Dr. Levenson is professor in the Departments of Psychiatry, Medicine, and Surgery, chair of the Division of Consultation-Liaison Psychiatry, and vice chair for clinical affairs in the Department of Psychiatry at Virginia Commonwealth University School of Medicine in Richmond.
Disclosure: Dr. Levenson is on the depression advisory board for Eli Lilly.
Psychiatrists and other clinicians working in general medical or specialized neurologic settings frequently encounter important psychiatric issues affecting diagnosis and management of patients with neurologic illnesses. These include cognitive impairment either as a primary presentation or as a secondary complication of a known neurologic condition such as multiple sclerosis; other psychiatric symptoms as a manifestation or complication of neurologic disease; and physical neurologic symptoms that do not correspond to any recognized pattern of neurologic disease, ie, conversion disorder or somatization disorder. In addition, behavioral, cognitive, or emotional symptoms may occur as a complication of drug therapy of neurologic disease. A more detailed coverage of these topics can be found elsewhere.1,2 This column illustrates the principles of evaluating and treating psychopathology in neurologic illness in the most common disorder affecting the central nervous system, stroke.
A cerebrovascular accident, or stroke, is defined as a focal disturbance of cerebral function of presumed vascular origin with rapid onset and lasting >24 hours, caused by cerebral infarction or hemorrhage. Infarction results from thrombosis of vessels or emboli. Infarctions are much more common than hemorrhages and, as a result of a lower immediate fatality rate, are a much greater source of enduring disability. Strokes are the third most common cause of death in the Western world.
Psychosocial factors influence the risk for stroke. Stroke is more common in widowers, divorcees, those with less education, those engaged in hard manual labor, and those with low social support. There is also evidence that depression and other psychological factors constitute risks for stroke, consistent with widespread lay and folk beliefs regarding stress and stroke. There is some evidence that anger/hostility may pose a risk for carotid atherosclerosis just as it may for coronary disease. In some longitudinal prospective epidemiologic studies, depression appears to significantly predict greater stroke frequency, but the finding sometimes disappears when other significant predictors are taken into consideration (eg, age, sex, smoking, hypertension, diabetes) As with many other major medical illnesses, stroke patients who have extensive social support have better functional outcomes than those who do not.
Cognitive Disorders After Stroke
Delirium occurs in 30% to 40% of patients during the first week after a stroke, especially after a hemorrhagic stroke. Delirium after a stroke is associated with poorer prognosis, longer hospital stays, and increased risk of dementia.1
Dementia is common following stroke, occurring in approximately 25% of patients at 3 months after stroke. Vascular dementia is an overarching term encompassing subcortical ischemic dementia, multi-infarct dementia, and dementia due to focal strategic infarction, ie, unexpectedly severe cognitive impairment following limited infarction in critical brain areas such as the thalamus, internal capsule, and basal ganglia.1
Psychiatric Issues that May Present After Stroke
A wide variety of focal cognitive deficits as well as emotional and behavioral changes may occur after stroke, depending on the location of the vascular occlusion or bleed. Such changes reflect the specific affected cerebral area and are not unique to stroke. These include aphasia, anosognosia, dysprosody, apathy, depression, anxiety, emotional incontinence, catastrophic reactions, psychosis, obsessive-compulsive symptoms, and hyposexuality.
Global aphasia occurs when all linguistic abilities have been lost, making communication extremely limited, and the physician must infer mental state from behavior and nonverbal communication. In expressive (Broca’s) aphasia, intense emotional frustration is common due to the difficulties in patients’ making themselves understood and the resulting problems in social interaction.3 In receptive (Wernicke’s) aphasia, patients manifest irritability and rage because they do not understand what others are saying, and therefore lack insight. Some recovered patients have reported that they thought their physicians were being deliberately incomprehensible.4
Anosognosia refers to partial or complete unawareness of a deficit. In extreme cases, patients may deny that a limb or an entire side of their body belongs to them, attributing it to someone else. Anosognosia occurs more frequently with nondominant parietal lobe strokes.
Dysprosodia is impairment of the production of those aspects of speech that communicate emotions,. It is characterized by alterations in intensity, timing, rhythm, cadence, melody, and intonation of words. Dysprosody is a deficit in the ability to communicate emotions, but is not associated with an actual deficit in the ability to experience emotions. Dysprosodic speech sounds flat and robotic. Others must infer the patient’s emotional state from the content of the patient’s speech and facial expressions.
Patients with apathy show absence of passion, emotion, or excitement. They lack interest in or concern for things that others find moving or exciting. Apathetic patients produce little spontaneous action or speech. Apathy is associated primarily with frontal lobe strokes.
