Help for victims of childhood abuse, spousal battery, and political terrorism.
by Brian Trappler, M.D.
What Happens to the Brain in PTSD
Neurobiology of the brain’s response to trauma
Published on December 21, 2010
Physiologically, the part of the brain that functions as the “fear center” is the amygdala (Davis. J. Neuropsychiatry Clin. Neurosc, 1997).
Once the limbic brain acquired advanced neocortex, mechanisms of survival evolved beyond visceral and simple reflective behaviors.
In primates, the Hippocampus, while located in the “limbic brain”, contains layers of advanced neocortex. It plays a crucial role in providing memory with context and emotional relevance, and also restrains the amygdala from activating the fear-cascade.
It is also responsible for notifying the prefrontal brain for response choices, which are both diverse and receptive to change (when comparing humans with other primates).
Activated stress-circuits in all vertebrates express themselves through the autonomic (sympathetic) nervous system (via brainstem nerve outlets) and via the Hypothalamic-Pituitary-Adrenal Axis.
Integrating intelligence into limbic functions allowed stimulus response reactions to support more complex responses to threat, including hesitation and response selection (Maclean. “Culminating Developments in the Evolution of the Limbic System.” Raven Press, 1986).
It appears as if in the brains of patients with PTSD, the hippocampus continues to remain on “high alert” to retrieve previous recollections when reminded of a similar threat (McNally, et al. “Selective Processing of Threat Cues in PTSD.” J Abnorm Psychol, 1990).
When cortisol overproduction continues (in conjunction with other neuro-excitatory transmitters such as glutamate), hippocampal cells degenerate and eventually die (apoptosis) (Bremner. “Alterations in Brain Structure and Function Associated with PTSD.” Seminars in Clinical Neuropsychiatry, 1999).
This has been demonstrated by Functional MRI studies showing hippocampal changes in the immediate aftermath of physical or sexual assault (Bremner, et al. “MRI Measurement of Hippocampal Volume in PTSD Related to Childhood Physical and Sexual Abuse.” Bio Psychiatry (1997): 41).
Rachel Yehuda and colleagues published several articles reporting low urinary excretion of cortisol in patients with PTSD (J Nerv Ment Dis (1990): 178, and Am J Psychiatry (1995): 152).
At first, findings of lower-than-expected cortisol in abuse victims were extremely counterintuitive.
With the advent of functional imagery studies such as PET scans, Functional MRI, and Magnetic Spectroscopy, patients with PTSD indeed showed significant Hippocampal dysfunction (Schuff, et al. “Decreased Hippocampal N-Acetyl-Aspartate in the Absence of Atrophy in PTSD.” Biological Psychiatry, 2001).
The damaging downstream effect of prolonged stress-activation is testimony to the importance of containing the physiologic stress cascade.
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