Sulkava R, Erkinjuntti T
Department of Neurology, University of Helsinki, Finland.
Acta Neurol Scand. 1987 Aug;76(2):123-8. doi: 10.1111/j.1600-0404.1987.tb03555.x.
Among 133 consecutive patients with the clinical diagnosis of vascular dementia there were 6 patients (4.5%) in whom dementia was judged to be associated with cerebral hypoperfusion due to cardiac arrhythmias and systemic hypotension. Patients with cardio-pulmonary arrest and resuscitation were excluded from this series. Our findings suggest that cerebral hypoperfusion is not an uncommon mechanism to contribute to the evolution of vascular dementia in the elderly. Besides arrhythmias, also hypovolaemia caused by diuretics medication might have been a contributory factor to hypoperfusion. It is evident that cerebral hypoperfusion is the predominant mechanism responsible for vascular dementia in some cases. It may be a contributing factor also in many cases of multi-infarct dementia. Thus, besides dementia after cardio-pulmonary arrest, vascular dementia of the haemodynamic type as a separate clinical entity is open to discussion.
在133例临床诊断为血管性痴呆的连续患者中,有6例(4.5%)被判定痴呆与心律失常和全身性低血压导致的脑灌注不足有关。本系列研究排除了心肺骤停及复苏患者。我们的研究结果表明,脑灌注不足是导致老年人血管性痴呆进展的一种常见机制。除心律失常外,利尿剂药物导致的血容量不足也可能是灌注不足的一个促成因素。显然,脑灌注不足在某些情况下是血管性痴呆的主要机制。在许多多发性梗死性痴呆病例中,它也可能是一个促成因素。因此,除了心肺骤停后的痴呆外,血流动力学型血管性痴呆作为一个独立的临床实体尚有待讨论。