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* Stroke
Psychosomatics 44:65-75, February 2003
© 2003 The Academy of Psychosomatic Medicine

Case Report

Acute Psychiatric Manifestations of Stroke: A Clinical Case Conference

Jeff Huffman, M.D., and Theodore A. Stern, M.D.

Received Jan. 18, 2002; revision received May 1, 2002; accepted May 16, 2002. From the Department of Psychiatry, Harvard Medical School and Massachusetts General Hospital; and McLean Hospital, Belmont, Mass. Address correspondence and reprint requests to Theodore A. Stern, M.D., Department of Psychiatry, Massachusetts General Hospital, Warren 605, Fruit St., Boston, MA 02114; TStern{at}partners.org (e-mail).

Cerebrovascular accidents are common and debilitating medical events that frequently result in significant functional impairment and medical comorbidity. Further, they are associated with substantial emotional and behavioral sequelae that significantly exacerbate such disability. Due to the high rates of psychiatric sequelae of stroke, the general hospital psychiatrist is frequently called on to evaluate and treat poststroke patients.

This report presents four cases that illustrate common poststroke scenarios and potential pitfalls in diagnosis and treatment. Each case highlights important clinical points in the evaluation of poststroke psychiatric symptoms.

Case Report 1
Mr. A, a 59-year-old African American man with hypertension and coronary artery disease (and a history of myocardial infarction) but no prior psychiatric illness was brought to the general hospital because of right lower extremity weakness and difficulty expressing himself that had progressed over 5 hours. On examination in the emergency room, he was found to have profound right lower extremity paresis and an expressive aphasia. Deep tendon reflexes in the right lower extremity were diminished. The results of the remainder of his physical examination, standard laboratory tests, and head computerized tomography (CT) scan without contrast were essentially normal. Treatment with heparin and aspirin was initiated, and Mr. A was admitted to the neurology service.

Over the first several days of his hospitalization, Mr. A's right-sided paresis partially improved, and he became able to express his thoughts, although he manifested some telegraphic speech. However, he became more withdrawn and did not participate actively in either occupational or physical therapy. Further, he exhibited psychomotor slowing, slept poorly (with both terminal and initial insomnia), and appeared depressed. A repeat CT scan of the head revealed infarction without edema in the left frontal lobe.

By hospital day 10, he was extremely withdrawn. He was nearly mute, was not eating, and refused to participate in rehabilitative activities. The neurology service physician felt that he was depressed and initiated treatment with 75 mg of venlafaxine twice a day; 2 days later, worsening diastolic hypertension led to discontinuation of venlafaxine. Psychiatric consultation was requested on hospital day 14 for treatment of his depression.

On consultation, Mr. A appeared sad with a constricted affect. He reported depressed mood, early morning awakening, poor energy, poor appetite, and difficulty concentrating. His movements were slow, and he reported passive suicidal ideation. He denied a history of similar symptoms, and there was no evidence of generalized anxiety, panic attacks, psychotic symptoms, or substance abuse. His only medications at the time of consultation were aspirin and enalapril.

Treatment with 2.5 mg/day of methylphenidate was initiated, and the dose was later increased to 10 mg/day. However, Mr. A's energy and mood improved only slightly over the next 7 days. Treatment options were discussed with his family, and they opted for a course of ECT, hoping for a rapid reversal of his debilitating symptoms. He received six ECT treatments over a 2-week period; by hospital day 38, all neurovegetative signs and symptoms of depression had remitted, and he was able to participate actively in his rehabilitation program.

Comments by Dr. Huffman
Mr. A, who had no history of psychiatric illness, developed a profound depression immediately after a stroke involving the left frontal lobe. His depression was not diagnosed in the crucial days immediately after the event, and it left him unable to participate in his treatment. Eventually his depression was recognized, and he had a marked recovery after ECT.

The case of Mr. A demonstrates the importance of prompt recognition and treatment of poststroke depression. Cerebrovascular accidents are common and debilitating. Each year between 600,000 and 700,000 persons suffer a thromboembolic stroke,1,2 making stroke the third leading cause of morbidity and mortality in the United States. Approximately 4 million stroke survivors exist at any given time,1 more than half of whom suffer from significant poststroke neuropsychiatric sequelae.3 Such sequelae require rapid diagnosis and treatment to maximize emotional and functional recovery.

