Traumatic Stress: A Chemical Approach
Web Paper 2
Traumatic Stress: A Chemical Approach
Treatment for the long-term effects of traumatic stress has long been a subject of debate among scientists and psychologists, and especially following the spike in post-traumatic stress experienced by those involved in combat during the First World War. Post-traumatic stress manifests in the patient’s vivid recurring dreams, emotional numbness, hyperarrousal, and frightening thoughts and memories (NIMH). Interestingly, experiences of post-traumatic stress exist most prevalently among those who experienced trauma in non-physical, but instead psychological ways; harm seems, in cases of PTSD, to have been caused, in other words, to the mind instead of the body from the traumatic experience or accident. Because the post-traumatic stress surfaces as a cognitive disorder, psychologists (at the frontline, Freud) first assumed the reins in diagnosing and treating the post-traumatic stress through hypnosis and psychotherapy, and now use cognitive therapy as a means to lessen the symptoms; in other words, the primary treatment for PTSD continues to be “working through” the reaction – or lack of time to have a reaction—to the traumatic event.
There exists a tension here between reactions in “the brain” and “the mind;” while post-traumatic stress disorder appears to alter behavior and thought (what we think of as “the mind”), the aforementioned symptoms are direct products of the limbic and nervous systems – the brain. It seems striking, then, that post-traumatic stress continues to be mainly treated with various sorts of psychotherapy, whereas there are currently no available pharmacological agents targeting the symptoms of the disorder. What do we make of this, then, if the limbic system and central nervous system are primarily at work in response to traumatic stress? If we think of traumatic stress as something that affects the brain, and not the “mind,” why haven’t our coping mechanisms altered more dramatically from their post-World War I stages?
It is now generally understood that the central nervous system functions to control, among many other things, the post-traumatic response through its enormous collection of structures and processes (Weiss). The after-effects of traumatic stress are, according to Weiss, chiefly experienced in the limbic system (most apparently the hypothalamic-pituitary-adrenal axis) and the central nervous system (specifically, monoamine neurotransmitters). The limbic system includes important parts of the brain, among which amygdala is most relevant to PTSD for its role in emotion, memory, and behavior (Medline). The hypothalamic-pituitary-adrenal axis (HPA axis) exists as a fundamental part of the neuroendocrine system, influencing and sending feedback between the hypothalamus, pituitary gland and adrenal gland, and a system to control stress response. Naturally, then, the HPA axis is altered both during after the traumatic event, altering stress levels in the body through the limbic system.
While the limbic system is largely at play during and following traumatic exposure, the central nervous system is also reacting extensively. Monoamine neurotransmitters, part of the central nervous system, are responsible for maintaining homeostasis in the central nervous system, an important function in the event of traumatic exposure. Monoamine neurotransmitters include serotonin, epinephrine, norepinephrine, and dopamine. These are functions of the amygdala, a part of the limbic system that activates the sympathetic nervous system and is responsible for our response to fear and remembering fear. During and after the traumatic exposure, monoamine transmitters are hugely instrumental because the network “determines and adjusts the overall behavioral state of a person, integrating autonomic, motor, cognitive, and emotional experience through long axons that reach throughout the brain” (Weiss). In particular, norepinephrine concentrations are, according to a 2001 study, “significantly higher” in subjects with PTSD than in those without the disorder, with a positive correlation between norepinephrine levels and severity of PTSD symptoms (Geracioti). This is extremely relevant because norepinephrine affects response in the brain and helps control the fight-or-flight response. It is not surprising, then, that norepinephrine levels are high during and immediately following the traumatic exposure; but that those levels remain high long after the experience suggests a perpetual and perhaps endless level of heightened fear in PTSD patients.
This is all to say that while therapeutic remedies for cognitive aid are helpful in lessening the effects of PTSD, there appears to be a need for a chemical response to the problem since the disorder is largely due to chemical alterations in the nervous and limbic systems. Doctors and neurobiologists are currently on the path of finding drugs to inhibit receptors implicated in post-traumatic stress disorder, including, most recently, drugs imitating ligands for the mGlutamate receptor, a receptor responsible for regulating axon potential such that neurons don’t remain perpetually excited (NIH). NIH has cited the drug as a likely near-future treatment for disorders and diseases with similar properties to PTSD: “anxiety, pain, depression, schizophrenia, Alzheimer's disease and Parkinson's disease” (NIH). It seems to be the beginning of a necessary focus on cell-signaling pathways in the brain as a supplement, at the very least, to the therapeutic treatment undergone by patients suffering from post-traumatic stress disorder.
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