PTSD has been in the news a lot recently, mostly because of Donald Trump's gaffe in which he alleged that people who have PTSD were not as "strong" as other people in the same situations who don't get PTSD. (Note: definitely not true.) As it so happens, there's a new theory that tries to explain the neurological basis of PTSD reactions, particularly that of the trigger: the sensory stimulus that sends PTSD sufferers into a "flashback" state, where they react in the same way that they did to the original traumatic event or events, or in ways that seem to fit with the stimulus.
The most well-known trigger is anything that sounds like a gunshot for people who have been in combat situations, but triggers can be extremely specific or very peculiar to outside observers. PTSDUK calls it "a memory filling error," and cite less obvious triggers like songs, experiences (being a passenger in a car at night), visually similar experiences and tastes. How these triggers actually work in the brain has been the subject of extensive scientific enquiry, and this new theory may bring together a lot of evidence to give shape to what really happens in a PTSD sufferer's neurology.
It's worth noting, as Mental Health America points out, that PTSD isn't just characterized by "reliving" traumatic events through triggers; it can also cause a constant state of panic and alertness, emotional isolation, depression, and other symptoms. We must also remember that PTSD is not a universal response to trauma, and is actually quite rare. With those things in mind, let's dive into what triggering actually does, why it might be involved with multiple areas of brain malfunction, and whether this new theory holds any weight.
What Really Happens In The Brains Of PTSD Sufferers?
The physical impacts of severe trauma on the brains of PTSD sufferers are generally found in three areas: the hippocampus, medial prefrontal cortex, and amygdala. The hippocampus, in a normal brain, is responsible for memory formation and storage, the amygdala monitors sensory input to determine correct fear responses, and the medial prefrontal cortex tends to deal with the "extinction" of fears (what happens when we're gradually exposed to something we fear and are shown it doesn't actually pose a threat, for instance). In a brain with PTSD, the amygdala is panicking all the time and the medial prefrontal cortex doesn't do its normal "this is OK" soothing; and the hippocampus part of the brain actually loses volume in some people with PTSD, inhibiting its proper function.
But there are several different theories about how these physical malfunctions may all draw together to create PTSD symptoms, and the new paper, from the University of Michigan School of Medicine, suggests they're all looking at a part of the picture, not the whole. The three they pick out for examination are the "abnormal fear learning model," the "exaggerated threat detection model," and the "diminished emotional regulation model". They're all convincing models, using overlapping ideas about brain damage in trauma and how PTSD sufferers react neurologically to triggers and fear. But, the Michigan scientists told Science Daily, while these theories seem pretty convincing, they may actually represent "searching under the streetlight," focusing on things that bolster their specific thinking without seeing the rest of the picture.
What's the rest of the picture? The Michigan scientists think it's something called context processing. Context processing is the way in which we determine things in certain situations to be a threat, and the same things in different situations to be benign. The researchers used the example of a mountain lion in a zoo (not a problem) and a mountain lion unexpectedly in your kitchen (big, BIG problem). This is actually one of the reasons people are capable of watching horror films: they can process the context and realize that the person on the screen with the machete isn't capable of killing them.
Even on the face of it, this makes perfect sense: PTSD triggers are all about things appearing threatening to the brain when they actually may not be, because of damage to memory and appropriate fear reactions. A person triggered by PTSD has been unable to use their context (the fact that it's a mall in broad daylight, not the place or scenario where the original trauma actually happened) to calm themselves down and "correct" their fear. Their brains can't use the information around them to create reassurance.
Could We Use This Information To Cure PTSD?
Lest you start breaking out the streamers and declaring PTSD to be solved, here's something to give you pause: the Michigan scientists are only suggesting a theory. Their next step will be to test it. But preliminary evidence suggests that there may be a good chance that they're onto something.
For one thing, the regions of the brain that are involved in PTSD are also the ones responsible for how we respond to contextual information. The hippocampus, amygdala, and medial prefrontal cortex (try saying those three times fast) all play important roles in how we assess our surroundings, determine if they're safe, and react accordingly. For another, we know that context processing can go wrong in other mental disorders, too. Problems with context processing have been seen to pop up persistently in people with schizophrenia and psychosis, though psychotic patients can improve if given medication. People with persecutory delusions showed difficulties with it too, and teenagers with high-functioning autism sometimes seem to find it hard (a study from this August suggests that it gives them "cognitive overload").
And there's one other thing: a study's already been done that might begin to prove them right. In 2012, the European Journal of Psychotraumatology published an experiment from Sweden that looked at whether context processing played a role in PTSD, in both humans and animals. They found that PTSD patients "exhibited decreased responses to contextual signals of safety and danger;" in other words, they couldn't pick up on context properly. If something indicated "nope" to a "normal" human, PTSD people weren't able to see it as clearly. Animals exposed to a "single prolonged stress" reacted in the same way.
Whether this means more effective treatment for PTSD remains to be seen. It's all a bit hypothetical at the moment. The antipsychotics that helped the psychosis patients with their context processing are likely not going to be helpful for PTSD patients, who face the same problem with very different origins and in a different form.
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