Current Psychiatry

Neurodevelopmental disorders are “life span” clinical syndromes¹ that may contribute to development of axis I and axis II disorders and are associated with high rates of psychiatric comorbidity. Behaviors and symptoms of neurodevelopmental disorders are enduring and difficult to recognize—particularly in their milder and attenuated forms—because patients often “age out” of obvious manifestations. High rates of comorbidity with other DSM-IV-TR disorders also can contribute to substantial underdiagnosis and under-recognition. Failure to accurately identify a residual neurodevelopmental disorder can cause problems establishing and maintaining a working alliance and may lead to poor treatment outcomes.

Clues to help identify patients with residual neurodevelopmental symptoms include:

• repeating grade levels, requiring special education services, and/or failing to graduate high school
• academic and/or career underachievement
• developing uneven sensory, motor, cognitive, and/or academic skills
• chronically distressed “high achiever”
• long-term social ostracism and/or peculiarity.

Classification and typology

Patients within the dyslexic spectrum typically have a history of difficulty reading, spelling, and writing. These problems cannot be explained adequately by socio-cultural factors and/or general limitations in cognition.

Nonverbal learning disability patients have selective deficits in math reasoning and visuospatial processing, motor planning problems, and, at times, weak social interaction skills.

Signs of suspected residual attention-deficit/hyperactivity disorder include a history—usually dating back to elementary school—of poor concentration and weak retention abilities. These patients also have difficulty organizing, planning, and completing activities, particularly those requiring multiple steps and/or sustained mental effort.

Socially ostracized patients with social peculiarity, especially if coupled with ≥1 specific information processing and learning problems, frequently have mild residual difficulties that fall within the pervasive developmental disorder (autistic) spectrum.

Patients with histories of “across-the-board” problems acquiring academic skills and a lack of compensatory success in at least some non-academic pursuits may have generalized intellectual disability. This may be so-called “borderline” intellectual functioning or, in a much smaller number of cases, mild mental retardation/ mild intellectual disability.

Making an accurate diagnosis

To more easily identify patients with a residual developmental disorder, take a more detailed academic/educational history that includes Scholastic Aptitude Test scores, previous “coding” for ≥1 special needs psychoeducational conditions, and/or a childhood/adolescent history of psychometric testing. Also, obtain your patient’s educational/psychoeducational records.

Complete a detailed developmental history that includes exploring subtle anomalies in acquiring language pragmatics, motor coordination/planning, and social interaction skills.

Interview parents, spouses, and friends who are familiar with your patient’s longitudinal neurodevelopmental functioning.

Review recent texts on residual neurodevelopmental disorders.² Consider referring your patient for psychometric testing to firm up diagnostic impressions and assist in treatment planning.

Neurodevelopmental disorders are “life span” clinical syndromes¹ that may contribute to development of axis I and axis II disorders and are associated with high rates of psychiatric comorbidity. Behaviors and symptoms of neurodevelopmental disorders are enduring and difficult to recognize—particularly in their milder and attenuated forms—because patients often “age out” of obvious manifestations. High rates of comorbidity with other DSM-IV-TR disorders also can contribute to substantial underdiagnosis and under-recognition. Failure to accurately identify a residual neurodevelopmental disorder can cause problems establishing and maintaining a working alliance and may lead to poor treatment outcomes.

Clues to help identify patients with residual neurodevelopmental symptoms include:

• repeating grade levels, requiring special education services, and/or failing to graduate high school
• academic and/or career underachievement
• developing uneven sensory, motor, cognitive, and/or academic skills
• chronically distressed “high achiever”
• long-term social ostracism and/or peculiarity.

Classification and typology

Patients within the dyslexic spectrum typically have a history of difficulty reading, spelling, and writing. These problems cannot be explained adequately by socio-cultural factors and/or general limitations in cognition.

Nonverbal learning disability patients have selective deficits in math reasoning and visuospatial processing, motor planning problems, and, at times, weak social interaction skills.

Signs of suspected residual attention-deficit/hyperactivity disorder include a history—usually dating back to elementary school—of poor concentration and weak retention abilities. These patients also have difficulty organizing, planning, and completing activities, particularly those requiring multiple steps and/or sustained mental effort.

Socially ostracized patients with social peculiarity, especially if coupled with ≥1 specific information processing and learning problems, frequently have mild residual difficulties that fall within the pervasive developmental disorder (autistic) spectrum.

Patients with histories of “across-the-board” problems acquiring academic skills and a lack of compensatory success in at least some non-academic pursuits may have generalized intellectual disability. This may be so-called “borderline” intellectual functioning or, in a much smaller number of cases, mild mental retardation/ mild intellectual disability.

Making an accurate diagnosis

To more easily identify patients with a residual developmental disorder, take a more detailed academic/educational history that includes Scholastic Aptitude Test scores, previous “coding” for ≥1 special needs psychoeducational conditions, and/or a childhood/adolescent history of psychometric testing. Also, obtain your patient’s educational/psychoeducational records.

Complete a detailed developmental history that includes exploring subtle anomalies in acquiring language pragmatics, motor coordination/planning, and social interaction skills.

Interview parents, spouses, and friends who are familiar with your patient’s longitudinal neurodevelopmental functioning.

Review recent texts on residual neurodevelopmental disorders.² Consider referring your patient for psychometric testing to firm up diagnostic impressions and assist in treatment planning.

Neurodevelopmental disorders are “life span” clinical syndromes¹ that may contribute to development of axis I and axis II disorders and are associated with high rates of psychiatric comorbidity. Behaviors and symptoms of neurodevelopmental disorders are enduring and difficult to recognize—particularly in their milder and attenuated forms—because patients often “age out” of obvious manifestations. High rates of comorbidity with other DSM-IV-TR disorders also can contribute to substantial underdiagnosis and under-recognition. Failure to accurately identify a residual neurodevelopmental disorder can cause problems establishing and maintaining a working alliance and may lead to poor treatment outcomes.

Clues to help identify patients with residual neurodevelopmental symptoms include:

• repeating grade levels, requiring special education services, and/or failing to graduate high school
• academic and/or career underachievement
• developing uneven sensory, motor, cognitive, and/or academic skills
• chronically distressed “high achiever”
• long-term social ostracism and/or peculiarity.

Classification and typology

Patients within the dyslexic spectrum typically have a history of difficulty reading, spelling, and writing. These problems cannot be explained adequately by socio-cultural factors and/or general limitations in cognition.

Nonverbal learning disability patients have selective deficits in math reasoning and visuospatial processing, motor planning problems, and, at times, weak social interaction skills.

Signs of suspected residual attention-deficit/hyperactivity disorder include a history—usually dating back to elementary school—of poor concentration and weak retention abilities. These patients also have difficulty organizing, planning, and completing activities, particularly those requiring multiple steps and/or sustained mental effort.

Socially ostracized patients with social peculiarity, especially if coupled with ≥1 specific information processing and learning problems, frequently have mild residual difficulties that fall within the pervasive developmental disorder (autistic) spectrum.

Patients with histories of “across-the-board” problems acquiring academic skills and a lack of compensatory success in at least some non-academic pursuits may have generalized intellectual disability. This may be so-called “borderline” intellectual functioning or, in a much smaller number of cases, mild mental retardation/ mild intellectual disability.

Making an accurate diagnosis

To more easily identify patients with a residual developmental disorder, take a more detailed academic/educational history that includes Scholastic Aptitude Test scores, previous “coding” for ≥1 special needs psychoeducational conditions, and/or a childhood/adolescent history of psychometric testing. Also, obtain your patient’s educational/psychoeducational records.

Complete a detailed developmental history that includes exploring subtle anomalies in acquiring language pragmatics, motor coordination/planning, and social interaction skills.

