Current Psychiatry

I read Dr. Henry Nasrallah’s plea for “disruptive” new drugs (“Innovation deficit disorder: Psychiatry needs ‘disruptive’ new drugs,” Current Psychiatry, May 2007) with incredulity. I do not know if Dr. Nasrallah has ties to the pharmaceutical industry, but I do know that only a fierce critic of pharmaceutical companies could credibly suggest that we take steps to make this enterprise more lucrative than it already is. With all due respect, his 3 ideas bore an uneasy resemblance to a corporate lobbyist’s speaking points.

His recommendation that drug companies receive a pass in terms of product liability particularly is outrageous. I shudder to contemplate the consequences of allowing pharmaceutical companies to introduce drugs to the market with no meaningful consequences should they turn out to be unsafe or inadequately investigated.

If our government was not dominated by special interests, we might be able to spend fewer public dollars on medication purchases and more money on research. A properly funded National Institute of Mental Health (NIMH) is quite capable of independently developing innovative drugs without the encumbrance of profit seekers. If we allow the private sector to guide research and development, then we should expect continued recycling of existing treatments—or slightly tweaked versions—to treat exciting newly created niches such as jumpy leg disorder, excessive daytime apathy, and involuntary emotional unavailability syndrome. There are plenty of well-heeled, neurotic people who are eager to spend their money on such maladies, especially if advertised on television.

As Dr. Nasrallah mentioned, we applaud the profitability of high-tech or apparel companies. But there is one key difference: the consumer can choose not to purchase new clothing. Any physician who cannot appreciate this dilemma should be spending more time with patients and less with pharmaceutical representatives.

Douglas F. Steenblock, MD
Staff psychiatrist Iowa Veterans Home
Marshalltown, IA

Dr. Nasrallah responds

My editorial critiqued the pharmaceutical industry and its recent lack of innovation, but I understand its need to make a profit—like any other corporation. If a pharmaceutical company is not profitable, it will not invest in research to develop new medications.

Let’s consider the following:

• The pharmaceutical industry is the only U.S. entity developing psychiatric drugs. If we suffocate this industry, our patients might not have treatment options and we could return to locking up the mentally ill as we did before the psychopharmacology era.
  
• I would love for the National Institutes of Health (NIH) to fund psychotropic drug development, but it will never happen. The budget of the National Institute of Mental Health (NIMH) is approximately $1.6 billion, and the entire NIH budget is approximately $30 billion. To replicate pharmaceutical companies’ CNS franchise, the NIMH budget would have to increase more than 50 fold to approximately $80 to $100 billion per year.
  
• I did my psychopharmacology post-residency research fellowship in neuropsychopharmacology at NIMH. If pharmaceutical companies did not exist, psychopharmacology researchers, teachers, and clinicians like myself would not be able to conduct research or teach and would not have medications to treat patients. Everybody suffers if we do not have an industry incentivized to “invent” new agents to treat serious mental illness.
  
• Gaps in knowledge about the biological causes of psychiatric brain disorders make designing and developing new treatments particularly difficult. This is why I suggested a private-public partnership between NIMH and the pharmaceutical industry to expedite progress in discovering drugs to help treat patients with any of the 88% of DSM-IV-TR diagnoses that do not have an FDA-approved drug.
  

Henry A. Nasrallah, MD
Editor-In-Chief

I read Dr. Henry Nasrallah’s plea for “disruptive” new drugs (“Innovation deficit disorder: Psychiatry needs ‘disruptive’ new drugs,” Current Psychiatry, May 2007) with incredulity. I do not know if Dr. Nasrallah has ties to the pharmaceutical industry, but I do know that only a fierce critic of pharmaceutical companies could credibly suggest that we take steps to make this enterprise more lucrative than it already is. With all due respect, his 3 ideas bore an uneasy resemblance to a corporate lobbyist’s speaking points.

His recommendation that drug companies receive a pass in terms of product liability particularly is outrageous. I shudder to contemplate the consequences of allowing pharmaceutical companies to introduce drugs to the market with no meaningful consequences should they turn out to be unsafe or inadequately investigated.

If our government was not dominated by special interests, we might be able to spend fewer public dollars on medication purchases and more money on research. A properly funded National Institute of Mental Health (NIMH) is quite capable of independently developing innovative drugs without the encumbrance of profit seekers. If we allow the private sector to guide research and development, then we should expect continued recycling of existing treatments—or slightly tweaked versions—to treat exciting newly created niches such as jumpy leg disorder, excessive daytime apathy, and involuntary emotional unavailability syndrome. There are plenty of well-heeled, neurotic people who are eager to spend their money on such maladies, especially if advertised on television.

As Dr. Nasrallah mentioned, we applaud the profitability of high-tech or apparel companies. But there is one key difference: the consumer can choose not to purchase new clothing. Any physician who cannot appreciate this dilemma should be spending more time with patients and less with pharmaceutical representatives.

Douglas F. Steenblock, MD
Staff psychiatrist Iowa Veterans Home
Marshalltown, IA

Dr. Nasrallah responds

My editorial critiqued the pharmaceutical industry and its recent lack of innovation, but I understand its need to make a profit—like any other corporation. If a pharmaceutical company is not profitable, it will not invest in research to develop new medications.

Let’s consider the following:

• The pharmaceutical industry is the only U.S. entity developing psychiatric drugs. If we suffocate this industry, our patients might not have treatment options and we could return to locking up the mentally ill as we did before the psychopharmacology era.
  
• I would love for the National Institutes of Health (NIH) to fund psychotropic drug development, but it will never happen. The budget of the National Institute of Mental Health (NIMH) is approximately $1.6 billion, and the entire NIH budget is approximately $30 billion. To replicate pharmaceutical companies’ CNS franchise, the NIMH budget would have to increase more than 50 fold to approximately $80 to $100 billion per year.
  
• I did my psychopharmacology post-residency research fellowship in neuropsychopharmacology at NIMH. If pharmaceutical companies did not exist, psychopharmacology researchers, teachers, and clinicians like myself would not be able to conduct research or teach and would not have medications to treat patients. Everybody suffers if we do not have an industry incentivized to “invent” new agents to treat serious mental illness.
  
• Gaps in knowledge about the biological causes of psychiatric brain disorders make designing and developing new treatments particularly difficult. This is why I suggested a private-public partnership between NIMH and the pharmaceutical industry to expedite progress in discovering drugs to help treat patients with any of the 88% of DSM-IV-TR diagnoses that do not have an FDA-approved drug.
  

Henry A. Nasrallah, MD
Editor-In-Chief

I read Dr. Henry Nasrallah’s plea for “disruptive” new drugs (“Innovation deficit disorder: Psychiatry needs ‘disruptive’ new drugs,” Current Psychiatry, May 2007) with incredulity. I do not know if Dr. Nasrallah has ties to the pharmaceutical industry, but I do know that only a fierce critic of pharmaceutical companies could credibly suggest that we take steps to make this enterprise more lucrative than it already is. With all due respect, his 3 ideas bore an uneasy resemblance to a corporate lobbyist’s speaking points.

His recommendation that drug companies receive a pass in terms of product liability particularly is outrageous. I shudder to contemplate the consequences of allowing pharmaceutical companies to introduce drugs to the market with no meaningful consequences should they turn out to be unsafe or inadequately investigated.

If our government was not dominated by special interests, we might be able to spend fewer public dollars on medication purchases and more money on research. A properly funded National Institute of Mental Health (NIMH) is quite capable of independently developing innovative drugs without the encumbrance of profit seekers. If we allow the private sector to guide research and development, then we should expect continued recycling of existing treatments—or slightly tweaked versions—to treat exciting newly created niches such as jumpy leg disorder, excessive daytime apathy, and involuntary emotional unavailability syndrome. There are plenty of well-heeled, neurotic people who are eager to spend their money on such maladies, especially if advertised on television.

As Dr. Nasrallah mentioned, we applaud the profitability of high-tech or apparel companies. But there is one key difference: the consumer can choose not to purchase new clothing. Any physician who cannot appreciate this dilemma should be spending more time with patients and less with pharmaceutical representatives.

Douglas F. Steenblock, MD
Staff psychiatrist Iowa Veterans Home
Marshalltown, IA

Dr. Nasrallah responds

My editorial critiqued the pharmaceutical industry and its recent lack of innovation, but I understand its need to make a profit—like any other corporation. If a pharmaceutical company is not profitable, it will not invest in research to develop new medications.

Let’s consider the following:

• The pharmaceutical industry is the only U.S. entity developing psychiatric drugs. If we suffocate this industry, our patients might not have treatment options and we could return to locking up the mentally ill as we did before the psychopharmacology era.
  
• I would love for the National Institutes of Health (NIH) to fund psychotropic drug development, but it will never happen. The budget of the National Institute of Mental Health (NIMH) is approximately $1.6 billion, and the entire NIH budget is approximately $30 billion. To replicate pharmaceutical companies’ CNS franchise, the NIMH budget would have to increase more than 50 fold to approximately $80 to $100 billion per year.
  
• I did my psychopharmacology post-residency research fellowship in neuropsychopharmacology at NIMH. If pharmaceutical companies did not exist, psychopharmacology researchers, teachers, and clinicians like myself would not be able to conduct research or teach and would not have medications to treat patients. Everybody suffers if we do not have an industry incentivized to “invent” new agents to treat serious mental illness.
  
• Gaps in knowledge about the biological causes of psychiatric brain disorders make designing and developing new treatments particularly difficult. This is why I suggested a private-public partnership between NIMH and the pharmaceutical industry to expedite progress in discovering drugs to help treat patients with any of the 88% of DSM-IV-TR diagnoses that do not have an FDA-approved drug.
  

Henry A. Nasrallah, MD
Editor-In-Chief

The article “Depression, medication and ‘bad blood’” (Current Psychiatry, May 2007) discussed a case of reduced white blood cell (WBC) count in a patient the authors ultimately diagnosed as having a mood disorder with depressive features secondary to a general medical condition. However, I believe the authors missed the extent of the patient’s manic features.

The first clue was that the patient had “become increasingly irritable and volatile, often arguing with a staff nurse and other patients.” This behavior possibly was iatrogenic and caused by venlafaxine treatment. The authors added lithium at a low dose of 300 mg bid (no lithium blood levels given). This measure was done to increase WBC count, but it fortuitously may have helped reduce manic symptoms. At follow-up, “after 3 months of continuous hospitalization,” the patient was still described as “at times oversensitive and combative.”

Missing manic symptoms because of nonclassical ways they can present is a major clinical concern. For example, a patient may feel irritable, hostile, or labile instead of expansive or euphoric. I wonder if this patient’s manic symptoms could have been better controlled with titrating the lithium dose and following up by monitoring blood levels.

Robert Barris, MD
East Meadow, NY

The article “Depression, medication and ‘bad blood’” (Current Psychiatry, May 2007) discussed a case of reduced white blood cell (WBC) count in a patient the authors ultimately diagnosed as having a mood disorder with depressive features secondary to a general medical condition. However, I believe the authors missed the extent of the patient’s manic features.

The first clue was that the patient had “become increasingly irritable and volatile, often arguing with a staff nurse and other patients.” This behavior possibly was iatrogenic and caused by venlafaxine treatment. The authors added lithium at a low dose of 300 mg bid (no lithium blood levels given). This measure was done to increase WBC count, but it fortuitously may have helped reduce manic symptoms. At follow-up, “after 3 months of continuous hospitalization,” the patient was still described as “at times oversensitive and combative.”

Missing manic symptoms because of nonclassical ways they can present is a major clinical concern. For example, a patient may feel irritable, hostile, or labile instead of expansive or euphoric. I wonder if this patient’s manic symptoms could have been better controlled with titrating the lithium dose and following up by monitoring blood levels.

Robert Barris, MD
East Meadow, NY

The article “Depression, medication and ‘bad blood’” (Current Psychiatry, May 2007) discussed a case of reduced white blood cell (WBC) count in a patient the authors ultimately diagnosed as having a mood disorder with depressive features secondary to a general medical condition. However, I believe the authors missed the extent of the patient’s manic features.

The first clue was that the patient had “become increasingly irritable and volatile, often arguing with a staff nurse and other patients.” This behavior possibly was iatrogenic and caused by venlafaxine treatment. The authors added lithium at a low dose of 300 mg bid (no lithium blood levels given). This measure was done to increase WBC count, but it fortuitously may have helped reduce manic symptoms. At follow-up, “after 3 months of continuous hospitalization,” the patient was still described as “at times oversensitive and combative.”

Missing manic symptoms because of nonclassical ways they can present is a major clinical concern. For example, a patient may feel irritable, hostile, or labile instead of expansive or euphoric. I wonder if this patient’s manic symptoms could have been better controlled with titrating the lithium dose and following up by monitoring blood levels.

Robert Barris, MD
East Meadow, NY

What is the future of psychiatric practice? The emerging trend in medicine is toward more and more specialization, but will psychiatry follow suit?

Explosive growth in scientific knowledge and increasingly technical aspects of treatment are making it harder than ever for specialists— let alone generalists—to remain current. Gone are the days of Marcus Welby, MD, television’s 1970s paragon of the “do-it-all” generalist.

Physicians now differentiate into specialists immediately after medical school and train for up to 7 additional years in fields such as psychiatry, surgery, internal medicine, radiology, pediatrics, or dermatology. Even family medicine—an advanced form of “general practice”—requires 3 additional years of post-MD residency. The Accreditation Council for Graduate Medical Education (ACGME) recognizes and regulates residency training in 26 medical specialties.

But the trend does not stop there. Specialists have differentiated further into subspecialists who focus on narrower areas that require additional qualifications. Internal medicine has 18 subspecialties that offer board certification (such as interventional cardiology, gastroenterology, infectious disease, and rheumatology). Psychiatry has 5 (child and adolescent psychiatry, geriatric psychiatry, forensic psychiatry, addiction psychiatry, and psychosomatic medicine).

The ACGME now accredits nearly 100 subspecialties! A unique feature of subspecialty training is that important research takes place in those programs, advancing knowledge at the molecular, translational, and clinical levels.

An emerging practice model. The trend towards subspecialization is likely to continue and could culminate in a “diseasologist” model of medicine. Already, a number of psychiatry “diseasologists” are focusing on only 1 disorder, such as anxiety, bipolar disorder, eating disorders, psychosis, or borderline personality disorders. Similarly:

• In our sister specialty, neurology, some clinicians are focusing on stroke, multiple sclerosis, dementia, movement disorders, or epilepsy.
• Ophthalmology—a superspecialty in its own right—has fractionated into “diseasologists” who restrict their practices to cataracts, vitreo-retinal diseases, corneal disorders, or onco-ophthalmology.

Is the day approaching when there will be 2,000 types of diseasology, one for each recognized medical illness?

In psychiatry, the diseasologist paradigm of clinical practice may be more difficult to implement than in other specialties. Clinical features overlap across many psychiatric disorders, and comorbidity is the rule. We need to maintain “big picture” competence in diagnosis and treatment, being mindful of the “forest” while addressing one or more “trees” with intertwining branches and/or roots.

Psychiatrists may decide to focus on a single major disorder, but we always will need broad-based knowledge of mental disorders. Perhaps we practice “mental primary care,” in which the diseasology model will not be as feasible as in other medical specialties.

What is the future of psychiatric practice? The emerging trend in medicine is toward more and more specialization, but will psychiatry follow suit?

Explosive growth in scientific knowledge and increasingly technical aspects of treatment are making it harder than ever for specialists— let alone generalists—to remain current. Gone are the days of Marcus Welby, MD, television’s 1970s paragon of the “do-it-all” generalist.

Physicians now differentiate into specialists immediately after medical school and train for up to 7 additional years in fields such as psychiatry, surgery, internal medicine, radiology, pediatrics, or dermatology. Even family medicine—an advanced form of “general practice”—requires 3 additional years of post-MD residency. The Accreditation Council for Graduate Medical Education (ACGME) recognizes and regulates residency training in 26 medical specialties.

But the trend does not stop there. Specialists have differentiated further into subspecialists who focus on narrower areas that require additional qualifications. Internal medicine has 18 subspecialties that offer board certification (such as interventional cardiology, gastroenterology, infectious disease, and rheumatology). Psychiatry has 5 (child and adolescent psychiatry, geriatric psychiatry, forensic psychiatry, addiction psychiatry, and psychosomatic medicine).

The ACGME now accredits nearly 100 subspecialties! A unique feature of subspecialty training is that important research takes place in those programs, advancing knowledge at the molecular, translational, and clinical levels.

An emerging practice model. The trend towards subspecialization is likely to continue and could culminate in a “diseasologist” model of medicine. Already, a number of psychiatry “diseasologists” are focusing on only 1 disorder, such as anxiety, bipolar disorder, eating disorders, psychosis, or borderline personality disorders. Similarly:

• In our sister specialty, neurology, some clinicians are focusing on stroke, multiple sclerosis, dementia, movement disorders, or epilepsy.
• Ophthalmology—a superspecialty in its own right—has fractionated into “diseasologists” who restrict their practices to cataracts, vitreo-retinal diseases, corneal disorders, or onco-ophthalmology.

