The main objective in these forms of ischemic cerebrovascular disease is the amelioration of the existing deficit and the prevention of future stroke. It is now a major goal of general medicine to reduce the incidence of stroke in the general population by the control of modifiable risk factors. In addition to reduction of known risk factors such as hypertension, smoking, and glucose control in diabetics, the widespread use of cholesterol-lowering statin medications has been shown in some studies to reduce stroke incidence (“primary prevention”) and recurrence of stroke (“secondary prevention”). The use of anticoagulants to prevent stroke in patient with atrial fibrillation is a component of primary prevention. Although the risk of recurrent stroke is dependent on the underlying mechanism, some insight has been gained by the study of a cohort of patients with mild stroke or what have been considered to be “high-risk” TIAs in the modern era by Amarenco and colleagues (2016 and 2018). They estimated recurrence rates of approximately 4 percent at 90 days, 5 percent at a year and another 6 percent between the end of the first year and the fifth year. The treatment of stroke may be divided into three broad parts: management in the acute phase by measures to restore the circulation and arrest the pathologic process, physical therapy and rehabilitation, and measures to prevent further strokes and progression of vascular disease.
Management in the Acute Phase
With the inception of thrombolytic agents for stroke and the advances in endovascular procedures for thrombectomy, acute stroke treatment has evolved to emphasize rapid restoration of perfusion through occluded cerebral vessels. The steps in the process are now dominated by rapidly determining the patient’s eligibility for intravenous and intra-arterial revascularization treatment and the timing of these steps has been derived from a series of randomized clinical trials. The current practice is to use intravenous thrombolysis within 3 h if there is no intracranial hemorrhage on CT and with additional qualifications, up to 4.5 h of stroke onset (Hacke et al, 2008). If vascular imaging performed during or after intravenous thrombolysis treatment shows large vessel occlusion (distal internal carotid or proximal middle cerebral arteries), the patient is eligible for endovascular thrombectomy or thrombolysis. If vascular imaging at that point shows no proximal arterial occlusion, no endovascular procedure is undertaken. Beyond 4.5 h (“outside the window”), intravenous thrombolysis is not used. If there is a large vessel occlusion and the patient is seen between 4.5 and 6 h of stroke onset, endovascular treatment is undertaken based on several trials including SWIFT-PRIME (see Saver et al). Beyond 6 h after stroke onset, and extending to at least 18 h and probably to 24 h, including if the patient awakens from sleep with a stroke (“last seen well”) and there is large vessel occlusion demonstrated by vascular imaging, endovascular treatment is possible but only of advanced imaging demonstrates a mismatch between the size of the infarction (diffusion volume) and a region of hypoperfused ischemic, but not yet infarcted tissue (perfusion defect). This has created a notion that imaging demonstration of perfusion defects could be a better gauge than the time interval from onset of symptoms for predicting response to treatment. There are also clinical and laboratory features that preclude various of these steps, as noted below. Medical systems have had to adapt to the resource requirements to carry out these therapies.