Interview parents, spouses, and friends who are familiar with your patient’s longitudinal neurodevelopmental functioning.

Review recent texts on residual neurodevelopmental disorders.² Consider referring your patient for psychometric testing to firm up diagnostic impressions and assist in treatment planning.

Many psychiatric patients present with substance abuse problems in addition to mood, anxiety, or psychotic disorders. Addiction to cocaine or methamphetamine is widespread and difficult to treat. Also, patients who abuse these substances frequently relapse.¹

Need for treatment. There are no FDA-approved medications for treating cocaine or methamphetamine addiction. Several compounds are being studied, including therapy for addiction–cocaine addiction (TA-CD), a potential cocaine vaccine. The vaccine produces anticocaine antibodies that attach to cocaine molecules in the blood, preventing them from passing the blood-brain barrier. This mechanism blocks cocaine-induced euphoria. Although promising, it is still under investigation and pharmaceutical companies have shown little interest in producing it.²

Initial treatment. Bupropion is a norepinephrine-dopamine reuptake inhibitor with a chemical structure similar to amphetamine. It is FDA-approved for treating major depressive disorder and nicotine addiction;³ however, some clinicians have found it helpful during the initial treatment of cocaine and methamphetamine addiction. If bupropion is initiated while the patient is detoxifying, the drug significantly reduces cravings and also treats depressive symptoms, which are common during withdrawal.⁴ The patient can safely remain on bupropion after discharge if the medication is taken continuously without a lapse in treatment.

Caveat. If a patient presents with depression or another mood disorder, take a careful addiction history before prescribing bupropion. If the patient has a recent history of cocaine addiction, but has been abstinent for ≥1 month, bupropion may not be the drug of choice. Because bupropion has a chemical structure similar to amphetamine, it can be a powerful trigger for relapse. To avoid this problem, take a careful history during the initial psychiatric evaluation. Timing is crucial for effective bupropion use and for maintaining continued abstinence among dual diagnosis patients.

Many psychiatric patients present with substance abuse problems in addition to mood, anxiety, or psychotic disorders. Addiction to cocaine or methamphetamine is widespread and difficult to treat. Also, patients who abuse these substances frequently relapse.¹

Need for treatment. There are no FDA-approved medications for treating cocaine or methamphetamine addiction. Several compounds are being studied, including therapy for addiction–cocaine addiction (TA-CD), a potential cocaine vaccine. The vaccine produces anticocaine antibodies that attach to cocaine molecules in the blood, preventing them from passing the blood-brain barrier. This mechanism blocks cocaine-induced euphoria. Although promising, it is still under investigation and pharmaceutical companies have shown little interest in producing it.²

Initial treatment. Bupropion is a norepinephrine-dopamine reuptake inhibitor with a chemical structure similar to amphetamine. It is FDA-approved for treating major depressive disorder and nicotine addiction;³ however, some clinicians have found it helpful during the initial treatment of cocaine and methamphetamine addiction. If bupropion is initiated while the patient is detoxifying, the drug significantly reduces cravings and also treats depressive symptoms, which are common during withdrawal.⁴ The patient can safely remain on bupropion after discharge if the medication is taken continuously without a lapse in treatment.

Caveat. If a patient presents with depression or another mood disorder, take a careful addiction history before prescribing bupropion. If the patient has a recent history of cocaine addiction, but has been abstinent for ≥1 month, bupropion may not be the drug of choice. Because bupropion has a chemical structure similar to amphetamine, it can be a powerful trigger for relapse. To avoid this problem, take a careful history during the initial psychiatric evaluation. Timing is crucial for effective bupropion use and for maintaining continued abstinence among dual diagnosis patients.

Many psychiatric patients present with substance abuse problems in addition to mood, anxiety, or psychotic disorders. Addiction to cocaine or methamphetamine is widespread and difficult to treat. Also, patients who abuse these substances frequently relapse.¹

Need for treatment. There are no FDA-approved medications for treating cocaine or methamphetamine addiction. Several compounds are being studied, including therapy for addiction–cocaine addiction (TA-CD), a potential cocaine vaccine. The vaccine produces anticocaine antibodies that attach to cocaine molecules in the blood, preventing them from passing the blood-brain barrier. This mechanism blocks cocaine-induced euphoria. Although promising, it is still under investigation and pharmaceutical companies have shown little interest in producing it.²

Initial treatment. Bupropion is a norepinephrine-dopamine reuptake inhibitor with a chemical structure similar to amphetamine. It is FDA-approved for treating major depressive disorder and nicotine addiction;³ however, some clinicians have found it helpful during the initial treatment of cocaine and methamphetamine addiction. If bupropion is initiated while the patient is detoxifying, the drug significantly reduces cravings and also treats depressive symptoms, which are common during withdrawal.⁴ The patient can safely remain on bupropion after discharge if the medication is taken continuously without a lapse in treatment.

Caveat. If a patient presents with depression or another mood disorder, take a careful addiction history before prescribing bupropion. If the patient has a recent history of cocaine addiction, but has been abstinent for ≥1 month, bupropion may not be the drug of choice. Because bupropion has a chemical structure similar to amphetamine, it can be a powerful trigger for relapse. To avoid this problem, take a careful history during the initial psychiatric evaluation. Timing is crucial for effective bupropion use and for maintaining continued abstinence among dual diagnosis patients.

Dr. Lau is chief resident and Dr. Han is residency training director, departments of family and community medicine and psychiatry and behavioral sciences, University of California, Davis, Sacramento, CA.

Low back pain is a common, unrelenting concern for many patients and accounts for a high percentage of health care visits. Although low back pain has a generally favorable prognosis, some patients develop long-term debilitating symptoms that exacerbate or initiate psychiatric conditions. Chronic low back pain has been associated with depression¹ and rising rates of depression may contribute to the increasing prevalence of low back pain.^2,3

The recent Stepped Care for Affective Disorders and Musculoskeletal Pain (SCAMP) trial showed that optimization of antidepressants in conjunction with a self-management behavioral program reduced depressive and pain symptoms.⁴ Understanding current diagnostic and treatment recommendations for physical aspects of low back pain will allow psychiatrists to intervene more effectively in somatic and behavioral aspects of the disease and improve functional outcomes.

This article reviews American College of Physicians guidelines on diagnosing and treating low back pain. Most episodes of acute low back pain are self-limited and do not require medical care, with symptom resolution and functional return occurring within the first month. However, 7.6% adult patients report at least 1 episode of severe acute low back pain over 1 year, and one-third of patients who have suffered an acute back pain episode report persistent, moderately intense symptoms and many suffer functional limitations.

Categorizing pain

Back pain can be grouped into 3 categories:

• non-specific low back pain
• back pain associated with radiculopathy or spinal stenosis
• back pain associated with another specific cause.

Low back pain frequently cannot be attributed to a specific disease or spinal abnormality, and conditions such as cancer, compression fracture, spinal stenosis, herniated disks, spinal infection, and ankylosing spondylitis comprise <10% of diagnosed causes of back pain.⁵ In the absence of “red flag” symptoms that may indicate more serious conditions (Table 1), there is no need to attribute low back pain symptoms to an anatomical source because often there is no associated improvement in outcomes.

Table 1

Back pain symptoms that may indicate a more serious condition

When imaging is warranted

Although patients often request imaging as part of their workup, routine imaging or other diagnostic tests do not improve outcomes in patients with nonspecific back pain. When patients present with “red flag” symptoms or you suspect another underlying condition, imaging is warranted. MRI generally is preferred over CT. In patients with possible malignancy but no signs of spinal cord compression, multiple strategies have been proposed but not validated. First check plain radiography or erythrocyte sedimentation rate, followed by MRI if abnormalities are found. For patients with low back pain and signs of radiculopathy or spinal stenosis, MRI or CT is appropriate only if patients are candidates for surgery or epidural steroid injection, because symptoms tend to improve within 4 weeks with conservative, noninvasive management.

