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. Recognition of this type of behavioral disruption and its proper treatment can lead to improved quality of life for these patients, maintain these patients in their homes and out of chronic care institutions longer, and facilitate the community's and caretaker's interactive roles with the patient.Transient global amnesia (TGA) is a clinically defined syndrome of acute hippocampal dysfunction lasting several hours. This report emphasizes the importance of recognizing transient epileptic amnesia as an easily treatable cause of episodic behavioral abnormalities responsive to antiepileptic therapy, especially in those patients who have a markedly inconsistent pattern of wandering, disorientation in familiar settings, and amnesia exacerbation manifested by no recall of the emotional stress of getting lost or of any information during these episodes. The authors suggest that transient wandering of this type may be caused by ictal events or postictal confusional states. These transient amnestic wandering events subsided after treatment with antiepileptic drugs in both patients. These clinical episodes and the bilateral interictal epileptiform electroencephalographic changes found in both patients led to the diagnosis of transient epileptic amnesia, a syndrome that can be diagnostically elusive.
The inability to recall any information during these episodes, and the marked difference of the episodic amnesia exacerbations from the progressive amnesia characteristic of Alzheimer disease seen in these patients led to their evaluation.
At other times these patients did not wander or become disoriented. The authors present two patients with dementia who displayed recurrent transient episodes of amnestic wandering and disorientation characterized by getting lost in familiar environments.
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