Articles: brain-injuries.
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Case Reports
[A case of subarachnoid hemorrhage with acute subdural hematoma due to head injury: a case report].
Acute intracranial hemorrhages can be caused by cerebrovascular disease or head injury. Diagnostic imaging is in both cases sometimes similar, so it is difficult to make an exact diagnosis. We report a case of acute subdural hematoma due to head injury after loss of consciousness due to an aneurysmal rupture. ⋯ Postoperative CT scan showed contusional hematoma at the left frontal lobe and plain skull X-ray films demonstrated a diastatic fracture of the right lambdoid suture. Acute subdural hematoma due to the rupture of a cerebral aneurysm is sometimes recognized, but the first CT findings are similar to those observed after head injury. When the clinical course of onset is unclear, we must keep in mind that the cause of acute subdural hematoma may be head injury, even if angiography demonstrates abnormal vessels.
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J. Neurol. Neurosurg. Psychiatr. · Feb 1995
Cerebral blood flow and metabolism in children with severe head injury. Part 1: Relation to age, Glasgow coma score, outcome, intracranial pressure, and time after injury.
Understanding the pathophysiology of paediatric head trauma is essential for rational acute management. It has been proposed that the response to severe head injury in children differs from that in adults, with increased cerebral blood flow (cerebral hyperaemia) representing the most common cause of raised intracranial pressure, but this has recently been disputed. The relation between the pathophysiological response and time after injury has not been defined in children. ⋯ These data represent the first evidence that the temporal change in cerebral metabolic rate reported in experimental models of traumatic brain injury also occurs in patients with head injury. The changes in the pathophysiological response over time suggest that the management may need to be modified accordingly. If cerebral metabolic rate and cerebral oxygen extraction are maximal shortly after injury in children with severe head injury then the children are most likely to sustain secondary damage during this period.
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Journal of neurotrauma · Feb 1995
The effect of acute cocaine or lidocaine on behavioral function following fluid percussion brain injury in rats.
One of the goals of our laboratory is to examine how the presence of drugs of abuse will influence traumatic brain injury. Previous studies in our laboratory have shown that cocaine or lidocaine treatment before experimental fluid percussion brain injury in rats reduces the cortical hypoperfusion normally found in the early posttraumatic period. The purpose of the current study was to determine if pretreatment with cocaine or lidocaine is also associated with changes in trauma-induced suppression of reflexes and motor and cognitive dysfunction that occurs following traumatic brain injury (TBI). ⋯ Lidocaine and cocaine did not affect cognitive function on days 11-15 postinjury. The mechanism by which lidocaine improves acute neurological and motor function following brain injury is unknown, but may involve improved posttraumatic cortical blood flow, as seen in our previous study. Our results, along with other studies showing lidocaine to be neuroprotective in animal models of ischemia, suggest that studies of the effect of posttraumatic administration of lidocaine are warranted.
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Two hundred and sixty-three consecutive head-injured patients aged over 65 years, admitted to a neurosurgical service, are reported. In contrast to younger age group the main cause was falls concomitant with a high rate of cardiovascular pre-existing disorders. The distribution of causes and grim results justify, in our opinion, regarding head injury in the elderly as a distinct entity requiring special surgical, medical, organizational and ethical considerations.
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Brain injury : [BI] · Feb 1995
Self-reported social networks and interpersonal support 2 years after severe traumatic brain injury.
Fifty-four patients with traumatic brain injury (TBI) consecutively admitted to a rehabilitation hospital were examined 2 years post-injury. Social interaction and support, subjective complaints, and functional status were assessed. A large variability in social interaction and support patterns was found. ⋯ Thirty-one patients (57.4%) reported that their social networks had markedly declined subsequent to injury. Relatively short duration of coma (< 1 week) and severe sequelae in terms of low functional status and poor emotional adjustment at follow-up, especially in terms of deficits in initiating behaviour, were found to be related to little interaction and support. The importance of both provider and patient initiative in order to establish and preserve a social support network is suggested, and clinical implications briefly discussed.