Lauren Swager, MD

CASE Paranoid and confused

Mr. P, age 46, presents to the emergency department (ED) with a chief complaint of feeling “very weird.” Although he has seen a number of psychiatrists in the past, he does not recall being given a specific diagnosis. He describes his feelings as “1 minute I am fine and the next minute I am confused.” He endorses feeling paranoid for the past 6 to 12 months and reports a history of passive suicidal ideations. On the day he presents to the ED, however, he has a specific plan to shoot himself. He does not report audiovisual hallucinations, but has noticed that he talks to himself often.

Mr. P reports feeling worthless at times. He has a history of manic symptoms, including decreased need for sleep and hypersexuality. He describes verbal and sexual abuse by his foster parents. Mr. P reports using Cannabis and opioids occasionally and to drinking every “now and then” but not every day. He denies using benzodiazepines. When he is evaluated, he is not taking any medication and has no significant medical problems. Mr. P reports a history of several hospitalizations, but he could not describe the reasons or timing of past admissions.

Mr. P has a 10^th-grade education. He lives with his fiancée, who reports that he has been behaving oddly for some time. She noticed that he has memory problems and describes violent behavior, such as shaking his fist at her, breaking the television, and attempting to cut his throat once when he was “intoxicated.” She says she does not feel safe around him because of his labile mood and history of
aggression. She confirms that Mr. P does not drink daily but binge-drinks at times.

Initial mental status examination of evaluation reveals hyperverbal, rapid speech. Mr. P is circumstantial and tangential in his thought process. He has poor judgment and insight and exhibits suicidal ideations with a plan. Toxicology screening reveals a blood alcohol level of 50 mg/dL and is positive for Cannabis and opiates.

Which condition most likely accounts for Mr. P’s presentation?
    a) bipolar disorder, currently manic
    b) substance-induced mood disorder
    c) cognitive disorder
    d) delirium


TREATMENT Rapid improvement

From the ED, Mr. P was admitted to an inpatient psychiatric unit, where he was found initially to be disoriented to time, place, and person. His thought process remained disorganized and irrational, with significant memory difficulties. He is noted to have an unsteady gait. Nursing staff observes that Mr. P has significant difficulties with activities of daily living and requires assistance. He talks in circles
and uses nonsensical words.

His serum vitamin B₁₂ level, folate level, rapid plasma reagin, magnesium level, and thiamine level are within normal limits; CT scan of the brain is unremarkable. Neuropsychological testing reveals significant and diffuse cognitive deficits suggestive of frontal lobe dysfunction. He is deemed to not have decision-making capacity; because he has no family, his fiancée is appointed as his temporary health care proxy.

Thiamine and lorazepam are prescribed as needed because of Mr. P’s history of alcohol abuse. However, it’s determined that he does not need lorazepam because his vital signs are stable and there is no evidence of alcohol withdrawal symptoms.

During the course of his 10-day hospitalization, Mr. P’s cognitive difficulties resolved. He regains orientation to time, place, and person. He gains skill in all his activities of daily living, to the point of independence, and is discharged with minimal supervision. Vitamin B supplementation is prescribed, with close follow up in an outpatient day program. MRI/SPECT scan is considered to rule out frontotemporal dementia as recommended by the results of his neurocognitive testing profile.

Which condition likely account for Mr. P’s presentation during inpatient hospitalization?
    a) Wernicke’s encephalopathy
    b) Korsakoff’s syndrome
    c) malingering
    d) frontotemporal dementia
    e) a neurodegenerative disease

The author's observations

Mr. P’s fluctuating mental status, gait instability, and confabulation create high suspicion for Wernicke’s encephalopathy; his dramatic improvement with IV thiamine supports that diagnosis. Mr. P attends the outpatient day program once after his discharge, and is then lost to follow-up.

During inpatient stay, Mr. P eventually admits to binge drinking several times a week, and drinking early in the morning, which would continue throughout the day. His significant cognitive deficits revealed by neuropsychological testing suggests consideration of a differential diagnosis of multifactorial cognitive dysfunction because of:
   • long-term substance use
   • Korsakoff’s syndrome
   • frontotemporal dementia
   • a neurodegenerative disease
   • malingering (Table 1).

Wernicke’s encephalopathy
Wernicke’s encephalopathy is a life-threatening neurologic disorder caused by thiamine deficiency. The disease is rare, catastrophic in onset, and clinically complex¹; as in Mr. P’s case, diagnosis often is delayed. In autopsy studies, the reported prevalence of Wernicke’s encephalopathy is 0.4% to 2.8%.1 Wernicke’s encephalopathy was suspected before death in 33% of alcohol-dependent patientsand 6% of nonalcoholics.¹ Other causes of Wernicke’s encephalopathy include cancer, gastrointestinal surgery, hyperemesis gravidarum, a starvation or malnutrition state, GI tract disease, AIDS, parenteral nutrition, repetitive vomiting, and infection.¹

Diagnosis. Making the correct diagnosis is challenging because the clinical presentation can be variable. No lab or imaging studies confirm the diagnosis. The triad of signs considered to support the diagnosis include ocular signs such as nystagmus, cerebellar signs, and confusion. These signs occur in only 8% to 10% of patients in whom the diagnosis likely.^1,2

Attempts to increase the likelihood of making an accurate lifetime diagnosis of
Wernicke’s encephalopathy include expanding the focus to 8 clinical domains:
   • dietary deficiency
   • eye signs
   • cerebellar signs
   • seizures
   • frontal lobe dysfunction
   • amnesia
   • mild memory impairment
   • altered mental status.¹

The sensitivity of making a correct diagnosis increases to 85% if at least 2 of 4 features—namely dietary deficiency, eye signs, cerebellar signs, memory impairment, and altered mental status—are present. These criteria can be applied to alcoholic and nonalcoholic patients.¹Table 2_³ lists common and uncommon symptoms of Wernicke’s encephalopathy.