Is the day approaching when there will be 2,000 types of diseasology, one for each recognized medical illness?

In psychiatry, the diseasologist paradigm of clinical practice may be more difficult to implement than in other specialties. Clinical features overlap across many psychiatric disorders, and comorbidity is the rule. We need to maintain “big picture” competence in diagnosis and treatment, being mindful of the “forest” while addressing one or more “trees” with intertwining branches and/or roots.

Psychiatrists may decide to focus on a single major disorder, but we always will need broad-based knowledge of mental disorders. Perhaps we practice “mental primary care,” in which the diseasology model will not be as feasible as in other medical specialties.

What is the future of psychiatric practice? The emerging trend in medicine is toward more and more specialization, but will psychiatry follow suit?

Explosive growth in scientific knowledge and increasingly technical aspects of treatment are making it harder than ever for specialists— let alone generalists—to remain current. Gone are the days of Marcus Welby, MD, television’s 1970s paragon of the “do-it-all” generalist.

Physicians now differentiate into specialists immediately after medical school and train for up to 7 additional years in fields such as psychiatry, surgery, internal medicine, radiology, pediatrics, or dermatology. Even family medicine—an advanced form of “general practice”—requires 3 additional years of post-MD residency. The Accreditation Council for Graduate Medical Education (ACGME) recognizes and regulates residency training in 26 medical specialties.

But the trend does not stop there. Specialists have differentiated further into subspecialists who focus on narrower areas that require additional qualifications. Internal medicine has 18 subspecialties that offer board certification (such as interventional cardiology, gastroenterology, infectious disease, and rheumatology). Psychiatry has 5 (child and adolescent psychiatry, geriatric psychiatry, forensic psychiatry, addiction psychiatry, and psychosomatic medicine).

The ACGME now accredits nearly 100 subspecialties! A unique feature of subspecialty training is that important research takes place in those programs, advancing knowledge at the molecular, translational, and clinical levels.

An emerging practice model. The trend towards subspecialization is likely to continue and could culminate in a “diseasologist” model of medicine. Already, a number of psychiatry “diseasologists” are focusing on only 1 disorder, such as anxiety, bipolar disorder, eating disorders, psychosis, or borderline personality disorders. Similarly:

• In our sister specialty, neurology, some clinicians are focusing on stroke, multiple sclerosis, dementia, movement disorders, or epilepsy.
• Ophthalmology—a superspecialty in its own right—has fractionated into “diseasologists” who restrict their practices to cataracts, vitreo-retinal diseases, corneal disorders, or onco-ophthalmology.

Is the day approaching when there will be 2,000 types of diseasology, one for each recognized medical illness?

In psychiatry, the diseasologist paradigm of clinical practice may be more difficult to implement than in other specialties. Clinical features overlap across many psychiatric disorders, and comorbidity is the rule. We need to maintain “big picture” competence in diagnosis and treatment, being mindful of the “forest” while addressing one or more “trees” with intertwining branches and/or roots.

Psychiatrists may decide to focus on a single major disorder, but we always will need broad-based knowledge of mental disorders. Perhaps we practice “mental primary care,” in which the diseasology model will not be as feasible as in other medical specialties.

CASE: The big freeze

Mr. Q, age 34, is afraid to cross the street. As he steps off the curb, his legs “cramp up.” As the cramping intensifies and his feet stiffen, his heart races, he begins to sweat, and he turns back for fear his legs will buckle in the street. While on the sidewalk, he stays within reach of a building or car in case he falls.

Six months before presentation, Mr. Q walked to church during a blizzard, only to find the church closed because of the storm. He returned home and shoveled snow for 1 hour, during which he repeatedly leaned forward and backward to dump the snow.

The following Sunday, Mr. Q’s legs started to “hurt” as he crossed the street. Thinking he had severely injured himself while shoveling, he began to fear street crossings. At work, he asked coworkers to help him cross over to the subway. By spring, he had become so humiliated by his dependence that he stopped working. His phobia intensified until he presented to us at his family’s urging.

During evaluation, Mr. Q says he can cross only side streets and holds on to his father while crossing. His father, who is retired, spends much of his day helping his son get around.

Complete physical exam by Mr. Q’s primary care physician reveals a possible pulled muscle in his right leg but no other medical problems. Neurologic exam results are normal, ruling out nerve damage.

Later in the evaluation, Mr. Q mentions that at age 10 he was struck by a car. The impact fractured the left side of his skull and left leg, and he temporarily lost consciousness.

Shortly after the accident, Mr. Q developed mild memory and concentration impairments and a moderate stutter. He also experienced nightmares, but they disappeared within days. He says he never received speech therapy or other psychiatric treatment because his family did not have medical insurance.

Mr. Q did not lose function after the accident, but in college his stuttering led to difficulty speaking in class and interacting socially. He suffered panic attacks while on the telephone or during job interviews. He now mostly stays home, where he lives with his parents and a nephew. He interacts only with family members.

During the evaluation, Mr. Q effortlessly walks around the therapist’s office and reports no trouble walking at home. He says the cramps almost never surface at home because he feels “calm” with walls close by. When trying to cross the street, he manages to turn back without falling despite the cramps.

Upon considering this conflict, Mr. Q seems to realize that his fear of street crossings protects him from social situations. His stuttering, however, confounds the evaluation because he has trouble communicating his symptoms.

Mr. Q’s affect is constricted as he describes his anxiety and fear. He says he feels limited and at times depressed by his inability to cross streets, yet shows little dysphoric affect or mourning and seems unusually calm when discussing the problem. He appears relaxed knowing that he can keep avoiding social situations.

The authors’ observations

Mr. Q’s history of fearing interviews and telephone conversations suggests social anxiety, and his fear and avoidance of street crossings suggest a specific phobia. Panic disorder with agoraphobia is not present because the patient never experienced spontaneous panic attacks.

Anxiety is more prevalent among persons who stutter than in fl uent speakers.^1,2

Persons who stutter:

• more commonly report speech anxiety³
  
• are significantly more uneasy in social situations and tend to avoid them^4,5
  
• might not be motivated to eliminate barriers that thwart social interaction.
  

Worse, his stuttering makes it difficult to ascertain his symptoms or plan treatment because it takes him so long to finish a sentence.

EVALUATION: Flashing back

Later in the evaluation, Mr. Q says that whenever he considers or tries crossing a street, he recalls his childhood vehicular injury and fears he will be struck again. He has nightmares of being run over, and these nightmares and flashbacks have been occurring twice weekly since the snowstorm.

During the mental status examination, Mr. Q is well related with fair to poor eye contact, probably because of his stutter; he looks away from the speaker when his stuttering intensifies. His nightmares and flashbacks suggest comorbid posttraumatic stress disorder (PTSD), although he has no persistent symptoms of increased arousal. He also shows no evidence of acute mood disorder, psychosis, or cognitive disturbance.

The authors’ observations

PTSD symptoms can develop months to years after a precipitating incident,^6,7 and repeated trauma can make patients more susceptible.

Interestingly, Mr. Q briefly suffered PTSD symptoms after the childhood accident but had no full-blown symptoms until adulthood. In addition to triggering avoidance behaviors, the muscle pull apparently reignited long-dormant PTSD symptoms (fl ashbacks, nightmares).

Mr. Q suffered no other PTSD symptoms. His stuttering might have signaled a psychogenic anxiety disorder, rather than being an incidental finding that developed after acute brain trauma at age 10.

Stuttering also might have contained Mr. Q’s PTSD symptoms for 24 years, until his snow-shoveling injury shattered that containment. Further, while shoveling in the street amid slippery conditions, he might have subconsciously feared he would have trouble eluding an oncoming vehicle.

The authors’ observations

We must address Mr. Q’s stuttering, phobia, and PTSD simultaneously to restore function. If we were to target his street-crossing phobia alone, we would face considerable resistance while exposing the underlying social phobia.

Supportive psychotherapy and exposure therapy—which would involve taking Mr. Q to an intersection and guiding him across—could help him overcome his fear of being run over. Cognitive-behavioral therapy (CBT) alone or with medications also could help.^8,9

Mr. Q’s anxiety, however, is severe enough to keep him from trying exposure therapy. Because staying home is his shield from social contact, he is not motivated to leave his apartment. Although he presented voluntarily, like many patients he is ambivalent toward exposure therapy.

Also, Mr. Q’s stutter makes it difficult to engage him in conversation. His stuttering is so severe that we have trouble doing an adequate CBT case formulation. At times his speech is almost incomprehensible.

Improving Mr. Q’s speech is crucial to completing an assessment, decreasing his social anxiety, and motivating him to conquer his fear of crossing streets. By addressing his stuttering and phobia simultaneously, we can treat his anxiety on 2 fronts:

• the stuttering that stemmed from his car accident at age 10
  
• the street-crossing phobia that developed after he pulled a leg muscle as an adult.
  

TREATMENT: 5-step approach

Negative medical results convince Mr. Q that anxiety is holding him back. This allows us to target his anxiety with CBT, in vivo exposure, deep breathing/relaxation, speech therapy, and pharmacotherapy, all of which we start immediately.

As part of Mr. Q’s psychoeducation, we reiterate his negative physical examination results and point out that his childhood vehicular injuries might be perpetuating his fears. We work on getting him to recognize that leg tightness does not predict falling and getting hit by a car.

Box 2

When his legs cramp up while trying to cross, we have him say out loud, “I can do it. I feel calm;” this helps him proceed across the street. We also teach self-empowerment by having him purposely cramp up his legs, then release them to stop the cramping.

Deep breathing/relaxation. We teach Mr. Q progressive muscle relaxation and slow rhythmic breathing exercises, which he does before crossing streets to reduce his anxiety. For homework, he practices these exercises and soaks his legs in warm water for 10 minutes twice daily to relax his muscles and prevent cramping.

Speech therapy. The primary therapist devotes 20 minutes of each session to speech therapy. She employs relaxation training and therapy techniques such as Easy Onset,¹⁰ in which the patient stretches each sound, syllable, or word for up to 2 seconds, allowing him to speak at a smooth, slow rate. Mr. Q also practices these speech exercises at home.

After 6 weeks, Mr. Q’s stutter improves slightly but he still has trouble communicating. We refer him to a consulting speech therapist, who sees him twice weekly and leads Easy Onset and relaxation exercises. This gives us more time for supportive psychotherapy.

As his speech becomes more fluent, Mr. Q’s social anxiety and fear of street crossings decreases.

Pharmacotherapy. We instruct Mr. Q to take paroxetine, 20 mg/d, and clonazepam, 0.25 mg bid, 30 minutes before in vivo work to manage his anxiety. We titrate clonazepam to 0.5 mg bid over 1 month. He responds well to this regimen but fears he will become dependent on it.

During therapy, Mr. Q and the therapist rank the above interventions from most to least therapeutic (Box 2) so that we can effectively treat him should he relapse.

The authors’ observations

Although Mr. Q’s case is unusual, we feel our diagnostic and treatment methods can be applied to similar cases. His stutter, however, prevented us from conducting a structured diagnostic interview—which would have uncovered his symptoms more quickly—or performing standard manualized therapy.

Some data¹¹ suggest that combination psychotropics and relaxation therapy can compromise long-term exposure therapy outcomes, as the patient’s fear could return once medication is stopped. Mr. Q’s anxiety was crippling, however, and had to be addressed before we could consider exposure therapy.

More research is needed on overcoming patient communication barriers that can hamper treatment. Rapport with patients often makes or breaks psychiatric treatment, and communication problems can prevent that connection. As clinicians, we must watch for linguistic, cognitive, and cultural impediments to treatment.

FOLLOW-UP: ‘I can cross’

Six months after presentation, Mr. Q crosses all types of streets—from 1-way streets to 6-lane intersections—with minimal anxiety. He has resumed his previous level of functioning and is searching for work. His stutter, though greatly improved, is still audible.

We see Mr. Q monthly. We stop paroxetine after 8 months but continue clonazepam to address his many underlying social anxieties. By November—approximately 1½ years after presentation—we have reduced clonazepam to 0.5 mg each morning. We try reducing the morning dose to 0.25 mg, but Mr. Q’s debilitating anxiety resurfaces.

In December, we increase clonazepam to 0.5 mg bid, then reduce it to 0.5 mg each morning 2 months later. In April, we cut clonazepam to 0.25 mg each morning. So far, Mr. Q is functioning well.

The authors’ observations

Patients who begin antistuttering intervention as adults have a poorer speech improvement prognosis than those who start speech therapy in childhood.¹² In leaving his stuttering untreated for 24 years, Mr. Q likely sacrificed quality of life. Speech intervention at an earlier age might have improved his speech and prognosis early on.

Related resources

• Anxiety Disorders Association of America. www.adaa.org.
  
• Beck AT, Emery G, Greenberg RL. Anxiety disorders and phobias: a cognitive perspective. New York: Basic Books; 1985.
  
• Leahy RL, Holland SJ. Treatment plans and interventions for depression and anxiety disorders. New York: Guilford Press; 2000.
  

• Clonazepam • Klonopin
  
• Paroxetine • Paxil
  

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

Acknowledgment

The authors thank Michael Garret, MD, for his assistance in preparing this article.

CASE: The big freeze

Mr. Q, age 34, is afraid to cross the street. As he steps off the curb, his legs “cramp up.” As the cramping intensifies and his feet stiffen, his heart races, he begins to sweat, and he turns back for fear his legs will buckle in the street. While on the sidewalk, he stays within reach of a building or car in case he falls.

Six months before presentation, Mr. Q walked to church during a blizzard, only to find the church closed because of the storm. He returned home and shoveled snow for 1 hour, during which he repeatedly leaned forward and backward to dump the snow.

The following Sunday, Mr. Q’s legs started to “hurt” as he crossed the street. Thinking he had severely injured himself while shoveling, he began to fear street crossings. At work, he asked coworkers to help him cross over to the subway. By spring, he had become so humiliated by his dependence that he stopped working. His phobia intensified until he presented to us at his family’s urging.

During evaluation, Mr. Q says he can cross only side streets and holds on to his father while crossing. His father, who is retired, spends much of his day helping his son get around.

Complete physical exam by Mr. Q’s primary care physician reveals a possible pulled muscle in his right leg but no other medical problems. Neurologic exam results are normal, ruling out nerve damage.

Later in the evaluation, Mr. Q mentions that at age 10 he was struck by a car. The impact fractured the left side of his skull and left leg, and he temporarily lost consciousness.

Shortly after the accident, Mr. Q developed mild memory and concentration impairments and a moderate stutter. He also experienced nightmares, but they disappeared within days. He says he never received speech therapy or other psychiatric treatment because his family did not have medical insurance.

Mr. Q did not lose function after the accident, but in college his stuttering led to difficulty speaking in class and interacting socially. He suffered panic attacks while on the telephone or during job interviews. He now mostly stays home, where he lives with his parents and a nephew. He interacts only with family members.

During the evaluation, Mr. Q effortlessly walks around the therapist’s office and reports no trouble walking at home. He says the cramps almost never surface at home because he feels “calm” with walls close by. When trying to cross the street, he manages to turn back without falling despite the cramps.

Upon considering this conflict, Mr. Q seems to realize that his fear of street crossings protects him from social situations. His stuttering, however, confounds the evaluation because he has trouble communicating his symptoms.

Mr. Q’s affect is constricted as he describes his anxiety and fear. He says he feels limited and at times depressed by his inability to cross streets, yet shows little dysphoric affect or mourning and seems unusually calm when discussing the problem. He appears relaxed knowing that he can keep avoiding social situations.

The authors’ observations

Mr. Q’s history of fearing interviews and telephone conversations suggests social anxiety, and his fear and avoidance of street crossings suggest a specific phobia. Panic disorder with agoraphobia is not present because the patient never experienced spontaneous panic attacks.

Anxiety is more prevalent among persons who stutter than in fl uent speakers.^1,2

Persons who stutter:

• more commonly report speech anxiety³
  
• are significantly more uneasy in social situations and tend to avoid them^4,5
  
• might not be motivated to eliminate barriers that thwart social interaction.
  

Worse, his stuttering makes it difficult to ascertain his symptoms or plan treatment because it takes him so long to finish a sentence.

EVALUATION: Flashing back

Later in the evaluation, Mr. Q says that whenever he considers or tries crossing a street, he recalls his childhood vehicular injury and fears he will be struck again. He has nightmares of being run over, and these nightmares and flashbacks have been occurring twice weekly since the snowstorm.

During the mental status examination, Mr. Q is well related with fair to poor eye contact, probably because of his stutter; he looks away from the speaker when his stuttering intensifies. His nightmares and flashbacks suggest comorbid posttraumatic stress disorder (PTSD), although he has no persistent symptoms of increased arousal. He also shows no evidence of acute mood disorder, psychosis, or cognitive disturbance.

The authors’ observations

PTSD symptoms can develop months to years after a precipitating incident,^6,7 and repeated trauma can make patients more susceptible.