Neuropsychiatric sequelae of strokes have been recognized for decades. In 1921, Kraepelin4 noted an association between cerebrovascular disease and manic-depressive illness. In 1939, Goldstein5 described the phenomenon of "catastrophic reaction," an emotional disorder that occurred after stroke and that was characterized by anger, frustration, denial, tearfulness, and, at times, by compensatory boasting. Bleuler,6 in 1924, noted poststroke melancholia that could last for months. Ironside,7 in 1956, was the first to describe pathologic crying and laughing associated with cerebral infarction; this phenomenon has become a well-described poststroke syndrome, termed pseudobulbar affect.

Despite the high incidence of these disorders and their frequent description in the literature, the acute emotional and behavioral sequelae of stroke are largely unrecognized and untreated. The literature has consistently found, for example, that more than 50% of nonpsychiatric physicians underdiagnose poststroke depression.8

Poststroke depression is the prototypical acute psychiatric manifestation of stroke. It is exceedingly common; approximately 20% of poststroke patients meet the criteria for major depression in the poststroke period, and another 20% meet the criteria for minor depression.9–15 Left untreated, episodes of poststroke major depression last approximately 9 months, and a minority of patients remain depressed for several years.16,17

Most studies of poststroke depression have found elevated rates of either personal or family histories of psychiatric disorders in patients with poststroke depression.12,13,18 A study of more than 300 patients admitted for stroke found that women suffered from poststroke depression at twice the rate of men, similar to the gender distribution of depression in the general population.19 Finally, a small study by Starkstein and associates20 of 26 matched stroke patients with and without poststroke depression found no difference in age, socioeconomic status, or education.

Poststroke depression has significant long-term negative effects on social functioning, motor abilities, and quality of life.19,21–24 The negative effect of depression on functional impairment continues for at least 2 years poststroke, i.e., more than a year after mood symptoms have abated in most patients.25–27 Multiple factors may cause the extended functional disability associated with poststroke depression. Poor initial rehabilitation efforts by patients with poststroke depression may have prolonged effects on function by limiting the recovery of strength and mobility. In addition, depression is associated with higher rates of medical illness;28,29 therefore, patients with poststroke depression are likely to have more poststroke medical illnesses that adversely affect function well beyond the duration of the depressive episode.

Despite the devastating consequences of untreated poststroke depression, it is vastly undertreated, both because of underdiagnosis and the fear of intolerable side effects of antidepressant medication. However, early and effective treatment of depression is perhaps even more crucial in this patient population than it is in other populations, given the need for full mobilization for occupational and physical therapy and other functional retraining early in the course of recovery.

A number of placebo-controlled trials have demonstrated that antidepressants are effective in the treatment of poststroke depression. Nortriptyline,30 citalopram,31 and fluoxetine32 have each been shown in at least one placebo-controlled, double-blind trial to relieve symptoms of poststroke depression to a significantly greater degree than placebo. Further, one study of trazodone resulted in improved functional outcome,33 and another of nortriptyline found that treatment of depression resulted in improved cognitive outcome.34 A recent study by Robinson and colleagues35 found that nortriptyline was more effective than either fluoxetine or placebo in treating poststroke depression and improving functional outcomes. These findings suggest that tricyclic antidepressants, despite higher rates of side effects than selective serotonin reuptake inhibitors (SSRIs), might be considered first-line agents for poststroke depression because of their potentially superior efficacy.

Hence, the literature indicates that antidepressants (e.g., tricyclic antidepressants and SSRIs) are effective treatments for poststroke depression. It appears that use of antidepressants results in improvement of both the mood symptoms and the functional impairment associated with poststroke depression. Studies of poststroke depression have found disruptions of both noradrenergic and serotonergic pathways;31 therefore, newer antidepressants with effects on both norepinephrine and serotonin, such as mirtazapine and venlafaxine, may also be effective in the treatment of poststroke depression. However, to our knowledge, there have been no clinical trials in which these medications have been used to treat poststroke depression.

