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* Stroke
Psychosomatics 41:5-14, February 2000
© 2000 The Academy of Psychosomatic Medicine

Special Article

The Neuropsychiatry of Stroke

Eran Chemerinski, M.D., and Robert G. Robinson, M.D.

Received and accepted September 2, 1999. From the Department of Psychiatry, The University of Iowa College of Medicine, Iowa City, Iowa 52242. Address reprint requests to Dr. Chemerinski, The University of Iowa, Medical Education Building, Iowa City, IA 52242. e-mail: eran-chemerinski{at}uiowa.edu


  ABSTRACT

 
TOP
 ABSTRACT
INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
 CONCLUSIONS
 REFERENCES
 
Stroke represents a major public health problem in the United States, but relatively little work has been directed toward identifying and treating the common neuropsychiatric disorders occurring after stroke. This review discusses clinical and pathological correlates of depression, anxiety disorder, catastrophic reactions, pathological affect, or psychosis after stroke, as well as their epidemiology. Depressive disorder and anxiety disorder have been shown to inhibit physical recovery from stroke. It seems likely that other psychiatric disorders also inhibit recovery and limit quality of life. There are very few controlled trials examining the effectiveness of treatments for these disorders after stroke. Both depression and pathological affect, however, can be effectively treated with antidepressant medications.

Key Words: Neuropsychiatry • Stroke

  INTRODUCTION

 
TOP
 ABSTRACT
 INTRODUCTION
POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
 CONCLUSIONS
 REFERENCES
 
The World Health Organization defines stroke as "rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin."1

Over the last 50 years, however, there has been a steady decline in stroke incidence and mortality. Improved control of hypertension and acute management of stroke patients are important factors contributing to this decline.2 The American Heart Association nevertheless estimates that 500,000 new cases of stroke appear in the United States per year. Also, although stroke ranks in the top three leading causes of death (behind heart disease and cancer), accounting for 150,000 fatalities per year, a population of around 3 million stroke survivors exists at any given time.3 Of the survivors, two-thirds have some degree of permanent disability that requires rehabilitation care.4

Recent studies have concluded that neuropsychiatric complications (i.e., emotional, behavioral, and cognitive disorders) may have a negative effect not only on the social functioning and overall quality of life of stroke survivors,5 but also on the recovery of their motor functioning, as well.6 This article will discuss a number of these neuropsychiatric disorders (Table 1), including their effects on recovery and methods of treatment.


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TABLE 1. Neuropsychiatric disorders associated with stroke




  POSTSTROKE DEPRESSION (PSD)

 
TOP
 ABSTRACT
 INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
 CONCLUSIONS
 REFERENCES
 
Depression is among the most common neuropsychiatric disorders occurring after stroke. Despite its high frequency and negative influence on the overall recovery of stroke patients, a study by Schubert et al.7 reported that poststroke depression (PSD) was underdiagnosed by nonpsychiatric physicians in 50%–80% of cases.

Epidemiology
The frequency of PSD has been examined in numerous studies. The frequency depends on whether patients are examined in hospital or in community surveys and whether they are studied during the acute poststroke period or many months after stroke (Table 2). Also, the use of cutoff scores to define the existence of PSD, rather than structured interviews and diagnostic criteria, have also contributed to reported differences in the prevalence rates of PSD.


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TABLE 2. Prevalence studies of poststroke depression



The mean prevalence in hospitalized acute stroke patients was 22% for major depression and 17% for minor depression. In outpatient populations, the mean prevalences were 23% for major depression and 35% for minor depression, whereas community samples showed 13% for major depression and 10% for minor depression (Table 2).

Diagnosis
The diagnosis of PSD may be difficult or impossible in some groups of patients with stroke. For instance, the presence of language comprehension disorders and/or cognitive impairment may prohibit the reliable assessment of symptoms of depression.8

Although the DSM-IV9 criteria for "mood disorders due to a medical condition" are applicable for the diagnosis of PSD,10 some investigators have suggested that several symptoms used by DSM-IV for the diagnosis of major depression, such as loss of energy and appetite, and insomnia, are also found among euthymic stroke patients secondary to hospital environment, the use of medications, other associated medical conditions, or the stroke itself.11 In 1991, a study by Fedoroff et al.12 examined the frequency of depressive symptoms among both depressed and nondepressed patients with acute stroke. This study found that, with the exception of morning awakening, all neurovegetative and psychological symptoms of depression were significantly more frequent among patients with depressed mood compared with patients without depressed mood. Even when the frequency of nonspecific symptoms among the nondepressed patients was taken into account, the frequency of major depression decreased only 2%, from 23% to 21%.