Selecting treatment

Education and counseling are essential when treating low back pain. Provide your patient with evidence-based information about low back pain, including self-care options such as support measures for pain relief (applying ice packs and heating or pads/blankets) and back-focused stretching and exercise programs (see Related Resources). Remaining as active as possible is more effective than prolonged (>1 to 2 days) bed rest in promoting return to function.⁶ Consider recommending self-care educational books such as The back book.⁷ The prognosis of acute low back pain with or without sciatica generally is favorable, and improvement is likely within the first month.⁸

Pharmacotherapy for low back pain is used in conjunction with—not in lieu of—back care education. However, there is a relative lack of long-term efficacy and safety. Acetaminophen or nonsteroidal anti-inflammatory drugs are typical first-line options.⁹ Other medications have moderate, mostly short-term benefits. Opioid analgesics or tramadol should be used occasionally and intermittently. When a patient does not respond to a time-limited opioid trial, reassess the symptoms and consider alternate therapies. Muscle relaxants such as cyclobenzaprine offer short-term relief but are associated with CNS side effects, most commonly drowsiness and dizziness but also fatigue, somnolence, confusion, and irritability. Tricyclic antidepressants are options to relieve chronic low back pain.¹⁰

Multiple nonpharmacologic therapies have small-to-moderate benefits for low back pain (Table 2). In acute low back pain (<4 weeks), spinal manipulation often is useful. Subacute low back pain (4 to 8 weeks) may improve with intensive interdisciplinary rehabilitation, including cognitive-behavioral therapy (CBT), and can increase functional status and reduce work absenteeism. For chronic low back pain, CBT or progressive relaxation, spinal manipulation, acupuncture, and other modalities have mild to moderate effectiveness.

Table 2

Nonpharmacologic modalities for low back pain

Related resources

• Last AR, Hulbert K. Chronic low back pain: evaluation and management. Am Fam Physician. 2009;79(12):1067-1074.
• Exercise for a better back. www.backcare.org.uk/CMS/files/702-exercise-for-a-better-back.pdf. Accessed April 12, 2010.

Drug brand names

• Cyclobenzaprine • Flexeril
• Tramadol • Ultram, Ultram ER

Disclosure

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

Dr. Lau is chief resident and Dr. Han is residency training director, departments of family and community medicine and psychiatry and behavioral sciences, University of California, Davis, Sacramento, CA.

Low back pain is a common, unrelenting concern for many patients and accounts for a high percentage of health care visits. Although low back pain has a generally favorable prognosis, some patients develop long-term debilitating symptoms that exacerbate or initiate psychiatric conditions. Chronic low back pain has been associated with depression¹ and rising rates of depression may contribute to the increasing prevalence of low back pain.^2,3

The recent Stepped Care for Affective Disorders and Musculoskeletal Pain (SCAMP) trial showed that optimization of antidepressants in conjunction with a self-management behavioral program reduced depressive and pain symptoms.⁴ Understanding current diagnostic and treatment recommendations for physical aspects of low back pain will allow psychiatrists to intervene more effectively in somatic and behavioral aspects of the disease and improve functional outcomes.

This article reviews American College of Physicians guidelines on diagnosing and treating low back pain. Most episodes of acute low back pain are self-limited and do not require medical care, with symptom resolution and functional return occurring within the first month. However, 7.6% adult patients report at least 1 episode of severe acute low back pain over 1 year, and one-third of patients who have suffered an acute back pain episode report persistent, moderately intense symptoms and many suffer functional limitations.

Categorizing pain

Back pain can be grouped into 3 categories:

• non-specific low back pain
• back pain associated with radiculopathy or spinal stenosis
• back pain associated with another specific cause.

Low back pain frequently cannot be attributed to a specific disease or spinal abnormality, and conditions such as cancer, compression fracture, spinal stenosis, herniated disks, spinal infection, and ankylosing spondylitis comprise <10% of diagnosed causes of back pain.⁵ In the absence of “red flag” symptoms that may indicate more serious conditions (Table 1), there is no need to attribute low back pain symptoms to an anatomical source because often there is no associated improvement in outcomes.

Table 1

Back pain symptoms that may indicate a more serious condition

When imaging is warranted

Although patients often request imaging as part of their workup, routine imaging or other diagnostic tests do not improve outcomes in patients with nonspecific back pain. When patients present with “red flag” symptoms or you suspect another underlying condition, imaging is warranted. MRI generally is preferred over CT. In patients with possible malignancy but no signs of spinal cord compression, multiple strategies have been proposed but not validated. First check plain radiography or erythrocyte sedimentation rate, followed by MRI if abnormalities are found. For patients with low back pain and signs of radiculopathy or spinal stenosis, MRI or CT is appropriate only if patients are candidates for surgery or epidural steroid injection, because symptoms tend to improve within 4 weeks with conservative, noninvasive management.

Selecting treatment

Education and counseling are essential when treating low back pain. Provide your patient with evidence-based information about low back pain, including self-care options such as support measures for pain relief (applying ice packs and heating or pads/blankets) and back-focused stretching and exercise programs (see Related Resources). Remaining as active as possible is more effective than prolonged (>1 to 2 days) bed rest in promoting return to function.⁶ Consider recommending self-care educational books such as The back book.⁷ The prognosis of acute low back pain with or without sciatica generally is favorable, and improvement is likely within the first month.⁸

Pharmacotherapy for low back pain is used in conjunction with—not in lieu of—back care education. However, there is a relative lack of long-term efficacy and safety. Acetaminophen or nonsteroidal anti-inflammatory drugs are typical first-line options.⁹ Other medications have moderate, mostly short-term benefits. Opioid analgesics or tramadol should be used occasionally and intermittently. When a patient does not respond to a time-limited opioid trial, reassess the symptoms and consider alternate therapies. Muscle relaxants such as cyclobenzaprine offer short-term relief but are associated with CNS side effects, most commonly drowsiness and dizziness but also fatigue, somnolence, confusion, and irritability. Tricyclic antidepressants are options to relieve chronic low back pain.¹⁰

Multiple nonpharmacologic therapies have small-to-moderate benefits for low back pain (Table 2). In acute low back pain (<4 weeks), spinal manipulation often is useful. Subacute low back pain (4 to 8 weeks) may improve with intensive interdisciplinary rehabilitation, including cognitive-behavioral therapy (CBT), and can increase functional status and reduce work absenteeism. For chronic low back pain, CBT or progressive relaxation, spinal manipulation, acupuncture, and other modalities have mild to moderate effectiveness.

Table 2

Nonpharmacologic modalities for low back pain

Related resources

• Last AR, Hulbert K. Chronic low back pain: evaluation and management. Am Fam Physician. 2009;79(12):1067-1074.
• Exercise for a better back. www.backcare.org.uk/CMS/files/702-exercise-for-a-better-back.pdf. Accessed April 12, 2010.

Drug brand names

• Cyclobenzaprine • Flexeril
• Tramadol • Ultram, Ultram ER

Disclosure

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

Dr. Lau is chief resident and Dr. Han is residency training director, departments of family and community medicine and psychiatry and behavioral sciences, University of California, Davis, Sacramento, CA.

Low back pain is a common, unrelenting concern for many patients and accounts for a high percentage of health care visits. Although low back pain has a generally favorable prognosis, some patients develop long-term debilitating symptoms that exacerbate or initiate psychiatric conditions. Chronic low back pain has been associated with depression¹ and rising rates of depression may contribute to the increasing prevalence of low back pain.^2,3

The recent Stepped Care for Affective Disorders and Musculoskeletal Pain (SCAMP) trial showed that optimization of antidepressants in conjunction with a self-management behavioral program reduced depressive and pain symptoms.⁴ Understanding current diagnostic and treatment recommendations for physical aspects of low back pain will allow psychiatrists to intervene more effectively in somatic and behavioral aspects of the disease and improve functional outcomes.