Although CT scan of the brain is not a reliable test for the disorder, MRI can be powerful tool that could support a diagnosis of acute Wernicke’s encephalopathy.¹ We did not consider MRI in Mr. P’s case because the consulting neurologist thought this was unnecessary because of the quick improvement in his cognitive status with IV thiamine—although MRI might have helped to detect the disease earlier. In some studies, brain MRI revealed lesions in two-thirds of Wernicke’s encephalopathy patients.¹ Typically, lesions are symmetrical and seen in the thalamus, mammillary body, and periaqueductal areas.^1,4 Atypical lesions commonly are seen in the cerebellum, dentate nuclei, caudate nucleus, and cerebral cortex.¹

Treatment. Evidence supports use of IV thiamine, 200 mg 3 times a day, when the disease is suspected or established.^1,2 Thiamine has been associated with sporadic anaphylactic reactions, and should be administered when resuscitation facilities are available. Do not delay treatment because resuscitation measures are unavailable because you risk causing irreversible brain damage.¹

In Mr. P’s case, prompt recognition of the need for thiamine likely led to a better outcome. Thiamine supplementation can prevent Wernicke’s encephalopathy in some patients. Prophylactic parenteral administration of thiamine before administration of glucose in the ED is recommended, as well as vitamin B supplementation with thiamine included upon discharge.^1,2 Studies support several treatment regimens for patients with Wernicke’s encephalopathy and those at risk of it.^1,3,5

Neither the optimal dosage of thiamine nor the appropriate duration of treatment have been determined by randomized, double-blind, controlled studies; empirical clinical practice and recommendations by Royal College of Physicians, London, suggest that a more prolonged course of thiamine—administered as long as improvement continues—might be beneficial.⁶

Left untreated, Wernicke’s encephalopathy can lead to irreversible brain damage.²
Mortality has been reported as 17% to 20%; 82% of patients develop Korsakoff’s syndrome, a chronic condition characterized by short-term memory loss. One-quarter of patients who develop Korsakoff’s syndrome require long-term residential care because of permanent brain damage.²

Making a diagnosis of Wernicke’s encephalopathy is a challenge because no specific symptom or diagnostic test can be relied upon to confirm the diagnosis. Also, patients might deny that they have an alcohol problem or give an inaccurate history of their alcohol use,² as Mr. P did. The disorder is substantially underdiagnosed; as a consequence, patients are at risk of brain damage.²

Bottom Line

Not all patients who present with aggressive behavior, mania, and psychiatric
symptoms have a primary psychiatric diagnosis. It is important to consider
nutritional deficiencies caused by chronic alcohol abuse in patients presenting
with acute onset of confusion or altered mental status. Wernicke’s encephalopathy
might be the result of alcohol abuse and can be treated with IV thiamine.

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

CASE Paranoid and confused

Mr. P, age 46, presents to the emergency department (ED) with a chief complaint of feeling “very weird.” Although he has seen a number of psychiatrists in the past, he does not recall being given a specific diagnosis. He describes his feelings as “1 minute I am fine and the next minute I am confused.” He endorses feeling paranoid for the past 6 to 12 months and reports a history of passive suicidal ideations. On the day he presents to the ED, however, he has a specific plan to shoot himself. He does not report audiovisual hallucinations, but has noticed that he talks to himself often.

Mr. P reports feeling worthless at times. He has a history of manic symptoms, including decreased need for sleep and hypersexuality. He describes verbal and sexual abuse by his foster parents. Mr. P reports using Cannabis and opioids occasionally and to drinking every “now and then” but not every day. He denies using benzodiazepines. When he is evaluated, he is not taking any medication and has no significant medical problems. Mr. P reports a history of several hospitalizations, but he could not describe the reasons or timing of past admissions.

Mr. P has a 10^th-grade education. He lives with his fiancée, who reports that he has been behaving oddly for some time. She noticed that he has memory problems and describes violent behavior, such as shaking his fist at her, breaking the television, and attempting to cut his throat once when he was “intoxicated.” She says she does not feel safe around him because of his labile mood and history of
aggression. She confirms that Mr. P does not drink daily but binge-drinks at times.

Initial mental status examination of evaluation reveals hyperverbal, rapid speech. Mr. P is circumstantial and tangential in his thought process. He has poor judgment and insight and exhibits suicidal ideations with a plan. Toxicology screening reveals a blood alcohol level of 50 mg/dL and is positive for Cannabis and opiates.

Which condition most likely accounts for Mr. P’s presentation?
    a) bipolar disorder, currently manic
    b) substance-induced mood disorder
    c) cognitive disorder
    d) delirium


TREATMENT Rapid improvement

From the ED, Mr. P was admitted to an inpatient psychiatric unit, where he was found initially to be disoriented to time, place, and person. His thought process remained disorganized and irrational, with significant memory difficulties. He is noted to have an unsteady gait. Nursing staff observes that Mr. P has significant difficulties with activities of daily living and requires assistance. He talks in circles
and uses nonsensical words.

His serum vitamin B₁₂ level, folate level, rapid plasma reagin, magnesium level, and thiamine level are within normal limits; CT scan of the brain is unremarkable. Neuropsychological testing reveals significant and diffuse cognitive deficits suggestive of frontal lobe dysfunction. He is deemed to not have decision-making capacity; because he has no family, his fiancée is appointed as his temporary health care proxy.

Thiamine and lorazepam are prescribed as needed because of Mr. P’s history of alcohol abuse. However, it’s determined that he does not need lorazepam because his vital signs are stable and there is no evidence of alcohol withdrawal symptoms.

During the course of his 10-day hospitalization, Mr. P’s cognitive difficulties resolved. He regains orientation to time, place, and person. He gains skill in all his activities of daily living, to the point of independence, and is discharged with minimal supervision. Vitamin B supplementation is prescribed, with close follow up in an outpatient day program. MRI/SPECT scan is considered to rule out frontotemporal dementia as recommended by the results of his neurocognitive testing profile.

Which condition likely account for Mr. P’s presentation during inpatient hospitalization?
    a) Wernicke’s encephalopathy
    b) Korsakoff’s syndrome
    c) malingering
    d) frontotemporal dementia
    e) a neurodegenerative disease

The author's observations

Mr. P’s fluctuating mental status, gait instability, and confabulation create high suspicion for Wernicke’s encephalopathy; his dramatic improvement with IV thiamine supports that diagnosis. Mr. P attends the outpatient day program once after his discharge, and is then lost to follow-up.