Interestingly, Mr. Q briefly suffered PTSD symptoms after the childhood accident but had no full-blown symptoms until adulthood. In addition to triggering avoidance behaviors, the muscle pull apparently reignited long-dormant PTSD symptoms (fl ashbacks, nightmares).

Mr. Q suffered no other PTSD symptoms. His stuttering might have signaled a psychogenic anxiety disorder, rather than being an incidental finding that developed after acute brain trauma at age 10.

Stuttering also might have contained Mr. Q’s PTSD symptoms for 24 years, until his snow-shoveling injury shattered that containment. Further, while shoveling in the street amid slippery conditions, he might have subconsciously feared he would have trouble eluding an oncoming vehicle.

The authors’ observations

We must address Mr. Q’s stuttering, phobia, and PTSD simultaneously to restore function. If we were to target his street-crossing phobia alone, we would face considerable resistance while exposing the underlying social phobia.

Supportive psychotherapy and exposure therapy—which would involve taking Mr. Q to an intersection and guiding him across—could help him overcome his fear of being run over. Cognitive-behavioral therapy (CBT) alone or with medications also could help.^8,9

Mr. Q’s anxiety, however, is severe enough to keep him from trying exposure therapy. Because staying home is his shield from social contact, he is not motivated to leave his apartment. Although he presented voluntarily, like many patients he is ambivalent toward exposure therapy.

Also, Mr. Q’s stutter makes it difficult to engage him in conversation. His stuttering is so severe that we have trouble doing an adequate CBT case formulation. At times his speech is almost incomprehensible.

Improving Mr. Q’s speech is crucial to completing an assessment, decreasing his social anxiety, and motivating him to conquer his fear of crossing streets. By addressing his stuttering and phobia simultaneously, we can treat his anxiety on 2 fronts:

• the stuttering that stemmed from his car accident at age 10
  
• the street-crossing phobia that developed after he pulled a leg muscle as an adult.
  

TREATMENT: 5-step approach

Negative medical results convince Mr. Q that anxiety is holding him back. This allows us to target his anxiety with CBT, in vivo exposure, deep breathing/relaxation, speech therapy, and pharmacotherapy, all of which we start immediately.

As part of Mr. Q’s psychoeducation, we reiterate his negative physical examination results and point out that his childhood vehicular injuries might be perpetuating his fears. We work on getting him to recognize that leg tightness does not predict falling and getting hit by a car.

Box 2

When his legs cramp up while trying to cross, we have him say out loud, “I can do it. I feel calm;” this helps him proceed across the street. We also teach self-empowerment by having him purposely cramp up his legs, then release them to stop the cramping.

Deep breathing/relaxation. We teach Mr. Q progressive muscle relaxation and slow rhythmic breathing exercises, which he does before crossing streets to reduce his anxiety. For homework, he practices these exercises and soaks his legs in warm water for 10 minutes twice daily to relax his muscles and prevent cramping.

Speech therapy. The primary therapist devotes 20 minutes of each session to speech therapy. She employs relaxation training and therapy techniques such as Easy Onset,¹⁰ in which the patient stretches each sound, syllable, or word for up to 2 seconds, allowing him to speak at a smooth, slow rate. Mr. Q also practices these speech exercises at home.

After 6 weeks, Mr. Q’s stutter improves slightly but he still has trouble communicating. We refer him to a consulting speech therapist, who sees him twice weekly and leads Easy Onset and relaxation exercises. This gives us more time for supportive psychotherapy.

As his speech becomes more fluent, Mr. Q’s social anxiety and fear of street crossings decreases.

Pharmacotherapy. We instruct Mr. Q to take paroxetine, 20 mg/d, and clonazepam, 0.25 mg bid, 30 minutes before in vivo work to manage his anxiety. We titrate clonazepam to 0.5 mg bid over 1 month. He responds well to this regimen but fears he will become dependent on it.

During therapy, Mr. Q and the therapist rank the above interventions from most to least therapeutic (Box 2) so that we can effectively treat him should he relapse.

The authors’ observations

Although Mr. Q’s case is unusual, we feel our diagnostic and treatment methods can be applied to similar cases. His stutter, however, prevented us from conducting a structured diagnostic interview—which would have uncovered his symptoms more quickly—or performing standard manualized therapy.

Some data¹¹ suggest that combination psychotropics and relaxation therapy can compromise long-term exposure therapy outcomes, as the patient’s fear could return once medication is stopped. Mr. Q’s anxiety was crippling, however, and had to be addressed before we could consider exposure therapy.

More research is needed on overcoming patient communication barriers that can hamper treatment. Rapport with patients often makes or breaks psychiatric treatment, and communication problems can prevent that connection. As clinicians, we must watch for linguistic, cognitive, and cultural impediments to treatment.

FOLLOW-UP: ‘I can cross’

Six months after presentation, Mr. Q crosses all types of streets—from 1-way streets to 6-lane intersections—with minimal anxiety. He has resumed his previous level of functioning and is searching for work. His stutter, though greatly improved, is still audible.

We see Mr. Q monthly. We stop paroxetine after 8 months but continue clonazepam to address his many underlying social anxieties. By November—approximately 1½ years after presentation—we have reduced clonazepam to 0.5 mg each morning. We try reducing the morning dose to 0.25 mg, but Mr. Q’s debilitating anxiety resurfaces.

In December, we increase clonazepam to 0.5 mg bid, then reduce it to 0.5 mg each morning 2 months later. In April, we cut clonazepam to 0.25 mg each morning. So far, Mr. Q is functioning well.

The authors’ observations

Patients who begin antistuttering intervention as adults have a poorer speech improvement prognosis than those who start speech therapy in childhood.¹² In leaving his stuttering untreated for 24 years, Mr. Q likely sacrificed quality of life. Speech intervention at an earlier age might have improved his speech and prognosis early on.

Related resources

• Anxiety Disorders Association of America. www.adaa.org.
  
• Beck AT, Emery G, Greenberg RL. Anxiety disorders and phobias: a cognitive perspective. New York: Basic Books; 1985.
  
• Leahy RL, Holland SJ. Treatment plans and interventions for depression and anxiety disorders. New York: Guilford Press; 2000.
  

• Clonazepam • Klonopin
  
• Paroxetine • Paxil
  

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

Acknowledgment

The authors thank Michael Garret, MD, for his assistance in preparing this article.

CASE: The big freeze

Mr. Q, age 34, is afraid to cross the street. As he steps off the curb, his legs “cramp up.” As the cramping intensifies and his feet stiffen, his heart races, he begins to sweat, and he turns back for fear his legs will buckle in the street. While on the sidewalk, he stays within reach of a building or car in case he falls.

Six months before presentation, Mr. Q walked to church during a blizzard, only to find the church closed because of the storm. He returned home and shoveled snow for 1 hour, during which he repeatedly leaned forward and backward to dump the snow.

The following Sunday, Mr. Q’s legs started to “hurt” as he crossed the street. Thinking he had severely injured himself while shoveling, he began to fear street crossings. At work, he asked coworkers to help him cross over to the subway. By spring, he had become so humiliated by his dependence that he stopped working. His phobia intensified until he presented to us at his family’s urging.

During evaluation, Mr. Q says he can cross only side streets and holds on to his father while crossing. His father, who is retired, spends much of his day helping his son get around.

Complete physical exam by Mr. Q’s primary care physician reveals a possible pulled muscle in his right leg but no other medical problems. Neurologic exam results are normal, ruling out nerve damage.

Later in the evaluation, Mr. Q mentions that at age 10 he was struck by a car. The impact fractured the left side of his skull and left leg, and he temporarily lost consciousness.

Shortly after the accident, Mr. Q developed mild memory and concentration impairments and a moderate stutter. He also experienced nightmares, but they disappeared within days. He says he never received speech therapy or other psychiatric treatment because his family did not have medical insurance.

Mr. Q did not lose function after the accident, but in college his stuttering led to difficulty speaking in class and interacting socially. He suffered panic attacks while on the telephone or during job interviews. He now mostly stays home, where he lives with his parents and a nephew. He interacts only with family members.

During the evaluation, Mr. Q effortlessly walks around the therapist’s office and reports no trouble walking at home. He says the cramps almost never surface at home because he feels “calm” with walls close by. When trying to cross the street, he manages to turn back without falling despite the cramps.

Upon considering this conflict, Mr. Q seems to realize that his fear of street crossings protects him from social situations. His stuttering, however, confounds the evaluation because he has trouble communicating his symptoms.

Mr. Q’s affect is constricted as he describes his anxiety and fear. He says he feels limited and at times depressed by his inability to cross streets, yet shows little dysphoric affect or mourning and seems unusually calm when discussing the problem. He appears relaxed knowing that he can keep avoiding social situations.

The authors’ observations

Mr. Q’s history of fearing interviews and telephone conversations suggests social anxiety, and his fear and avoidance of street crossings suggest a specific phobia. Panic disorder with agoraphobia is not present because the patient never experienced spontaneous panic attacks.

Anxiety is more prevalent among persons who stutter than in fl uent speakers.^1,2

Persons who stutter:

• more commonly report speech anxiety³
  
• are significantly more uneasy in social situations and tend to avoid them^4,5
  
• might not be motivated to eliminate barriers that thwart social interaction.
  

Worse, his stuttering makes it difficult to ascertain his symptoms or plan treatment because it takes him so long to finish a sentence.

EVALUATION: Flashing back

Later in the evaluation, Mr. Q says that whenever he considers or tries crossing a street, he recalls his childhood vehicular injury and fears he will be struck again. He has nightmares of being run over, and these nightmares and flashbacks have been occurring twice weekly since the snowstorm.

During the mental status examination, Mr. Q is well related with fair to poor eye contact, probably because of his stutter; he looks away from the speaker when his stuttering intensifies. His nightmares and flashbacks suggest comorbid posttraumatic stress disorder (PTSD), although he has no persistent symptoms of increased arousal. He also shows no evidence of acute mood disorder, psychosis, or cognitive disturbance.

The authors’ observations

PTSD symptoms can develop months to years after a precipitating incident,^6,7 and repeated trauma can make patients more susceptible.

Interestingly, Mr. Q briefly suffered PTSD symptoms after the childhood accident but had no full-blown symptoms until adulthood. In addition to triggering avoidance behaviors, the muscle pull apparently reignited long-dormant PTSD symptoms (fl ashbacks, nightmares).

Mr. Q suffered no other PTSD symptoms. His stuttering might have signaled a psychogenic anxiety disorder, rather than being an incidental finding that developed after acute brain trauma at age 10.

Stuttering also might have contained Mr. Q’s PTSD symptoms for 24 years, until his snow-shoveling injury shattered that containment. Further, while shoveling in the street amid slippery conditions, he might have subconsciously feared he would have trouble eluding an oncoming vehicle.

The authors’ observations

We must address Mr. Q’s stuttering, phobia, and PTSD simultaneously to restore function. If we were to target his street-crossing phobia alone, we would face considerable resistance while exposing the underlying social phobia.

Supportive psychotherapy and exposure therapy—which would involve taking Mr. Q to an intersection and guiding him across—could help him overcome his fear of being run over. Cognitive-behavioral therapy (CBT) alone or with medications also could help.^8,9

Mr. Q’s anxiety, however, is severe enough to keep him from trying exposure therapy. Because staying home is his shield from social contact, he is not motivated to leave his apartment. Although he presented voluntarily, like many patients he is ambivalent toward exposure therapy.

Also, Mr. Q’s stutter makes it difficult to engage him in conversation. His stuttering is so severe that we have trouble doing an adequate CBT case formulation. At times his speech is almost incomprehensible.

Improving Mr. Q’s speech is crucial to completing an assessment, decreasing his social anxiety, and motivating him to conquer his fear of crossing streets. By addressing his stuttering and phobia simultaneously, we can treat his anxiety on 2 fronts:

• the stuttering that stemmed from his car accident at age 10
  
• the street-crossing phobia that developed after he pulled a leg muscle as an adult.
  

TREATMENT: 5-step approach

Negative medical results convince Mr. Q that anxiety is holding him back. This allows us to target his anxiety with CBT, in vivo exposure, deep breathing/relaxation, speech therapy, and pharmacotherapy, all of which we start immediately.

As part of Mr. Q’s psychoeducation, we reiterate his negative physical examination results and point out that his childhood vehicular injuries might be perpetuating his fears. We work on getting him to recognize that leg tightness does not predict falling and getting hit by a car.

Box 2

When his legs cramp up while trying to cross, we have him say out loud, “I can do it. I feel calm;” this helps him proceed across the street. We also teach self-empowerment by having him purposely cramp up his legs, then release them to stop the cramping.

Deep breathing/relaxation. We teach Mr. Q progressive muscle relaxation and slow rhythmic breathing exercises, which he does before crossing streets to reduce his anxiety. For homework, he practices these exercises and soaks his legs in warm water for 10 minutes twice daily to relax his muscles and prevent cramping.

Speech therapy. The primary therapist devotes 20 minutes of each session to speech therapy. She employs relaxation training and therapy techniques such as Easy Onset,¹⁰ in which the patient stretches each sound, syllable, or word for up to 2 seconds, allowing him to speak at a smooth, slow rate. Mr. Q also practices these speech exercises at home.

After 6 weeks, Mr. Q’s stutter improves slightly but he still has trouble communicating. We refer him to a consulting speech therapist, who sees him twice weekly and leads Easy Onset and relaxation exercises. This gives us more time for supportive psychotherapy.

As his speech becomes more fluent, Mr. Q’s social anxiety and fear of street crossings decreases.

Pharmacotherapy. We instruct Mr. Q to take paroxetine, 20 mg/d, and clonazepam, 0.25 mg bid, 30 minutes before in vivo work to manage his anxiety. We titrate clonazepam to 0.5 mg bid over 1 month. He responds well to this regimen but fears he will become dependent on it.

During therapy, Mr. Q and the therapist rank the above interventions from most to least therapeutic (Box 2) so that we can effectively treat him should he relapse.

The authors’ observations

Although Mr. Q’s case is unusual, we feel our diagnostic and treatment methods can be applied to similar cases. His stutter, however, prevented us from conducting a structured diagnostic interview—which would have uncovered his symptoms more quickly—or performing standard manualized therapy.

Some data¹¹ suggest that combination psychotropics and relaxation therapy can compromise long-term exposure therapy outcomes, as the patient’s fear could return once medication is stopped. Mr. Q’s anxiety was crippling, however, and had to be addressed before we could consider exposure therapy.

More research is needed on overcoming patient communication barriers that can hamper treatment. Rapport with patients often makes or breaks psychiatric treatment, and communication problems can prevent that connection. As clinicians, we must watch for linguistic, cognitive, and cultural impediments to treatment.

FOLLOW-UP: ‘I can cross’

Six months after presentation, Mr. Q crosses all types of streets—from 1-way streets to 6-lane intersections—with minimal anxiety. He has resumed his previous level of functioning and is searching for work. His stutter, though greatly improved, is still audible.

We see Mr. Q monthly. We stop paroxetine after 8 months but continue clonazepam to address his many underlying social anxieties. By November—approximately 1½ years after presentation—we have reduced clonazepam to 0.5 mg each morning. We try reducing the morning dose to 0.25 mg, but Mr. Q’s debilitating anxiety resurfaces.

In December, we increase clonazepam to 0.5 mg bid, then reduce it to 0.5 mg each morning 2 months later. In April, we cut clonazepam to 0.25 mg each morning. So far, Mr. Q is functioning well.

The authors’ observations

Patients who begin antistuttering intervention as adults have a poorer speech improvement prognosis than those who start speech therapy in childhood.¹² In leaving his stuttering untreated for 24 years, Mr. Q likely sacrificed quality of life. Speech intervention at an earlier age might have improved his speech and prognosis early on.

Related resources

• Anxiety Disorders Association of America. www.adaa.org.
  
• Beck AT, Emery G, Greenberg RL. Anxiety disorders and phobias: a cognitive perspective. New York: Basic Books; 1985.
  
• Leahy RL, Holland SJ. Treatment plans and interventions for depression and anxiety disorders. New York: Guilford Press; 2000.
  

• Clonazepam • Klonopin
  
• Paroxetine • Paxil
  

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

Acknowledgment

The authors thank Michael Garret, MD, for his assistance in preparing this article.

Mr. V, age 49, has stable but symptomatic schizophrenia and a 33-year cigarette smoking history. He is very concerned because his primary care physician told him he has 2 serious smoking-related health problems: diabetes and hypertension. He tried a smoking cessation program for the general public, but it was a poor fit because of his schizophrenia symptoms.

Despite adhering to his medications (ziprasidone, 20 mg hs; perphenazine, 8 mg hs; lorazepam, 1 mg hs; zonisamide, 200 mg/d, and benztropine mesylate, 2 mg hs), Mr. V has residual auditory hallucinations, paranoid ideation, and impaired concentration and attention. He smokes approximately 1.5 packs per day, particularly when very ill, to alleviate chronic boredom, and to diminish distress from the hallucinations. All of his friends smoke, and they do not support his attempts to quit.

