Steven, age 6, lives in a foster home and attends an intensive day program for treatment of severe aggressive and violent episodes, for which he has been hospitalized several times. The boy has been separated from his biological mother for 2 years, and her parental rights have been terminated because of allegations of neglect and severe abuse.

Steven’s mother has a long history of substance abuse. Her boyfriend, who lived with her, abused Steven physically and sexually. He beat him, tortured him, and burned him. He once inserted a hot curling iron into the boy’s rectum, causing severe burns.

It is not unusual for psychiatrists to encounter children such as Steven who have experienced abuse, trauma, or a life-threatening event, but the psychological aftermath of these experiences has only recently been fully recognized. Diagnostic criteria continue to change with evidence that posttraumatic stress disorder (PTSD) manifests differently in children and adolescents than in adults. Now research is showing changes in brain physiology in children who have experienced maltreatment.

Based on our experience and recent evidence, we discuss important features of PTSD that are being recognized in children and adolescents and describe trends and acceptable practices in treating this chronic, debilitating illness.

Diagnostic criteria

PTSD is reported to occur in 1 to 14% of the general population of children¹ and in 3 to 100% of children at risk (those exposed to violence, trauma, or abuse).^2,3 As diagnostic criteria have changed over the years, so may have prevalence rates.

PTSD was recognized as a diagnostic entity in adults in DSM-III and in children and adolescents in DSM-III-R. PTSD in children has a somewhat different presentation and expression of symptoms than in adults. According to DSM-IV-TR diagnostic criteria:

• A child’s response to a stressful event may be expressed as disorganized or agitated behavior instead of intense fear, helplessness, or horror.
• Children re-experience and express the traumatic event or aspects of it through repetitive play.
• Children’s dreams may be frightening but without recognizable content, or they may change into generalized nightmares of monsters, of rescuing others, or of threats to self or others.
• Children also tend to have more psychosomatic complaints, such as headaches and stomachaches, than adults with PTSD.¹

Box 1

Age-related symptoms. Appropriate diagnostic criteria for childhood PTSD have been debated for some time, in part because of differences in children’s symptoms at different ages and developmental stages. Since DSM-IV was introduced in 1994, several researchers have recommended modifications to its diagnostic characterizations of childhood PTSD.

To accommodate the developmental stage of children younger than age 4, for example, Scheeringa et al suggested changes to DSM-IV criteria for PTSD.^4,5 These changes (Boxes 1-5) are included in the American Academy of Child and Adolescent Psychiatry’s guidelines for assessing and treating PTSD⁶ and may be a valuable tool for the clinician treating young children.

Subsyndromal cases. Children whose symptoms fall below the diagnostic criteria for PTSD may demonstrate substantial functional impairment and distress, according to Carrion et al.⁷ In fact, these researchers found that children who fulfill the requirements for two of three symptom clusters—Cluster B, re-experiencing (Box 2); Cluster C, avoidance and numbing (Box 3); and Cluster D, hyperarousal (Box 4)—do not differ significantly from children who meet criteria for all three symptom clusters. Therefore—the researchers reported—the absence of this triad does not necessarily indicate a lack of posttraumatic stress in children but may stem from “developmental differences in symptom expression.”

Vulnerability. Traumatic experience contributes to PTSD development, and the “vulnerable, anxious child who is exposed to violence appears to be at greater risk,” according to Silva et al.⁸ After a regression analysis of 59 traumatized children, the research team concluded that PTSD risk is greatest when violence occurs within the family.

A review of 25 studies found that three factors appear to mediate the development of PTSD in children:

• the severity of the trauma exposure
• trauma related to parental distress
• temporal proximity to the traumatic event.⁹

Chronicity. PTSD is a long-lasting, chronic disorder for young patients. Symptoms have been found to persist in one-third of children 2 years after the initial diagnosis.¹⁰

Comorbidity in childhood PTSD is the norm. Among the conditions frequently encountered with childhood PTSD are major depression, dysthymia, substance abuse, anxiety disorder, attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and oppositional defiant disorder.

Steven’s story, continued. At psychiatric referral, Steven had a history of aggression towards other children. He had no friends and usually played alone. He had difficulty sleeping and awoke frequently during the night. Several times daily he displayed temper tantrums with kicking and screaming.

The boy was unable to discuss the abuse that had happened to him but displayed severe aggression when playing with dolls in the office. He stripped off their clothes, examined their private parts, then ripped them apart or threw them across the room. His language development showed significant delays, both in expression and comprehension.

Organic basis for PTSD in children?

Studies of the hypothalamic-pituitary-adrenal (HPA) axis and of brain volume have revealed physiologic changes that may indicate PTSD in children. These changes could be the result of PTSD or a risk factor for its development.

HPA axis dysregulation. One of the first controlled studies of biological and physiologic changes in children with PTSD found elevated levels of dopamine, norepinephrine, and free cortisol in 24-hour urine specimens of maltreated children. Urinary catecholamine and free cortisol concentrations were positively correlated with the duration of PTSD trauma and symptom severity.^11,12

Elevated afternoon salivary cortisol levels have been found in depressed, maltreated children compared with depressed children who had not been maltreated.¹³ Girls ages 5 to 7 who had been abused in the past 2 months were found to have lower salivary cortisol levels than normal controls.¹⁴ A controlled study found significantly elevated salivary cortisol levels in 51 children with PTSD, compared with 31 controls. Interestingly, cortisol levels in the PTSD group were significantly higher in girls than in boys.¹⁵

The effect of trauma on the HPA axis in children requires more research. Although these studies produced contradicting results, elevated cortisol levels seem to be found more consistently than depressed cortisol levels. The differences in outcome could be related to the groups studied or to variations in adrenal system response among subjects.

Brain volume. Changes in brain volume have been measured in maltreated children using MRI readings analyzed with IMAGE software developed by the National Institutes of Health. Intracranial and cerebral volumes of 44 children with PTSD were found to be smaller than those of 61 matched controls.¹² Specifically:

• Children who experienced abuse at the earliest ages and for the longest periods had the smallest brain volumes.
• Maltreated children with the smallest brain and corpus callosum volumes displayed the most severe PTSD symptoms (intrusive thoughts, avoidance, hyperarousal, and dissociation).
• Corpus callosum areas and cerebral volumes were reduced more in maltreated boys than in maltreated girls.
• Hippocampal volumes were not decreased in maltreated children, unlike findings reported in adults with a history of PTSD.

Box 2

In a recent study, the same researchers¹⁶ reported that superior temporal gyrus gray matter volumes measured with MRI were larger in 43 maltreated children and adolescents compared with controls, but white matter volumes were smaller in the maltreated group. The authors suggested these findings may represent developmental alterations in maltreated children. Other MRI studies have found:

Box 3

DSM-IV-TR: POSTTRAUMATIC STRESS DISORDER Criterion C: Avoidance and numbing

Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:

1. efforts to avoid thoughts, feelings, or conversations associated with the trauma
2. efforts to avoid activities, places, or people that arouse recollections of the trauma
3. inability to recall an important aspect of the trauma
4. markedly diminished interest toward participation in significant activity
5. feeling of detachment or estrangement from others
6. restricted range of affect (e.g., unable to have loving feelings)
7. sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)

PROPOSED CHANGE FOR YOUNG CHILDREN

Only one symptom is needed from the following:

1. constriction of play
2. socially more withdrawn
3. restricted range of affect
4. loss of acquired developmental skills (especially language and toilet training)

Source: Adapted from DSM-IV-TR and Scheeringa et al. J Am Acad Child Adolesc Psychiatry 1995;34:191-200.

• attenuation in frontal lobe asymmetry and smaller total brain and cerebral volumes in children with PTSD, compared with controls¹⁷
• a lower N-acetylaspartate/creatine ratio in children with PTSD, which suggests altered anterior cingulate neuronal metabolism.¹⁸

These apparent changes in brain architecture and metabolism may have functional implications. Children with PTSD have been found to perform more poorly than do controls on measures of attention, abstract reasoning, and executive functioning.¹⁶

PTSD treatment in children

Treatment of PTSD in children is strongly influenced by the adult literature and practice guidelines. Most psychiatrists who treat children endorse drug therapy as the first line of treatment, followed by psychodynamic psychotherapy and cognitive-behavioral therapy (CBT). In a recent survey of treatment practices in childhood PTSD, 95% of psychiatrists endorsed the use of medications such as selective serotonin reuptake inhibitors (SSRIs) (47 to 49%), alpha-agonists (16 to 38%), tricyclic antidepressants (11 to 15%), and anxiolytics (12%).

Nonmedical therapists who were included in the survey endorsed the use of eye movement desensitization and reprocessing, CBT, family therapy, and nondirective play therapy.¹⁹

Psychotherapy. Preliminary evidence from five controlled trialsindicates that CBT may be an effective first-line treatment for children and adolescents with PTSD:

• In a study of 100 sexually abused children, PTSD symptoms improved significantly more when children received CBT alone or with their parents, compared with when only their parents received CBT.²⁰ Externalizing and depressive symptoms improved greatly when a parent was included in the child’s treatment, and this improvement was maintained 2 years later.²¹
• A randomized study of 80 sexually abused children found little difference between those who received traditional group therapy and others who received group therapy plus CBT.²²
• CBT was found more effective than nondirective supportive therapy in sexually abused preschool children, both initially and at 6- and 12-month intervals, as well as in children ages 7 to 14.^23,24
• After an earthquake in Armenia, children treated with school-based, grief/trauma-focused CBT showed significant improvement on self-reported measures of PTSD and depressive symptoms, compared with children who received no such treatment.²⁵

Pharmacotherapy

Open-label case reports and case series have examined a variety of pharmacotherapies in childhood PTSD, but no double-blind, placebo-controlled studies have been published.

Propranolol. Eleven children with histories of sexual and/or physical abuse exhibited significantly fewer PTSD symptoms during a 5-week regimen of the beta blocker propranolol than either before or after they received the medication.²⁶

Carbamazepine was given to 28 children and adolescents ages 8 to 17 with a primary diagnosis of PTSD. Complete symptom remission was observed in 22 children, and the other 6 had significant improvement—reporting only abuse-related nightmares. Carbamazepine dosages of 300 to 1,200 mg/d yielded serum levels of 10 to 11.5 mcg/ml.

Subjects with comorbid conditions (one-half the sample) required additional medications. Four children with ADHD received stimulants, three with major depressive disorder received SSRIs, and one patient was given imipramine.²⁷

Clonidine treatment resulted in moderate or greater improvement in target symptoms of PTSD in seven preschool children ages 3 to 6 with a history of severe sexual and/or physical abuse. Clonidine dosages ranged from 0.1 mg at bedtime to 0.05 bid plus 0.1 at bedtime.²⁸

SSRIs and other antidepressants. Citalopram was given in a comparison study to 24 children and adolescents and 14 adults with PTSD, with symptoms assessed every 2 weeks based on Clinician Administered PTSD Scale (CAPS) and Clinical Global Impression (CGI) scores. Mean CAPS total score, symptom cluster score, and CGI ratings were significantly reduced in both age groups. Children and adolescents showed greater improvement than adults in hyperarousal symptoms but less in re-experiencing and avoidance symptoms.²⁹

An 8-year-old girl with PTSD and comorbid anxiety disorder initially responded to fluvoxamine. When she relapsed, mirtazapine was added and her overall symptoms improved.³⁰

An adolescent with PTSD treated with nefazodone, up to 600 mg/d, showed improvement in hyperarousal symptoms and anhedonia.³¹

Summary. In the absence of conclusive scientific evidence—i.e., double-blind, placebo-controlled studies—these case reports reflect common practices in treating PTSD in children and adolescents. American Academy of Child and Adolescent Psychiatry practice guidelines defer to the psychiatrist’s judgment to determine the best pharmacologic approach.⁶ In most cases, evidence from the adult literature influences treatment decisions, and in some cases treatment targets comorbidities such as depression, panic disorder, ADHD, and anxiety.

Box 4

Confronting Steven’s demons. Steven was treated with paroxetine, 15 mg/d, targeting both his depressive and PTSD symptoms; clonidine, 0.05 mg at bedtime, targeting hyperarousal symptoms and ADHD; and risperidone, 0.5 mg bid, which was added last to target his severe aggression and violent behavior.

He also received speech therapy, milieu treatment with the structured setting at the day program, and individual play therapy from the day program’s interns. At home, wrap-around services—including a behavioral specialist and a therapeutic staff support worker—were provided to help his foster family deal with his aggression and difficult behavior.

Conclusion

Current approaches to diagnosis, assessment, and treatment of PTSD in children and adolescents depend in large part on the few available studies conducted in adults, which may not necessarily apply to younger patients. We need more clinical trials involving children and adolescents, better diagnostic instruments, and accurate symptom severity rating scales.

Box 5

Research is leading to new understandings of PTSD in childhood, from more refined diagnostic criteria to observations of changes in brain volume and secretion of stress hormones in maltreated children. Case reports are exploring the safety and efficacy of drug and psychotherapeutic treatments.

Acceptable treatment and management—as indicated by case reports and recommended by the American Academy of Child and Adolescent Psychiatry—includes CBT or dynamic psychotherapy, group therapy, and drug treatment, especially for PTSD’s comorbidities.

Related resources

• National Center for PTSD. www.ncptsd.org
• International Society for Traumatic Stress Studies. www.istss.org
• The PTSD Alliance. http://www.ptsdalliance.org
• National Center for Children Exposed to Violence (NCCEV) http://www.nccev.org

Drug brand names

• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonidine • Catapres
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Mirtazapine • Remeron
• Nefazodone • Serzone
• Paroxetine • Paxil
• Propranolol • Inderal
• Risperidone • Risperdal

Disclosure

Dr. Elizabeth Weller reports that she receives research/grant support from Forest Pharmaceuticals, Organon, and Wyeth Pharmaceuticals, and serves as a consultant to Johnson & Johnson, GlaxoSmithKline, and Novartis Pharmaceuticals Corp.

