Lanzone et al 8 retrospectively analysed clinical and other data of 83 patients with an abrupt occurrence of amnesia that was initially diagnosed as TGA in their emergency department. Given the potential long-term consequences of amnesia, the threshold for an MRI scan with DWI sequences in acutely amnesic patients should be low, particularly in scenarios such as an unusual duration of amnesia, the presence of further cognitive or neurological signs and/or high vascular risk factor load. The authors concluded that although ischaemic amnesia could mimic TGA, it is a “rare” occurrence.īut the true rate of underdiagnosis (missing ischaemic stroke or TIA and diagnosing TGA instead) could not be estimated, as less than 25% of the 164 clinically diagnosed TGA patients underwent magnetic resonance imaging with DWI. This one patient demonstrated an isolated hippocampal lesion (20 hours after onset) that “was brighter and more linear than the usual punctuate TGA lesions and showed Gadolinium uptake on repeat MRI at eight days, leading to the diagnosis of ischaemic amnesia”. All but 1 of the 13 patients demonstrated DWI lesions distinct from the pattern that is thought to be characteristic for TGA. During long-term follow-up, cognitive assessment demonstrated persistent amnesia in 4/13 patients. Clues pointing to ischaemic amnesia were: minor additional cognitive signs (executive deficits and mild anomia), minor neurological signs and/or an unusual duration of amnesia (<1 and over 24 hours). In 7 out of these 13 cases it was difficult if not sometimes impossible to distinguish them from TGA on a purely clinical basis. The gold standard for the diagnosis of ischaemic amnesia (as opposed to TGA), was the DWI pattern seen in MRI scans (see below). They identified 13 patients who met their inclusion criteria and also had witnessed episodes. They utilised hospital records and in particular their large stroke data base (3804 patients at the time) to identify clinical clues that might differentiate certain forms of acute ischaemic stroke and transient ischaemic attacks (TIA) presenting predominantly with amnesia (ischaemic amnesia) from transient global amnesia (TGA). Michel et al 7 published a retrospective case series of patients with amnesia as the predominant presenting symptom. When trying to answer these questions, we will also look at the role – and limitations – of EEG in the diagnostic process, and discuss the issue of diffusion-weighted MRI (DWI) lesions in the hippocampus due to amnestic episodes. 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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