The research showing how exposure to extreme stress affects brain function is making important contributions to understanding the nature of traumatic stress. This includes the notion that traumatized individuals are vulnerable to react to sensory information with subcortically initiated responses that are irrelevant, and often harmful, in the present. Reminders of traumatic experiences activate brain regions that support intense emotions, and decrease activation in the central nervous system (CNS) regions involved in (a) the integration of sensory input with motor output, (b) the modulation of physiological arousal, and (c) the capacity to communicate experience in words.Source: Clinical Implications of Neuroscience Research in PTSD- New York Academy of Sciences
PTSD displays biochemical changes in the brain and body, which are different from other psychiatric disorders such as major depression.In PTSD patients, the dexamethasone cortisol suppression is strong, while it is weak in patients with major depression. In most PTSD patients the urine secretion of cortisol is low, at the same time as the catecholamine secretion is high, and the norepinephrine/cortisol ratio is increased. Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. There is also an increased sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis, with a strong negative feedback of cortisol, due to a generally increased sensitivity of cortisol receptors (Yehuda, 2001).
The response to stress in PTSD is abnormal with long-term high levels of norepinephrine, at the same time as cortisol levels are low, a pattern associated with facilitated learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response (Yehuda 2002). With this deduction follows that the clinical picture of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA-axis.
Swedish United Nations soldiers serving in Bosnia with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels (Aardal-Eriksson 2001).
Source: US News and World Report
Some studies have suggested that disorders in the peripheral and central metabolism of serotonin (5-HT) and noradrenaline (NE) may play roles in the pathophysiology of post-traumatic stress disorder (PTSD).
The impact of early environment through epigenetic programming by maternal behavior, and glucocorticoid programming of the fetus on the later development of PTSD is discussed in a brief by Jonathan R. Seckl and Michael J. Meaney
Disturbed regulation of both the hypothalamic-pituitary-adrenal (HPA) axis and sympathoadrenomedullary system in posttraumatic stress disorder (PTSD) suggests that immune function, which is modulated by these systems, may also be dysregulated.
US News and World Report cites
D-Cycloserine (DCS) as an effective and lasting treatment for anxiety disorders without side effects in an article titled
DCS- Amygdala and the
Hippocampus; The Biological Underpinnings of Paralyzing Fears
Source: US News and World Report Source: Amygdala, Medial Prefrontal Cortex, and Hippocampal Function in PTSD, a brief by Lisa M Shin, Scott L Rauch, and Rodger K. Pitman published in the New York Acadamy of Sciences
In animal research as well as human studies, the amygdala has been shown to be strongly
involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans
have revealed both morphological and functional aspects of PTSD. The amygdalocentric model of PTSD proposes that
it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal
cortex and the hippocampus. Further animal and clinical research into the c and fear conditioning may
suggest additional treatments for the condition.
The last decade of neuroimaging research has yielded important
information concerning the structure, neurochemistry, and function of the amygdala, medial prefrontal cortex,
and hippocampus in posttraumatic stress disorder (PTSD). Neuroimaging research reviewed in this article reveals
heightened amygdala responsivity in PTSD during symptomatic states and during the processing of trauma-unrelated
affective information. Importantly, amygdala responsivity is positively associated with symptom severity in PTSD.
In contrast, medial prefrontal cortex appears to be volumetrically smaller and is hyporesponsive during
symptomatic states and the performance of emotional cognitive tasks in PTSD. Medial prefrontal cortex
responsivity is inversely associated with PTSD symptom severity. Lastly, the reviewed research suggests
diminished volumes, neuronal integrity, and functional integrity of the hippocampus in PTSD.
A study done by Cohen H., Kaplan Z.,Kotler M., Kouperman I. , Moisa R.,Grisaru N. notes that "a
number of structural and functional neuroimaging studies which have shown that abnormalities in the prefrontal cortex can be found in patients with PTSD. Low metabolism was found at baseline in temporal and prefrontal
cortical areas according to PET scans. PTSD patients showed increased regional cerebral blood flow (rCBF) in
the amygdala and decreased rCBF in prefrontal cortex in response to provocation of symptoms by script driven
imagery. Also proton magnetic resonance spectroscopy (MRS) measurement of medial cneural density
in Vietnam combat veterans with PTSD and in healthy controls showed the ratio of N-acetyl-L-aspartic acid to
creatinine ratio was lower in the right hemisphere vs. left as well as in comparison with healthy control subjects. This lower ratio is suggestive of neuronal loss.
Additionally, prefrontal and limbic abnormalities is suggested by neuropsychological testing sensitive to frontal lobe damage., which demonstrate impaired performance on tests reflecting abnormalities of the dorsolateral prefrontal cortex, the orbitofrontal cortex as well as the limbic system generally.
Taken together these studies suggest that the right limbic and paralimbic structures are involved in the pathophysiology of PTSD and that stimulation of the right dorsolateral prefrontal cortex may result in improvement of symptoms."
The study tested Transcortical magnetic stimulation (TMS) "a noninvasive technique for directly stimulating
cortical neurons. Electrical energy crosses the brain almost painlessly, without causing convulsions or
cognitive impairment but causing depolarization of neurons with resultant changes in monoamines. The authors
cite prior pilot studies that lend credence to the idea that repetitive TMS (rTMS) may be an
effective alternative for treating patients with PTSD.