

• 34% had depression
• 22% had attention-deficit/hyperactivity disorder (ADHD)
• 21% had disruptive behavior disorders
• 23% had other diagnoses.⁶

Studies suggest that children who have hallucinations but no other psychotic symptoms have a better long-term prognosis than those with additional psychotic symptoms.⁷ A 17-year longitudinal study of children with hallucinations and concurrent emotional and conduct problems found:

• up to 50% of patients still experience hallucinations at age 30
• hallucinations did not significantly predict clinical outcome at age 30
• childhood hallucinations did not increase the risk for psychosis, depression, organic brain disorder, or other psychiatric illnesses.⁷

In a study of children with psychosis and disruptive disorders, at 2- to 8-years follow-up 50% met criteria for major depressive disorder, bipolar disorder, or schizophreniform disorders.⁸ In a 15-year longitudinal study of 11-year-olds, self-reported psychotic symptoms—such as delusional beliefs and hallucinatory experiences—predicted a high risk of schizophreniform disorder at age 26.⁹ These studies suggest that experiencing significant disruptions in thoughts and perceptions during childhood may be related to later development of prominent mood and thought disorders.

Differential diagnosis

Table 1 lists possible causes of hallucination in children.^6,10-13 Hallucinations during childhood can occur in the context of several psychiatric disorders, including:

• schizophrenia
• schizophreniform disorders
• mood disorders with psychotic features (Table 2).¹⁴

They can also manifest as comorbid or associated symptoms of disorders not commonly associated with hallucinations, such as ADHD, disruptive disorders, anxiety disorders, and prodromal clinical states. Medications, substance use, and organic and metabolic disorders also must be considered in the differential diagnosis (Table 3).

Hallucinations may occur in low-functioning or anxious children, in the context of psychosocial adversity or abuse, and during bereavement of a deceased parent when the surviving parent is emotionally unavailable.^11-13,15-17 Rule out hypnagogic and hypnopompic hallucinations, which are predominantly visual hallucinations that occur immediately before falling asleep and during the transition from sleep to wakefulness, respectively.¹⁸ Rarely, a child who has had hallucinations for some time may learn to complain of them when he or she is not hallucinating in order to obtain a primary or secondary gain, such as getting attention from caregivers.

Little is known about psychosis and hallucinations in preschoolers (age ≤5); therefore, their language use may help assessment. Because of cognitive immaturity, children often use illogical thinking and loose association and may describe their thoughts as “voices.” This is common in children with language disorders—and sometimes in healthy patients—who may talk about voices because they cannot describe their own thoughts.

Children with ADHD and/or oppositional defiant disorder often are impulsive and show poor judgment and may blame voices for telling them to do bad things. These “hallucinations” may represent internal thoughts battling with the child’s conscience.⁶ Auditory and visual hallucinations have been reported in children with Tourette syndrome, especially when associated with ADHD or obsessive-compulsive disorder.¹⁹

Medical causes. Electrolyte disturbances, metabolic disorders, fever, and serious infections are common nonpsychiatric causes of hallucinations.²⁰ Brain neoplasm—particularly in visual association areas, the temporal lobe, or portions of the optic nerve or retina—also may produce hallucinations, which can be complex with full images.²¹

Medications such as steroids and anticholinergics may cause hallucinations. Case studies report visual and tactile hallucinations with methylphenidate therapy that resolve after discontinuing the medication.²² Illicit substances, including cannabis, lysergic acid diethylamide (LSD), cocaine, amphetamines, 3,4-methylenedioxymeth-amphetamine (ecstasy), opiates, and barbiturates, can induce hallucinations.

Suspect substance-induced hallucinations if your patient shows:

• acute onset of hallucinations
• dilated pupils
• extreme agitation or drowsiness
• other signs of intoxication.

Hallucinations caused by seizure disorders are rare but can be somatosensory, visual (occipital lobe focus), auditory, olfactory (uncinate, complex partial), or gustatory. The hallucinations may be unformed (flashing lights or rushing noises) or formed (images, spoken words, or music) and could be part of the aura arising from the temporal lobe (dreamlike, flashbacks). Command hallucinations are rare and adult and pediatric patients usually sense they are not real.²³

Migraines occur in approximately 5% of prepubertal children and often are comorbid with affective and anxiety disorders.²⁴ Hallucinations associated with migraine commonly are visual, but gustatory, olfactory, and auditory hallucinations also can occur, with or without headaches.³ Any hallucination associated with headaches should be investigated neurologically. Other diagnostic aspects of hallucinations to consider while interviewing children are listed in Table 4.^25-28

Table 1

Possible causes of hallucinations in children and adolescents

Table 2

Content of hallucinations may point to their cause

Table 3

Hallucinations in young patients: Differential diagnoses

Table 4

Diagnostic considerations when assessing a hallucinating child

Psychotic disorder not otherwise specified

(NOS) in children often is overused and misused. One reason could be that DSM-IV-TR does not have a category for hallucinations in nonpsychotic children or for children who are at risk for psychosis. However, recommendations regarding the diagnosis of psychotic disorder NOS note it:

• may be used if uncertainty persists after ruling out all other diagnoses
• should be avoided when hallucinations occur in nonpsychotic children
• should not be used longitudinally if a clinician later determines a specific disorder accounts for the hallucinations.²⁹

Treatment

Addressing underlying medical or psychiatric illness, including substance use, is primary. Some adolescents or children may think that cannabis use is relatively benign. Discuss the risks of cannabis use in an age-appropriate manner.

In the ED. Children or adolescents who present with hallucinations in the ED should undergo a thorough evaluation that explores the differential diagnoses. Suggestions for evaluating patients in this setting appear in Table 5.²¹

Prodromal or at-risk children. There is no consensus on how early to initiate treatment for children in the prodromal stages of psychosis. Early identification and treatment is imperative because duration of untreated psychosis (DUP) is a primary predictor of treatment response in first-admission patients, and longer DUP corresponds to poorer prognosis in children.³⁰

Assessment scales for early identification of psychosis have limitations because most are not standardized for use in children age <14. To assess symptoms and predict future psychosis in children consider using:

• Scale of Prodromal Symptoms
• Structured Interview for Prodromal Symptoms
• Comprehensive Assessment of At-Risk Mental States
• Bonn Scale for the Assessment of Basic Symptoms.

A hallucinating child may be considered prodromal if he or she has:

• 30% drop in Global Assessment Functioning score in the past month
• a first-degree relative with affective or nonaffective psychotic disorder or schizotypal personality disorder.³¹

Antipsychotics. When treating children, use antipsychotics with caution and consider short- and long-term risks and benefits. Early treatment is indicated when hallucinations are among a patient’s psychotic symptoms; however, antipsychotic use for children in the prodromal phase lacks consensus. McGlashan et al³² showed that in 60 high-risk patients (mean age 16), olanzapine, 5 to 15 mg/d, reduced conversion to psychosis by 50% over 6 months. McGorry et al³³ observed that in 59 ultra-high risk patients (mean age 20), adding low-dose risperidone (1 to 2 mg/d) and cognitive-behavioral therapy (CBT) was superior to case management and supportive psychotherapy in preventing psychosis after 6 months of treatment, but this difference was not maintained at 6 months of follow-up.

CBT slows progression to psychosis in ultra-high risk patients and reduces positive symptoms more specifically than it improves emotional dysfunction.³⁴ CBT for psychosis is based on the concept that auditory hallucinations have an underlying personalized meaning or cognitive schema.³⁵ The initial goal of treatment is to engage the child and understand:

• What do the hallucinations mean to the patient?
• How did they start?
• Can the child start or stop them?
• What does the patient think they are?

The clinician then strives to help the child identify alternative explanations for these hallucinations and develop coping strategies.³⁶ “Normalizing” the voices helps the child attribute these voices to a less anxiety-provoking cause.³⁷ Consider suggesting common reasons for the hallucinations, such as:

• lack of sleep
• isolation
• dehydration
• extreme stress
• strong thoughts (obsessions)
• fever and illness
• lack of food
• drugs and alcohol.

If your patient learns that any of these reasons could explain the hallucinations, he or she may start to have a less delusional understanding of them. Suggest that the voices are “real” only if your patient believes it.

Help children develop coping strategies to control auditory hallucinations such as:

• humming
• listening to music
• reading (forwards and backwards)
• talking to others
• exercising
• singing
• medication
• ignoring the voices.