During inpatient stay, Mr. P eventually admits to binge drinking several times a week, and drinking early in the morning, which would continue throughout the day. His significant cognitive deficits revealed by neuropsychological testing suggests consideration of a differential diagnosis of multifactorial cognitive dysfunction because of:
   • long-term substance use
   • Korsakoff’s syndrome
   • frontotemporal dementia
   • a neurodegenerative disease
   • malingering (Table 1).

Wernicke’s encephalopathy
Wernicke’s encephalopathy is a life-threatening neurologic disorder caused by thiamine deficiency. The disease is rare, catastrophic in onset, and clinically complex¹; as in Mr. P’s case, diagnosis often is delayed. In autopsy studies, the reported prevalence of Wernicke’s encephalopathy is 0.4% to 2.8%.1 Wernicke’s encephalopathy was suspected before death in 33% of alcohol-dependent patientsand 6% of nonalcoholics.¹ Other causes of Wernicke’s encephalopathy include cancer, gastrointestinal surgery, hyperemesis gravidarum, a starvation or malnutrition state, GI tract disease, AIDS, parenteral nutrition, repetitive vomiting, and infection.¹

Diagnosis. Making the correct diagnosis is challenging because the clinical presentation can be variable. No lab or imaging studies confirm the diagnosis. The triad of signs considered to support the diagnosis include ocular signs such as nystagmus, cerebellar signs, and confusion. These signs occur in only 8% to 10% of patients in whom the diagnosis likely.^1,2

Attempts to increase the likelihood of making an accurate lifetime diagnosis of
Wernicke’s encephalopathy include expanding the focus to 8 clinical domains:
   • dietary deficiency
   • eye signs
   • cerebellar signs
   • seizures
   • frontal lobe dysfunction
   • amnesia
   • mild memory impairment
   • altered mental status.¹

The sensitivity of making a correct diagnosis increases to 85% if at least 2 of 4 features—namely dietary deficiency, eye signs, cerebellar signs, memory impairment, and altered mental status—are present. These criteria can be applied to alcoholic and nonalcoholic patients.¹Table 2_³ lists common and uncommon symptoms of Wernicke’s encephalopathy.

Although CT scan of the brain is not a reliable test for the disorder, MRI can be powerful tool that could support a diagnosis of acute Wernicke’s encephalopathy.¹ We did not consider MRI in Mr. P’s case because the consulting neurologist thought this was unnecessary because of the quick improvement in his cognitive status with IV thiamine—although MRI might have helped to detect the disease earlier. In some studies, brain MRI revealed lesions in two-thirds of Wernicke’s encephalopathy patients.¹ Typically, lesions are symmetrical and seen in the thalamus, mammillary body, and periaqueductal areas.^1,4 Atypical lesions commonly are seen in the cerebellum, dentate nuclei, caudate nucleus, and cerebral cortex.¹

Treatment. Evidence supports use of IV thiamine, 200 mg 3 times a day, when the disease is suspected or established.^1,2 Thiamine has been associated with sporadic anaphylactic reactions, and should be administered when resuscitation facilities are available. Do not delay treatment because resuscitation measures are unavailable because you risk causing irreversible brain damage.¹

In Mr. P’s case, prompt recognition of the need for thiamine likely led to a better outcome. Thiamine supplementation can prevent Wernicke’s encephalopathy in some patients. Prophylactic parenteral administration of thiamine before administration of glucose in the ED is recommended, as well as vitamin B supplementation with thiamine included upon discharge.^1,2 Studies support several treatment regimens for patients with Wernicke’s encephalopathy and those at risk of it.^1,3,5

Neither the optimal dosage of thiamine nor the appropriate duration of treatment have been determined by randomized, double-blind, controlled studies; empirical clinical practice and recommendations by Royal College of Physicians, London, suggest that a more prolonged course of thiamine—administered as long as improvement continues—might be beneficial.⁶

Left untreated, Wernicke’s encephalopathy can lead to irreversible brain damage.²
Mortality has been reported as 17% to 20%; 82% of patients develop Korsakoff’s syndrome, a chronic condition characterized by short-term memory loss. One-quarter of patients who develop Korsakoff’s syndrome require long-term residential care because of permanent brain damage.²

Making a diagnosis of Wernicke’s encephalopathy is a challenge because no specific symptom or diagnostic test can be relied upon to confirm the diagnosis. Also, patients might deny that they have an alcohol problem or give an inaccurate history of their alcohol use,² as Mr. P did. The disorder is substantially underdiagnosed; as a consequence, patients are at risk of brain damage.²

Bottom Line

Not all patients who present with aggressive behavior, mania, and psychiatric
symptoms have a primary psychiatric diagnosis. It is important to consider
nutritional deficiencies caused by chronic alcohol abuse in patients presenting
with acute onset of confusion or altered mental status. Wernicke’s encephalopathy
might be the result of alcohol abuse and can be treated with IV thiamine.

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

CASE Paranoid and confused

Mr. P, age 46, presents to the emergency department (ED) with a chief complaint of feeling “very weird.” Although he has seen a number of psychiatrists in the past, he does not recall being given a specific diagnosis. He describes his feelings as “1 minute I am fine and the next minute I am confused.” He endorses feeling paranoid for the past 6 to 12 months and reports a history of passive suicidal ideations. On the day he presents to the ED, however, he has a specific plan to shoot himself. He does not report audiovisual hallucinations, but has noticed that he talks to himself often.

Mr. P reports feeling worthless at times. He has a history of manic symptoms, including decreased need for sleep and hypersexuality. He describes verbal and sexual abuse by his foster parents. Mr. P reports using Cannabis and opioids occasionally and to drinking every “now and then” but not every day. He denies using benzodiazepines. When he is evaluated, he is not taking any medication and has no significant medical problems. Mr. P reports a history of several hospitalizations, but he could not describe the reasons or timing of past admissions.

Mr. P has a 10^th-grade education. He lives with his fiancée, who reports that he has been behaving oddly for some time. She noticed that he has memory problems and describes violent behavior, such as shaking his fist at her, breaking the television, and attempting to cut his throat once when he was “intoxicated.” She says she does not feel safe around him because of his labile mood and history of
aggression. She confirms that Mr. P does not drink daily but binge-drinks at times.

Initial mental status examination of evaluation reveals hyperverbal, rapid speech. Mr. P is circumstantial and tangential in his thought process. He has poor judgment and insight and exhibits suicidal ideations with a plan. Toxicology screening reveals a blood alcohol level of 50 mg/dL and is positive for Cannabis and opiates.

