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DOI 10.1161/01.str.30.7.1429

Медицинская библиотека · Stroke · 1999

A decrease in regional cerebral blood volume and hematocrit in crossed cerebellar diaschisis.

Yamauchi H, Fukuyama H, Nagahama Y, Okazawa H, Konishi J

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND AND PURPOSE: The pathophysiology of crossed cerebellar diaschisis (CCD) remains to be elucidated. In CCD, the metabolic suppression resulting from deafferentation may cause vasoconstriction, which may result in a decrease in cerebral blood volume (CBV) and may differentially affect the flows of red blood cells and of plasma. The purpose of this study was to investigate whether CCD decreases the total CBV (cerebral red blood cell volume [CRCV] plus cerebral plasma volume [CPV]) and, if so, whether CCD differentially affects the CRCV and CPV, resulting in a change in hematocrit.

METHODS

We used positron emission tomography to study 7 patients with a unilateral supratentorial infarct and CCD. The distributions of CRCV and CPV were assessed by using 15O-labeled carbon monoxide and 62Cu-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The CRCV, CPV, and calculated hematocrit values were compared between the cerebellar hemispheres.

RESULTS

In the cerebellar cortex contralateral to the supratentorial infarct, the values of CRCV, CPV, and total CBV were significantly decreased compared with those in the ipsilateral cerebellar cortex. The CRCV was decreased to a greater degree than the CPV, and the value of the hematocrit was decreased in the contralateral cerebellar cortex.

CONCLUSIONS

CCD may decrease the total CBV, which may reflect vasoconstriction caused by decreased metabolism due to deafferentation. In addition, the more pronounced decrease in CRCV than in CPV may result in a decrease in hematocrit in CCD.

Для цитирования: Yamauchi H, Fukuyama H, Nagahama Y, Okazawa H, Konishi J. A decrease in regional cerebral blood volume and hematocrit in crossed cerebellar diaschisis.. Stroke. 1999. DOI: 10.1161/01.str.30.7.1429.

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