With normalization and other coping strategies, children with visual hallucinations can learn to transform in their mind the frightful image to a funnier one, which is less anxiety-provoking and gives them a sense of control.

Table 5

Suggestions for evaluating hallucinating children in the ED

Related Resources

• Bartels-Velthuis AA, Jenner JA, van de Willige G, et al. Prevalence and correlates of auditory vocal hallucinations in middle childhood. Br J Psychiatry. 2010;196(1):41-46.
• Cepeda C. Psychotic symptoms in children and adolescents: assessment, differential diagnosis, and treatment. New York, NY: Routledge; 2007.

Drug Brand Names

• Methylphenidate • Ritalin
• Olanzapine • Zyprexa
• 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 http://currentpsychiatry.blogspot.com/2010/10/re-envisioning-psychosis-new-language.html#comments

“I haven’t wanted to call it psychosis yet…”
“I’m not sure if this is psychosis or neurosis.”
“I wonder if there’s a psychotic process underneath all of this?”
“Psychotherapy won’t help psychosis.”

In our experience as practitioners in an early psychosis program, the above statements are common among mental health care providers. In our opinion, they are examples of vestiges of an archaic, overly simplistic clinical language that is not representative of current conceptions of psychosis as being on a continuum with normal experience.^1,2

The above quotes speak of psychosis as an all-or-none distinction: a “switch,” something fundamentally different from other psychological processes. In this article, we highlight common “all-or-none” myths about psychosis and argue for a more fluid, normalized psychosis language, where impairment is defined not by the absolute presence or absence of “weirdness” but instead by distress, conviction, preoccupation, and behavioral disturbance. We challenge the notion that the presence of psychosis mandates a “fast track” diagnosis that ignores the complexity of human experience.

Power of language

The word “psychosis” has enormous power for patients, families, clinicians, and the public. It often is used interchangeably with “craziness,” “insanity,” or “madness.” Mental health clinicians use psychosis to describe many phenomena, including:

• breaks with reality testing
• odd or delusional beliefs
• abnormal sensations
• catatonia
• bizarre behaviors
• so-called formal thought disorders.

It is likely one of the most heterogeneous symptom terms in psychiatry. DSM-IV-TR notes “the term psychotic has historically received a number of different definitions, none of which has achieved universal acceptance.”³

Psychosis myths. In addition to its phenomenological usage, the word psychosis also has various theoretical interpretations and often is used to demonstrate a fundamental pivot point for making qualitative distinctions. For example, clinicians and theorists have used “psychotic” to assume that someone experiencing psychosis:

• is operating on a core or primitive mode of thought, the so-called “primary process”⁴
• has a belief that is beyond understanding, one for which empathy is meaningless and misplaced⁵
• has clear convictions that violate social norms and refuses to accept society’s “proper” rules for logic and emotion⁶
• is in a state of “brain toxicity” with an “organic” cause (this comes from discussing psychosis with other clinicians, not from the literature).

Such seemingly disparate definitions share the assumption that psychosis represents a shift in categorical status, whether the category is developmental (advanced vs primitive), interpersonal judgment (able to be empathized with or not), sociopolitical status (conformist or not), or functional brain state (organic or non-organic).

Even the etymological basis for schizophrenia (its Greek roots signify “split mind,” which arguably spawned the long-held erroneous view that schizophrenia is a “split personality”) exemplifies this stance and reinforces the notion of discrete “all-or-none” categories of experience. In our view, such assumptions do not adequately reflect the reality of psychosis as a continuum of human experience, and could lead to serious, if unintended, stigmatization and oversimplification of persons who have psychotic symptoms. We argue that such all-or-none thinking reifies 2 clinical “myths” about what psychosis represents:

• Psychosis represents a fundamentally different type of cognitive process.
• Psychosis is so different from normal human experience that mood and anxiety symptoms become “subsumed” by it and treated as “secondary.”

Our goal is not to redefine psychosis or present an argument for diagnostically recategorizing schizophrenia, schizoaffective disorder, and bipolar disorder, which others have already done well.^7-10 Instead we want to reinforce the evidence-based and clinically relevant concept that psychosis exists on a definable continuum of human experience and to offer practitioners a clinical language of psychosis for assessing and treating psychotic symptoms that avoids unsupported all-or-none distinctions.

Defining ‘the schizophrenic’

In our experience, an unintended consequence of assuming psychosis is an all-or-none state is the clinician’s perpetual search for “real psychosis” as separate from “psychosis for which I have a good explanation.” Although this distinction is reminiscent of earlier arguments regarding “neurotic” vs “endogenous” depression, we feel that in this case “real or not” acts at a more basic level: the characterization of person types.

We assume that every clinician—ourselves included—who has worked with seriously mentally ill patients has heard an individual with schizophrenia referred to as “a schizophrenic.” Although the problem of defining a person as an illness is not unique to psychosis, we think that you will agree that the phrases “a depressive,” “a bipolar,” or “a generalized anxiotic” [sic] are rare.

DSM-IV-TR specifically avoids using expressions such as “a schizophrenic…and [instead uses]…an individual with schizophrenia.”¹¹ But we believe that DSM-IV-TR accidentally encourages the distinction of a “psychotic person type” by making schizoaffective disorder—a disorder that suggests a continuum—use Criterion A for schizophrenia as its defining feature. The implicit assumption is that “something categorical”—in this case defined by Criterion A—identifies a “psychotic person type,” as opposed to a person who simply has psychotic symptoms. If we see evidence of Criterion A, then the person is naturally moved into the realm of “schizophrenia and other psychotic disorders.” In other words, Criterion A subsumes other types of symptoms. In contrast, the presence of 1 month of social anxiety or obsessions and compulsions does not subsume other symptoms into primary anxiety disorders. To make this example explicit, we have developed a set of criteria for hypothetical disorders that overlap major categories of DSM-IV-TR (Table 1).

Table 1

The ‘logic’ of schizoaffective disorder applied to anxiety and OCD

A continuum approach

As a way out of this inductive logic trap, we suggest the following statements as evidence-based and clinically realistic ways of approaching psychosis assessment.

‘Normal sadness’ and ‘normal psychosis’ are equivalent. The DSM-IV-TR description of major depressive disorder, states that “periods of sadness are inherent aspects of the human experience.”¹² However, descriptions of psychosis rarely reflect that psychotic-like experiences are quite common^13-19 and easily induced in otherwise healthy people.²⁰ Psychotic symptoms are widely described as being genetically linked to normally distributed personality traits.^21-24 Finally, research on risk for developing chronic psychosis has identified that most patients who develop attenuated psychotic symptoms do not experience them chronically.^25-28 Together, these data argue strongly for a concept of psychosis as common and continuously distributed across large groups.

A psychosis screen can be much more than ‘+/- AH/VH/PI.’ We reject the idea that psychotic phenomena are fundamentally different from “normal” occurrences such as imagined or inner speech, perceptual fluctuations, distorted or rigid beliefs, or inability to accurately express one’s emotional state. Yet abnormal perception, affect flattening, and delusions often are viewed as “really weird,” which suggests most people never experience these phenomena, only “affected” people. This easily can lead to cognitive errors that associate psychosis as a state of mind that is fundamentally different from non-psychosis. In fact, DSMIV-TR categorizes the presence of persistent psychotic symptoms as evidence of disorder until proven otherwise.³

We feel that this simplistic language describing psychosis as inherently pathological ignores the clinical richness of psychotic experience. In our experience, many individuals who have been diagnosed with chronic psychosis have never been asked:

• about the timing, intensity, and character of their abnormal sensory experiences²⁹
• how their beliefs and schemas affect day-to-day behavior and choices
• if their psychotic symptoms are bothersome or troubling.

We worry that a person experiencing impairing psychotic symptoms could become overshadowed by all-or-none assumptions about the symptoms themselves.

We propose Table 2 as a guideline for approaching psychotic symptoms as expressions along a continuum of experience, one that shares much in common with recent well-developed biopsychosocial models of psychotic phenomena.³⁰ In our view, this allows for a therapeutic alliance that focuses on patient recovery, as opposed to seeing psychotic symptoms as the only treatment targets. By moving beyond all-or-none myths and approaching psychosis as a continuum with normal experience, we believe that patient recovery can become a realistic goal.

