6 Does this statement really apply: Could TGA not be a form of NCSE or maybe a post-ictal phenomenon? 4īased on my previous work 5 and further study of the literature on TGA the following questions will be discussed in this paper:ġ) Are the Hodges & Warlow 4 diagnostic criteria for TGA specific enough to exclude the risk of missing a mimic such as TEA or ischaemic amnesia?Ģ) In a comprehensive review of non-convulsive status epilepticus (NCSE), Kinney et al stated that TGA can be readily distinguished from NCSE. Box 1 summarises the clinical TGA criteria based on the work of Hodges & Warlow. 2 The chance of re-occurrence is minimal 3 (estimated to be <10% annually), there are no known means of prevention or treatment, and due to its benign nature there is no need for further investigations. ![]() 1 “TGA does not increase the long-term risk of cerebrovascular events, seizures, or cognitive impairment”. The whole episode resolves spontaneously leaving only a memory gap of a few hours. They realise that something is wrong with them, become anxious and repeatedly ask the same questions, as they cannot memorise the answer. The neurological examination is unremarkable. Patients, typically between 50 and 80 years of age, are suddenly unable to encode new information, without impairment of attention, self-identity or previously learned skills such as driving or using their phone. We will look at a few arguments that could explain why TGA is possibly an epileptic phenomenon and maybe even a form of non-convulsive status epilepticus.Ĭonsistent with our knowledge of memory formation, transient global amnesia (TGA) is a temporary loss of hippocampal function lasting several hours. But hypothetically TGA might share a common mechanism with its closest mimic, namely transient epileptic amnesia. Its pathophysiology remains elusive, and current hypotheses favour a non-epileptic cause. ![]() Transient global amnesia (TGA) is a clinically defined syndrome of acute hippocampal dysfunction lasting several hours.
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