Thus, although PSD cannot be reliably diagnosed in patients with severe comprehension impairments, the DSM-IV diagnostic criteria for major depression are applicable to patients with PSD, and the depressions appear to be similar to those found in elderly patients with primary depressions. The DSM-IV criteria for major depression require the presence of either depressed mood or apathy during 2 or more weeks, accompanied by at least four of the following symptoms: decreased or increased appetite or weight; insomnia or hypersomnia; psychomotor agitation or retardation; loss of energy; feelings of worthlessness or inappropriate guilt; loss of concentration; and recurrent suicidal ideation.

Minor depression is a DSM-IV research diagnosis that requires the presence of more than two, but fewer than five, depressive symptoms, including either a depressed mood or loss of interest. Although it excludes depressions "due to a general medical condition," we have used this diagnosis to identify stroke patients with milder (subsyndromal) forms of depression. Our studies have validated this diagnosis by identifying differences between major and minor depression in the frequency of past personal history of depression,13 the association with cognitive impairment,14 and association with lesion location.15

Duration
The duration of depression has been examined in several longitudinal studies. In a prospective study of mood disorders in 65 acute stroke patients,16 we found that 9 patients (14%) had an in-hospital symptom cluster of major depression, whereas 12 patients (18%) had a symptom cluster of minor depression. All of the follow-up patients with major in-hospital depression were improved after 2 years, whereas only three patients (30%) with in-hospital minor depression recovered by this time (Figure 1).



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FIGURE 1.  Outcome of stroke patients with in-hospital major vsminor depression. Note: The majority of patients with major depression are improved by 1 year, whereas the majority of minor depression patients were still depressed at 2-year follow-up


Morris et al.17 found that the mean duration of poststroke major depression was 34 weeks, whereas the mean duration of minor depression was only 13 weeks. Aström et al.18 also found that the majority of major depressions remitted by the 1-year follow-up. However, 30% of patients with in-hospital major depression remained depressed at the 1-year follow-up; 25% were depressed at 2-year follow-up; and 20% were still depressed at the 3-year follow-up.

Thus, although the mean duration of major depression appears to be about 9 months, there are a significant number of patients with major or minor in-hospital depression who remain depressed for several years after stroke.

Anatomical Correlates
Over the last two decades there has been a growing interest in finding a correlation between lesion location and PSD in order to delineate a pathophysiological hypothesis to explain this disorder.

In a study of acute stroke, we found that 14 of 22 patients with left-hemisphere lesions suffered either major or minor depression, whereas these disorders occurred in only 2 of 14 patients with right-hemisphere lesions. Later, 13 PSD patients with left-sided lesions and a group of stroke patients without depression, matched for age, lesion size, and location, were compared. We found that subcortical atrophy (as evidenced by increased ventricular–brain ratios) was associated with the presence of PSD.19 In a still later study of 93 patients with right-sided lesions, both right-frontal (i.e., 6 of 17 depressed patients and 1 of 25 nondepressed patients had a frontal lesion) and right-parietal lesions (i.e., 11 of 17 depressed and 9 of 25 nondepressed had a parietal lesion) were associated with PSD.20

Although these findings have been replicated by several authors,21,22 several others have not found lateralized effects.23 We have recently shown that laterality effects are present only during the acute stroke period, and studying patients several months or several years after stroke has led to this failure to find laterality effects.

Mechanism
Although the cause of PSD remains unknown, we have hypothesized24 that the depletion of monoaminergic amines occurring after lesions in the frontal lobe or basal ganglia of the brain may play a role in PSD. Norepinephrine and serotonin nuclei send ascending projections from their location in the brain stem to the frontal cortex through the median forebrain bundle. These ascending axons then arc posteriorly, running through the deep layers of the cortex, where they arborize and send terminal projections into the superficial cortical layers.

Lesions of the frontal lobe or basal ganglia have been shown in animal models to disrupt these pathways.25 Furthermore, we reported higher serotonin-receptor binding in the ipsilateral, non-injured, temporal, and parietal cortex of patients with right- compared with left-sided lesions. Among patients with left-hemisphere stroke, we found a significant correlation between severity of depression and the absence (i.e., decreased amount) of serotonin-receptor binding.26 Disruptions of dopaminergic pathways ascending from the ventral tegmental area have also been implicated in the pathogenesis of PSD.27

Association Between Physical Impairment and PSD
Stroke survivors often suffer some degree of long-term impairment. Approximately 80% of patients with acute stroke present with weakness or paralysis of either the upper or lower extremity. The relationship between PSD and functional impairment is complex. The measurement of physical impairment usually involves both neurological motor and sensory examinations and quantification of deficits in the performance of activities of daily living (ADL). In one of our earliest studies of PSD,28 we found a significant correlation among 130 patients between the severity of depressive symptoms as measured by the Zung Depression Scale, the Hamilton Rating Scale for Depression (Ham-D), or the Present State Examination and the severity of impairment in ADL, including the patients' ability to dress and feed themselves, walk, find their way around, express needs, read and write, keep their room in order, and maintain sphincter control.