Depression is very common following stroke but its diagnosis is problematic because it can be unclear which symptoms are attributable to the stroke and which are attributable to depression. In patients with strokes that result in significant deficits, one must also distinguish between normal or adjustment reactions and major depressive disorder (MDD). Persistent dysphoric mood, anhedonia, vegetative symptoms (eg, insomnia, anorexia), and poor participation in rehabilitation point to a diagnosis of MDD. The 9-item Patient Health Questionnaire performs well as a screening instrument for poststroke depression.5 Depression after stroke has been associated with increased disability6 and mortality.7
Many studies have examined whether depression is associated with the location of the stroke lesion (particularly the left frontal lobe), but a consensus has not been reached in the literature. Meta-analyses have both supported8 and not supported a relationship between stroke location and incidence of subsequent depression.9,10
Treatment for depression should be started early after stroke in order to improve participation in rehabilitation and maximize functional outcome. There is some evidence that effective treatment of depression leads to a reduction in overall disability1 and even reduction in mortality.11 However, in many patients, poststroke depression tends to improve over time irrespective of treatment. While there have been several randomized placebo-controlled trials demonstrating the effectiveness of selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs) in poststroke depression,12,13 antidepressants have not been more effective than placebo for treatment of poststroke depression in numerous recent controlled trials.14-16
Antidepressants have been demonstrated to improve some of the related symptoms that may accompany poststroke depressive states, including emotional incontinence,15 anger proneness,15 and executive dysfunction,17 but not fatigue.18 There have also been mixed results in controlled trials to determine if early antidepressant therapy after stroke can prevent the development of depression16,19; however, a recent meta-analysis concluded that antidepressant prophylaxis is associated with a significant reduction in the occurrence rate of newly developed poststroke depression.20
Randomized controlled trials have also supported the efficacy of exercise,21 case management,22 and acupuncture23 in the treatment of poststroke depression. Cognitive-behavioral therapy may offer an alternative to antidepressants, but has not received adequate study of its efficacy in postroke depression.24
Clinically significant anxiety is common in ischemic stroke patients, frequently co-occurs with depression, and may interfere with rehabilitation. Anxiety after stroke is usually in the form of generalized anxiety and appears to share risk factors with depression.25 Reported rates of prevalence of generalized anxiety disorder (GAD) after stroke range from 4% to 28%, with a higher percentage of patients experiencing anxiety symptoms.1
Poststroke anxiety may include posttraumatic stress symptoms, anticipatory anxiety about the risk of recurrence, and somatization. There is a lack of randomized controlled trial data to guide treatment of anxiety after stroke, but there is no reason not to apply the usual psychotherapeutic and psychopharmacologic treatments. When GAD is comorbid with poststroke depression, it appears to respond to antidepressant therapy.26
Emotional incontinence (also referred to as pathological crying or laughing, emotional diarrhea, emotional lability, pseudobulbar affect, or, more recently, involuntary emotional expression disorder [IEED]27) is a syndrome of uncontrollable episodes of emotional expression that occur after stroke and in a variety of other neurologic conditions. IEED is characterized by episodes of crying or laughing that are unrelated to or out of proportion to the eliciting stimulus. The crying or laughing are disinhibited and experienced by the patient as unwanted and a struggle to stop. In addition to stroke, this syndrome is common in patients with frontal lobe lesions due to traumatic brain injury, multiple sclerosis, pseudobulbar palsy, and amyotrophic lateral sclerosis.
Pathological crying or laughing can have a significant impact on individuals’ social functioning and their relationships with others. Unpredictable and uncontrollable outbursts of affect often cause severe embarrassment and avoidance of social interactions and may result in subsequent agoraphobia.
Treatment options include TCAs, SSRIs, dopamine agonists, and a combination of dextromethorphan and quinidine.28
Catastrophic reactions are outbursts of frustration, dysphoria, and anger when confronted with a frustrating (usually cognitive) task, often appearing suddenly and unexpectedly, startling caregivers and relatives. Catastrophic reactions, emotional incontinence, and poststroke depression share some symptoms in common and often co-occur but are distinct clinical syndromes. One prospective study of patients with a first stroke identified catastrophic reactions in 12 of 326 patients within 48 hours from onset of the stroke, and were associated with nonfluent aphasias.29 Another study found that catastrophic reactions after acute stroke were significantly associated with depression, a personal and family history of psychiatric disorder, and subcortical lesions which were mostly located in the basal ganglia.30
Psychosis can be caused by stroke but is very uncommon, with an incidence of approximately 1%. Pre-existing cortical atrophy increases the risk for poststroke psychosis. Auditory hallucinations can be directly caused by acute stroke, mostly described after lesions of the brain stem, but rarely reported after cortical strokes. A cross-sectional study of 641 stroke patients identified four patients who developed postcortical stroke auditory hallucinations.31 All of them occurred after an ischemic lesion of the right temporal lobe, and all resolved without pharmacotherapy in a few months. Stroke can also cause delusions, which sometimes are persistent to the point of constituting a delusional disorder, eg, delusions of parasitosis.32 If psychotic symptoms appearing soon after stroke are mild and not distressing to the patient, drug treatment may not be necessary. Significant persistent or disruptive psychosis should usually be treated with antipsychotics since the risk of untreated psychosis usually is greater than the risk of increased mortality reported in some studies of patients with dementia receiving antipsychotics. However, long-term treatment may not be needed since most poststroke psychotic symptoms in patients without dementia will resolve.
Obsessive-compulsive disorder has been reported after strokes, most often those affecting the basal ganglia or brainstem. Case reports suggest that both antidepressants33 and behavior therapy34 can be effective.
Decline in sexual interest and activity is common after stroke, with greater declines in those who are older or disabled. Psychological rather than physical aspects account for most of the decline in sexual activity in stroke survivors.35 Patients’ partners play a substantial role in the decline of sexual activity, related to their own anguish and anxiety over risk for recurrence of stroke. Patients and their partners can be counseled that sexual intercourse does not increase risk for stroke.36 Sexual dysfunction after stroke frequently occurs alongside depression; therefore, treatment for depression is likely to help restore normal sexual functioning37 unless the sexual dysfunction has been caused by an antidepressant. Patients with stroke may also have major medical comorbidities contributing to sexual dysfunction, including diabetes mellitus, peripheral vascular disease, and hypertension (with sexual dysfunction due to antihypertensives such as β-blockers).
Conversion Disorder and Stroke
Because some patients with conversion disorder present with acute onset of neurologic symptoms, they may be misdiagnosed as having transient ischemic attacks or strokes. In one study of 151 consecutive patients presenting to an emergency room initially diagnosed with stroke who received tissue plasminogen activator, four turned out to have conversion disorder instead.38 Careful neurologic examination and imaging studies permit distinguishing which patients really have strokes. The older the patient, the less likely it is that the diagnosis is conversion disorder. PP
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