Transient global amnesia may be caused by cerebral vein thrombosis.
Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.
Solheim
Ole
O
Department of Neurosurgery, University Hospital of Trondheim, St. Olavs Hospital, Olav Kyrres gt 17, N-7005 Trondheim, Norway. ole.solheim@stolav.no
Skeidsvoll
Tora
T
D020236:Amnesia, Transient Global / Q000453:epidemiology* / Q000503:physiopathology*; D001921:Brain / Q000098:blood supply / Q000503:physiopathology; D015984:Causality; D002550:Cerebral Veins / Q000503:physiopathology; D002986:Clinical Trials as Topic; D015897:Comorbidity; D019317:Evidence-Based Medicine; D006801:Humans; D020767:Intracranial Thrombosis / Q000453:epidemiology* / Q000503:physiopathology*; D008954:Models, Biological; D015995:Prevalence; D018570:Risk Assessment / Q000379:methods*; D012307:Risk Factors; D020246:Venous Thrombosis / Q000453:epidemiology* / Q000503:physiopathology*