Successfully treating nicotine dependence can seem a formidable challenge in patients with schizophrenia:

• 72% to 90% smoke cigarettes, compared with 21% of the general population¹ (Box).^2-12
  
• They tend to smoke heavily, spending about one-third of their incomes on cigarettes.¹³
  
• Their negative symptoms (such as apathy), positive symptoms (such as disorganized thinking), and cognitive impairment can reduce motivation to quit and adhere to a smoking cessation strategy.
  
• Sociologic and physiologic aspects of schizophrenia reinforce their smoking habit (Table 1).^9,12,14-17
  

Even so, smokers with schizophrenia can be highly motivated and persistent in attempting to quit.¹⁸ Promising results have been reported in trials when psychopharmacologic treatments are combined with cognitive and behavioral interventions.

Box

This article reviews these empiric studies and suggests practical ways for clinicians to create smoking cessation and relapse prevention plans for individuals with schizophrenia.

Table 1

Why up to 90% of schizophrenia patients smoke cigarettes

Clinical trials of smoking cessation

Inadequate interventions. Conventional regimens—consisting of 8 to 12 weeks with sustained-release bupropion or nicotine replacement therapy (NRT) added to supportive or cognitive-behavioral therapy (CBT)¹⁹—are well-tolerated by patients with schizophrenia but only modestly effective. CBT alone (or with placebo) has not been effective for smoking cessation in schizophrenia. In clinical trials, abstinence rates have been:

• 4% to 19% after 3 to 6 months with bupropion or NRT and CBT
  
• ≤6% with placebo and CBT.^20-23
  

In a double-blind, placebo-controlled trial,²⁷ 51 smokers with schizophrenia were randomly assigned to receive combination NRT (21-mg NRT patch plus ≤18 mg/d NRT polacrilex gum prn) added to bupropion SR, 150 mg bid, or placebo. Smoking cessation—defined as quitting on the assigned date and maintaining continuous abstinence for 4 weeks (measured by expired air carbon monoxide

• 52% of those receiving bupropion and dual NRT
  
• 19% who received placebo and the 2 forms of NRT.
  

In one clinical trial, >50% of patients achieved 4 weeks of continuous abstinence on a regimen of bupropion SR, 150 mg bid; nicotine patch (21 mg/d); and as-needed nicotine gum (≤18 mg/d). However:

• 31% relapsed to smoking while NRT was being tapered from ~40 to 20 mg/d
  
• 77% relapsed after nicotine dependence treatment was discontinued.²⁷
  

Table 2

Suggested pharmacologic approaches for smoking cessation in patients with schizophrenia

CASE CONTINUED: Treating nicotine dependence

Mr. V cut down to 10 cigarettes a day during a 4-week motivational enhancement/psychoeducation intervention for smokers with major mental illness.²⁹ He then enrolled in a 12-week study in which subjects received high-dose dual NRT and bupropion SR or placebo.

He received bupropion SR, 150 mg bid; NRT patch, 21 mg/d; and nicotine polacrilex gum, up to 18 mg/d as needed, and tolerated the regimen well. After 4 weeks, he quit smoking on the quit date. His blood pressure—monitored weekly for the first month then monthly thereafter—remained stable throughout the intervention.

Prescribing considerations

Metabolic changes. Smoking—but not NRT—induces hepatic clearance of many psychotropics, and smoking cessation can be associated with increased drug serum levels. Polycyclic aromatic hydrocarbons present in cigarette smoke—but not NRT—induce hepatic aryl hydrocarbon hydroxylases and cytochrome P (CYP)-450 isozymes, primarily CYP 1A1, 1A2, and 2E1, thereby increasing metabolic clearance of medications—such as clozapine—that are substrates for these enzymes.

Smoking cessation is associated with a 30% to 42% reduction in activity of CYP 1A2, and the half-life of this reduction is 27 to 54 hours. Thus, therapeutic drug monitoring and dose reduction of 10% over the first 4 days of tobacco abstinence is recommended to avoid toxicity. If the patient remains abstinent from tobacco, further reducing the antipsychotic dose may be warranted, based on individual assessment.

Weight gain. Patients who quit smoking gain an average of 3 to 5 kg.³⁰

Nicotine withdrawal. Patients are used to thinking that nicotine is calming, whereas in reality nicotine and smoking are anxiogenic, and cigarette smoking alleviates the anxiety that comes from nicotine withdrawal.³¹ Educate patients about nicotine withdrawal symptoms, which easily can be confused with early signs of a psychotic relapse but are much more time-limited:

• dysphoria and irritability
  
• anxiety
  
• insomnia
  
• reduced heart rate
  
• restlessness
  
• difficulty concentrating.
  

NRT in a variety of delivery forms has been well tolerated and modestly effective for smoking cessation in schizophrenia.^23,27,28 Combinations of short-acting NRT (gum, lozenge, inhaler, or nasal spray) with the long-acting NRT patch improve long-term abstinence rates in smokers in the general population²⁶ and may improve abstinence rates in those with schizophrenia.²⁷ Maintaining the pharmacotherapy used to achieve abstinence may also improve sustained abstinence rates.

Varenicline is a partial nicotinic receptor agonist approved for treating tobacco dependence. No reports have been published on its safety and efficacy for smoking cessation in persons with schizophrenia.

In our experience with open-label varenicline for nicotine dependence in schizophrenia, 8 of 9 patients quit smoking, reported reduced cravings, and remained clinically stable on the agent for 6 to 9 months. All had previously relapsed after discontinuing NRT, bupropion, or the combination.

Controlled trials are needed to discern this agent’s place in the treatment hierarchy for smokers with schizophrenia, and several such trials are underway.

10-step office-based approach

CBT alone is not effective for smoking cessation in the schizophrenia population,^22,28 but pharmacologic interventions have not been shown to succeed without concurrent behavioral treatment.

The 10 behavioral treatments described below and the tools listed in Table 3 can be covered in 1 or 2 visits and individualized for a relatively brief, office-based approach. Using the complete list may be ideal, but you can deliver a reasonable behavioral intervention by choosing tasks tailored to each patient’s needs. After the initial session, review these interventions at follow-up appointments to reinforce skills.

1 Send a clear and simple message to your patients to quit smoking. If possible, provide a handout about health risks of smoking and benefits of quitting.

2 Elicit the patient’s reasons for wanting to quit, and help him or her list these reasons as specifically as possible, such as:

• “I want to have more spending money.”
  
• “I want to improve my health.”
  
• “I want to make my sister proud.”
  

3 Prescribe pharmacotherapy, as supported by clinical trial results. Explain the rationale for its use, and encourage adherence. Review proper techniques for using NRT patches and gum, lozenge, inhaler, or nasal spray.

4 Teach the patient skills to cope with cravings. The “4 Ds” are a helpful mnemonic:

• Deep breathe.
  
• Drink fluids.
  
• Delay (smoking).
  
• Do something else.
  

5 Discuss the patient’s smoking triggers and risky situations. These vary from patient to patient, but common triggers include:

• finishing a meal or drinking coffee
  
• seeing other people smoking
  
• psychological stressors or psychiatric symptoms such as anxiety or auditory hallucinations
  
• boredom, such as waiting for a bus.
  

• going to a day treatment center where most patients and staff smoke
  
• visiting a family member who smokes
  
• dealing with a stressful situation.
  

Plan the day, often hour by hour, to help the patient make new choices (such as go to the park in the morning instead of the convenience store, do a puzzle while watching TV at night). Schedule in some rewards and pleasant activities to substitute for cigarettes.

7 Work on ‘refusal skills.’ Patients will likely need to practice saying no to cigarettes offered to them in their social environments. Discuss these skills, and role-play to increase patients’ likelihood of success.

9 Discuss rewards patients can give themselves instead of cigarettes. This concept will be new to many but is important to help patients depend less on cigarettes for gratification.

10 Call patients on their quit date or the day after to make sure they are on track.

Table 3

CBT tools to help schizophrenia patients quit smoking

6-step problem-solving skills to help prevent smoking relapse

CASE CONTINUED: An improving picture

With CBT, Mr. V grasped that he had to make important changes to quit smoking and reduce his risk of relapse. He embraced the “4 Ds” and successfully adhered to the plan for his quit date. He maintained abstinence through the 12-month relapse prevention treatment period with the same bupropion and NRT dosage he had used to quit smoking (and tapered CBT sessions).

Mr. V realized early in treatment that if he quit smoking he could save $1,000 per year in the price of cigarettes. The camera he bought with the money he saved served as a motivator and helped alleviate the boredom that had kept him smoking.

Related resources

• U.S. Public Health Service. Clinical practice guideline. Treating tobacco use and dependence. www.surgeongeneral.gov/tobacco/tobaqrg.htm.
  
• Agency for Healthcare Research and Quality. Treating tobacco use and dependence: clinician’s packet. A how-to guide for implementing the Public Health Service Clinical Practice Guideline. www.ahcpr.gov/clinic/tobacco.
  
• Massachusetts Department of Public Health. www.trytostop.org.
  
• Centers for Disease Control and Prevention. Tobacco Information and Prevention Source (TIPS). www.cdc.gov/obacco.
  

• Benztropine mesylate • Cogentin
  
• Bupropion SR • Zyban
  
• Clozapine • Clozaril
  
• Lorazepam • Ativan
  
• Nicotine/transdermal • Nicotrol, Prostep
  
• Nicotine/nasal spray • Nicotrol NS
  
• Nicotine/polacrilex • Nicorette
  
• Perphenazine • various
  
• Varenicline • Chantix
  
• Ziprasidone • Geodon
  
• Zonisamide • Zonegram
  

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

Dr. Evins receives research support from Janssen Pharmaceutica.

Mr. V, age 49, has stable but symptomatic schizophrenia and a 33-year cigarette smoking history. He is very concerned because his primary care physician told him he has 2 serious smoking-related health problems: diabetes and hypertension. He tried a smoking cessation program for the general public, but it was a poor fit because of his schizophrenia symptoms.

Despite adhering to his medications (ziprasidone, 20 mg hs; perphenazine, 8 mg hs; lorazepam, 1 mg hs; zonisamide, 200 mg/d, and benztropine mesylate, 2 mg hs), Mr. V has residual auditory hallucinations, paranoid ideation, and impaired concentration and attention. He smokes approximately 1.5 packs per day, particularly when very ill, to alleviate chronic boredom, and to diminish distress from the hallucinations. All of his friends smoke, and they do not support his attempts to quit.

Successfully treating nicotine dependence can seem a formidable challenge in patients with schizophrenia:

• 72% to 90% smoke cigarettes, compared with 21% of the general population¹ (Box).^2-12
  
• They tend to smoke heavily, spending about one-third of their incomes on cigarettes.¹³
  
• Their negative symptoms (such as apathy), positive symptoms (such as disorganized thinking), and cognitive impairment can reduce motivation to quit and adhere to a smoking cessation strategy.
  
• Sociologic and physiologic aspects of schizophrenia reinforce their smoking habit (Table 1).^9,12,14-17
  

Even so, smokers with schizophrenia can be highly motivated and persistent in attempting to quit.¹⁸ Promising results have been reported in trials when psychopharmacologic treatments are combined with cognitive and behavioral interventions.

Box

This article reviews these empiric studies and suggests practical ways for clinicians to create smoking cessation and relapse prevention plans for individuals with schizophrenia.

Table 1

Why up to 90% of schizophrenia patients smoke cigarettes

Clinical trials of smoking cessation

Inadequate interventions. Conventional regimens—consisting of 8 to 12 weeks with sustained-release bupropion or nicotine replacement therapy (NRT) added to supportive or cognitive-behavioral therapy (CBT)¹⁹—are well-tolerated by patients with schizophrenia but only modestly effective. CBT alone (or with placebo) has not been effective for smoking cessation in schizophrenia. In clinical trials, abstinence rates have been:

• 4% to 19% after 3 to 6 months with bupropion or NRT and CBT
  
• ≤6% with placebo and CBT.^20-23
  

In a double-blind, placebo-controlled trial,²⁷ 51 smokers with schizophrenia were randomly assigned to receive combination NRT (21-mg NRT patch plus ≤18 mg/d NRT polacrilex gum prn) added to bupropion SR, 150 mg bid, or placebo. Smoking cessation—defined as quitting on the assigned date and maintaining continuous abstinence for 4 weeks (measured by expired air carbon monoxide

• 52% of those receiving bupropion and dual NRT
  
• 19% who received placebo and the 2 forms of NRT.
  

In one clinical trial, >50% of patients achieved 4 weeks of continuous abstinence on a regimen of bupropion SR, 150 mg bid; nicotine patch (21 mg/d); and as-needed nicotine gum (≤18 mg/d). However:

• 31% relapsed to smoking while NRT was being tapered from ~40 to 20 mg/d
  
• 77% relapsed after nicotine dependence treatment was discontinued.²⁷
  

Table 2

Suggested pharmacologic approaches for smoking cessation in patients with schizophrenia

CASE CONTINUED: Treating nicotine dependence

Mr. V cut down to 10 cigarettes a day during a 4-week motivational enhancement/psychoeducation intervention for smokers with major mental illness.²⁹ He then enrolled in a 12-week study in which subjects received high-dose dual NRT and bupropion SR or placebo.

He received bupropion SR, 150 mg bid; NRT patch, 21 mg/d; and nicotine polacrilex gum, up to 18 mg/d as needed, and tolerated the regimen well. After 4 weeks, he quit smoking on the quit date. His blood pressure—monitored weekly for the first month then monthly thereafter—remained stable throughout the intervention.

Prescribing considerations

Metabolic changes. Smoking—but not NRT—induces hepatic clearance of many psychotropics, and smoking cessation can be associated with increased drug serum levels. Polycyclic aromatic hydrocarbons present in cigarette smoke—but not NRT—induce hepatic aryl hydrocarbon hydroxylases and cytochrome P (CYP)-450 isozymes, primarily CYP 1A1, 1A2, and 2E1, thereby increasing metabolic clearance of medications—such as clozapine—that are substrates for these enzymes.

Smoking cessation is associated with a 30% to 42% reduction in activity of CYP 1A2, and the half-life of this reduction is 27 to 54 hours. Thus, therapeutic drug monitoring and dose reduction of 10% over the first 4 days of tobacco abstinence is recommended to avoid toxicity. If the patient remains abstinent from tobacco, further reducing the antipsychotic dose may be warranted, based on individual assessment.

Weight gain. Patients who quit smoking gain an average of 3 to 5 kg.³⁰

Nicotine withdrawal. Patients are used to thinking that nicotine is calming, whereas in reality nicotine and smoking are anxiogenic, and cigarette smoking alleviates the anxiety that comes from nicotine withdrawal.³¹ Educate patients about nicotine withdrawal symptoms, which easily can be confused with early signs of a psychotic relapse but are much more time-limited:

• dysphoria and irritability
  
• anxiety
  
• insomnia
  
• reduced heart rate
  
• restlessness
  
• difficulty concentrating.
  

NRT in a variety of delivery forms has been well tolerated and modestly effective for smoking cessation in schizophrenia.^23,27,28 Combinations of short-acting NRT (gum, lozenge, inhaler, or nasal spray) with the long-acting NRT patch improve long-term abstinence rates in smokers in the general population²⁶ and may improve abstinence rates in those with schizophrenia.²⁷ Maintaining the pharmacotherapy used to achieve abstinence may also improve sustained abstinence rates.

Varenicline is a partial nicotinic receptor agonist approved for treating tobacco dependence. No reports have been published on its safety and efficacy for smoking cessation in persons with schizophrenia.

In our experience with open-label varenicline for nicotine dependence in schizophrenia, 8 of 9 patients quit smoking, reported reduced cravings, and remained clinically stable on the agent for 6 to 9 months. All had previously relapsed after discontinuing NRT, bupropion, or the combination.

Controlled trials are needed to discern this agent’s place in the treatment hierarchy for smokers with schizophrenia, and several such trials are underway.

10-step office-based approach

CBT alone is not effective for smoking cessation in the schizophrenia population,^22,28 but pharmacologic interventions have not been shown to succeed without concurrent behavioral treatment.

The 10 behavioral treatments described below and the tools listed in Table 3 can be covered in 1 or 2 visits and individualized for a relatively brief, office-based approach. Using the complete list may be ideal, but you can deliver a reasonable behavioral intervention by choosing tasks tailored to each patient’s needs. After the initial session, review these interventions at follow-up appointments to reinforce skills.

1 Send a clear and simple message to your patients to quit smoking. If possible, provide a handout about health risks of smoking and benefits of quitting.

2 Elicit the patient’s reasons for wanting to quit, and help him or her list these reasons as specifically as possible, such as:

• “I want to have more spending money.”
  
• “I want to improve my health.”
  
• “I want to make my sister proud.”
  

3 Prescribe pharmacotherapy, as supported by clinical trial results. Explain the rationale for its use, and encourage adherence. Review proper techniques for using NRT patches and gum, lozenge, inhaler, or nasal spray.

4 Teach the patient skills to cope with cravings. The “4 Ds” are a helpful mnemonic:

• Deep breathe.
  