Although most stroke patients experience some natural recovery of their neurologic functioning and ability to perform ADL, we have reported that at 2-year follow-up, patients with major or minor depression after acute stroke were significantly more impaired in their ADL than comparably impaired patients without depression. Also, however, in-hospital impairment in ADL was found to correlate with severity of depression at both 3- and 6-month follow-up.25 These findings suggest that depression influences ADL recovery. They also suggest that severity of ADL impairment influences the duration and severity of depression.

Association Between Cognitive Impairment and PSD
Deficits in one or more domains of cognitive functioning are, along with motor impairment, the most common complications of stroke. We first reported a specific association between cognitive impairment and major PSD in 1986.29 In this study, 38 patients who had single infarcts in the left hemisphere, as documented by either computed tomography (CT) scan or clinical history, were grouped according to whether they had major depression (n=11), minor depression (n=10), or no depression (n=17). Although there were no significant differences in terms of background characteristics and neurological findings among groups, patients with major depression had significantly more cognitive impairment, as measured with the Mini-Mental State Exam, than did those with minor depression or no depression.30

Using a comprehensive neuropsychological battery,31 we subsequently found that patients with major depression and left-hemisphere infarcts had significantly greater deficits in tasks involving language, temporal orientation, executive motor, and frontal lobe functions than patients with comparable lesions but without depression.

Longitudinal studies of the course of cognitive impairment and PSD found that this association tended to decline with time. House et al.,32 for example, found that the high correlation between depression, measured with the Beck Depression Inventory, and cognitive impairment that was seen in 76 patients at 1 month after stroke failed to reach significance at the 1-year follow-up. In a 2-year longitudinal study of 103 stroke patients, we found that patients with an in-hospital diagnosis of major depression after a left-hemisphere stroke had significantly greater cognitive impairment at the in-hospital, 6-month (P=0.03), and 12-month (P=0.02) follow-up, but no difference in cognitive functioning at the 2-year follow-up.33

Treatment
The widespread belief that depression is an understandable psychological reaction to the physical impairments of stroke and the increased frequency and severity of side effects that psychotropic drugs (e.g., tricyclic antidepressants) might produce in this mostly advanced-age patient population are factors that probably account for the reluctance by many physicians to use antidepressant medications in PSD.

There are currently at least three double-blind, placebo-controlled studies that have examined the efficacy of antidepressant medication in PSD. We conducted the first study, reported in 1984,34 in which patients given nortriptyline showed a significantly greater improvement on the Ham-D, the Zung Self-Rating Depression Scale, and the profile of depressive symptoms assessed by the PSE than placebo-treated subjects. It is worth noting that 3 of the original 14 patients treated with nortriptyline dropped out of the study. Two patients developed delirium, and one had a sudden syncopal episode of unknown etiology.

In a controlled study by Redding et al.,35 seven PSD patients with an abnormal Dexamethasone Suppression Test treated with trazodone had a significantly greater improvement in ADL at 2–3 months after stroke, as measured with the Barthel ADL scale, compared with nine comparable patients treated with placebo.

Andersen et al.36 assessed the efficacy and tolerability of the selective serotonin-reuptake inhibitor (SSRI) antidepressant citalopram in a controlled study of 66 patients with stroke. The Ham-D and the Melancholia Scale scores were significantly better at both 3 and 6 weeks among patients who received citalopram compared with patients given placebo.

Although other treatment modalities, such as stimulant medication and electroconvulsive therapy (ECT) have been used for PSD, they have not been evaluated in controlled studies; therefore most clinicians agree that antidepressant drugs constitute the first choice for the treatment of PSD. Because depressive symptoms have a negative influence on functional recovery, medication should be administered as soon as these symptoms are recognized in order to diminish the risk of long-term impairment. Finally, in our treatment study,34 patients who received active treatment for 6 weeks showed significantly lower depression scores than patients who were treated for 4 weeks, suggesting that longer duration of treatment may improve outcome.


