The answer to the first question is based primarily on the temporal profile of the patient’s presenting symptoms. The classic vascular profile involves sudden onset with rapid progression to maximal deficit (instantaneously or in seconds). All the affected areas of the body are involved from the onset. The rapid onset and evolution usually apply to all types of cerebrovascular episodes, regardless of the total duration of symptoms. The prototype for brief ischemic spells is the transient ischemic attack (TIA), defined as a temporary episode of focal neurologic dysfunction caused by focal cerebral ischemia that resolves completely without permanent cerebral infarction. Such episodes were previously defined as lasting less than 24 hours. It is important to distinguish TIA from an episode of generalized cerebral ischemia (syncope) and from spells such as seizures or migraine, both of which may appear as episodes of transient focal neurologic dysfunction. The temporal profile of focal seizures generally involves progression and evolution within a few minutes (˜2 to 3 minutes), whereas the focal deficit that sometimes
occurs with migraine usually builds or moves for 15 to 20 minutes (e.g., increasing scintillating scotomata or marching numbness starting in one hand) before subsiding and is often associated with localized headache, normally occurring after the focal neurologic deficit. Migraine aura that occurs without subsequent headache is often referred to as a migraine equivalent.

Another distinguishing characteristic of vascular spells is that most tend to produce negative phenomena (e.g., weakness, reduced sensation or numbness, visual loss), but focal seizures tend to produce positive phenomena (e.g., tonic-clonic movements, tingling, visual hallucinations, scintillating scotomata), and migraine may produce either phenomena (more commonly positive).

There are rare exceptions to these guidelines. Some TIAs may present with rhythmic jerking of the arm or the leg, often occurring when the patient arises from a sitting or a lying position. A contralateral high-grade carotid stenosis or an occlusion is often detected (the so-called limb-shaking TIA). Likewise, seizures may present with speech arrest, or weakness may occur after a seizure (Todd’s paralysis).

A focal neurologic deficit caused by brain ischemia that results in imaging or pathologic evidence of brain injury is called a cerebral infarction (ischemic stroke).

An exception to the usual rapid evolution of ischemic cerebrovascular events occurs in patients who have increasing neurologic deficit for as long as 72 hours after the onset of symptoms. These patients are classified as having progressing cerebral infarction, a phenomenon that is more common in strokes involving the vertebrobasilar system. In this situation, the clinician should carefully consider the possibility of an underlying mass lesion (e.g., subdural hematoma, neoplasm, and abscess), a demyelinating disease, or a superimposed encephalopathy.