Headache as a manifestation of transient cerebral ischemia is relatively common (7,10), but the focal neurologic symptoms of the attack need to be differentiated from an aura of migraine. The motor or sensory symptoms contralateral to hemispheric ischemia, like the weakness or subjective sense of heaviness and the paresthesias of a migraine aura, can involve the face, limbs, or trunk. A motor or sensory march of symptoms may occur but tends to be much quicker in a transient ischemic attack (TIA) than in migraine. The motor or sensory spread of a TIA is rapid, taking at most only seconds to a minute to move from the face to the hand, then marching up the arm to the trunk. Progression down the trunk to the lower limb can occur in both conditions. The march of motor and sensory changes in migraine is slow, taking a number of minutes to reach to its maximum distribution. The sensory symptoms in migraine are commonly a positive phenomenon, that is, a tingling sensation rather than a sense of numbness or sensory loss. Although the former can occur in a TIA, a sense of numbness or deadness is more often described. In both conditions, although more common in migraine, the sensory disturbances still can be spreading to new areas of involvement while simultaneously clearing from previously involved areas.

The weakness of a TIA is usually far greater than in a migrainous aura, but in the case of hemiplegic migraine, the difference can be minor and not diagnostic. Recovery can be over a similar period in both TIAs and migraine, but most TIAs are very short lived, and recovery is within minutes. A long history of similar attacks, onset in youth or early adult life, a personal or family history of migraine, and a normal clinical and noninvasive neurovascular examination all point to a migraine aura as the cause of the transient symptoms. Even in later life, when TIAs are more common, migraine can be the cause of such events (8,9).

Hemianopia is a relatively rare manifestation of a TIA and does not generally have the scintillating and spreading features of the visual aura of migraine. The visual loss of a TIA is usually a negative scotoma (black) rather than the
positive scotoma (bright) of migraine. Amaurosis fugax is a sudden onset of monocular blindness followed by gradual clearing of vision in 5 to 10 minutes. This pattern of visual disturbance is contrasted with an initial small area of scintillating scotoma that spreads gradually in the visual field in migraine.

Transient ischemic events can result in brainstem and temporooccipital dysfunction, leading to vertigo, tinnitus, bilateral visual disturbances, weakness of both sides of the body, and brainstem symptoms such as dysarthria, dysphagia, and diplopia. A similar constellation of symptoms occurs in basilar artery migraine (2). Headache can occur in both conditions, but in basilar migraine the headache is severe and almost always presents as the neurologic symptoms subside. Basilar migraine is most common in teenagers or in early adult life, whereas vertebrobasilar TIAs usually occur later in life. An overlap does occur; therefore, age alone is not an arbiter. Arteriography (MR or conventional) may be required for clarification.

Cerebral infarction, particularly cerebral embolism, often is associated with headache (7,19) and sometimes with positive visual symptoms, such as phosphenes or other visual hallucinations, when the vertebrobasilar arterial system is involved. It is rarely confused with migraine, because the resulting neurologic deficit generally suggests the presence of the structural lesion. Arteriography or noninvasive vascular studies, echocardiography, and coagulation studies may be required for final diagnosis. The dominantly inherited arteriopathy associated with recurrent subcortical infarction (CADASIL) can, in its course, be manifested by migraine attacks. The family history, the progressive course, and the characteristic subcortical infarcts shown on MRI make the diagnosis clear.