Unfortunately, there are today no neuroanatomic or physiologic measurements that can be used to precisely determine the extent of injury in concussion or the severity of metabolic dysfunction or precisely when it has cleared.
Precisely how long this period of metabolic dysfunction lasts is not presently fully understood. While the precise mechanisms of this dysfunction are still not fully understood, it is now clear that, although concussion in and of itself may not produce extensive neuronal damage, the surviving cells are in a state of vulnerability characterized by a metabolic dysfunction, which can be thought of as a breakdown between energy demand and production. 1 – 5 This vulnerability appears to be due to an uncoupling of the demand for glucose, which is increased after injury, with a relative reduction in cerebral blood flow. Animal studies have shown that, during this period of vulnerability, which may last as long as a week with a minor head injury such as a concussion, a minor reduction in cerebral blood flow that would normally be well tolerated now produces extensive neuronal cell loss. These cells are particularly vulnerable to minor changes in cerebral blood flow, increases in intracranial pressure, and especially anoxia. It has become clear that, in the minutes to days after concussive brain injury, brain cells that are not irreversibly destroyed remain alive but in a vulnerable state. In the last several years, the neurobiology of cerebral concussion has been advanced predominantly in animal studies but also in studies in man as well. We now know that structural damage with loss of brain cells does occur with some concussions. Initially, it was thought to produce only a temporary disturbance of brain function due to neuronal, chemical, or neuroelectrical changes without gross structural change. Concussion is derived from the Latin word concussus, which means to shake violently.
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