Aphasia, depression, and non-verbal cognitive impairment in ischaemic stroke.

Aphasia, depression, and cognitive dysfunction are common consequences of stroke, but knowledge of their interrelationship is limited. This 1-year prospective study was designed to evaluate prevalence and course of post-stroke aphasia and to study its psychiatric, neurological, and cognitive correlates. We studied a series of 106 consecutive patients (46 women and 60 men, mean age 65. 8 years) with first-ever ischaemic brain infarction. The patients were clinically examined, and presence and type of aphasia were evaluated during the 1st week after stroke and 3 and 12 months later. Psychiatric and neuropsychological evaluations were performed 3 and 12 months after stroke. Aphasia was diagnosed in 34% of the patients during the acute phase, and two thirds of them remained so 12 months later. Seventy percent of the aphasic patients fulfilled the DSM-III-R criteria of depression 3 months and 62% 12 months after stroke. The prevalence of major depression increased from 11 to 33% during the 12-month follow-up period. The non-verbal neuropsychological test performance in the aphasic patients was significantly inferior to that of the patients with dominant hemisphere lesion without aphasia. One third of the patients with ischaemic stroke suffer from communicative disorders which seem to increase the risk of depression and non-verbal cognitive deficits. Although the prevalence of depression in aphasic patients decreases in the long term, the proportion of patients suffering from major depression seems to increase. We emphasize the importance of the multidimensional evaluation of aphasic stroke patients.

Auditory P300 event related potential in minor ischemic stroke.

OBJECTIVE: Various degenerative cerebral diseases and even depression may cause abnormalities of the cognitive event related potentials (ERPs). We conducted the present study to elucidate the effects of ischemic stroke on the P300 ERP component. MATERIAL AND METHODS: We recorded the P300 wave using an auditory oddball paradigm in 38 consecutive brain infarct patients with mild neurological deficits at 3 and 12 months post-stroke, and in 29 healthy control subjects. RESULTS: Brain infarction slightly prolonged the P300 latency, and the observed delay was related to the presence and degree of post-stroke depression evaluated with the Zung Depression Scale and the DSM-III criteria. Infarction did not affect the P300 amplitude or its distribution on the scalp. The results of the patients with hemispheric brain infarction and those of the patients with brainstem infarction were similar, and also the values of the patients with the left- and right-sided lesions. The normal physiological correlation between subject age and the P300 latency was absent at 3 months post-stroke, but was present at 12 months post-stroke. CONCLUSION: Brain infarction delays the P300 ERP and temporarily distorts its age-related physiology. The increase of the P300 latency seems to be associated with the post-stroke depression.

Poststroke depression correlates with cognitive impairment and neurological deficits.

BACKGROUND AND PURPOSE: The prevalence of poststroke depression is known to be high, but the knowledge of its neuropsychological correlates is limited. This 12-month prospective study was designed to evaluate the natural history of poststroke depression and to study its neuropsychological, clinical, and functional associates. METHODS: We studied a series of 106 consecutive patients (46 women and 60 men, mean age 65.8 years) with acute first-ever ischemic stroke. The patients underwent a neurological, psychiatric, and neuropsychological examination at 3 and 12 months after the stroke. The psychiatric diagnosis of depression was based on DSM-III-R-criteria. RESULTS: Depression was diagnosed in 53% of the patients at 3 months and in 42% of the patients at 12 months after the stroke. The prevalence of major depression was 9% at 3 months and 16% at 12 months. There was an association between poststroke depression and cognitive impairment; the domains most likely to be defective in stroke-related depression were memory (P=0.022), nonverbal problem solving (P=0.039), and attention and psychomotor speed (P=0.020). The presence of dysphasia increased the risk of major depression. The depressive patients were more dependent in ADL and had more severe impairment and handicap than the nondepressive patients. CONCLUSIONS: More than half of the patients suffer from depression after stroke, and the frequency of major depression seems to increase during the first year. In addition to dysphasia, poststroke depression is correlated with other cognitive deficits. We emphasize the importance of psychiatric evaluation of stroke patients.