Psychostimulants have also been used in the treatment of poststroke depression. Four retrospective studies using psychostimulants (methylphenidate and dextroamphetamine) to treat poststroke depression found these medications to be effective; response rates in these studies were between 47% and 80%.36–39 Response to psychostimulants was rapid (usually within 48 hours), and adverse events were rare. However, unlike SSRIs and tricyclic antidepressants, psychostimulants for the treatment of poststroke depression have not been studied under placebo-controlled, double-blind conditions.

ECT also appears to be an effective treatment for poststroke depression. Three articles have discussed the successful use of ECT in poststroke depression,40–42 with two retrospective studies finding response rates of 86%–95%. Furthermore, according to a review by Hsiao and colleagues,43 there have been approximately 50 case reports describing the use of ECT to treat poststroke depression. Rates of ECT-related medical complications were low in these studies.

While there are no absolute contraindications to the use of ECT, some relative risk factors must be considered when contemplating the use of ECT for patients with recent stroke. Poststroke patients may have space-occupying lesions, intracranial hemorrhage, or recent myocardial infarction. Each of these conditions has been considered a contraindication to ECT in the past,44 but with careful monitoring, patients with these conditions can be safely treated with ECT.45–48 In general, a patient's relative risk factors for adverse events from ECT must be weighed against the morbidity and mortality of ongoing depression. There is no established poststroke waiting period for ECT; Welch,45 in a review of ECT in the general hospital, noted that the interval between the time of the stroke and the administration of ECT is determined by the urgency of treatment for depression.

In addition to the previously discussed somatic treatments of poststroke depression, group and family psychotherapy have also been reported to safely and effectively treat poststroke depression.49,50 However, these modalities have not yet been evaluated in controlled trials. Furthermore, individual psychotherapy, a safe and effective treatment for depression, has not yet been evaluated for patients with poststroke depression.

Comments by Dr. Stern
In this case of poststroke depression, several treatment modalities were tried, and ECT was the most successful. The bottom line is that poststroke depression should be treated the same way that depression would be treated in a patient who has not had a stroke. A variety of treatments for depression are equally efficacious. Treatment is tailored to the patient and his or her specific needs. Moreover, the side effect profile of the treatment can be used to advantage to treat specific target symptoms. For example, if the patient suffers from insomnia or poor appetite, a sedating antidepressant (e.g., nortriptyline or mirtazapine) that also increases appetite can be used. If the patient suffers from anergia, an activating antidepressant or a psychostimulant may be employed.

In this case, venlafaxine was chosen as the initial treatment. Although this medication was used appropriately, it led to worsening of hypertension, a known side effect. Next, methylphenidate was used. Alternatively, dextroamphetamine could have been tried. However, in this case, the dose of methylphenidate was increased to only 10 mg/day. Thus, treatment with this medication should not be considered to have failed, as an adequate trial was not conducted.

Finally, ECT was used with good effect. Even stroke is not an absolute contraindication to ECT. Numerous patients with poststroke depression have been treated safely and effectively with ECT in the general hospital. ECT is a rapidly effective treatment for poststroke depression. It is important to note, however, that even though this patient responded fully within six treatments, the complete trial took 2 weeks, and remission of depression did not occur until nearly 6 weeks poststroke.

Case Report 2
Mr. B, a 63-year-old man with hypertension, diabetes mellitus, transient ischemic attacks, and no history of psychiatric problems was brought to the emergency room 30 minutes after the sudden onset of left-sided face, arm, and leg weakness. Examination revealed a dense left hemiparesis and deviation of gaze to the right. Deep tendon reflexes were diminished in the left extremities, and sensation to temperature and light touch was impaired throughout the left side, as well. The results of the remainder of the initial physical examination were normal, as were the results of standard laboratory tests. A head CT scan without contrast was unremarkable. Tissue plasminogen activator was administered, and Mr. B was admitted to the neurology service. By the second hospital day, Mr. B's gaze had normalized, and he had some improvement of his hemiparesis and sensory deficits. More thorough neurologic examination revealed a constructional apraxia and some hemineglect of the left side. Mr. B denied that he had any new medical problem at all and stated, "Maybe there was a problem earlier, but I'm back to 100%." His speech was monotonous, and he had no emotional inflection. A magnetic resonance imaging (MRI) scan revealed infarction in the right frontal and parietal lobes. The neurology service noted that Mr. B had psychomotor slowing and early morning awakening. Given these symptoms and his monotone speech, treatment with citalopram (20 mg/day) was initiated for a presumptive diagnosis of depression. When these symptoms had not improved after 7 days of treatment, psychiatric consultation was requested on hospital day 10 for treatment of what appeared to be ongoing depression.

