Neurobiology of Post-traumatic Stress disorder (PTSD)

Neurobiology of Post-traumatic Stress disorder (PTSD)
Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop following exposure to a traumatic event, including terrifying or life-threatening situations such as sexual assault or natural disasters. The disorder is characterized by a reaction of intense fear, helplessness, or horror when the individual experiences, testifies about, or is faced with one or more events that involve death, severe wounds, or a threat to one's own or another's physical integrity.
One of the most important symptoms of PTSD is the revival of the traumatic event, which has been interpreted as an inability to downregulate negative emotions. Neuroimaging studies that probed the ability to regulate emotions in healthy volunteers have found a pattern characterized by activation of the prefrontal cortex associated with a reduction in amygdala activity. This suggests an inhibitory prefrontal cortex-amygdala circuit that underlies emotional regulation. The hypothesis that increased amygdala activation associated with PTSD results from dysfunction in the inhibitory mechanism exerted by the prefrontal cortex has been the topic of debate.
As neuroscience advances and the understanding of neurobiology improves, so too has insight into the etiology, pathogenesis, and neural substrates of PTSD. Increasingly, as with other psychiatric and neurological illnesses, PTSD is framed within the context of dysfunctional brain networks and circuitry. Non-invasive brain imaging has played a pivotal role in uncovering the neurobiological circuitry involved in psychiatric illness, driven by magnetic resonance imaging (MRI), which can image brain anatomy. This technological revolution - along with extensive preclinical work - led to the neurocircuitry model of PTSD,13 which posited that the emergent behaviour and cognitive phenotypes of PTSD primarily arise from the interactions among three key neurobiological structures in the brain: the amygdalae, prefrontal cortices, and hippocampi. This theory states the following: that exaggerated amygdalae activity is responsible for maladaptive fear responses and conditioned associations with traumatic stimuli; that the frontal cortices do not sufficiently suppress reflexive fear and startle responses and fail to extinguish dysfunctional attention and orienting responses; and that atypical hippocampal functioning is responsible for the consolidation and recollection of episodic memories that underlie traumatic re-experiencing and nightmares.
The studies provide evidence that the amygdala and prefrontal cortex exhibit distinct activation patterns in PTSD, thus supporting the model of a dysfunctional circuit. Inconsistencies in the literature may be attributable to distinct PTSD subgroups, different experimental approaches, different contrasts employed in neuroimaging studies, and small sample sizes.

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[@SureshBadaMath]

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[@vrindasugandhi1646]

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[@SureshBadaMath]

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[@SunilPatil-rr1cz]

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[@rafal8921]

Thank you

[@SureshBadaMath]

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[@SureshBadaMath]

Welcome

[@PunmasterSTP]

Thank you for sharing that information.

[@SureshBadaMath]

Welcome

[@mohammedkhan1150]

According to a theory, the reduced gray matter volume reflects a preexisting vulnerability that increases the propensity to develop PTSD. A study on identical twins reported that a previously smaller hippocampus was the risk factor for developing stress-related psychopathology.

[@mohammedkhan1150]

YOUR concept is wrong,,,,,, it is pre existing structural defecit.

[@SureshBadaMath]

Thank you very much for your input and appreciate your expert opinion

[@ishitagoyal8553]

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[@SureshBadaMath]

Thank you very much for your suggestions. Will start working on it