Table 2

Revising the clinical language of psychosis to separate presence from pathology

Re-envisioning psychosis

We conclude with a reiteration of recovery in the language of the US Surgeon General almost 10 years ago: “…hope and restoration of a meaningful life are possible, despite serious mental illness… Instead of focusing primarily on symptom relief…recovery casts a much wider spotlight on restoration of self-esteem and identity and on attaining meaningful roles in society.”³¹ We see no reason why people cannot live meaningful lives while also having symptoms of psychosis. Data from well-designed studies³² and accounts from individuals who have experienced or continue to experience psychosis³³ suggest that this is realistic.

By dispelling all-or-none myths, revealing the flawed logic of psychosis as “subsumer” of mood and anxiety, and describing the continuum of psychotic symptoms, we hope to encourage clinicians to be more positive and proactive in their approach to people experiencing impairing psychotic symptoms. Through assertive alliance and informed clinical technique, we envision a landscape in which psychosis is seen as a “normal” part of outpatient psychiatric practice.

Related resources

• Bentall R. Madness explained: psychosis and human nature. London, United Kingdom: Penguin Books; 2003.
• Gleeson JFM, McGorry PD, eds. Psychological interventions in early psychosis: a treatment handbook. West Sussex, United Kingdom: John Wiley & Sons; 2004.
• Wright JH, Kingdon D, Turkington D, et al. Cognitive-behavior therapy for severe mental illness. Arlington, VA: American Psychiatric Publishing, Inc; 2008.

Disclosure

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

Acknowledgement

The authors wish to acknowledge Dr. Carol Mathews for her comments on this manuscript.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/10/re-envisioning-psychosis-new-language.html#comments

“I haven’t wanted to call it psychosis yet…”
“I’m not sure if this is psychosis or neurosis.”
“I wonder if there’s a psychotic process underneath all of this?”
“Psychotherapy won’t help psychosis.”

In our experience as practitioners in an early psychosis program, the above statements are common among mental health care providers. In our opinion, they are examples of vestiges of an archaic, overly simplistic clinical language that is not representative of current conceptions of psychosis as being on a continuum with normal experience.^1,2

The above quotes speak of psychosis as an all-or-none distinction: a “switch,” something fundamentally different from other psychological processes. In this article, we highlight common “all-or-none” myths about psychosis and argue for a more fluid, normalized psychosis language, where impairment is defined not by the absolute presence or absence of “weirdness” but instead by distress, conviction, preoccupation, and behavioral disturbance. We challenge the notion that the presence of psychosis mandates a “fast track” diagnosis that ignores the complexity of human experience.

Power of language

The word “psychosis” has enormous power for patients, families, clinicians, and the public. It often is used interchangeably with “craziness,” “insanity,” or “madness.” Mental health clinicians use psychosis to describe many phenomena, including:

• breaks with reality testing
• odd or delusional beliefs
• abnormal sensations
• catatonia
• bizarre behaviors
• so-called formal thought disorders.

It is likely one of the most heterogeneous symptom terms in psychiatry. DSM-IV-TR notes “the term psychotic has historically received a number of different definitions, none of which has achieved universal acceptance.”³

Psychosis myths. In addition to its phenomenological usage, the word psychosis also has various theoretical interpretations and often is used to demonstrate a fundamental pivot point for making qualitative distinctions. For example, clinicians and theorists have used “psychotic” to assume that someone experiencing psychosis:

• is operating on a core or primitive mode of thought, the so-called “primary process”⁴
• has a belief that is beyond understanding, one for which empathy is meaningless and misplaced⁵
• has clear convictions that violate social norms and refuses to accept society’s “proper” rules for logic and emotion⁶
• is in a state of “brain toxicity” with an “organic” cause (this comes from discussing psychosis with other clinicians, not from the literature).

Such seemingly disparate definitions share the assumption that psychosis represents a shift in categorical status, whether the category is developmental (advanced vs primitive), interpersonal judgment (able to be empathized with or not), sociopolitical status (conformist or not), or functional brain state (organic or non-organic).

Even the etymological basis for schizophrenia (its Greek roots signify “split mind,” which arguably spawned the long-held erroneous view that schizophrenia is a “split personality”) exemplifies this stance and reinforces the notion of discrete “all-or-none” categories of experience. In our view, such assumptions do not adequately reflect the reality of psychosis as a continuum of human experience, and could lead to serious, if unintended, stigmatization and oversimplification of persons who have psychotic symptoms. We argue that such all-or-none thinking reifies 2 clinical “myths” about what psychosis represents:

• Psychosis represents a fundamentally different type of cognitive process.
• Psychosis is so different from normal human experience that mood and anxiety symptoms become “subsumed” by it and treated as “secondary.”

Our goal is not to redefine psychosis or present an argument for diagnostically recategorizing schizophrenia, schizoaffective disorder, and bipolar disorder, which others have already done well.^7-10 Instead we want to reinforce the evidence-based and clinically relevant concept that psychosis exists on a definable continuum of human experience and to offer practitioners a clinical language of psychosis for assessing and treating psychotic symptoms that avoids unsupported all-or-none distinctions.

Defining ‘the schizophrenic’

In our experience, an unintended consequence of assuming psychosis is an all-or-none state is the clinician’s perpetual search for “real psychosis” as separate from “psychosis for which I have a good explanation.” Although this distinction is reminiscent of earlier arguments regarding “neurotic” vs “endogenous” depression, we feel that in this case “real or not” acts at a more basic level: the characterization of person types.

We assume that every clinician—ourselves included—who has worked with seriously mentally ill patients has heard an individual with schizophrenia referred to as “a schizophrenic.” Although the problem of defining a person as an illness is not unique to psychosis, we think that you will agree that the phrases “a depressive,” “a bipolar,” or “a generalized anxiotic” [sic] are rare.

DSM-IV-TR specifically avoids using expressions such as “a schizophrenic…and [instead uses]…an individual with schizophrenia.”¹¹ But we believe that DSM-IV-TR accidentally encourages the distinction of a “psychotic person type” by making schizoaffective disorder—a disorder that suggests a continuum—use Criterion A for schizophrenia as its defining feature. The implicit assumption is that “something categorical”—in this case defined by Criterion A—identifies a “psychotic person type,” as opposed to a person who simply has psychotic symptoms. If we see evidence of Criterion A, then the person is naturally moved into the realm of “schizophrenia and other psychotic disorders.” In other words, Criterion A subsumes other types of symptoms. In contrast, the presence of 1 month of social anxiety or obsessions and compulsions does not subsume other symptoms into primary anxiety disorders. To make this example explicit, we have developed a set of criteria for hypothetical disorders that overlap major categories of DSM-IV-TR (Table 1).

Table 1

The ‘logic’ of schizoaffective disorder applied to anxiety and OCD

A continuum approach

As a way out of this inductive logic trap, we suggest the following statements as evidence-based and clinically realistic ways of approaching psychosis assessment.

‘Normal sadness’ and ‘normal psychosis’ are equivalent. The DSM-IV-TR description of major depressive disorder, states that “periods of sadness are inherent aspects of the human experience.”¹² However, descriptions of psychosis rarely reflect that psychotic-like experiences are quite common^13-19 and easily induced in otherwise healthy people.²⁰ Psychotic symptoms are widely described as being genetically linked to normally distributed personality traits.^21-24 Finally, research on risk for developing chronic psychosis has identified that most patients who develop attenuated psychotic symptoms do not experience them chronically.^25-28 Together, these data argue strongly for a concept of psychosis as common and continuously distributed across large groups.

A psychosis screen can be much more than ‘+/- AH/VH/PI.’ We reject the idea that psychotic phenomena are fundamentally different from “normal” occurrences such as imagined or inner speech, perceptual fluctuations, distorted or rigid beliefs, or inability to accurately express one’s emotional state. Yet abnormal perception, affect flattening, and delusions often are viewed as “really weird,” which suggests most people never experience these phenomena, only “affected” people. This easily can lead to cognitive errors that associate psychosis as a state of mind that is fundamentally different from non-psychosis. In fact, DSMIV-TR categorizes the presence of persistent psychotic symptoms as evidence of disorder until proven otherwise.³

We feel that this simplistic language describing psychosis as inherently pathological ignores the clinical richness of psychotic experience. In our experience, many individuals who have been diagnosed with chronic psychosis have never been asked:

• about the timing, intensity, and character of their abnormal sensory experiences²⁹
• how their beliefs and schemas affect day-to-day behavior and choices
• if their psychotic symptoms are bothersome or troubling.