Which condition most likely accounts for Mr. P’s presentation?
    a) bipolar disorder, currently manic
    b) substance-induced mood disorder
    c) cognitive disorder
    d) delirium


TREATMENT Rapid improvement

From the ED, Mr. P was admitted to an inpatient psychiatric unit, where he was found initially to be disoriented to time, place, and person. His thought process remained disorganized and irrational, with significant memory difficulties. He is noted to have an unsteady gait. Nursing staff observes that Mr. P has significant difficulties with activities of daily living and requires assistance. He talks in circles
and uses nonsensical words.

His serum vitamin B₁₂ level, folate level, rapid plasma reagin, magnesium level, and thiamine level are within normal limits; CT scan of the brain is unremarkable. Neuropsychological testing reveals significant and diffuse cognitive deficits suggestive of frontal lobe dysfunction. He is deemed to not have decision-making capacity; because he has no family, his fiancée is appointed as his temporary health care proxy.

Thiamine and lorazepam are prescribed as needed because of Mr. P’s history of alcohol abuse. However, it’s determined that he does not need lorazepam because his vital signs are stable and there is no evidence of alcohol withdrawal symptoms.

During the course of his 10-day hospitalization, Mr. P’s cognitive difficulties resolved. He regains orientation to time, place, and person. He gains skill in all his activities of daily living, to the point of independence, and is discharged with minimal supervision. Vitamin B supplementation is prescribed, with close follow up in an outpatient day program. MRI/SPECT scan is considered to rule out frontotemporal dementia as recommended by the results of his neurocognitive testing profile.

Which condition likely account for Mr. P’s presentation during inpatient hospitalization?
    a) Wernicke’s encephalopathy
    b) Korsakoff’s syndrome
    c) malingering
    d) frontotemporal dementia
    e) a neurodegenerative disease

The author's observations

Mr. P’s fluctuating mental status, gait instability, and confabulation create high suspicion for Wernicke’s encephalopathy; his dramatic improvement with IV thiamine supports that diagnosis. Mr. P attends the outpatient day program once after his discharge, and is then lost to follow-up.

During inpatient stay, Mr. P eventually admits to binge drinking several times a week, and drinking early in the morning, which would continue throughout the day. His significant cognitive deficits revealed by neuropsychological testing suggests consideration of a differential diagnosis of multifactorial cognitive dysfunction because of:
   • long-term substance use
   • Korsakoff’s syndrome
   • frontotemporal dementia
   • a neurodegenerative disease
   • malingering (Table 1).

Wernicke’s encephalopathy
Wernicke’s encephalopathy is a life-threatening neurologic disorder caused by thiamine deficiency. The disease is rare, catastrophic in onset, and clinically complex¹; as in Mr. P’s case, diagnosis often is delayed. In autopsy studies, the reported prevalence of Wernicke’s encephalopathy is 0.4% to 2.8%.1 Wernicke’s encephalopathy was suspected before death in 33% of alcohol-dependent patientsand 6% of nonalcoholics.¹ Other causes of Wernicke’s encephalopathy include cancer, gastrointestinal surgery, hyperemesis gravidarum, a starvation or malnutrition state, GI tract disease, AIDS, parenteral nutrition, repetitive vomiting, and infection.¹

Diagnosis. Making the correct diagnosis is challenging because the clinical presentation can be variable. No lab or imaging studies confirm the diagnosis. The triad of signs considered to support the diagnosis include ocular signs such as nystagmus, cerebellar signs, and confusion. These signs occur in only 8% to 10% of patients in whom the diagnosis likely.^1,2

Attempts to increase the likelihood of making an accurate lifetime diagnosis of
Wernicke’s encephalopathy include expanding the focus to 8 clinical domains:
   • dietary deficiency
   • eye signs
   • cerebellar signs
   • seizures
   • frontal lobe dysfunction
   • amnesia
   • mild memory impairment
   • altered mental status.¹

The sensitivity of making a correct diagnosis increases to 85% if at least 2 of 4 features—namely dietary deficiency, eye signs, cerebellar signs, memory impairment, and altered mental status—are present. These criteria can be applied to alcoholic and nonalcoholic patients.¹Table 2_³ lists common and uncommon symptoms of Wernicke’s encephalopathy.

Although CT scan of the brain is not a reliable test for the disorder, MRI can be powerful tool that could support a diagnosis of acute Wernicke’s encephalopathy.¹ We did not consider MRI in Mr. P’s case because the consulting neurologist thought this was unnecessary because of the quick improvement in his cognitive status with IV thiamine—although MRI might have helped to detect the disease earlier. In some studies, brain MRI revealed lesions in two-thirds of Wernicke’s encephalopathy patients.¹ Typically, lesions are symmetrical and seen in the thalamus, mammillary body, and periaqueductal areas.^1,4 Atypical lesions commonly are seen in the cerebellum, dentate nuclei, caudate nucleus, and cerebral cortex.¹

Treatment. Evidence supports use of IV thiamine, 200 mg 3 times a day, when the disease is suspected or established.^1,2 Thiamine has been associated with sporadic anaphylactic reactions, and should be administered when resuscitation facilities are available. Do not delay treatment because resuscitation measures are unavailable because you risk causing irreversible brain damage.¹

In Mr. P’s case, prompt recognition of the need for thiamine likely led to a better outcome. Thiamine supplementation can prevent Wernicke’s encephalopathy in some patients. Prophylactic parenteral administration of thiamine before administration of glucose in the ED is recommended, as well as vitamin B supplementation with thiamine included upon discharge.^1,2 Studies support several treatment regimens for patients with Wernicke’s encephalopathy and those at risk of it.^1,3,5

Neither the optimal dosage of thiamine nor the appropriate duration of treatment have been determined by randomized, double-blind, controlled studies; empirical clinical practice and recommendations by Royal College of Physicians, London, suggest that a more prolonged course of thiamine—administered as long as improvement continues—might be beneficial.⁶

Left untreated, Wernicke’s encephalopathy can lead to irreversible brain damage.²
Mortality has been reported as 17% to 20%; 82% of patients develop Korsakoff’s syndrome, a chronic condition characterized by short-term memory loss. One-quarter of patients who develop Korsakoff’s syndrome require long-term residential care because of permanent brain damage.²

Making a diagnosis of Wernicke’s encephalopathy is a challenge because no specific symptom or diagnostic test can be relied upon to confirm the diagnosis. Also, patients might deny that they have an alcohol problem or give an inaccurate history of their alcohol use,² as Mr. P did. The disorder is substantially underdiagnosed; as a consequence, patients are at risk of brain damage.²

Bottom Line

Not all patients who present with aggressive behavior, mania, and psychiatric
symptoms have a primary psychiatric diagnosis. It is important to consider
nutritional deficiencies caused by chronic alcohol abuse in patients presenting
with acute onset of confusion or altered mental status. Wernicke’s encephalopathy
might be the result of alcohol abuse and can be treated with IV thiamine.