On consultation, Mr. B endorsed psychomotor slowing and sleep disturbance (with early morning awakening). He denied depressed mood, anhedonia, or problems with concentration, appetite, or energy. Further, he denied suicidal ideation, anxiety, or psychotic symptoms. Despite findings of continued left-sided weakness from a physical examination, he continued to deny that he had any motor dysfunction and manifested left-sided hemineglect. His speech was fluent, but it lacked emotional inflection. He was able to comprehend the inflection of others.

The consultant made a diagnosis of motor aprosodia and anosognosia consistent with the location of his infarction, and she discontinued the antidepressant. She visited the patient daily and helped him gain insight into his illness; further, she reinforced the necessity of his treatment and rehabilitation. Mr. B recovered successfully without the use of psychotropics; he was able to understand better the events leading to his hospitalization and the neurologic deficits that followed.

Comments by Dr. Huffman
This case highlights two confounding factors in the diagnosis of poststroke depression. The first is the presence of neurovegetative signs and symptoms in the absence of depressed mood. It has been suggested that several neurovegetative symptoms (e.g., poor appetite, low energy, psychomotor slowing, and sleep disturbance) can be seen in euthymic poststroke patients.51 Such symptoms can occur as a result of comorbid medical conditions, medication effects, deconditioning in the hospital setting, or the stroke itself. For this reason, there has been concern that the use of DSM-IV criteria for depression in evaluating medically ill patients may result in a high rate of inappropriate diagnosis of depression.

However, a study of 205 poststroke patients found that the 85 patients who endorsed depressed mood were significantly more likely to endorse other neurovegetative symptoms, compared with the 120 patients who reported euthymic mood.52 Less than 5% of the patients in the euthymic group met the criteria for major depressive disorder except for depressed mood. Therefore, euthymic patients with neurovegetative symptoms associated with their stroke appear not to be erroneously given a diagnosis of major depressive disorder when DSM-IV criteria are applied.

The second confounding factor in the diagnosis of poststroke depression is that nondepressive neurologic stroke sequelae (such as anosognosia, aphasia, and aprosodia) can appear similar to symptoms of depression. Patients with motor aprosodias can appear sad or withdrawn, and their affect may appear blunted. The presence of anosognosia may look like denial associated with depression, and this symptom can itself lead to frustration and anger when others insist that the patient has a problem that he or she simply cannot recognize. Finally, aphasias can make the diagnosis of depression—or any diagnosis—more difficult because of the difficulty of communicating with such patients.

Comments by Dr. Stern
It can be difficult to make a diagnosis of poststroke depression. However, a consideration of diagnostic criteria and potential confounding factors can lead to the appropriate diagnosis. To meet the criteria for major depressive disorder, the patient must have either depressed mood or anhedonia, along with at least four other symptoms for at least 2 weeks. If the patient does not describe depressed mood or diminished interest in activities that he or she typically enjoys, then that person does not, by definition, have major depressive disorder. Certainly, someone can be intermittently angry or frustrated about his or her condition, but these states are not synonymous with depression.

Nondepressive neurologic phenomena, such as aphasia, impede effective communication and interfere with accurate clinical assessment. Of the aphasias, Wernicke's aphasia, in which comprehension is impaired, occurs as a result of damage to the left superior posterior temporal lobe. With pure Broca's aphasia (secondary to a left frontal lesion), the patient is able to comprehend questions about symptoms and may be able to express answers telegraphically. Some patients with Broca's aphasia are better able to express themselves while singing than while speaking.

Several types of aprosodia exist. In receptive aprosodia, associated with right parietal lesions, a patient may be unable to tell whether a phrase sounds happy, sad, or angry. With expressive aprosodias, associated with right frontal lesions, the patient's own statements have no emotional inflection. When a patient is asked to say something as if he or she were very happy, sad, or angry, the patient is unable to express the desired emotional inflection. In the case of Mr. B, an expressive aprosodia led to a constricted affect that was erroneously diagnosed as a manifestation of depression.