This article reviews American College of Physicians guidelines on diagnosing and treating low back pain. Most episodes of acute low back pain are self-limited and do not require medical care, with symptom resolution and functional return occurring within the first month. However, 7.6% adult patients report at least 1 episode of severe acute low back pain over 1 year, and one-third of patients who have suffered an acute back pain episode report persistent, moderately intense symptoms and many suffer functional limitations.

Categorizing pain

Back pain can be grouped into 3 categories:

• non-specific low back pain
• back pain associated with radiculopathy or spinal stenosis
• back pain associated with another specific cause.

Low back pain frequently cannot be attributed to a specific disease or spinal abnormality, and conditions such as cancer, compression fracture, spinal stenosis, herniated disks, spinal infection, and ankylosing spondylitis comprise <10% of diagnosed causes of back pain.⁵ In the absence of “red flag” symptoms that may indicate more serious conditions (Table 1), there is no need to attribute low back pain symptoms to an anatomical source because often there is no associated improvement in outcomes.

Table 1

Back pain symptoms that may indicate a more serious condition

When imaging is warranted

Although patients often request imaging as part of their workup, routine imaging or other diagnostic tests do not improve outcomes in patients with nonspecific back pain. When patients present with “red flag” symptoms or you suspect another underlying condition, imaging is warranted. MRI generally is preferred over CT. In patients with possible malignancy but no signs of spinal cord compression, multiple strategies have been proposed but not validated. First check plain radiography or erythrocyte sedimentation rate, followed by MRI if abnormalities are found. For patients with low back pain and signs of radiculopathy or spinal stenosis, MRI or CT is appropriate only if patients are candidates for surgery or epidural steroid injection, because symptoms tend to improve within 4 weeks with conservative, noninvasive management.

Selecting treatment

Education and counseling are essential when treating low back pain. Provide your patient with evidence-based information about low back pain, including self-care options such as support measures for pain relief (applying ice packs and heating or pads/blankets) and back-focused stretching and exercise programs (see Related Resources). Remaining as active as possible is more effective than prolonged (>1 to 2 days) bed rest in promoting return to function.⁶ Consider recommending self-care educational books such as The back book.⁷ The prognosis of acute low back pain with or without sciatica generally is favorable, and improvement is likely within the first month.⁸

Pharmacotherapy for low back pain is used in conjunction with—not in lieu of—back care education. However, there is a relative lack of long-term efficacy and safety. Acetaminophen or nonsteroidal anti-inflammatory drugs are typical first-line options.⁹ Other medications have moderate, mostly short-term benefits. Opioid analgesics or tramadol should be used occasionally and intermittently. When a patient does not respond to a time-limited opioid trial, reassess the symptoms and consider alternate therapies. Muscle relaxants such as cyclobenzaprine offer short-term relief but are associated with CNS side effects, most commonly drowsiness and dizziness but also fatigue, somnolence, confusion, and irritability. Tricyclic antidepressants are options to relieve chronic low back pain.¹⁰

Multiple nonpharmacologic therapies have small-to-moderate benefits for low back pain (Table 2). In acute low back pain (<4 weeks), spinal manipulation often is useful. Subacute low back pain (4 to 8 weeks) may improve with intensive interdisciplinary rehabilitation, including cognitive-behavioral therapy (CBT), and can increase functional status and reduce work absenteeism. For chronic low back pain, CBT or progressive relaxation, spinal manipulation, acupuncture, and other modalities have mild to moderate effectiveness.

Table 2

Nonpharmacologic modalities for low back pain

Related resources

• Last AR, Hulbert K. Chronic low back pain: evaluation and management. Am Fam Physician. 2009;79(12):1067-1074.
• Exercise for a better back. www.backcare.org.uk/CMS/files/702-exercise-for-a-better-back.pdf. Accessed April 12, 2010.

Drug brand names

• Cyclobenzaprine • Flexeril
• Tramadol • Ultram, Ultram ER

Disclosure

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

Few things capture the imagination like the future. I recall how after reading Alvin Toffler’s seminal book Future Shock in college, I was fascinated by how the future could change us as people and as a culture.

During medical school and psychiatric residency, the breathless pace of scientific discoveries—especially in neuroscience—prompted me to dream about the potentially stunning medical breakthroughs of the future. My frustrations about severe, disabling psychiatric brain disorders were tempered by hope that tomorrow will unfold new knowledge that will unravel the dark mysteries of psychotic delusions, obsessive-compulsive disorder (OCD) rituals, intractable narcissism, suicidal urges, and homicidal impulses. The future, I frequently mused, will provide all answers for definitive diagnoses, effective treatments, prevention, and cures for all psychiatric disorders.

Hope for restoring wellness for our suffering patients continues to sustain me and my fellow psychiatrists. The ongoing gush of neuroscience advances that elucidate the divine details of brain and mind continue to inspire us. However, we are getting impatient with the slow translation of groundbreaking basic science discoveries into new and dramatic clinical applications for our long-suffering patients. A collective mantra is building up: We want our future and we want it now!

Evolving advances are lurking in our future, some of which already are palpable and we hope may soon become clinical realities.

Diagnostic lab tests. Biomarkers for psychiatric disorders will, in the near future, help our specialty transcend the DSM’s syndromal approach and help us more decisively clinch diagnoses and proceed to specific treatment. The biggest challenge remains the etiologic heterogeneity of psychiatric disorders, which can undermine the reliability of a single test. I predict that a combination of tests will have to be used to confirm a given clinical diagnosis.

Pharmacogenetics. Momentous advances have been made in identifying cytochrome enzyme mutations that render individuals poor metabolizers or extensive metabolizers; yet few clinicians have access to a laboratory to provide them with their patients’ cytochrome activity profile so they can select the right dose to maximize response and minimize side effects. Furthermore, research is proceeding to identify genes and single nucleotide polymorphisms that predict response to a given antipsychotic, antidepressant, or mood stabilizer. Similarly, pharmacogenetic research is pursuing methods of predicting patients’ potential to develop a specific adverse event but these methods are not yet accessible in clinical settings and the cost remains prohibitive.

Brave new formulations. Despite evidence of high rates of nonadherence with oral medications among schizophrenia patients, long-acting antipsychotics that ensure adherence are used infrequently. Patches and sublingual tablets are now available. The future may bring additional formulations with advantages such as immediate onset of action (eg, intravenous antidepressants or mood stabilizers) or more localized CNS activity (eg, intrathecal antipsychotic drug administration) to avoid organ-system complications. Inhalable formulations may be around the corner and could offer quicker onset of efficacy.

Neuroimaging-guided psychotherapy. Functional magnetic resonance imaging (fMRI), which shows what brain region is activated, some day will enable psychotherapists to visualize their patients’ brain activity in real time as they evoke memories, elicit insight, or trigger anger or sadness. The emotional and cognitive circuitry will provide a road map of patients’ mental archaeology and may help document psychotherapeutic response and recovery.

Brain repair. Evidence indicates that ailing brains can be structurally repaired. Brain disorders such as schizophrenia, bipolar disorder, unipolar depression, and OCD show gray and white matter deterioration, and acute episodes often are associated with detrimental neuroplastic changes. Advances in neuroprotection, neurogenesis, neurotrophic factors, and antiapoptotic cascades will give psychiatrists a toolbox to regenerate, reconnect, and resculpt brain regions in their patients by using specific pharmacologic agents and evidence-based psychotherapy.