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

CASE Angry and depressed

Y is a 16-year-old male who presents with his mother to our clinic for medication evaluation because of anger issues and problems learning in school. He says he has been feeling depressed for several months and noticed significant irritability. Y sleeps excessively, sometimes for more than 12 hours a day, and eats more than he usually does. He reports feeling hopeless, helpless, and guilty for letting his family down. Y, who is in the 10th grade, acknowledges trouble focusing and concentrating but attributed this to a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD). He stopped taking his stimulant medication several months ago because he did not like taking it. He denies thoughts of self-harm or thinking about death.

Y’s mother reports that her son had been athletic but had to stop playing football because he has had 5 concussions. Y’s inability to play sports appears to be a precipitating factor in his decline in mood (Box). He had his first concussion at age 13; the last one was several months before his presenting to the clinic. Y experienced loss of consciousness and unsteady gait after his concussions and was hospitalized for some of them. Y says his life goals are “playing sports and being a marine,” which may be compromised because of his head injuries.

His mother reports Y is having more anger outbursts and says his personality is changing. Y viewed this change as just being more assertive and fails to see that others may be scared by his behavior. He is getting into more fights at school and is more impulsive and unpredictable, according to his mother. Y is struggling in school with cognitive deficits and memory problems; his grade point average (GPA) drops from 3.5 to 0.3 over several months. He had been homeschooled initially because of uncontrolled impulsivity and aggression, but was reintegrated to public school. Y has a history of a mathematics disorder but had done well without school accommodations before the head injuries. Lack of access to his peers and poor self-esteem because of his declining grades are making his mood worse. He denies a history of substance use and his urine drug screen is negative.

Recently, Y’s grandfather, with whom he had been close, died and 2 friends were killed in car accidents in the last few years. Y has no history of psychiatric hospitalization. He had seen a psychotherapist for depression. He had been on lisdexamfetamine, 30 mg/d, citalopram, 10 mg/d, and an unknown dose of dextroamphetamine. He had no major medical comorbidities. He lives with his mother. His parents are separated but he has frequent contact with his father. His developmental history is unremarkable. There was a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. There was no family history of suicide.

On his initial mental status examination, Y appears to be his stated age and is dressed appropriately. He is well dressed, suggesting that he puts a lot of care into his personal appearance. He is alert and oriented. He is cooperative and has fair eye contact. His gait is normal and no motor abnormalities are evident. His speech is normal in rate, rhythm, and volume. He can remember events with great accuracy. He reports that his mood is depressed and “down.” His affect appears irritable and he has low frustration tolerance, especially towards his mother. He is easy to anger but is re-directable. He does not endorse thoughts of suicidality or harm to others. He denies auditory or visual hallucinations, and paranoia. He does not appear to be responding to internal stimuli. His judgment and insight are fair.

The authors' observations

Traumatic brain injury (TBI) affects 1.7 to 3.8 million people in the United States. More than 473,000 children present to the emergency room annually with TBI, approximately 75% of whom are given a label of mild TBI in the United States.^1-3 TBI patients present with varying degrees of problems ranging from headaches to cognitive deficits and death. Symptoms may be transient or permanent.⁴ Prepubescent children are at higher risk and are more likely to sustain permanent damage post-TBI, with problems in attention, executive functioning, memory, and cognition.^5-7

Prognosis depends on severity of injury and environmental factors, including socioeconomic status, family dysfunction, and access to resources.⁸ Patients may present during the acute concussion phase with physical symptoms, such as headaches, nausea, vomiting, sensitivity to light and sounds, and memory deficits, and psychiatric complaints such as anger, irritability, and mood swings. Symptoms may persist post-concussion, leading to problems in personal relationships and social and occupational functioning, and neuropsychiatric manifestations, including changes in personality, depression, suicidal thoughts, and substance dependence. As seen in this case, Y had neuropsychiatric manifestations after his TBI but other factors, such as his ADHD diagnosis and the death of his grandfather and friends, may have contributed to his presentation.

Up to one-half of children with brain injuries may be at increased risk for unfavorable behavioral outcomes, which include internalizing and externalizing presentations.⁹ These behavioral problems may emerge several years after the injury and often persist or get worse with time. Behavioral functioning before injury usually dictates long-term outcomes post injury. The American Academy of Neurology recently released guidelines for the assessment and treatment of athletes with concussions (see Related Resources).

TREATMENT Restart medication

We restart Y on citalopram, 10 mg/d, which he tolerated in the past, and increase it to 20 mg/d after 4 days to address his depression and irritability. He also is restarted on lisdexamfetamine, 30 mg/d, for his ADHD. We give his mother the Child Behavior Checklist and Teacher’s Report Forms to gather additional collateral information. We ask Y to follow up in 1 month and we encourage him to continue seeing his psychotherapist.

EVALUATION Testing

Although Y denies feeling depressed to the neuropsychologist, the examiner notes her concerns about his depression based on his mental status examination during testing.

Neuropsychological testing reveals a discrepancy noted between normal verbal skills and perceptual intellectual skills that were in the borderline range (Table). Testing revealed results supporting executive dysfunction and distractibility, which are consistent with his history of ADHD. Y’s broad reading scores are in the 20th percentile and math scores in the 30th percentile. Although he has a history of a mathematics disorder, his reading deficits are considered a decline compared with his previous performance.

