Vinpocetine is a derivative of the alkaloid (extracted from Vinca minor) vincamine, and is used in many countries in the treatment and prevention of stroke and vascular dementia. Although there has not been one single mechanism of action agreed upon for vinpocetine, there are many known activities that contribute to its use such as dilating blood vessels, enhancing circulation to the brain, improving oxygen utilization and reducing blood clotting, and inhibition of platelet aggregation. Vinpocetine works on altering the ischemic cascade in several different areas, including ATP depletion, activation of voltage-sensitive sodium and calcium channels, glutamate and free radicals release. The most important of these effects to its neuroprotective activity seems to be the interference of voltage-sensitive sodium channels, and possibly also its strong antioxidant activity (Hadjiev, 2003).
One main Hungarian company markets vinpocetine in Europe as a drug (Cavinton) for improving several types of cerebral insufficiency conditions, and for improving cerebral metabolism. In studies involving vinpocetine’s use in chronic stroke patients, positron emission tomography (PET) scans showed that it improves the brain metabolism and blood flow, especially around the stroke-damaged areas (Szakal et al., 1998; Vas et al., 2002; Gulyas et al., 2002).
There seems to be a good amount of preclinical science and little clincial science to back vinpocetine’s use in cerebrovascular disorders. However, with its low toxicity and side effects, it shows excellent potential for the future use of prevention and treatment of stroke. Its effects on memory on healthy individuals has some merit, but yet needs more clinical backing.
Hadjiev (2003) reviewed the actions of vinpocetine on the ischemic cascade, and discussed how it may be a new therapeutic approach to treatment and prophylactic neuroprevention in patients with asymtomatic ischemic cerebrovascular disorders (AICVD) and cerebrovascular disease. A subclinical noninvasive diagnosis of AICVD has been recently introduced by the American Heart Association and its treatment was identified as being important in prevention of ischemic stroke and cognitive decline. As a potential treatment to AICVD, the neuroprotective effects of vinpocetine were discussed.
Szapary et al. (2003) examined the high and low dose therapy of vinpocetine on rheological parameters in acute and chronic stroke patients. Vinpocetine is used mainly in a preventative manner, and this study sought to determine if it had value as a treatment for chronic disease. The authors concluded that after parenteral administration with low (30 mg/day) and high (70 mg/day) doses of vinpocetine, the high dose showed significant decreases in hematocrit, the whole blood and plasma viscosity and red blood cell aggregation, indicating a beneficial role in the treatment of chronic cerebrovascular disease.
A pilot clinical study involving the treatment of 30 patients with vinpocetine was conducted in order to determine the safety and feasibility of a full-scale clinical study. Patients were given either dextran alone or dextran in combination with vinpocetine and it was found that the two treatment groups were comparable in their major prognostic variables. However, the National Institute of Health Stroke Scale score was slightly improved in the vinpocetine group at 3 months of follow-up, and no significant side effects were seen. A full-scale clinical study was concluded to be warranted (Feigin et al., 2001).
A systematic review of the literature and researchers in the field (including drug companies) was conducted to determine if therapy with vinpocetine on stroke was effective. Only one trial was found that was of an unconfounded randomized, placebo controlled design. The authors concluded that there were no deaths found, nor drug dependencies, but that there were not enough studies conducted to determine the efficacy of vinpocetine in stroke patients (Bereczki and Fekete, 2000; Bereczki and Fekete, 1999).
As vinpocetine had been used for over 20 years in the treatment of cognitive impairment due to vascular diseases, and there had been many preclinical findings to suggest several important mechanisms of action, no consensus had been reached on its efficacy. Therefore this search was conducted to review the existing literature world-wide to analyze unconfounded double-blind studies pertaining to vinpocetine treatment of vascular dementia, Alzheimer’s dementia and other dementias. The authors concluded that although the preclinical science done on vinpocetine was persuasive and few adverse effects were found, the clinical science was inconclusive and did not support clinical use. The authors called for more clinical work on well-defined types of cognitive impairment. (Szatmari and Whitehouse, 2003).
Twelve healthy females were given vinpocetine in the dosages of 10, 20, or 40 mg for two days or placebo and assessed for psychopharmacological effects in a randomized, double-blind crossover study. Assessment parameters were measured on the third day, and included Critical Flicker Fusion (CFF), Choice Reaction Time (CRT), Subjective Ratings of Drug Effects (LARS), and Sternberg Memory Scanning Test. Significant improvements were found in memory as a function of the Sternberg test at the dosage level of 40 mg. The results suggested that vinpocetine has a specific effect on the serial comparison stage of the reaction process (Subhan and Hindmarch, 1985).
Safety / Dosage
For the use of improving mild to moderate dementia in patients, 5-10 mg, taken 2-3 times daily, is the typical dosage recommendation, however larger dosages have been used clinically for acute treatment. Because vinpocetine is difficult to absorb in large quantities, it is recommended to divide the daily doses as suggested.
Side effects of vinpocetine are rare and transient (with discontinued use) at the recommended dosages. Typically these side effects may include gastrointestinal upset, low blood pressure, dry mouth, insomnia, headaches and heart palpitations. Persons on anti-coagulant therapy should not use vinpocetine, as it may interfere with clotting.
The safety or efficacy of vinpocetine for pregnant or lactating women is undocumented.
1.Bereczki D, Fekete I. Vinpocetine for acute ischaemic stroke. Cochrane Database Syst Rev. 2000;(2):CD000480.
2.Bereczki D, Fekete I. A systematic review of vinpocetine therapy in acute ischaemic stroke. Eur J Clin Pharmacol. 1999 Jul;55(5):349-52.
3.Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol. 2001 Jan;8(1):81-5.
4.Gulyas B, Halldin C, Sandell J, Karlsson P, Sovago J, Karpati E, Kiss B, Vas A, Cselenyi Z, Farde L. PET studies on the brain uptake and regional distribution of [11C]vinpocetine in human subjects. Acta Neurol Scand. 2002 Dec;106(6):325-32.
5.Hadjiev D. Asymptomatic ischemic cerebrovascular disorders and neuroprotection with vinpocetine. Ideggyogy Sz. 2003 May 20;56(5-6):166-72
6.Subhan Z, Hindmarch I. Psychopharmacological effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol. 1985;28(5):567-71.
7.Szapary L, Horvath B, Alexy T, Marton Z, Kesmarky G, Szots M, Nagy F, Czopf J, Toth K. [Effect of vinpocetin on the hemorheologic parameters in patients with chronic cerebrovascular disease] Orv Hetil. 2003 May 18;144(20):973-8.
8.Szakall S, Boros I, Balkay L, Emri M, Fekete I, Kerenyi L, Lehel S, Marian T, Molnar T, Varga J, Galuska L, Tron L, Bereczki D, Csiba L, Gulyas B. Cerebral effects of a single dose of intravenous vinpocetine in chronic stroke patients: a PET study. J Neuroimaging. 1998 Oct;8(4):197-204.
9.Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database Syst Rev. 2003;(1):CD003119.
10.Vas A, Sovago J, Halldin C, Sandell J, Karlsson P, Karpati E, Kiss B, Cselenyi Z, Farde L, Gulyas B. Cerebral uptake and regional distribution of [11C]-vinpocetin after intravenous administration to healthy men: a PET study. Orv Hetil. 2002 Nov 24;143(47):2631-6.
EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.