Effects of interhemispheric and intrahemispheric lesion location

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We first examined the effect of unilateral ischemic lesions on depression in a series of patients who had no known risk factors for depression and were admitted to hospital after an acute stroke lesion (Robinson et al. 1984a). All patients were right-handed and had a single stroke lesion of the right or left hemisphere which was visible on computed tomography (CT) scan. Patients were included only if they had no previous personal or family history of psychiatric disorder.

Major or minor depression was found in 14 of 22 patients with left hemisphere lesions and 2 of 14 patients with right hemisphere lesions (p < 0.01) (Robinson et al. 1984a). In addition to the increased frequency of depression in patients with left hemisphere lesions, the intrahemispheric lesion location was also an important determinant of the existence of depression. Among 10 patients who had left anterior lesions (i.e., the anterior border of the lesion was rostral to 40% of the overall anterior-posterior length of the brain on CT scan), 6 had depression as compared to only one of eight patients with left posterior lesions (i.e., the anterior border of the lesion was caudal to 40% of the anterior-posterior distance) (p < 0.05). Thus, patients with left anterior hemisphere injuries were found to have a significantly greater frequency of major depression than patients with any other lesion location.

We also looked at this issue in another study of 45 patients with single lesions restricted to either cortical or subcortical structures in the right or left hemisphere (Starkstein et al. 1987). The background characteristics of these patients who are grouped according to whether they had a cortical or subcortical lesion location are shown in Table 10.1. Patients with subcortical lesions had infarcts limited to the basal ganglia, thalamus, or white matter of the internal capsule without any involvement of cortical gray matter or subcortical white matter. Patients with cortical lesions had ischemic damage of the cerebral cortical gray matter or underlying white matter.

We found that 44% of patients with left cortical lesions were depressed (i.e., 4 of 16 had major depression) and 39% of patients with left subcortical lesions were similarly depressed (i.e., 4 of 13 with major and 1 of 13 with minor depression). In contrast, only 11% of patients with right cortical lesions (none of nine with major and one of nine with minor depression) and 14% of patients with right subcortical lesions were depressed (one of seven with major, zero of seven with minor

Table 10.1. Characteristics of patients: lesion location

Left Cortical

Right Cortical

Left Subcortical

Right Subcortical

(n = 16)

(n = 9)

(n = 13)

(n = 7)

Age (mean ± SD)

59 ± 12

54 ± 13

63 ± 12

54 ± 8

Sex (% male)





Race (% black)





Marital status (% married)





Mean # children





Origin (% rural)





Mean # siblings





Tobacco use (% >pack/day)





Previous medical illness





(% life threatening)

Time since stroke

23 ± 25

18 ± 14

19 ± 21

20 ± 19

(mean days ± SD)

Education (mean years ± SD)


11 ± 4

9 ± 3

8 ± 3

Family history of psychiatric





disorder (% positive)

Personal history of psychiatric

disorder (% positive)










CS 0

□ Major depression □ Minor depression *p < 0.05

Figure 10.1 The percent of patients with major or minor depression divided by stroke lesion location.

LC = left cortical, LS = left subcortical, RC = right cortical, RS = right subcortical. Patients with either left cortical or left subcortical lesions had a significantly higher frequency of major depression during the acute post-stroke period than patients with right hemisphere lesions (data from Starkstein, Brain 1987).

depression) (Fig. 10.1). Patients with lesions of the left hemisphere had significantly higher rates of depression than patients with right hemisphere lesions, regardless of the cortical or subcortical location of the lesion (p < 0.01).

The patients were further grouped according to whether they had anterior and posterior lesions using the anatomical criteria that the anterior border of the lesion was located in the frontal lobe. All five patients with left cortical anterior lesions involving the frontal lobe had depression (three major and two minor depression) as compared to only 2 of 11 patients with left cortical posterior lesions whose rostral border involved the temporal, parietal, and/or occipital cortex (one major, one minor depression, p < 0.01). Moreover, four of the six patients with left subcortical anterior lesions had major depression (none had minor depression) as compared to one minor depression (none with major depression) among seven patients with left subcortical posterior lesions (p < 0.01).

In a subsequent study (Starkstein et al. 1988) which included the 20 patients with subcortical lesions from the previous study as well as five new patients, we compared patients with lesions limited entirely to the basal ganglia/internal capsule with those having thalamic lesions of the right or left hemisphere with no evidence of other brain lesions. Basal ganglia (caudate and/or putamen) lesions produced major depression in seven of eight patients with left hemisphere lesions but in only one of seven patients with right hemisphere lesions. None of the patients with left (n = 6) or right (n = 4) thalamic lesions had major depression (p < 0.001).

The largest study examining clinical-pathological correlations in patients with stroke was reported by Vataja et al. (2001). Twelve to twenty weeks following stroke, 275 patients were examined, using the Structured Interview for Clinical Assessment in Neuropsychiatry (SCAN) and diagnostic and statistical manual (DSM)-IV

diagnostic criteria for depressive disorders. The authors did not evaluate the hypotheses that patients with left frontal or left basal ganglia lesions in the first 2 months following stroke would have a greater frequency of major depressive disorder than patients with comparable right hemisphere lesions and that there would be a significant correlation between the proximity of the lesion to the frontal pole and severity of depression. Of the 275 patients, 83 (30%) had prior stroke and 54 (20%) had prior depression. A logistic regression analysis examining independent magnetic resonance imaging (MRI) correlates of the existence of depression was conducted. Depressed patients (n = 71) with major depression and (n = 38) with minor depression were found to have an increased mean frequency of infarcts in the genu of the internal capsule on the left side (OR: 3.2; 95% CI: 1.0-10.1) and in the pallidum of either side (OR: 1.6; 95% CI and over 1.1-2.3). In addition, the mean volume of infarcts in right occipital lobe was smaller in depressed compared with non-depressed patients (OR: 0.98; CI: 0.96-0.99). These authors have recently published a secondary analysis of this data utilizing the 70 who had a single infarct on magnetic resonance (MR) scan. A logistic regression analysis found that infarct localization in the pallidum of either side was the only correlate of poststroke major or minor depression. When a separate analysis of each hemisphere was done, lesions of the caudate and pallidum on the left hemisphere were significantly associated with depression while lesions of these structures in the right hemisphere were not (Vataja et al. 2004).

Studies by other investigators have sometimes shown similar lateralized effects of stroke lesions but sometimes have not. The variable which seemed most likely to account for differences in findings between studies was "time since stroke". For example, in contrast to our studies of acute stroke patients examined 1-2 weeks following stroke, a study of 88 Australian patients seen in a rehabilitation hospital 8.4 weeks (average) following stroke found that 43% of patients with left hemisphere lesions had major or minor depression and 38% of patients with right hemisphere lesions had depression (Morris et al. 1990). Similarly, Eastwood et al. (1989) examined 87 patients admitted to rehabilitation hospital 12 weeks (average) after stroke. Of 28 patients with left hemisphere lesions, 50% had either major or minor depression while among 45 patients with right hemisphere stroke 62% had major or minor depression. Thus, both of these studies which examined patients in rehabilitation hospitals at approximately 2-3 months poststroke failed to show a lateralized effect of hemispheric brain injury on frequency of depression.

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