In today’s post, we’re turning our attention towards a (yet another) mental disorder relatively often portrayed in the media, but still not fully understood or easily treatable: posttraumatic stress disorder (or PTSD, in short). The article addresses the following questions:
- What is PTSD?
- Who can get PTSD?
- What are the symptoms of PTSD?
- What factors could increase our risk of developing PTSD?
- What are common PTSD comorbidities?
- How does PTSD manifest in the brain?
- How can we treat PTSD?
What is PTSD?
Posttraumatic stress disorder or, in short, PTSD, is a mental and behavioural disorder which appears as a consequence of trauma. According to the Diagnostic and Statistical Manual 5 (DSM-5), i.e. one of the two reference manuals based on which all mental disorders are diagnosed, a person must present symptoms from eight sets of criteria in order to be diagnosed with PTSD.
You can imagine the process of diagnosing someone with PTSD like a flowchart. In fact, as most mental disorders still lack reliable biomarker-based tests (think brain scans or blood tests), the diagnostic methods are exactly like flowcharts (or bingo cards, if you want). But this acute problem of psychiatry belongs to a different discussion. For now, let’s turn our attention back to PTSD.
As you can also see in the image below, the first condition for a PTSD diagnosis to even be considered is exposure to trauma. Afterwards, the doctor needs to make sure that the patient actually has symptoms of PTSD (duh!), but more on that later. The final three criteria are not specific to PTSD. For most mental illnesses, the symptoms need to have been present for some time, they have to carry functional significance (i.e. actually affect your life) and the medical team should make sure they aren’t caused by an organic illness, medication or substance abuse.
Who can get PTSD?
Of course, as the first diagnosis criterion (and the “posttraumatic” in the name) already inform us, only people who have been exposed to trauma can develop PTSD. But for a complete answer to this question, both “trauma” and “exposure” need further clarification.
Trauma includes, but is not limited to warfare, assault, abuse, as well as other forms of violence (either experienced or threatened), natural disasters, or death. As pop culture often presents war veterans as suffering from PTSD, I feel that this clarification was needed to underscore how varied trauma sources, and by extension, people afflicted by PTSD, can be. That is not to say that war isn’t a major contributor to PTSD. For example, while PTSD prevalence in the United States is estimated to be up to 10%, this number is approximately three times higher when looking at countries which have experienced direct combat, such as Syria or countries in Sub-Saharan Africa.
In terms of exposure, we need to clarify that the DSM-5 doesn’t recognize just direct or primary exposure, but also secondhand or secondary exposure, otherwise referred to as vicarious trauma. The term vicarious trauma was coined to refer to the traumatization experienced by trauma counsellors working with traumatized individuals. Since then, it has been expanded to include many other categories, such as first responders, relief workers, and even foster parents or children exposed to the trauma of their parents. Some studies even go as far as to consider tertiary exposure (such as, for example, that experienced by spouses of first responders) as a potential source of trauma for PTSD. In other words, potentially anyone who interacts with a traumatized person and is exposed to the details of their experience could end up developing PTSD.
Now that we’ve clarified the trauma exposure criterion, we can turn our attention to the actual PTSD symptoms. These are classified into four categories (also depicted below): intrusion, avoidance, cognition and mood, and arousal and reactivity symptoms. In order to meet the criteria for PTSD, a person needs to have at least one symptom of intrusion, one of avoidance, two related to cognition and mood, as well two related to changes in arousal and reactivity.
As with any other mental disorder, the clinical presentation of PTSD can be quite different from person to person. For example, while one might suffer from nightmares, avoid external reminders, suffer from trauma-related memory loss, blame the world for it, and be incredibly irritable, another might suffer more from emotional distress from reminders, avoid thinking about it all together, feel depressed and isolated, and engage in self-destructive behaviour.
Additionally, other factors can contribute to clinical heterogeneity. For example, trauma exposure during childhood usually leads to more severe PTSD symptoms. Certain types of trauma, such as adult sexual assault, also lead to more severe PTSD. Finally, repeated trauma exposure usually affects individuals more than single trauma exposure.
Risk factors and comorbidities
We’ve mentioned above that, in theory, anyone exposed to trauma can develop PTSD. But while that’s true, it comes with a footnote: not everyone has the same chance of developing it. To conceptualize this in an easier manner, imagine that you’re competing against a friend to see who can score more hoops. But there’s a catch: while you throw the basketball from three meters away, your friend throws it from ten. In theory, either of you can win, but you definitely have higher chances. So what are the factors that shorten one’s distance from the basketball hoop?
For one, genetics. In order to determine whether a disorder has a genetic component or not, researchers often conduct so-called twin studies, on both monozygotic (identical twins) and dizygotic (non-identical or fraternal twins). Depending on the proportion of mono- and dizygotic twins who develop a certain disorder, researchers can calculate the heritability of that particular disorder. For PTSD, this is approximately 40-50%. This means that about 40-50% of the risk of getting PTSD after trauma exposure is explained by your genes.
