A neuropsychological hypothesis explaining posttraumatic stress disorders.
The author reports findings from recent psychophysiological and biochemical research on Vietnam combat veterans with chronic posttraumatic stress disorder. Applying these data and the analogy of the known functional and structural defects in the peripheral (cranial) sensory system consequent to high-intensity stimulation, he hypothesizes that cortical neuronal and synaptic changes occur in posttraumatic stress disorder as the consequence of excessive and prolonged sensitizing stimulation leading to depression of habituating learning. He postulates that the "constant" symptoms of the disorder are due to the changes in the agonistic neuronal system which impair cortical control of hindbrain structures concerned with aggressive expression and the sleep-dream cycle.
D000374:Aggression / Q000502:physiology; D002540:Cerebral Cortex / Q000503:physiopathology*; D003130:Combat Disorders / Q000209:etiology* / Q000503:physiopathology; D006185:Habituation, Psychophysiologic / Q000502:physiology*; D006801:Humans; D007858:Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology; D008959:Models, Neurological; D009434:Neural Pathways / Q000503:physiopathology; D012249:Rhombencephalon / Q000503:physiopathology; D013313:Stress Disorders, Post-Traumatic / Q000209:etiology*