Deep brain stimulation (DBS). Of all neurostimulation techniques, DBS may have the most promising psychiatric applications. Studies suggest applications for refractory depression, OCD, or psychosis. The future will bring insights into how DBS can used to bring back to life a dormant corner of the brain or turn off a rogue neural circuit. DBS is a standard treatment for Parkinson’s disease and may become so for psychiatric conditions.

The future can fulfill our dreams and aspirations for curing or preventing psychiatric illness. But let us not forget that only intensive research can accelerate our future. Everything we know today was a research project a few years ago and the research of today is the treatment of tomorrow. Thus, recruiting more psychiatrists into research careers is a key and indispensable ingredient for a brighter future for us and our patients.

Few things capture the imagination like the future. I recall how after reading Alvin Toffler’s seminal book Future Shock in college, I was fascinated by how the future could change us as people and as a culture.

During medical school and psychiatric residency, the breathless pace of scientific discoveries—especially in neuroscience—prompted me to dream about the potentially stunning medical breakthroughs of the future. My frustrations about severe, disabling psychiatric brain disorders were tempered by hope that tomorrow will unfold new knowledge that will unravel the dark mysteries of psychotic delusions, obsessive-compulsive disorder (OCD) rituals, intractable narcissism, suicidal urges, and homicidal impulses. The future, I frequently mused, will provide all answers for definitive diagnoses, effective treatments, prevention, and cures for all psychiatric disorders.

Hope for restoring wellness for our suffering patients continues to sustain me and my fellow psychiatrists. The ongoing gush of neuroscience advances that elucidate the divine details of brain and mind continue to inspire us. However, we are getting impatient with the slow translation of groundbreaking basic science discoveries into new and dramatic clinical applications for our long-suffering patients. A collective mantra is building up: We want our future and we want it now!

Evolving advances are lurking in our future, some of which already are palpable and we hope may soon become clinical realities.

Diagnostic lab tests. Biomarkers for psychiatric disorders will, in the near future, help our specialty transcend the DSM’s syndromal approach and help us more decisively clinch diagnoses and proceed to specific treatment. The biggest challenge remains the etiologic heterogeneity of psychiatric disorders, which can undermine the reliability of a single test. I predict that a combination of tests will have to be used to confirm a given clinical diagnosis.

Pharmacogenetics. Momentous advances have been made in identifying cytochrome enzyme mutations that render individuals poor metabolizers or extensive metabolizers; yet few clinicians have access to a laboratory to provide them with their patients’ cytochrome activity profile so they can select the right dose to maximize response and minimize side effects. Furthermore, research is proceeding to identify genes and single nucleotide polymorphisms that predict response to a given antipsychotic, antidepressant, or mood stabilizer. Similarly, pharmacogenetic research is pursuing methods of predicting patients’ potential to develop a specific adverse event but these methods are not yet accessible in clinical settings and the cost remains prohibitive.

Brave new formulations. Despite evidence of high rates of nonadherence with oral medications among schizophrenia patients, long-acting antipsychotics that ensure adherence are used infrequently. Patches and sublingual tablets are now available. The future may bring additional formulations with advantages such as immediate onset of action (eg, intravenous antidepressants or mood stabilizers) or more localized CNS activity (eg, intrathecal antipsychotic drug administration) to avoid organ-system complications. Inhalable formulations may be around the corner and could offer quicker onset of efficacy.

Neuroimaging-guided psychotherapy. Functional magnetic resonance imaging (fMRI), which shows what brain region is activated, some day will enable psychotherapists to visualize their patients’ brain activity in real time as they evoke memories, elicit insight, or trigger anger or sadness. The emotional and cognitive circuitry will provide a road map of patients’ mental archaeology and may help document psychotherapeutic response and recovery.

Brain repair. Evidence indicates that ailing brains can be structurally repaired. Brain disorders such as schizophrenia, bipolar disorder, unipolar depression, and OCD show gray and white matter deterioration, and acute episodes often are associated with detrimental neuroplastic changes. Advances in neuroprotection, neurogenesis, neurotrophic factors, and antiapoptotic cascades will give psychiatrists a toolbox to regenerate, reconnect, and resculpt brain regions in their patients by using specific pharmacologic agents and evidence-based psychotherapy.

Deep brain stimulation (DBS). Of all neurostimulation techniques, DBS may have the most promising psychiatric applications. Studies suggest applications for refractory depression, OCD, or psychosis. The future will bring insights into how DBS can used to bring back to life a dormant corner of the brain or turn off a rogue neural circuit. DBS is a standard treatment for Parkinson’s disease and may become so for psychiatric conditions.

The future can fulfill our dreams and aspirations for curing or preventing psychiatric illness. But let us not forget that only intensive research can accelerate our future. Everything we know today was a research project a few years ago and the research of today is the treatment of tomorrow. Thus, recruiting more psychiatrists into research careers is a key and indispensable ingredient for a brighter future for us and our patients.

Few things capture the imagination like the future. I recall how after reading Alvin Toffler’s seminal book Future Shock in college, I was fascinated by how the future could change us as people and as a culture.

During medical school and psychiatric residency, the breathless pace of scientific discoveries—especially in neuroscience—prompted me to dream about the potentially stunning medical breakthroughs of the future. My frustrations about severe, disabling psychiatric brain disorders were tempered by hope that tomorrow will unfold new knowledge that will unravel the dark mysteries of psychotic delusions, obsessive-compulsive disorder (OCD) rituals, intractable narcissism, suicidal urges, and homicidal impulses. The future, I frequently mused, will provide all answers for definitive diagnoses, effective treatments, prevention, and cures for all psychiatric disorders.

Hope for restoring wellness for our suffering patients continues to sustain me and my fellow psychiatrists. The ongoing gush of neuroscience advances that elucidate the divine details of brain and mind continue to inspire us. However, we are getting impatient with the slow translation of groundbreaking basic science discoveries into new and dramatic clinical applications for our long-suffering patients. A collective mantra is building up: We want our future and we want it now!

Evolving advances are lurking in our future, some of which already are palpable and we hope may soon become clinical realities.

Diagnostic lab tests. Biomarkers for psychiatric disorders will, in the near future, help our specialty transcend the DSM’s syndromal approach and help us more decisively clinch diagnoses and proceed to specific treatment. The biggest challenge remains the etiologic heterogeneity of psychiatric disorders, which can undermine the reliability of a single test. I predict that a combination of tests will have to be used to confirm a given clinical diagnosis.

Pharmacogenetics. Momentous advances have been made in identifying cytochrome enzyme mutations that render individuals poor metabolizers or extensive metabolizers; yet few clinicians have access to a laboratory to provide them with their patients’ cytochrome activity profile so they can select the right dose to maximize response and minimize side effects. Furthermore, research is proceeding to identify genes and single nucleotide polymorphisms that predict response to a given antipsychotic, antidepressant, or mood stabilizer. Similarly, pharmacogenetic research is pursuing methods of predicting patients’ potential to develop a specific adverse event but these methods are not yet accessible in clinical settings and the cost remains prohibitive.

Brave new formulations. Despite evidence of high rates of nonadherence with oral medications among schizophrenia patients, long-acting antipsychotics that ensure adherence are used infrequently. Patches and sublingual tablets are now available. The future may bring additional formulations with advantages such as immediate onset of action (eg, intravenous antidepressants or mood stabilizers) or more localized CNS activity (eg, intrathecal antipsychotic drug administration) to avoid organ-system complications. Inhalable formulations may be around the corner and could offer quicker onset of efficacy.

Neuroimaging-guided psychotherapy. Functional magnetic resonance imaging (fMRI), which shows what brain region is activated, some day will enable psychotherapists to visualize their patients’ brain activity in real time as they evoke memories, elicit insight, or trigger anger or sadness. The emotional and cognitive circuitry will provide a road map of patients’ mental archaeology and may help document psychotherapeutic response and recovery.