• Drink fluids.
  
• Delay (smoking).
  
• Do something else.
  

5 Discuss the patient’s smoking triggers and risky situations. These vary from patient to patient, but common triggers include:

• finishing a meal or drinking coffee
  
• seeing other people smoking
  
• psychological stressors or psychiatric symptoms such as anxiety or auditory hallucinations
  
• boredom, such as waiting for a bus.
  

• going to a day treatment center where most patients and staff smoke
  
• visiting a family member who smokes
  
• dealing with a stressful situation.
  

Plan the day, often hour by hour, to help the patient make new choices (such as go to the park in the morning instead of the convenience store, do a puzzle while watching TV at night). Schedule in some rewards and pleasant activities to substitute for cigarettes.

7 Work on ‘refusal skills.’ Patients will likely need to practice saying no to cigarettes offered to them in their social environments. Discuss these skills, and role-play to increase patients’ likelihood of success.

9 Discuss rewards patients can give themselves instead of cigarettes. This concept will be new to many but is important to help patients depend less on cigarettes for gratification.

10 Call patients on their quit date or the day after to make sure they are on track.

Table 3

CBT tools to help schizophrenia patients quit smoking

6-step problem-solving skills to help prevent smoking relapse

CASE CONTINUED: An improving picture

With CBT, Mr. V grasped that he had to make important changes to quit smoking and reduce his risk of relapse. He embraced the “4 Ds” and successfully adhered to the plan for his quit date. He maintained abstinence through the 12-month relapse prevention treatment period with the same bupropion and NRT dosage he had used to quit smoking (and tapered CBT sessions).

Mr. V realized early in treatment that if he quit smoking he could save $1,000 per year in the price of cigarettes. The camera he bought with the money he saved served as a motivator and helped alleviate the boredom that had kept him smoking.

Related resources

• U.S. Public Health Service. Clinical practice guideline. Treating tobacco use and dependence. www.surgeongeneral.gov/tobacco/tobaqrg.htm.
  
• Agency for Healthcare Research and Quality. Treating tobacco use and dependence: clinician’s packet. A how-to guide for implementing the Public Health Service Clinical Practice Guideline. www.ahcpr.gov/clinic/tobacco.
  
• Massachusetts Department of Public Health. www.trytostop.org.
  
• Centers for Disease Control and Prevention. Tobacco Information and Prevention Source (TIPS). www.cdc.gov/obacco.
  

• Benztropine mesylate • Cogentin
  
• Bupropion SR • Zyban
  
• Clozapine • Clozaril
  
• Lorazepam • Ativan
  
• Nicotine/transdermal • Nicotrol, Prostep
  
• Nicotine/nasal spray • Nicotrol NS
  
• Nicotine/polacrilex • Nicorette
  
• Perphenazine • various
  
• Varenicline • Chantix
  
• Ziprasidone • Geodon
  
• Zonisamide • Zonegram
  

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

Dr. Evins receives research support from Janssen Pharmaceutica.

Mr. V, age 49, has stable but symptomatic schizophrenia and a 33-year cigarette smoking history. He is very concerned because his primary care physician told him he has 2 serious smoking-related health problems: diabetes and hypertension. He tried a smoking cessation program for the general public, but it was a poor fit because of his schizophrenia symptoms.

Despite adhering to his medications (ziprasidone, 20 mg hs; perphenazine, 8 mg hs; lorazepam, 1 mg hs; zonisamide, 200 mg/d, and benztropine mesylate, 2 mg hs), Mr. V has residual auditory hallucinations, paranoid ideation, and impaired concentration and attention. He smokes approximately 1.5 packs per day, particularly when very ill, to alleviate chronic boredom, and to diminish distress from the hallucinations. All of his friends smoke, and they do not support his attempts to quit.

Successfully treating nicotine dependence can seem a formidable challenge in patients with schizophrenia:

• 72% to 90% smoke cigarettes, compared with 21% of the general population¹ (Box).^2-12
  
• They tend to smoke heavily, spending about one-third of their incomes on cigarettes.¹³
  
• Their negative symptoms (such as apathy), positive symptoms (such as disorganized thinking), and cognitive impairment can reduce motivation to quit and adhere to a smoking cessation strategy.
  
• Sociologic and physiologic aspects of schizophrenia reinforce their smoking habit (Table 1).^9,12,14-17
  

Even so, smokers with schizophrenia can be highly motivated and persistent in attempting to quit.¹⁸ Promising results have been reported in trials when psychopharmacologic treatments are combined with cognitive and behavioral interventions.

Box

This article reviews these empiric studies and suggests practical ways for clinicians to create smoking cessation and relapse prevention plans for individuals with schizophrenia.

Table 1

Why up to 90% of schizophrenia patients smoke cigarettes

Clinical trials of smoking cessation

Inadequate interventions. Conventional regimens—consisting of 8 to 12 weeks with sustained-release bupropion or nicotine replacement therapy (NRT) added to supportive or cognitive-behavioral therapy (CBT)¹⁹—are well-tolerated by patients with schizophrenia but only modestly effective. CBT alone (or with placebo) has not been effective for smoking cessation in schizophrenia. In clinical trials, abstinence rates have been:

• 4% to 19% after 3 to 6 months with bupropion or NRT and CBT
  
• ≤6% with placebo and CBT.^20-23
  

In a double-blind, placebo-controlled trial,²⁷ 51 smokers with schizophrenia were randomly assigned to receive combination NRT (21-mg NRT patch plus ≤18 mg/d NRT polacrilex gum prn) added to bupropion SR, 150 mg bid, or placebo. Smoking cessation—defined as quitting on the assigned date and maintaining continuous abstinence for 4 weeks (measured by expired air carbon monoxide

• 52% of those receiving bupropion and dual NRT
  
• 19% who received placebo and the 2 forms of NRT.
  

In one clinical trial, >50% of patients achieved 4 weeks of continuous abstinence on a regimen of bupropion SR, 150 mg bid; nicotine patch (21 mg/d); and as-needed nicotine gum (≤18 mg/d). However:

• 31% relapsed to smoking while NRT was being tapered from ~40 to 20 mg/d
  
• 77% relapsed after nicotine dependence treatment was discontinued.²⁷
  

Table 2

Suggested pharmacologic approaches for smoking cessation in patients with schizophrenia

CASE CONTINUED: Treating nicotine dependence

Mr. V cut down to 10 cigarettes a day during a 4-week motivational enhancement/psychoeducation intervention for smokers with major mental illness.²⁹ He then enrolled in a 12-week study in which subjects received high-dose dual NRT and bupropion SR or placebo.

He received bupropion SR, 150 mg bid; NRT patch, 21 mg/d; and nicotine polacrilex gum, up to 18 mg/d as needed, and tolerated the regimen well. After 4 weeks, he quit smoking on the quit date. His blood pressure—monitored weekly for the first month then monthly thereafter—remained stable throughout the intervention.

Prescribing considerations

Metabolic changes. Smoking—but not NRT—induces hepatic clearance of many psychotropics, and smoking cessation can be associated with increased drug serum levels. Polycyclic aromatic hydrocarbons present in cigarette smoke—but not NRT—induce hepatic aryl hydrocarbon hydroxylases and cytochrome P (CYP)-450 isozymes, primarily CYP 1A1, 1A2, and 2E1, thereby increasing metabolic clearance of medications—such as clozapine—that are substrates for these enzymes.

Smoking cessation is associated with a 30% to 42% reduction in activity of CYP 1A2, and the half-life of this reduction is 27 to 54 hours. Thus, therapeutic drug monitoring and dose reduction of 10% over the first 4 days of tobacco abstinence is recommended to avoid toxicity. If the patient remains abstinent from tobacco, further reducing the antipsychotic dose may be warranted, based on individual assessment.

Weight gain. Patients who quit smoking gain an average of 3 to 5 kg.³⁰

Nicotine withdrawal. Patients are used to thinking that nicotine is calming, whereas in reality nicotine and smoking are anxiogenic, and cigarette smoking alleviates the anxiety that comes from nicotine withdrawal.³¹ Educate patients about nicotine withdrawal symptoms, which easily can be confused with early signs of a psychotic relapse but are much more time-limited:

• dysphoria and irritability
  
• anxiety
  
• insomnia
  
• reduced heart rate
  
• restlessness
  
• difficulty concentrating.
  

NRT in a variety of delivery forms has been well tolerated and modestly effective for smoking cessation in schizophrenia.^23,27,28 Combinations of short-acting NRT (gum, lozenge, inhaler, or nasal spray) with the long-acting NRT patch improve long-term abstinence rates in smokers in the general population²⁶ and may improve abstinence rates in those with schizophrenia.²⁷ Maintaining the pharmacotherapy used to achieve abstinence may also improve sustained abstinence rates.

Varenicline is a partial nicotinic receptor agonist approved for treating tobacco dependence. No reports have been published on its safety and efficacy for smoking cessation in persons with schizophrenia.

In our experience with open-label varenicline for nicotine dependence in schizophrenia, 8 of 9 patients quit smoking, reported reduced cravings, and remained clinically stable on the agent for 6 to 9 months. All had previously relapsed after discontinuing NRT, bupropion, or the combination.

Controlled trials are needed to discern this agent’s place in the treatment hierarchy for smokers with schizophrenia, and several such trials are underway.

10-step office-based approach

CBT alone is not effective for smoking cessation in the schizophrenia population,^22,28 but pharmacologic interventions have not been shown to succeed without concurrent behavioral treatment.

The 10 behavioral treatments described below and the tools listed in Table 3 can be covered in 1 or 2 visits and individualized for a relatively brief, office-based approach. Using the complete list may be ideal, but you can deliver a reasonable behavioral intervention by choosing tasks tailored to each patient’s needs. After the initial session, review these interventions at follow-up appointments to reinforce skills.

1 Send a clear and simple message to your patients to quit smoking. If possible, provide a handout about health risks of smoking and benefits of quitting.

2 Elicit the patient’s reasons for wanting to quit, and help him or her list these reasons as specifically as possible, such as:

• “I want to have more spending money.”
  
• “I want to improve my health.”
  
• “I want to make my sister proud.”
  

3 Prescribe pharmacotherapy, as supported by clinical trial results. Explain the rationale for its use, and encourage adherence. Review proper techniques for using NRT patches and gum, lozenge, inhaler, or nasal spray.

4 Teach the patient skills to cope with cravings. The “4 Ds” are a helpful mnemonic:

• Deep breathe.
  
• Drink fluids.
  
• Delay (smoking).
  
• Do something else.
  

5 Discuss the patient’s smoking triggers and risky situations. These vary from patient to patient, but common triggers include:

• finishing a meal or drinking coffee
  
• seeing other people smoking
  
• psychological stressors or psychiatric symptoms such as anxiety or auditory hallucinations
  
• boredom, such as waiting for a bus.
  

• going to a day treatment center where most patients and staff smoke
  
• visiting a family member who smokes
  
• dealing with a stressful situation.
  

Plan the day, often hour by hour, to help the patient make new choices (such as go to the park in the morning instead of the convenience store, do a puzzle while watching TV at night). Schedule in some rewards and pleasant activities to substitute for cigarettes.

7 Work on ‘refusal skills.’ Patients will likely need to practice saying no to cigarettes offered to them in their social environments. Discuss these skills, and role-play to increase patients’ likelihood of success.

9 Discuss rewards patients can give themselves instead of cigarettes. This concept will be new to many but is important to help patients depend less on cigarettes for gratification.

10 Call patients on their quit date or the day after to make sure they are on track.

Table 3

CBT tools to help schizophrenia patients quit smoking

6-step problem-solving skills to help prevent smoking relapse

CASE CONTINUED: An improving picture

With CBT, Mr. V grasped that he had to make important changes to quit smoking and reduce his risk of relapse. He embraced the “4 Ds” and successfully adhered to the plan for his quit date. He maintained abstinence through the 12-month relapse prevention treatment period with the same bupropion and NRT dosage he had used to quit smoking (and tapered CBT sessions).

Mr. V realized early in treatment that if he quit smoking he could save $1,000 per year in the price of cigarettes. The camera he bought with the money he saved served as a motivator and helped alleviate the boredom that had kept him smoking.

Related resources

• U.S. Public Health Service. Clinical practice guideline. Treating tobacco use and dependence. www.surgeongeneral.gov/tobacco/tobaqrg.htm.
  
• Agency for Healthcare Research and Quality. Treating tobacco use and dependence: clinician’s packet. A how-to guide for implementing the Public Health Service Clinical Practice Guideline. www.ahcpr.gov/clinic/tobacco.
  
• Massachusetts Department of Public Health. www.trytostop.org.
  
• Centers for Disease Control and Prevention. Tobacco Information and Prevention Source (TIPS). www.cdc.gov/obacco.
  

• Benztropine mesylate • Cogentin
  
• Bupropion SR • Zyban
  
• Clozapine • Clozaril
  
• Lorazepam • Ativan
  
• Nicotine/transdermal • Nicotrol, Prostep
  
• Nicotine/nasal spray • Nicotrol NS
  
• Nicotine/polacrilex • Nicorette
  
• Perphenazine • various
  
• Varenicline • Chantix
  
• Ziprasidone • Geodon
  
• Zonisamide • Zonegram
  

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

Dr. Evins receives research support from Janssen Pharmaceutica.

Mr. C is a 50-year-old professional writer who recently made a serious suicide attempt. At his initial session, Mr. C was hesitant to discuss his situation and reason for attending. He did, however, bring a copy of his résumé so the therapist could “get to know him quickly.”

He said he had been depressed for a long time, especially since he found an error in one of his published works. His confidence and writing abilities seemed to decline after this discovery, his career took a downturn, and ultimately he was fired from his position. He described often being at odds with his supervisors at work, whom he saw as critical and condescending. He was mortified by his job loss and did not inform his wife or friends of his firing.

Mr. C had always been a bit of a loner, and after losing his job he further distanced himself from others. He began drinking heavily to avoid the pain of “letting everyone down.” His wife, family, and friends were shocked at the suicide attempt and expressed dismay that Mr. C had not confided in anyone.

Mr. C describes himself as being perfectionistic throughout his life and never being quite good enough in any of his pursuits. This leads to self-recriminations and persistent feelings of shame.

Far from being a positive attribute, perfectionism is a neurotic personality style that can result in serious psychopathology, including relationship problems, depression, anorexia nervosa, and suicide. Determining a patient’s perfectionistic traits is essential when evaluating those who seek treatment specifically for this distressing behavior as well as patients in treatment for other issues who may have a perfectionistic personality. Accurately assessing perfectionism can help you predict and forestall noncompliance, assess suicide risk, determine appropriate treatment and identify circumstances under which a patient might be particularly vulnerable to relapse.

This article describes:

• 3 traits of perfectionism
  
• 3 dimensions of perfectionistic self-presentation
  
• perfectionistic cognitions
  
• useful self-report tools for clinical practice
  
• effective treatments.
  

Characteristics of perfectionism

Although perfectionism initially was viewed as self-related cognitions, recent models suggest it incorporates intrapersonal and interpersonal dimensions.¹ A person with perfectionism has a marked need for absolute perfection for the self and/or others in many—if not all—pursuits that is strongly rooted in his or her intrapersonal and interpersonal worlds. Other characteristics of perfectionism include:

• equating self-worth or esteem with performance
  
• self-punishment in failure and a lack of satisfaction in success
  
• maintaining and needing to strive for unrealistic expectations
  
• unrealistic criteria for success and broad criteria for failure.
  

We define perfectionism as a neurotic personality style involving perfectionist traits, self-presentation styles, and cognitions that is a core vulnerability factor for a variety of psychological, physical, achievement, and relationship problems (Table 2).^1,3

3 traits. Three traits of perfectionism reflect the desire for the self or others to be perfect:

• self-oriented perfectionism—a requirement for the self to be perfect
  
• other-oriented perfectionism—a requirement for others to be perfect
  
• socially prescribed perfectionism—a perception that others require perfection of oneself.
  

3 self-presentational dimensions. The interpersonal expression of perfectionism is perfectionistic self-presentation. In our model, the 3 facets of perfectionistic self-presentation are:

• perfectionistic self-promotion—overt displays and statements of one’s supposed “perfection”
  
• nondisplay of imperfections—hiding any imperfections
  
• nondisclosure of imperfections—avoiding disclosure or discussion of any imperfection.³
  

Table 1

How perfectionism differs from conscientiousness

Psychopathologies associated with perfectionism

Traits tied to psychopathology

Each of the 3 traits of perfectionism in our model has been associated with psychopathology in multiple studies.

Self-oriented perfectionism is often involved in Axis I disorders, including unipolar depression. This trait is elevated among adults and children diagnosed with major depressive disorder and may be pernicious in the presence of stressors, particularly achievement-related ones.⁶ In other words, self-oriented perfectionism appears to be a risk factor for unipolar depression.^7,8

It also is elevated in women with anorexia nervosa compared with normal and psychiatric controls.⁹ Individuals with anorexia nervosa appear to have the highest levels of self-oriented perfectionism among clinical groups.

