the syndrome of transient global amnesia ( tga ) , first described as such by fisher and adams   in 1964 , is characterised by abrupt and temporary ( < 24 h ) disruption of anterograde memory without clouding of consciousness or focal neurological signs . patients typically present with repetition of the same questions or statements , followed by full recovery but without memory for the amnesic period . the pathophysiology of tga is uncertain , but probably involves transient hypoperfusion of memory - eloquent brain structures including the medial temporal lobe and hippocampus , as evidenced by sophisticated neuroimaging studies . despite its sudden onset , there is no evidence for an epileptic aetiology in tga , although misdiagnosis as epilepsy or stroke by clinicians unfamiliar with tga is not uncommon . a possible relationship to migraine , particularly in younger patients , has been noted . familial cases of tga have rarely been reported [ 7 , 8 , 9 , 10 , 11 , 12 ] . we present further familial tga cases , survey prior publications on this topic , and consider the possible aetiology of familial tga . a 54-year - old female had an episode of neurological disturbance of about 2.5 h duration after taking her dog for a walk . an eyewitness of the attack reported that the patient was repeatedly asking the same questions . she had little recollection of the episode after recovery but had a vague recollection of being fearful . she had a mild migraine tendency but was otherwise in good health and took no regular medication . neurological examination 1 month after the event was normal . as the patient was well , no further investigation ( brain mri , dopplers , eeg and blood tests for stress hormones ) was undertaken . based on the history , proposed diagnostic criteria for tga   were felt to be fulfilled . the patient reported that in the family history , 2 maternal aunts had had similar symptoms at similar ages to herself and had both been diagnosed with tga . familial occurrence of tga has been reported on occasion ( table 1 ) [ 7 , 8 , 9 , 10 , 11 , 12 ] , but all prior reports have involved siblings , with only occasional definite   or possible   instances of parental involvement . prior accounts of familial involvement with more distant relatives , as in the current report , have not been identified . summing all the 22 patients in these 7 reports , there is a slight female preponderance ( f : m = 14:8 ) , with all episodes occurring in the 6th8th decades of life . although details are incomplete , at least 6 of these individuals ( 5 f , 1 m ) had a history of migraine , and 1 patient had migraine - type headaches immediately after two tga episodes . typical precipitating factors for tga ( physical exercise and emotional upset ) were recorded in 13/22 familial cases . no details on whether our patient had undertaken strenuous physical exertion whilst walking her dog were available some clinicians are of the view that  tga is probably a migraine aura in most cases , in which case a familial tendency to tga would not be surprising . likewise , a female preponderance of cases , as noted in some prior surveys of tga [ 6 , 14 ] , might be deemed consistent with a migrainous aetiology . comorbidity with migraine has been noted in some of the reports of familial tga [ 9 , 10 ] , but only in some family members in other reports   or not at all ; still other reports make no comment on migraine [ 8 , 11 ] . since migraine is a highly prevalent condition , it can not be assumed that the presence of this variable necessarily influences the occurrence of tga . it may be that in some families , a genetically determined migraine tendency may also predispose to attacks of tga . if this were the case , then it is perhaps surprising that familial tga is so rare when migraine is so common . other genetically influenced developmental factors , perhaps related to local blood vessel structure or innervation , which rendered the hippocampal blood supply particularly vulnerable , might predispose only certain families . if routine questioning of all tga patients about a family history of similar events proved positive , then these patients might be submitted to further investigation ( brain mri , dopplers , eeg and blood tests for stress hormones ) to address the proposed tga aetiologies .
following an episode of typical transient global amnesia ( tga ) , a female patient reported similar clinical attacks in 2 maternal aunts . 
 prior reports of familial tga are few , and no previous account of affected relatives more distant than siblings or parents was discovered in a literature survey . 
 the aetiology of familial tga is unknown . 
 a pathophysiological mechanism akin to that in migraine attacks , comorbidity reported in a number of the examples of familial tga , is one possibility . 
 the study of familial tga cases might facilitate the understanding of tga aetiology .