However, it should be noted that the presence of these nondepressive neurologic phenomena does not rule out depression. Depending on the location of a stroke, a patient meeting the criteria for depression may be unaware of being sad (due to anosognosia) or be unable to show sadness (from masked facies). In such cases, the diagnosis of depression may be missed as a result of the neurologic consequences of the stroke.

The key to diagnosis is what the patient expresses (i.e., both the words and the music). In this case, Mr. B displayed neurologic sequelae of stroke that can confound diagnosis of depression. He endorsed neither depression nor anhedonia, and he did not meet enough of the other criteria for depression. Hence, Mr. B did not have major depressive disorder.

Case Report 3
Ms. C, a 74-year-old woman with a history of hypertension, peptic ulcer disease, depression, and alcohol dependence was brought to the emergency room by paramedics after she reported weakness and sensory loss progressing over the prior 24 hours in her entire left leg and foot. Examination revealed profound weakness and lack of sensation to temperature and light touch throughout her left lower extremity; in addition, she had a grasp reflex in her left hand. She had an up-going toe on the left, and her deep tendon reflexes were hyperactive (patella and ankle jerk), but she was without clonus in the left lower extremity. The results of the remainder of her physical examination, standard laboratory tests, and a head CT scan without contrast were normal. She was admitted to the neurology service.

By the third hospital day, her left-sided weakness had improved, although she still had moderate residual weakness in her left foot. An MRI scan revealed infarction in the right frontal lobe. However, over the next 3 days she reported progressive depression, anhedonia, poor sleep, low energy, inability to concentrate, and intermittent suicidal ideation. She also reported anxiety, which lasted nearly all day, every day, involving worry about several different subjects and rumination about her neurologic symptoms. Psychiatric consultation was requested for treatment of depression and anxiety.

On consultation, Ms. C endorsed symptoms of depression and anxiety, and she noted that her anxiety seemed to coincide with her depressive symptoms. Because she had reported drinking approximately three drinks daily before her admission, she had been placed on alcohol withdrawal precautions (1 to 2 mg of lorazepam every 2 hours as needed for symptoms of withdrawal). Ms. C required 1 mg of lorazepam each day for the first 2 days of her hospitalization but showed no further symptoms of withdrawal (aside from anxiety). Ms. C denied symptoms of panic, psychosis, mania, or other symptoms of psychiatric conditions. She reported that she had in the past suffered from depression, which had been successfully treated with sertraline, but never to this degree; she had never had similar anxiety or been suicidal.

Ms. C's level of thyroid-stimulating hormone (TSH) was checked and found to be normal. Treatment with 50 mg/day of sertraline was initiated, and the dose was increased to 100 mg/day after 1 week. Her symptoms of anxiety and depression improved over the next 3 weeks; within 1 month of her cerebrovascular accident she was euthymic. By this time, she had a full neurologic recovery and was able to return to work.

Comments by Dr. Huffman
This case demonstrates another presentation of poststroke depression, i.e., depression complicated by superimposed features of anxiety. In contrast to Mr. A, who had poststroke depression after a left frontal lobe infarction, Ms. C had depression associated with infarction in the right frontal lobe. The difference in neuroanatomic stroke location raises the issue of the relationship between the location of a central nervous system (CNS) lesion and the resulting depression.

The relationship between lesion location and rates of depression remains controversial. Initial studies showed increased rates of depression in patients with left hemispheric strokes. Two studies by Starkstein and colleagues53,54 that included a total of 81 stroke patients found that 41%–59% of patients with left-hemispheric strokes had depression, compared with 13%–14% of patients with right-hemispheric strokes. A subsequent study of 124 patients with comparable small lesions similarly found significantly higher rates of depression in those with left-hemispheric strokes (31% versus 16%).55

Further study found higher rates of poststroke depression in two specific regions of the left hemisphere—the left frontal lobe and the basal ganglia. A pair of small studies (with a total of 63 patients) found that 70%–86% of patients with left anterior lesions had depression, compared with 0%–14% of those with left posterior or right-hemispheric lesions.10,11 Furthermore, five studies found increasing rates of depression with increased proximity to the left frontal pole.11,12,56–58 Studies of right-hemispheric lesions, in contrast, showed mixed results.12,56,59

Finally, Starkstein and associates60 compared rates of depression in patients with lesions of specific subcortical nuclei and found that seven of eight patients with left basal ganglia lesions had poststroke depression, while only one of 17 patients with right basal ganglia or thalamic lesions was depressed. In contrast, other studies have found no such correlation between lesion location and poststroke depression. A meta-analysis by Carson and co-workers61 of 143 studies found "no support for the hypothesis that the risk of depression after stroke is affected by location of the brain lesion."

