ABSTRACT

Aetiology does not influence the hyperacute management of ischemic stroke, but establishing a cause is essential in order to reduce or prevent recurrence. There is ample epidemiological evidence of a genetic predisposition to stroke. Genome-wide association studies have identified a genetic locus on chromosome 12p13 to be associated with total, ischemic, and atherothrombotic stroke in white subjects. Gene therapy for stroke remains remote from clinical practice but gene markers may allow more effective screening and risk profiling and may play a role in the prevention and investigation of stroke. Cerebral oedema may also follow an ischemic stroke, and oedema may add to the neurological damage and injury. Atherosclerosis ranks among the disorders leading to stroke and transient ischemic attack. Severe heart failure and cardiomyopathy are also associated with myocardial dyskinesia that promotes mural thrombi. Embolism may accompany cardioversion, and the risk is higher shortly after development of atrial fibrillation.