Dr. Shlewiet reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Ronald Weller reports that he receives research/grant support from Wyeth Pharmaceuticals, Organon, and Forest Pharmaceuticals.

Steven, age 6, lives in a foster home and attends an intensive day program for treatment of severe aggressive and violent episodes, for which he has been hospitalized several times. The boy has been separated from his biological mother for 2 years, and her parental rights have been terminated because of allegations of neglect and severe abuse.

Steven’s mother has a long history of substance abuse. Her boyfriend, who lived with her, abused Steven physically and sexually. He beat him, tortured him, and burned him. He once inserted a hot curling iron into the boy’s rectum, causing severe burns.

It is not unusual for psychiatrists to encounter children such as Steven who have experienced abuse, trauma, or a life-threatening event, but the psychological aftermath of these experiences has only recently been fully recognized. Diagnostic criteria continue to change with evidence that posttraumatic stress disorder (PTSD) manifests differently in children and adolescents than in adults. Now research is showing changes in brain physiology in children who have experienced maltreatment.

Based on our experience and recent evidence, we discuss important features of PTSD that are being recognized in children and adolescents and describe trends and acceptable practices in treating this chronic, debilitating illness.

Diagnostic criteria

PTSD is reported to occur in 1 to 14% of the general population of children¹ and in 3 to 100% of children at risk (those exposed to violence, trauma, or abuse).^2,3 As diagnostic criteria have changed over the years, so may have prevalence rates.

PTSD was recognized as a diagnostic entity in adults in DSM-III and in children and adolescents in DSM-III-R. PTSD in children has a somewhat different presentation and expression of symptoms than in adults. According to DSM-IV-TR diagnostic criteria:

• A child’s response to a stressful event may be expressed as disorganized or agitated behavior instead of intense fear, helplessness, or horror.
• Children re-experience and express the traumatic event or aspects of it through repetitive play.
• Children’s dreams may be frightening but without recognizable content, or they may change into generalized nightmares of monsters, of rescuing others, or of threats to self or others.
• Children also tend to have more psychosomatic complaints, such as headaches and stomachaches, than adults with PTSD.¹

Box 1

Age-related symptoms. Appropriate diagnostic criteria for childhood PTSD have been debated for some time, in part because of differences in children’s symptoms at different ages and developmental stages. Since DSM-IV was introduced in 1994, several researchers have recommended modifications to its diagnostic characterizations of childhood PTSD.

To accommodate the developmental stage of children younger than age 4, for example, Scheeringa et al suggested changes to DSM-IV criteria for PTSD.^4,5 These changes (Boxes 1-5) are included in the American Academy of Child and Adolescent Psychiatry’s guidelines for assessing and treating PTSD⁶ and may be a valuable tool for the clinician treating young children.

Subsyndromal cases. Children whose symptoms fall below the diagnostic criteria for PTSD may demonstrate substantial functional impairment and distress, according to Carrion et al.⁷ In fact, these researchers found that children who fulfill the requirements for two of three symptom clusters—Cluster B, re-experiencing (Box 2); Cluster C, avoidance and numbing (Box 3); and Cluster D, hyperarousal (Box 4)—do not differ significantly from children who meet criteria for all three symptom clusters. Therefore—the researchers reported—the absence of this triad does not necessarily indicate a lack of posttraumatic stress in children but may stem from “developmental differences in symptom expression.”

Vulnerability. Traumatic experience contributes to PTSD development, and the “vulnerable, anxious child who is exposed to violence appears to be at greater risk,” according to Silva et al.⁸ After a regression analysis of 59 traumatized children, the research team concluded that PTSD risk is greatest when violence occurs within the family.

A review of 25 studies found that three factors appear to mediate the development of PTSD in children:

• the severity of the trauma exposure
• trauma related to parental distress
• temporal proximity to the traumatic event.⁹

Chronicity. PTSD is a long-lasting, chronic disorder for young patients. Symptoms have been found to persist in one-third of children 2 years after the initial diagnosis.¹⁰

Comorbidity in childhood PTSD is the norm. Among the conditions frequently encountered with childhood PTSD are major depression, dysthymia, substance abuse, anxiety disorder, attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and oppositional defiant disorder.

Steven’s story, continued. At psychiatric referral, Steven had a history of aggression towards other children. He had no friends and usually played alone. He had difficulty sleeping and awoke frequently during the night. Several times daily he displayed temper tantrums with kicking and screaming.

The boy was unable to discuss the abuse that had happened to him but displayed severe aggression when playing with dolls in the office. He stripped off their clothes, examined their private parts, then ripped them apart or threw them across the room. His language development showed significant delays, both in expression and comprehension.

Organic basis for PTSD in children?

Studies of the hypothalamic-pituitary-adrenal (HPA) axis and of brain volume have revealed physiologic changes that may indicate PTSD in children. These changes could be the result of PTSD or a risk factor for its development.

HPA axis dysregulation. One of the first controlled studies of biological and physiologic changes in children with PTSD found elevated levels of dopamine, norepinephrine, and free cortisol in 24-hour urine specimens of maltreated children. Urinary catecholamine and free cortisol concentrations were positively correlated with the duration of PTSD trauma and symptom severity.^11,12

Elevated afternoon salivary cortisol levels have been found in depressed, maltreated children compared with depressed children who had not been maltreated.¹³ Girls ages 5 to 7 who had been abused in the past 2 months were found to have lower salivary cortisol levels than normal controls.¹⁴ A controlled study found significantly elevated salivary cortisol levels in 51 children with PTSD, compared with 31 controls. Interestingly, cortisol levels in the PTSD group were significantly higher in girls than in boys.¹⁵

The effect of trauma on the HPA axis in children requires more research. Although these studies produced contradicting results, elevated cortisol levels seem to be found more consistently than depressed cortisol levels. The differences in outcome could be related to the groups studied or to variations in adrenal system response among subjects.

Brain volume. Changes in brain volume have been measured in maltreated children using MRI readings analyzed with IMAGE software developed by the National Institutes of Health. Intracranial and cerebral volumes of 44 children with PTSD were found to be smaller than those of 61 matched controls.¹² Specifically:

• Children who experienced abuse at the earliest ages and for the longest periods had the smallest brain volumes.
• Maltreated children with the smallest brain and corpus callosum volumes displayed the most severe PTSD symptoms (intrusive thoughts, avoidance, hyperarousal, and dissociation).
• Corpus callosum areas and cerebral volumes were reduced more in maltreated boys than in maltreated girls.
• Hippocampal volumes were not decreased in maltreated children, unlike findings reported in adults with a history of PTSD.

Box 2

In a recent study, the same researchers¹⁶ reported that superior temporal gyrus gray matter volumes measured with MRI were larger in 43 maltreated children and adolescents compared with controls, but white matter volumes were smaller in the maltreated group. The authors suggested these findings may represent developmental alterations in maltreated children. Other MRI studies have found:

Box 3

DSM-IV-TR: POSTTRAUMATIC STRESS DISORDER Criterion C: Avoidance and numbing

Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:

1. efforts to avoid thoughts, feelings, or conversations associated with the trauma
2. efforts to avoid activities, places, or people that arouse recollections of the trauma
3. inability to recall an important aspect of the trauma
4. markedly diminished interest toward participation in significant activity
5. feeling of detachment or estrangement from others
6. restricted range of affect (e.g., unable to have loving feelings)
7. sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)

PROPOSED CHANGE FOR YOUNG CHILDREN

Only one symptom is needed from the following:

1. constriction of play
2. socially more withdrawn
3. restricted range of affect
4. loss of acquired developmental skills (especially language and toilet training)

Source: Adapted from DSM-IV-TR and Scheeringa et al. J Am Acad Child Adolesc Psychiatry 1995;34:191-200.

• attenuation in frontal lobe asymmetry and smaller total brain and cerebral volumes in children with PTSD, compared with controls¹⁷
• a lower N-acetylaspartate/creatine ratio in children with PTSD, which suggests altered anterior cingulate neuronal metabolism.¹⁸

These apparent changes in brain architecture and metabolism may have functional implications. Children with PTSD have been found to perform more poorly than do controls on measures of attention, abstract reasoning, and executive functioning.¹⁶

PTSD treatment in children

Treatment of PTSD in children is strongly influenced by the adult literature and practice guidelines. Most psychiatrists who treat children endorse drug therapy as the first line of treatment, followed by psychodynamic psychotherapy and cognitive-behavioral therapy (CBT). In a recent survey of treatment practices in childhood PTSD, 95% of psychiatrists endorsed the use of medications such as selective serotonin reuptake inhibitors (SSRIs) (47 to 49%), alpha-agonists (16 to 38%), tricyclic antidepressants (11 to 15%), and anxiolytics (12%).

Nonmedical therapists who were included in the survey endorsed the use of eye movement desensitization and reprocessing, CBT, family therapy, and nondirective play therapy.¹⁹

Psychotherapy. Preliminary evidence from five controlled trialsindicates that CBT may be an effective first-line treatment for children and adolescents with PTSD:

• In a study of 100 sexually abused children, PTSD symptoms improved significantly more when children received CBT alone or with their parents, compared with when only their parents received CBT.²⁰ Externalizing and depressive symptoms improved greatly when a parent was included in the child’s treatment, and this improvement was maintained 2 years later.²¹
• A randomized study of 80 sexually abused children found little difference between those who received traditional group therapy and others who received group therapy plus CBT.²²
• CBT was found more effective than nondirective supportive therapy in sexually abused preschool children, both initially and at 6- and 12-month intervals, as well as in children ages 7 to 14.^23,24
• After an earthquake in Armenia, children treated with school-based, grief/trauma-focused CBT showed significant improvement on self-reported measures of PTSD and depressive symptoms, compared with children who received no such treatment.²⁵

Pharmacotherapy

Open-label case reports and case series have examined a variety of pharmacotherapies in childhood PTSD, but no double-blind, placebo-controlled studies have been published.

Propranolol. Eleven children with histories of sexual and/or physical abuse exhibited significantly fewer PTSD symptoms during a 5-week regimen of the beta blocker propranolol than either before or after they received the medication.²⁶

Carbamazepine was given to 28 children and adolescents ages 8 to 17 with a primary diagnosis of PTSD. Complete symptom remission was observed in 22 children, and the other 6 had significant improvement—reporting only abuse-related nightmares. Carbamazepine dosages of 300 to 1,200 mg/d yielded serum levels of 10 to 11.5 mcg/ml.

Subjects with comorbid conditions (one-half the sample) required additional medications. Four children with ADHD received stimulants, three with major depressive disorder received SSRIs, and one patient was given imipramine.²⁷

Clonidine treatment resulted in moderate or greater improvement in target symptoms of PTSD in seven preschool children ages 3 to 6 with a history of severe sexual and/or physical abuse. Clonidine dosages ranged from 0.1 mg at bedtime to 0.05 bid plus 0.1 at bedtime.²⁸

SSRIs and other antidepressants. Citalopram was given in a comparison study to 24 children and adolescents and 14 adults with PTSD, with symptoms assessed every 2 weeks based on Clinician Administered PTSD Scale (CAPS) and Clinical Global Impression (CGI) scores. Mean CAPS total score, symptom cluster score, and CGI ratings were significantly reduced in both age groups. Children and adolescents showed greater improvement than adults in hyperarousal symptoms but less in re-experiencing and avoidance symptoms.²⁹

An 8-year-old girl with PTSD and comorbid anxiety disorder initially responded to fluvoxamine. When she relapsed, mirtazapine was added and her overall symptoms improved.³⁰

An adolescent with PTSD treated with nefazodone, up to 600 mg/d, showed improvement in hyperarousal symptoms and anhedonia.³¹

Summary. In the absence of conclusive scientific evidence—i.e., double-blind, placebo-controlled studies—these case reports reflect common practices in treating PTSD in children and adolescents. American Academy of Child and Adolescent Psychiatry practice guidelines defer to the psychiatrist’s judgment to determine the best pharmacologic approach.⁶ In most cases, evidence from the adult literature influences treatment decisions, and in some cases treatment targets comorbidities such as depression, panic disorder, ADHD, and anxiety.

Box 4

Confronting Steven’s demons. Steven was treated with paroxetine, 15 mg/d, targeting both his depressive and PTSD symptoms; clonidine, 0.05 mg at bedtime, targeting hyperarousal symptoms and ADHD; and risperidone, 0.5 mg bid, which was added last to target his severe aggression and violent behavior.

He also received speech therapy, milieu treatment with the structured setting at the day program, and individual play therapy from the day program’s interns. At home, wrap-around services—including a behavioral specialist and a therapeutic staff support worker—were provided to help his foster family deal with his aggression and difficult behavior.

Conclusion

Current approaches to diagnosis, assessment, and treatment of PTSD in children and adolescents depend in large part on the few available studies conducted in adults, which may not necessarily apply to younger patients. We need more clinical trials involving children and adolescents, better diagnostic instruments, and accurate symptom severity rating scales.

Box 5

Research is leading to new understandings of PTSD in childhood, from more refined diagnostic criteria to observations of changes in brain volume and secretion of stress hormones in maltreated children. Case reports are exploring the safety and efficacy of drug and psychotherapeutic treatments.

Acceptable treatment and management—as indicated by case reports and recommended by the American Academy of Child and Adolescent Psychiatry—includes CBT or dynamic psychotherapy, group therapy, and drug treatment, especially for PTSD’s comorbidities.