We worry that a person experiencing impairing psychotic symptoms could become overshadowed by all-or-none assumptions about the symptoms themselves.

We propose Table 2 as a guideline for approaching psychotic symptoms as expressions along a continuum of experience, one that shares much in common with recent well-developed biopsychosocial models of psychotic phenomena.³⁰ In our view, this allows for a therapeutic alliance that focuses on patient recovery, as opposed to seeing psychotic symptoms as the only treatment targets. By moving beyond all-or-none myths and approaching psychosis as a continuum with normal experience, we believe that patient recovery can become a realistic goal.

Table 2

Revising the clinical language of psychosis to separate presence from pathology

Re-envisioning psychosis

We conclude with a reiteration of recovery in the language of the US Surgeon General almost 10 years ago: “…hope and restoration of a meaningful life are possible, despite serious mental illness… Instead of focusing primarily on symptom relief…recovery casts a much wider spotlight on restoration of self-esteem and identity and on attaining meaningful roles in society.”³¹ We see no reason why people cannot live meaningful lives while also having symptoms of psychosis. Data from well-designed studies³² and accounts from individuals who have experienced or continue to experience psychosis³³ suggest that this is realistic.

By dispelling all-or-none myths, revealing the flawed logic of psychosis as “subsumer” of mood and anxiety, and describing the continuum of psychotic symptoms, we hope to encourage clinicians to be more positive and proactive in their approach to people experiencing impairing psychotic symptoms. Through assertive alliance and informed clinical technique, we envision a landscape in which psychosis is seen as a “normal” part of outpatient psychiatric practice.

Related resources

• Bentall R. Madness explained: psychosis and human nature. London, United Kingdom: Penguin Books; 2003.
• Gleeson JFM, McGorry PD, eds. Psychological interventions in early psychosis: a treatment handbook. West Sussex, United Kingdom: John Wiley & Sons; 2004.
• Wright JH, Kingdon D, Turkington D, et al. Cognitive-behavior therapy for severe mental illness. Arlington, VA: American Psychiatric Publishing, Inc; 2008.

Disclosure

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

Acknowledgement

The authors wish to acknowledge Dr. Carol Mathews for her comments on this manuscript.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/10/re-envisioning-psychosis-new-language.html#comments

“I haven’t wanted to call it psychosis yet…”
“I’m not sure if this is psychosis or neurosis.”
“I wonder if there’s a psychotic process underneath all of this?”
“Psychotherapy won’t help psychosis.”

In our experience as practitioners in an early psychosis program, the above statements are common among mental health care providers. In our opinion, they are examples of vestiges of an archaic, overly simplistic clinical language that is not representative of current conceptions of psychosis as being on a continuum with normal experience.^1,2

The above quotes speak of psychosis as an all-or-none distinction: a “switch,” something fundamentally different from other psychological processes. In this article, we highlight common “all-or-none” myths about psychosis and argue for a more fluid, normalized psychosis language, where impairment is defined not by the absolute presence or absence of “weirdness” but instead by distress, conviction, preoccupation, and behavioral disturbance. We challenge the notion that the presence of psychosis mandates a “fast track” diagnosis that ignores the complexity of human experience.

Power of language

The word “psychosis” has enormous power for patients, families, clinicians, and the public. It often is used interchangeably with “craziness,” “insanity,” or “madness.” Mental health clinicians use psychosis to describe many phenomena, including:

• breaks with reality testing
• odd or delusional beliefs
• abnormal sensations
• catatonia
• bizarre behaviors
• so-called formal thought disorders.

It is likely one of the most heterogeneous symptom terms in psychiatry. DSM-IV-TR notes “the term psychotic has historically received a number of different definitions, none of which has achieved universal acceptance.”³

Psychosis myths. In addition to its phenomenological usage, the word psychosis also has various theoretical interpretations and often is used to demonstrate a fundamental pivot point for making qualitative distinctions. For example, clinicians and theorists have used “psychotic” to assume that someone experiencing psychosis:

• is operating on a core or primitive mode of thought, the so-called “primary process”⁴
• has a belief that is beyond understanding, one for which empathy is meaningless and misplaced⁵
• has clear convictions that violate social norms and refuses to accept society’s “proper” rules for logic and emotion⁶
• is in a state of “brain toxicity” with an “organic” cause (this comes from discussing psychosis with other clinicians, not from the literature).

Such seemingly disparate definitions share the assumption that psychosis represents a shift in categorical status, whether the category is developmental (advanced vs primitive), interpersonal judgment (able to be empathized with or not), sociopolitical status (conformist or not), or functional brain state (organic or non-organic).

Even the etymological basis for schizophrenia (its Greek roots signify “split mind,” which arguably spawned the long-held erroneous view that schizophrenia is a “split personality”) exemplifies this stance and reinforces the notion of discrete “all-or-none” categories of experience. In our view, such assumptions do not adequately reflect the reality of psychosis as a continuum of human experience, and could lead to serious, if unintended, stigmatization and oversimplification of persons who have psychotic symptoms. We argue that such all-or-none thinking reifies 2 clinical “myths” about what psychosis represents:

• Psychosis represents a fundamentally different type of cognitive process.
• Psychosis is so different from normal human experience that mood and anxiety symptoms become “subsumed” by it and treated as “secondary.”

Our goal is not to redefine psychosis or present an argument for diagnostically recategorizing schizophrenia, schizoaffective disorder, and bipolar disorder, which others have already done well.^7-10 Instead we want to reinforce the evidence-based and clinically relevant concept that psychosis exists on a definable continuum of human experience and to offer practitioners a clinical language of psychosis for assessing and treating psychotic symptoms that avoids unsupported all-or-none distinctions.

Defining ‘the schizophrenic’

In our experience, an unintended consequence of assuming psychosis is an all-or-none state is the clinician’s perpetual search for “real psychosis” as separate from “psychosis for which I have a good explanation.” Although this distinction is reminiscent of earlier arguments regarding “neurotic” vs “endogenous” depression, we feel that in this case “real or not” acts at a more basic level: the characterization of person types.

We assume that every clinician—ourselves included—who has worked with seriously mentally ill patients has heard an individual with schizophrenia referred to as “a schizophrenic.” Although the problem of defining a person as an illness is not unique to psychosis, we think that you will agree that the phrases “a depressive,” “a bipolar,” or “a generalized anxiotic” [sic] are rare.

DSM-IV-TR specifically avoids using expressions such as “a schizophrenic…and [instead uses]…an individual with schizophrenia.”¹¹ But we believe that DSM-IV-TR accidentally encourages the distinction of a “psychotic person type” by making schizoaffective disorder—a disorder that suggests a continuum—use Criterion A for schizophrenia as its defining feature. The implicit assumption is that “something categorical”—in this case defined by Criterion A—identifies a “psychotic person type,” as opposed to a person who simply has psychotic symptoms. If we see evidence of Criterion A, then the person is naturally moved into the realm of “schizophrenia and other psychotic disorders.” In other words, Criterion A subsumes other types of symptoms. In contrast, the presence of 1 month of social anxiety or obsessions and compulsions does not subsume other symptoms into primary anxiety disorders. To make this example explicit, we have developed a set of criteria for hypothetical disorders that overlap major categories of DSM-IV-TR (Table 1).

Table 1

The ‘logic’ of schizoaffective disorder applied to anxiety and OCD

A continuum approach

As a way out of this inductive logic trap, we suggest the following statements as evidence-based and clinically realistic ways of approaching psychosis assessment.

‘Normal sadness’ and ‘normal psychosis’ are equivalent. The DSM-IV-TR description of major depressive disorder, states that “periods of sadness are inherent aspects of the human experience.”¹² However, descriptions of psychosis rarely reflect that psychotic-like experiences are quite common^13-19 and easily induced in otherwise healthy people.²⁰ Psychotic symptoms are widely described as being genetically linked to normally distributed personality traits.^21-24 Finally, research on risk for developing chronic psychosis has identified that most patients who develop attenuated psychotic symptoms do not experience them chronically.^25-28 Together, these data argue strongly for a concept of psychosis as common and continuously distributed across large groups.

