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How Ptsd Affects The Body
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Chronic Pain After Trauma May Depend On What Stress Gene Variation You Carry
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I. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 8/2 Trubetskaya Str., 119991 Moscow, Russia
How Ptsd Affects The Brain
Institute of Physiological Compounds of the Russian Academy of Sciences, Severny pr. 1, Chernogolovka, 142432 Moscow Region, Russia
Department of Biology, Center of Excellence in Regenerative Medicine and Molecular Biology (CEMR), JSS College of Higher Education and Research (JSS AHER), Mysuru 570015, Karnataka, India.
Received: May 20, 2020 / Revised: August 10, 2020 / Accepted: September 4, 2020 / Published: September 12, 2020
(This article belongs to the special issue Pharmacogenomics and mitochondrial genomics as a strategy for diagnosis and treatment of PTSD)
Post-traumatic stress disorder (PTSD) is a well-known mental illness that affects millions of people worldwide. Pharmacodynamic and cognitive behavioral therapy (CBT) has been used to treat patients with PTSD. However, it remains unclear whether there are simultaneous changes in psychological and neurophysiological factors associated with PTSD patients. Previous reports explained that PTSD patients with efficient fatty acid metabolism, neurogenesis, and mitochondrial energy balance can improve the ability to cope with the response to fear situations and traumatic memories. In addition, cognitive, behavioral, cellular, and molecular testing can be combined to create personalized treatments for PTSD patients with or without comorbidities such as depression or memory impairment. Unfortunately, there is still no evidence to establish a complete understanding of the basic neurophysiological and psychopathological aspects associated with PTSD. This review has discussed in detail the single nucleotide polymorphism (SNP) of genetic factors that cause PTSD, inflammatory reactions, neurotransmitter genomics, metabolic changes, neuroendocrine changes (hypothalamic-pituitary-adrenal (HPA) axis), mitochondrial dynamics, neurogenesis and premature aging. for PTSD-induced psychopathology and neurophysiology. In addition, the review described the importance of CBT and various pharmacodynamic treatments in reducing PTSD symptoms.
Post-traumatic stress disorder (PTSD) consists of a set of changes in cognition and emotion . PTSD is associated with a large constellation of symptoms resulting from continuous and long-term exposure to traumatic events that directly or indirectly induce stress . PTSD has been reclassified in the Diagnostic and Statistical Manual 5 (DSM-5). It is no longer classified as an anxiety disorder, but instead is classified as a “Stress or Trauma Related Disorder.” This classification was based on negative effects similar to other stress-related disorders, as well as new diagnostic criteria [3, 4]. According to the DSM-5, the diagnostic criteria for PTSD are exposure to actual or threatened death, serious injury or sexual assault. According to the American Psychiatric Association, exposure must be based on one or more of the following conditions where the person:
The above list is not exhaustive. There are other examples of traumatic events such as violent crimes, accidents, emotional and social abuse, physical attacks, military conflicts, civil unrest, natural disasters, child abuse that can cause PTSD in some people. . Therefore, PTSD is known as a mental disorder that can be characterized by severe social impairment, inability to work, or decreased mental ability to perform other daily tasks . Events that an individual experiences as terrifying are not negotiable. There are no thresholds or criteria for judging whether an event is traumatic enough to cause PTSD. Currently, approximately 24 million people have been diagnosed with PTSD in the United States (or about 8% of the population). In addition, the public costs of treating PTSD have increased by nearly 43 billion dollars annually .
PTSD is characterized by a spectrum of psychological and neurophysiological effects, such as re-experiencing the trauma through vivid memories, flashbacks, or nightmares . These events are often followed by intense fear and intense physical sensations. PTSD patients often try to suppress memories or avoid activities that remind them of traumatic events and withdraw from society. PTSD patients also report a sense of fear of current threats, for example, hypervigilance and overreaction to unexpected noises. These symptoms greatly affect personal, family, social, educational, occupational and other important areas of performance and quality of life [3, 4].
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Neurophysiological deficits are associated with imbalances in the functional aspects of the hypothalamic-pituitary-adrenal (HPA) axis , immune changes, neurotransmitter and neurotropic functions , increased thyroid activity , sensitization high nervous. system, accelerated aging. processes due to increased DNA damage and telomere shortening . In addition, PTSD is associated with osteoporosis, migraine, sleep disorders, respiratory disorders, cardiovascular disease, autoimmune disease, chronic inflammation, metabolic syndrome, and early death of unknown causes [7, 8].
The psychology and pathophysiology of PTSD is associated with deep feelings or memories of a traumatic event that remain vivid. Memories don’t just fade over time, but can last or even grow over years . These effects may be associated with ongoing damage within the central nervous system that facilitates the occurrence of chronic PTSD. A smaller hippocampus in PTSD patients may be the reason for the development of strong fear perceptions and the acquisition of avoidance feelings associated with auditory signals as well as shock [9, 10]. Additionally, hippocampal volume is related to fear-based performance and may predispose a person to decreased neural activity through the HPA axis. This is seen in many people with PTSD who experienced childhood trauma due to elevated cortisol levels . Therefore, a small hippocampal volume is associated with physiological changes and may prepare patients to experience persistent physiological responses to stress signals caused by hormones [12, 13].
Various clinical changes have been reported in PTSD patients and these changes are reported to overlap with the clinical manifestations seen in patients with traumatic brain injury (TBI) . In addition, pathophysiological changes in the amygdala, hippocampus, and associated brain structures are associated with PTSD [14, 15, 16, 17]. Networks with these brain regions and the parahippocampal gyrus and the visual processing stream have been reported to be involved in the processing of fearful information and the recall of fearful memories [18, 19]. Involuntary memory interference may be mediated by the processing of visual traumatic memories [20, 21, 22].
Brain scans using single-photon computed tomography (SPECT) can contribute to the diagnosis of PTSD with higher accuracy compared to other MRI and CT scans, which often provide normal results in PTSD patients. SPECT imaging has been shown to differentiate PTSD from traumatic brain injury (TBI) of varying severity in large patient groups. SPECT studies can reveal a relative increase in permeability in limbic areas, basal ganglia, thalamus, and temporal lobes of PTSD patients compared to TBI subjects . Clinicians should seek more accurate diagnostic methods to select appropriate treatment options targeting PTSD . In addition, brain tissue recovery is enhanced in PTSD patients who interact socially to acquire new learning skills, exercise regularly, avoid potential threats and negative thoughts, and actively develop skills to perform challenging tasks [1, 3 ]. These healthy lifestyles are complemented by good nutrition and weight management
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