Other-oriented perfectionism is associated with antisocial and narcissistic personality disorders.^10,11 It also is related to interpersonal problems and difficulties with marriage and intimate relationships.¹²

Socially prescribed perfectionism is highly elevated in patients with social phobia¹³ and narcissistic¹¹ or borderline personality disorder.¹⁰ It also is associated with severity of depression, anxiety, and symptoms of hostility.⁷

Perhaps most important, determining a patient’s level of socially prescribed perfectionism can aid in assessing suicide risk. Socially prescribed perfectionism has been shown to be highly relevant in suicide ideation, ratings of suicide risk, and moderate- to high-intent suicide attempts in adults,¹⁴ adolescents, and children.¹⁵ Socially prescribed perfectionism has been found to be a unique predictor of suicide behaviors even after controlling for common predictors such as depression severity and hopelessness.

In addition, perfectionistic self-presentation appears to impair patients’ ability to access and benefit from treatment. Researchers (Hewitt PL, Lee-Baggley D, Sherry SB, et al., unpublished data, 2007) have found that the various dimensions of perfectionistic self-presentation are associated with:

• difficulty in seeking help for psychological problems
  
• increased distress in clinical interviews
  
• fears of psychotherapy and psychotherapists
  
• early termination of treatment.
  

Assessing perfectionistic behavior

A variety of brief self-report measures of perfectionism components—and at least one interview measure—can aid your assessment. These are brief instruments and take only a few minutes to complete. Each self-report measure assesses different aspects of perfectionism, such as traits, self-presentational styles, or cognitions (Table 3). The interview can be used as an alternative to the self-report tools.

Mr. C’s scores on several of these measures appear in Table 4. Interpretive information is available from the authors (see Related Resources). Empirical evidence supports the reliability and validity of these measures in clinical samples of both adults and children/adolescents.

Table 3

Perfectionism self-report assessment tools

Interpreting scores on perfectionism self-reports

Limited data on treatments

Few treatments for perfectionistic behavior have been systematically evaluated. Numerous studies have attempted to assess changes in perfectionism as the result of treatment for a specific Axis I disorder, but few have addressed treatment for perfectionism as a clinical entity.

Overall, it seems reasonable to expect that because perfectionism is a personality style, improvement would require fairly intensive, long-term treatment that explicitly emphasizes reducing dimensions of perfectionism.

Psychodynamic treatments focus on perfectionism’s underlying mechanisms and attempt to alter the patient’s personality structure. Studies suggest that intensive psychotherapy is most appropriate.

One of the first treatment evaluations from a reanalysis of Menninger Clinic data found the greatest improvements in patients receiving intensive psychoanalytically oriented treatment, compared with short-term psychotherapy or other treatments.¹⁶ More recent evaluations suggest that highly perfectionistic individuals can be treated effectively only with intensive, long-term psychodynamically oriented treatment¹⁷ and short-term interpersonal, cognitive, and medication therapies do little to alter perfectionistic behavior.

In our experience [PLH] perfectionistic individuals can improve significantly with long-term intensive treatment. On the other hand, we recently completed a study of the efficacy of a short-term, intensive psychodynamic/interpersonal group approach for treating perfectionism and its sequelae.

In this study,¹⁸ we focused on treating the interpersonal precursors or causes of perfectionism, such as attachment styles; interpersonal needs for respect, caring, acceptance, and belonging; and need to avoid rejection, abandonment, and humiliation. In 70 patients with high levels of perfectionism, this treatment significantly decreased perfectionism, symptoms of depression and anxiety, and interpersonal problems. These symptoms continued to be reduced from baseline 6 months later.

Cognitive-behavioral approaches. Several researchers’ findings suggest that cognitive restructuring, bibliotherapy, role-playing, coping strategies, homework assignments, and relaxation may help reduce the cognitive component of perfectionism.^19,20 Other work indicates that cognitive interventions can reduce perfectionism. One study linked reductions in socially prescribed perfectionism to concomitant reductions in depression.²¹

Cognitive interventions can reduce perfectionistic concerns about mistakes and doubting actions, but other aspects of perfectionism—such as perceived parental unrealistic standards and criticisms—remain elevated and appear more treatment-resistant.²⁴

Collectively, these data suggest that some treated patients may be at risk for relapse because persistent perfectionism contributes to a vulnerability to distress.

Medication. No studies have specifically assessed whether medications might reduce perfectionism. Imipramine did not have a significant effect on perfectionistic attitudes when used in the medication protocol of the National Institute of Mental Health Collaborative Study on Depression.¹⁷ Amitriptyline has alleviated some dysfunctional attitudes in depressed patients but not perfectionism.²⁵

Research is needed to evaluate the efficacy of various treatments. At this early stage, it appears that:

• short-term gains might be achieved by reducing symptoms
  
• long-term, intensive psychodynamic treatment may be required to change the perfectionistic personality and its vulnerability effects.
  

Table 5

Treating perfectionism: Common patient challenges

• Flett GL, Hewitt PL. Perfectionism: theory, research and treatment. Washington, DC: American Psychological Association; 2002.
  
• Greenspon T. Freeing our families from perfectionism. Minneapolis: Free Spirit Publishing; 2002.
  
• For more information on interpreting self-report measures of perfectionism, contact Dr. Paul Hewitt, [email protected]; 604-822-5827.
  

• Amitriptyline • Elavil, Endep
  
• Imipramine • Tofranil
  

The authors thank Jonathan Blasberg for his help with this paper and the Social Sciences and Humanities Research Council of Canada for supporting this work.

Mr. C is a 50-year-old professional writer who recently made a serious suicide attempt. At his initial session, Mr. C was hesitant to discuss his situation and reason for attending. He did, however, bring a copy of his résumé so the therapist could “get to know him quickly.”

He said he had been depressed for a long time, especially since he found an error in one of his published works. His confidence and writing abilities seemed to decline after this discovery, his career took a downturn, and ultimately he was fired from his position. He described often being at odds with his supervisors at work, whom he saw as critical and condescending. He was mortified by his job loss and did not inform his wife or friends of his firing.

Mr. C had always been a bit of a loner, and after losing his job he further distanced himself from others. He began drinking heavily to avoid the pain of “letting everyone down.” His wife, family, and friends were shocked at the suicide attempt and expressed dismay that Mr. C had not confided in anyone.

Mr. C describes himself as being perfectionistic throughout his life and never being quite good enough in any of his pursuits. This leads to self-recriminations and persistent feelings of shame.

Far from being a positive attribute, perfectionism is a neurotic personality style that can result in serious psychopathology, including relationship problems, depression, anorexia nervosa, and suicide. Determining a patient’s perfectionistic traits is essential when evaluating those who seek treatment specifically for this distressing behavior as well as patients in treatment for other issues who may have a perfectionistic personality. Accurately assessing perfectionism can help you predict and forestall noncompliance, assess suicide risk, determine appropriate treatment and identify circumstances under which a patient might be particularly vulnerable to relapse.

This article describes:

• 3 traits of perfectionism
  
• 3 dimensions of perfectionistic self-presentation
  
• perfectionistic cognitions
  
• useful self-report tools for clinical practice
  
• effective treatments.
  

Characteristics of perfectionism

Although perfectionism initially was viewed as self-related cognitions, recent models suggest it incorporates intrapersonal and interpersonal dimensions.¹ A person with perfectionism has a marked need for absolute perfection for the self and/or others in many—if not all—pursuits that is strongly rooted in his or her intrapersonal and interpersonal worlds. Other characteristics of perfectionism include:

• equating self-worth or esteem with performance
  
• self-punishment in failure and a lack of satisfaction in success
  
• maintaining and needing to strive for unrealistic expectations
  
• unrealistic criteria for success and broad criteria for failure.
  

We define perfectionism as a neurotic personality style involving perfectionist traits, self-presentation styles, and cognitions that is a core vulnerability factor for a variety of psychological, physical, achievement, and relationship problems (Table 2).^1,3

3 traits. Three traits of perfectionism reflect the desire for the self or others to be perfect:

• self-oriented perfectionism—a requirement for the self to be perfect
  
• other-oriented perfectionism—a requirement for others to be perfect
  
• socially prescribed perfectionism—a perception that others require perfection of oneself.
  

3 self-presentational dimensions. The interpersonal expression of perfectionism is perfectionistic self-presentation. In our model, the 3 facets of perfectionistic self-presentation are:

• perfectionistic self-promotion—overt displays and statements of one’s supposed “perfection”
  
• nondisplay of imperfections—hiding any imperfections
  
• nondisclosure of imperfections—avoiding disclosure or discussion of any imperfection.³
  

Table 1

How perfectionism differs from conscientiousness

Psychopathologies associated with perfectionism

Traits tied to psychopathology

Each of the 3 traits of perfectionism in our model has been associated with psychopathology in multiple studies.

Self-oriented perfectionism is often involved in Axis I disorders, including unipolar depression. This trait is elevated among adults and children diagnosed with major depressive disorder and may be pernicious in the presence of stressors, particularly achievement-related ones.⁶ In other words, self-oriented perfectionism appears to be a risk factor for unipolar depression.^7,8

It also is elevated in women with anorexia nervosa compared with normal and psychiatric controls.⁹ Individuals with anorexia nervosa appear to have the highest levels of self-oriented perfectionism among clinical groups.

Other-oriented perfectionism is associated with antisocial and narcissistic personality disorders.^10,11 It also is related to interpersonal problems and difficulties with marriage and intimate relationships.¹²

Socially prescribed perfectionism is highly elevated in patients with social phobia¹³ and narcissistic¹¹ or borderline personality disorder.¹⁰ It also is associated with severity of depression, anxiety, and symptoms of hostility.⁷

Perhaps most important, determining a patient’s level of socially prescribed perfectionism can aid in assessing suicide risk. Socially prescribed perfectionism has been shown to be highly relevant in suicide ideation, ratings of suicide risk, and moderate- to high-intent suicide attempts in adults,¹⁴ adolescents, and children.¹⁵ Socially prescribed perfectionism has been found to be a unique predictor of suicide behaviors even after controlling for common predictors such as depression severity and hopelessness.

In addition, perfectionistic self-presentation appears to impair patients’ ability to access and benefit from treatment. Researchers (Hewitt PL, Lee-Baggley D, Sherry SB, et al., unpublished data, 2007) have found that the various dimensions of perfectionistic self-presentation are associated with:

• difficulty in seeking help for psychological problems
  
• increased distress in clinical interviews
  
• fears of psychotherapy and psychotherapists
  
• early termination of treatment.
  

Assessing perfectionistic behavior

A variety of brief self-report measures of perfectionism components—and at least one interview measure—can aid your assessment. These are brief instruments and take only a few minutes to complete. Each self-report measure assesses different aspects of perfectionism, such as traits, self-presentational styles, or cognitions (Table 3). The interview can be used as an alternative to the self-report tools.

Mr. C’s scores on several of these measures appear in Table 4. Interpretive information is available from the authors (see Related Resources). Empirical evidence supports the reliability and validity of these measures in clinical samples of both adults and children/adolescents.

Table 3

Perfectionism self-report assessment tools

Interpreting scores on perfectionism self-reports

Limited data on treatments

Few treatments for perfectionistic behavior have been systematically evaluated. Numerous studies have attempted to assess changes in perfectionism as the result of treatment for a specific Axis I disorder, but few have addressed treatment for perfectionism as a clinical entity.

Overall, it seems reasonable to expect that because perfectionism is a personality style, improvement would require fairly intensive, long-term treatment that explicitly emphasizes reducing dimensions of perfectionism.

Psychodynamic treatments focus on perfectionism’s underlying mechanisms and attempt to alter the patient’s personality structure. Studies suggest that intensive psychotherapy is most appropriate.

One of the first treatment evaluations from a reanalysis of Menninger Clinic data found the greatest improvements in patients receiving intensive psychoanalytically oriented treatment, compared with short-term psychotherapy or other treatments.¹⁶ More recent evaluations suggest that highly perfectionistic individuals can be treated effectively only with intensive, long-term psychodynamically oriented treatment¹⁷ and short-term interpersonal, cognitive, and medication therapies do little to alter perfectionistic behavior.

In our experience [PLH] perfectionistic individuals can improve significantly with long-term intensive treatment. On the other hand, we recently completed a study of the efficacy of a short-term, intensive psychodynamic/interpersonal group approach for treating perfectionism and its sequelae.

In this study,¹⁸ we focused on treating the interpersonal precursors or causes of perfectionism, such as attachment styles; interpersonal needs for respect, caring, acceptance, and belonging; and need to avoid rejection, abandonment, and humiliation. In 70 patients with high levels of perfectionism, this treatment significantly decreased perfectionism, symptoms of depression and anxiety, and interpersonal problems. These symptoms continued to be reduced from baseline 6 months later.

Cognitive-behavioral approaches. Several researchers’ findings suggest that cognitive restructuring, bibliotherapy, role-playing, coping strategies, homework assignments, and relaxation may help reduce the cognitive component of perfectionism.^19,20 Other work indicates that cognitive interventions can reduce perfectionism. One study linked reductions in socially prescribed perfectionism to concomitant reductions in depression.²¹

Cognitive interventions can reduce perfectionistic concerns about mistakes and doubting actions, but other aspects of perfectionism—such as perceived parental unrealistic standards and criticisms—remain elevated and appear more treatment-resistant.²⁴

Collectively, these data suggest that some treated patients may be at risk for relapse because persistent perfectionism contributes to a vulnerability to distress.

Medication. No studies have specifically assessed whether medications might reduce perfectionism. Imipramine did not have a significant effect on perfectionistic attitudes when used in the medication protocol of the National Institute of Mental Health Collaborative Study on Depression.¹⁷ Amitriptyline has alleviated some dysfunctional attitudes in depressed patients but not perfectionism.²⁵

Research is needed to evaluate the efficacy of various treatments. At this early stage, it appears that:

• short-term gains might be achieved by reducing symptoms
  
• long-term, intensive psychodynamic treatment may be required to change the perfectionistic personality and its vulnerability effects.
  

Table 5

Treating perfectionism: Common patient challenges

• Flett GL, Hewitt PL. Perfectionism: theory, research and treatment. Washington, DC: American Psychological Association; 2002.
  
• Greenspon T. Freeing our families from perfectionism. Minneapolis: Free Spirit Publishing; 2002.
  
• For more information on interpreting self-report measures of perfectionism, contact Dr. Paul Hewitt, [email protected]; 604-822-5827.
  

• Amitriptyline • Elavil, Endep
  
• Imipramine • Tofranil
  

The authors thank Jonathan Blasberg for his help with this paper and the Social Sciences and Humanities Research Council of Canada for supporting this work.

Mr. C is a 50-year-old professional writer who recently made a serious suicide attempt. At his initial session, Mr. C was hesitant to discuss his situation and reason for attending. He did, however, bring a copy of his résumé so the therapist could “get to know him quickly.”

He said he had been depressed for a long time, especially since he found an error in one of his published works. His confidence and writing abilities seemed to decline after this discovery, his career took a downturn, and ultimately he was fired from his position. He described often being at odds with his supervisors at work, whom he saw as critical and condescending. He was mortified by his job loss and did not inform his wife or friends of his firing.

Mr. C had always been a bit of a loner, and after losing his job he further distanced himself from others. He began drinking heavily to avoid the pain of “letting everyone down.” His wife, family, and friends were shocked at the suicide attempt and expressed dismay that Mr. C had not confided in anyone.

Mr. C describes himself as being perfectionistic throughout his life and never being quite good enough in any of his pursuits. This leads to self-recriminations and persistent feelings of shame.

Far from being a positive attribute, perfectionism is a neurotic personality style that can result in serious psychopathology, including relationship problems, depression, anorexia nervosa, and suicide. Determining a patient’s perfectionistic traits is essential when evaluating those who seek treatment specifically for this distressing behavior as well as patients in treatment for other issues who may have a perfectionistic personality. Accurately assessing perfectionism can help you predict and forestall noncompliance, assess suicide risk, determine appropriate treatment and identify circumstances under which a patient might be particularly vulnerable to relapse.

This article describes:

• 3 traits of perfectionism
  
• 3 dimensions of perfectionistic self-presentation
  
• perfectionistic cognitions
  
• useful self-report tools for clinical practice
  
• effective treatments.
  

Characteristics of perfectionism

Although perfectionism initially was viewed as self-related cognitions, recent models suggest it incorporates intrapersonal and interpersonal dimensions.¹ A person with perfectionism has a marked need for absolute perfection for the self and/or others in many—if not all—pursuits that is strongly rooted in his or her intrapersonal and interpersonal worlds. Other characteristics of perfectionism include:

• equating self-worth or esteem with performance
  
• self-punishment in failure and a lack of satisfaction in success
  
• maintaining and needing to strive for unrealistic expectations
  
• unrealistic criteria for success and broad criteria for failure.
  