Related resources

• National Center for PTSD. www.ncptsd.org
• International Society for Traumatic Stress Studies. www.istss.org
• The PTSD Alliance. http://www.ptsdalliance.org
• National Center for Children Exposed to Violence (NCCEV) http://www.nccev.org

Drug brand names

• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonidine • Catapres
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Mirtazapine • Remeron
• Nefazodone • Serzone
• Paroxetine • Paxil
• Propranolol • Inderal
• Risperidone • Risperdal

Disclosure

Dr. Elizabeth Weller reports that she receives research/grant support from Forest Pharmaceuticals, Organon, and Wyeth Pharmaceuticals, and serves as a consultant to Johnson & Johnson, GlaxoSmithKline, and Novartis Pharmaceuticals Corp.

Dr. Shlewiet reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Ronald Weller reports that he receives research/grant support from Wyeth Pharmaceuticals, Organon, and Forest Pharmaceuticals.

Steven, age 6, lives in a foster home and attends an intensive day program for treatment of severe aggressive and violent episodes, for which he has been hospitalized several times. The boy has been separated from his biological mother for 2 years, and her parental rights have been terminated because of allegations of neglect and severe abuse.

Steven’s mother has a long history of substance abuse. Her boyfriend, who lived with her, abused Steven physically and sexually. He beat him, tortured him, and burned him. He once inserted a hot curling iron into the boy’s rectum, causing severe burns.

It is not unusual for psychiatrists to encounter children such as Steven who have experienced abuse, trauma, or a life-threatening event, but the psychological aftermath of these experiences has only recently been fully recognized. Diagnostic criteria continue to change with evidence that posttraumatic stress disorder (PTSD) manifests differently in children and adolescents than in adults. Now research is showing changes in brain physiology in children who have experienced maltreatment.

Based on our experience and recent evidence, we discuss important features of PTSD that are being recognized in children and adolescents and describe trends and acceptable practices in treating this chronic, debilitating illness.

Diagnostic criteria

PTSD is reported to occur in 1 to 14% of the general population of children¹ and in 3 to 100% of children at risk (those exposed to violence, trauma, or abuse).^2,3 As diagnostic criteria have changed over the years, so may have prevalence rates.

PTSD was recognized as a diagnostic entity in adults in DSM-III and in children and adolescents in DSM-III-R. PTSD in children has a somewhat different presentation and expression of symptoms than in adults. According to DSM-IV-TR diagnostic criteria:

• A child’s response to a stressful event may be expressed as disorganized or agitated behavior instead of intense fear, helplessness, or horror.
• Children re-experience and express the traumatic event or aspects of it through repetitive play.
• Children’s dreams may be frightening but without recognizable content, or they may change into generalized nightmares of monsters, of rescuing others, or of threats to self or others.
• Children also tend to have more psychosomatic complaints, such as headaches and stomachaches, than adults with PTSD.¹

Box 1

Age-related symptoms. Appropriate diagnostic criteria for childhood PTSD have been debated for some time, in part because of differences in children’s symptoms at different ages and developmental stages. Since DSM-IV was introduced in 1994, several researchers have recommended modifications to its diagnostic characterizations of childhood PTSD.

To accommodate the developmental stage of children younger than age 4, for example, Scheeringa et al suggested changes to DSM-IV criteria for PTSD.^4,5 These changes (Boxes 1-5) are included in the American Academy of Child and Adolescent Psychiatry’s guidelines for assessing and treating PTSD⁶ and may be a valuable tool for the clinician treating young children.

Subsyndromal cases. Children whose symptoms fall below the diagnostic criteria for PTSD may demonstrate substantial functional impairment and distress, according to Carrion et al.⁷ In fact, these researchers found that children who fulfill the requirements for two of three symptom clusters—Cluster B, re-experiencing (Box 2); Cluster C, avoidance and numbing (Box 3); and Cluster D, hyperarousal (Box 4)—do not differ significantly from children who meet criteria for all three symptom clusters. Therefore—the researchers reported—the absence of this triad does not necessarily indicate a lack of posttraumatic stress in children but may stem from “developmental differences in symptom expression.”

Vulnerability. Traumatic experience contributes to PTSD development, and the “vulnerable, anxious child who is exposed to violence appears to be at greater risk,” according to Silva et al.⁸ After a regression analysis of 59 traumatized children, the research team concluded that PTSD risk is greatest when violence occurs within the family.

A review of 25 studies found that three factors appear to mediate the development of PTSD in children:

• the severity of the trauma exposure
• trauma related to parental distress
• temporal proximity to the traumatic event.⁹

Chronicity. PTSD is a long-lasting, chronic disorder for young patients. Symptoms have been found to persist in one-third of children 2 years after the initial diagnosis.¹⁰

Comorbidity in childhood PTSD is the norm. Among the conditions frequently encountered with childhood PTSD are major depression, dysthymia, substance abuse, anxiety disorder, attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and oppositional defiant disorder.

Steven’s story, continued. At psychiatric referral, Steven had a history of aggression towards other children. He had no friends and usually played alone. He had difficulty sleeping and awoke frequently during the night. Several times daily he displayed temper tantrums with kicking and screaming.

The boy was unable to discuss the abuse that had happened to him but displayed severe aggression when playing with dolls in the office. He stripped off their clothes, examined their private parts, then ripped them apart or threw them across the room. His language development showed significant delays, both in expression and comprehension.

Organic basis for PTSD in children?

Studies of the hypothalamic-pituitary-adrenal (HPA) axis and of brain volume have revealed physiologic changes that may indicate PTSD in children. These changes could be the result of PTSD or a risk factor for its development.

HPA axis dysregulation. One of the first controlled studies of biological and physiologic changes in children with PTSD found elevated levels of dopamine, norepinephrine, and free cortisol in 24-hour urine specimens of maltreated children. Urinary catecholamine and free cortisol concentrations were positively correlated with the duration of PTSD trauma and symptom severity.^11,12

Elevated afternoon salivary cortisol levels have been found in depressed, maltreated children compared with depressed children who had not been maltreated.¹³ Girls ages 5 to 7 who had been abused in the past 2 months were found to have lower salivary cortisol levels than normal controls.¹⁴ A controlled study found significantly elevated salivary cortisol levels in 51 children with PTSD, compared with 31 controls. Interestingly, cortisol levels in the PTSD group were significantly higher in girls than in boys.¹⁵

The effect of trauma on the HPA axis in children requires more research. Although these studies produced contradicting results, elevated cortisol levels seem to be found more consistently than depressed cortisol levels. The differences in outcome could be related to the groups studied or to variations in adrenal system response among subjects.

Brain volume. Changes in brain volume have been measured in maltreated children using MRI readings analyzed with IMAGE software developed by the National Institutes of Health. Intracranial and cerebral volumes of 44 children with PTSD were found to be smaller than those of 61 matched controls.¹² Specifically:

• Children who experienced abuse at the earliest ages and for the longest periods had the smallest brain volumes.
• Maltreated children with the smallest brain and corpus callosum volumes displayed the most severe PTSD symptoms (intrusive thoughts, avoidance, hyperarousal, and dissociation).
• Corpus callosum areas and cerebral volumes were reduced more in maltreated boys than in maltreated girls.
• Hippocampal volumes were not decreased in maltreated children, unlike findings reported in adults with a history of PTSD.

Box 2

In a recent study, the same researchers¹⁶ reported that superior temporal gyrus gray matter volumes measured with MRI were larger in 43 maltreated children and adolescents compared with controls, but white matter volumes were smaller in the maltreated group. The authors suggested these findings may represent developmental alterations in maltreated children. Other MRI studies have found:

Box 3

DSM-IV-TR: POSTTRAUMATIC STRESS DISORDER Criterion C: Avoidance and numbing

Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:

1. efforts to avoid thoughts, feelings, or conversations associated with the trauma
2. efforts to avoid activities, places, or people that arouse recollections of the trauma
3. inability to recall an important aspect of the trauma
4. markedly diminished interest toward participation in significant activity
5. feeling of detachment or estrangement from others
6. restricted range of affect (e.g., unable to have loving feelings)
7. sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)

PROPOSED CHANGE FOR YOUNG CHILDREN

Only one symptom is needed from the following:

1. constriction of play
2. socially more withdrawn
3. restricted range of affect
4. loss of acquired developmental skills (especially language and toilet training)

Source: Adapted from DSM-IV-TR and Scheeringa et al. J Am Acad Child Adolesc Psychiatry 1995;34:191-200.

• attenuation in frontal lobe asymmetry and smaller total brain and cerebral volumes in children with PTSD, compared with controls¹⁷
• a lower N-acetylaspartate/creatine ratio in children with PTSD, which suggests altered anterior cingulate neuronal metabolism.¹⁸

These apparent changes in brain architecture and metabolism may have functional implications. Children with PTSD have been found to perform more poorly than do controls on measures of attention, abstract reasoning, and executive functioning.¹⁶

PTSD treatment in children

Treatment of PTSD in children is strongly influenced by the adult literature and practice guidelines. Most psychiatrists who treat children endorse drug therapy as the first line of treatment, followed by psychodynamic psychotherapy and cognitive-behavioral therapy (CBT). In a recent survey of treatment practices in childhood PTSD, 95% of psychiatrists endorsed the use of medications such as selective serotonin reuptake inhibitors (SSRIs) (47 to 49%), alpha-agonists (16 to 38%), tricyclic antidepressants (11 to 15%), and anxiolytics (12%).

Nonmedical therapists who were included in the survey endorsed the use of eye movement desensitization and reprocessing, CBT, family therapy, and nondirective play therapy.¹⁹

Psychotherapy. Preliminary evidence from five controlled trialsindicates that CBT may be an effective first-line treatment for children and adolescents with PTSD:

• In a study of 100 sexually abused children, PTSD symptoms improved significantly more when children received CBT alone or with their parents, compared with when only their parents received CBT.²⁰ Externalizing and depressive symptoms improved greatly when a parent was included in the child’s treatment, and this improvement was maintained 2 years later.²¹
• A randomized study of 80 sexually abused children found little difference between those who received traditional group therapy and others who received group therapy plus CBT.²²
• CBT was found more effective than nondirective supportive therapy in sexually abused preschool children, both initially and at 6- and 12-month intervals, as well as in children ages 7 to 14.^23,24
• After an earthquake in Armenia, children treated with school-based, grief/trauma-focused CBT showed significant improvement on self-reported measures of PTSD and depressive symptoms, compared with children who received no such treatment.²⁵

Pharmacotherapy

Open-label case reports and case series have examined a variety of pharmacotherapies in childhood PTSD, but no double-blind, placebo-controlled studies have been published.

Propranolol. Eleven children with histories of sexual and/or physical abuse exhibited significantly fewer PTSD symptoms during a 5-week regimen of the beta blocker propranolol than either before or after they received the medication.²⁶

Carbamazepine was given to 28 children and adolescents ages 8 to 17 with a primary diagnosis of PTSD. Complete symptom remission was observed in 22 children, and the other 6 had significant improvement—reporting only abuse-related nightmares. Carbamazepine dosages of 300 to 1,200 mg/d yielded serum levels of 10 to 11.5 mcg/ml.

Subjects with comorbid conditions (one-half the sample) required additional medications. Four children with ADHD received stimulants, three with major depressive disorder received SSRIs, and one patient was given imipramine.²⁷

Clonidine treatment resulted in moderate or greater improvement in target symptoms of PTSD in seven preschool children ages 3 to 6 with a history of severe sexual and/or physical abuse. Clonidine dosages ranged from 0.1 mg at bedtime to 0.05 bid plus 0.1 at bedtime.²⁸

SSRIs and other antidepressants. Citalopram was given in a comparison study to 24 children and adolescents and 14 adults with PTSD, with symptoms assessed every 2 weeks based on Clinician Administered PTSD Scale (CAPS) and Clinical Global Impression (CGI) scores. Mean CAPS total score, symptom cluster score, and CGI ratings were significantly reduced in both age groups. Children and adolescents showed greater improvement than adults in hyperarousal symptoms but less in re-experiencing and avoidance symptoms.²⁹

An 8-year-old girl with PTSD and comorbid anxiety disorder initially responded to fluvoxamine. When she relapsed, mirtazapine was added and her overall symptoms improved.³⁰

An adolescent with PTSD treated with nefazodone, up to 600 mg/d, showed improvement in hyperarousal symptoms and anhedonia.³¹

Summary. In the absence of conclusive scientific evidence—i.e., double-blind, placebo-controlled studies—these case reports reflect common practices in treating PTSD in children and adolescents. American Academy of Child and Adolescent Psychiatry practice guidelines defer to the psychiatrist’s judgment to determine the best pharmacologic approach.⁶ In most cases, evidence from the adult literature influences treatment decisions, and in some cases treatment targets comorbidities such as depression, panic disorder, ADHD, and anxiety.

Box 4

Confronting Steven’s demons. Steven was treated with paroxetine, 15 mg/d, targeting both his depressive and PTSD symptoms; clonidine, 0.05 mg at bedtime, targeting hyperarousal symptoms and ADHD; and risperidone, 0.5 mg bid, which was added last to target his severe aggression and violent behavior.

He also received speech therapy, milieu treatment with the structured setting at the day program, and individual play therapy from the day program’s interns. At home, wrap-around services—including a behavioral specialist and a therapeutic staff support worker—were provided to help his foster family deal with his aggression and difficult behavior.

Conclusion

Current approaches to diagnosis, assessment, and treatment of PTSD in children and adolescents depend in large part on the few available studies conducted in adults, which may not necessarily apply to younger patients. We need more clinical trials involving children and adolescents, better diagnostic instruments, and accurate symptom severity rating scales.

Box 5

Research is leading to new understandings of PTSD in childhood, from more refined diagnostic criteria to observations of changes in brain volume and secretion of stress hormones in maltreated children. Case reports are exploring the safety and efficacy of drug and psychotherapeutic treatments.

