15
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Aphasia remains one of the most perplexing problems for investigators of neu-ropsychiatric disorders following stroke. Since the diagnoses of all neuropsychi-atric disorders requires subjective responses by the patient to verbal or written questions, the existence of even a moderate degree of comprehension deficit may represent a severe obstacle to the diagnoses of numerous neuropsychiatric disor-ders. This conundrum has led almost all investigators of poststroke neuropsychi-atric disorders to exclude patients with moderate or severe comprehension deficits from their studies (Robinson et al. 1983; House et al. 1990; Astrom et al. 1993).
In spite of the fact that almost all investigations of poststroke depression have excluded patients with comprehension aphasia, the hypothesized cause of many poststroke depressive disorders has been aphasia (Gainotti 1972; Benson 1979).
Gainotti (1972) hypothesized that the depressive-catastrophic reaction associated with left hemisphere lesions represented an understandable response of depression and angry outbursts to the loss of language because language represents one of the most important elements of the patient’s life. Similarly, Benson (1979) hypothe-sized that depression sometimes represents a secondary psychological reaction to the loss of language. As a result of the exclusion of patients with comprehensive aphasia (e.g., fluent aphasias and global aphasias) two major questions arise. First, what is the true prevalence of depression among patients with aphasia. Does the exclusion of these patients significantly alter our estimates of prevalence rates, as well as clinical and pathological correlates of depression. The second question aris-ing from the exclusion of patients with comprehension impairment is whether alternative means can be devised to diagnose depression in this population of patients that will withstand tests of reliability and validity? Although patients with moderate to severe comprehension deficits have been excluded from our studies, we have included patients with at least mild forms of fluent, non-fluent and global aphasia in most of our studies.
In our initial studies, the existence of moderate to severe comprehension deficit was determined by requiring the patient to score within 10 points following verbal
readministration of the Zung depression scale approximately 10 min apart. For the past 20 years, however, we have utilized the Token test which is specifically designed to assess comprehension. The Token test examines the patient’s ability to comprehend and carry out verbal instructions related to the shape and color of plastic tokens. For example, in Part 1, patients are asked to point to the red square or the blue triangle. Patients who are unable to pass Part 1 of the Token test which involves only these simple tasks are excluded from our studies. Our studies, there-fore, have included patients with mild fluent (i.e., Wernicke’s) aphasia, global aphasia, and transcortical sensory aphasia as well as patients with any severity of non-fluent (Broca’s) aphasia. Patients with Broca’s aphasia are asked the standard questions in the psychiatric interview but their responses may include such non-verbal behaviors as pointing appropriately to yes or no responses or communicat-ing uscommunicat-ing non-verbal gestures or limited verbal responses.
In our study of 103 patients with acute stroke, 42% of the patients who met study inclusion criteria and had left hemisphere lesions were diagnosed as having fluent, non-fluent, transcortical, or global aphasia, or severe anomia (this does not include the patients who were excluded from the study due to comprehension deficits). Our latest data on the relationship between aphasia and depression is shown in Table 15.1 (Part A). These findings indicate that among patients without significant comprehension deficits, neither major nor minor depression was more common among aphasic as compared to non-aphasic patients.
We also examined the relationship between depression and aphasia in another group of 25 patients who were examined approximately 3 months following stroke.
Based on findings from the Boston aphasia examination, patients were grouped according to whether they had non-fluent (n 7), fluent (n 8), or global (n 9) aphasia (Robinson and Benson 1981). Although the groups were not significantly different with respect to their background characteristics, patients with non-fluent aphasia had significantly higher Zung, Hamilton, and Nurses’ depression rating scale scores than the other two groups (Fig. 15.1). There were, however, no differ-ences in mean depression scores between patients with fluent aphasia and patients with global aphasia. There were no statistically significant differences between flu-ent, non-fluflu-ent, and global aphasic patients in terms of their severity of impair-ment in activities of daily living (ADL) (i.e., Johns Hopkins functioning inventory or JHFI score) or severity of cognitive impairment (i.e., mini-mental state exam score). Thus, this study demonstrated that non-fluent aphasic patients had signif-icantly greater severity of depression than fluent or global aphasic patients in the absence of significant differences in their physical or cognitive deficits.
