PTSD can result from many stressors. Part of the issue is genetics, and some of the issue is “situational”. In some studies of military combatants when compared to blood relatives, the person with combat-related PTSD will have a greater than average risk for mood or anxiety disorder – the non-combatant blood relative will have mood or anxiety disorder but not the PTSD syndrome. In other studies, the PTSD patient will have more mood or anxiety symptoms than the non-combatant – which might raise the question of susceptibility to psychiatric illness.
In 2012, Janine Flory looked for at the effect of childhood abuse + family history of depression – she reported that: The results from this observational study contribute to a growing understanding of predisposing factors for the development of PTSD and suggest that joint effects of family history of MDD and childhood abuse on PTSD are greater than either factor alone.
PTSD is associated with changes in the very matter of the brain. In a 2008 study, Roger Pitman found that: “The results point to gray matter volume diminutions in limbic and paralimbic structures in PTSD. The pattern of results obtained for pregenual ACC suggests that gray matter reduction in this region represents an acquired sign of PTSD that is consistent with stress-induced loss.” And as long ago as 2000 we knew that traumatic stress could “sensitize” the nervous system and create PTSD symptoms.
Victor Wiegant reported that stressful experiences in humans can result in a spectrum of long-term changes in behavioral, autonomic and hormonal responsivity. An extreme form of such alterations is found in patients with post-traumatic stress disorder PTSD.. A number of animal models has been developed in which intense stressful experiences shocks, social confrontations. result in long-term altered responsivity of behavioural, autonomic and hormonal responses to aversive challenges which mimic many of the changes seen in PTSD.
These models of stress-induced sensitisation are beginning to generate a better understanding of the vulnerability factors, time-course and underlying neuronal substrates of the long-term disturbances experienced by humans as a result of stressful life events. In 2009 Momahmmed Milad reported that specific brain mechanisms were impaired in PTSD – in that research he found a neurobiological basis for the impairment in fear extinction – which may tell us more about why PTSD patients have trouble benefitting from traditional psychological therapy.
So, trauma can also alter brain function in a number of other ways: altering size or functional activity of they amygdala, hippocampus, prefrontal cortex; and altering the chemical environment of the brain through neurochemical stress response systems such as cortisol and norepinephrine.
As we examine the psychoneuroimmunology of PTSD patients, we know that they are more likely to develop immunity problems and autoimmune disease. Interestingly, certain pro-inflammatory cytokines can induce neurochemical and behavioral changes that resemble some key features of PTSD. In 2010 Sandro Galea reported on the alterations of genetic (epigenetic) and immune function that can be associated with PTSD. They attributed the alterations to stress and consequent methylation of usually non-methylated gene sequences including the clusters related to immune response and also another cluster related to sensory perception of sound.
When examining the specific symptom of Chronic Widespread Pain, it appears that PTSD symptoms are strongly linked to CWP. This association was not explained by a common familial or genetic vulnerability to both conditions. We do know that CWP is associated with increased pro-inflammatory cytokine levels.
Bowirrat studied PTSD and reported that: “We propose that successful treatment of PTSD will involve preliminary genetic testing for specific polymorphisms. Early detection is especially important, because early treatment can improve outcome. When genetic testing reveals deficiencies, vulnerable individuals can be recommended for treatment with “body friendly” pharmacologic substances and/or nutrients. Results of our research suggest the following genes should be tested: serotonergic, dopaminergic (DRD2, DAT, DBH), glucocorticoid, GABAergic (GABRB), apolipoprotein systems (APOE2), brain-derived neurotrophic factor, Monamine B, CNR1, Myo6, CRF-1 and CRF-2 receptors, and neuropeptide Y (NPY).”
PTSD is frequently co-morbid to: depression, anxiety, bipolar disorder, schizophrenia, concussion, chronic pain syndromes, and substance abuse disorders. It needs to be treated in order for a person to re-gain robustness and resilience. Treatments are varied but require neurological well-being so that the physiological conditions of the brain are most conducive to effective exploration of trauma, and then un-learning of abnormal responses. In this clinic, a typical work-up of a complicated, or treatment resistant condition includes objective evaluation using EEG/QEEG, Brain SPECT, and specific lab testing for intensity of inflammation.
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