Acceptable treatment and management—as indicated by case reports and recommended by the American Academy of Child and Adolescent Psychiatry—includes CBT or dynamic psychotherapy, group therapy, and drug treatment, especially for PTSD’s comorbidities.

Related resources

• National Center for PTSD. www.ncptsd.org
• International Society for Traumatic Stress Studies. www.istss.org
• The PTSD Alliance. http://www.ptsdalliance.org
• National Center for Children Exposed to Violence (NCCEV) http://www.nccev.org

Drug brand names

• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonidine • Catapres
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Mirtazapine • Remeron
• Nefazodone • Serzone
• Paroxetine • Paxil
• Propranolol • Inderal
• Risperidone • Risperdal

Disclosure

Dr. Elizabeth Weller reports that she receives research/grant support from Forest Pharmaceuticals, Organon, and Wyeth Pharmaceuticals, and serves as a consultant to Johnson & Johnson, GlaxoSmithKline, and Novartis Pharmaceuticals Corp.

Dr. Shlewiet reports no affiliation or financial arrangement with any of the companies whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Ronald Weller reports that he receives research/grant support from Wyeth Pharmaceuticals, Organon, and Forest Pharmaceuticals.

Sport psychiatry—a relatively new subspecialty—emphasizes treating mental illness caused in athletes by a pre-existing disposition, stressors unique to sports, or use of anabolic steroids or other substances. Sport psychiatrists do not set out to enhance an athlete’s performance, although effective therapy may produce that outcome.

Athletes of all ages and levels, from Little League to the Olympics, are vulnerable to psychiatric disorders. Using real-life examples, let’s look at the practice of sport psychiatry and examine common psychopathologies in athletes.

Psychiatry in the gym

Psychiatric illness in an amateur or professional athlete may arise from coincidence, a predisposing pathology that first attracted the athlete to the arena, or a psychopathology caused by the sport itself. Some athletes succumb to suicide (Box 1),¹ although insufficient data exist to establish the prevalence.

Educating athletes, their families, coaches, and trainers about mental illness is key to identifying at-risk athletes and referring them for treatment. To that end, think of sports and psychiatry in a consultation-liaison model.² A psychiatrist working alongside an orthopedist at the gym would help remove the stigma of psychiatric illness in sports and allow for timely diagnosis and treatment.

Box 1

Special stressors of athletes

Stressors unique to athletes that may cause, trigger, or worsen psychopathology include pressure to win, constant risk of injury, and the specter of sudden retirement at an early age.

Pressure to win. Parents and coaches pursuing vicarious aspirations may push a child athlete to physical and emotional extremes, a dynamic that Tofler calls “achievement by proxy.”³ These adults may send children away from home for training or remove them from school in the hope that they will excel at a sport. Intense training may preclude normal childhood friendships and pursuits and may become frankly abusive.⁴

Gymnast Christy Henrich competed in one World Cup gymnastics meet with a broken foot and ultimately died of complications of anorexia nervosa. During the girl’s training, her mother was quoted as saying, “A gymnast without a high pain threshold is a gymnast without a career. Their body is a machine, and they are a person. The two are separate.”⁵

Injuries can threaten the athlete’s career and are a major cause of stress. Olympic diver Greg Louganis was devastated by knee injuries that ended his gymnastics career at a young age, before he switched to diving.⁶

Retirement. Even in the absence of injuries, most athletic careers are relatively short because of their physical demands. Professional athletes may be so focused on their sports careers that they are ill-equipped to face life without athletic competition. Retirement, with its abrupt change in emotional support and finances, can be overwhelming.

Golden Gloves boxer Gerry Cooney recalls a difficult descent into retirement, complicated by alcohol. He received treatment and now runs an organization designed to help other boxers through the transition to a life without sports.

Affective disorders in athletes

Unipolar and bipolar affective disorders occur in athletes, as in any population. Sometimes athletes with depression find temporary relief in athletic involvement—in some cases for substantial periods.

Depression. U.S. Olympic diver Wendy Williams describes years of denying and coping with depression. Eventually, however, her affective symptoms required psychiatric intervention. Refusing medication, she first tried psychotherapy alone. Several years later, after a worsening of symptoms and several episodes of suicidal ideation, Williams relented to drug therapy to good effect.⁷

Bipolar disorder. Bipolar mania can cause the same behavioral disturbances in athletes as in anyone else. Stressors in professional athletes’ lives can trigger a manic episode, however, and the public may witness the episode’s manifestations. When this occurs, the athlete’s mental illness is generally misunderstood by the public and misrepresented in the media.

In discussing the use of psychological screens for prospective National Football League players, for example, a sportswriter explained the rationale as going for “…the right mix of on-field aggression and off-field character. No team wants to draft the next Dimitrius Underwood.”⁸

Underwood, who reportedly has bipolar disorder, slashed his throat under the pressure of being a first-round draft pick while a member of the Miami Dolphins. He survived and went on to play 19 NFL games before being released this season by the Dallas Cowboys.⁹

Anxiety disorders

Obsessive-compulsive disorder may have unique manifestations on the baseball diamond, where the batter wears his “lucky socks” to every game, spits his tobacco juice in a particular pattern, or taps his bat on the ground a requisite number of times before approaching the plate. It is easy to imagine that the features of obsessive-compulsive personality disorder, present in a subset of those with obsessive-compulsive disorder, can contribute to athletic success.

Repetition and perfectionism are required for the athlete who aspires to succeed at the elite level. U.S. speed skater Eric Hayden wore grooves into a wooden board on which he tirelessly practiced the side-to-side motion that hypertrophied his quadriceps en route to the Olympic gold medal.

Social phobia. Some athletes with social phobia appear to express a counterphobic response on the field or find an escape from their anxiety in this forum. Perhaps Ricky Williams, who has acknowledged that he is being treated for social anxiety disorder, takes refuge behind the armor of his helmet and uniform as a running back for the NFL’s Miami Dolphins.¹⁰

Panic disorder. Earl Campbell, a former NFL running back, developed panic disorder after his retirement from professional football. The chest pain and palpitations he experienced caused him to seek help, but he told a newspaper reporter, “I didn’t realize I was going to a shrink, and when I found out, I almost slugged him.”¹¹ After an initial prescription of alprazolam, Campbell’s panic symptoms were well managed through relaxation techniques and exercise.

Posttraumatic stress disorder (PTSD). Julie Krone, the celebrated female jockey, developed PTSD after two falls from her mount: a serious spill from which she recovered, and later a more minor fall that resulted in two broken wrists.¹² Her anxiety symptoms were treated, and she went on to race horses again before her retirement. She now participates in the Women’s Sports Foundation-sponsored Minds in Motion Depression Campaign to remove the stigma of PTSD.

Other disorders in athletes

ADHD. Children and adolescents with attention-deficit/ hyperactivity disorder (ADHD) may find sports to be adaptive, even therapeutic. Though this theory is untested, anecdotal reports, as in Box 1, are suggestive.

Eating disorders. Certain athletic environments foster eating disorders, especially in athletes who are psychodynamically or genetically predisposed to disordered eating. Eating disorders appear to arise in three major sports categories:

• Where low body fat provides an advantage, including track and field, swimming, and distance running. Distance runner Mary Wazeter developed an eating disorder while attending Georgetown University on a track scholarship.¹³
• Where it is imperative to “make weight,” including wrestling, horse racing, and crew. Thoroughbred jockey Herb McCauley recalls his bulimia developing when he was a high school wrestler, running in rubber suits and vomiting to keep his weight down. Later he won more than 3,000 races at major horse tracks, using diuretics and laxatives on his way to less than 2% body fat.¹⁴
• Where scoring may be based in part on aesthetics, including gymnastics, figure skating, diving, synchronized swimming, and—though not a competitive sport—ballet.

In aesthetic sports, the onset of an athlete’s eating disorder often can be traced to a single, critical comment (Box 2).⁵

Box 2

Psychotic disorders also arise in athletes, sometimes after abuse of anabolic steroids or other substances or in association with bipolar disorder or schizophrenia. There is nothing more poignant than treating a first episode of schizophrenia in an adolescent who dreams of becoming the high school’s next great quarterback. The illness itself and necessary drug interventions can pose insurmountable obstacles, although the newer antipsychotics offer reduced side effects compared with older medications.

Substance abuse

Anabolic steroids. At the start of the 2002 baseball season, former Atlanta Braves third baseman Ken Caminiti shocked the sports world with allegations that “at least 50 percent” of Major League Baseball players use anabolic steroids to enhance their performance. Use of anabolic steroids is illegal without a prescription; the National Football League requires screening for steroid use, but Major League Baseball does not.

The use of performance-enhancing drugs is not unique to baseball¹⁵ or to professional athletes. A significant percentage of high school athletes also is believed to be using anabolic steroids,¹⁶ which cause psychiatric symptoms ranging from depression to psychosis (“roid rage”) to suicide. Other commonly used performance-enhancing drugs include caffeine, human growth hormone, and erythropoietin.¹⁶

Alcohol and drugs. For some professional athletes, alcohol and drug abuse is as much a part of sports culture as sweat and fame. Former Major League Baseball outfielder Darryl Strawberry spent more time in treatment for alcohol and cocaine addiction than he did playing baseball toward the end of his career. He was sentenced in April 2002 to 18 months in prison after 3 years of repeated drug-related offenses and probation violations.

Psychiatric therapy for athletes

Psychotherapy. A range of psychotherapeutic techniques—from cognitive-behavioral and family therapy to insight-oriented psychotherapy—can help the troubled athlete.

Drug therapy. When prescribing psychotropic medications to an athlete, remember that the physiologic effects of exertion—such as fluid loss, increases in VO₂ max, and cardiac output—can alter drug metabolism and distribution. These effects need to be assessed case by case.

Psychotropic side effects to avoid in the athlete include sedation, extrapyramidal symptoms, orthostasis, tremor, and cardiac arrhythmias. We know little about the potential for psychotropic drugs to enhance athletic performance, and research is needed.^1\7

Related resources

• Mind Body and Sports (promotes sportsmanship and addresses the emotional needs of athletes of all ages). www.mindbodyandsports.com
• USA Gymnastics Athlete Wellness Program. www.usa-gymnastics.org/wellness
• Fuentes RJ, Rosenberg JM (eds). Athletic drug reference. Durham, NC: Clean Data, Inc., 1999.

Drug brand names

• Alprazolam • Xanax

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Sport psychiatry—a relatively new subspecialty—emphasizes treating mental illness caused in athletes by a pre-existing disposition, stressors unique to sports, or use of anabolic steroids or other substances. Sport psychiatrists do not set out to enhance an athlete’s performance, although effective therapy may produce that outcome.

Athletes of all ages and levels, from Little League to the Olympics, are vulnerable to psychiatric disorders. Using real-life examples, let’s look at the practice of sport psychiatry and examine common psychopathologies in athletes.

Psychiatry in the gym

Psychiatric illness in an amateur or professional athlete may arise from coincidence, a predisposing pathology that first attracted the athlete to the arena, or a psychopathology caused by the sport itself. Some athletes succumb to suicide (Box 1),¹ although insufficient data exist to establish the prevalence.

Educating athletes, their families, coaches, and trainers about mental illness is key to identifying at-risk athletes and referring them for treatment. To that end, think of sports and psychiatry in a consultation-liaison model.² A psychiatrist working alongside an orthopedist at the gym would help remove the stigma of psychiatric illness in sports and allow for timely diagnosis and treatment.

Box 1

Special stressors of athletes

Stressors unique to athletes that may cause, trigger, or worsen psychopathology include pressure to win, constant risk of injury, and the specter of sudden retirement at an early age.

Pressure to win. Parents and coaches pursuing vicarious aspirations may push a child athlete to physical and emotional extremes, a dynamic that Tofler calls “achievement by proxy.”³ These adults may send children away from home for training or remove them from school in the hope that they will excel at a sport. Intense training may preclude normal childhood friendships and pursuits and may become frankly abusive.⁴

Gymnast Christy Henrich competed in one World Cup gymnastics meet with a broken foot and ultimately died of complications of anorexia nervosa. During the girl’s training, her mother was quoted as saying, “A gymnast without a high pain threshold is a gymnast without a career. Their body is a machine, and they are a person. The two are separate.”⁵

Injuries can threaten the athlete’s career and are a major cause of stress. Olympic diver Greg Louganis was devastated by knee injuries that ended his gymnastics career at a young age, before he switched to diving.⁶

Retirement. Even in the absence of injuries, most athletic careers are relatively short because of their physical demands. Professional athletes may be so focused on their sports careers that they are ill-equipped to face life without athletic competition. Retirement, with its abrupt change in emotional support and finances, can be overwhelming.

Golden Gloves boxer Gerry Cooney recalls a difficult descent into retirement, complicated by alcohol. He received treatment and now runs an organization designed to help other boxers through the transition to a life without sports.

Affective disorders in athletes

Unipolar and bipolar affective disorders occur in athletes, as in any population. Sometimes athletes with depression find temporary relief in athletic involvement—in some cases for substantial periods.

Depression. U.S. Olympic diver Wendy Williams describes years of denying and coping with depression. Eventually, however, her affective symptoms required psychiatric intervention. Refusing medication, she first tried psychotherapy alone. Several years later, after a worsening of symptoms and several episodes of suicidal ideation, Williams relented to drug therapy to good effect.⁷

Bipolar disorder. Bipolar mania can cause the same behavioral disturbances in athletes as in anyone else. Stressors in professional athletes’ lives can trigger a manic episode, however, and the public may witness the episode’s manifestations. When this occurs, the athlete’s mental illness is generally misunderstood by the public and misrepresented in the media.