A psychosis screen can be much more than ‘+/- AH/VH/PI.’ We reject the idea that psychotic phenomena are fundamentally different from “normal” occurrences such as imagined or inner speech, perceptual fluctuations, distorted or rigid beliefs, or inability to accurately express one’s emotional state. Yet abnormal perception, affect flattening, and delusions often are viewed as “really weird,” which suggests most people never experience these phenomena, only “affected” people. This easily can lead to cognitive errors that associate psychosis as a state of mind that is fundamentally different from non-psychosis. In fact, DSMIV-TR categorizes the presence of persistent psychotic symptoms as evidence of disorder until proven otherwise.³

We feel that this simplistic language describing psychosis as inherently pathological ignores the clinical richness of psychotic experience. In our experience, many individuals who have been diagnosed with chronic psychosis have never been asked:

• about the timing, intensity, and character of their abnormal sensory experiences²⁹
• how their beliefs and schemas affect day-to-day behavior and choices
• if their psychotic symptoms are bothersome or troubling.

We worry that a person experiencing impairing psychotic symptoms could become overshadowed by all-or-none assumptions about the symptoms themselves.

We propose Table 2 as a guideline for approaching psychotic symptoms as expressions along a continuum of experience, one that shares much in common with recent well-developed biopsychosocial models of psychotic phenomena.³⁰ In our view, this allows for a therapeutic alliance that focuses on patient recovery, as opposed to seeing psychotic symptoms as the only treatment targets. By moving beyond all-or-none myths and approaching psychosis as a continuum with normal experience, we believe that patient recovery can become a realistic goal.

Table 2

Revising the clinical language of psychosis to separate presence from pathology

Re-envisioning psychosis

We conclude with a reiteration of recovery in the language of the US Surgeon General almost 10 years ago: “…hope and restoration of a meaningful life are possible, despite serious mental illness… Instead of focusing primarily on symptom relief…recovery casts a much wider spotlight on restoration of self-esteem and identity and on attaining meaningful roles in society.”³¹ We see no reason why people cannot live meaningful lives while also having symptoms of psychosis. Data from well-designed studies³² and accounts from individuals who have experienced or continue to experience psychosis³³ suggest that this is realistic.

By dispelling all-or-none myths, revealing the flawed logic of psychosis as “subsumer” of mood and anxiety, and describing the continuum of psychotic symptoms, we hope to encourage clinicians to be more positive and proactive in their approach to people experiencing impairing psychotic symptoms. Through assertive alliance and informed clinical technique, we envision a landscape in which psychosis is seen as a “normal” part of outpatient psychiatric practice.

Related resources

• Bentall R. Madness explained: psychosis and human nature. London, United Kingdom: Penguin Books; 2003.
• Gleeson JFM, McGorry PD, eds. Psychological interventions in early psychosis: a treatment handbook. West Sussex, United Kingdom: John Wiley & Sons; 2004.
• Wright JH, Kingdon D, Turkington D, et al. Cognitive-behavior therapy for severe mental illness. Arlington, VA: American Psychiatric Publishing, Inc; 2008.

Disclosure

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

Acknowledgement

The authors wish to acknowledge Dr. Carol Mathews for her comments on this manuscript.

CASE: Scared and confused

Mr. C, age 28, presents to the emergency department (ED) in police custody with agitation and altered mental status. Earlier that evening, Mr. C’s girlfriend noticed he was talking to himself while watching television. A few hours later, Mr. C thought someone was breaking into his house. Mr. C ran out of the house screaming for help, broke his neighbor’s window, and eventually called the police. When the police arrived Mr. C was wearing only his underwear, shaking, and bleeding from his hands. He said he was afraid and refused to respond to police instructions. Police officers used an electronic stun gun to facilitate transport to the hospital.

Mr. C admits to smoking 3 to 4 marijuana joints daily for the past 16 years. His last drug use was 2 hours before his symptoms began. Mr. C suggests that someone may have adulterated his marijuana joint but he has no factual basis for this accusation. He denies using alcohol and other illicit drugs and has no personal or family psychiatric history. He denies recent fever, loss of consciousness, chest pain, weakness, myalgia, or headache. Medically stable, his only complaint is mild hand pain.

Mr. C is alert, awake, and oriented to his name, and he responds properly to questions. He is tachycardic (101 bpm), his blood pressure is 149/57 mm Hg with normal S1 and S2 sounds, and he has no meningismus or nystagmus. Glasgow Coma Scale score is 15. He has increased deep tendon reflexes on the right upper and lower limb with good hand-grip and multiple abrasions and lacerations on his hands.

The authors’ observations

New-onset psychosis can have a wide differential diagnosis, particularly when reliable history is not available. Mr. C’s allegation that someone tampered with his marijuana raises 2 possibilities: embalming fluid (form-aldehyde) toxicity or PCP intoxication.

Embalming fluid toxicity can cause:

• agitation and sudden unpredictable behavior
• confusion or toxic delirium
• coma or seizure
• cerebral and pulmonary edema or death in severe cases.

The terms “wet,” “sherm,” “fly,” “amp,” or “illy” are used to describe a marijuana cigarette that has been dipped into embalming fluid, dried, and then smoked.¹ The effect is similar to that of PCP and causes extreme hallucinations. Reported highs last 30 minutes to 1 hour.²

Symptomatology of PCP intoxication may be indistinguishable from functional psychosis (Table 1).³ Visual, auditory, and tactile misperceptions are common and highly changeable disorientation often is accompanied by alternating periods of lethargy and fearful agitation. These patients typically show catatonic posturing and/or stereotyped movement. Somatic sensations appear to be disassociated; patients may misperceive pain, distance, and time. Patients taking PCP rarely admit to true hallucinations; however their thinking usually is grossly disoriented.⁴ Symptoms of delirium may last from 30 minutes to 6 hours in 80% of cases; 12% of patients may remain symptomatic for 12 hours. Violent behavior and agitation usually lasts only a few hours.⁵

Long-term marijuana abuse can lead to psychosis⁶ but acute onset is not typical, and recent prospective trials raised doubts that cannabis would be a sole factor.⁷ Instead, cannabis may be 1 of several factors that contribute to psychosis, particularly in patients who are predisposed.

Table 1

Phencyclidine (PCP) intoxication: What to look for

Possible neurologic causes

Complex partial seizures—also known as psychomotor epilepsy—are caused by a surge of electrical activity in the brain. Seizures often involve 1 of the brain’s temporal lobes but can affect any brain region. Symptoms include:

• impaired social interaction
• inability to control one’s movements
• alogia
• amnesia.

Episodes typically start with a blank stare followed by automatisms. The actions and movements often are unorganized or confused. Motor symptoms typically last for 1 to 2 minutes and confusion persists for another 1 to 2 minutes.⁸ In rare cases, a patient may become agitated or engage in behaviors such as undressing. Complex partial seizures may cause a person to run in apparent fear, cry out, or repeat a phrase.⁹ Electroencephalogram, CT, MRI, or positron-emission tomography scan could reveal any intracranial focus of complex partial seizures.

We suspect PCP or embalming fluid intoxication and initiate supportive therapy.

EVALUATION: Still confused

Initial baseline labs include a urine drug screen (UDS), chest radiography, ECG, and head CT. Mr. C’s UDS is positive for cannabis. A specific PCP assay is negative. White blood cell count (WBC) is 22,000/μL with high neutrophil count (88%), creatine kinase (CK) is 458 U/L, and urinalyis reveals protein 75 mg/dL and ketone 50 mg/dL. Head CT is negative for any acute process (click here for detailed description of Mr. C�s hospital course while in the ED).

During psychiatric evaluation 7 hours after presentation, Mr. C’s speech is loose and somewhat pressured, but intelligible. He cannot follow commands. Mr. C is delusional and appears to be hallucinating. He can repeat 3 words immediately but not after 3 minutes. We start Mr. C on divalproex, 1,500 mg/d, haloperidol, 6 mg/d, and IV lorazepam, 2 mg as needed for agitation. Although mildly disoriented, he gradually becomes less agitated.

The authors’ observations

At this point further evaluation is needed. Mr. C’s elevated WBC count could explain his fluctuating symptoms. He cannot provide further history and his family denies any past psychiatric episodes. Thyroid-stimulating hormone, B12, and folate levels are within normal limits. A negative LP rules out meningitic infection. We give Mr. C a diagnosis of psychosis NOS (Table 2).¹⁰

Table 2

DSM-IV-TR criteria for psychotic disorder, not otherwise specified

TREATMENT: Medication choices

After 8 hours in the ED, Mr. C is transferred to the medical unit, where he becomes agitated and complains of auditory and visual hallucinations. He receives divalproex, 750 mg, haloperidol, 3 mg, and IM diphenhydramine, 50 mg, to calm him. He remains agitated but not violent until bedtime. At midnight he is agitated and violent and receives another dose of haloperidol and IM diphenhydramine with IV lorazepam, 2 mg. These medications calm him and he is able to sleep until morning.

