I T IS difficult to determine how long the premonitory symptoms of stroke have been recognized by medical writers and neurologists. It is probable that their recognition came hand in hand with the developing understanding of the varieties of apoplexy; the differentiation between cerebral infarction or acute cerebral softening and cerebral hemorrhage. Certainly, as early as the middle of the last century the premonitory symptoms of cerebral softening or cerebral infarction were written about and recognized in such authoritative references as Gowers’s textbook, A Manual of Diseases of the Nervous System. In his edition of 1893, he states as follows, “In thrombosis from atheroma on the other hand, the premonitory symptoms are frequent. They depend on the interference with the supply of blood due to the disease of the vessels. They may exist for months before the onset or only for a few hours. The most common are dull general headache, giddiness, tingling, numbness, slight weakness in one half of the body, sometimes limited to a single limb and often, but not always corresponding in seat to the subsequent paralysis; less commonly. there is defective articulation or some mental change, failure of memory or irritability due to the general malnutrition of the brain that is produced by widespread arterial disease. In all cases, there presence is far more significant than their absence.“’ This description by Gowers would certainly be well recognized as quite accurate by most medical and neurologic clinicians in 1979. Wilson, in his textbook on neurology noted that “Premonitory signs, lacking in embolism, are often conspicuous in thrombotic cases, more so than in hemorrhagic; days or weeks beforehand, they may give the observer an inkling of what is likely to occur. Here are comprised headache, not infrequently on the same side as the commencing damage, vertigo, defective memory, transient confusion of thought and more specifically heaviness or momentary weakness, numb feeling or other paresthesia in the limb or limbs on the verge of becoming involved. Whether such symptoms constitute minor antecedent attacks or merely indicate general vascular trouble is immaterial; they are the straws which show how the intracranial wind is blowing.“2 Hunt, in his classic 1914 article pointing out the importance of carotid occlusion in the genesis of stroke, wrote that “it is also important to note that the visual disturbance and vascular changes in the optic nerve may precede other organic cerebral symptoms, the collateral circulation, failing to develop in the distribution of the ophthalmic artery. Unilateral headaches and vertigo, especially in assuming the upright posture, epileptiform attacks, failing memory, attacks of threatened hemiplegia, cerebral intermittent claudication are some of the vascular symptoms that should suggest the possibility of carotid obstruction.“3 These descriptions of symptoms are clearly identifiable today with what we consider to be transient ischemic attacks. Between the time of these writings and 1950, there was some recognition of the fact that patients with stroke often had preceding symptoms that suggested a threatened stroke. These were generally believed to be related to cerebral vasospasm. It was only with more careful and detailed inspection of the state of patients with stroke and their premonitory symptoms beginning in 1951 that a better understanding of transient ischemic attacks was possible. In 1951, Miller Fisher4 wrote that frequently in his autopsy studies of patients with occlusion of the cervical portion of the internal carotid artery, patients had reported premonitory fleeting symptoms including paresthesia, paralysis, monocular blindness, and aphasia. In his series of seven patients with carotid occlusion in the neck, ali patients but one had experienced transient numbness, tingling, speechlessness, unilateral blindness, or dizziness. These symptoms, Fisher pointed out were very characteristic of the onset of carotid occlusion. He also pointed out
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May 1, 1988
F Strik 
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