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Showing posts with label PTSD. Show all posts
Showing posts with label PTSD. Show all posts

Monday, January 28, 2019

Learning to Learn Emotional Stability


Educated people know about Pavlov's classical conditioning studies. But few people realize the pervasive implications that apply even today.

The key initial observation made by Pavlov was that when dogs saw objects that looked like (and probably smelled like) food, they salivated. He immediately seized on the concept of ASSOCATION that somehow caused nervous systems to learn. He had no way to know if dogs actually "thought" about the association. It did not matter whether the dogs did or not. The biological adaptiveness of such a learning system was obvious. Pavlov realized he needed to pursue this, instead of digestive physiology, as it was something new and fundamental. He went on to perform experiments that lead to the ideas of UCS/CS and UCR/CR.

The idea he missed was positive reinforcement. In fact, it took some 50 years for others to realize that reinforcement was an underlying mechanism in classical conditioning. This led of course to the idea that you could produce learning by manipulating reinforcement (i.e., operant conditioning).

Pavlov's work, old as it is, is still finding applications today. A couple years ago I got an up-date in the area of PTSD research at a seminar by Gregory Quick from the Department of Psychiatry at the University of Puerto Rico. As Pavlov showed, memory extinction is a basic phenomenon even in simple animals. If you repeatedly flash a light and then stress a rat, it soon learns to become distressed the next time it sees the flash, even after you stop the stress. In the lab, this is manifested by the rat showing freeze behavior. But, if you repeat flash cue enough times without the stress, the conditioned response (CR) (freeze behavior) eventually becomes extinguished.

At first, scientists thought that extinction erases the memory of the CR. But extinction really creates a new memory that competes with memory of the original CR. Both memories co-exist. Over time the extinction memory may be lost, and the CR can return. The implication is that, just as ordinary learning needs rehearsal, so does extinction learning.

Therapy for emotional trauma and PTSD might be more effective if therapy were approached like a conventional learning experience whose memory is affected in all the usual ways. Recall what was said about extinction being a case of new learning. Re-learning of an extinguished response occurs much more readily than it does for initial extinction learning. This is an example of priming. It’s like re-learning a foreign language. It goes easier the second time and the memory might be even more dependable. 

Since memory of an emotional CR learning experience and its extinction can co-exist, these two memories compete for which one is strong enough to survive long-term. Sadly, the CR memory that causes the PTSD is often stronger. Cues are extremely important to both forming and retrieving all kinds of memory. It seems likely there are many more explicit cues for CR memories than for extinction memories. Therapy should be aimed at enriching the number and variety of cues associated with extinction learning. Rehearsal is likewise important. So far, nobody seems to have given that much thought.

There is another aspect to emotional learning: learning to learn. If you have multiple anxieties, they may generalize and "spread" to facilitate learning new anxieties. In other words, the brain is learning to become emotionally dysfunctional. The corollary would be that learning how to promote extinction could also generalize and thus increase the general ability to cope with emotional trauma. Obviously, for one's brain to learn how to do that, one would need to begin with a single relatively easy extinction learning task, and then apply that learning-to-extinguish experience to other situations. Extinction learning needs to be repeated in order to become firmly established.

Monday, May 23, 2016

A Potential New Area for PTSD Research

Post-traumatic stress disorder (PTSD) is a common form of fear memory, in which a pervasive emotional stress is created by remembering experiences that evoked fear. If our brains could forget the fear memory, PTSD would decay away. Why can't we forget fear memories? In part, it is because they keep getting rehearsed, and much of this rehearsal occurs during our dreams. One major normal function of sleep is to help the brain to strengthen memory of things, good and bad, that happened during wakefulness.

Recent animal research suggests how the brain accomplishes this memory strengthening (called consolidation). More importantly, consolidation is manipulable. The study began with the established understanding that memories are of two kinds: explicit (episodic) and implicit (procedural). Fear memories are episodic; that is, we remember the episodes in our life that were traumatic. Episodic memories are laid down by a structure in the brain known as the hippocampus, a part of the cerebral cortex that is folded underneath the main cortex and has different internal structure and connections with other parts of brain. Moreover, the hippocampal consolidation effect is exerted when it generates a voltage rhythm of roughly 6-10 waves per second that also contains nested higher frequencies (gamma) of about 30-90.