In discussing the use of psychological screens for prospective National Football League players, for example, a sportswriter explained the rationale as going for “…the right mix of on-field aggression and off-field character. No team wants to draft the next Dimitrius Underwood.”⁸

Underwood, who reportedly has bipolar disorder, slashed his throat under the pressure of being a first-round draft pick while a member of the Miami Dolphins. He survived and went on to play 19 NFL games before being released this season by the Dallas Cowboys.⁹

Anxiety disorders

Obsessive-compulsive disorder may have unique manifestations on the baseball diamond, where the batter wears his “lucky socks” to every game, spits his tobacco juice in a particular pattern, or taps his bat on the ground a requisite number of times before approaching the plate. It is easy to imagine that the features of obsessive-compulsive personality disorder, present in a subset of those with obsessive-compulsive disorder, can contribute to athletic success.

Repetition and perfectionism are required for the athlete who aspires to succeed at the elite level. U.S. speed skater Eric Hayden wore grooves into a wooden board on which he tirelessly practiced the side-to-side motion that hypertrophied his quadriceps en route to the Olympic gold medal.

Social phobia. Some athletes with social phobia appear to express a counterphobic response on the field or find an escape from their anxiety in this forum. Perhaps Ricky Williams, who has acknowledged that he is being treated for social anxiety disorder, takes refuge behind the armor of his helmet and uniform as a running back for the NFL’s Miami Dolphins.¹⁰

Panic disorder. Earl Campbell, a former NFL running back, developed panic disorder after his retirement from professional football. The chest pain and palpitations he experienced caused him to seek help, but he told a newspaper reporter, “I didn’t realize I was going to a shrink, and when I found out, I almost slugged him.”¹¹ After an initial prescription of alprazolam, Campbell’s panic symptoms were well managed through relaxation techniques and exercise.

Posttraumatic stress disorder (PTSD). Julie Krone, the celebrated female jockey, developed PTSD after two falls from her mount: a serious spill from which she recovered, and later a more minor fall that resulted in two broken wrists.¹² Her anxiety symptoms were treated, and she went on to race horses again before her retirement. She now participates in the Women’s Sports Foundation-sponsored Minds in Motion Depression Campaign to remove the stigma of PTSD.

Other disorders in athletes

ADHD. Children and adolescents with attention-deficit/ hyperactivity disorder (ADHD) may find sports to be adaptive, even therapeutic. Though this theory is untested, anecdotal reports, as in Box 1, are suggestive.

Eating disorders. Certain athletic environments foster eating disorders, especially in athletes who are psychodynamically or genetically predisposed to disordered eating. Eating disorders appear to arise in three major sports categories:

• Where low body fat provides an advantage, including track and field, swimming, and distance running. Distance runner Mary Wazeter developed an eating disorder while attending Georgetown University on a track scholarship.¹³
• Where it is imperative to “make weight,” including wrestling, horse racing, and crew. Thoroughbred jockey Herb McCauley recalls his bulimia developing when he was a high school wrestler, running in rubber suits and vomiting to keep his weight down. Later he won more than 3,000 races at major horse tracks, using diuretics and laxatives on his way to less than 2% body fat.¹⁴
• Where scoring may be based in part on aesthetics, including gymnastics, figure skating, diving, synchronized swimming, and—though not a competitive sport—ballet.

In aesthetic sports, the onset of an athlete’s eating disorder often can be traced to a single, critical comment (Box 2).⁵

Box 2

Psychotic disorders also arise in athletes, sometimes after abuse of anabolic steroids or other substances or in association with bipolar disorder or schizophrenia. There is nothing more poignant than treating a first episode of schizophrenia in an adolescent who dreams of becoming the high school’s next great quarterback. The illness itself and necessary drug interventions can pose insurmountable obstacles, although the newer antipsychotics offer reduced side effects compared with older medications.

Substance abuse

Anabolic steroids. At the start of the 2002 baseball season, former Atlanta Braves third baseman Ken Caminiti shocked the sports world with allegations that “at least 50 percent” of Major League Baseball players use anabolic steroids to enhance their performance. Use of anabolic steroids is illegal without a prescription; the National Football League requires screening for steroid use, but Major League Baseball does not.

The use of performance-enhancing drugs is not unique to baseball¹⁵ or to professional athletes. A significant percentage of high school athletes also is believed to be using anabolic steroids,¹⁶ which cause psychiatric symptoms ranging from depression to psychosis (“roid rage”) to suicide. Other commonly used performance-enhancing drugs include caffeine, human growth hormone, and erythropoietin.¹⁶

Alcohol and drugs. For some professional athletes, alcohol and drug abuse is as much a part of sports culture as sweat and fame. Former Major League Baseball outfielder Darryl Strawberry spent more time in treatment for alcohol and cocaine addiction than he did playing baseball toward the end of his career. He was sentenced in April 2002 to 18 months in prison after 3 years of repeated drug-related offenses and probation violations.

Psychiatric therapy for athletes

Psychotherapy. A range of psychotherapeutic techniques—from cognitive-behavioral and family therapy to insight-oriented psychotherapy—can help the troubled athlete.

Drug therapy. When prescribing psychotropic medications to an athlete, remember that the physiologic effects of exertion—such as fluid loss, increases in VO₂ max, and cardiac output—can alter drug metabolism and distribution. These effects need to be assessed case by case.

Psychotropic side effects to avoid in the athlete include sedation, extrapyramidal symptoms, orthostasis, tremor, and cardiac arrhythmias. We know little about the potential for psychotropic drugs to enhance athletic performance, and research is needed.^1\7

Related resources

• Mind Body and Sports (promotes sportsmanship and addresses the emotional needs of athletes of all ages). www.mindbodyandsports.com
• USA Gymnastics Athlete Wellness Program. www.usa-gymnastics.org/wellness
• Fuentes RJ, Rosenberg JM (eds). Athletic drug reference. Durham, NC: Clean Data, Inc., 1999.

Drug brand names

• Alprazolam • Xanax

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Sport psychiatry—a relatively new subspecialty—emphasizes treating mental illness caused in athletes by a pre-existing disposition, stressors unique to sports, or use of anabolic steroids or other substances. Sport psychiatrists do not set out to enhance an athlete’s performance, although effective therapy may produce that outcome.

Athletes of all ages and levels, from Little League to the Olympics, are vulnerable to psychiatric disorders. Using real-life examples, let’s look at the practice of sport psychiatry and examine common psychopathologies in athletes.

Psychiatry in the gym

Psychiatric illness in an amateur or professional athlete may arise from coincidence, a predisposing pathology that first attracted the athlete to the arena, or a psychopathology caused by the sport itself. Some athletes succumb to suicide (Box 1),¹ although insufficient data exist to establish the prevalence.

Educating athletes, their families, coaches, and trainers about mental illness is key to identifying at-risk athletes and referring them for treatment. To that end, think of sports and psychiatry in a consultation-liaison model.² A psychiatrist working alongside an orthopedist at the gym would help remove the stigma of psychiatric illness in sports and allow for timely diagnosis and treatment.

Box 1

Special stressors of athletes

Stressors unique to athletes that may cause, trigger, or worsen psychopathology include pressure to win, constant risk of injury, and the specter of sudden retirement at an early age.

Pressure to win. Parents and coaches pursuing vicarious aspirations may push a child athlete to physical and emotional extremes, a dynamic that Tofler calls “achievement by proxy.”³ These adults may send children away from home for training or remove them from school in the hope that they will excel at a sport. Intense training may preclude normal childhood friendships and pursuits and may become frankly abusive.⁴

Gymnast Christy Henrich competed in one World Cup gymnastics meet with a broken foot and ultimately died of complications of anorexia nervosa. During the girl’s training, her mother was quoted as saying, “A gymnast without a high pain threshold is a gymnast without a career. Their body is a machine, and they are a person. The two are separate.”⁵

Injuries can threaten the athlete’s career and are a major cause of stress. Olympic diver Greg Louganis was devastated by knee injuries that ended his gymnastics career at a young age, before he switched to diving.⁶

Retirement. Even in the absence of injuries, most athletic careers are relatively short because of their physical demands. Professional athletes may be so focused on their sports careers that they are ill-equipped to face life without athletic competition. Retirement, with its abrupt change in emotional support and finances, can be overwhelming.

Golden Gloves boxer Gerry Cooney recalls a difficult descent into retirement, complicated by alcohol. He received treatment and now runs an organization designed to help other boxers through the transition to a life without sports.

Affective disorders in athletes

Unipolar and bipolar affective disorders occur in athletes, as in any population. Sometimes athletes with depression find temporary relief in athletic involvement—in some cases for substantial periods.

Depression. U.S. Olympic diver Wendy Williams describes years of denying and coping with depression. Eventually, however, her affective symptoms required psychiatric intervention. Refusing medication, she first tried psychotherapy alone. Several years later, after a worsening of symptoms and several episodes of suicidal ideation, Williams relented to drug therapy to good effect.⁷

Bipolar disorder. Bipolar mania can cause the same behavioral disturbances in athletes as in anyone else. Stressors in professional athletes’ lives can trigger a manic episode, however, and the public may witness the episode’s manifestations. When this occurs, the athlete’s mental illness is generally misunderstood by the public and misrepresented in the media.

In discussing the use of psychological screens for prospective National Football League players, for example, a sportswriter explained the rationale as going for “…the right mix of on-field aggression and off-field character. No team wants to draft the next Dimitrius Underwood.”⁸

Underwood, who reportedly has bipolar disorder, slashed his throat under the pressure of being a first-round draft pick while a member of the Miami Dolphins. He survived and went on to play 19 NFL games before being released this season by the Dallas Cowboys.⁹

Anxiety disorders

Obsessive-compulsive disorder may have unique manifestations on the baseball diamond, where the batter wears his “lucky socks” to every game, spits his tobacco juice in a particular pattern, or taps his bat on the ground a requisite number of times before approaching the plate. It is easy to imagine that the features of obsessive-compulsive personality disorder, present in a subset of those with obsessive-compulsive disorder, can contribute to athletic success.

Repetition and perfectionism are required for the athlete who aspires to succeed at the elite level. U.S. speed skater Eric Hayden wore grooves into a wooden board on which he tirelessly practiced the side-to-side motion that hypertrophied his quadriceps en route to the Olympic gold medal.

Social phobia. Some athletes with social phobia appear to express a counterphobic response on the field or find an escape from their anxiety in this forum. Perhaps Ricky Williams, who has acknowledged that he is being treated for social anxiety disorder, takes refuge behind the armor of his helmet and uniform as a running back for the NFL’s Miami Dolphins.¹⁰

Panic disorder. Earl Campbell, a former NFL running back, developed panic disorder after his retirement from professional football. The chest pain and palpitations he experienced caused him to seek help, but he told a newspaper reporter, “I didn’t realize I was going to a shrink, and when I found out, I almost slugged him.”¹¹ After an initial prescription of alprazolam, Campbell’s panic symptoms were well managed through relaxation techniques and exercise.

Posttraumatic stress disorder (PTSD). Julie Krone, the celebrated female jockey, developed PTSD after two falls from her mount: a serious spill from which she recovered, and later a more minor fall that resulted in two broken wrists.¹² Her anxiety symptoms were treated, and she went on to race horses again before her retirement. She now participates in the Women’s Sports Foundation-sponsored Minds in Motion Depression Campaign to remove the stigma of PTSD.

Other disorders in athletes

ADHD. Children and adolescents with attention-deficit/ hyperactivity disorder (ADHD) may find sports to be adaptive, even therapeutic. Though this theory is untested, anecdotal reports, as in Box 1, are suggestive.

Eating disorders. Certain athletic environments foster eating disorders, especially in athletes who are psychodynamically or genetically predisposed to disordered eating. Eating disorders appear to arise in three major sports categories:

• Where low body fat provides an advantage, including track and field, swimming, and distance running. Distance runner Mary Wazeter developed an eating disorder while attending Georgetown University on a track scholarship.¹³
• Where it is imperative to “make weight,” including wrestling, horse racing, and crew. Thoroughbred jockey Herb McCauley recalls his bulimia developing when he was a high school wrestler, running in rubber suits and vomiting to keep his weight down. Later he won more than 3,000 races at major horse tracks, using diuretics and laxatives on his way to less than 2% body fat.¹⁴
• Where scoring may be based in part on aesthetics, including gymnastics, figure skating, diving, synchronized swimming, and—though not a competitive sport—ballet.

In aesthetic sports, the onset of an athlete’s eating disorder often can be traced to a single, critical comment (Box 2).⁵

Box 2

Psychotic disorders also arise in athletes, sometimes after abuse of anabolic steroids or other substances or in association with bipolar disorder or schizophrenia. There is nothing more poignant than treating a first episode of schizophrenia in an adolescent who dreams of becoming the high school’s next great quarterback. The illness itself and necessary drug interventions can pose insurmountable obstacles, although the newer antipsychotics offer reduced side effects compared with older medications.

Substance abuse

Anabolic steroids. At the start of the 2002 baseball season, former Atlanta Braves third baseman Ken Caminiti shocked the sports world with allegations that “at least 50 percent” of Major League Baseball players use anabolic steroids to enhance their performance. Use of anabolic steroids is illegal without a prescription; the National Football League requires screening for steroid use, but Major League Baseball does not.

The use of performance-enhancing drugs is not unique to baseball¹⁵ or to professional athletes. A significant percentage of high school athletes also is believed to be using anabolic steroids,¹⁶ which cause psychiatric symptoms ranging from depression to psychosis (“roid rage”) to suicide. Other commonly used performance-enhancing drugs include caffeine, human growth hormone, and erythropoietin.¹⁶

Alcohol and drugs. For some professional athletes, alcohol and drug abuse is as much a part of sports culture as sweat and fame. Former Major League Baseball outfielder Darryl Strawberry spent more time in treatment for alcohol and cocaine addiction than he did playing baseball toward the end of his career. He was sentenced in April 2002 to 18 months in prison after 3 years of repeated drug-related offenses and probation violations.