Brain repair. Evidence indicates that ailing brains can be structurally repaired. Brain disorders such as schizophrenia, bipolar disorder, unipolar depression, and OCD show gray and white matter deterioration, and acute episodes often are associated with detrimental neuroplastic changes. Advances in neuroprotection, neurogenesis, neurotrophic factors, and antiapoptotic cascades will give psychiatrists a toolbox to regenerate, reconnect, and resculpt brain regions in their patients by using specific pharmacologic agents and evidence-based psychotherapy.

Deep brain stimulation (DBS). Of all neurostimulation techniques, DBS may have the most promising psychiatric applications. Studies suggest applications for refractory depression, OCD, or psychosis. The future will bring insights into how DBS can used to bring back to life a dormant corner of the brain or turn off a rogue neural circuit. DBS is a standard treatment for Parkinson’s disease and may become so for psychiatric conditions.

The future can fulfill our dreams and aspirations for curing or preventing psychiatric illness. But let us not forget that only intensive research can accelerate our future. Everything we know today was a research project a few years ago and the research of today is the treatment of tomorrow. Thus, recruiting more psychiatrists into research careers is a key and indispensable ingredient for a brighter future for us and our patients.

It is interesting to look at other agents that aide in treating alcohol withdrawal (AW) (“Alcohol withdrawal: When to choose an adjunctive anticonvulsant,” Current Psychiatry, April 2010). However, it would be more important to stress using chlordiazepoxide instead of lorazepam as long as there are no contraindications, because there is conclusive evidence that patients receiving chlordiazepoxide are hospitalized for fewer days. Presumably, there should be less morbidity and a smoother withdrawal likely related to chlordiazepoxide’s longer half-life. What do the authors think about using chlordiazepoxide more often and what cutoff for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) would they suggest for not using chlordiazepoxide?

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

Chlordiazepoxide and diazepam are time-honored choices for AW. Advantages include long half-lives, which allow for uniform blood levels across the day and reduce risk of withdrawal symptoms, including seizures, that may arise when blood levels drop. At the same time, this long half-life combined with the presence of active metabolites, dependence on Phase I metabolism, and higher lipophilicity could result in increased drug accumulation and redistribution into lipid storage reservoirs, which could complicate the clinical picture. Alternatively, lorazepam, an intermediate-acting benzodiazepine that depends primarily on Phase 2 metabolism, is less affected by liver disease. Additional advantages of lorazepam are its lower lipophilicity compared with chlordiazepoxide and diazepam, and no active metabolites. For these pharmacokinetic benefits, in a group where liver dysfunction is presumed, lorazepam has grown in favor.²

Although there is a dearth of head-to-head efficacy comparisons between lorazepam and chlordiazepoxide/diazepam, a study of chlordiazepoxide and lorazepam in AW supported that during detoxification the longer-acting diazepam produced no withdrawal seizures; the lorazepam group had patients who developed seizures. However, when the initial lorazepam dosage was increased in a later study, patients’ withdrawal was seizure-free. Efficacy was otherwise equal among treatment groups.¹

The evidence seems to lead to an overall generalization that when dosed correctly, shorter- and longer-acting benzodiazepines (ie, lorazepam and chlordiazepoxide, respectively) are effective and safe, with the caveat that older patients and those with liver dysfunction should be treated with lorazepam.³ However, is there a reliable and quick assessment of liver dysfunction in patients with alcohol use disorders?

Although the Child-Pugh classification score can be used, it typically is used to assess prognosis of chronic liver disease.⁴ Using traditional serum biomarkers to predict hepatic dysfunction offers advantages and disadvantages. I offer the following guidelines: gamma-glutamyl transpeptidase (GGTP) ≥177 U/L, AST ≥63 U/L, and ALT ≥67 U/L, statistically separates (P < .001) heavy drinkers from moderate drinkers and abstainers; the former group is at greatest risk for alcoholic liver disease.⁵ The majority of long-term heavy drinkers develop fatty liver disease, but only 10% to 35% develop hepatitis and 8% to 20% progress to cirrhosis.⁶ Additionally, other limitations with using a priori serum biomarkers’ range include the role of genetics, gender, race, and medical comorbidities⁷ (ie, other causes of acute hepatitis, cholestasis, and liver congestion) in the development of alcoholic liver disease and their effect on these biomarkers.⁶

David R. Spiegel, MD
Associate professor of clinical psychiatry and behavioral sciences

Daiana Radac, MD
Resident

Eastern Virginia Medical School
Norfolk, VA

It is interesting to look at other agents that aide in treating alcohol withdrawal (AW) (“Alcohol withdrawal: When to choose an adjunctive anticonvulsant,” Current Psychiatry, April 2010). However, it would be more important to stress using chlordiazepoxide instead of lorazepam as long as there are no contraindications, because there is conclusive evidence that patients receiving chlordiazepoxide are hospitalized for fewer days. Presumably, there should be less morbidity and a smoother withdrawal likely related to chlordiazepoxide’s longer half-life. What do the authors think about using chlordiazepoxide more often and what cutoff for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) would they suggest for not using chlordiazepoxide?

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

Chlordiazepoxide and diazepam are time-honored choices for AW. Advantages include long half-lives, which allow for uniform blood levels across the day and reduce risk of withdrawal symptoms, including seizures, that may arise when blood levels drop. At the same time, this long half-life combined with the presence of active metabolites, dependence on Phase I metabolism, and higher lipophilicity could result in increased drug accumulation and redistribution into lipid storage reservoirs, which could complicate the clinical picture. Alternatively, lorazepam, an intermediate-acting benzodiazepine that depends primarily on Phase 2 metabolism, is less affected by liver disease. Additional advantages of lorazepam are its lower lipophilicity compared with chlordiazepoxide and diazepam, and no active metabolites. For these pharmacokinetic benefits, in a group where liver dysfunction is presumed, lorazepam has grown in favor.²

Although there is a dearth of head-to-head efficacy comparisons between lorazepam and chlordiazepoxide/diazepam, a study of chlordiazepoxide and lorazepam in AW supported that during detoxification the longer-acting diazepam produced no withdrawal seizures; the lorazepam group had patients who developed seizures. However, when the initial lorazepam dosage was increased in a later study, patients’ withdrawal was seizure-free. Efficacy was otherwise equal among treatment groups.¹

The evidence seems to lead to an overall generalization that when dosed correctly, shorter- and longer-acting benzodiazepines (ie, lorazepam and chlordiazepoxide, respectively) are effective and safe, with the caveat that older patients and those with liver dysfunction should be treated with lorazepam.³ However, is there a reliable and quick assessment of liver dysfunction in patients with alcohol use disorders?

Although the Child-Pugh classification score can be used, it typically is used to assess prognosis of chronic liver disease.⁴ Using traditional serum biomarkers to predict hepatic dysfunction offers advantages and disadvantages. I offer the following guidelines: gamma-glutamyl transpeptidase (GGTP) ≥177 U/L, AST ≥63 U/L, and ALT ≥67 U/L, statistically separates (P < .001) heavy drinkers from moderate drinkers and abstainers; the former group is at greatest risk for alcoholic liver disease.⁵ The majority of long-term heavy drinkers develop fatty liver disease, but only 10% to 35% develop hepatitis and 8% to 20% progress to cirrhosis.⁶ Additionally, other limitations with using a priori serum biomarkers’ range include the role of genetics, gender, race, and medical comorbidities⁷ (ie, other causes of acute hepatitis, cholestasis, and liver congestion) in the development of alcoholic liver disease and their effect on these biomarkers.⁶

David R. Spiegel, MD
Associate professor of clinical psychiatry and behavioral sciences

Daiana Radac, MD
Resident

Eastern Virginia Medical School
Norfolk, VA

It is interesting to look at other agents that aide in treating alcohol withdrawal (AW) (“Alcohol withdrawal: When to choose an adjunctive anticonvulsant,” Current Psychiatry, April 2010). However, it would be more important to stress using chlordiazepoxide instead of lorazepam as long as there are no contraindications, because there is conclusive evidence that patients receiving chlordiazepoxide are hospitalized for fewer days. Presumably, there should be less morbidity and a smoother withdrawal likely related to chlordiazepoxide’s longer half-life. What do the authors think about using chlordiazepoxide more often and what cutoff for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) would they suggest for not using chlordiazepoxide?