  POSTSTROKE ANXIETY DISORDER

 
TOP
 ABSTRACT
 INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
OTHER POSTSTROKE...
 CONCLUSIONS
 REFERENCES
 
Epidemiology
A significant comorbidity exists between poststroke anxiety and PSD. In a study of 98 acute stroke patients,37 we found that, whereas only 6 patients met modified DSM-III criteria for generalized anxiety disorder (GAD; excluding the 6-month duration criterion) in the absence of any mood disorder, 23 of 47 patients with major depression also met criteria for GAD.

In another study,38 we reported that 78 patients (27%) of a population of 288 stroke patients met the modified DSM-III criteria for GAD (excluding the 6-month duration criterion). Major or minor depression was also present in most of them (58 of 78 GAD patients).

These results were replicated by Aström39 in a 3-year longitudinal study of 80 patients with acute stroke. In this study, the prevalence of GAD in the acute stage was 28%, with no significant decrease through the 3-year follow-up. Criteria for major depression were met by 85% of those poststroke GAD patients at some time during the 3-year follow-up period.

Diagnosis
The DSM-IV categorizes poststroke GAD as "anxiety disorder due to stroke, with generalized anxiety." The criteria for primary GAD require the presence of a sustained worrying state associated with at least three anxiety symptoms, including restlessness, decreased energy, difficulties in concentration, irritability, muscle tension, and sleep disturbance, for a period of at least 6 months. In order to study patients in the acute poststroke stage, most studies of poststroke GAD have not required the 6-month duration.

Using our overall population of stroke patients, we examined the frequency of symptoms of GAD among patients who acknowledged the symptoms of anxiety or worry. With the exception of decreased energy, all the individual symptoms of GAD were significantly more frequent among patients with anxiety.25 Thus, given that anxiety symptoms are not associated with the stroke itself, poststroke GAD can be diagnosed using DSM-IV symptom criteria.

Anatomical Correlates
Our original population of 98 stroke patients was divided into those with anxiety only, those with anxiety plus depression, those with depression only, and those with no mood disorder.37 Examination of the CT scans of these patients showed that anxious–depressed patients had a significantly higher frequency of cortical lesions than did either the depression-only group or the control group (Figure 2). Moreover, the depression-only group showed a significantly higher frequency of subcortical lesions than did the anxious–depressed group.



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FIGURE 2.  Lesion location among patients with left-side lesionNote: The frequency of cortical and subcortical lesions of the left hemisphere among patients with depression (major or minor) and generalized anxiety disorder. Depression without anxiety was associated with subcortical left-hemisphere lesions, whereas the combination of anxiety and depression was associated with left-cortical lesions (Reprinted with permission from Robinson RG: The Clinical Neuropsychiatry of Stroke, Cambridge University Press, 1998)25


We subsequently reported, in our overall group of 288 patients, that depression plus anxiety was associated with left-cortical lesions, whereas anxiety-alone was associated with right-hemisphere lesions.38

In the 3-year longitudinal study of stroke patients by Aström,39 similar findings were reported. In the acute poststroke period, pure GAD was significantly associated with right-hemisphere lesions, whereas comorbid anxiety/depression was significantly associated with left-hemisphere lesions. Another important finding of this study was that, at 3 years after stroke, GAD was significantly associated with both cortical and subcortical atrophy. Aström suggested that this atrophy might play a role in the prolonged maintenance of GAD after stroke.

Risk Factors and Effect on Recovery
Longitudinal studies of poststroke GAD have shown that functional recovery of patients with stroke was negatively affected by the presence of GAD. For example, in her 3-year longitudinal study, Aström39 found that ADL impairment was associated with GAD not only in the acute period but at all time periods after discharge from the hospital. Thus, anxiety was more than an immediate reaction to loss of function. In another study, with 142 patients, we found that patients with GAD and depression (n=18) had significantly greater impairment in ADL at a 2-year follow-up than patients with PSD alone (n=9).40 We suggested that one possible explanation was that the comorbidity of PSD and GAD produced a longer duration of depression than PSD alone, and this prolonged depression might lead to more profound adverse physical and social functioning outcomes.

Treatment
Because there have not been any systematic treatment studies of poststroke GAD, the only information available is from treatment studies of GAD patients without brain lesions. Benzodiazepines are the most commonly prescribed medications for the treatment of GAD, but these tend to accumulate in older people. Given the fact that stroke patients constitute an older population, benzodiazepines should be used as a time-limited treatment.

Buspirone, an anxiolytic medication with partial serotonin-agonist properties, has been reported41 to have an efficacy similar to diazepam in the treatment of GAD but with a more tolerable side-effects profile. The utility of buspirone in this population has not been examined.


