The localisation of this pathological process to the CA1 area on imaging may give an indication to its causation. 8,9 In fact in cases where the initial MRI performed within 24 h is normal, however clinical suspicion for TGA remains high, repeat imaging is recommended. These include high-resolution DWI, higher B-values, thin slice thickness (2–3 mm) and a delay of 48–72 h between symptom onset and scanning. 7 Since that time, various studies have been carried out and shown that certain factors may improve the visibility of these findings on MRI. These changes were first described in 1998 by Strupp et al. 6 Classic DWI findings in TGA consist of unilateral or bilateral small punctuate hyper-intense lesions in the CA1 region of the hippocampal cornu ammonis. CA1 (Sommer’s sector) is known as the vulnerable zone, CA2 and CA3 as the resistant sector and CA4 as the medium vulnerability sector. Structurally, the cornu ammonis or hippocampus proper is divided into four distinct zones, based upon their sensitivity to hypoxia and histological differences. While imaging in such cases is usually normal, it is now well-known that TGA may be accompanied by characteristic MRI changes involving the hippocampus. 5 MRI is nonetheless recommended to exclude stroke or structural pathology, where there is diagnostic uncertainty. Criteria, such as those established by Hodges and Warlow, serve as guidance. The diagnosis of TGA is based on its clinical features. None of these however clearly explain all the condition's characteristics. Various theories have been postulated, including venous congestion (secondary to retrograde cerebral venous blood flow), 3 focal ischaemia, migraine as well as epilepsy. While this is a well-described disorder, the exact aetiology of this condition remains obscure. Cited precipitating factors include emotional stress, physical exertion, pain and the Valsalva manoeuvre. The reported incidence is of 5–10 per 100 000 population. This syndrome usually occurs between the fifth and seventh decade of life and there is no significant gender predilection. Episodes characteristically resolve completely within 24 hours, with return to baseline cognition. Long-term memory, language, visual-spatial orientation and executive functions are typically preserved, with no other associated focal neurological deficit. Transient global amnesia is a clinical disorder characterised by sudden onset anterograde amnesia with temporal disorientation and iterative questioning due to inability to form new memories. Parameters including blood pressure were normal and full neurological examination was unremarkable. On examination, he was fully alert, oriented and cognitively intact. There was no previous history of transient ischaemic attacks, strokes or migraine. His medical history was notable for hypertension, diabetes and a 20-pack-year history of smoking. The patient also denied any recent stressful event or head injury and this was the first such episode of memory impairment. There was no witnessed loss of consciousness or seizure activity. He denied any associated headache, weakness, speech problems or sensory disturbance. This lasted for about 30 min, after which his memory slowly returned however, he could not remember what had happened during this episode. There were no features of retrograde amnesia, with the patient still being able to recall his identity, recognise his family members and carry out usual functions. According to his wife, he went to work as usual that morning, however on returning home in the afternoon he was forgetting a number of recent events and was asking a number of questions repeatedly. A 61-year-old gentleman presented to the Mater Dei Hospital emergency department following a short episode of transient memory loss.
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