Transient global amnesia may be ischemic or perhaps migrainous in nature, though not of the usual atherosclerotic-thrombotic, and rarely (if ever) do the attacks progress to stroke. There are certainly comparable memory deficits with ischemia in the territory of the posterior cerebral artery branches to the medial temporal lobe and thalamus but they lack many of the characteristic aspects of TGA including completely normal functioning otherwise. We have, however, cared for several patients with unusual basilar artery ischemic syndromes who displayed the repetitive questioning typical of TGA at longer intervals than customary for the latter. Regarding cerebrovascular disease and TGA, Hinge and associates and Hodges and Warlow, in a case-control study of 114 patients with TGA, found no evidence of an association with cerebrovascular disease; there was, however, an 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 flow in the internal jugular arteries during the Valsalva maneuver (the maneuver occasionally precipitates an attack), Sander and colleagues and Chung and coworkers have suggested that venous congestion of the temporal lobes was operative. Other studies suggest that the draining veins in the neck lack valves in patients who have had TGA, which permits venous ischemia in the temporal lobes (Schreiber et al); rare cases associated with lateral sinus thrombosis also implicate derangements in venous blood flow in the genesis of TGA. None of these is definitive and they are mentioned here for completeness.
Perhaps the most persuasive cases for an ischemic basis, perhaps most relevant to migraine, come from Stillhard and colleagues, who demonstrated bitemporal hypoperfusion during an attack of TGA, and from Strupp and associates and Sedlaczek and colleagues, who demonstrated hippocampal and peri-hippocampal lesions (interpreted as cellular edema) with diffusion-weighted MRI, but only 2 days following an attack, not acutely. Like the clinical syndrome, the MRI findings are reversible (Fig. 20-2). The precipitation, rarely, of attacks by vertebrobasilar and coronary angiography is also suggestive of an ischemic or migrainous causation.
A hypothesis generated by the authors of studies on delayed MRI lesions is of a mismatch between cerebral blood supply and demand in the limbic regions. This provides a potential explanation for the association of highly emotional events prior to an episode.
The benignity of transient 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 briefly to be certain that the episode clears without further incident. The diagnosis of TGA should not be accepted if there has been ataxia, vertigo, diplopia, or other visual complaints, or if there are deficits in cognition that extend beyond the limited retrograde and complete anterograde amnesia.
The physician presented with a patient suffering from dementia must adopt an examination technique designed to expose the intellectual defect fully. Abnormalities of posture, movement, sensation, and reflexes 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 fit 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.
Three categories of data are useful for the recognition and differential diagnosis of dementing brain disease: 1. A reliable history of the illness and its impact on daily life 2. Findings on mental examination 3. Ancillary examinations: CT, MRI, functional imaging, sometimes lumbar puncture, EEG, and appropriate laboratory procedures, as described in Chap. 2.