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

Chlordiazepoxide and diazepam are time-honored choices for AW. Advantages include long half-lives, which allow for uniform blood levels across the day and reduce risk of withdrawal symptoms, including seizures, that may arise when blood levels drop. At the same time, this long half-life combined with the presence of active metabolites, dependence on Phase I metabolism, and higher lipophilicity could result in increased drug accumulation and redistribution into lipid storage reservoirs, which could complicate the clinical picture. Alternatively, lorazepam, an intermediate-acting benzodiazepine that depends primarily on Phase 2 metabolism, is less affected by liver disease. Additional advantages of lorazepam are its lower lipophilicity compared with chlordiazepoxide and diazepam, and no active metabolites. For these pharmacokinetic benefits, in a group where liver dysfunction is presumed, lorazepam has grown in favor.²

Although there is a dearth of head-to-head efficacy comparisons between lorazepam and chlordiazepoxide/diazepam, a study of chlordiazepoxide and lorazepam in AW supported that during detoxification the longer-acting diazepam produced no withdrawal seizures; the lorazepam group had patients who developed seizures. However, when the initial lorazepam dosage was increased in a later study, patients’ withdrawal was seizure-free. Efficacy was otherwise equal among treatment groups.¹

The evidence seems to lead to an overall generalization that when dosed correctly, shorter- and longer-acting benzodiazepines (ie, lorazepam and chlordiazepoxide, respectively) are effective and safe, with the caveat that older patients and those with liver dysfunction should be treated with lorazepam.³ However, is there a reliable and quick assessment of liver dysfunction in patients with alcohol use disorders?

Although the Child-Pugh classification score can be used, it typically is used to assess prognosis of chronic liver disease.⁴ Using traditional serum biomarkers to predict hepatic dysfunction offers advantages and disadvantages. I offer the following guidelines: gamma-glutamyl transpeptidase (GGTP) ≥177 U/L, AST ≥63 U/L, and ALT ≥67 U/L, statistically separates (P < .001) heavy drinkers from moderate drinkers and abstainers; the former group is at greatest risk for alcoholic liver disease.⁵ The majority of long-term heavy drinkers develop fatty liver disease, but only 10% to 35% develop hepatitis and 8% to 20% progress to cirrhosis.⁶ Additionally, other limitations with using a priori serum biomarkers’ range include the role of genetics, gender, race, and medical comorbidities⁷ (ie, other causes of acute hepatitis, cholestasis, and liver congestion) in the development of alcoholic liver disease and their effect on these biomarkers.⁶

David R. Spiegel, MD
Associate professor of clinical psychiatry and behavioral sciences

Daiana Radac, MD
Resident

Eastern Virginia Medical School
Norfolk, VA

I commend Dr. Douglas Mossman on his balanced perspective in “Navigating the 15-minute ‘med check’” (Current Psychiatry, June 2010). Dr. Mossman was kind enough to cite my editorial¹ on the “prescriptive bond,” in which I use the term “infamous” to describe the 15-minute med check. Indeed, there are instances when a brief encounter is inadequate to address the multitude of biologic, psychological, and social issues faced by a complex patient. However, I agree with Dr. Mossman that, for some patients, a well-managed 15-minute med check may be appropriate and useful. Much depends on how well the time is structured, as Dr. Mossman’s article nicely describes. Indeed, some psychotic patients or those with extreme social phobic symptoms may not tolerate longer encounters. We must learn to do the best we can with the resources we have, while still advocating for greater access to appropriate mental health care for our patients.

Ronald Pies, MD
Professor of psychiatry
SUNY Upstate Medical University
Clinical professor of psychiatry
Tufts University School of Medicine
Boston, MA

I commend Dr. Douglas Mossman on his balanced perspective in “Navigating the 15-minute ‘med check’” (Current Psychiatry, June 2010). Dr. Mossman was kind enough to cite my editorial¹ on the “prescriptive bond,” in which I use the term “infamous” to describe the 15-minute med check. Indeed, there are instances when a brief encounter is inadequate to address the multitude of biologic, psychological, and social issues faced by a complex patient. However, I agree with Dr. Mossman that, for some patients, a well-managed 15-minute med check may be appropriate and useful. Much depends on how well the time is structured, as Dr. Mossman’s article nicely describes. Indeed, some psychotic patients or those with extreme social phobic symptoms may not tolerate longer encounters. We must learn to do the best we can with the resources we have, while still advocating for greater access to appropriate mental health care for our patients.

Ronald Pies, MD
Professor of psychiatry
SUNY Upstate Medical University
Clinical professor of psychiatry
Tufts University School of Medicine
Boston, MA

I commend Dr. Douglas Mossman on his balanced perspective in “Navigating the 15-minute ‘med check’” (Current Psychiatry, June 2010). Dr. Mossman was kind enough to cite my editorial¹ on the “prescriptive bond,” in which I use the term “infamous” to describe the 15-minute med check. Indeed, there are instances when a brief encounter is inadequate to address the multitude of biologic, psychological, and social issues faced by a complex patient. However, I agree with Dr. Mossman that, for some patients, a well-managed 15-minute med check may be appropriate and useful. Much depends on how well the time is structured, as Dr. Mossman’s article nicely describes. Indeed, some psychotic patients or those with extreme social phobic symptoms may not tolerate longer encounters. We must learn to do the best we can with the resources we have, while still advocating for greater access to appropriate mental health care for our patients.

Ronald Pies, MD
Professor of psychiatry
SUNY Upstate Medical University
Clinical professor of psychiatry
Tufts University School of Medicine
Boston, MA

I treat adults with bipolar II and cyclothymic disorders; I am concerned about the dogmatic view that antidepressants should not be used to treat bipolar spectrum disorders (“Antidepressants in bipolar disorder: 7 myths and realities,” Current Psychiatry, May 2010). As I have been advising my patients, managed care reviewers, and even a few psychiatric editors during the past several years, it is a flawed dogma for reasons identified by the author of this article, Dr. Joseph F. Goldberg. He correctly cites Tohen et al,¹ who showed a 56% response rate for fluoxetine plus olanzapine in treating bipolar depression vs olanzapine alone or placebo. He also cites another study by Amsterdam² on the efficacy of venlafaxine in bipolar II depression.

I would add 2 observations to Dr. Goldberg’s critique. The frequently cited Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study by Sachs et al³ argues antidepressants are not effective for bipolar depression. What many colleagues may not know is that STEP-BD achieved only a 28% positive treatment response. Also, only 6% of subjects were taking atypical antipsychotics, usually high doses—typically olanzapine, >10 mg. These doses of olanzapine—like high doses of other mood stabilizers—may exacerbate fatigue and depressive symptoms. Secondly, the scant research and dogmatism about antidepressants in bipolar treatment has tended to focus on bipolar I disorder, as Dr. Goldberg points out. In addition, it tends to ignore the issue of highly prevalent comorbid anxiety disorders and attention-deficit/hyperactivity disorder in early-onset bipolar spectrum disorders.

