It has been questioned whether traumatic brain injury forms a model of acquired psychiatric illness. Neurosurgieal care in the U.S. has markedly progressed in the last 25 years. The good news from this progress is that the survival rate of traumatically brain-injured persons has increased dramatically.
The bad news is that improved survival rates have led to a dramatic increase in the number of cognitively and behaviorally impaired persons with long-term neuropsyehiatrie disorders as a consequence of traumatic brain injury. Roughly 2 million cases of head trauma oceur in the U.S. each year. Traumatic brain injury results principally from vehicular accidents, falls, acts of violence, and sports injuries and is twiee as likely to occur in men than women.
The estimated ineidenee is 100 per 100,000 persons, with 52,000 annual deaths. The highest incidence is among persons aged 15 to 24 years and those older than 75 years, with a less striking peak at age 5 years. Prevalence 2.5 to 6.5 million persons.” Of these injuries, almost 25% require hospitalization and 80,000 to 90,000 persons are left with some level of chronic disability.
In terms of neuropathology of head injuries, structural and functional abnormalities develop progressively after brain trauma, which suggests that the resulting brain injury is a dynamie process of events rather than a single event. Numerous types of neuropathologies can occur in the same brain, in the same individual, from the same injury.
Neuropathological damage can occur by direct damage caused by excitotoxic-mediated calcium influx into cells, free radical-mediated damage, receptor-mediated damage, and inflammatory processes.’ Furthermore, the direct consequences of trauma may be complicated by secondary injuries oceurring after head trauma. These include intracranial hypertension, vascular failure, ischemia, endogenous brain defenses, axonal injury, and neuronal injury.
Head injury classification has no universally accepted system. Many classification schemes have been proposed. All existing classification systems have limitations. The types of brain trauma are straightforward, and these include damage from skull fractures.
Focal brain damage is a result of contusions, hemorrhage, hematoma, or tissue tears. Diffuse brain damage may be the result of diffuse axonal injury, ischemic injury, or the complications of brain edema. Lastly, there is the apparent relationship between traumatic brain injury and late-appearing neurodegeneration of the Alzheimer’s type.”
This chapter focuses on the key concepts of the epidemiology of brain injury and the pathophysiology of traumatic brain injury. Various classification systems for categorizing the severity of brain injury arc expressed. The serious neurosurgical consequences of acute brain injury are demonstrated, and their relationships to cellular and neuronal injury are exemplified.
The current apparent relationship between traumatic brain injury and the later expression of Alzheimer’s-like neurodegeneration is explored.
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Free download Traumatic Brain Injury : Methods for Clinical and Forensic Neuropsychiatric Assessment by Robert P. Granacher, Jr.