Based on these findings, one might wonder why there is a greater severity of depression in patients with non-fluent as compared to fluent or global aphasia. It might be proposed, for example, that patients with non-fluent aphasia were most 172 Poststroke depression
depressed because of their greater awareness of their impairments. Another possi-ble explanation, however, is based on lesion location. Patients with fluent and non-fluent aphasias generally have different lesion locations and the lesion locations which are frequently involved in non-fluent aphasia might explain the increased association of this type of aphasia with depression. In an effort to answer this ques-tion, we conducted another study of 25 consecutive patients with aphasia evalu-ated using the Western aphasia battery (Kertesz 1982; Starkstein and Robinson 1988). Seven patients had anomia, six had Wernicke’s aphasia, six had Broca’s aphasia, four had global aphasia, and two had transcortical sensory aphasia. The depressive diagnoses are shown in Part B of Table 15.1. There was no significant difference in the frequency of depression among patients with milder forms of aphasia (i.e., anomia or transcortical sensory aphasia) compared with more severe forms of aphasia (i.e., Broca’s, Wernicke’s, or global aphasia). On the other hand, when we examined the relationship with lesion location, there was a consistent 173 Relationship of aphasia to depression
Table 15.1. The relationship between the existence of aphasia and depression
No of patients with
Major Minor No mood
depression depression disorder A. Patients with acute stroke (n 265) (n 44) (n 51) (n 170)
Aphasia 8 7 13
No aphasia 36 44 157
(depressed versus non-depressed, NS, p 0.1079) B. Patients given Western aphasia
(n 25)
Anomia (n 7) 2 2 3
Broca’s (n 6) 3 1 2
Wernicke (n 6) 0 3 3
Global (n 4) 2 0 2
TCS (n 2) 2 0 0
(depressed versus non-depressed, p NS) C. Patients with subcortical lesions (n 25)
Basal ganglia
Aphasia 3 0 0
No aphasia 5 2 5
Thalamus
Aphasia 0 1 1
No aphasia 0 1 7
(depressed versus non-depressed, p NS) TCS transcortical sensory aphasia.
association between depression and left frontal or left basal ganglia injury. Of the seven patients with major depression and positive computed tomography (CT) scans, all had lesions involving the left anterior brain region (i.e., the left frontal cortex in five cases, and the left basal ganglia in two cases). On the other hand, only one of the 10 non-depressed patients had a left anterior brain injury (p 0.01).
These findings suggest that lesion location rather than type of aphasia may be the most relevant variable in poststroke major depression. The association between Broca’s aphasia and the severity of depression reported in the Robinson and Benson study (1981) may be explained by the fact that Broca’s area is located in the posterior-inferior aspect of the left frontal lobe (see Fig. 2.1). As discussed in Chapter 10 on the relationship of depression to lesion location during the first two months following stroke, left frontal and left basal ganglia lesions are significantly more frequent among patients with major depression than any other lesion location.
We have also examined the role of subcortical structures in depression and aphasia. The role of subcortical structures in the production and comprehension of language has been the subject of numerous studies [e.g. (Crosson 1985)]. In an effort to clarify the relationship between aphasia and depression, we examined patients with lesions restricted to the subcortical grey nuclei with or without involvement of the white matter of the internal capsule (Starkstein and Robinson 1988). If aphasia led to the development of depression, one would expect that, whether the aphasia was produced by a subcortical lesion or a cortical lesion, depression should follow. Included in this study were eight patients with lesions of 174 Poststroke depression
0 5 10 15 20
Hamilton depression
0 25 50 75
Non-fluent aphasia Fluent aphasia Global aphasia
Increasing depression score Zung and analogue score
Nurses’
mood
Overall depression
Analogue mood
Zung depression Type of scale
p 0.05
Figure 15.1 Mean SEM depression scores using four different measurement scales and an overall scale factoring together the four instruments grouped by type of aphasia. Patients with Broca’s (i.e., non-fluent) aphasia (n 7) had the highest depression scores on all scales (significant on four of the five measures) compared to Wernicke’s (i.e., fluent) aphasia (n 8) or global aphasia (n 9) (reprinted from Robinson and Benson 1981 with permission from Elsevier).
the left basal ganglia and seven with lesions of the right basal ganglia. In addition, there were six patients with lesions restricted to the left thalamus and four with right thalamic lesions. Aphasia occurred only in patients with left hemisphere lesions.
