A central feature of PTSD is a state of persistent hyperarousal that chronically persists following a traumatic event. Individuals with PTSD have been found to have important physiologic changes of the hypothalamic-pituitary axis (HPA) and sympathoadrenal system including increased levels of sympathetic neurotransmitters such as norepinephrine and increased activity of α2-adrenergic and glucocortocoid receptors. Both the HPA and sympathetic nervous system are associated with attention and arousal. Prolonged activation of these systems has been shown to induce important biochemical changes associated with disordered sleep. Indeed, studies in norepinephrine deficient knockout mice have demonstrated that increased stimulus is required to induce cortical arousal in the norepinephrine deficient mice and results in higher acoustic ArTH when compared to controls. Our hypothesis is that patients suffering from PTSD will have a lower ArTH when compared to subjects without PTSD. This work is significant because if lower ArTH is associated with PTSD these patients may benefit from therapies that raise the ArTH.