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Prof. Dr. Carlo Loeb, Istituto di Clinica Neurologica dell’Università di Genova, I-16132 Genova (Italy) Over the last few years various definitions have been coined to indicate ischemic attacks receding later than 24 h from their onset: strokes with full recovery (6th International Salzburg Conference, 1972), reversible ischemic neurological deficit (Handbook of Clinical Neurology, 1972; Ad hoc Committee on Cerebrovascular Diseases, 1975), prolonged reversible ischemic neurological deficits (International Symposium on Microsurgical Anastomoses for Cerebral Ischemia, 1974). In spite of the relative dearth of pertinent data which permits hardly more than a preliminary formulation of the problem an attempt at placing the whole topic into proper perspective seems indeed justified. Historical Review A glimpse at the historical evolution of the concept of transient cerebrovascular episodes turns out to be rather disappointing. Even the interesting review by Schiller (1970) of the concept of stroke before and after Virchow did not touch upon this problem. From ancient Greek and Roman students to the founders of the modern anatomoclinical investigation (17th-18th centuries) all who dealt with cerebrovascular disorders seemed most concerned with severe hemorrhagic apoplexies or, at the most, with the harbingers of stroke (Caelius Aurelianus, 5th century AD; Morgagni and Boheraave, 18th century). Transient episodes were either indirectly mentioned (42nd aphorism of Hippocrates) or briefly recalled in the clinical history (see Zani case of Morgagni letter IV) almost always being overlooked in favor of pathological studies of the completed stroke. Only during the second half of the 19th century did transient cerebrovascular episodes come somewhat to the fore, their possible causes being grouped as follows: (a) massive extracranial hemorrhages (Durand-Fardell, 1843; Andral, 1853;Bouveret, 1899); (b) cardiac alterations (Rokitansky, 1856; Andral, 1853); (c) cerebral arterial spasms: this hypothesis put forward by Raynaud (1862) to account for the transient loss of vision was subsequently accepted by many authors (Weiss, 1882; Bland, 1889; Peabody, 1891; Osier, 1896) as the most convincing pathophysiological explanation of cerebrovascular transient episodes; in fact Wilson and Bruce (1955) devoted a whole chapter of their treatise to the cerebral spasm, and (d) neurolues (apoplectiform episodes of general palsy: Neisser, 1894; syphilithic hemiplegia: Jackson, 1888/1958). 2 Loeb The vasospasm theory held sway although among controversies (Oppenheim, 1905; Ala-jouanine and Thurel, 1936; Fazio and Loeb, 1948) up to the 1950s, being unanimously rejected when Corday and Rothenberg (1957) introduced the successful label of ‘cerebrovascular insufficiency’ following a similar cardiological definition by Rein (1931) and Buchner (1939). During the 2nd Princeton Conference along with other terms such as ‘intermittent vascular insufficiency’, ‘ischemic recurrent attacks’, ‘recurrent focal cerebral ischemic attacks’, ‘transient cerebral ischemia’, the definition of’transient ischemic attacks’ (Miller Fisher, 1958) was employed for the first time. Such definition was popularized gradually: in 1958 the ‘Ad hoc Committee’ established by the NIH indicated the transient episodes as ‘transient cerebral ischemia’, in the 1961 3rd Princeton Conference the term ‘focal intermittent insufficiency or ischemic attack’ was still used, with only Miller Fisher employing the TIA acronym (absent from the analytical index); it was only in the 4th Princeton Conference of 1965, however, that the definition of’transient ischemic attacks’ gained unanimous acceptance. With respect to the duration of the episode, as long ago as 1928 Lhermitte stated that rarely it lasted more than 24 h; on the other hand Alajouanine et al. (1960) dealing with ‘transient cerebral ischemia’ wrote that ‘in a few cases the attacks may be more prolonged persisting for several days’. Quite recently attention has been focused on a number of cases exhibiting transient episodes which cleared completely later than 24 h from the onset and were labelled as ‘stroke with full recovery’ (6th Salzburg Conference, 1972). In the same year similar cases, although devoid of a complete clinical evaluation and follow-up were mentioned by Meyer, Guiraud and Bauer in Vinken and de-Bruyrts Handbook of Neurology as ‘reversible ischemic neurological deficits’. A few years later the same terminology was employed by an official classification of the ‘Ad hoc Committee on Cerebrovascular Diseases’, headed by Millikan (1975). Clinical Definition The transient ischemic attack was classically defined as a cerebral dysfunction of ischemic nature lasting not longer than 24 h with a tendency to recur. The following were therefore the features essential to the definition: ischemic pathogenesis, complete reversibility, and 24 h duration. To conform to the definition the completeness of the regression should, first of all, be verified by the neurological examination, which should be unrevealing altogether: in other words, free from even slight abnormalities — unequality of tendon reflexes, slight pronator drifts, etc. (Loeb, 1977a). In fact, episodes which do not recede completely, often labelled as ‘minor strokes’ can be brought about by small infarctions or even hemorrhages (van der Drift and Kok, 1973; Yates, 1976; Russell, 1976; Loeb, 1978b) and large softenings (Loeb, 1978b) and cannot therefore be considered as proper TIA.