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Biomedical subjects

W F Caveness

Publications and source records attributed to W F Caveness.

At least 19 recordsLinked to original sources
PubMed1979

Cranioplasty: a review of 1030 cases of penetrating head injury.

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. Complication 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.

Acrylic Resins↗
PubMed1977

Effects of single dose supervoltage whole brain radiation in Macaca mulatta.

Three groups of four Macaca mulatta were exposed respectively to a single dose of 1000, 1500, and 2000 rads of 20 MeV whole brain radiation with one animal from each group and a control scheduled for sacrifice at 6, 12, 18, and 24 months. With 1000 rads there were no abnormalities. The characteristic lesions in the animals exposed to 1500 and 2000 rads were small foci of delayed radiation necrosis that in the acute phase were relatively large due to marked local accumulation of edema fluid and at later stages were decreased in volume and showed early mineralization. Correspondingly the monkeys frequently showed papilledema, evidently from brain swelling, as the initial clinical finding, and upon histological examination at later stages, brain atrophy and ventricular dilatation. After exposure to 1500 rads the necrotic process was primarily in the white matter of the cerebral hemisphere and progressed from a small number of lesions in this location at 6 months to confluent necrosis at 12 months. At 18 and 24 months, although there was no evidence of further necrosis, there was evidence of increasing gliosis and at 24 months the occurrence of three independent glioblastomas. With exposure to 2000 rads there was a profuse wide scatter of focal necrotic lesions with a predilection for the basis pontis and a clinical deficit inconsistent with survival past 6 months. Accumulation of minute mineral deposits and atherosclerotic plaques were also noted in these monkeys and appeared to be related to both dose and survival time.

Animals↗
PubMed1977

Pathology of radiation damage to the normal brain of the monkey.

Model I: A portion of the monkey brain, the right occipital lobe, was exposed to 3,500 rads of orthovoltage radiation in a single dose. This demonstrated a) the delayed, 4 to 5 months, massive break in blood-brain barrier with extravasation of plasmatic fluid throughout the right hemisphere causing gross brain distortion, and b) after a protracted course, a remaining impairment in function extending beyond the irradiation lesion. Model II: The whole brain was exposed to supervoltage radiation in single doses of 1,000, 1,500, and 2,000 rads, respectively. This demonstrated a) the lack of effect from 1,000 rads; b) the wide scatter of necrotic lesions in the forebrain white matter from 1,500 rads at 6 months, followed by confluent necrosis in the cerebral hemispheres at 12 months; and c) the numerous focal lesions throughout the brain from 2,000 rads, with the lesions in the brain stem precluding survival beyond 6 months. Model III: The whole brain was exposed to fractionated doses of 4,000, 6,000 and 8,000 rads in 4, 6, and 8 weeks, respectively. This demonstrated a) the lack of effect from 4,000 rads; b) the wide scatter of small focal lesions at different stages of breakdown and repair accompanied by focal edema from 6,000 rads at 6 months, followed by more of the reparative processes including mineralization of focal lesions, and widespread telangiectasia, at 12 months; and c) with 8,000 rads, at 6 months, focal lesions similar to those from 6,000 rads, but at 12 months, gross brain loss from coalescing necrosis.

Animals↗
PubMed1976

Epilepsy, a product of trauma in our time.

Using data obtained by the National Center for Health Statistics through household interviews, an estimate of 8,100,000 cases of head injury was determined for the civilian population of the United States in 1974. Excluding contusions and lacerations of the scalp, face, and neck; there remained 1,900,000 with concussion, skull fractures, intracranial hemorrhage, cerebral laceration, or other intracranial injury. Extrapolating from the military experience with craniocerebral trauma admittedly a rough approximation, it is estimated that in 30% of this latter group one more seizures will develop. Both severity of the injury and the predisposition of the injured are thought to play a part in the occurrence of seizures, with the predisposition playing the dominant role in the persistence of seizures. The following gradation of posttraumatic epilepsy is predicted for the 1,900,000 with the greater implication of brain damage: 1,340,000 will never have a seizure; 560,000 will develop one or more attacks, most of which will begin in 1974, 1975, or 1976. In 280,000 of these, the attacks will be transient and of little consequence. In an equal number, the attacks will require medical attention, and in some 140,000 the seizures will be intractable to therapy. This latter group represents 7% of the 1,900,000 cases. Attention is directed to the practical problems in the control of carniocerebral trauma and of posttraumatic epilepsy.

Adolescent↗
PubMed1976

Monkey brain damage from radiation in the therapeutic range.

Twelve Macaca mulatta monkeys received 200 rads of supervoltage radiation to the whole brain per day, 5 days a week. The course in 4 monkeys was 4 weeks for a total dose of 4000 rads; in 4 monkeys, 6 weeks for 6000 rads; and in 4 monkeys, 8 weeks for 8000 rads. Four unirradiated monkeys served as controls. One from each group, sacrificed at 6 and 12 months from start of irradiation, are reported here. The results from 4000 rads were negligible; those from 8000 rads, profound, with gross brain destruction. The results from 6000 rads, within the therapeutic range, included at 6 months punctate necrotic lesions, 1 mm or less, widely scattered but with a predilection for the forebrain white matter. The reaction to these lesions ranged from an early macrophage response to calcification. Some were accompanied by focal edema. There were occasional examples of vascular endothelial proliferation. In addition, there were patches of dilated capillaries or telangiectasia. Twelve months after 6000 rads there were a few mineralized lesions and innumerable minute deposits of calcium and iron. A more active process was suggested by widely disseminated areas of telangiectasia, 6 to 12 mm in extent. The clinical course from this exposure included papilledema from the third to the sixth month and depressed visual evoked response accompanied by delta activity in the electroencephalogram from the sixth to the twelfth month.

Animals↗
PubMed1975

Regional cerebral blood flow in delayed brain swelling following x-irradiation of the right occipital lobe in the monkey.

Four to 5 months after exposure of the right occipital lobe of the monkey to 3500 rads of X-irradiation there is a proliferative and degenerative lesion accompanied by a massive break in the blood-brain barrier. The resulting vasogenic edema causes gross swelling in the ipsilateral hemisphere, compression of the contralateral hemisphere with ventricular dilatation, and distortion of midline structures, which may result in herniation through the incisura and foramen magnum. The regional cerebral blood flow, determined by [14C]antipyrine method, at successive stages in the development and resolution of the delayed brain swelling shows a reduction of blood flow in white and gray matter, first regionally, then throughout the ipsilateral hemisphere and finally throughout the brain. This is accompanied by an increase in CSF pressure, CSF lactic dehydrogenase and total protein, and clinical signs of increased intracranial pressure. With resolution of CSF pressure, there is a return to baseline of CSF chemistry and partial resolution of the other parameters. The cerebral blood flow shows a greater recovery in gray than white matter, but there remains a diffuse depression suggesting a long-term impairment in cellular metabolism and/or blood flow regulatory mechanisms.

Animals↗