The authors' observations

Y is a 16-year-old male who presented with anger, depression, and academic problems. He had genetic loading with a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. Other than his concussions, Y was healthy, however, he had pre-morbid, untreated ADHD. He was doing well academically until his concussions, after which he started to see a steep decline in his grades. He was struggling with low self-esteem, which affected his mood. Multiple contributors perpetuated his difficulties, including, his inability to play sports; being home-schooled; removal from his friends; deaths of close friends and family; and a concern that his medical limitation to refrain from physical activities was affecting his career ambitions, contributing to his sense of hopelessness.

Y responded well to the stimulant and antidepressant, but it is important to note the increased risk of non-compliance in teenagers, even when they report seemingly minor side effects, despite doing well clinically. Y required frequent psychiatric follow up and repeat neuropsychological evaluation to monitor his progress.

OUTCOME Back on the playing field

At Y’s 1 month follow up, he reports feeling less depressed but citalopram, 20 mg/d, makes him feel “plain.” His GPA increases to 2.5 and he completes 10th grade. Lisdexamfetamine is titrated to 60 mg/d, he is focusing at school, and his anger is better controlled. Y’s mother is hesitant to change any medications because of her son’s overall improvement.

A few weeks before his next follow up appointment, Y’s mother calls stating that his depression is worse as he has not been taking citalopram because he doesn’t like how it makes him feel. He is started on fluoxetine, 10 mg/d. At his next appointment, Y says that he tolerates fluoxetine. His mood improves substantially and he is doing much better. Y’s mother says she feel that her son is more social, smiling more, and sleeping and eating better.

Several months after Y’s school performance, mood, and behaviors improve, his physicians give him permission to play non-contact sports. He is excited to play baseball. Because of his symptoms, we recommend continuing treating his ADHD and depressive symptoms and monitoring the need for medication. We discussed with Y nonpharmacotherapeutic options, including access to an individualized education plan at school, individual therapy, and formalized cognitive training.

Bottom Line

Traumatic brain injury (TBI) affects children and adults with long-term sequelae, which affects outcomes. Outcome is dependent on several risk factors. Many patients with TBI also suffer from neuropsychiatric symptoms that affect their functioning at home and in social and occupational settings. Those with premorbid psychiatric conditions need to be closely monitored because they may be at greater risk for problems with mood and executive function. Treatment should be targeted to individual complaints.

Related Resources

• Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24): 2250-2257.
• Reardon CL, Factor RM. Sport psychiatry: a systematic review of diagnosis and medical treatment of mental illness in athletes. Sports Med. 2010;40(11):961-980.

Drug Brand Names

Citalopram • Celexa            Dextroamphetamine • Adderall

Fluoxetine • Prozac             Lisdexamfetamine dimesylate • Vyvanse

Disclosure

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

CASE Angry and depressed

Y is a 16-year-old male who presents with his mother to our clinic for medication evaluation because of anger issues and problems learning in school. He says he has been feeling depressed for several months and noticed significant irritability. Y sleeps excessively, sometimes for more than 12 hours a day, and eats more than he usually does. He reports feeling hopeless, helpless, and guilty for letting his family down. Y, who is in the 10th grade, acknowledges trouble focusing and concentrating but attributed this to a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD). He stopped taking his stimulant medication several months ago because he did not like taking it. He denies thoughts of self-harm or thinking about death.

Y’s mother reports that her son had been athletic but had to stop playing football because he has had 5 concussions. Y’s inability to play sports appears to be a precipitating factor in his decline in mood (Box). He had his first concussion at age 13; the last one was several months before his presenting to the clinic. Y experienced loss of consciousness and unsteady gait after his concussions and was hospitalized for some of them. Y says his life goals are “playing sports and being a marine,” which may be compromised because of his head injuries.

His mother reports Y is having more anger outbursts and says his personality is changing. Y viewed this change as just being more assertive and fails to see that others may be scared by his behavior. He is getting into more fights at school and is more impulsive and unpredictable, according to his mother. Y is struggling in school with cognitive deficits and memory problems; his grade point average (GPA) drops from 3.5 to 0.3 over several months. He had been homeschooled initially because of uncontrolled impulsivity and aggression, but was reintegrated to public school. Y has a history of a mathematics disorder but had done well without school accommodations before the head injuries. Lack of access to his peers and poor self-esteem because of his declining grades are making his mood worse. He denies a history of substance use and his urine drug screen is negative.

Recently, Y’s grandfather, with whom he had been close, died and 2 friends were killed in car accidents in the last few years. Y has no history of psychiatric hospitalization. He had seen a psychotherapist for depression. He had been on lisdexamfetamine, 30 mg/d, citalopram, 10 mg/d, and an unknown dose of dextroamphetamine. He had no major medical comorbidities. He lives with his mother. His parents are separated but he has frequent contact with his father. His developmental history is unremarkable. There was a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. There was no family history of suicide.

On his initial mental status examination, Y appears to be his stated age and is dressed appropriately. He is well dressed, suggesting that he puts a lot of care into his personal appearance. He is alert and oriented. He is cooperative and has fair eye contact. His gait is normal and no motor abnormalities are evident. His speech is normal in rate, rhythm, and volume. He can remember events with great accuracy. He reports that his mood is depressed and “down.” His affect appears irritable and he has low frustration tolerance, especially towards his mother. He is easy to anger but is re-directable. He does not endorse thoughts of suicidality or harm to others. He denies auditory or visual hallucinations, and paranoia. He does not appear to be responding to internal stimuli. His judgment and insight are fair.

The authors' observations

Traumatic brain injury (TBI) affects 1.7 to 3.8 million people in the United States. More than 473,000 children present to the emergency room annually with TBI, approximately 75% of whom are given a label of mild TBI in the United States.^1-3 TBI patients present with varying degrees of problems ranging from headaches to cognitive deficits and death. Symptoms may be transient or permanent.⁴ Prepubescent children are at higher risk and are more likely to sustain permanent damage post-TBI, with problems in attention, executive functioning, memory, and cognition.^5-7

Prognosis depends on severity of injury and environmental factors, including socioeconomic status, family dysfunction, and access to resources.⁸ Patients may present during the acute concussion phase with physical symptoms, such as headaches, nausea, vomiting, sensitivity to light and sounds, and memory deficits, and psychiatric complaints such as anger, irritability, and mood swings. Symptoms may persist post-concussion, leading to problems in personal relationships and social and occupational functioning, and neuropsychiatric manifestations, including changes in personality, depression, suicidal thoughts, and substance dependence. As seen in this case, Y had neuropsychiatric manifestations after his TBI but other factors, such as his ADHD diagnosis and the death of his grandfather and friends, may have contributed to his presentation.

