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BACKGROUND: Stroke patients commonly suffer from neuropsychiatric disorders, such as depression, that negatively influence stroke outcome. Diagnosis, treatment and prevention of post-stroke psychiatric disorders including depression are under debate. OBJECTIVE: To study the course of depression after stroke. METHODS: One hundred and ninety first-ever stroke patients were screened for depressive symptoms at 1, 3, 6, 9, and 12 months after stroke. Diagnosis of depression was made according to the DSM-IV criteria of major and minor depression. RESULTS: Follow-up was completed in 138 patients. The cumulative incidence of post-stroke depression (PSD) in 1 year was 36.2%. One month after stroke the prevalence of PSD was 18.8%. Thirty percent of patients who were depressed in the first three months did not reach cut-off levels on depression screening instruments at the following assessments. In 44% of these patients symptoms recurred. Recurrent cases were older than patients with limited disease. In 40% of PSD patients depression persisted for at least two consecutive following follow-up visits. Persistent cases were more disabled and suffered more often from major depression. CONCLUSION: Half of PSD patients become depressed within the first month after stroke. Although most patients recover, a clinician has to be aware that symptoms can recur especially in older patients and that in patients with major depression symptoms may be persistent. In these patients treatment should be considered, whereas in patients with limited disease an observational approach may suffice.

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BACKGROUND: Depression is a frequent problem in stroke patients but, all too often, the problem goes unrecognized. How depression-like symptoms in post-stroke depression (PSD) should be interpreted is still subject to debate. If PSD has a distinct symptom profile of depression accompanying other chronic vascular somatic conditions then this could imply that PSD is a specific disease entity. OBJECTIVE: To study whether depressed stroke patients exhibit other signs and symptoms than patients suffering from depression after myocardial infarction (MI). METHODS: Depressive signs and symptoms were measured using the Hospital Anxiety and Depression Scale and the 17-item Hamilton Depression Rating Scale. The results of 190 stroke patients were compared with the results of 198 MI patients every 3 months during the first year after the event. RESULTS: Depressed stroke patients exhibited more loss of interest, psychomotor retardation, and gastro-intestinal complaints as compared to depressed MI patients. However, in multivariate analyses including both depressed and non-depressed stroke and MI patients, no specific symptom profile was found to differentiate between the two depressive syndromes by looking at the modifying effect of stroke vs MI on the occurrence of specific symptoms in depression. CONCLUSION: Although in their clinical presentation, depressed stroke patients exhibit a symptom profile different from depressed MI patients, this is not due to differences in the depressive syndrome in these two patient groups but it reflects differences between stroke and MI patients in general.

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BACKGROUND: Both the lesion location hypothesis and the vascular depression hypothesis have been proposed to explain the high incidence of depression in stroke patients. However, research studying both hypotheses in a single cohort is, at present, scarce. OBJECTIVE: To test the independent effects of lesion location (left hemisphere, anterior region) and of co-occurring generalized vascular damage on the development of depression in the first year after ischemic stroke, while other risk factors for depression are controlled for. METHODS: One hundred and ninety consecutive patients with a first-ever, supratentorial infarct were followed up for one year. CT was performed in the acute phase of stroke, while in 75 patients an additional MRI scan was also available. Depression was assessed at 1, 3, 6, 9, and 12 months after stroke using self-rating scales as screening tools and the SCID-I to diagnose depression according to DSM-IV criteria. RESULTS: Separate analyses of the lesion location hypothesis and the vascular depression hypothesis failed to reveal significant support for either of these biological models of post-stroke depression. Similar negative results appeared from one overall, multivariate analysis including variables of both focal and generalized vascular brain damage, as well as other non-cerebral risk factors. In addition, level of handicap and neuroticism were independent predictors of depression in this cohort, as has been reported previously. CONCLUSION: This study supports neither the lesion location nor the vascular depression hypothesis of post-stroke depression. A biopsychosocial model including both premorbid (prior to stroke) vulnerability factors, such as neuroticism and (family) history of depression, as well as post-stroke stressors, such as level of handicap, may be more appropriate and deserves further study.

