.png)
Written by Isabelle Strachan
This post will be an overview of the science behind anxiety disorders, why they occur, and the chemistry and dysfunctions behind them.
The "fight, flight, or freeze" response is a well-known reaction in all of the animal kingdom. ¹ When faced with danger, our amygdala (a little pea-sized nugget in the center of our brains responsible for many emotions, such as fear), will send out a distress signal, which our hypothalamus responds to by notifying our nervous system that we are in danger. ² This sends a signal to our adrenal glands, which release a hormone called epinephrine (also known as adrenaline). ² The sudden surge of adrenaline causes us to, as we all know, do one of three things: fight well-known and try to defend ourselves from the threat; "flight", and run away from or avoid the threat; or freeze and not respond, like a "deer caught in the headlights". ¹ This evolutionary response is a very logical reaction that is responsible for saving lives when the situation arises. ¹ But what would happen if this reaction were to occur excessively, pathologically, or inappropriately when there was no real threat and one's life was not in danger?
Well, as you may have guessed, when that occurs, it causes what is referred to as anxiety, or more specifically, disordered anxiety. Anxiety is defined by MedlinePlus as "a feeling of fear, dread, and uneasiness." ⁴, and when it is felt in unreasonable and/or non-threatening circumstances, it is characterized as disordered anxiety, which, when experienced chronically, causes anxiety disorders. ³ Some anxiety disorders, such as OCD (obsessive-compulsive disorder) and GAD (generalized anxiety disorder), are characterized by feelings of excessive anxiety. ³ Other anxiety disorders, however, such as PTSD (post-traumatic stress disorder), social anxiety disorders, and specific phobias, are characterized by excessive and inappropriate feelings of fear and anxiety. ³ But, in these situations, why does the amygdala send out a distress signal when there is no reason to?
The answer is pretty simple. In occurrences of anxiety disorders, it has been observed that one's amygdala presents as hyperactive. ³ This has been studied multiple times and observed through a variety of medical scans, such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scans, that are able to monitor neural activity and cerebral blood flow. ³
For example, individuals suffering from social anxiety disorder show heightened amygdala responses to both social and non-social highly emotive stimuli, compared to healthy control groups, which display significantly lower responses. ³ This kind of reaction displayed in social anxiety disorders has been related to trait anxiety, leading researchers to believe that social anxiety disorder is characterized by a more general dysfunction in emotional processing capabilities as well as altered processing of social stimuli and situations. ³ This theory was further reinforced when reduced symptoms in public speaking situations were observed in people with social anxiety disorder following medicinal treatments intended to reduce amygdala reactivity. ³ This further suggests a tight link between symptomology and amygdala reactivity in social anxiety disorder. ³
Like social anxiety disorder, similar reactions were observed in various PTSD populations. ³ Hyperactivity of the amygdala in response to trauma-related stimuli was commonly observed. ³ Similar to PTSD and social anxiety disorder, amygdala hyperactivity as a result of the presentation of highly emotional stimuli or strategies such as symptom provocation has been observed in disorders such as specific phobia, panic disorder, pediatric GAD, and OCD. ³ And so, you may assume that amygdala hyperactivity is the leading cause of all anxiety disorders; however, this doesn't seem to be the case. ³
Amygdala hyperactivity has not been commonly observed in adults with GAD (generalized anxiety disorder). ³ This is surprising because of the prevalence of this disorder; however, after many studies, it has been theorized that amygdala hypofunction in adult GAD might be better revealed by visual studies that create anxiogenic or conflict situations rather than the standard presentation of fearful stimuli. ³ While this conclusion requires direct testing, the findings that anxiogenic but not fearful stimuli reveal hypofunction of the amygdala in GAD, whereas fearful stimuli consistently elicit amygdala hyper-reactivity in other anxiety disorders (such as social anxiety disorder, PTSD, and pediatric GAD) suggest a neural dichotomy between GAD and other anxiety disorders on the anxiety-to-fear continuum (as stated by the authors of "The Role of the Amygdala in Anxiety Disorders"). ³
In conclusion, the current leading theory of the neurobiological cause behind anxiety disorders is hyperactivity of the amygdala when presented with fearful stimuli, in all cases except for adult GAD, which is more effectively triggered by anxiogenic and conflict-based stimuli.
About the author:
My name is Isabelle Strachan, and I am currently a rising junior based in Ontario! I enjoy doing research on neuropsychology-based subjects in my free time and have been doing such since I was 10 years old. I also enjoy music and the arts and have participated in multiple local musical theater productions in the past few years. I've been nominated for awards and had the amazing opportunity to perform at the National Arts Center! I hope to be a research-based neuroscientist when I grow up, and I am very excited about this opportunity the WOWIS organization has presented me with :)
Sources:
Comentarios