Psychiatric therapy for athletes

Psychotherapy. A range of psychotherapeutic techniques—from cognitive-behavioral and family therapy to insight-oriented psychotherapy—can help the troubled athlete.

Drug therapy. When prescribing psychotropic medications to an athlete, remember that the physiologic effects of exertion—such as fluid loss, increases in VO₂ max, and cardiac output—can alter drug metabolism and distribution. These effects need to be assessed case by case.

Psychotropic side effects to avoid in the athlete include sedation, extrapyramidal symptoms, orthostasis, tremor, and cardiac arrhythmias. We know little about the potential for psychotropic drugs to enhance athletic performance, and research is needed.^1\7

Related resources

• Mind Body and Sports (promotes sportsmanship and addresses the emotional needs of athletes of all ages). www.mindbodyandsports.com
• USA Gymnastics Athlete Wellness Program. www.usa-gymnastics.org/wellness
• Fuentes RJ, Rosenberg JM (eds). Athletic drug reference. Durham, NC: Clean Data, Inc., 1999.

Drug brand names

• Alprazolam • Xanax

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

History: A fading memory

Mrs. S, 85, lives alone in her home of 40 years. Over the past 3 years, she has complained increasingly about headaches, fatigue, and back pain. The cause of these vague physical difficulties has not been determined.

Her daughters say that Mrs. S has become increasingly forgetful. She often does not remember family visits, has difficulty organizing her bank accounts, repeatedly misplaces her pocketbook, and on one occasion became lost on her way to the supermarket. Once fairly social, she has become increasingly isolated.

How would you address Mrs. S’ impaired memory? What medical or psychiatric problems might her forgetfulness indicate?

Dr. Verma’s observations

This case illustrates the fundamentals of geriatric care, the first of which is to preserve—if not enhance—the patient’s function (Box). Forty years ago, Kral¹ identified “benign senescent forgetfulness” as a normal aspect of aging. Current research, however, suggests that “senescent forgetfulness” is not always benign. Alexopoulos, Krishnan, and others^2,3 have shown that depression manifesting in late life is accompanied by significant white-matter change and substantially increases the risk of developing dementia.

Well past the point of isolated forgetfulness, Mrs. S is exhibiting functional decline and cognitive impairment in multiple domains. The question is, are these symptoms the result of a medical problem such as Alzheimer’s disease or dementia, a psychiatric disorder, or both? The workup and management of these complaints can dramatically affect subsequent outcomes.

Vague medical complaints of unknown cause should not necessarily imply that the problem is psychiatric. The clinician should rule out common medical causes of cognitive decline, including:

• drug toxicity, especially after anxiolytic and sedative-hypnotic agents have been administered
• endocrine dysfunction, such as hypothyroidism
• and CNS neoplasms (Table 1).

Box

A detailed history (still the best diagnostic procedure), a thorough physical evaluation, and routine lab tests can usually help rule out most of these causes. On the other hand, affirmative diagnosis when psychiatric symptoms are evident can minimize testing that can be emotionally, physically, and financially draining to the patient. In Mrs. S’ case, the prominence of the cognitive decline and attendant social withdrawal clearly point to depression or dementia.

The significant overlap between depression and dementia further complicates the diagnosis. Neuropsychological testing can uncover distinguishing factors, but it may help to empirically consider that all late-life depression with cognitive impairment may be secondary to early dementia.

Initiating early drug treatment of dementia with a cholinesterase inhibitor such as donepezil, galantamine, or rivastigmine may slow the trajectory of decline. Vascular risk factors—hypertension and diabetes in particular—also need to be controlled. Low-dose aspirin may help prevent microembolic phenomena.

A selective serotonin reuptake inhibitor (SSRI) can alleviate the depression. If mild paranoia is noted, adding an atypical antipsychotic at a low dosage (olanzapine, 1.25 to 5 mg once daily or risperidone, 0.5 to 1.0 mg/d divided in two doses) may help.

Above all, encourage the patient to remain physically and mentally active. To this end, the clinician should enlist the family and other caregivers to help motivate the patient. Involvement in a day program or similar program may alleviate the patient’s social isolation.

Treatment: New surroundings

Since her initial evaluation 1 year ago, Mrs. S reluctantly has moved into an assisted living facility at her daughters’ insistence. She adjusted well—at least for the first month or so. She then starting calling her daughters at all hours, complaining of being alone and scared. She was taken to a new internist, who prescribed oxazepam, 15 mg bid, for an “anxiety disorder.”

Instead of adjusting to her new surroundings, Mrs. S began to withdraw further. She stayed in her room most days, not even venturing to the dining room for meals. Her personal hygiene deteriorated. According to staff reports, “Mrs. S did not mix with the other residents,” and was becoming “increasingly paranoid.” Her calls to her family had escalated into bitter complaints that people were stealing her belongings.

Table 1

COMMON CAUSES OF DEMENTIA

Mrs. S again visited the internist who, upon hearing that the patient was becoming more paranoid, assumed that she was exhibiting psychotic features. The internist diagnosed Mrs. S as having late-onset Alzheimer’s-type dementia with delusions and added haloperidol, 0.5 mg tid, to her regimen.

How would you help Mrs. S adjust to her new surroundings? How would your treatment plan differ from that of the internist?Table 2

ANTIPSYCHOTICS: SIDE-EFFECT PROFILES

Dr. Verma’s observations

The decision to transfer a loved one to a nursing home is difficult for all concerned. I have often seen caregiver “burnout” play a major role in the family’s decision.

After 40 years in her own home, Mrs. S is not likely to adjust readily to living in a “regimented” environment, no matter how comfortable and elegant it may seem. The phenomenon is often called “transfer trauma” and manifests as a sharp decline in function upon moving to a new environment. Most individuals do adapt with time; involving Mrs. S. in a socialization program and insisting on her presence during meals and at other facility events would have hastened her adjustment. Above all, clinicians should be supportive and avoid resorting to medication too soon.

Because Mrs. S’ functional decline was so sharp, however, trying a nondrug therapy would have been easier said than done. Indeed, the internist resorted too quickly to medication, prescribing a short-acting benzodiazepine at first and, when this was perceived as ineffective, adding a neuroleptic antipsychotic.

Psychotropics are a double-edged sword. Used appropriately, they can reduce distressing symptoms and enhance function. Drugs, however, are increasingly replacing human contact. As we see here, medication side effects in nursing homes can be deleterious. Federal regulations enforced under the Omnibus Budget Reconciliation Act of 1987 have helped reduce the inappropriate use of psychotropics as “chemical restraints.” Still, the emotional distress for patient and caretaker during transitions often leads to inappropriate reliance on psychotropics for predictable adjustment symptoms.

Benzodiazepines have been found to cause sedation, falls, and cognitive clouding and thus should be avoided in older patients. Haloperidol has long been used in psychosis, but its use in older patients is contraindicated because of its side-effect profile. Extrapyramidal symptoms (EPS) are a common side effect of neuroleptics in older persons and are associated with a high incidence of tardive dyskinesia, gait disturbance, akathisia, and cognitive impairment.

Atypical antipsychotics have a more benign side-effect profile (Table 2) and should constitute first-line treatment—but only after human contact, stimulation, and care have been attempted.

Continued treatment: Another setback

A week after starting on haloperidol, Mrs. S fell and fractured her hip. She was transferred to the general hospital, where a surgical repair was performed. Her recovery was slow and difficult. She would not participate in physical therapy and required much coaxing to walk or stand up, often insisting that she could no longer do either. She developed urinary incontinence and became increasingly unable to care for herself. She remained in the hospital for 1 week, then was transferred to a rehabilitation facility.

Dr. Verma’s observations

A causal relationship between Mrs. S’ fall and the haloperidol/oxazepam combination is more than likely. Older persons have diminished pro-prioception, walk on a wider base, and struggle with postural sway. EPS combined with sedation can therefore have disastrous consequences, as this case clearly illustrates. Benzodiazepines, anticholinergics, antihistamines, and the typical neuroleptics are known to impair mobility. Many antidepressants, especially tertiary tricyclics such as amitriptyline and imipramine, may lead to falls by causing orthostatic hypotension secondary to alpha-adrenergic receptor blockade.

Check for pre-treatment orthostatic changes in blood pressure before prescribing psychotropics to older patients. An ECG can also help rule out rhythm abnormalities and assess baseline QTc interval. Agents with the most benign side-effect profiles—atypical antipsychotics, SSRIs, and newer antidepressants such as bupropion and venlafaxine—are recommended for older patients. For Mrs. S, a low dosage of a novel antipsychotic instead of haloperidol and oxazepam would have preserved her physical function and might have greatly reduced her chances of falling.

Follow-up ‘:Not helping’

Mrs. S has been in the nursing home for about 3 1/2 weeks. Staff members consistently report that she “is not helping herself,” is “always weepy,” and “feels her family (has) abandoned her.” She is now taking oxazepam, 15 mg bid, haloperidol, 0.5 mg bid and 1.0 mg at bedtime, and diphenhydramine, 50 mg at bedtime, to help her sleep.

Staff members also report that Mrs. S is “confused and very forgetful … (she) may have Alzheimer’s disease.” Urinary and bowel incontinence are an increasing problem, and she has lost about 15 pounds since she entered the facility. Laboratory readings are normal, but oral intake is poor.

Could Mrs. S’ functional decline have been avoided? How would you improve her function at this point?

Dr. Verma’s observations

A well-intentioned but ill-conceived drug regimen has compounded problems caused by the prior intervention. As Mrs. S becomes increasingly unable to function—and the staff becomes more frustrated with her deterioration and lack of initiative—more drugs are added. The three agents she is taking all carry a significant risk for sedation, and the anticholinergic effects of both haloperidol and diphenhydramine compound Mrs S’ difficulties by causing delirium and cognitive difficulties.

If this regimen is not modified, Mrs. S likely will stay bed-bound, her cognition will remain impaired or worsen, and her incontinence will continue unchecked. She will require more and more nursing time as her condition deteriorates further. Decubiti, sepsis, and even premature death are all likely sequelae.

In retrospect, an initial intervention with an antidepressant and/or an acetylcholinesterase inhibitor might have prevented such a precipitous decline. It is conceivable that Mrs. S could even have avoided institutional placement. At this point, I would gradually wean her off haloperidol and oxazepam, then aggressively treat her depression, resorting to electroconvulsive therapy if necessary.

In today’s atmosphere of cost containment, care decisions are too often dictated by shortsighted formulary lists, not sound clinical reasoning. In this case, the use of more cost-effective drugs with well-documented higher toxicity ultimately led to excess disability, which in turn required increased effort (and cost) by the treatment team.

Psychosocial interventions can be time-consuming, but they might have prevented Mrs. S’ rapid decline and saved substantial staff time. A higher-functioning patient uses far fewer staff resources, and the added expense of treating a hip fracture exceeds any savings from the use of a lessexpensive medication.

Related resources

• Salzman C. Psychiatric medications for older adults–the concise guide. New York: Guilford Press, 2001
• Jacobson SA, Pies RW, Greenblatt DJ. Handbook of geriatric psychopharmacology. Washington DC: American Psychiatric Publishing, 2002.

Drug brand names

• Amitriptyline • Elavil
• Bupropion • Wellbutrin
• Clozapine • Clozaril
• Donepezil • Aricept
• Galantamine • Reminyl
• Haloperidol • Haldol
• Imipramine • Tofranil
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Rivastigmine • Exelon
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

Dr. Verma reports that he is on the speakers bureau of Eli Lilly and Co. and Abbott Laboratories, serves as a consultant to Eli Lilly and Co., and receives grant support from Eli Lilly and Co. and GlaxoSmithKline.

History: A fading memory

Mrs. S, 85, lives alone in her home of 40 years. Over the past 3 years, she has complained increasingly about headaches, fatigue, and back pain. The cause of these vague physical difficulties has not been determined.

Her daughters say that Mrs. S has become increasingly forgetful. She often does not remember family visits, has difficulty organizing her bank accounts, repeatedly misplaces her pocketbook, and on one occasion became lost on her way to the supermarket. Once fairly social, she has become increasingly isolated.

How would you address Mrs. S’ impaired memory? What medical or psychiatric problems might her forgetfulness indicate?

Dr. Verma’s observations

This case illustrates the fundamentals of geriatric care, the first of which is to preserve—if not enhance—the patient’s function (Box). Forty years ago, Kral¹ identified “benign senescent forgetfulness” as a normal aspect of aging. Current research, however, suggests that “senescent forgetfulness” is not always benign. Alexopoulos, Krishnan, and others^2,3 have shown that depression manifesting in late life is accompanied by significant white-matter change and substantially increases the risk of developing dementia.

Well past the point of isolated forgetfulness, Mrs. S is exhibiting functional decline and cognitive impairment in multiple domains. The question is, are these symptoms the result of a medical problem such as Alzheimer’s disease or dementia, a psychiatric disorder, or both? The workup and management of these complaints can dramatically affect subsequent outcomes.

Vague medical complaints of unknown cause should not necessarily imply that the problem is psychiatric. The clinician should rule out common medical causes of cognitive decline, including:

• drug toxicity, especially after anxiolytic and sedative-hypnotic agents have been administered
• endocrine dysfunction, such as hypothyroidism
• and CNS neoplasms (Table 1).

Box

A detailed history (still the best diagnostic procedure), a thorough physical evaluation, and routine lab tests can usually help rule out most of these causes. On the other hand, affirmative diagnosis when psychiatric symptoms are evident can minimize testing that can be emotionally, physically, and financially draining to the patient. In Mrs. S’ case, the prominence of the cognitive decline and attendant social withdrawal clearly point to depression or dementia.

