Transient ischemic attacks due to increased platelet aggregation and adhesiveness. Ultrastructural and functional correlation.

The authors report 22 cases of transient ischemic attacks (TIA's) manifested by amaurosis fugax or hemiparesis or paresthesia of less than 24 hours' duration. None of the patients demonstrated 1) evidence of atherosclerotic cerebral vascular disease on angiography, 2) evidence of intracranial lesion on brain scan, 3) cardiac source of emboli, 4) arteritis or collagen disease, or 5) history of migraine. The only abnormalities found to explain the TIA's were abnormally increased platelet adhesiveness and/or aggregation. All of these patients were followed from 1 to 5 years, and had repeated coagulation studies. Treatment with antiplatelet drugs showed an excellent clinical response with associated decrease in platelet adhesiveness and aggregation. Discontinuance of the antiplatelet drug resulted in a recurrence of the TIA's which coincided with an increase in aggregation and adhesiveness. In two cases the platelet morphology was studied by transmission and scanning electron microscopy. It appears that there is a specific group of patients with TIA's in whom the sole cause of the attack is an abnormality of platelet function. For these people there is a specific therapy and a method monitoring the treatment.