Clinical Neuroscience

[Diagnostic criteria and differential diagnosis of Parkinson’s disease]

TAKÁTS Annamária

JUNE 20, 2003

Clinical Neuroscience - 2003;56(05-06)

[The clinical diagnosis of Parkinson’s disease is based on the identification of some combination of the clinical motor signs of bradykinesia, rigidity, tremor and postural instability. Three levels of diagnostic confidence are differentiated: possible, probable, and definite. The diagnosis of possible and probable Parkinson’s disease based on clinical criteria alone, while definite diagnosis requires neuropathologic confirmation. To differentiate Parkinson’s disease (idiopathic Parkinsonian syndrome) and other Parkinsonian syndromes is of increasing importance considering the therapy and life expectancy of the patients. Recently the functional imaging technics have been more and more helpful in the early differential diagnosis of Parkinson’s disease.]

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[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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