Morning labs reveal CK is 674 U/L and WBC decreased to 13,200/μL. Mr. C denies any distress but after the fourth dose of haloperidol, he develops dystonia of his arms so we discontinue this medication. We start aripiprazole, 10 mg/d gradually increased to 30 mg/d, and Mr. C receives 1 injection of diphenhydramine. He responds well to the treatment.

The next few hours are uneventful but then Mr. C becomes verbally abusive to his relatives and sitter; physical restraints are ordered and he receives IM ziprasidone, 20 mg, and IV lorazepam, 2 mg. He remains awake and babbling. His perception continues to wax and wane and his words are jumbled. He remains calm until the next morning (click here for detailed description of Mr. C�s hospital course while on the medical unit).

After 4 days on the medical unit Mr. C is transferred to the psychiatry unit, where he is angry, belligerent, and hostile, but not placed in restraints. His symptoms resolve in 2 days without any further episodes of violent behavior.

OUTCOME: Solving the puzzle

When Mr. C becomes cooperative, he gives a detailed history. He repeats his suspicion of smoking adulterated marijuana, but during detailed questioning, he admits to using alprazolam, which he purchased illegally, to sleep for the past 6 to 7 months. He started with 1 or 2 “footballs” (1 to 2 mg) and gradually increased to 3 or 4 “bars” (6 to 8 mg) each day. Mr. C could no longer afford the drug and last took alprazolam 6 days before his symptoms began. He says that after stopping alprazolam he felt anxious and could not sleep. His girlfriend adds that he was irritable and “he had not been acting himself” several days before admission. She says he complained of hearing the voice of God, particularly when he was not taking alprazolam.

Mr. C’s hand wounds heal and his vitals are normal during his 1-week stay on the psychiatric unit. His interactions with staff and peers improve. Aripiprazole is tapered and discontinued; divalproex is reduced to 1,000 mg/d. Mr. C is discharged 11 days after presentation and prescribed divalproex, 1,000 mg/d, with instructions to taper the drug over several days to prevent withdrawal seizures before stopping it in 1 week.

Mr. C does not return for his follow-up appointment; however, in a telephone follow-up 6 months later, he denies experiencing withdrawal symptoms after discharge. Mr. C is now undergoing drug rehabilitation.

The authors’ observations

Benzodiazepine withdrawal symptoms occur 7 to 10 days after abrupt cessation (Table 3).¹⁰ Symptoms are similar to those of alcohol withdrawal and include tachycardia, hypertension, clouding of consciousness, and auditory and visual hallucinations.¹¹ Serious reactions to benzodiazepine withdrawal include seizures and death.¹²

Because of the high prevalence of poly-substance misuse, obtain a detailed substance use history in patients undergoing benzodiazepine withdrawal to determine the likelihood of polysubstance withdrawal.¹³ A cross-tolerant sedative such as clonazepam could prevent withdrawal symptoms as the dose is gradually decreased. Long-acting benzodiazepines such as clonazepam or diazepam are recommended.¹⁴

In Mr. C’s case, minor withdrawal symptoms, such as disturbed sleep and irritability, began 3 to 4 days after discontinuing benzodiazepines¹⁵ and preceded development of psychosis. Withdrawal symptoms usually resolve after 2 weeks.¹⁶ Mr. C responded only partially to IV lorazepam because he did not receive the total replacement dose. Had we known he was experiencing benzodiazepine withdrawal, Mr. C could have been managed with detoxi"cation of the primary drug, alprazolam, with diazepam substitution and tapering over 3 weeks.¹⁷

Table 3

Criteria for sedative, hypnotic, or anxiolytic withdrawal

Related Resource

• Vikander B, Koechling UM, Borg S, et al. Benzodiazepine tapering: a prospective study. Nord J Psychiatry. 2010; 64(4):273-282.

Drug Brand Names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Chlordiazepoxide • Librium
• Diazepam • Valium
• Diphenhydramine • Diphenhydramine injection
• Divalproex • Depakote
• Haloperidol • Haldol
• Lorazepam • Ativan
• Ziprasidone • Geodon

Acknowledgements

The authors wish to thank Reena Kumar, MD, and Sonja Gennuso, fourth-year medical student at Louisiana State University Health Sciences Center, Shreveport, for their help in preparing this manuscript.

Disclosure

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

Table 1

Mr. C’s hospital course in the emergency department

Table 2

Mr. C’s hospital course on the medical unit

CASE: Scared and confused

Mr. C, age 28, presents to the emergency department (ED) in police custody with agitation and altered mental status. Earlier that evening, Mr. C’s girlfriend noticed he was talking to himself while watching television. A few hours later, Mr. C thought someone was breaking into his house. Mr. C ran out of the house screaming for help, broke his neighbor’s window, and eventually called the police. When the police arrived Mr. C was wearing only his underwear, shaking, and bleeding from his hands. He said he was afraid and refused to respond to police instructions. Police officers used an electronic stun gun to facilitate transport to the hospital.

Mr. C admits to smoking 3 to 4 marijuana joints daily for the past 16 years. His last drug use was 2 hours before his symptoms began. Mr. C suggests that someone may have adulterated his marijuana joint but he has no factual basis for this accusation. He denies using alcohol and other illicit drugs and has no personal or family psychiatric history. He denies recent fever, loss of consciousness, chest pain, weakness, myalgia, or headache. Medically stable, his only complaint is mild hand pain.

Mr. C is alert, awake, and oriented to his name, and he responds properly to questions. He is tachycardic (101 bpm), his blood pressure is 149/57 mm Hg with normal S1 and S2 sounds, and he has no meningismus or nystagmus. Glasgow Coma Scale score is 15. He has increased deep tendon reflexes on the right upper and lower limb with good hand-grip and multiple abrasions and lacerations on his hands.

The authors’ observations

New-onset psychosis can have a wide differential diagnosis, particularly when reliable history is not available. Mr. C’s allegation that someone tampered with his marijuana raises 2 possibilities: embalming fluid (form-aldehyde) toxicity or PCP intoxication.

Embalming fluid toxicity can cause:

• agitation and sudden unpredictable behavior
• confusion or toxic delirium
• coma or seizure
• cerebral and pulmonary edema or death in severe cases.

The terms “wet,” “sherm,” “fly,” “amp,” or “illy” are used to describe a marijuana cigarette that has been dipped into embalming fluid, dried, and then smoked.¹ The effect is similar to that of PCP and causes extreme hallucinations. Reported highs last 30 minutes to 1 hour.²

Symptomatology of PCP intoxication may be indistinguishable from functional psychosis (Table 1).³ Visual, auditory, and tactile misperceptions are common and highly changeable disorientation often is accompanied by alternating periods of lethargy and fearful agitation. These patients typically show catatonic posturing and/or stereotyped movement. Somatic sensations appear to be disassociated; patients may misperceive pain, distance, and time. Patients taking PCP rarely admit to true hallucinations; however their thinking usually is grossly disoriented.⁴ Symptoms of delirium may last from 30 minutes to 6 hours in 80% of cases; 12% of patients may remain symptomatic for 12 hours. Violent behavior and agitation usually lasts only a few hours.⁵

Long-term marijuana abuse can lead to psychosis⁶ but acute onset is not typical, and recent prospective trials raised doubts that cannabis would be a sole factor.⁷ Instead, cannabis may be 1 of several factors that contribute to psychosis, particularly in patients who are predisposed.

Table 1

Phencyclidine (PCP) intoxication: What to look for

Possible neurologic causes

Complex partial seizures—also known as psychomotor epilepsy—are caused by a surge of electrical activity in the brain. Seizures often involve 1 of the brain’s temporal lobes but can affect any brain region. Symptoms include:

• impaired social interaction
• inability to control one’s movements
• alogia
• amnesia.

Episodes typically start with a blank stare followed by automatisms. The actions and movements often are unorganized or confused. Motor symptoms typically last for 1 to 2 minutes and confusion persists for another 1 to 2 minutes.⁸ In rare cases, a patient may become agitated or engage in behaviors such as undressing. Complex partial seizures may cause a person to run in apparent fear, cry out, or repeat a phrase.⁹ Electroencephalogram, CT, MRI, or positron-emission tomography scan could reveal any intracranial focus of complex partial seizures.