With this background of information, researchers at McGill University in Canada* decided to see how fear memory might be affected by disrupting hippocampal theta rhythm, which in sleep occurs during the REM (dream) stage of sleep. The study was conducted in mice, monitored during their sleep, soon after they were trained to remember certain objects and also after they had learned a conditioned fear memory. The object-learning task was to remember where a novel object had been placed (the hippocampus is also known to provide the brain with spatial location information). The other learning task, and the one relevant to PTSD, involved exposing awake mice to a sound warning followed by electrical shock to their feet. They manifested the associated fear learning by freezing all movement as soon as the sound cue was heard, before the foot-shock was actually delivered.

The key part of the experiment was the ability to shut down theta activity. Other workers had shown that neurons can be made hypersensitive to laser light by injecting their environment with a virus that is fused to a fluorescent protein. The location of neurons that drive theta rhythm is known, and so the researchers injected such a virus into that area and also implanted a fiber optic that could deliver laser light on those neurons. Neuronal activity in this area could be stopped whenever laser light activated the protein.

With both memories of object location and conditioned fear, testing for recall on the next day revealed that memory formation was prevented by blocking theta activity during the preceding REM sleep when the blocking occurred during a critical four-hour period immediately after initial learning. Similar activity disruption during the non-dream, non-theta, stage of sleeping did not prevent either form of memory.

Even if you could use this laser-light technique in humans (and theoretically you can), you might say this approach could not work because it is usually not practical to institute formal therapy within four hours after an initial emotionally traumatic experience. But, a common current PTSD therapy is based on the established phenomenon of re-consolidation of memory. Every time you recall a memory, it has to be re-stored, and thus it is susceptible to modification (by talk therapy, for example). The revised memory can replace the original fear memory. A therapist could have a patient recall the bad experience, go to sleep right away, and receive light blocking of theta to disrupt the re-storage of the bad memory. Perhaps a simpler approach would be to get good dream sleep soon after talk therapy, which might help cement the revised, less traumatic memory.

*It was at McGill, about a half-century ago, that the role of the hippocampus in memory formation was first discovered.


Source:

Boyce, Richard, et al. (2016) Causal evidence for the role of REM sleep theta rhythm in contextual memory consolidation. Science. 352, 812-815.


For more information about learning and memory, consult Memory Medic’s recent book, Memory Power 101.

Monday, November 10, 2008

Negative Emotions and Memory

I have a big section in my memory book on the interference with memory formation caused by negative emotions. I have seen first hand how emotional crises cause the grades of college students to plummet. Whenever a good student suddenly starts making poor grades, I know this student has recently had an emotional trauma. Common problems for college students include trouble making friends, boy/girl problems, parent divorce, homesickness, financial worries―grades invariably suffer.

Recently, I had a reader of this blog challenge my position, pointing out that the most severe form of negative emotions, post-traumatic stress (PTSD), has as its main problem the inability to forget the events that triggered the PTSD. My reader is of course correct. But so also is all the evidence that negative emotions interfere with memory. How do I reconcile these incompatible views?

What is so well-remembered in PTSD are the traumatic events that caused the negative emotions. That is not the same as saying that PTSD patients have exceptional ability to remember other things or learn new things. I contend that their memory for new learning is impaired because of their distressed emotional state. The reason they remember the PTSD events so well is because they rehearse them so often.

All intense situations, even happy ones, tend to be well-remembered because of the intensity of the stimuli and the fact that such situations are repeatedly rehearsed. Rehearsal usually occurs immediately, because of the intensity of stimulation, and is repeated frequently, because the situation had such a big emotional impact. It is not so much the positive or negative aspect of the situation that matters for memory formation, but rather the timing and frequency of rehearsal.

Why do negative emotions interfere with new learning? I haven’t seen formal studies of this question, but what I know about memory allows some useful speculation. First, feelings such as worry, fear, depression, loneliness, and the like, have devastating effects on motivation. Under such conditions, nobody feels much like taking on challenges. Negative feelings also make it hard to pay attention to anything else besides what is causing the emotional distress. Attentiveness is pre-requisite for forming memories of new learning. Negative feelings lead to persistent negative thoughts, and thinking about one thing while trying to memorize another just doesn’t work. Negative feelings also erode confidence and sense of well being, both of which are essential for optimal memory ability. Why confidence and sense of well being are important is unclear, but I suspect they motivate a person to do what it takes to achieve personal goals. In the case of memory ability, it is easier for an up-beat person to take on learning challenges and to do the right things for promoting memory formation.