t,' The development, recession, and residua of posttraumatic epilepsy follow natural laws that are imperfectly defined. However, studies from World War I, World War II, the Korean conflict, and the Vietnam War demonstrate the following patterns: 1) The onset of seizures is significantly related to local brain destruction and its location, and to diffuse brain damage, reflected by alteration in consciousness. 2) The incidence of seizures has remained the same from one war to another, in spite of marked improvement in patient transport, surgical techniques, medical management, and the prophylactic use of anticonvulsants in Vietnam. 3) After injuries incurred in combat and support activities, the onset of new cases of epilepsy rises sharply, with approximately 5% having a seizure in the first week, 10% in the first 3 months, 16% in the first 6 months, 23% in the first year, 29% in the first 2 years; after that there is a low, but protracted rate of new cases of epilepsy. 4) Those cases that occur in the first week are less influenced by the agent of injury or local brain damage, thereafter there is a sharp divergence with the more extensive injuries providing the greater number of patients with seizures. 5) In the population at risk, 65% to 75% never have a seizure. In those that do, the development varies in degree, adjudged from frequency of seizures. The latter ranges from a single seizure to a number that defies an accurate count. 6) As new patients with seizures accumulate, earlier patients cease having seizures. Within 5 to 10 years, one-half of the patients have ceased having seizures, with or without therapy. Half of the remainder, about 8% of the injured, have intractable seizures. 7) While there is a clear correlation between severity of injury and onset of seizures, there is no correlation between severity of injury and cessation of attacks. However, there is a correlation between the attack frequency and persistence of seizures. 8) From the preceding, two principal determinants are evident: the constitutional tendency toward seizures (probably a multifactorial genetic trait), and the brain damage. In onset of seizures, both play a part, the constitutional factor apparently determining severity of attacks. In cessation or persistence of seizures, the constitutional factor plays the dominant role.
A total of 491 cranioplasties performed in a population of 1030 cases of penetrating head injury are reviewed. The morbidity rate was 5.5%, and the mortality rate was 0.2%. The clinical criteria of improving cosmetic defects and restoring craniocerebral protection are established, based on the location and size of the skull defect. Cranioplasty after penetrating head injury should be deferred for a minimum of 1 year to control morbidity. Complications of the original injury and surgical debridement increase the morbidity rate of cranioplasty. Post-traumatic epilepsy is not related to skull defects per se; neither is it affected by cranioplasty. Acrylic is an acceptable cranioplasty material if there is strict adherence to good surgical technique.
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