William Niederhut, MD
Denver, CO

I treat adults with bipolar II and cyclothymic disorders; I am concerned about the dogmatic view that antidepressants should not be used to treat bipolar spectrum disorders (“Antidepressants in bipolar disorder: 7 myths and realities,” Current Psychiatry, May 2010). As I have been advising my patients, managed care reviewers, and even a few psychiatric editors during the past several years, it is a flawed dogma for reasons identified by the author of this article, Dr. Joseph F. Goldberg. He correctly cites Tohen et al,¹ who showed a 56% response rate for fluoxetine plus olanzapine in treating bipolar depression vs olanzapine alone or placebo. He also cites another study by Amsterdam² on the efficacy of venlafaxine in bipolar II depression.

I would add 2 observations to Dr. Goldberg’s critique. The frequently cited Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study by Sachs et al³ argues antidepressants are not effective for bipolar depression. What many colleagues may not know is that STEP-BD achieved only a 28% positive treatment response. Also, only 6% of subjects were taking atypical antipsychotics, usually high doses—typically olanzapine, >10 mg. These doses of olanzapine—like high doses of other mood stabilizers—may exacerbate fatigue and depressive symptoms. Secondly, the scant research and dogmatism about antidepressants in bipolar treatment has tended to focus on bipolar I disorder, as Dr. Goldberg points out. In addition, it tends to ignore the issue of highly prevalent comorbid anxiety disorders and attention-deficit/hyperactivity disorder in early-onset bipolar spectrum disorders.

William Niederhut, MD
Denver, CO

I treat adults with bipolar II and cyclothymic disorders; I am concerned about the dogmatic view that antidepressants should not be used to treat bipolar spectrum disorders (“Antidepressants in bipolar disorder: 7 myths and realities,” Current Psychiatry, May 2010). As I have been advising my patients, managed care reviewers, and even a few psychiatric editors during the past several years, it is a flawed dogma for reasons identified by the author of this article, Dr. Joseph F. Goldberg. He correctly cites Tohen et al,¹ who showed a 56% response rate for fluoxetine plus olanzapine in treating bipolar depression vs olanzapine alone or placebo. He also cites another study by Amsterdam² on the efficacy of venlafaxine in bipolar II depression.

I would add 2 observations to Dr. Goldberg’s critique. The frequently cited Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study by Sachs et al³ argues antidepressants are not effective for bipolar depression. What many colleagues may not know is that STEP-BD achieved only a 28% positive treatment response. Also, only 6% of subjects were taking atypical antipsychotics, usually high doses—typically olanzapine, >10 mg. These doses of olanzapine—like high doses of other mood stabilizers—may exacerbate fatigue and depressive symptoms. Secondly, the scant research and dogmatism about antidepressants in bipolar treatment has tended to focus on bipolar I disorder, as Dr. Goldberg points out. In addition, it tends to ignore the issue of highly prevalent comorbid anxiety disorders and attention-deficit/hyperactivity disorder in early-onset bipolar spectrum disorders.

William Niederhut, MD
Denver, CO

Propranolol is used to treat thyroid storm specifically because of its action in blocking conversion of prohormone thyroxine (T4) to triiodothyronine (T3) (“Do beta blockers cause depression?” Medicine in Brief, Current Psychiatry, May 2010). Because T3 is the basis of the basal metabolic rate, if T3 were decreased then the only other mechanism for energy is adrenaline. This would cause depression when adrenaline wasn’t in use and anxiety when it was. This sounds like a direct link to depression and anxiety to me. The thyroid function test would show no change in thyroid-stimulating hormone, but an increase in T4 to compensate for the decrease in T3. There are no medical standards to routinely look at T3 and the effect would not be seen anyway. I am not aware of research that explores this connection between beta blockers and depression.

John V. Billings, ARNP
Spokane, WA

Propranolol is used to treat thyroid storm specifically because of its action in blocking conversion of prohormone thyroxine (T4) to triiodothyronine (T3) (“Do beta blockers cause depression?” Medicine in Brief, Current Psychiatry, May 2010). Because T3 is the basis of the basal metabolic rate, if T3 were decreased then the only other mechanism for energy is adrenaline. This would cause depression when adrenaline wasn’t in use and anxiety when it was. This sounds like a direct link to depression and anxiety to me. The thyroid function test would show no change in thyroid-stimulating hormone, but an increase in T4 to compensate for the decrease in T3. There are no medical standards to routinely look at T3 and the effect would not be seen anyway. I am not aware of research that explores this connection between beta blockers and depression.

John V. Billings, ARNP
Spokane, WA

Propranolol is used to treat thyroid storm specifically because of its action in blocking conversion of prohormone thyroxine (T4) to triiodothyronine (T3) (“Do beta blockers cause depression?” Medicine in Brief, Current Psychiatry, May 2010). Because T3 is the basis of the basal metabolic rate, if T3 were decreased then the only other mechanism for energy is adrenaline. This would cause depression when adrenaline wasn’t in use and anxiety when it was. This sounds like a direct link to depression and anxiety to me. The thyroid function test would show no change in thyroid-stimulating hormone, but an increase in T4 to compensate for the decrease in T3. There are no medical standards to routinely look at T3 and the effect would not be seen anyway. I am not aware of research that explores this connection between beta blockers and depression.

John V. Billings, ARNP
Spokane, WA

Dr. Henry A. Nasrallah is on target in his editorial, “Combination therapies are here to stay” (From the Editor, Current Psychiatry, May 2010). Psychosis in the context of dementia is another area of interest. We have been thoroughly steeped in the “black-box” warning about antipsychotic use in dementia. The most common discussion point among psychiatrists in consideration of the managing complex dementia with psychotic disturbances is which medications to use and how to use antipsychotics when there is no other choice. The warning is certainly judicious; however, the fact is that almost every day this clinical situation could arise, placing us in a difficult position of weighing a complex risk vs safety analysis with no viable guidance and no real option other than to make decisions and involve family members in complicated informed consent discussions. Evidence also suggests that functional capacity in dementia may be enhanced by combining donepezil and memantine, which also is of consequence in dementia polypharmacy.

John Hendrick, MD
Assistant professor of psychiatry
East Tennessee State University
Johnson City, TN

Dr. Henry A. Nasrallah is on target in his editorial, “Combination therapies are here to stay” (From the Editor, Current Psychiatry, May 2010). Psychosis in the context of dementia is another area of interest. We have been thoroughly steeped in the “black-box” warning about antipsychotic use in dementia. The most common discussion point among psychiatrists in consideration of the managing complex dementia with psychotic disturbances is which medications to use and how to use antipsychotics when there is no other choice. The warning is certainly judicious; however, the fact is that almost every day this clinical situation could arise, placing us in a difficult position of weighing a complex risk vs safety analysis with no viable guidance and no real option other than to make decisions and involve family members in complicated informed consent discussions. Evidence also suggests that functional capacity in dementia may be enhanced by combining donepezil and memantine, which also is of consequence in dementia polypharmacy.

John Hendrick, MD
Assistant professor of psychiatry
East Tennessee State University
Johnson City, TN

Dr. Henry A. Nasrallah is on target in his editorial, “Combination therapies are here to stay” (From the Editor, Current Psychiatry, May 2010). Psychosis in the context of dementia is another area of interest. We have been thoroughly steeped in the “black-box” warning about antipsychotic use in dementia. The most common discussion point among psychiatrists in consideration of the managing complex dementia with psychotic disturbances is which medications to use and how to use antipsychotics when there is no other choice. The warning is certainly judicious; however, the fact is that almost every day this clinical situation could arise, placing us in a difficult position of weighing a complex risk vs safety analysis with no viable guidance and no real option other than to make decisions and involve family members in complicated informed consent discussions. Evidence also suggests that functional capacity in dementia may be enhanced by combining donepezil and memantine, which also is of consequence in dementia polypharmacy.

John Hendrick, MD
Assistant professor of psychiatry
East Tennessee State University
Johnson City, TN