03/07/2018
A reappraisal of a Transient Global Amnesia (TGA*) episode
The function of human memory is, as we would all agree, to remember. But paradoxically the neurological mechanism to achieve this memory function is actually to erase the vast majority of incoming data. In more frivolous terms we are constructed in such a way to be good at forgetting nearly everything our sense organs register. What our eyes see, our ears hear, our nose smells, our tong tastes and our body feels, all that will never reach conscious memory apart from a tiny fraction of which we craftily construct our personal narrative.
This created narrative, a miniature sample of our sensory observations, provides us with a sense of continuous awareness of presence both in place and time, furthermore it constructs an understandable and manageable relation to other human beings.
Too much sensory input makes an erratic narrative and in extreme cases a psychotic episode. Less input disables us to form coherent narrative. People who have had one or more TGA episodes, are painfully aware how diminishing the imprint to an even lower degree than the already by default extremely selective neuro mechanism of memorising, dilute or nearly completely breaks our ability of narrative continuity, luckily only for a relatively short period of time on average two to six hours.
We are naturally inclined to refer all exceptional and painful events in our life to the category “dis-ease” and even more inclined to blame this to malfunctioning due to a detectable physical cause. Is this the case with TGA, and if so, is this justified?
Several nuances are to be made before “medicalisation” of events like high blood pressure, palpitations, fear, fainting, just to name a few.
Since we encounter the above mentioned often, we now discern the frequency and intensity of these phenomena's as criteria for labeling them as pathological instead of functional. It is clear we have not reached this level of nuance about TGA yet.
Contrary to our primitive intuitions, for many condition like high blood pressure we have accepted multi causal explanations leading to a final common pathway. This is not the case for TGA yet, as it is rare and recently discovered we are still inclined to find the one common determinant.
A broadening of our understanding, and maybe, even more significant, an efficient way to cope with a TGA experience could be to approach such an episode from a functional point of view.
If we faint at a funeral of a loved one we would not be inclined to go to the emergency room to see what bodily disfunction was responsible. We would instead consider it as a sign that somehow the experience became too painful to sustain consciousness. If our GP measures high blood pressure he will ask you to come back twice at different times of the day to get a better impression of your blood pressure in the course of time because there is nothing wrong with being able to rise your blood pressure but the only problem for your health is if you are not able to lower it (e.g. during sleep).
Could a similar approach benefit those, who experienced a TGA? Could we accept that a TGA is maybe just an (exaggerated?) normal physiological possibility of our complex brain?
Well, I do not know. But since narrative continuity is our framework for consciousness it is very well possible that the continuous flow of narration needs interruption, like it naturally does in sleeping and dreaming. Maybe like fainting is an exaggerated interruption of consciousness, TGA could be an abrupt interruption of the narrative proces.
* A person having an attack of TGA has almost no capacity to establish new memories, but generally appears otherwise mentally alert and lucid, possessing full knowledge of self-identity and identity of close family, and maintaining intact perceptual skills and a wide repertoire of complex learned behavior. The individual simply cannot recall anything that happened outside the last few minutes, while memory for more temporally distant events may or may not be largely intact. The degree of amnesia is profound, and, in the interval during which the individual is aware of his or her condition, is often accompanied by anxiety. The five diagnostic criteria for TGA, are:
The attack was witnessed by a capable observer and reported as being a definite loss of recent memory (anterograde amnesia).
There was an absence of clouding of consciousness or other cognitive impairment other than amnesia.
There were no focal neurological signs or deficits during or after the attack.
There were no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.
The attack resolved within 24 hours. (wikipedia)