The frequency of depression in patients with non-fluent, fluent or global aphasia and lesions of the basal ganglia or thalamus is shown in Part C of Table15.1. There was a significant association between major depression and basal ganglia lesions as compared to thalamic lesions (p 0.01). On the other hand, there was no significant increase in the frequency of depression among patients with basal ganglia or thal-amic lesions based on the presence or absence of aphasia. Thus, these findings suggest that, as with cortical lesions, the location of the lesion appears to be a more important factor in determining the frequency of depression than the existence of aphasia.
Herrmann et al. (1993) reported on the results of a study of 21 acute and 21 chronic aphasic patients with single stroke lesions of the left hemisphere. The acute stroke patients had significantly higher depression scores (i.e., Cornell depression scale) compared to the chronic stroke patients with non-fluent aphasias (i.e., Broca’s or global aphasia) who also had a greater frequency of major depression compared to patients with fluent aphasias (i.e., Wernicke’s or anomic aphasia) (p 0.0014). These authors also found a significant linear correlation between the severity of depression and the proximity of the lesion to the frontal pole. These findings are in agreement with our previously described studies of aphasia and are consistent with the hypothesis that non-fluent aphasia does not cause depression but frequently coexists with it because lesion sites associated with depression and non-fluent aphasia are anatomically close.
Astrom et al. (1993) also reported a significant association between major depression and aphasia in seven patients with language impairment who could be assessed for depression. Dysphasic patients were significantly more likely to be depressed than non-dysphasic patients both during the acute hospitalization period (p 0.001) and at 3 months follow-up (p 0.001) but not at 1, 2, or 3 years follow-up. Patients, however, were not grouped according to whether they had fluent or non-fluent aphasia, and the relationship between depression and anterior left hemisphere lesions, independent of aphasia, was not examined.
Dam et al. (1989) examined 92 patients between 8 and 1280 days since their stroke. Aphasia severity was rated on a 4-point scale ranging from none to severe.
These investigators found no significant correlation between Hamilton depression (Ham-D) score and the severity of aphasia.
Damecour and Caplan (1991) examined 54 patients with fluent or non-fluent (n 32) aphasia, who were less than (n 23) or more than (n 31) 6 months poststroke. Zung depression rating scales from significant others and speech pathologists were obtained. Depression was determined using a cutoff score on the Zung. Overall 15% of the population was depressed, but using mean rating scores 175 Relationship of aphasia to depression
or frequency of depression, no significant differences were found among the groups either in the acute or chronic stroke period. They concluded that patients with Wernicke’s aphasia do not experience depression more frequently than patients with Broca’s aphasia and that depression is not frequent in this population. Of the fluent aphasics, 84% were interviewed but the reliability of responses was not reported.
Kauhanen et al. (2000) examined a consecutive series of 106 patients (46 women and 60 men, mean age 65.8 years) with first ever ischemic stroke. Patients were evaluated for aphasia during the first week after stoke and for aphasia plus psychi-atric and neuropsychological impairment at 3 and 12 months poststroke. Aphasia was diagnosed in 34% of the patients during the acute phase and two-thirds of these patients remained aphasic 12 months later. Seventy percent of the aphasic patients fulfilled DSM-III-R criteria for depression at 3 months and 62% at 12 months poststroke. During this time, the prevalence of major depression in the overall population increased from 11% at 3 months to 33% at 12 months. They concluded that aphasia represented a significant risk factor for poststroke depres-sion. Furthermore, although the overall prevalence of depression decreased from 3–12 months poststroke, patients who continued to have aphasia are increasingly likely to have major depressive disorder. The difficulty in evaluating this study is that the diagnosis of depression was based on observation by relatives or hospital staff without showing the reliability or validity of these assessments.