In short, some studies have found a correlation between left anterior cortex/basal ganglia lesions and increased rates of poststroke depression. These findings have coincided with preliminary reports from functional imaging studies that found a correlation between hypoperfusion of the left dorsolateral prefrontal cortex/basal ganglia and depression. However, other studies, and a recent meta-analysis, found no such correlation.

The pathophysiologic mechanism of poststroke depression remains poorly understood. Most researchers believe that poststroke depression results from disruptions of pathways associated with biogenic amines, especially serotonin and norepinephrine. Noradrenergic and serotonergic cell bodies located in the brainstem send projections through forebrain bundles into the frontal cortex.62 Lesions in the frontal cortex or basal ganglia that disrupt these pathways may affect downstream fibers and lead to depletions of norepinephrine and serotonin, resulting in a clinical syndrome of depression.59

Laboratory studies of rats have revealed disruption of these noradrenergic and serotonergic pathways with lesions of the frontal lobe or basal ganglia.63 Further, it appears that left-hemispheric lesions can result in both depletion of biogenic amines and low rates of compensatory serotonergic receptor upregulation.3,16,64 Still, definitive details of the mechanism of poststroke depression remain unclear.

Another interesting facet of Ms. C's case is her poststroke anxiety. Three major studies that included a total of 466 stroke patients found that approximately one-fourth of patients met the criteria for generalized anxiety disorder (except for the duration criterion) in the acute poststroke period.65–67 Each study found that at least three-fourths of the patients with generalized anxiety disorder had comorbid depression, as was the case with Ms. C. The studies also found that patients with both poststroke generalized anxiety disorder and depression most commonly had left hemispheric lesions, while the small subset of patients with isolated poststroke anxiety had right hemispheric lesions.65,66 These patients with isolated anxiety also had high rates of preexisting anxiety disorders and alcohol dependence.67

Such poststroke anxiety has a negative impact on the functional recovery of stroke victims. In one study, poststroke generalized anxiety disorder was associated with impairment in activities of daily living up to 3 years after the event,66 and, in another, patients with both generalized anxiety disorder and poststroke depression had greater impairment in activities of daily living at 2-year follow-up than did patients who had poststroke depression alone.68

Ms. C's case had features that were more typical of isolated poststroke anxiety than coexisting anxiety and depression. She had a right hemispheric infarction, as well as a history of both a preexisting anxiety disorder and alcohol dependence, each of which was seen in studies of patients with isolated poststroke anxiety. However, she presented with comorbid anxiety and depression. Fortunately, her symptoms of anxiety and depression remitted with SSRI treatment, and she had full recovery of her activities of daily living 1 month after her stroke.

Comments by Dr. Stern
The literature reveals three sites most closely linked with poststroke depression—the left frontal lobe, the right parietal lobe, and the right frontal lobe. In my experience, such lesions do seem to result in depression more often than do cortical lesions in other locations. However, poststroke depression can occur with a stroke in any location. Clinically, it makes little difference where the lesion is; if it causes a depressive syndrome, the depression must be treated.

In the case of Ms. C, the diagnosis of depression was made with the DSM-IV criteria, and appropriate treatment followed. Information about the lesion location can prepare the clinician to be aware of confounding symptoms and syndromes (e.g., aphasia or aprosodia) that can interfere with diagnosis and treatment. A rule of thumb is to treat the clinical syndrome manifested by the patient, regardless of the lesion's location.

Poststroke anxiety can be treated in the same away as any primary anxiety syndrome is treated. In the case of Ms. C, treatment was with an SSRI. SSRIs are effective in the treatment of a variety of anxiety disorders as well as depression; they can be used for comorbid panic disorder, obsessive-compulsive disorder, and social anxiety, as well as generalized anxiety disorder. In general, SSRIs are well tolerated and have a favorable side effect profile. However, recent studies have found elevated rates of falls69 and hip fractures70 among elderly persons taking SSRIs; these rates are equal to those seen in elderly persons taking tricyclic antidepressants. Prescribers must be aware of these risks when prescribing SSRIs.

