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present and the recent past coupled with an ongoing anterograde amnesia During the attack, there was no impairment in the state of consciousness, no other sign of confusion, and no overt seizure activity; personal identi cation was intact, as are motor, sensory, and re ex functions The patient s behavior is normal except for incessant, repetitive questioning about his immediate circumstances (eg, What am I doing here ; How did we get here ) Unlike those with psychomotor epilepsy, the patient is alert, in contact with his surroundings, and capable of high-level intellectual activity and language function during the attack As soon as the attack has ended, no abnormality of mental function is apparent except for a permanent gap in memory for the period of the attack itself and for a brief period (hours or days) preceding the attack The patient may be left with a mild headache Incomplete or mild attacks are not seen Only the recent retrograde and complete anterograde amnesia stand out The condition is among the most curious in neurology but is often mistaken for a psychiatric episode Hodges and Ward have made detailed psychologic observations in ve patients during an episode The psychologic de cit, except for its transience, was much the same as that in the permanent amnesia syndrome Personality, cognition involving highlevel functioning, semantic language, and visuospatial discrimination were all preserved So-called immediate memory ie, registration (see above) was intact, but retentive memory was severely deranged The extent of retrograde amnesia was highly variable, but characteristically it shrank after the attack, leaving a permanent retrograde gap of about 1 h However, some mild impairment of new learning persisted for up to a week after the acute attack In a survey conducted in the Rochester, Minnesota, area, transient global amnesia (TGA) occurred at an annual rate of 52 cases per 100,000 population The recurrence of such attacks is not uncommon, having been noted in 66 of 277 patients who were observed for an average period of 80 months (Miller et al) and in 16 of 74 patients followed for 7 to 210 months (Hinge et al) The latter authors estimate the mean annual recurrence rate to be so low (47 percent) that most elderly patients are likely to experience only one attack One of our patients had more than 50 attacks, but among all the rest (more than 100 cases), 5 was the maximum It seems children are not susceptible to the condition; however, a 13-yearold and 16-year-old with migraine were reported to have had similar attacks during participation in sports (Tosi and Righetti) No consistent antecedent events have been identi ed, but certain ones such as a highly emotional experience, pain, exposure to cold water, sexual intercourse, and mild head trauma have been reported in some cases (Haas and Ross; Fisher) The similarity to postconcussive amnesia is notable We have also seen several patients in whom the attacks appeared after minor diagnostic procedures such as colonoscopy, but the residual effects of sedation are suspect in some of these instances Several cases have been reported in high-altitude climbers and created dif culty in distinguishing TGA from altitude sickness One of the dif culties in judging the accuracy of the many published reports is whether, during the attack, the patient was or was not in contact with the environment and capable of high-level mental performance and whether a retrograde amnesia was present important features in differentiating the attack from a partial complex seizure The pathogenesis of TGA has not been settled It has been suggested that it represents an unusual form of temporal lobe epilepsy (transient epileptic amnesia, TEA), but this seems unlikely A large number of patients have been studied with EEGs during.

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an attack or shortly thereafter and have not shown seizure activity (Miller et al) Moreover, amnesic episodes due to seizures are usually much briefer than those of TGA, and most or all temporal lobe seizures are associated with impairment of consciousness and an inability to interact fully with the social and physical environment Using EEG and nasopharyngeal leads, Rowan and Protass found mesiotemporal spike discharges in 5 of 7 patients Curiously, they attributed the discharges to ischemic lesions during drug-induced sleep, making the observations ambiguous Palmini and coworkers cite exceptional cases of pure amnesic seizures in temporal lobe epilepsy, but even in their best examples, ictal and postictal function was not normal More likely in our view, transient global amnesia is ischemic or perhaps migrainous in nature, though not atherosclerotic-thrombotic Rarely (if ever) do the attacks progress to stroke Regarding cerebrovascular disease and TGA, Hinge and associates and Hodges and Warlow, in a case-control study of 114 patients with transient global amnesia, found no evidence of an association with cerebrovascular disease; there was, however, a signi cantly increased history of migraine, as there was in the series of Miller and coworkers (14 percent) and of Caplan and colleagues From indirect evidence of retrograde blood ow in the internal jugular arteries during the Valsalva maneuver (occasionally reported to precipitate an attack), Sander and colleagues suggested that venous congestion of the temporal lobes was operative The most compelling cases for an ischemic basis of TGA, perhaps most relevant to migraine, comes from Stillhard and colleagues, who demonstrated bitemporal hypoperfusion during an attack of TGA, and from Strupp et al and Sedlaczek and others, who have demonstrated left mediotemporal changes (interpreted as cellular edema) with diffusion-weighted MRI In the study by the latter authors, signal changes in the hippocampi were delayed for 48 h The precipitation of identical attacks by vertebrobasilar and coronary angiography is also suggestive of an ischemic or migrainous causation The benignity of episodic global amnesia in most patients is noteworthy Once the history and examination have excluded vertebrobasilar ischemia and temporal lobe epilepsy, no treatment is required other than an explanation of the nature of the attack and reassurance, although we often hospitalize such patients brie y to be certain that the episode clears without further incident The diagnosis should not be accepted if there has been ataxia, vertigo, diplopia, or other visual complaints, or if there are de cits in cognition that extend beyond the limited retrograde and complete anterograde amnesia.

The physician presented with a patient suffering from dementia and amnesia must adopt an examination technique designed to expose the intellectual defect fully Abnormalities of posture, movement, sensation, and re exes cannot be relied on to disclose the disease process Suspicion of a dementing disease is aroused when the patient presents multiple complaints that seem totally unrelated to one another and to any known syndrome; when symptoms of irritability, nervousness, and anxiety are vaguely described and do not t exactly into one of the major psychiatric syndromes; and when the patient is incoherent in describing the illness and the reasons for consulting a physician

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Three categories of data are required for the recognition and differential diagnosis of dementing brain disease: 1 2 3 A reliable history of the illness Findings on mental examination, ie, the mental status as well as on the rest of the neurologic examination Ancillary examinations: CT, MRI, sometimes lumbar puncture, EEG, and appropriate laboratory procedures, as described in Chap 2

certain amount of coverage for your car, an option has a similar theory You are paying a premium for the right, but not the obligation, to the market This premium is determined by supply and demand in the market Like other securities, options are bid, offered, and traded actively on the market They are traded separately from their underlying instruments and often on different trading exchanges

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