Transient Global Amnesia (TGA)

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website
to see the anatomical information referred to in this post.

The criteria used to diagnose follow:
There is clear anterograde amnesia.
The attack must last no longer than 24 hours.
The individual must not have clouding of consciousness (drowsiness) and they must know their personal identity.
The attack must be witnessed by another person.
There should be no other neurological symptoms during or after the attack (problems speaking or partial paralysis).
There should be no recent history of head injury or epilepsy.

TGA patients often have retrograde amnesia for hours before the attack and have anterograde amnesia for 1 to 10 hours. They usually repeat the same questions, such as “where am I?” and “why am I here?” because they forget that they had already asked a question and received an answer. The most common events that precipitate an attack are emotional stress, physical effort, contact with hot or cold water, or sexual intercourse. TGA patients are usually middle-aged or elderly adults. Accompanying symptoms can include headache, nausea, and dizziness. After diagnosis, the course of treatment is to wait for the amnesia to resolve on its own.

Research provides compelling evidence that TGA is caused by a temporary lesion in the CA1 region of the hippocampus. This is consistent with the important role of the hippocampus in long term memory. The mechanism underlying hippocampal lesions in TGA patients remains unknown. One hypothesis is that TGA patients have blood flow problems due to vascular blockage, but TGA patients do not have greater vascular risk
factors, such as high blood pressure, high cholesterol, than healthy control participants.

Dr. Slotnick writes, “The only identified risk factor is a history of migraine headaches. As emotional or physical stress almost always triggers TGA attacks and stress can produce changes in blood flow, it may be that hippocampal CA2 lesions are due to stress-induced decreases in blood flow to this sub-region. The hippocampal CA1 sub-region may be particularly susceptible to reductions in blood flow because it is supplied by one large artery, while the other hippocampal sub-regions are supplied by one large artery and many small arteries. The temporary focal lesions in the hipocampas CA1 sub-region of TGA patients provide a unique opportunity for future collaborations between cognitive neuroscientists and neurologists to investigate the specific role of this region in long-term memory.

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