We define perfectionism as a neurotic personality style involving perfectionist traits, self-presentation styles, and cognitions that is a core vulnerability factor for a variety of psychological, physical, achievement, and relationship problems (Table 2).^1,3

3 traits. Three traits of perfectionism reflect the desire for the self or others to be perfect:

• self-oriented perfectionism—a requirement for the self to be perfect
  
• other-oriented perfectionism—a requirement for others to be perfect
  
• socially prescribed perfectionism—a perception that others require perfection of oneself.
  

3 self-presentational dimensions. The interpersonal expression of perfectionism is perfectionistic self-presentation. In our model, the 3 facets of perfectionistic self-presentation are:

• perfectionistic self-promotion—overt displays and statements of one’s supposed “perfection”
  
• nondisplay of imperfections—hiding any imperfections
  
• nondisclosure of imperfections—avoiding disclosure or discussion of any imperfection.³
  

Table 1

How perfectionism differs from conscientiousness

Psychopathologies associated with perfectionism

Traits tied to psychopathology

Each of the 3 traits of perfectionism in our model has been associated with psychopathology in multiple studies.

Self-oriented perfectionism is often involved in Axis I disorders, including unipolar depression. This trait is elevated among adults and children diagnosed with major depressive disorder and may be pernicious in the presence of stressors, particularly achievement-related ones.⁶ In other words, self-oriented perfectionism appears to be a risk factor for unipolar depression.^7,8

It also is elevated in women with anorexia nervosa compared with normal and psychiatric controls.⁹ Individuals with anorexia nervosa appear to have the highest levels of self-oriented perfectionism among clinical groups.

Other-oriented perfectionism is associated with antisocial and narcissistic personality disorders.^10,11 It also is related to interpersonal problems and difficulties with marriage and intimate relationships.¹²

Socially prescribed perfectionism is highly elevated in patients with social phobia¹³ and narcissistic¹¹ or borderline personality disorder.¹⁰ It also is associated with severity of depression, anxiety, and symptoms of hostility.⁷

Perhaps most important, determining a patient’s level of socially prescribed perfectionism can aid in assessing suicide risk. Socially prescribed perfectionism has been shown to be highly relevant in suicide ideation, ratings of suicide risk, and moderate- to high-intent suicide attempts in adults,¹⁴ adolescents, and children.¹⁵ Socially prescribed perfectionism has been found to be a unique predictor of suicide behaviors even after controlling for common predictors such as depression severity and hopelessness.

In addition, perfectionistic self-presentation appears to impair patients’ ability to access and benefit from treatment. Researchers (Hewitt PL, Lee-Baggley D, Sherry SB, et al., unpublished data, 2007) have found that the various dimensions of perfectionistic self-presentation are associated with:

• difficulty in seeking help for psychological problems
  
• increased distress in clinical interviews
  
• fears of psychotherapy and psychotherapists
  
• early termination of treatment.
  

Assessing perfectionistic behavior

A variety of brief self-report measures of perfectionism components—and at least one interview measure—can aid your assessment. These are brief instruments and take only a few minutes to complete. Each self-report measure assesses different aspects of perfectionism, such as traits, self-presentational styles, or cognitions (Table 3). The interview can be used as an alternative to the self-report tools.

Mr. C’s scores on several of these measures appear in Table 4. Interpretive information is available from the authors (see Related Resources). Empirical evidence supports the reliability and validity of these measures in clinical samples of both adults and children/adolescents.

Table 3

Perfectionism self-report assessment tools

Interpreting scores on perfectionism self-reports

Limited data on treatments

Few treatments for perfectionistic behavior have been systematically evaluated. Numerous studies have attempted to assess changes in perfectionism as the result of treatment for a specific Axis I disorder, but few have addressed treatment for perfectionism as a clinical entity.

Overall, it seems reasonable to expect that because perfectionism is a personality style, improvement would require fairly intensive, long-term treatment that explicitly emphasizes reducing dimensions of perfectionism.

Psychodynamic treatments focus on perfectionism’s underlying mechanisms and attempt to alter the patient’s personality structure. Studies suggest that intensive psychotherapy is most appropriate.

One of the first treatment evaluations from a reanalysis of Menninger Clinic data found the greatest improvements in patients receiving intensive psychoanalytically oriented treatment, compared with short-term psychotherapy or other treatments.¹⁶ More recent evaluations suggest that highly perfectionistic individuals can be treated effectively only with intensive, long-term psychodynamically oriented treatment¹⁷ and short-term interpersonal, cognitive, and medication therapies do little to alter perfectionistic behavior.

In our experience [PLH] perfectionistic individuals can improve significantly with long-term intensive treatment. On the other hand, we recently completed a study of the efficacy of a short-term, intensive psychodynamic/interpersonal group approach for treating perfectionism and its sequelae.

In this study,¹⁸ we focused on treating the interpersonal precursors or causes of perfectionism, such as attachment styles; interpersonal needs for respect, caring, acceptance, and belonging; and need to avoid rejection, abandonment, and humiliation. In 70 patients with high levels of perfectionism, this treatment significantly decreased perfectionism, symptoms of depression and anxiety, and interpersonal problems. These symptoms continued to be reduced from baseline 6 months later.

Cognitive-behavioral approaches. Several researchers’ findings suggest that cognitive restructuring, bibliotherapy, role-playing, coping strategies, homework assignments, and relaxation may help reduce the cognitive component of perfectionism.^19,20 Other work indicates that cognitive interventions can reduce perfectionism. One study linked reductions in socially prescribed perfectionism to concomitant reductions in depression.²¹

Cognitive interventions can reduce perfectionistic concerns about mistakes and doubting actions, but other aspects of perfectionism—such as perceived parental unrealistic standards and criticisms—remain elevated and appear more treatment-resistant.²⁴

Collectively, these data suggest that some treated patients may be at risk for relapse because persistent perfectionism contributes to a vulnerability to distress.

Medication. No studies have specifically assessed whether medications might reduce perfectionism. Imipramine did not have a significant effect on perfectionistic attitudes when used in the medication protocol of the National Institute of Mental Health Collaborative Study on Depression.¹⁷ Amitriptyline has alleviated some dysfunctional attitudes in depressed patients but not perfectionism.²⁵

Research is needed to evaluate the efficacy of various treatments. At this early stage, it appears that:

• short-term gains might be achieved by reducing symptoms
  
• long-term, intensive psychodynamic treatment may be required to change the perfectionistic personality and its vulnerability effects.
  

Table 5

Treating perfectionism: Common patient challenges

• Flett GL, Hewitt PL. Perfectionism: theory, research and treatment. Washington, DC: American Psychological Association; 2002.
  
• Greenspon T. Freeing our families from perfectionism. Minneapolis: Free Spirit Publishing; 2002.
  
• For more information on interpreting self-report measures of perfectionism, contact Dr. Paul Hewitt, [email protected]; 604-822-5827.
  

• Amitriptyline • Elavil, Endep
  
• Imipramine • Tofranil
  

The authors thank Jonathan Blasberg for his help with this paper and the Social Sciences and Humanities Research Council of Canada for supporting this work.

Clinicians could become discouraged when confronting methamphetamine-dependent patients’ wide-ranging psychiatric symptoms.

These patients often present with:

• overlapping primary psychiatric syndromes and secondary substance abuse
  
• complex histories fraught with psychological trauma, limited social supports, and court involvement.
  

Treatment can be successful, however, and patients can change their addictive behaviors with a chronic disease management approach that targets the drug’s cognitive sequelae and psychiatric effects. Medications show limited benefit (Box 1),^1-8 but behavioral treatments—including cognitive behavioral therapy (CBT) and motivational incentives—have proven efficacy in treating methamphetamine addiction.

This article discusses how to counteract methamphetamine’s negative cognitive effects and enable patients to engage in psychosocial treatment. Our discussion is informed by an extensive literature search and clinical experience from treating patients in the Midwest—at the geographic heart of the “meth” epidemic.

CASE REPORT: Overwhelmed and suicidal

Ms. D, age 27, presents to the emergency department with anxiety, dysphoria, and a plan to commit suicide by overdose. She feels overwhelmed by her 4-hour-a-day customer service job—a prerequisite for staying at the halfway house where she has lived for 2 months. She has a 13-year history of polysubstance dependence and is under court order to complete chemical dependence treatment or go to jail.

Box 1

Ms. D began using drugs at age 14 and has 3 convictions for driving under the influence of alcohol. An average student, she dropped out of high school but obtained a GED certificate. She first had psychiatric contact at age 16 and has been diagnosed at various times with attention deficit/hyperactivity disorder, bipolar disorder, and anxiety disorder. She also has been violently sexually assaulted while engaging in prostitution to support her drug habit.

Ms. D has been hospitalized multiple times—voluntarily and involuntarily—in dual diagnosis treatment centers. Her 5-year-old son no longer lives with her, and she has limited social supports beyond her parents, who live in a neighboring state.

Table 1

Antidepressant trials for treating methamphetamine dependence

3-step approach

For patients such as Ms. D, clinical evidence supports a 3-step approach to treating methamphetamine dependence:

• step 1: institute acute management and stabilization
  
• step 2: eliminate or decrease methamphetamine use to “move the frontal lobe back to the front”
  
• step 3: identify and target psychiatric and psychosocial comorbidities.
  

• help her eliminate or decrease methamphetamine use to allow neuronal systems to recover
  
• target maladaptive behaviors that hinder sobriety while providing motivational incentives to help her maintain a methamphetamine-free life.
  

How ‘meth’ affects cognition

Methamphetamine use has been associated with cognitive dysfunction at initial abstinence and even years later in some patients.¹⁰ Ms. D’s cognitive limitations in a fast-paced customer service job—even though hours are limited—lead to anxiety, dysphoria, and loss of self-esteem when she can’t manage patrons’ requests.

Methamphetamine has profound acute and chronic effects on the sympathetic nervous system, and dopaminergic, serotonergic, and noradrenergic neuronal networks. Most evidence of chronic neuronal effects comes from animal research and reflects toxic damage to dopaminergic and serotonergic neuronal systems. Postmortem human studies of direct neurotoxicity from chronic methamphetamine exposure show:

• decreased dopamine and tyrosine hydroxylase levels
  
• reduced concentrations of dopamine transporters.¹¹
  

• changes in neurotransmitter, protein, brain metabolism, and transporter levels
  
• damage in multiple brain areas including the frontal region, basal ganglia, grey matter, corpus callosum, and striatum; smaller hippocampi; and cerebral vasculature changes.^14-16
  

CASE CONTINUED: Does she understand?

After Ms. D is stabilized, her case manager expresses concern about her ability to follow through with treatment planning. He says, “I just don’t think she understands some of the things we discuss.” She then is referred for neuropsychological testing, which shows clear cognitive impairment. Specifically, she has a slowed rate of thinking, general cognitive ineficiency, deficits in learning and memory retention, and mild impulsivity.

Patients with a history of extensive methamphetamine abuse are ruled by the limbic system and may have higher cortical damage that complicates initiating, maintaining, and fully participating in treatment. Patients’ deficits in memory, executive functioning, attention, and cognitive speed may require you to simplify, repeat, and otherwise modify your treatment plan. You will need to provide clear instructions and consistent support—individually and psychosocially—and to recognize and reinforce patients’ treatment gains.

Even before using methamphetamine, patients may have had academic problems or learning disabilities that will compromise their ability to participate in treatment. Infection with HIV, syphilis, or hepatitis C can further hamper cognitive function.¹⁸

What treatments are effective?

Medications. Evidence is extremely limited, and no medications are approved to treat methamphetamine-addicted patients. Bupropion has shown some efficacy (Table 1),^2-4,7 but other drugs such as sertraline and topiramate may aggravate rather than diminish methamphetamine dependence (Table 2).^5,6,8,19

Behavioral treatments supply the evidence basis for methamphetamine dependence treatment. Cognitive behavioral therapy (CBT),²⁰ contingency management (CM),^21,22 and a manualized structured treatment—the Matrix Model²³—all have proven efficacy.

CBT involves functional analysis and skills training. Patients are guided through analyzing their drug use and associated cognitions, emotions, and expectations and in identifying situations that trigger methamphetamine use or relapse. Skills training involves identifying, reinforcing, and practicing coping skills to help the patient avoid drug use and reinforce the ability to refuse use.

CM is based on operant conditioning—the use of consequences to modify behavior. It involves establishing a “contingent” relationship between a desired behavior/outcome (such as methamphetamine-free urinalysis) and delivering a positive reinforcing event to promote abstinence:

• Vouchers, privileges, or small amounts of money linked to healthy behaviors serve as incentives for negative urine testing.
  
• Rewards increase as periods of confirmed abstinence lengthen and are reset to smaller rewards if relapse occurs.
  

CM does not require extensive staff training and has been described as relatively simple to implement. CM also has been used successfully in urban gay and bisexual men with methamphetamine dependence (Box 2).^18,25-29

Although CM’s efficacy is well-supported by clinical trials, we have encountered some resistance to the idea of “paying individuals to not use drugs” when training medical students, allied health staff, and residents. The National Institute on Drug Abuse (NIDA) supports the use of motivational incentives in treating substance abuse and offers support materials, resources, and training on this approach (see Related Resources).

Multiple studies show that CBT and CM are equally effective for treating chronic methamphetamine abuse at a 1-year follow-up, although CM may be more effective than CBT for acute treatment.

The Matrix model is a 4-month intensive, manualized treatment program that uses CBT, education on drug effects, positive reinforcement for intended behavioral change, and a 12-step approach.

Methamphetamine dependence outcomes based on the Matrix treatment model were compared with community treatment as usual in a project sponsored by The Center for Substance Abuse Treatment of the Substance Abuse and Mental Health Services Administration, U.S. Department of Health and Human Services.³⁰ End-point outcomes were similar, but the Matrix treatment was more effective in early treatment, including decreased urinalyses positive for methamphetamine and increased abstinence.

Box 2

In patients such as Ms. D, the structure of court-ordered treatment can provide accountability, enforced abstinence, and mandated treatment resources. This, in turn, may give your patient a better chance to engage a recovering and better functioning frontal lobe to inhibit urges for methamphetamine use and manage stress.

Table 2

Other agents studied in methamphetamine dependence trials

CASE CONTINUED: Racing thoughts and psychosis

Before hospital admission, Ms. D was being treated with gabapentin, 300 mg bid, and sustained-release bupropion, 150 mg/d, for anxiety and dysphoria. Previously, she has received multiple antidepressants and mood stabilizers with reportedly little effect.

Initially guarded, she at first denies psychotic symptoms but acknowledges their extent several days later. She describes periods of 6 months or more when she feels “lost.” The treatment team titrates quetiapine up to 200 mg/d and restarts duloxetine, 30 mg/d, for depressive symptoms, based on her past positive response to this antidepressant.

Box 3

Targeting psychiatric symptoms

Step 3 in the chronic disease management approach to methamphetamine dependence is to identify and target psychiatric and psychosocial comorbidities. When approaching psychiatric symptoms, high priorities are to aim for abstinence and manage the patient’s stress (Box 3).^31-33

In clinical practice, we find it difficult to diagnostically categorize and treat methamphetamine-abusing patients who show residual post-acute psychotic symptoms. Some appear to have no risk factors for primary psychotic illness, and their symptoms show an association with the severity of their past methamphetamine abuse.

Other patient presentations can be difficult to separate from family histories of psychotic illness. Research suggests that genetic risk factors may be associated with methamphetamine psychosis in some vulnerable patients.³⁵

Unfortunately, no data exist to guide the use of antipsychotics to maintain symptom control. Some patients may need low-dose antipsychotics for maintenance treatment, and second-generation antipsychotics may have a theoretical advantage over first-generation antipsychotics. Use your clinical judgment in determining dosing and treatment duration, and in weighing risks and benefits of continued treatment.

Using imaging, researchers found aggression severity to be directly correlated with past total methamphetamine use and globally decreased serotonin transporter density.³⁶ Serotonin transporter densities were 30% lower in methamphetamine users vs controls after >1 year of abstinence.

CASE CONTINUED: Discharge plans

Because of the severity of her psychiatric symptoms, Ms. D is unable to return to the halfway house after discharge. As her treatment team works to coordinate discharge placement, Ms. D continues to improve. Her psychotic and dysphoria symptoms resolve, and she shows increased spontaneity. These changes—attributed to supports during hospitalization, decreased stressors, and quetiapine treatment—continue until her discharge to a combined mental illness and chemical dependence program.

Related resources

• Methamphetamine use and sexually transmitted diseases. Centers for Disease Control and Prevention. www.cdc.gov/std/DearColleagueRiskBehaviorMetUse8-18-2006.pdf.
  
• National Institute on Drug Abuse Blending Initiative. Promoting Awareness of Motivational Incentives (PAMI). www.drugabuse.gov/blending/PAMI.html.
  

• Aripiprazole • Abilify
  
• Baclofen • various
  
• Bupropion • Wellbutrin
  
• Duloxetine • Cymbalta
  
• Gabapentin • Neurontin
  
• Modafinil • Provigil
  
• Quetiapine • Seroquel
  
• Sertraline • Zoloft
  
• Topiramate • Topamax
  
• Trazodone • Desyrel
  

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

Clinicians could become discouraged when confronting methamphetamine-dependent patients’ wide-ranging psychiatric symptoms.

