Articles: brain-injuries.
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Computed tomography has replaced the invasive techniques of angiography and ventriculography as the diagnostic study of choice in head injury. It has proven not only accurate but extremely safe. ⋯ Respresentative examples of common lesions seen in trauma are presented along with the errors in diagnosis most frequently made and how to avoid them. The common artifacts, including movement, are also discussed.
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A successfully managed case of posterior fossa subdural hematoma occurring in a hemophiliac is reported, and the rarity of this lesion is mentioned. The management of the hemophiliac who is a victim of craniocerebral trauma is discussed, with emphasis on the use of computerized tomographic scanning to obtain rapid diagnosis. The importance of prophylactic Factor VIII replacement is emphasized, and appropriate methods of Factor VIII administration are outlined.
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Zh Vopr Neirokhir Im N N Burdenko · Sep 1978
[Effect of protective helmets and head guards on localization of injuries to the skull and brain in cranio-cerebral injuries].
The results of post-mortem examination of 140 cadavers of persons who had died of craniocerebral injuries are appraised. It was established that in injury inflicted through a protective head-piece, the proportion of damage to the bones of the base of the skull, basally located structures of the large hemispheres and stem of the brain in the total number of injuries increases. The study is supplemented with mathematical calculations which explain the dependence observed.
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Journal of neurosurgery · May 1978
Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury.
Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. ⋯ The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with imparied CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.