Monday, May 23, 2022

Infantile Amnesia, Trauma and the Recontextualization of Broad and Generalized Anxiety and PTSD

Dr. Lynn Nadel at UBC answering a question
After a hiatus of more than a couple of years - yes, you guessed it: due to the pandemic - it was finally back to (relative) normal for me with a long-overdue (masked) in-person attendance of one of my favorite traditions of psychology, the annual Quinn Memorial Lecture! This year’s talk was about memory, and it was presented by Dr. Lynn Nadel from the University of Arizona entitled “Brain Development and the Emergence of Learning and Memory in Humans and Other Animals.” And yes, humans are animals, hence the deliberate use of the word “other.”

Getting out and getting to the location was more challenging than expected. It was one of my first large-group outings since the onset of the pandemic, and I was slightly nervous. It did not help much to encounter continuous construction sites and the rerouting of traffic due to construction and closures. It was with some difficulty I managed to get to the university site and with UBC’s mandatory masking rules in place for another month, this year’s lecture was in equal measure familiar and unfamiliar. 

But the main thing was that I was finally able to be there in person and ready to take in another interesting and insightful lecture with the added bonus of a complimentary glass of (red) wine and psychological chit-chat during the subsequent reception.

The lecture started with an interesting tidbit of trivia that was new to me: hippocampus actually means “seahorse" due to the similarity in terms of its shape, and, for better or for worse, it has nothing to do with hippos. The other bit of surprising information was that the hippocampus does not develop for the first two years of life - its function emerges only after 18 to 24 months with its fully adult function from 10 to 12 years - which explains not only pre-adolescent forgetfulness but also why we cannot remember anything from our first few years of infancy, and which also implies that those who claim they do are either misguided, misled or they are simply lying to you.

I was pleased to hear Freud’s name mentioned during the lecture, but sadly, it was not done with the sufficient respect I had hoped for. And yet, there were three reasons given by the father of psychoanalysis, and all of them contain at least a ring if not a shout of truth to them. Freud hypothesized three potential reasons for the dead zone of infantile amnesia, namely that it could be because of repression (a plausibility but not applicable to all cases and situations), the second reason was the non-translatability of experiences due to an absence of and recourse to language, and finally, that it may have been due to biological development and mechanisms.

We now know that the last two are certainly of importance here. We should not forget that Freud himself was a neurologist and to be able to see things clearly in a time and age where neuroscience was in its own infancy is truly impressive. It is evident now that the hippocampus develops and matures later than various other parts of the brain and that language and self-consciousness and self-awareness do not make an impact until after the second year of life. Adding to this, it is not just a matter of being unable to form episode memories but memory, as a rule, and as a function, is not meant to capture events photographically but rather to be used as a tool for predicting future events and essentially setting up conditions and opportunities for overall learning. 

This also has serious ramifications for the experience of stress and traumatic experiences in the first fragile and impressionable years of human life. Any neglect and trauma become stored not as a concrete memory but as waves of vague, uneasy, and seemingly impenetrable feelings. This is different from the usual and regular issues and matters that the unconscious is tasked to deal with because the experiences have not been formed and are shapeless in this case.

The unconscious is the convenient and useful placeholder for and reservoir of unwanted memories, feelings, desires, wishes, and traumatic experiences. Although they seem to be locked away, the contents often leak and seep through and may create a number of neuroses, neurotic afflictions, and anxiety. But in his lecture, Dr. Nadel was claiming that our fears and anxieties may usually have a traceable cause, such as fear of dogs resulting and emanating from a memory of a dog bite in childhood. But the problem is what if we cannot find or trace our fears, phobias, and anxieties back to any specific event? For instance, what would cause the prevalent fear of spiders even though the person in question may have never had any negative contact or experience with those insects?

Of course, we could refer to Jung’s collective unconscious and that there are archetypical fears that regardless of personal experience, we collectively inherit and operate within. But another possible explanation could be that we might have had a negative experience say of a bite but since it occurred at a time where we did not have access to a) any memory - remember we are still lacking that capacity before the age of 2 - and in addition to having no access or recourse to b) the benefits and clarity of language.

When we experience fear-inducing moments with a clear and distinct sense of threat, a road accident, burglary, or attack by an animal, we do not need language to tell us what to do, but we instinctively and automatically engage in fight, flight, or freeze behaviors. But what if it is something that is at least from a rational perspective a non-threatening and often benign-seeming situation? We understand how the sight of dogs can be fear-inducing for some but few of us would feel that way about puppies. So how to make sense of that kind of seemingly irrational fear?

In this case, we sense not only concrete, specific, plausible, and traceable triggering experiences of fear but also the vague, broad, and generalized forms of anxiety in which threats are sensed and perceived where none of them seem to exist except in our own perception and minds.

This may be due to traumatic experiences at a point in time where we were either too young to process them or too overwhelmed by them. Infants may internalize the dread alongside feelings of fear and since they have no context nor nothing to compare it with and have nothing to express nor make sense of it, it remains floating and elusive as a general sense of ominous and foreboding threat. This could lead to panic attacks and the fear of open spaces, with agoraphobia being a less common form of fear as opposed to claustrophobia and the fear of spiders and heights, which many of us commonly experience. 

This would be then due to the amygdala being switched on without the mediation and aid of the hippocampus in the form of stored memory as well as a lack of rational thinking via language and logic in the prefrontal cortex. And yet, the feeling of unease might get imprinted and recorded across various parts of the brain and hand in hand with sensations stored in the body. In an experiment where rats were stressed early on (poor things), the effects of early environmental stress could be demonstrated as well as how the hippocampus is loaded with stress receptors and how stress affects and weakens the development of the hippocampus. 

In fact, a similar process may occur even with adults who experience significant stress and trauma. The clearest example in history would be when perfectly healthy adults came back from World War I and were shell-shocked, i.e., simply not being able to shake off, process and digest their feelings of fear and dread and making it difficult for them to function in daily life. Those “shell-shocked” individuals did not have any issues or precursors with mental health, and we know now that they were suffering from post-traumatic stress disorder (PTSD).

When seemingly random events trigger those events (and it may not even have a trigger or provocation, to begin with), the afflicted person is not simply remembering what happened to them, but they are reliving the whole stressful and traumatizing experience repeatedly. It is not a case of episodic memory, but it seems that they are not able to recall it without the mental anguish and debilitating bodily sensations that are intimately linked and associated with the original experience.

This is often due to stress downregulating the hippocampus, which would usually give it a label and a context, and increasing the amygdala, which is connected with sensations of fear. In other words, the reactions to threats are isolated and taken out of any and all context, and this enhances emotional memory in the amygdala. The hippocampus is further weakened and affected due to exposure to too much cortisol.

As a potential form of treatment, people suffering from this condition could be encouraged, helped, and guided to contextualize and in some cases even re-contextualize those experiences, that is to give them a definite form and shape and then be able to store them properly in memory and be able to understand and process them more effectively. Evidently, this boils down not just to a matter of reason and rational thinking, but it can help to understand it and to put it into context; then, one can gradually deal with the emotional aspects and counterparts without being overwhelmed by those paralyzing feelings of dread and fear.

As you can see, this year’s Quinn Memorial Lecture was another wonderful opportunity to learn more about the brain and psychological processes and where I was once again able to mix and mingle with like-minded and interesting people. It was indeed a most memorable lecture!