In an attempt to establish an instrument to assess depression in aphasic patients with stroke, Sutcliffe and Lincoln (1998) developed an observer based depression rating scale called the stroke aphasic depression questionnaire (SADQ). Seventy patients who were discharged to home following acute stroke were evaluated using the SADQ, the hospital anxiety and depression scale (HADS) and the Wakefield depression inventory. The correlation between the aphasia questionnaire score and the HADS was 0.32 using a shortened 10-item version of the scale and 0.67 with the Wakefield depression inventory. Seventeen aphasic patients examined at 4-week intervals demonstrated a test-retest reliability of 0.72.
Although Sutcliffe and Lincoln (Sutcliffe and Lincoln 1998) found a relationship between the SADQ and severity of depression, Leeds et al. (2004) examined 65 stroke patients without significant aphasia using the shortened version of the SADQ. The Geriatric depression scale correlated with the SADQ score with a cor-relation coefficient of 0.40. This relatively weak corcor-relation between patient’s self report of depression and relatives scores on the SADQ led the authors to conclude that the SADQ-10 did not appear to be a valid measure of depression. The fact that both the Sutcliffe and Lincoln (1998) and the Leeds (2004) studies found only weak to moderate correlations between self reported depression severity and observer rated depressive symptoms indicates that the problem of assessment of depression in patients with comprehension impairment remains a significant obstacle to the investigation of depressive disorders in these patients.
176 Poststroke depression
It has been suggested that the exclusion of aphasic patients with severe compre-hension deficits following parietal-temporal lesions may have skewed the association between depression and lesion location to more anterior (i.e., frontal) brain regions (Ross et al. 1986). If one assumes that the correlation between depression and anterior-posterior lesion location was an artifact produced by excluding depressed patients with posterior lesions (i.e., fluent aphasics), there would have to be a very high frequency of depression in these excluded aphasic patients to negate the cor-relation of depression with proximity of the lesion to the frontal pole. Since the fre-quency of major depression among patients with acute left anterior lesions was found to be approximately 60%, the rate of major depression among patients with comprehension disorders would have to be equally high. If findings in studies of patients with mild forms of fluent and global aphasia are extrapolated, however, the frequency of depression in these groups of patients is significantly lower than that among patients with non-fluent aphasia (Robinson and Benson 1981; Herrmann et al. 1993). This conclusion, however, is based on the assumption that patients with mild fluent aphasias had the same rate of depression as patients with severe non-fluent aphasia (Robinson and Benson 1981). However, in the Damecour and Caplan study there was a modest correlation between depression severity and fluent aphasia severity (r 0.3–0.6 depending on the scale). The affective appearance and behavior of patients with severe fluent aphasias have been described by Benson (1973) as cheer-ful or even euphoric and in rare instances as fearcheer-ful or paranoid, but not depressed.
Thus, although it is possible that these patients who cannot be examined could have a very different frequency of depression compared with patients with mild fluent aphasias, the available data suggest that this is not the case.
Although aphasia does not appear to be a cause of depression, depression and apha-sia may interact significantly throughout the course of poststroke recovery. In Chapter 14, I discussed in detail our finding concerning the effect of depression on recovery from impairment in ADL (Parikh et al. 1990). One of the factors derived from the activities of daily living scale (ADLs) JHFI was language. We found that patients who were depressed (major or minor depression, n 25) immediately after stroke had not recovered in language function to the same extent as patients who were not depressed (n 38) even when other relevant factors were controlled. Thus, although further research, including treatment studies, are needed, there is some evidence to support the hypothesis that there are important effects of depression on recovery from aphasia.
In summary, aphasia is a common sequelae of dominant hemisphere brain injury. Although the loss of language might understandably lead to depression, the available evidence suggests that non-fluent (Broca’s) aphasia appears to be associ-ated with the highest frequency of depression. The true prevalence, however, of depression in patients with aphasia and comprehension deficits remains uncertain.
The association between non-fluent (Broca’s) aphasia and depression may be due to the fact that both depression and non-fluent aphasia result from lesions of the 177 Relationship of aphasia to depression
left frontal lobe. The development of alternative diagnostic instruments based on relatives’ observations has not led to valid measures of depression in patients with comprehension deficits. Although much of the emphasis has been placed on the effect of aphasia in producing depression, it seems likely that poststroke depression may have a significant impact on patients’ recovery from aphasia. Future studies should examine the effect of antidepressant treatment on the clinical manifesta-tions and longitudinal recovery from aphasic disorders.
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178 Poststroke depression