Vinpocetine

Acute Cerebro-Vascular Accidents (Strokes) : Ischaemic strokes due to cerebral thrombosis, cerebral embolism, acute circulatory disorder, hypertensive crisis; the acute cardiovascular disorders, ischaemic neurological defcit, complete stroke (CS), multiinfarct dementia, cerebral arteriosclerosis ... Read more Acute Cerebro-Vascular Accidents (Strokes) : Ischaemic strokes due to cerebral thrombosis, cerebral embolism, acute circulatory disorder, hypertensive crisis; the acute cardiovascular disorders, ischaemic neurological defcit, complete stroke (CS), multiinfarct dementia, cerebral arteriosclerosis, hypertensive encephalopathy, post-apoplectic conditions with the background of haemorrhagic strokes etc. Senile Disorder : For relief of psychosomatic symptoms in the elderly due to cerebral insufciency eg. forgetfulness, memory disturbances, slow thinking, lack of concentration, dizziness, mood instability, aphasia, sleep disturbances, vasovegetative symptoms of menopausal syndrome etc. Visual Disorder : Vascular disorders of the choroid and retina due to arteriosclerosis. Vasospasm, macula degenerations, arterial or venous thrombosis or embolism and glaucoma secondary to the above mentioned disorders. Hearing Disorder : For the treatment of impaired hearing of vascular or toxic (iatrogenic) origin presbyacusis, meniere's disease, cochleovestibular neuritis, tinnitus and dizziness of labirynth origin.

Vinpocetine increases cerebral metabolism; it increases glucose and O2 consumption; improves cerebral hypoxia tolerance; shifts glucose metabolism to the energetically more favourable aerobic pathway, but it increases the anaerobic pathway as well; it elevates the ATP concentration and the ATP/AMP ratio in the brain, and elevates the cerebral norepinephrine, dopamine and serotonin levels. Vinpocetine considerably improves cerebral microcirculation by inhibiting platelet aggregation, reducing the pathologically increased blood viscosity, and increases erythrocyte deformability. It also promotes O 2 transport into the tissues by reducing the O 2 affinity of erythrocytes. It selectively and intensely increases cerebral blood flow and the share of the brain in cardiac output, it reduces cerebral vascular resistance without affecting systemic circulation (blood pressure, heart rate, cardiac output, total peripheral resistance). It does not elicit steal phenomenon; on the contrary, it primarily improves the blood supply of the injured and ischaemic area while it remains unchanged in the intact areas (inverse steal effect). It further increases blood flow which is already increased as a result of hypoxia.