For more acute anxiety, benzodiazepines can be used, though one must be somewhat cautious with their use in this generally older and medically compromised population. One problem with benzodiazepines is their propensity to induce disinhibition and confusion in elderly patients who have sustained a CNS injury. Other problems, such as ataxia and falls, may occur. The risk of respiratory depression with benzodiazepines is quite low, especially at the doses generally used for anxiety relief. The risk of adverse cardiovascular events, such as hypotension, is also quite low. Other psychotropics that can be used to treat anxiety include quetiapine and gabapentin, although they must be used with caution because of potential adverse effects, for example, orthostasis with quetiapine and ataxia with gabapentin.

Case Report 4
Mr. D, a 57-year-old man with hypertension and depression who was taking 300 mg/day of nefazodone, was brought by his family to the emergency room for "out-of-control behavior." Over the preceding 4 days, he had needed less sleep, had manifested rapid speech and increased energy, and had been irritable and paranoid (i.e., believing that his neighbors were spying on him in an attempt to steal his new business idea for "downsized mini-motels"). When he was examined in the emergency room, he showed pressured speech, grandiosity, psychomotor agitation, and paranoia (e.g., he said, "You doctors are getting involved in my business ideas"). The results of a neurologic and general physical examination were normal. Discussion with the patient's family revealed that Mr. D had never before manifested similar behavior. He had previously suffered four or five episodes of depression, but he had experienced no significant depressive symptoms for at least 2 years. He had no recent physical complaints and no change in his usual medication regimen (atenolol and nefazodone), and he did not use either alcohol or illicit substances. His family history was notable for bipolar disorder in his maternal aunt and grandmother.

The results of laboratory tests, including serum and urine toxicological screenings and liver function and TSH tests, were within normal limits. A head CT scan without contrast was unremarkable. The patient was admitted to the psychiatric service for treatment of his manic symptoms.

Mr. D was given an oral loading dose of valproic acid (1500 mg/day), and he received risperidone and clonazepam for adjunctive control of his mania. Nefazodone was discontinued. An MRI scan on the second hospital day revealed an infarction along the central and medial aspects of the right thalamus. No evidence of the infarction had been found on an MRI done 2 years earlier. Over the next 15 days, Mr. D's manic symptoms subsided, and he gained insight into the episode. By the 10th hospital day, his valproic acid level was 89 µg/ml (therapeutic level, 50–100 µg/ml), and follow-up liver function tests and a complete blood count were normal. Risperidone and clonazepam were tapered, and treatment with aspirin for secondary stroke prophylaxis was started. He was discharged on the 17th hospital day.

Comments by Dr. Huffman
The case of Mr. D highlights a less common manifestation of acute stroke, poststroke mania. In this case, a middle-aged man with no history of bipolar disorder presented with new-onset mania. Such a presentation warranted a thorough workup for secondary mania, and a new right thalamic lesion was visible on an MRI scan, compared with a scan obtained 2 years earlier. Mr. D's manic symptoms were likely a result of his thalamic infarction; the radiographic change, the lack of prior mania, and a lesion location conducive to the development of mania were all highly suggestive that his infarction was the cause of his manic episode.

In general, mania is a rare complication of cerebral infarction; it occurs in less than 1% of all strokes.3 Symptoms of poststroke mania are identical to those of primary mania, with flight of ideas, pressured speech, a decreased need for sleep, grandiosity, and associated psychotic symptoms.27 Lesions resulting in mania tend to reside within the right hemisphere, and lesions in the right orbitofrontal cortex and thalamus appear to be most often associated with poststroke mania.71–73

While patients with poststroke depression may not have higher rates of affective illness in their families, one study of poststroke mania found significantly higher rates of affective disorders in family members of afflicted patients.71 We are aware of no studies that have specifically examined rates of premorbid affective illness among patients with poststroke mania. One study of 17 patients with secondary mania after a head injury found that seven (41%) had postinjury depression before developing mania.71 This finding may suggest that patients with prior depression are at higher risk for developing poststroke mania, although more study of this topic is necessary.

