What clinical features differentiate Transient Global Amnesia (TGA) from other causes of acute memory loss?

Transient Global Amnesia (TGA) is a distinct clinical syndrome primarily characterised by a sudden onset of profound anterograde amnesia, which is the inability to form new memories, often accompanied by some retrograde amnesia for recent events [Faust et al., 2016]. A crucial differentiating feature of TGA is the preservation of personal identity and other cognitive functions, such as attention, language, and visuospatial skills [Faust et al., 2016]. Patients typically engage in repeated questioning about their current situation and recent past due to their memory impairment [Faust et al., 2016].

TGA is differentiated from other causes of acute memory loss by the absence of focal neurological deficits, such as weakness, sensory loss, or speech disturbance, which would typically prompt investigation for conditions like stroke or transient ischaemic attack (TIA) [NG127, Faust et al., 2016]. Unlike epileptic seizures, TGA does not involve loss of consciousness, automatisms, or significant post-ictal confusion [CG109, Faust et al., 2016]. The memory impairment in TGA is characteristically transient, resolving completely within 24 hours, often much sooner, with no residual memory deficits [Faust et al., 2016].

Other conditions causing acute memory loss, such as head injury, toxic/metabolic encephalopathy, or complex partial seizures, usually present with additional features not seen in TGA [NG127, CG109]. For instance, a head injury would have a clear history of trauma, while toxic/metabolic causes often involve altered consciousness and diffuse cognitive impairment beyond just memory [NG127]. While psychogenic amnesia can present with memory loss, it often involves a loss of personal identity or selective memory for traumatic events, which differs from the global amnesia and preserved identity observed in TGA [Faust et al., 2016].