Up to one-half of children with brain injuries may be at increased risk for unfavorable behavioral outcomes, which include internalizing and externalizing presentations.⁹ These behavioral problems may emerge several years after the injury and often persist or get worse with time. Behavioral functioning before injury usually dictates long-term outcomes post injury. The American Academy of Neurology recently released guidelines for the assessment and treatment of athletes with concussions (see Related Resources).

TREATMENT Restart medication

We restart Y on citalopram, 10 mg/d, which he tolerated in the past, and increase it to 20 mg/d after 4 days to address his depression and irritability. He also is restarted on lisdexamfetamine, 30 mg/d, for his ADHD. We give his mother the Child Behavior Checklist and Teacher’s Report Forms to gather additional collateral information. We ask Y to follow up in 1 month and we encourage him to continue seeing his psychotherapist.

EVALUATION Testing

Although Y denies feeling depressed to the neuropsychologist, the examiner notes her concerns about his depression based on his mental status examination during testing.

Neuropsychological testing reveals a discrepancy noted between normal verbal skills and perceptual intellectual skills that were in the borderline range (Table). Testing revealed results supporting executive dysfunction and distractibility, which are consistent with his history of ADHD. Y’s broad reading scores are in the 20th percentile and math scores in the 30th percentile. Although he has a history of a mathematics disorder, his reading deficits are considered a decline compared with his previous performance.

The authors' observations

Y is a 16-year-old male who presented with anger, depression, and academic problems. He had genetic loading with a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. Other than his concussions, Y was healthy, however, he had pre-morbid, untreated ADHD. He was doing well academically until his concussions, after which he started to see a steep decline in his grades. He was struggling with low self-esteem, which affected his mood. Multiple contributors perpetuated his difficulties, including, his inability to play sports; being home-schooled; removal from his friends; deaths of close friends and family; and a concern that his medical limitation to refrain from physical activities was affecting his career ambitions, contributing to his sense of hopelessness.

Y responded well to the stimulant and antidepressant, but it is important to note the increased risk of non-compliance in teenagers, even when they report seemingly minor side effects, despite doing well clinically. Y required frequent psychiatric follow up and repeat neuropsychological evaluation to monitor his progress.

OUTCOME Back on the playing field

At Y’s 1 month follow up, he reports feeling less depressed but citalopram, 20 mg/d, makes him feel “plain.” His GPA increases to 2.5 and he completes 10th grade. Lisdexamfetamine is titrated to 60 mg/d, he is focusing at school, and his anger is better controlled. Y’s mother is hesitant to change any medications because of her son’s overall improvement.

A few weeks before his next follow up appointment, Y’s mother calls stating that his depression is worse as he has not been taking citalopram because he doesn’t like how it makes him feel. He is started on fluoxetine, 10 mg/d. At his next appointment, Y says that he tolerates fluoxetine. His mood improves substantially and he is doing much better. Y’s mother says she feel that her son is more social, smiling more, and sleeping and eating better.

Several months after Y’s school performance, mood, and behaviors improve, his physicians give him permission to play non-contact sports. He is excited to play baseball. Because of his symptoms, we recommend continuing treating his ADHD and depressive symptoms and monitoring the need for medication. We discussed with Y nonpharmacotherapeutic options, including access to an individualized education plan at school, individual therapy, and formalized cognitive training.

Bottom Line

Traumatic brain injury (TBI) affects children and adults with long-term sequelae, which affects outcomes. Outcome is dependent on several risk factors. Many patients with TBI also suffer from neuropsychiatric symptoms that affect their functioning at home and in social and occupational settings. Those with premorbid psychiatric conditions need to be closely monitored because they may be at greater risk for problems with mood and executive function. Treatment should be targeted to individual complaints.

Related Resources

• Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24): 2250-2257.
• Reardon CL, Factor RM. Sport psychiatry: a systematic review of diagnosis and medical treatment of mental illness in athletes. Sports Med. 2010;40(11):961-980.

Drug Brand Names

Citalopram • Celexa            Dextroamphetamine • Adderall

Fluoxetine • Prozac             Lisdexamfetamine dimesylate • Vyvanse

Disclosure

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

CASE Angry and depressed

Y is a 16-year-old male who presents with his mother to our clinic for medication evaluation because of anger issues and problems learning in school. He says he has been feeling depressed for several months and noticed significant irritability. Y sleeps excessively, sometimes for more than 12 hours a day, and eats more than he usually does. He reports feeling hopeless, helpless, and guilty for letting his family down. Y, who is in the 10th grade, acknowledges trouble focusing and concentrating but attributed this to a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD). He stopped taking his stimulant medication several months ago because he did not like taking it. He denies thoughts of self-harm or thinking about death.

Y’s mother reports that her son had been athletic but had to stop playing football because he has had 5 concussions. Y’s inability to play sports appears to be a precipitating factor in his decline in mood (Box). He had his first concussion at age 13; the last one was several months before his presenting to the clinic. Y experienced loss of consciousness and unsteady gait after his concussions and was hospitalized for some of them. Y says his life goals are “playing sports and being a marine,” which may be compromised because of his head injuries.

His mother reports Y is having more anger outbursts and says his personality is changing. Y viewed this change as just being more assertive and fails to see that others may be scared by his behavior. He is getting into more fights at school and is more impulsive and unpredictable, according to his mother. Y is struggling in school with cognitive deficits and memory problems; his grade point average (GPA) drops from 3.5 to 0.3 over several months. He had been homeschooled initially because of uncontrolled impulsivity and aggression, but was reintegrated to public school. Y has a history of a mathematics disorder but had done well without school accommodations before the head injuries. Lack of access to his peers and poor self-esteem because of his declining grades are making his mood worse. He denies a history of substance use and his urine drug screen is negative.

Recently, Y’s grandfather, with whom he had been close, died and 2 friends were killed in car accidents in the last few years. Y has no history of psychiatric hospitalization. He had seen a psychotherapist for depression. He had been on lisdexamfetamine, 30 mg/d, citalopram, 10 mg/d, and an unknown dose of dextroamphetamine. He had no major medical comorbidities. He lives with his mother. His parents are separated but he has frequent contact with his father. His developmental history is unremarkable. There was a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. There was no family history of suicide.