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Manipulation of blood pressure (BP) in acute stroke may improve outcome. Despite various studies, data on the prognostic significance of early BP in stroke remain unclear. Therefore, we studied the relationship between various BP variables in the acute phase of stroke and functional outcome at 3 months. Blood pressures were collected by reviewing BP records of 817 patients who were admitted to our stroke unit between 1987 and 1992. Besides the first systolic and diastolic admission BP (SBP and DBP), we also used the mean of the daytime as well as the night-time systolic and diastolic BP values. Finally, we studied the relationship between the decrease in BP between day 0 and 4 and outcome. As dependent outcome variable we used the Rankin handicap score at 3 months dichotomized in a score >3 (poor outcome) vs a score 3 (good outcome). A total of 430 patients were admitted within 24 h following stroke onset. There was no significant relationship between the systolic and diastolic BP and the outcome at 3 months. Only night-time systolic BP 165 mm Hg (odds ratio (OR) 2.8; 95% CI 1.1-6.8), night-time diastolic BP 60 mm Hg (OR 8.1; 95% CI 1.1-58.3), and a decrease in daytime diastolic BP between day 0 and 4 of 10 mm Hg (OR 3.0; 95% CI 1.1-7.9) showed a significant relationship with poor outcome. Our findings suggest that admission BP values may not reliably reflect any impact of BP on stroke outcome. They also suggest a potential differential effect of BP manipulation: increasing or decreasing BP may be beneficial for patients with BP extremes in one direction, but detrimental for those with BP values in the opposite direction.

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Data on the relationship between idiopathic Parkinson's disease (IPD) and stroke are conflicting. In this study, we examined the frequency of IPD in stroke patients registered in the Maastricht Stroke Registry. With the use of three different search strategies, we found eight individuals with IPD amongst a total of 1,516 stroke patients. We had expected to find approximately 30 IPD patients (relative risk 0.27; 95% confidence interval 0.11-0.53), based on IPD prevalence figures from a Dutch population-based study. We speculate that dopamine deficiency may protect against ischaemic brain damage, perhaps by reducing the effects of excitotoxicity.

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Blood pressure (BP) is often elevated in acute stroke. However, predictors of BP level and BP course during the first week after a stroke remain unknown. Knowledge of such factors may be of relevance when manipulation of early BP levels are considered as potentially therapeutic in acute stroke. In this study, BP data was collected by reviewing BP records of patients who were admitted with a first cerebral infarct to our stroke unit and who had their first BP recordings within 24 hours after stroke onset. Age and known hypertension before stroke were significantly associated with elevated poststroke BP level, whereas ischemic heart disease was associated with a lower BP level. BP decline in the poststroke period related to the initial BP elevation. BP in hypertensive patients remained higher than in nonhypertensive patients during the first poststroke week. Between day 0 and day 4 after stroke onset, only the daytime systolic BP decline showed a significant association with previously established hypertension. There was no difference in initial BP level, nor in the rate of BP decline between day 0 and 4 in patients with a lacunar infarct and those with an infarct involving the cortex. These findings indicate that BP increase poststroke is not a general phenomenon, nor is BP decline in the first poststroke week. Known hypertension is probably the strongest predictor of poststroke BP increase. Hypertensive patients are more sensitive to sympathetic stimulation. Therefore, when lowering of elevated BP early poststroke is tested as a potential neuroprotective modality, it may best be achieved by treating patients with sympathicolytic, antihypertensive drugs.

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We studied the relationship between infarct size and degree of internal carotid artery stenosis in 227 stroke patients without a source of embolism in the heart, who had a CT-verified territorial brain infarct. We used logistic regression analysis adjusting for differences between groups in co-associated variables such as age, sex, hypertension, diabetes mellitus, and a history of ischaemic heart disease. Ipsilateral carotid stenosis greater than 50% was more strongly associated with large than small infarcts; adjusted odds ration [(a)OR]: 4.56; 95% confidence interval (CI): 1.21-17.2; P = 0.02. For ipsilateral carotid occlusion the association was even stronger--(a)OR: 36.80; 95% CI: 2.54-533; P = 0.007. When large infarcts were compared with infarcts of small and moderate size together the ORs were 2.29, 95% CI 1.14-4.58 and 2.57, 95% CI 1.17-5.67 for carotid stenosis or occlusion, respectively. Our data show a relationship between greater than 50% carotid stenosis or occlusion and large brain infarcts. We suggest that haemodynamic impairment may contribute to infarct size in territorial infarcts of non-cardiac origin.

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A patient developed a severe chorea whilst taking Chien Pu Wan pills. At examination only a high blood level of manganese (3 times the normal value) was found. Chemical analysis of these Chinese herbal pills showed that each pill contained 14 micrograms of manganese. By taking 3 to 5 pills a day, our patient was receiving 42 to 70 micrograms of manganese over and above the normal absorbed quantity of 60-90 micrograms daily. Because the chorea developed during the use of these pills and resolved when the blood levels of manganese went down, and because the high manganese blood levels were the only abnormality we found, we assumed these Chien Pu Wan pills and the subsequent manganese intoxication to be the cause of the chorea. Manganese poisoning may cause extrapyramidal signs such as parkinsonism, dystonia and chorea. This form of alternative therapy is not yet subject to legislation. In order to be able to control the nature and (side) effects of this kind of therapy, legislation is required.

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