  OTHER POSTSTROKE NEUROPSYCHIATRIC DISORDERS

 
TOP
 ABSTRACT
 INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
CONCLUSIONS
 REFERENCES
 
Catastrophic Reaction
In 1939, Goldstein42 created the term "catastrophic reaction" to describe a series of symptoms (i.e., anxiety, aggressiveness, refusal, and renouncement) that may occur in patients with brain injury and appear to be due to the "inability of the organism to cope with physical or cognitive deficits."

Starkstein et al.43 developed a scale (the Catastrophic Reaction Scale) for the assessment of the existence and severity of catastrophic reactions. Using this scale, we reported that a catastrophic reaction was present in 19% (n=12) of a consecutive series of 62 patients with acute stroke. Moreover, because catastrophic reactions were significantly associated with both major depression and basal ganglia lesions, we suggested that this phenomenon might represent the release of depressive emotions provoked by anterior subcortical damage.

The preferred treatment for the catastrophic reaction is prophylactic.44 Because this condition appears frequently in patients with nonfluent aphasia after stroke, language testing or therapy should not be pushed too hard in patients frustrated and depressed because of continual failure during the rehabilitation period.

Pathological Affect
Pathological affect is characterized by frequent and easily provoked episodes of crying and/or laughing that are not appropriate to the situation or are in excess of the underlying emotion. Several studies45,46 have reported that 15% of acute stroke patients manifest his condition. We demonstrated the reliability and validity of the Pathological Crying and Laughing Scale (PLACS)47 for the assessment of emotional lability in 54 patients with acute stroke. Furthermore, in a double-blind drug trial of nortriptyline vs. placebo, patients receiving nortriptyline (n=14) showed a significantly greater decrease in PLACS scores (i.e., fewer pathological affect symptoms) at 4–6 weeks of treatment than patients receiving placebo (n=14; Figure 3). In another double-blind drug trial using a crossover design, Andersen et al.48 reported that all 13 patients treated with the SSRI responded to treatment with a reduction in the number of crying episodes by at least 50%, as compared with 2 responders in the placebo group. Although significant improvement in the Ham-D scores was also seen in our treatment study, analysis of the data to exclude the effect of depression demonstrated that nortriptyline was an effective treatment for pathological emotions.



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FIGURE 3.  Comparison of Pathological Laughter And Crying Scale (PLACS) scores over 6 weeks of double-blind treatment with nortriptyline or placeboNote: The nortriptyline was superior to placebo at both 4 and 6 weeks of treatment (Reprinted with permission from Robinson RG: The Clinical Neuropsychiatry of Stroke, Cambridge University Press, 1998)25


Poststroke Psychosis
Psychosis (i.e., delusions and hallucinations) is a rare complication of stroke. Rabins et al.49 screened all individuals >=60 years old who were admitted to a hospital during a 9-year period and identified five patients with poststroke psychosis. All of them had right frontoparietal lesions and showed a significantly greater degree of subcortical atrophy than five stroke patients without psychosis, matched for age and lesion size and location. Moreover, three of the five patients with poststroke psychosis had seizures, whereas no seizures were seen in any of the five nonpsychotic patients.

Generally, patients respond to treatment with neuroleptic medications, although, in some treatment-resistant cases, anticonvulsant medications have been reported to be useful.50


  CONCLUSIONS

 
TOP
 ABSTRACT
 INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
 CONCLUSIONS
REFERENCES
 
There are numerous neuropsychiatric disorders that may occur after stroke (Table 1). The limited space for this review has restricted us to examining only a few of these disorders. Depression and anxiety disorder are two of the most common poststroke neuropsychiatric disorders, and they frequently occur as comorbid conditions. In addition to producing a significant degree of psychological distress, both of these disorders have been shown to be associated with particular lesion locations and to adversely affect the physical recovery from stroke.

Similarly, catastrophic reactions, pathological affect, and poststroke psychosis are disorders that may occur after stroke and probably influence the course of recovery as well as quality of life. Given the frequent occurrence of these disorders and the magnitude of the public health problem produced by stroke, it is remarkable how few treatment studies have been conducted. Apart from the early treatment interventions to prevent infarction, treatment of neuropsychiatric poststroke disorders appears to have the greatest potential for improving the outcome and quality of life for people who have suffered a stroke.


  ACKNOWLEDGMENTS

 
This work was supported in part by the following National Institute of Mental Health grants: MH40355, MH52879, and MH53592.


  REFERENCES

 
TOP
 ABSTRACT
 INTRODUCTION
 POSTSTROKE DEPRESSION (PSD)
 POSTSTROKE ANXIETY DISORDER
 OTHER POSTSTROKE...
 CONCLUSIONS
 REFERENCES
 

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