These patients often present with:

• overlapping primary psychiatric syndromes and secondary substance abuse
  
• complex histories fraught with psychological trauma, limited social supports, and court involvement.
  

Treatment can be successful, however, and patients can change their addictive behaviors with a chronic disease management approach that targets the drug’s cognitive sequelae and psychiatric effects. Medications show limited benefit (Box 1),^1-8 but behavioral treatments—including cognitive behavioral therapy (CBT) and motivational incentives—have proven efficacy in treating methamphetamine addiction.

This article discusses how to counteract methamphetamine’s negative cognitive effects and enable patients to engage in psychosocial treatment. Our discussion is informed by an extensive literature search and clinical experience from treating patients in the Midwest—at the geographic heart of the “meth” epidemic.

CASE REPORT: Overwhelmed and suicidal

Ms. D, age 27, presents to the emergency department with anxiety, dysphoria, and a plan to commit suicide by overdose. She feels overwhelmed by her 4-hour-a-day customer service job—a prerequisite for staying at the halfway house where she has lived for 2 months. She has a 13-year history of polysubstance dependence and is under court order to complete chemical dependence treatment or go to jail.

Box 1

Ms. D began using drugs at age 14 and has 3 convictions for driving under the influence of alcohol. An average student, she dropped out of high school but obtained a GED certificate. She first had psychiatric contact at age 16 and has been diagnosed at various times with attention deficit/hyperactivity disorder, bipolar disorder, and anxiety disorder. She also has been violently sexually assaulted while engaging in prostitution to support her drug habit.

Ms. D has been hospitalized multiple times—voluntarily and involuntarily—in dual diagnosis treatment centers. Her 5-year-old son no longer lives with her, and she has limited social supports beyond her parents, who live in a neighboring state.

Table 1

Antidepressant trials for treating methamphetamine dependence

3-step approach

For patients such as Ms. D, clinical evidence supports a 3-step approach to treating methamphetamine dependence:

• step 1: institute acute management and stabilization
  
• step 2: eliminate or decrease methamphetamine use to “move the frontal lobe back to the front”
  
• step 3: identify and target psychiatric and psychosocial comorbidities.
  

• help her eliminate or decrease methamphetamine use to allow neuronal systems to recover
  
• target maladaptive behaviors that hinder sobriety while providing motivational incentives to help her maintain a methamphetamine-free life.
  

How ‘meth’ affects cognition

Methamphetamine use has been associated with cognitive dysfunction at initial abstinence and even years later in some patients.¹⁰ Ms. D’s cognitive limitations in a fast-paced customer service job—even though hours are limited—lead to anxiety, dysphoria, and loss of self-esteem when she can’t manage patrons’ requests.

Methamphetamine has profound acute and chronic effects on the sympathetic nervous system, and dopaminergic, serotonergic, and noradrenergic neuronal networks. Most evidence of chronic neuronal effects comes from animal research and reflects toxic damage to dopaminergic and serotonergic neuronal systems. Postmortem human studies of direct neurotoxicity from chronic methamphetamine exposure show:

• decreased dopamine and tyrosine hydroxylase levels
  
• reduced concentrations of dopamine transporters.¹¹
  

• changes in neurotransmitter, protein, brain metabolism, and transporter levels
  
• damage in multiple brain areas including the frontal region, basal ganglia, grey matter, corpus callosum, and striatum; smaller hippocampi; and cerebral vasculature changes.^14-16
  

CASE CONTINUED: Does she understand?

After Ms. D is stabilized, her case manager expresses concern about her ability to follow through with treatment planning. He says, “I just don’t think she understands some of the things we discuss.” She then is referred for neuropsychological testing, which shows clear cognitive impairment. Specifically, she has a slowed rate of thinking, general cognitive ineficiency, deficits in learning and memory retention, and mild impulsivity.

Patients with a history of extensive methamphetamine abuse are ruled by the limbic system and may have higher cortical damage that complicates initiating, maintaining, and fully participating in treatment. Patients’ deficits in memory, executive functioning, attention, and cognitive speed may require you to simplify, repeat, and otherwise modify your treatment plan. You will need to provide clear instructions and consistent support—individually and psychosocially—and to recognize and reinforce patients’ treatment gains.

Even before using methamphetamine, patients may have had academic problems or learning disabilities that will compromise their ability to participate in treatment. Infection with HIV, syphilis, or hepatitis C can further hamper cognitive function.¹⁸

What treatments are effective?

Medications. Evidence is extremely limited, and no medications are approved to treat methamphetamine-addicted patients. Bupropion has shown some efficacy (Table 1),^2-4,7 but other drugs such as sertraline and topiramate may aggravate rather than diminish methamphetamine dependence (Table 2).^5,6,8,19

Behavioral treatments supply the evidence basis for methamphetamine dependence treatment. Cognitive behavioral therapy (CBT),²⁰ contingency management (CM),^21,22 and a manualized structured treatment—the Matrix Model²³—all have proven efficacy.

CBT involves functional analysis and skills training. Patients are guided through analyzing their drug use and associated cognitions, emotions, and expectations and in identifying situations that trigger methamphetamine use or relapse. Skills training involves identifying, reinforcing, and practicing coping skills to help the patient avoid drug use and reinforce the ability to refuse use.

CM is based on operant conditioning—the use of consequences to modify behavior. It involves establishing a “contingent” relationship between a desired behavior/outcome (such as methamphetamine-free urinalysis) and delivering a positive reinforcing event to promote abstinence:

• Vouchers, privileges, or small amounts of money linked to healthy behaviors serve as incentives for negative urine testing.
  
• Rewards increase as periods of confirmed abstinence lengthen and are reset to smaller rewards if relapse occurs.
  

CM does not require extensive staff training and has been described as relatively simple to implement. CM also has been used successfully in urban gay and bisexual men with methamphetamine dependence (Box 2).^18,25-29

Although CM’s efficacy is well-supported by clinical trials, we have encountered some resistance to the idea of “paying individuals to not use drugs” when training medical students, allied health staff, and residents. The National Institute on Drug Abuse (NIDA) supports the use of motivational incentives in treating substance abuse and offers support materials, resources, and training on this approach (see Related Resources).

Multiple studies show that CBT and CM are equally effective for treating chronic methamphetamine abuse at a 1-year follow-up, although CM may be more effective than CBT for acute treatment.

The Matrix model is a 4-month intensive, manualized treatment program that uses CBT, education on drug effects, positive reinforcement for intended behavioral change, and a 12-step approach.

Methamphetamine dependence outcomes based on the Matrix treatment model were compared with community treatment as usual in a project sponsored by The Center for Substance Abuse Treatment of the Substance Abuse and Mental Health Services Administration, U.S. Department of Health and Human Services.³⁰ End-point outcomes were similar, but the Matrix treatment was more effective in early treatment, including decreased urinalyses positive for methamphetamine and increased abstinence.

Box 2

In patients such as Ms. D, the structure of court-ordered treatment can provide accountability, enforced abstinence, and mandated treatment resources. This, in turn, may give your patient a better chance to engage a recovering and better functioning frontal lobe to inhibit urges for methamphetamine use and manage stress.

Table 2

Other agents studied in methamphetamine dependence trials

CASE CONTINUED: Racing thoughts and psychosis

Before hospital admission, Ms. D was being treated with gabapentin, 300 mg bid, and sustained-release bupropion, 150 mg/d, for anxiety and dysphoria. Previously, she has received multiple antidepressants and mood stabilizers with reportedly little effect.

Initially guarded, she at first denies psychotic symptoms but acknowledges their extent several days later. She describes periods of 6 months or more when she feels “lost.” The treatment team titrates quetiapine up to 200 mg/d and restarts duloxetine, 30 mg/d, for depressive symptoms, based on her past positive response to this antidepressant.

Box 3

Targeting psychiatric symptoms

Step 3 in the chronic disease management approach to methamphetamine dependence is to identify and target psychiatric and psychosocial comorbidities. When approaching psychiatric symptoms, high priorities are to aim for abstinence and manage the patient’s stress (Box 3).^31-33

In clinical practice, we find it difficult to diagnostically categorize and treat methamphetamine-abusing patients who show residual post-acute psychotic symptoms. Some appear to have no risk factors for primary psychotic illness, and their symptoms show an association with the severity of their past methamphetamine abuse.

Other patient presentations can be difficult to separate from family histories of psychotic illness. Research suggests that genetic risk factors may be associated with methamphetamine psychosis in some vulnerable patients.³⁵

Unfortunately, no data exist to guide the use of antipsychotics to maintain symptom control. Some patients may need low-dose antipsychotics for maintenance treatment, and second-generation antipsychotics may have a theoretical advantage over first-generation antipsychotics. Use your clinical judgment in determining dosing and treatment duration, and in weighing risks and benefits of continued treatment.

Using imaging, researchers found aggression severity to be directly correlated with past total methamphetamine use and globally decreased serotonin transporter density.³⁶ Serotonin transporter densities were 30% lower in methamphetamine users vs controls after >1 year of abstinence.

CASE CONTINUED: Discharge plans

Because of the severity of her psychiatric symptoms, Ms. D is unable to return to the halfway house after discharge. As her treatment team works to coordinate discharge placement, Ms. D continues to improve. Her psychotic and dysphoria symptoms resolve, and she shows increased spontaneity. These changes—attributed to supports during hospitalization, decreased stressors, and quetiapine treatment—continue until her discharge to a combined mental illness and chemical dependence program.

Related resources

• Methamphetamine use and sexually transmitted diseases. Centers for Disease Control and Prevention. www.cdc.gov/std/DearColleagueRiskBehaviorMetUse8-18-2006.pdf.
  
• National Institute on Drug Abuse Blending Initiative. Promoting Awareness of Motivational Incentives (PAMI). www.drugabuse.gov/blending/PAMI.html.
  

• Aripiprazole • Abilify
  
• Baclofen • various
  
• Bupropion • Wellbutrin
  
• Duloxetine • Cymbalta
  
• Gabapentin • Neurontin
  
• Modafinil • Provigil
  
• Quetiapine • Seroquel
  
• Sertraline • Zoloft
  
• Topiramate • Topamax
  
• Trazodone • Desyrel
  

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

Clinicians could become discouraged when confronting methamphetamine-dependent patients’ wide-ranging psychiatric symptoms.

These patients often present with:

• overlapping primary psychiatric syndromes and secondary substance abuse
  
• complex histories fraught with psychological trauma, limited social supports, and court involvement.
  

Treatment can be successful, however, and patients can change their addictive behaviors with a chronic disease management approach that targets the drug’s cognitive sequelae and psychiatric effects. Medications show limited benefit (Box 1),^1-8 but behavioral treatments—including cognitive behavioral therapy (CBT) and motivational incentives—have proven efficacy in treating methamphetamine addiction.

This article discusses how to counteract methamphetamine’s negative cognitive effects and enable patients to engage in psychosocial treatment. Our discussion is informed by an extensive literature search and clinical experience from treating patients in the Midwest—at the geographic heart of the “meth” epidemic.

CASE REPORT: Overwhelmed and suicidal

Ms. D, age 27, presents to the emergency department with anxiety, dysphoria, and a plan to commit suicide by overdose. She feels overwhelmed by her 4-hour-a-day customer service job—a prerequisite for staying at the halfway house where she has lived for 2 months. She has a 13-year history of polysubstance dependence and is under court order to complete chemical dependence treatment or go to jail.

Box 1

Ms. D began using drugs at age 14 and has 3 convictions for driving under the influence of alcohol. An average student, she dropped out of high school but obtained a GED certificate. She first had psychiatric contact at age 16 and has been diagnosed at various times with attention deficit/hyperactivity disorder, bipolar disorder, and anxiety disorder. She also has been violently sexually assaulted while engaging in prostitution to support her drug habit.

Ms. D has been hospitalized multiple times—voluntarily and involuntarily—in dual diagnosis treatment centers. Her 5-year-old son no longer lives with her, and she has limited social supports beyond her parents, who live in a neighboring state.

Table 1

Antidepressant trials for treating methamphetamine dependence

3-step approach

For patients such as Ms. D, clinical evidence supports a 3-step approach to treating methamphetamine dependence:

• step 1: institute acute management and stabilization
  
• step 2: eliminate or decrease methamphetamine use to “move the frontal lobe back to the front”
  
• step 3: identify and target psychiatric and psychosocial comorbidities.
  

• help her eliminate or decrease methamphetamine use to allow neuronal systems to recover
  
• target maladaptive behaviors that hinder sobriety while providing motivational incentives to help her maintain a methamphetamine-free life.
  

How ‘meth’ affects cognition

Methamphetamine use has been associated with cognitive dysfunction at initial abstinence and even years later in some patients.¹⁰ Ms. D’s cognitive limitations in a fast-paced customer service job—even though hours are limited—lead to anxiety, dysphoria, and loss of self-esteem when she can’t manage patrons’ requests.

Methamphetamine has profound acute and chronic effects on the sympathetic nervous system, and dopaminergic, serotonergic, and noradrenergic neuronal networks. Most evidence of chronic neuronal effects comes from animal research and reflects toxic damage to dopaminergic and serotonergic neuronal systems. Postmortem human studies of direct neurotoxicity from chronic methamphetamine exposure show:

• decreased dopamine and tyrosine hydroxylase levels
  
• reduced concentrations of dopamine transporters.¹¹
  

• changes in neurotransmitter, protein, brain metabolism, and transporter levels
  
• damage in multiple brain areas including the frontal region, basal ganglia, grey matter, corpus callosum, and striatum; smaller hippocampi; and cerebral vasculature changes.^14-16
  

CASE CONTINUED: Does she understand?

After Ms. D is stabilized, her case manager expresses concern about her ability to follow through with treatment planning. He says, “I just don’t think she understands some of the things we discuss.” She then is referred for neuropsychological testing, which shows clear cognitive impairment. Specifically, she has a slowed rate of thinking, general cognitive ineficiency, deficits in learning and memory retention, and mild impulsivity.

Patients with a history of extensive methamphetamine abuse are ruled by the limbic system and may have higher cortical damage that complicates initiating, maintaining, and fully participating in treatment. Patients’ deficits in memory, executive functioning, attention, and cognitive speed may require you to simplify, repeat, and otherwise modify your treatment plan. You will need to provide clear instructions and consistent support—individually and psychosocially—and to recognize and reinforce patients’ treatment gains.

Even before using methamphetamine, patients may have had academic problems or learning disabilities that will compromise their ability to participate in treatment. Infection with HIV, syphilis, or hepatitis C can further hamper cognitive function.¹⁸

What treatments are effective?

Medications. Evidence is extremely limited, and no medications are approved to treat methamphetamine-addicted patients. Bupropion has shown some efficacy (Table 1),^2-4,7 but other drugs such as sertraline and topiramate may aggravate rather than diminish methamphetamine dependence (Table 2).^5,6,8,19

Behavioral treatments supply the evidence basis for methamphetamine dependence treatment. Cognitive behavioral therapy (CBT),²⁰ contingency management (CM),^21,22 and a manualized structured treatment—the Matrix Model²³—all have proven efficacy.

CBT involves functional analysis and skills training. Patients are guided through analyzing their drug use and associated cognitions, emotions, and expectations and in identifying situations that trigger methamphetamine use or relapse. Skills training involves identifying, reinforcing, and practicing coping skills to help the patient avoid drug use and reinforce the ability to refuse use.

CM is based on operant conditioning—the use of consequences to modify behavior. It involves establishing a “contingent” relationship between a desired behavior/outcome (such as methamphetamine-free urinalysis) and delivering a positive reinforcing event to promote abstinence:

• Vouchers, privileges, or small amounts of money linked to healthy behaviors serve as incentives for negative urine testing.
  
• Rewards increase as periods of confirmed abstinence lengthen and are reset to smaller rewards if relapse occurs.
  

CM does not require extensive staff training and has been described as relatively simple to implement. CM also has been used successfully in urban gay and bisexual men with methamphetamine dependence (Box 2).^18,25-29

Although CM’s efficacy is well-supported by clinical trials, we have encountered some resistance to the idea of “paying individuals to not use drugs” when training medical students, allied health staff, and residents. The National Institute on Drug Abuse (NIDA) supports the use of motivational incentives in treating substance abuse and offers support materials, resources, and training on this approach (see Related Resources).

Multiple studies show that CBT and CM are equally effective for treating chronic methamphetamine abuse at a 1-year follow-up, although CM may be more effective than CBT for acute treatment.

The Matrix model is a 4-month intensive, manualized treatment program that uses CBT, education on drug effects, positive reinforcement for intended behavioral change, and a 12-step approach.

Methamphetamine dependence outcomes based on the Matrix treatment model were compared with community treatment as usual in a project sponsored by The Center for Substance Abuse Treatment of the Substance Abuse and Mental Health Services Administration, U.S. Department of Health and Human Services.³⁰ End-point outcomes were similar, but the Matrix treatment was more effective in early treatment, including decreased urinalyses positive for methamphetamine and increased abstinence.