Acute stress disorder (ASD, also known as acute stress reaction, psychological shock, mental shock, or simply shock) is a psychological response to a terrifying, traumatic or surprising experience. It may bring about delayed stress reactions (better known as post-traumatic stress disorder, or PTSD) if not correctly addressed. Types
Sympathetic
Sympathetic acute stress disorder is caused by the release of excessive adrenaline and norepinephrine into the nervous system. These hormones may speed up a persons pulse and respiratory rate, dilate pupils, or temporarily mask pain. This type of ASD developed as an evolutionary advantage to help humans survive dangerous situations. The "fight or flight" response may allow for temporarily-enhanced physical output, even in the face of severe injury. However, other physical illnesses become more difficult to diagnose, as ASD masks the pain and other vital signs that would otherwise be symptomatic. Parasympathetic
Parasympathetic acute stress disorder is characterised by feeling faint and nauseated. This response is fairly often triggered by the sight of blood. In this stress response, the body releases acetylcholine. In many ways, this reaction is the opposite of the sympathetic response, in that it slows the heart rate and can cause the patient to either regurgitate or temporarily lose consciousness. The evolutionary value of this is unclear, although it may have allowed for prey to appear dead to avoid being eaten. Signs and symptoms
The DSM-IV specifies that acute stress disorder must be accompanied by the presence of dissociative symptoms, which largely differentiates it from post-traumatic stress disorder.
History
Phenytoin, in both its acidic and sodium salt forms, is erratically bioavailable whether it is injected or taken orally due to its high melting point, weak acidity, and its being only sparingly soluble in water. Simply putting patients on other drugs is not always an option; this was especially true before 1993, when the number of anticonvulsants available was much more limited. One solution was to develop a prodrug that did not have these drawbacks. Fosphenytoin was approved by the Food and Drug Administration (FDA) on August 5, 1996, for use in epilepsy. See also
Ethotoin
Hydantoin
Mephenytoin
Phenytoin

References
External links
"Fosphenytoin". Drug Information Portal. U.S. National Library of Medicine. "Fosphenytoin sodium". Drug Information Portal. U.S. National Library of Medicine.