The significant overlap between depression and dementia further complicates the diagnosis. Neuropsychological testing can uncover distinguishing factors, but it may help to empirically consider that all late-life depression with cognitive impairment may be secondary to early dementia.

Initiating early drug treatment of dementia with a cholinesterase inhibitor such as donepezil, galantamine, or rivastigmine may slow the trajectory of decline. Vascular risk factors—hypertension and diabetes in particular—also need to be controlled. Low-dose aspirin may help prevent microembolic phenomena.

A selective serotonin reuptake inhibitor (SSRI) can alleviate the depression. If mild paranoia is noted, adding an atypical antipsychotic at a low dosage (olanzapine, 1.25 to 5 mg once daily or risperidone, 0.5 to 1.0 mg/d divided in two doses) may help.

Above all, encourage the patient to remain physically and mentally active. To this end, the clinician should enlist the family and other caregivers to help motivate the patient. Involvement in a day program or similar program may alleviate the patient’s social isolation.

Treatment: New surroundings

Since her initial evaluation 1 year ago, Mrs. S reluctantly has moved into an assisted living facility at her daughters’ insistence. She adjusted well—at least for the first month or so. She then starting calling her daughters at all hours, complaining of being alone and scared. She was taken to a new internist, who prescribed oxazepam, 15 mg bid, for an “anxiety disorder.”

Instead of adjusting to her new surroundings, Mrs. S began to withdraw further. She stayed in her room most days, not even venturing to the dining room for meals. Her personal hygiene deteriorated. According to staff reports, “Mrs. S did not mix with the other residents,” and was becoming “increasingly paranoid.” Her calls to her family had escalated into bitter complaints that people were stealing her belongings.

Table 1

COMMON CAUSES OF DEMENTIA

Mrs. S again visited the internist who, upon hearing that the patient was becoming more paranoid, assumed that she was exhibiting psychotic features. The internist diagnosed Mrs. S as having late-onset Alzheimer’s-type dementia with delusions and added haloperidol, 0.5 mg tid, to her regimen.

How would you help Mrs. S adjust to her new surroundings? How would your treatment plan differ from that of the internist?Table 2

ANTIPSYCHOTICS: SIDE-EFFECT PROFILES

Dr. Verma’s observations

The decision to transfer a loved one to a nursing home is difficult for all concerned. I have often seen caregiver “burnout” play a major role in the family’s decision.

After 40 years in her own home, Mrs. S is not likely to adjust readily to living in a “regimented” environment, no matter how comfortable and elegant it may seem. The phenomenon is often called “transfer trauma” and manifests as a sharp decline in function upon moving to a new environment. Most individuals do adapt with time; involving Mrs. S. in a socialization program and insisting on her presence during meals and at other facility events would have hastened her adjustment. Above all, clinicians should be supportive and avoid resorting to medication too soon.

Because Mrs. S’ functional decline was so sharp, however, trying a nondrug therapy would have been easier said than done. Indeed, the internist resorted too quickly to medication, prescribing a short-acting benzodiazepine at first and, when this was perceived as ineffective, adding a neuroleptic antipsychotic.

Psychotropics are a double-edged sword. Used appropriately, they can reduce distressing symptoms and enhance function. Drugs, however, are increasingly replacing human contact. As we see here, medication side effects in nursing homes can be deleterious. Federal regulations enforced under the Omnibus Budget Reconciliation Act of 1987 have helped reduce the inappropriate use of psychotropics as “chemical restraints.” Still, the emotional distress for patient and caretaker during transitions often leads to inappropriate reliance on psychotropics for predictable adjustment symptoms.

Benzodiazepines have been found to cause sedation, falls, and cognitive clouding and thus should be avoided in older patients. Haloperidol has long been used in psychosis, but its use in older patients is contraindicated because of its side-effect profile. Extrapyramidal symptoms (EPS) are a common side effect of neuroleptics in older persons and are associated with a high incidence of tardive dyskinesia, gait disturbance, akathisia, and cognitive impairment.

Atypical antipsychotics have a more benign side-effect profile (Table 2) and should constitute first-line treatment—but only after human contact, stimulation, and care have been attempted.

Continued treatment: Another setback

A week after starting on haloperidol, Mrs. S fell and fractured her hip. She was transferred to the general hospital, where a surgical repair was performed. Her recovery was slow and difficult. She would not participate in physical therapy and required much coaxing to walk or stand up, often insisting that she could no longer do either. She developed urinary incontinence and became increasingly unable to care for herself. She remained in the hospital for 1 week, then was transferred to a rehabilitation facility.

Dr. Verma’s observations

A causal relationship between Mrs. S’ fall and the haloperidol/oxazepam combination is more than likely. Older persons have diminished pro-prioception, walk on a wider base, and struggle with postural sway. EPS combined with sedation can therefore have disastrous consequences, as this case clearly illustrates. Benzodiazepines, anticholinergics, antihistamines, and the typical neuroleptics are known to impair mobility. Many antidepressants, especially tertiary tricyclics such as amitriptyline and imipramine, may lead to falls by causing orthostatic hypotension secondary to alpha-adrenergic receptor blockade.

Check for pre-treatment orthostatic changes in blood pressure before prescribing psychotropics to older patients. An ECG can also help rule out rhythm abnormalities and assess baseline QTc interval. Agents with the most benign side-effect profiles—atypical antipsychotics, SSRIs, and newer antidepressants such as bupropion and venlafaxine—are recommended for older patients. For Mrs. S, a low dosage of a novel antipsychotic instead of haloperidol and oxazepam would have preserved her physical function and might have greatly reduced her chances of falling.

Follow-up ‘:Not helping’

Mrs. S has been in the nursing home for about 3 1/2 weeks. Staff members consistently report that she “is not helping herself,” is “always weepy,” and “feels her family (has) abandoned her.” She is now taking oxazepam, 15 mg bid, haloperidol, 0.5 mg bid and 1.0 mg at bedtime, and diphenhydramine, 50 mg at bedtime, to help her sleep.

Staff members also report that Mrs. S is “confused and very forgetful … (she) may have Alzheimer’s disease.” Urinary and bowel incontinence are an increasing problem, and she has lost about 15 pounds since she entered the facility. Laboratory readings are normal, but oral intake is poor.

Could Mrs. S’ functional decline have been avoided? How would you improve her function at this point?

Dr. Verma’s observations

A well-intentioned but ill-conceived drug regimen has compounded problems caused by the prior intervention. As Mrs. S becomes increasingly unable to function—and the staff becomes more frustrated with her deterioration and lack of initiative—more drugs are added. The three agents she is taking all carry a significant risk for sedation, and the anticholinergic effects of both haloperidol and diphenhydramine compound Mrs S’ difficulties by causing delirium and cognitive difficulties.

If this regimen is not modified, Mrs. S likely will stay bed-bound, her cognition will remain impaired or worsen, and her incontinence will continue unchecked. She will require more and more nursing time as her condition deteriorates further. Decubiti, sepsis, and even premature death are all likely sequelae.

In retrospect, an initial intervention with an antidepressant and/or an acetylcholinesterase inhibitor might have prevented such a precipitous decline. It is conceivable that Mrs. S could even have avoided institutional placement. At this point, I would gradually wean her off haloperidol and oxazepam, then aggressively treat her depression, resorting to electroconvulsive therapy if necessary.

In today’s atmosphere of cost containment, care decisions are too often dictated by shortsighted formulary lists, not sound clinical reasoning. In this case, the use of more cost-effective drugs with well-documented higher toxicity ultimately led to excess disability, which in turn required increased effort (and cost) by the treatment team.

Psychosocial interventions can be time-consuming, but they might have prevented Mrs. S’ rapid decline and saved substantial staff time. A higher-functioning patient uses far fewer staff resources, and the added expense of treating a hip fracture exceeds any savings from the use of a lessexpensive medication.

Related resources

• Salzman C. Psychiatric medications for older adults–the concise guide. New York: Guilford Press, 2001
• Jacobson SA, Pies RW, Greenblatt DJ. Handbook of geriatric psychopharmacology. Washington DC: American Psychiatric Publishing, 2002.

Drug brand names

• Amitriptyline • Elavil
• Bupropion • Wellbutrin
• Clozapine • Clozaril
• Donepezil • Aricept
• Galantamine • Reminyl
• Haloperidol • Haldol
• Imipramine • Tofranil
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Rivastigmine • Exelon
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

Dr. Verma reports that he is on the speakers bureau of Eli Lilly and Co. and Abbott Laboratories, serves as a consultant to Eli Lilly and Co., and receives grant support from Eli Lilly and Co. and GlaxoSmithKline.

History: A fading memory

Mrs. S, 85, lives alone in her home of 40 years. Over the past 3 years, she has complained increasingly about headaches, fatigue, and back pain. The cause of these vague physical difficulties has not been determined.

Her daughters say that Mrs. S has become increasingly forgetful. She often does not remember family visits, has difficulty organizing her bank accounts, repeatedly misplaces her pocketbook, and on one occasion became lost on her way to the supermarket. Once fairly social, she has become increasingly isolated.

How would you address Mrs. S’ impaired memory? What medical or psychiatric problems might her forgetfulness indicate?

Dr. Verma’s observations

This case illustrates the fundamentals of geriatric care, the first of which is to preserve—if not enhance—the patient’s function (Box). Forty years ago, Kral¹ identified “benign senescent forgetfulness” as a normal aspect of aging. Current research, however, suggests that “senescent forgetfulness” is not always benign. Alexopoulos, Krishnan, and others^2,3 have shown that depression manifesting in late life is accompanied by significant white-matter change and substantially increases the risk of developing dementia.

Well past the point of isolated forgetfulness, Mrs. S is exhibiting functional decline and cognitive impairment in multiple domains. The question is, are these symptoms the result of a medical problem such as Alzheimer’s disease or dementia, a psychiatric disorder, or both? The workup and management of these complaints can dramatically affect subsequent outcomes.

Vague medical complaints of unknown cause should not necessarily imply that the problem is psychiatric. The clinician should rule out common medical causes of cognitive decline, including:

• drug toxicity, especially after anxiolytic and sedative-hypnotic agents have been administered
• endocrine dysfunction, such as hypothyroidism
• and CNS neoplasms (Table 1).

Box

A detailed history (still the best diagnostic procedure), a thorough physical evaluation, and routine lab tests can usually help rule out most of these causes. On the other hand, affirmative diagnosis when psychiatric symptoms are evident can minimize testing that can be emotionally, physically, and financially draining to the patient. In Mrs. S’ case, the prominence of the cognitive decline and attendant social withdrawal clearly point to depression or dementia.

The significant overlap between depression and dementia further complicates the diagnosis. Neuropsychological testing can uncover distinguishing factors, but it may help to empirically consider that all late-life depression with cognitive impairment may be secondary to early dementia.

Initiating early drug treatment of dementia with a cholinesterase inhibitor such as donepezil, galantamine, or rivastigmine may slow the trajectory of decline. Vascular risk factors—hypertension and diabetes in particular—also need to be controlled. Low-dose aspirin may help prevent microembolic phenomena.

A selective serotonin reuptake inhibitor (SSRI) can alleviate the depression. If mild paranoia is noted, adding an atypical antipsychotic at a low dosage (olanzapine, 1.25 to 5 mg once daily or risperidone, 0.5 to 1.0 mg/d divided in two doses) may help.

Above all, encourage the patient to remain physically and mentally active. To this end, the clinician should enlist the family and other caregivers to help motivate the patient. Involvement in a day program or similar program may alleviate the patient’s social isolation.

Treatment: New surroundings

Since her initial evaluation 1 year ago, Mrs. S reluctantly has moved into an assisted living facility at her daughters’ insistence. She adjusted well—at least for the first month or so. She then starting calling her daughters at all hours, complaining of being alone and scared. She was taken to a new internist, who prescribed oxazepam, 15 mg bid, for an “anxiety disorder.”

Instead of adjusting to her new surroundings, Mrs. S began to withdraw further. She stayed in her room most days, not even venturing to the dining room for meals. Her personal hygiene deteriorated. According to staff reports, “Mrs. S did not mix with the other residents,” and was becoming “increasingly paranoid.” Her calls to her family had escalated into bitter complaints that people were stealing her belongings.

Table 1

COMMON CAUSES OF DEMENTIA

Mrs. S again visited the internist who, upon hearing that the patient was becoming more paranoid, assumed that she was exhibiting psychotic features. The internist diagnosed Mrs. S as having late-onset Alzheimer’s-type dementia with delusions and added haloperidol, 0.5 mg tid, to her regimen.

How would you help Mrs. S adjust to her new surroundings? How would your treatment plan differ from that of the internist?Table 2

ANTIPSYCHOTICS: SIDE-EFFECT PROFILES

Dr. Verma’s observations

The decision to transfer a loved one to a nursing home is difficult for all concerned. I have often seen caregiver “burnout” play a major role in the family’s decision.

After 40 years in her own home, Mrs. S is not likely to adjust readily to living in a “regimented” environment, no matter how comfortable and elegant it may seem. The phenomenon is often called “transfer trauma” and manifests as a sharp decline in function upon moving to a new environment. Most individuals do adapt with time; involving Mrs. S. in a socialization program and insisting on her presence during meals and at other facility events would have hastened her adjustment. Above all, clinicians should be supportive and avoid resorting to medication too soon.

Because Mrs. S’ functional decline was so sharp, however, trying a nondrug therapy would have been easier said than done. Indeed, the internist resorted too quickly to medication, prescribing a short-acting benzodiazepine at first and, when this was perceived as ineffective, adding a neuroleptic antipsychotic.

Psychotropics are a double-edged sword. Used appropriately, they can reduce distressing symptoms and enhance function. Drugs, however, are increasingly replacing human contact. As we see here, medication side effects in nursing homes can be deleterious. Federal regulations enforced under the Omnibus Budget Reconciliation Act of 1987 have helped reduce the inappropriate use of psychotropics as “chemical restraints.” Still, the emotional distress for patient and caretaker during transitions often leads to inappropriate reliance on psychotropics for predictable adjustment symptoms.