We suspect PCP or embalming fluid intoxication and initiate supportive therapy.

EVALUATION: Still confused

Initial baseline labs include a urine drug screen (UDS), chest radiography, ECG, and head CT. Mr. C’s UDS is positive for cannabis. A specific PCP assay is negative. White blood cell count (WBC) is 22,000/μL with high neutrophil count (88%), creatine kinase (CK) is 458 U/L, and urinalyis reveals protein 75 mg/dL and ketone 50 mg/dL. Head CT is negative for any acute process (click here for detailed description of Mr. C�s hospital course while in the ED).

During psychiatric evaluation 7 hours after presentation, Mr. C’s speech is loose and somewhat pressured, but intelligible. He cannot follow commands. Mr. C is delusional and appears to be hallucinating. He can repeat 3 words immediately but not after 3 minutes. We start Mr. C on divalproex, 1,500 mg/d, haloperidol, 6 mg/d, and IV lorazepam, 2 mg as needed for agitation. Although mildly disoriented, he gradually becomes less agitated.

The authors’ observations

At this point further evaluation is needed. Mr. C’s elevated WBC count could explain his fluctuating symptoms. He cannot provide further history and his family denies any past psychiatric episodes. Thyroid-stimulating hormone, B12, and folate levels are within normal limits. A negative LP rules out meningitic infection. We give Mr. C a diagnosis of psychosis NOS (Table 2).¹⁰

Table 2

DSM-IV-TR criteria for psychotic disorder, not otherwise specified

TREATMENT: Medication choices

After 8 hours in the ED, Mr. C is transferred to the medical unit, where he becomes agitated and complains of auditory and visual hallucinations. He receives divalproex, 750 mg, haloperidol, 3 mg, and IM diphenhydramine, 50 mg, to calm him. He remains agitated but not violent until bedtime. At midnight he is agitated and violent and receives another dose of haloperidol and IM diphenhydramine with IV lorazepam, 2 mg. These medications calm him and he is able to sleep until morning.

Morning labs reveal CK is 674 U/L and WBC decreased to 13,200/μL. Mr. C denies any distress but after the fourth dose of haloperidol, he develops dystonia of his arms so we discontinue this medication. We start aripiprazole, 10 mg/d gradually increased to 30 mg/d, and Mr. C receives 1 injection of diphenhydramine. He responds well to the treatment.

The next few hours are uneventful but then Mr. C becomes verbally abusive to his relatives and sitter; physical restraints are ordered and he receives IM ziprasidone, 20 mg, and IV lorazepam, 2 mg. He remains awake and babbling. His perception continues to wax and wane and his words are jumbled. He remains calm until the next morning (click here for detailed description of Mr. C�s hospital course while on the medical unit).

After 4 days on the medical unit Mr. C is transferred to the psychiatry unit, where he is angry, belligerent, and hostile, but not placed in restraints. His symptoms resolve in 2 days without any further episodes of violent behavior.

OUTCOME: Solving the puzzle

When Mr. C becomes cooperative, he gives a detailed history. He repeats his suspicion of smoking adulterated marijuana, but during detailed questioning, he admits to using alprazolam, which he purchased illegally, to sleep for the past 6 to 7 months. He started with 1 or 2 “footballs” (1 to 2 mg) and gradually increased to 3 or 4 “bars” (6 to 8 mg) each day. Mr. C could no longer afford the drug and last took alprazolam 6 days before his symptoms began. He says that after stopping alprazolam he felt anxious and could not sleep. His girlfriend adds that he was irritable and “he had not been acting himself” several days before admission. She says he complained of hearing the voice of God, particularly when he was not taking alprazolam.

Mr. C’s hand wounds heal and his vitals are normal during his 1-week stay on the psychiatric unit. His interactions with staff and peers improve. Aripiprazole is tapered and discontinued; divalproex is reduced to 1,000 mg/d. Mr. C is discharged 11 days after presentation and prescribed divalproex, 1,000 mg/d, with instructions to taper the drug over several days to prevent withdrawal seizures before stopping it in 1 week.

Mr. C does not return for his follow-up appointment; however, in a telephone follow-up 6 months later, he denies experiencing withdrawal symptoms after discharge. Mr. C is now undergoing drug rehabilitation.

The authors’ observations

Benzodiazepine withdrawal symptoms occur 7 to 10 days after abrupt cessation (Table 3).¹⁰ Symptoms are similar to those of alcohol withdrawal and include tachycardia, hypertension, clouding of consciousness, and auditory and visual hallucinations.¹¹ Serious reactions to benzodiazepine withdrawal include seizures and death.¹²

Because of the high prevalence of poly-substance misuse, obtain a detailed substance use history in patients undergoing benzodiazepine withdrawal to determine the likelihood of polysubstance withdrawal.¹³ A cross-tolerant sedative such as clonazepam could prevent withdrawal symptoms as the dose is gradually decreased. Long-acting benzodiazepines such as clonazepam or diazepam are recommended.¹⁴

In Mr. C’s case, minor withdrawal symptoms, such as disturbed sleep and irritability, began 3 to 4 days after discontinuing benzodiazepines¹⁵ and preceded development of psychosis. Withdrawal symptoms usually resolve after 2 weeks.¹⁶ Mr. C responded only partially to IV lorazepam because he did not receive the total replacement dose. Had we known he was experiencing benzodiazepine withdrawal, Mr. C could have been managed with detoxi"cation of the primary drug, alprazolam, with diazepam substitution and tapering over 3 weeks.¹⁷

Table 3

Criteria for sedative, hypnotic, or anxiolytic withdrawal

Related Resource

• Vikander B, Koechling UM, Borg S, et al. Benzodiazepine tapering: a prospective study. Nord J Psychiatry. 2010; 64(4):273-282.

Drug Brand Names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Chlordiazepoxide • Librium
• Diazepam • Valium
• Diphenhydramine • Diphenhydramine injection
• Divalproex • Depakote
• Haloperidol • Haldol
• Lorazepam • Ativan
• Ziprasidone • Geodon

Acknowledgements

The authors wish to thank Reena Kumar, MD, and Sonja Gennuso, fourth-year medical student at Louisiana State University Health Sciences Center, Shreveport, for their help in preparing this manuscript.

Disclosure

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

Table 1

Mr. C’s hospital course in the emergency department

Table 2

Mr. C’s hospital course on the medical unit

CASE: Scared and confused

Mr. C, age 28, presents to the emergency department (ED) in police custody with agitation and altered mental status. Earlier that evening, Mr. C’s girlfriend noticed he was talking to himself while watching television. A few hours later, Mr. C thought someone was breaking into his house. Mr. C ran out of the house screaming for help, broke his neighbor’s window, and eventually called the police. When the police arrived Mr. C was wearing only his underwear, shaking, and bleeding from his hands. He said he was afraid and refused to respond to police instructions. Police officers used an electronic stun gun to facilitate transport to the hospital.

Mr. C admits to smoking 3 to 4 marijuana joints daily for the past 16 years. His last drug use was 2 hours before his symptoms began. Mr. C suggests that someone may have adulterated his marijuana joint but he has no factual basis for this accusation. He denies using alcohol and other illicit drugs and has no personal or family psychiatric history. He denies recent fever, loss of consciousness, chest pain, weakness, myalgia, or headache. Medically stable, his only complaint is mild hand pain.

Mr. C is alert, awake, and oriented to his name, and he responds properly to questions. He is tachycardic (101 bpm), his blood pressure is 149/57 mm Hg with normal S1 and S2 sounds, and he has no meningismus or nystagmus. Glasgow Coma Scale score is 15. He has increased deep tendon reflexes on the right upper and lower limb with good hand-grip and multiple abrasions and lacerations on his hands.

The authors’ observations

New-onset psychosis can have a wide differential diagnosis, particularly when reliable history is not available. Mr. C’s allegation that someone tampered with his marijuana raises 2 possibilities: embalming fluid (form-aldehyde) toxicity or PCP intoxication.

Embalming fluid toxicity can cause:

• agitation and sudden unpredictable behavior
• confusion or toxic delirium
• coma or seizure
• cerebral and pulmonary edema or death in severe cases.

