Transient ischemic attacks (TIAs) are sudden, transitory losses of neurologic function that come on without headache and resolve spontaneously leaving no neurologic sequela. The specific symptoms depend on the area of the brain affected, which is in turn related to the vessels involved. The most common origin is high-grade stenosis (70% or above) of the internal carotid, or ulcerated plaque, at the carotid bifurcation. The importance of TIAs is that they are predictors of stroke, and timely elective carotid endarterectomy may prevent or minimize that possibility. Workup starts with noninvasive Duplex studies (high-quality sonogram plus Doppler). Surgery (carotid endarterectomy) is indicated if the lesions described above are found in the location that explains the neurologic symptoms. Angioplasty and stent can be done if a filter is first deployed to prevent embolization of debris to the brain.
Ischemic stroke also has sudden onset without headache, but the neurologic deficits are present for a longer time, leaving permanent sequelae. Ischemic strokes that have been present for longer than 3 hours are not amenable to revascularization procedures. An ischemic infarct may be complicated by a hemorrhagic infarct if blood supply to the brain is suddenly increased. Vascular workup will eventually be done to identify lesions that might produce another stroke (and treat them), but for the existing infarct, assessment is by CT scan and therapy is centered on rehabilitation. Treatment of an early ongoing stroke has now become standard practice, with one or more hospitals in each major city equipped with the necessary resources and staff and designated as the places to do it. At the first sign of a sudden-onset neurological deficit, the patient is urged to report immediately to the emergency room. CT scan is done first to rule out infarcts that are too extensive to be treated, and to confirm that there is no hemorrhage. If at any time during this evaluation the neurological functions spontaneously return, the case is reclassified as a TIA and managed accordingly. But if not, no time should be wasted. Intravenous infusion of tissue-type plasminogen activator (t-PA) is best if started within 90 minutes, but it can still be done up to 3 hours after the onset of symptoms.
Hemorrhagic stroke is seen in the uncontrolled hypertensive who complains of very severe headache of sudden onset and goes on to develop severe neurologic deficits. CT scan is used to evaluate the location and extent of the hemorrhage, and therapy is directed at control of the hypertension and rehabilitation efforts.
Subarachnoid bleeding from intracranial aneurysms has a wide spectrum of severity when it first presents, and some patients are not salvageable—but in many cases a high index of suspicion and a timely diagnosis can be lifesaving. That sort of salvageable patient shows up complaining of extremely severe headache of sudden onset, like no other ever experienced before (a “thunderclap,” a headache that is “sudden, severe, and singular”). Because the blood is in the subarachnoid space (there is no hematoma pressing on the brain), there may be no neurologic findings at all, and the patient is sent home. Luckier patients may have meningeal irritation and nuchal rigidity, and be recognized. Those not recognized often return in 10 days with another bleed, perhaps this time a much worse one (the early one is referred to as the “sentinel bleed”). Workup begins with CT scan looking for blood in the subarachnoid space (spinal tap can identify old blood or small amounts of current blood, but it should never be the first test; always start with the CT) and follows with arteriogram to locate the aneurysm (a little devil off the circle of Willis). Clipping is the surgical therapy, and endovascular coiling is the radiological alternative.