Dementia of depression or depression of dementia in stroke?

This study describes the correlation between changes in mood symptoms assessed by the Hamilton Depression Rating Scale (HDRS) and intellectual impairment assessed by the Brief Cognitive Rating Scale (BCRS) and Mattis Dementia Rating Scale (MDRS) in 166 unselected 1-year survivors after stroke, in whom post-stroke depression (PSD) has previously been described and validated. The course of intellectual impairment associated with PSD was compared with the course of intellectual impairment in non-PSD patients. In general, improvement in mood symptoms was correlated with an improvement in intellectual function. However, in 53 PSD patients improvement in intellectual performance was absent, despite the fact that the patients reported being significantly less distressed by dementia symptoms. Antidepressive medication did not lead to any improvement in MDRS score. No evidence was found to support the hypothesis of 'dementia of depression'. To the contrary, the findings indicate 'depression of dementia'.

Pathoanatomic correlation between poststroke pathological crying and damage to brain areas involved in serotonergic neurotransmission.

BACKGROUND AND PURPOSE: The aim of the study was to correlate the severity of poststroke pathological crying with lesion size and location. METHODS: Twelve selected stroke patients were ranked in terms of overall clinical severity of the syndrome of pathological crying, and the size and location of the stroke lesion(s) were determined by magnetic resonance imaging. RESULTS: The patients with the clinically most severe pathological crying had relatively large bilateral pontine lesions without lesions in the hemispheres. The intermediate group had bilateral central hemispheric lesions, and the clinically least affected patients had mainly unilateral large subcortical lesions. CONCLUSIONS: Poststroke pathological crying may be attributable to stroke-induced partial destruction of the serotonergic raphe nuclei in the brain stem or their ascending projections to the hemispheres.

Citalopram for post-stroke pathological crying.

Post-stroke pathological crying is a distressing condition in which episodes occur in response to minor stimuli without associated mood changes. There is preliminary evidence of disturbed serotoninergic neurotransmission in such cases. We investigated the effect of the selective serotonin reuptake inhibitor citalopram on uncontrolled crying in stroke patients in a double-blind placebo-controlled crossover study. 16 consecutive patients (median age 58.5 years, range 40-83) entered the 9-week study a median of 168 days (range 6-913) post stroke and were treated with citalopram 10-20 mg daily for 3 weeks. Crying history was determined from semistructured interviews and from diaries kept by the patients. Psychiatric assessment was made with the Hamilton depression scale (HDS), and unwanted effects were measured with the UKU side-effect scale. In 13 patients in whom frequency of crying could be assessed, the number of daily crying episodes decreased by at least 50% in all cases during citalopram treatment vs 2 patients during placebo treatment (p < 0.005, McNemar's test), the effect being rapid (1-3 days) and pronounced in 11 (73%). There was a concomitant significant decrease in depression rating from HDS 8.9 to 5.3 (p < 0.005, Wilcoxon's test). Citalopram was well tolerated, the few side-effects being mild and transient. We conclude that serotoninergic neurotransmission plays an important part in post-stroke pathological crying and that citalopram is an effective and well-tolerated treatment.

"Pure alexia" without hemianopia or colour anomia.

We report a case of "pure alexia" without hemianopia or colour anomia, caused by a small subcortical haematoma in the dorso-lateral part of the occipital lobe, not affecting the splenium of the corpus callosum. It is argued that the reading disorder was due to a visual-verbal disconnection in spite of the fact that this typically is caused by a lesion in the medial part of the left occipital lobe including the splenium.