Treatment studies of poststroke mania have found lithium, valproic acid, carbamazepine, neuroleptics, and clonidine to be efficacious,74,75 although, to our knowledge, none of these treatments has been examined in placebo-controlled, double-blind trials. The case of Mr. D includes many of the prototypical features of poststroke mania, as well as a right thalamic lesion. Mr. D's symptoms responded to standard treatments for mania (in this case, valproic acid, risperidone, and clonazepam).

Along with poststroke mania, poststroke psychosis is a rare complication, occurring at a rate of approximately 1%–2%.76 Such patients have a high rate of associated seizures, and these symptoms are usually associated with a right temporoparietal lesion.76,77 These findings suggest that temporal lobe damage, leading to partial complex seizures and to associated psychosis, may account for symptoms in a significant percentage of patients.

Finally, two clinical syndromes seen in the poststroke period are both common and specific to cerebrovascular events. The first is pseudobulbar affect, also termed pseudobulbar palsy or pathologic affect. This syndrome is common in the poststroke period, occurring to some degree in approximately 15% of patients.78,79 The syndrome consists of frequent and easily provoked spells of laughing or crying. It is usually seen in a mild form, with brief fits of crying or laughing with appropriate changes in mood, but, in more serious cases, it may involve frequent and spontaneous fits of laughing and crying inappropriate to the context. Two studies of pseudobulbar affect found significant improvement after treatment with nortriptyline80 and citalopram.81 The second clinical scenario associated with stroke is termed "catastrophic reaction," a collection of symptoms involving patient desperation and frustration. Such symptoms include anxiety, aggression, refusal of reassurance and treatment, and compensatory boasting. This syndrome was first described by Ironside7 in 1939 and is relatively common; studies have found rates of poststroke catastrophic reaction between 3% and 20%.82,83

Catastrophic reaction appears to be associated with poststroke depression. A study of 62 stroke patients found that 26% of 50 patients without catastrophic reaction had depression, but fully 91% (11 of 12) of the patients manifesting catastrophic reactions had comorbid depression.82 A second study of 326 patients with first-time stroke found that 66% (eight of 12) of patients with catastrophic reaction developed poststroke depression or pseudobulbar affect.83 Catastrophic reaction is also associated with a personal and family history of psychiatric disorders.82

Catastrophic reactions also appear to be associated with anterior subcortical lesions.62 These reactions are also seen almost exclusively in patients with left-hemispheric damage.82–84 Given the strong association of catastrophic reaction and depression, some feel that such a reaction is a behavioral symptom of depression (provoked by anterior subcortical damage) rather than a discrete syndrome. Others feel that catastrophic reactions result from damage to left-hemispheric areas that are involved in regulating emotions related to social communication.83

Comments by Dr. Stern
The case of Mr. D was that of a classic manic episode in the context of a radiologic finding consistent with stroke. Mr. D met the diagnostic criteria for mania, which can be remembered by the mnemonic DTRHIGH—because the clinician wants to "deter the high"—distractibility, talkativeness, reckless behavior, hyposomnia, ideas that race, grandiosity, and hypersexuality. Mr. D clearly manifested three of these symptoms in conjunction with an elevated mood. When someone the age of Mr. D has a first manic episode, one must seriously consider secondary causes of mania; the thalamic lesion may well have been related to the patient's presenting symptoms.

In any case, treatment of poststroke mania follows the same rules as treatment of primary affective illness (manic type). A mood stabilizer and adjunctive antipsychotic medications or benzodiazepines are used to control symptoms. In the case of Mr. D, all of these types of treatments were used. Valproic acid was his primary mood stabilizer, administered along with the atypical antipsychotic risperidone and the mood-stabilizing benzodiazepine clonazepam. This was appropriate treatment, and the treatment team was able to taper the adjunctive medications successfully by the end of the hospitalization.

In short, the treatment of poststroke mania and poststroke psychosis involves treatment of the underlying condition. The patient should receive maximal treatment for the medical condition; psychiatric medication is used to treat the behavioral symptoms.

In summary, affective presentations after stroke are common. Moreover, attention to diagnosis and treatment facilitates timely and appropriate patient care. Treatment of these affective presentations in stroke patients frequently results in significantly improved rehabilitation and quality of life.

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