Clinical Neuroscience

[Asymptomatic ischemic cerebrovascular disorders and neuroprotection with vinpocetine]

HADJIEV Dimiter

JUNE 20, 2003

Clinical Neuroscience - 2003;56(05-06)

[The asymptomatic ischemic cerebrovascular disorders (AICVD) is an early manifestation of cerebrovascular disease. It is also known as latent insufficiency of the cerebrovascular circulation or as asymptomatic cerebrovascular disorders. Recently, the term subclinical disease, detected noninvasively, has been introduced by American Heart Association. The diagnosis is based on the following criteria: evidence of vascular risk factors; episodic nonspecific complaints without any focal cerebral symptoms; mild cognitive deficit, detected by neuropsychological tests; carotid ultrasonography often shows intimal-medial thickening, atherosclerotic plaques and carotid stenosis; CT and MRI occasionally reveal silent cerebral infarctions, white matter hyperintensities or cerebral atrophy; regional hypoperfusion above the ischemic threshold is also seen by rCBF measurements. Treatment of the AICVD, modifying the vascular risk factors and using neuroprotective agents, should be the cornerstone of primary prevention of ischemic stroke and cognitive decline, caused by cerebrovascular disorders. Vinpocetine has been found to interfere with various stages of the ischemic cascade: ATP depletion, activation of voltagesensitive Na+- and Ca++-channels, glutamate and free radicals release. The inhibition of the voltage-sensitive Na+- channels appears to be especially relevant to the neuroprotective effect of vinpocetine. Pronounced antioxidant activity of the drug could also contribute to the neuroprotection. PET studies in primates and man showed that 11C labelled vinpocetine passes the blood-brain barrier rapidly. Heterogeneous brain distribution of the compound was observed mainly in the thalamus, basal ganglia, occipital, parietal and temporal cortex, regions which are closely related to the cognitive functions. PET studies in chronic ischemic stroke patients revealed favourable effects of vinpocetine on rCBF and glucose metabolism in the thalamus, basal ganglia and primary visual cortex. It seems, vinpocetine, affecting the multiple mechanisms of the AICVD, could be of benefit for the treatment in this early stage of cerebrovascular disease. Vinpocetine may also become a new therapeutic approach to prophylactic neuroprotection in patients at high risk of ischemic stroke.]

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[Background - There are conflicting data about the role of Leiden mutation in the pathogenesis of cerebral arterial thrombosis. In order to obtain relevant data, authors investigated the prevalency of factor V Leiden (A506G) both in healthy subjects and in a subgroup of ischaemic stroke patients. Matherial and methods - Blood samples of 171 healthy persons and 254 ischaemic stroke patients were examined by PCR method for Leiden mutation. Ischaemic lesions in the stroke group were documented by CT or MRI. A routin questionnaire was used to study the family history of vascular events (hypertension, diabetes, POAD, stroke, myocardial infarction) of patients. Conventional vascular risk factors of patients were also documented. Results - The prevalence of Leiden mutation was 7.2% in healthy persons and 11.9% in stroke patients. The OR for 254 patient was 1,45 (0.71-2.97). In the subgroup of young patients: age <50 (n=134) the OR was 1.67 (0.75-3.70) and in the elderly patients group: age >50 (n=120) the OR was 1.21 (0.50-2.89). In the family history of stroke patients having Leiden mutation (hetero- and homozigosity) the stroke prevalence was higher (p=0.01). In the ischaemic stroke group, age<50 with polymorphism a tight correlation with hyperlipidaemia (p=0.03) was found. In the group of age<50 with heterozigosity for Leiden, a lower plasma fibrinogen concentration (p=0.02) was found. The polymorphism showed no correlation with the hypertension, hyperuricaemia, migraine, diabetes mellitus, smoking, alcohol consumption and CDS status of patients. Conclusion - When comparing stroke patients to control population there is no significant increase in the frequency of Leiden mutation. Leiden mutation together with hyperlipidaemia and stroke in the family history results in high risk for ischaemic stroke in young patients.]

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