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Poststroke Depression and Emotional Incontinence: Correlation with Lesion Location

Overview
Journal Neurology
Specialty Neurology
Date 2000 May 10
PMID 10802788
Citations 66
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Abstract

Objective: To correlate the location of stroke with poststroke depression (PSD) and emotional incontinence (PSEI).

Methods: The authors prospectively studied 148 patients (94 men and 54 women, mean age 62 years) with single, unilateral stroke (126 infarcts and 22 hemorrhages) at 2 to 4 months poststroke with regard to the presence of PSD (using Diagnostic and Statistical Manual of Mental Disorders IV criteria and Beck Depression Inventory) and PSEI. The lesion location was analyzed by CT or MRI.

Results: Twenty-seven patients (18%) had PSD and 50 (34%) had PSEI. The presence of PSD and PSEI was not related to the nature, laterality, or size of the lesion. The frequency of PSEI, but not of PSD, was higher in women than in men and in ischemic rather than hemorrhagic stroke (p < 0. 05). Although both PSD and PSEI were related to motor dysfunction and location (anterior versus posterior cortex) of the lesion, location was a stronger determinant for PSD (p < 0.05). The prevalence of PSD/PSEI in each location was 75%/100% in frontal lobe of anterior cerebral artery territory, 50%/0 in temporal lobe, 30%/40% in frontal-middle cerebral artery territory, 13%/0 in occipital lobe, 19%/45% in lenticulocapsular area, 11%/16% in thalamus, 16%/53% in pontine base, 36%/55% in medulla, and 0/22% in cerebellum. Parietal and dorsal pontine lesions were not associated with PSD or PSEI. PSEI was more closely associated with lenticulocapsular strokes than was PSD (p < 0.01).

Conclusion: Development of PSD and PSEI is strongly influenced by lesion location, probably associated with the chemical neuroanatomy related to the frontal/temporal lobe-basal ganglia-ventral brainstem circuitry. Although the lesion distribution is similar, PSEI is more closely related to lenticulocapsular strokes than is PSD.

Citing Articles

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Vision-related quality of life after unilateral occipital stroke.

Dogra N, Redmond B, Lilley S, Johnson B, Lam B, Tamhankar M Brain Behav. 2024; 14(7):e3582.

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Unraveling the Pathogenesis of Post-Stroke Depression in a Hemorrhagic Mouse Model through Frontal Lobe Circuitry and JAK-STAT Signaling.

Wu Y, Deng J, Ma J, Chen Y, Hu N, Hao S Adv Sci (Weinh). 2024; 11(33):e2402152.

PMID: 38946585 PMC: 11434213. DOI: 10.1002/advs.202402152.


Post-stroke emotionalism: Diagnosis, pathophysiology, and treatment.

Broomfield N, Blake J, Gracey F, Steverson T Int J Stroke. 2024; 19(8):857-866.

PMID: 38503711 PMC: 11408949. DOI: 10.1177/17474930241242952.


Neuroinflammation and Post-Stroke Depression: Focus on the Microglia and Astrocytes.

Lu W, Wen J Aging Dis. 2024; .

PMID: 38421829 PMC: 11745440. DOI: 10.14336/AD.2024.0214-1.