Brain and Trauma

Psychological trauma can have lasting effects on the brain. These effects underlie symptoms of posttrau-matic stress disorder (PTSD), as well as depression, substance abuse, dissociative disorders, and borderline personality disorder (BPD). Brain areas affected by trauma that also mediate the stress response include the amygdala, hippocampus, and medial prefrontal cortex (including the anterior cingulate).

Trauma spectrum psychiatric disorders represent the behavioral manifestation of stress-induced changes in brain structure and function. Stress results in acute and chronic changes in neurochemical systems and specific brain regions, which result in long-term changes in brain “circuits” involved in the stress response.

Hormones (including norepinephrine and cortisol) play a critical role in the stress response. However, chronic stress can lead to dysfunction of these systems. Norepinephrine (adrenaline) is released in both the brain and the body, and has several functions that are critical for survival. Norepinephrine sharpens the senses, focuses attention, raises the level of fear, quickens the heart rate and blood pressure, and in general prepares us for the worst. The norepinephrine system is like a fire alarm that alerts all areas of the brain simultaneously. This system sacrifices the ability to convey specific information to specific parts of the brain in order to obtain more speed. Norepinephrine focuses the senses by activating the neurons that collect information, preparing the body for fight or flight. At the same time, it stimulates the heart to beat more rapidly and blood pressure to increase, causing a rapid transfer of oxygen and nutrients needed for survival to all the cells of the body. Chronic stress in animals leads to increased levels of norepinephrine.

PTSD is associated with long-term dysregulation of the noradrenergic system. Psychophysiology studies have demonstrated an increase in sympathetic nervous system responses (e.g., heart rate, blood pressure, and galvanic skin response) to traumatic reminders. Other studies showed increased nor-epinephrine in plasma and urine at baseline and in response to traumatic reminders. Administration of the alpha2 antagonist yohimbine, which causes [Page 67]an increased release of norepinephrine in the brain, resulted in an increase in PTSD-specific symptomatology, as well as greater release of norepinephrine metabolites in plasma, in PTSD patients. Alterations in brain responses to stimulation of the norepinephrine system with yohimbine were also found in PTSD patients as measured with positron emission tomography (PET).

Figure 1 Impact of Trauma on the Brain. Trauma has lasting effects on the brain, including norepinephrine and cortisol systems and brain areas including the hippocampus, amygdala, and medial prefrontal cortex (mPFC).

The cortisol system also plays an important role in the stress response. Cortisol redistributes energy to enhance survival, suppressing functions not needed for immediate survival, such as reproduction, the body's immune response, digestion, and the feeling of pain, and shunting energy to the brain and muscles. Although useful in the short run, this may occur at the expense of long-term viability of the body. With chronic cortisol elevation, there is increased risk of gastric ulcers, thinning of the bones, cognitive dysfunction, and other problems.

The corticotropin-releasing factor (CRF) is released in the brain during stress, and causes release of adrenocorticotropin-releasing hormone (ACTH) from the pituitary, which in turn stimulates release of cortisol from the adrenal gland. Stress can result in long-term increases in CRF-potentiated release of cortisol with subsequent stressors. PTSD has been associated with long-term dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Baseline levels of urinary cortisol were either decreased or unchanged in chronic PTSD, but decreased levels were found in 24-hour samples of plasma cortisol levels, and stressors or traumatic reminders are associated with potentiated release of cortisol. PTSD was associated with a super-suppression of the cortisol response to lower doses of the synthetic form of cortisol, dexamethasone (0.5 mg), a finding that is the opposite of patients with major depression who are nonsuppressors with the standard 1 mg DST test. PTSD patients also had elevated levels of CRF in the cerebrospinal fluid.

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