The rest 50-60% of the risk comes from environmental factors. For example, as mentioned above, certain types of trauma, as well as repeated trauma exposure increase one’s risk of developing PTSD.
Studies have also shown that females and people who already suffered from another psychiatric disorder prior to the trauma or have a relative with another psychiatric disorder are more likely to develop PTSD.
In this context, it comes as no surprise that PTSD is highly comorbid with other mental disorders, in particular depression and anxiety disorders. Additionally, substance abuse is often seen in these patients and it represents a leading cause of suicide.
PTSD in the brain
Discovering and understanding brain differences/changes between healthy individuals and individuals with PTSD can help in two directions. For one, scientists hope we can actually develop a more objective diagnostic method. After all, the DSM-5 has been around for a long time and just between us, it’s not the best (but that’s a conversation for another time). For another, if we can pinpoint which exact brain regions are stepping out of line, the hope is we can develop more targeted therapies for these regions alone, instead of bathing the entire brain in various drug cocktails. This is applicable to neuropsychiatric disorders in general.
Similar to other mental disorders, PTSD is increasingly recognized as a disorder of circuits. Practically, what that means is that PTSD doesn’t affect just a single region in the brain, but the connections and interactions between several regions. More specifically, researchers look for two types of changes:
- structural; examples include the decrease in volume of some regions or the thinning of the wiring between them. Changes in structure usually lead to changes in function as well;
- functional; as the name suggests, the function of certain regions is affected: they might become either underactive or overactive. In response, other regions try to compensate for this abnormal function, and they might become affected themselves. And like that, an entire brain circuit becomes dysfunctional.
Not surprisingly, regions (and by extension, circuits) affected by PTSD are those involved in emotion regulation, as well as those supporting memory.
Scientists have observed that individuals who suffer from PTSD have smaller volumes and reduced connectivity in the amygdala, anterior cingulate cortex, insula, and hippocampus. Additionally, functional changes have been reported in many of these regions and different theories exist for how they relate to some of the PTSD symptoms presented above.
For example, the amygdala is normally responsible for our fear responses. However, it is also under direct control of the prefrontal cortex. The first time when we are exposed to a novel, frightening stimulus, the amygdala goes into overdrive. However, over time, the prefrontal cortex becomes used to the stimulus and signals to the amygdala to tone it down. But in PTSD patients, this doesn’t happen. The prefrontal cortex doesn’t properly inhibit the amygdala. This leads then to some of the intrusion symptoms mentioned above, such as emotional distress or physical reactivity after being exposed to trauma.
Unfortunately, while researchers are constantly making progress by creating more and more detailed models of the underlying brain circuitry altered in PTSD, we still have a long way to go before completely understanding the brain-behaviour relation in this disorder.
But although we don’t fully understand the neural intricacies of PTSD, that doesn’t mean that we cannot develop treatment options. The two current standard approaches towards treating PTSD are either through psychotherapy or medication. Current research does not support the notion that a combination of therapy and medication would be superior to each of them separately.
Psychotherapy approaches include cognitive therapy and exposure therapy. The former is focused on helping individuals with PTSD identify unhealthy patterns of thinking which hold them back and teaching them how to change these patterns. The latter refers to the gradual and safe exposure to triggering situations and memories with the ultimate purpose of decreasing the fear response and, in effect, “re-training” the amygdala and prefrontal cortex and bringing them back to baseline. Usually, cognitive and exposure therapies are used together.
Common medications administered in PTSD are antidepressants, which are particularly useful for the cluster of symptoms related to cognition and mood, as well as anti-anxiety medications for coping with the anxiety-related symptoms.
As psychotherapy and medication are not always successful in treating PTSD (plus, medications often come with unwanted side effects), researchers are currently exploring alternative forms of treatment. A new avenue of research for PTSD treatment is that of non-invasive brain stimulation, either magnetic or electric. Although not routinely used in clinical settings, some studies show that this form of therapy is very useful in reducing PTSD symptoms. However, more clinical studies on its effectiveness, as well as comparisons with current forms of treatment are needed before this form of treatment becomes routinely used.
As prevention is usually better than treatment, several studies have investigated whether there is something we could do to prevent PTSD. In particular, researchers looked at the effect of early psychological interventions on individuals who had been exposed to trauma. Unfortunately, the results were deeply disappointing: early psychological interventions did nothing to prevent PTSD. So at least for now, PTSD remains unpreventable.
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You might also like:
American Psychiatric Association, D. S., & American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5 (Vol. 5). Washington, DC: American psychiatric association.
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Hoppen, T. H., Priebe, S., Vetter, I., & Morina, N. (2021). Global burden of post-traumatic stress disorder and major depression in countries affected by war between 1989 and 2019: a systematic review and meta-analysis. BMJ global health, 6(7), e006303.
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