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Stroke is a leading cause of disability and death in women, despite progress in its prevention and treatment. As with coronary artery disease, the incidence of stroke rises after the menopause, in parallel with metabolic changes that add up to create an unfavourable risk factor profile for cardiovascular disease. The menopause metabolic syndrome, which includes weight gain and changes in lipids, insulin resistance, endothelial dysfunction, increased levels of homocysteine, lipoprotein (a) and several coagulation factors, may in part be attributable to estrogen deficiency, and may be reversible with hormone replacement therapy (HRT). As for blood pressure, a major detrimental risk factor for stroke, it is probably not affected by either the menopause per se or by HRT. Abundant experimental data exist indicating that estrogens have both anti-atherosclerotic and neuroprotective effects. The width or thickness of the carotid wall is a good indicator of carotid atherosclerosis; it increases after the menopause transition, and decreases with HRT. Estrogens may enhance cerebral blood flow and reduce vascular resistance. In animal models of stroke, estrogen induced anti-ischaemic effects. Several large-scale epidemiological studies have verified the concept of primary protection of stroke by HRT, though others have failed to do so. In light of these contradictory data, several recent reports were highly significant (Nurses' Health Study, HERS Study, Cancer Prevention II Trial, WEST Trial). Despite the known neural and vascular benefits of estrogen, it is uncertain whether HRT is associated with stroke protection. At present, prevention of stroke should involve proven risk reduction strategies.

Menopause and ischaemic stroke: basic, clinical and epidemiological considerations. The role of hormone replacement