Scientists have long recognized that stress can have long-term effects on the brain and on physiology. Often the scientists themselves did not think about the possible implications for the effects of stress on humans. However, recent research has shown that humans with a history of exposure to extreme trauma and who develop post-traumatic stress disorder (PTSD), with its associated nightmares, intrusive memories, avoidance of reminders of the trauma, sleep disturbance, hypervigilance, and other symptoms, have changes in actual brain structure and function. Research shows changes in brain areas including the hippocampus and frontal cortex, as well as alterations in levels of the stress hormones cortisol and norepinephrine, all of which underlie symptoms of PTSD.
In 1980 the American Psychiatric Association (APA) classified PTSD as a psychiatric disorder for the first time and listed criteria for inclusion in the Diagnostic and Statistical Manual III (DSMIII). This inclusion was the first time that psychological trauma (that is, things that happen to you when there is no physical injury) was recognized as having the potential to cause long-term changes in mental balance.
ROLE OF THE HIPPOCAMPUS
Research on the effects of stress on the brain in animals has a long history; however, such research on humans has just begun to catch up. Studies in animals exposed to stress show deficits in hippocampal-based memory function and damage to a part of the brain called the hippocampus that mediates memory. A variety of mechanisms has been proposed for these findings, including elevated levels of the stress-hormone cortisol or an inhibition of the ability to grow new neurons in the hippocampus, something called neurogenesis. Stress has been shown to inhibit neurogenesis, while antidepressants have the opposite effect. In fact, research suggests that antidepressants may cure depression by promoting neurogenesis in the hippocampus, although scientists continue to debate this fact.
The role of the hippocampus in learning and memory and the wide range of memory alterations seen in PTSD patients led to the hypothesis of hippocampal dysfunction in PTSD. Neuroimaging studies showed hippocampal atrophy in PTSD patients, with deficits in hippocampal-based learning and memory. Other studies provoked symptoms of PTSD by showing traumatic pictures, reading back personalized scripts of trauma, or other methods. These studies most consistently showed a failure of activation in the frontal cortex, the part of the brain involved in shutting off the fear response by inhibiting the amygdala, which mediates the fear response.
Considering findings related to the effects of antidepressants on neurogenesis, we assessed the effects of the antidepressant paroxetine (Paxil) on outcomes related to function of the hippocampus. Patients with PTSD showed a significant improvement in PTSD symptoms with treatment. Treatment resulted in significant improvements in verbal-declarative memory and a 4.6 percent increase in mean hippocampal volume. These findings suggest that long-term treatment with paroxetine is associated with improvement of verbal-declarative memory deficits and an increase in hippocampal volume in PTSD.
STRESS AND HORMONES
Hormones (including norepinephrine and cortisol) play a critical role in the stress response. Norepinephrine (commonly known as 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, raises 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 so that it can obtain more speed.
Norepinephrine focuses the senses by activating the neurons that collect information from the senses so that we may rapidly and efficiently obtain information about dangers in the environment. …