Benzodiazepines have been found to cause sedation, falls, and cognitive clouding and thus should be avoided in older patients. Haloperidol has long been used in psychosis, but its use in older patients is contraindicated because of its side-effect profile. Extrapyramidal symptoms (EPS) are a common side effect of neuroleptics in older persons and are associated with a high incidence of tardive dyskinesia, gait disturbance, akathisia, and cognitive impairment.

Atypical antipsychotics have a more benign side-effect profile (Table 2) and should constitute first-line treatment—but only after human contact, stimulation, and care have been attempted.

Continued treatment: Another setback

A week after starting on haloperidol, Mrs. S fell and fractured her hip. She was transferred to the general hospital, where a surgical repair was performed. Her recovery was slow and difficult. She would not participate in physical therapy and required much coaxing to walk or stand up, often insisting that she could no longer do either. She developed urinary incontinence and became increasingly unable to care for herself. She remained in the hospital for 1 week, then was transferred to a rehabilitation facility.

Dr. Verma’s observations

A causal relationship between Mrs. S’ fall and the haloperidol/oxazepam combination is more than likely. Older persons have diminished pro-prioception, walk on a wider base, and struggle with postural sway. EPS combined with sedation can therefore have disastrous consequences, as this case clearly illustrates. Benzodiazepines, anticholinergics, antihistamines, and the typical neuroleptics are known to impair mobility. Many antidepressants, especially tertiary tricyclics such as amitriptyline and imipramine, may lead to falls by causing orthostatic hypotension secondary to alpha-adrenergic receptor blockade.

Check for pre-treatment orthostatic changes in blood pressure before prescribing psychotropics to older patients. An ECG can also help rule out rhythm abnormalities and assess baseline QTc interval. Agents with the most benign side-effect profiles—atypical antipsychotics, SSRIs, and newer antidepressants such as bupropion and venlafaxine—are recommended for older patients. For Mrs. S, a low dosage of a novel antipsychotic instead of haloperidol and oxazepam would have preserved her physical function and might have greatly reduced her chances of falling.

Follow-up ‘:Not helping’

Mrs. S has been in the nursing home for about 3 1/2 weeks. Staff members consistently report that she “is not helping herself,” is “always weepy,” and “feels her family (has) abandoned her.” She is now taking oxazepam, 15 mg bid, haloperidol, 0.5 mg bid and 1.0 mg at bedtime, and diphenhydramine, 50 mg at bedtime, to help her sleep.

Staff members also report that Mrs. S is “confused and very forgetful … (she) may have Alzheimer’s disease.” Urinary and bowel incontinence are an increasing problem, and she has lost about 15 pounds since she entered the facility. Laboratory readings are normal, but oral intake is poor.

Could Mrs. S’ functional decline have been avoided? How would you improve her function at this point?

Dr. Verma’s observations

A well-intentioned but ill-conceived drug regimen has compounded problems caused by the prior intervention. As Mrs. S becomes increasingly unable to function—and the staff becomes more frustrated with her deterioration and lack of initiative—more drugs are added. The three agents she is taking all carry a significant risk for sedation, and the anticholinergic effects of both haloperidol and diphenhydramine compound Mrs S’ difficulties by causing delirium and cognitive difficulties.

If this regimen is not modified, Mrs. S likely will stay bed-bound, her cognition will remain impaired or worsen, and her incontinence will continue unchecked. She will require more and more nursing time as her condition deteriorates further. Decubiti, sepsis, and even premature death are all likely sequelae.

In retrospect, an initial intervention with an antidepressant and/or an acetylcholinesterase inhibitor might have prevented such a precipitous decline. It is conceivable that Mrs. S could even have avoided institutional placement. At this point, I would gradually wean her off haloperidol and oxazepam, then aggressively treat her depression, resorting to electroconvulsive therapy if necessary.

In today’s atmosphere of cost containment, care decisions are too often dictated by shortsighted formulary lists, not sound clinical reasoning. In this case, the use of more cost-effective drugs with well-documented higher toxicity ultimately led to excess disability, which in turn required increased effort (and cost) by the treatment team.

Psychosocial interventions can be time-consuming, but they might have prevented Mrs. S’ rapid decline and saved substantial staff time. A higher-functioning patient uses far fewer staff resources, and the added expense of treating a hip fracture exceeds any savings from the use of a lessexpensive medication.

Related resources

• Salzman C. Psychiatric medications for older adults–the concise guide. New York: Guilford Press, 2001
• Jacobson SA, Pies RW, Greenblatt DJ. Handbook of geriatric psychopharmacology. Washington DC: American Psychiatric Publishing, 2002.

Drug brand names

• Amitriptyline • Elavil
• Bupropion • Wellbutrin
• Clozapine • Clozaril
• Donepezil • Aricept
• Galantamine • Reminyl
• Haloperidol • Haldol
• Imipramine • Tofranil
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Rivastigmine • Exelon
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

Dr. Verma reports that he is on the speakers bureau of Eli Lilly and Co. and Abbott Laboratories, serves as a consultant to Eli Lilly and Co., and receives grant support from Eli Lilly and Co. and GlaxoSmithKline.

With obesity on the rise, more people are seeking alternatives to failed diets, grueling exercise regimens, and prescription weight-loss agents with troublesome side effects.

Bariatric surgery offers hope to morbidly obese persons (defined as having a body mass index [BMI] 40 kg/m²) and to those with a BMI >34 kg/m² who suffer hypertension, diabetes, and other comorbidities. The procedure produces significant short-term gains (diminished binge eating, weight loss, alleviation of depressed mood) and long-term benefits (improved self-image; increased HDL; lower apoprotein beta-containing lipoproteins; and lower LDL, blood pressure, and fasting blood glucose).

Too often, however, patients see bariatric surgery as a quick fix. Although hunger and stomach capacity are reduced, some patients do eat compulsively,¹ and many regain weight after surgery. Patients also may not realize that they must make extensive lifestyle changes and adjust psychologically to life as a normal-weight person.

Suicide is a major cause of postoperative death, either because of poor psychosocial adjustment or the emergence of an occult personality disorder. Continued alcohol consumption and noncompliance with prescribed vitamin or mineral regimens can also be fatal.

Gauging patient readiness

A preoperative psychiatric evaluation can uncover mental disorders and other risk factors for postoperative noncompliance. Evaluate the following issues:

• What caused or contributed to the patient’s obesity? Bariatric surgery candidates have a high prevalence of psychopathology, including major depression, binge eating, and personality disorders.^2,3 Untreated depression, bulimia, suicidality, and substance abuse are contraindications to bariatric surgery. Pre-existing major depression and binge-eating disorder are not, however.
• How does the patient perceive his or her body? Patients who have unrealistic perceptions about their bodies, such as those with eating disorders or psychoses, are poor surgical candidates. Such patients are unlikely to be satisfied with their postoperative body size.
• Why has the patient chosen to undergo bariatric surgery at this time? Ask whether he or she views it as a major procedure, and determine his or her level of conviction about receiving the surgery.
• Can the patient expect support from family and friends? Undue pressure from family members, such as a significant other’s dissatisfaction with the patient’s pre-operative body size, may lead to postoperative psychosocial maladjustment. A collateral history may be useful.
• Is the patient aware that postoperative behavioral changes will be needed? People will treat the patient differently and may even comment frequently about his or her new body size. Moreover, instead of eating as a coping mechanism, patients will need to find other ways to deal with unpleasant emotions.
• Does the patient understand the postoperative requirements? Reiterate that the patient must participate in group psychotherapy and follow postoperative instructions. The patient’s history of dieting, exercise, and weight-loss prescriptions may offer clues to prospective post-op compliance. Patients who have not complied with less invasive measures are not likely to be compliant after bariatric surgery.

Finally, to prevent miscommunication between patient and provider, ask the surgeon what he or she has told the patient about the procedure. A Minnesota Multiphasic Personality Inventory test can help confirm psychiatric diagnoses and determine whether the patient is being candid.

With obesity on the rise, more people are seeking alternatives to failed diets, grueling exercise regimens, and prescription weight-loss agents with troublesome side effects.

Bariatric surgery offers hope to morbidly obese persons (defined as having a body mass index [BMI] 40 kg/m²) and to those with a BMI >34 kg/m² who suffer hypertension, diabetes, and other comorbidities. The procedure produces significant short-term gains (diminished binge eating, weight loss, alleviation of depressed mood) and long-term benefits (improved self-image; increased HDL; lower apoprotein beta-containing lipoproteins; and lower LDL, blood pressure, and fasting blood glucose).

Too often, however, patients see bariatric surgery as a quick fix. Although hunger and stomach capacity are reduced, some patients do eat compulsively,¹ and many regain weight after surgery. Patients also may not realize that they must make extensive lifestyle changes and adjust psychologically to life as a normal-weight person.

Suicide is a major cause of postoperative death, either because of poor psychosocial adjustment or the emergence of an occult personality disorder. Continued alcohol consumption and noncompliance with prescribed vitamin or mineral regimens can also be fatal.

Gauging patient readiness

A preoperative psychiatric evaluation can uncover mental disorders and other risk factors for postoperative noncompliance. Evaluate the following issues:

• What caused or contributed to the patient’s obesity? Bariatric surgery candidates have a high prevalence of psychopathology, including major depression, binge eating, and personality disorders.^2,3 Untreated depression, bulimia, suicidality, and substance abuse are contraindications to bariatric surgery. Pre-existing major depression and binge-eating disorder are not, however.
• How does the patient perceive his or her body? Patients who have unrealistic perceptions about their bodies, such as those with eating disorders or psychoses, are poor surgical candidates. Such patients are unlikely to be satisfied with their postoperative body size.
• Why has the patient chosen to undergo bariatric surgery at this time? Ask whether he or she views it as a major procedure, and determine his or her level of conviction about receiving the surgery.
• Can the patient expect support from family and friends? Undue pressure from family members, such as a significant other’s dissatisfaction with the patient’s pre-operative body size, may lead to postoperative psychosocial maladjustment. A collateral history may be useful.
• Is the patient aware that postoperative behavioral changes will be needed? People will treat the patient differently and may even comment frequently about his or her new body size. Moreover, instead of eating as a coping mechanism, patients will need to find other ways to deal with unpleasant emotions.
• Does the patient understand the postoperative requirements? Reiterate that the patient must participate in group psychotherapy and follow postoperative instructions. The patient’s history of dieting, exercise, and weight-loss prescriptions may offer clues to prospective post-op compliance. Patients who have not complied with less invasive measures are not likely to be compliant after bariatric surgery.

Finally, to prevent miscommunication between patient and provider, ask the surgeon what he or she has told the patient about the procedure. A Minnesota Multiphasic Personality Inventory test can help confirm psychiatric diagnoses and determine whether the patient is being candid.

With obesity on the rise, more people are seeking alternatives to failed diets, grueling exercise regimens, and prescription weight-loss agents with troublesome side effects.

Bariatric surgery offers hope to morbidly obese persons (defined as having a body mass index [BMI] 40 kg/m²) and to those with a BMI >34 kg/m² who suffer hypertension, diabetes, and other comorbidities. The procedure produces significant short-term gains (diminished binge eating, weight loss, alleviation of depressed mood) and long-term benefits (improved self-image; increased HDL; lower apoprotein beta-containing lipoproteins; and lower LDL, blood pressure, and fasting blood glucose).

Too often, however, patients see bariatric surgery as a quick fix. Although hunger and stomach capacity are reduced, some patients do eat compulsively,¹ and many regain weight after surgery. Patients also may not realize that they must make extensive lifestyle changes and adjust psychologically to life as a normal-weight person.

Suicide is a major cause of postoperative death, either because of poor psychosocial adjustment or the emergence of an occult personality disorder. Continued alcohol consumption and noncompliance with prescribed vitamin or mineral regimens can also be fatal.

Gauging patient readiness

A preoperative psychiatric evaluation can uncover mental disorders and other risk factors for postoperative noncompliance. Evaluate the following issues:

• What caused or contributed to the patient’s obesity? Bariatric surgery candidates have a high prevalence of psychopathology, including major depression, binge eating, and personality disorders.^2,3 Untreated depression, bulimia, suicidality, and substance abuse are contraindications to bariatric surgery. Pre-existing major depression and binge-eating disorder are not, however.
• How does the patient perceive his or her body? Patients who have unrealistic perceptions about their bodies, such as those with eating disorders or psychoses, are poor surgical candidates. Such patients are unlikely to be satisfied with their postoperative body size.
• Why has the patient chosen to undergo bariatric surgery at this time? Ask whether he or she views it as a major procedure, and determine his or her level of conviction about receiving the surgery.
• Can the patient expect support from family and friends? Undue pressure from family members, such as a significant other’s dissatisfaction with the patient’s pre-operative body size, may lead to postoperative psychosocial maladjustment. A collateral history may be useful.
• Is the patient aware that postoperative behavioral changes will be needed? People will treat the patient differently and may even comment frequently about his or her new body size. Moreover, instead of eating as a coping mechanism, patients will need to find other ways to deal with unpleasant emotions.
• Does the patient understand the postoperative requirements? Reiterate that the patient must participate in group psychotherapy and follow postoperative instructions. The patient’s history of dieting, exercise, and weight-loss prescriptions may offer clues to prospective post-op compliance. Patients who have not complied with less invasive measures are not likely to be compliant after bariatric surgery.

Finally, to prevent miscommunication between patient and provider, ask the surgeon what he or she has told the patient about the procedure. A Minnesota Multiphasic Personality Inventory test can help confirm psychiatric diagnoses and determine whether the patient is being candid.