The terms “wet,” “sherm,” “fly,” “amp,” or “illy” are used to describe a marijuana cigarette that has been dipped into embalming fluid, dried, and then smoked.¹ The effect is similar to that of PCP and causes extreme hallucinations. Reported highs last 30 minutes to 1 hour.²

Symptomatology of PCP intoxication may be indistinguishable from functional psychosis (Table 1).³ Visual, auditory, and tactile misperceptions are common and highly changeable disorientation often is accompanied by alternating periods of lethargy and fearful agitation. These patients typically show catatonic posturing and/or stereotyped movement. Somatic sensations appear to be disassociated; patients may misperceive pain, distance, and time. Patients taking PCP rarely admit to true hallucinations; however their thinking usually is grossly disoriented.⁴ Symptoms of delirium may last from 30 minutes to 6 hours in 80% of cases; 12% of patients may remain symptomatic for 12 hours. Violent behavior and agitation usually lasts only a few hours.⁵

Long-term marijuana abuse can lead to psychosis⁶ but acute onset is not typical, and recent prospective trials raised doubts that cannabis would be a sole factor.⁷ Instead, cannabis may be 1 of several factors that contribute to psychosis, particularly in patients who are predisposed.

Table 1

Phencyclidine (PCP) intoxication: What to look for

Possible neurologic causes

Complex partial seizures—also known as psychomotor epilepsy—are caused by a surge of electrical activity in the brain. Seizures often involve 1 of the brain’s temporal lobes but can affect any brain region. Symptoms include:

• impaired social interaction
• inability to control one’s movements
• alogia
• amnesia.

Episodes typically start with a blank stare followed by automatisms. The actions and movements often are unorganized or confused. Motor symptoms typically last for 1 to 2 minutes and confusion persists for another 1 to 2 minutes.⁸ In rare cases, a patient may become agitated or engage in behaviors such as undressing. Complex partial seizures may cause a person to run in apparent fear, cry out, or repeat a phrase.⁹ Electroencephalogram, CT, MRI, or positron-emission tomography scan could reveal any intracranial focus of complex partial seizures.

We suspect PCP or embalming fluid intoxication and initiate supportive therapy.

EVALUATION: Still confused

Initial baseline labs include a urine drug screen (UDS), chest radiography, ECG, and head CT. Mr. C’s UDS is positive for cannabis. A specific PCP assay is negative. White blood cell count (WBC) is 22,000/μL with high neutrophil count (88%), creatine kinase (CK) is 458 U/L, and urinalyis reveals protein 75 mg/dL and ketone 50 mg/dL. Head CT is negative for any acute process (click here for detailed description of Mr. C�s hospital course while in the ED).

During psychiatric evaluation 7 hours after presentation, Mr. C’s speech is loose and somewhat pressured, but intelligible. He cannot follow commands. Mr. C is delusional and appears to be hallucinating. He can repeat 3 words immediately but not after 3 minutes. We start Mr. C on divalproex, 1,500 mg/d, haloperidol, 6 mg/d, and IV lorazepam, 2 mg as needed for agitation. Although mildly disoriented, he gradually becomes less agitated.

The authors’ observations

At this point further evaluation is needed. Mr. C’s elevated WBC count could explain his fluctuating symptoms. He cannot provide further history and his family denies any past psychiatric episodes. Thyroid-stimulating hormone, B12, and folate levels are within normal limits. A negative LP rules out meningitic infection. We give Mr. C a diagnosis of psychosis NOS (Table 2).¹⁰

Table 2

DSM-IV-TR criteria for psychotic disorder, not otherwise specified

TREATMENT: Medication choices

After 8 hours in the ED, Mr. C is transferred to the medical unit, where he becomes agitated and complains of auditory and visual hallucinations. He receives divalproex, 750 mg, haloperidol, 3 mg, and IM diphenhydramine, 50 mg, to calm him. He remains agitated but not violent until bedtime. At midnight he is agitated and violent and receives another dose of haloperidol and IM diphenhydramine with IV lorazepam, 2 mg. These medications calm him and he is able to sleep until morning.

Morning labs reveal CK is 674 U/L and WBC decreased to 13,200/μL. Mr. C denies any distress but after the fourth dose of haloperidol, he develops dystonia of his arms so we discontinue this medication. We start aripiprazole, 10 mg/d gradually increased to 30 mg/d, and Mr. C receives 1 injection of diphenhydramine. He responds well to the treatment.

The next few hours are uneventful but then Mr. C becomes verbally abusive to his relatives and sitter; physical restraints are ordered and he receives IM ziprasidone, 20 mg, and IV lorazepam, 2 mg. He remains awake and babbling. His perception continues to wax and wane and his words are jumbled. He remains calm until the next morning (click here for detailed description of Mr. C�s hospital course while on the medical unit).

After 4 days on the medical unit Mr. C is transferred to the psychiatry unit, where he is angry, belligerent, and hostile, but not placed in restraints. His symptoms resolve in 2 days without any further episodes of violent behavior.

OUTCOME: Solving the puzzle

When Mr. C becomes cooperative, he gives a detailed history. He repeats his suspicion of smoking adulterated marijuana, but during detailed questioning, he admits to using alprazolam, which he purchased illegally, to sleep for the past 6 to 7 months. He started with 1 or 2 “footballs” (1 to 2 mg) and gradually increased to 3 or 4 “bars” (6 to 8 mg) each day. Mr. C could no longer afford the drug and last took alprazolam 6 days before his symptoms began. He says that after stopping alprazolam he felt anxious and could not sleep. His girlfriend adds that he was irritable and “he had not been acting himself” several days before admission. She says he complained of hearing the voice of God, particularly when he was not taking alprazolam.

Mr. C’s hand wounds heal and his vitals are normal during his 1-week stay on the psychiatric unit. His interactions with staff and peers improve. Aripiprazole is tapered and discontinued; divalproex is reduced to 1,000 mg/d. Mr. C is discharged 11 days after presentation and prescribed divalproex, 1,000 mg/d, with instructions to taper the drug over several days to prevent withdrawal seizures before stopping it in 1 week.

Mr. C does not return for his follow-up appointment; however, in a telephone follow-up 6 months later, he denies experiencing withdrawal symptoms after discharge. Mr. C is now undergoing drug rehabilitation.

The authors’ observations

Benzodiazepine withdrawal symptoms occur 7 to 10 days after abrupt cessation (Table 3).¹⁰ Symptoms are similar to those of alcohol withdrawal and include tachycardia, hypertension, clouding of consciousness, and auditory and visual hallucinations.¹¹ Serious reactions to benzodiazepine withdrawal include seizures and death.¹²

Because of the high prevalence of poly-substance misuse, obtain a detailed substance use history in patients undergoing benzodiazepine withdrawal to determine the likelihood of polysubstance withdrawal.¹³ A cross-tolerant sedative such as clonazepam could prevent withdrawal symptoms as the dose is gradually decreased. Long-acting benzodiazepines such as clonazepam or diazepam are recommended.¹⁴

In Mr. C’s case, minor withdrawal symptoms, such as disturbed sleep and irritability, began 3 to 4 days after discontinuing benzodiazepines¹⁵ and preceded development of psychosis. Withdrawal symptoms usually resolve after 2 weeks.¹⁶ Mr. C responded only partially to IV lorazepam because he did not receive the total replacement dose. Had we known he was experiencing benzodiazepine withdrawal, Mr. C could have been managed with detoxi"cation of the primary drug, alprazolam, with diazepam substitution and tapering over 3 weeks.¹⁷

Table 3

Criteria for sedative, hypnotic, or anxiolytic withdrawal

Related Resource

• Vikander B, Koechling UM, Borg S, et al. Benzodiazepine tapering: a prospective study. Nord J Psychiatry. 2010; 64(4):273-282.

Drug Brand Names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Chlordiazepoxide • Librium
• Diazepam • Valium
• Diphenhydramine • Diphenhydramine injection
• Divalproex • Depakote
• Haloperidol • Haldol
• Lorazepam • Ativan
• Ziprasidone • Geodon

Acknowledgements

The authors wish to thank Reena Kumar, MD, and Sonja Gennuso, fourth-year medical student at Louisiana State University Health Sciences Center, Shreveport, for their help in preparing this manuscript.

Disclosure

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

Table 1

Mr. C’s hospital course in the emergency department

Table 2

Mr. C’s hospital course on the medical unit