Biological Etiology of PTSD: Abnormalities in the brain

Updated, July 2020

After teaching my unit on PTSD (Chapter 4), I found that my students developed a really good understanding of how PTSD is not explainable by a single etiology, but rather it is the product of multiple-interacting factors. While this is great, it does mean that when the question asks about “one” specific etiology, they found it difficult to address this question adequately. To rectify this, I have found some basic studies that make it very easy to show how specific etiologies are linked to PTSD. 

Etiology – Brain abnormalities

Numerous studies have shown that the following brain abnormalities have all been associated with a higher chance of developing PTSD:

• The Hippocampus: low function and volume in the hippocampus is commonly correlated with PTSD symptoms. This could explain symptoms of PTSD associated with loss of memory of the event, as the hippocampus is an essential part of the brain that is involved with memory consolidation.
  

  Explaining why abnormalities in three areas of the brain may be linked to PTSD shows deep understanding of one biological etiology (brain abnormalities). However, there is probably enough to write about just the hippocampus, especially if you include how it is affected by sociocultural factors.

 

• The amygdala: Decreased volume but hyper-responsivity (i.e. increased activity) in the amygdala is a common finding in people with PTSD. This could explain symptoms associated with increased arousal and anxiety as the amygdala is responsible for triggering the stress response. When the amygdala responds to emotional stimuli it activates the HPA-axis and stress hormones (e.g. cortisol and adrenaline) are released. This increases feelings of arousal and anxiety, which are symptoms of PTSD.

 

• The vmPFC: Decreased volume and hypo-responsivity in the vmPFC have been correlated with symptoms of PTSD. This could be because of the role of the vmPFC in cognitive reappraisal – the ability to reassess the danger or threat of an emotional stimulus. An inability to reappraise an emotional stimulus in a positive way could keep stress levels high, which may explain symptoms related to anxiety and arousal.

Fear conditioning: These three areas of the brain are also involved in the process of fear conditioning and fear extinction. The abnormalities may explain why some people are more likely to develop conditioned fears, which can explain symptoms of PTSD associated with increased arousal and anxiety. It may also explain why their symptoms remain, because the fear extinction process doesn’t function properly.

If you study strategically, you can prepare for Abnormal Psychology in Paper 2 using only five studies. Our revision book will help show you how (available here).

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Key Studies

• Meta-analysis of MRI studies on patients with PTSD (Karl et al. 2006): This meta-analysis gathered data from 50 different studies that investigated correlations between PTSD and brain regions (23 hippocampal studies and 27 other, including 18 amygdala studies). All studies used MRI and the DSM IV to diagnose symptoms of PTSD. The results showed that the strongest correlation was between reduced hippocampal volume and PTSD (with an effect size of -0.28). There was also a correlation between reduced amygdala volume and PTSD symptoms, although the effect size was smaller. The meta-analysis also included studies on children that found a correlation between reduced frontal lobe volume and PTSD symptoms (but interestingly these studies didn’t find a link between the hippocampus and PTSD).

 

• Meta-analysis of hippocampal volume and PTSD by Smith (2005): A common biological correlate of PTSD is reduced volume in the hippocampus. This could explain a common symptom of PTSD, which is amnesia of the traumatic event and/or events after the traumatic event. Smith conducted a meta-analysis of 13 studies that all used MRIs to study the brains of patients with PTSD. The results showed that there were significant differences in volumes of patients with PTSD when compared with healthy controls: on average the left hippocampus was 6.9% smaller and the right was 6.6% smaller.

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• Case-control study of hippocampal volume and PTSD (Gilbertson et al. 2002): To aim of this study was to see if low volume in the hippocampus is a risk factor for PTSD using 34 sets of identical twins. The study compared the hippocampal volume of veterans with PTSD. All pairs of twins had one twin who did not go to war (trauma unexposed) while the other did go to war (trauma exposed). Some trauma exposed twins developed PTSD, while the others didn’t. The researchers used MRI to find the volume of their hippocampi and they compared this across the twins. The results showed that veterans with PTSD had an average hippocampal volume 10% smaller than veterans without PTSD. There was also a negative correlation between symptom severity and hippocampal volume. Furthermore, trauma unexposed twins of veterans with PTSD had smaller hippocampal volume than trauma unexposed twins of veterans without PTSD. This suggests that the hippocampal volume is a pre-existing risk factor for the development of PTSD symptoms.

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Critical Thinking…

• What factors could be affecting the size of the hippocampus? How do we know (Hint: genetics, stress and poverty).
• How do each of these examples also show that cognition is an important factor?
• What alternative explanations are there for PTSD? For example, how can external factors affect the development of the brain?
• Why is it difficult to know if these are etiologies or symptoms? How might a small hippocampus be a symptom, not an etiology? (Hint: cortisol and the hippocampus).

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Karl, Anke & Schaefer, Michael & Malta, Loretta & Dörfel, Denise & Rohleder, Nicolas & Werner, Annett. (2006). A meta-analysis of structural brain abnormalities in PTSD. Neuroscience and biobehavioral reviews. 30. 1004-31. 10.1016/j.neubiorev.2006.03.004.(Link)

Gilbertson, Mark W et al. “Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma” Nature neuroscience vol. 5,11 (2002): 1242-7.(Link)