On his initial mental status examination, Y appears to be his stated age and is dressed appropriately. He is well dressed, suggesting that he puts a lot of care into his personal appearance. He is alert and oriented. He is cooperative and has fair eye contact. His gait is normal and no motor abnormalities are evident. His speech is normal in rate, rhythm, and volume. He can remember events with great accuracy. He reports that his mood is depressed and “down.” His affect appears irritable and he has low frustration tolerance, especially towards his mother. He is easy to anger but is re-directable. He does not endorse thoughts of suicidality or harm to others. He denies auditory or visual hallucinations, and paranoia. He does not appear to be responding to internal stimuli. His judgment and insight are fair.

The authors' observations

Traumatic brain injury (TBI) affects 1.7 to 3.8 million people in the United States. More than 473,000 children present to the emergency room annually with TBI, approximately 75% of whom are given a label of mild TBI in the United States.^1-3 TBI patients present with varying degrees of problems ranging from headaches to cognitive deficits and death. Symptoms may be transient or permanent.⁴ Prepubescent children are at higher risk and are more likely to sustain permanent damage post-TBI, with problems in attention, executive functioning, memory, and cognition.^5-7

Prognosis depends on severity of injury and environmental factors, including socioeconomic status, family dysfunction, and access to resources.⁸ Patients may present during the acute concussion phase with physical symptoms, such as headaches, nausea, vomiting, sensitivity to light and sounds, and memory deficits, and psychiatric complaints such as anger, irritability, and mood swings. Symptoms may persist post-concussion, leading to problems in personal relationships and social and occupational functioning, and neuropsychiatric manifestations, including changes in personality, depression, suicidal thoughts, and substance dependence. As seen in this case, Y had neuropsychiatric manifestations after his TBI but other factors, such as his ADHD diagnosis and the death of his grandfather and friends, may have contributed to his presentation.

Up to one-half of children with brain injuries may be at increased risk for unfavorable behavioral outcomes, which include internalizing and externalizing presentations.⁹ These behavioral problems may emerge several years after the injury and often persist or get worse with time. Behavioral functioning before injury usually dictates long-term outcomes post injury. The American Academy of Neurology recently released guidelines for the assessment and treatment of athletes with concussions (see Related Resources).

TREATMENT Restart medication

We restart Y on citalopram, 10 mg/d, which he tolerated in the past, and increase it to 20 mg/d after 4 days to address his depression and irritability. He also is restarted on lisdexamfetamine, 30 mg/d, for his ADHD. We give his mother the Child Behavior Checklist and Teacher’s Report Forms to gather additional collateral information. We ask Y to follow up in 1 month and we encourage him to continue seeing his psychotherapist.

EVALUATION Testing

Although Y denies feeling depressed to the neuropsychologist, the examiner notes her concerns about his depression based on his mental status examination during testing.

Neuropsychological testing reveals a discrepancy noted between normal verbal skills and perceptual intellectual skills that were in the borderline range (Table). Testing revealed results supporting executive dysfunction and distractibility, which are consistent with his history of ADHD. Y’s broad reading scores are in the 20th percentile and math scores in the 30th percentile. Although he has a history of a mathematics disorder, his reading deficits are considered a decline compared with his previous performance.

The authors' observations

Y is a 16-year-old male who presented with anger, depression, and academic problems. He had genetic loading with a questionable family history of schizophrenia, “nervous breakdowns,” depression, and bipolar disorder. Other than his concussions, Y was healthy, however, he had pre-morbid, untreated ADHD. He was doing well academically until his concussions, after which he started to see a steep decline in his grades. He was struggling with low self-esteem, which affected his mood. Multiple contributors perpetuated his difficulties, including, his inability to play sports; being home-schooled; removal from his friends; deaths of close friends and family; and a concern that his medical limitation to refrain from physical activities was affecting his career ambitions, contributing to his sense of hopelessness.

Y responded well to the stimulant and antidepressant, but it is important to note the increased risk of non-compliance in teenagers, even when they report seemingly minor side effects, despite doing well clinically. Y required frequent psychiatric follow up and repeat neuropsychological evaluation to monitor his progress.

OUTCOME Back on the playing field

At Y’s 1 month follow up, he reports feeling less depressed but citalopram, 20 mg/d, makes him feel “plain.” His GPA increases to 2.5 and he completes 10th grade. Lisdexamfetamine is titrated to 60 mg/d, he is focusing at school, and his anger is better controlled. Y’s mother is hesitant to change any medications because of her son’s overall improvement.

A few weeks before his next follow up appointment, Y’s mother calls stating that his depression is worse as he has not been taking citalopram because he doesn’t like how it makes him feel. He is started on fluoxetine, 10 mg/d. At his next appointment, Y says that he tolerates fluoxetine. His mood improves substantially and he is doing much better. Y’s mother says she feel that her son is more social, smiling more, and sleeping and eating better.

Several months after Y’s school performance, mood, and behaviors improve, his physicians give him permission to play non-contact sports. He is excited to play baseball. Because of his symptoms, we recommend continuing treating his ADHD and depressive symptoms and monitoring the need for medication. We discussed with Y nonpharmacotherapeutic options, including access to an individualized education plan at school, individual therapy, and formalized cognitive training.

Bottom Line

Traumatic brain injury (TBI) affects children and adults with long-term sequelae, which affects outcomes. Outcome is dependent on several risk factors. Many patients with TBI also suffer from neuropsychiatric symptoms that affect their functioning at home and in social and occupational settings. Those with premorbid psychiatric conditions need to be closely monitored because they may be at greater risk for problems with mood and executive function. Treatment should be targeted to individual complaints.

Related Resources

• Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24): 2250-2257.
• Reardon CL, Factor RM. Sport psychiatry: a systematic review of diagnosis and medical treatment of mental illness in athletes. Sports Med. 2010;40(11):961-980.

Drug Brand Names

Citalopram • Celexa            Dextroamphetamine • Adderall

Fluoxetine • Prozac             Lisdexamfetamine dimesylate • Vyvanse

Disclosure

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