Articles: brain-injuries.
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After acute brain injury there may be increased intracranial production of cytokines, with activation of inflammatory cascades. We have sought to determine if a transcranial cytokine gradient was demonstrable in paired sera of 32 patients requiring intensive care after acute brain injury. ⋯ This suggests that there is significant production of IL-6 by intracranial cells after acute brain injury. Therapy directed towards combatting the negative effects of IL-6 may potentially benefit patients who have sustained an acute brain injury.
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Arch Phys Med Rehabil · May 1997
Case ReportsCerebral salt wasting syndrome in brain injury patients: a potential cause of hyponatremia.
Hyponatremia is a common neuromedical problem seen in survivors of central nervous system injury. The etiology of this hyponatremia is often diagnosed as syndrome of inappropriate diuretic hormone (SIADH). Fluid restriction is usually the first line of treatment. ⋯ Cerebral salt wasting is a syndrome of renal sodium loss that may occur commonly after central nervous system injury, yet remains unrecognized. Treatment of cerebral salt wasting consists of hydration and salt replacement. This article uses a case report to discuss the importance of recognition of this syndrome, and treatment concerns are reviewed.
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Pediatric neurosurgery · May 1997
Intracranial neurological injuries associated with orbital fracture.
We attempted to define the central nervous system (CNS) concomitants of various types of orbital fractures in children by reviewing the records of 95 inpatients with admission diagnoses including orbital fracture who presented to the Children's National Medical Center from 1987 through 1994. Patients were divided into three age groups: group I: 0-5 years; group II: 6-12 years; group III: older than 12 years. Orbital fractures were classified by location: roof alone (A); orbital roof plus another orbital wall (B), and orbital fractures sparing the roof (C). ⋯ Seven of the patients with intracranial injury required emergent neurosurgical procedures. Younger children with maxillofacial injury sparing the orbital roof appear more likely to have coexisting intracranial injury, as reflected by CT findings and GCS on admission, than their older cohorts with similar injuries. Fracture of more than one orbital wall greatly increases risk of concurrent intracranial injury in all age groups.
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Pediatric neurosurgery · Apr 1997
Cerebrovascular response in infants and young children following severe traumatic brain injury: a preliminary report.
To further describe the pathophysiologic processes that occur in infants and young children after severe traumatic brain injury (TBI), we retrospectively reviewed the cerebral blood flow (CBF) values and 6-month Glasgow Outcome Scores (GOS) in 30 children < or = 8 years old (25 were < or = 4 years old) with a Glasgow Coma Score (GCS) on admission of < or = 8. Twelve females and 18 males (mean age 2.1 years, range 1 month to 8 years) underwent 61 CBF studies using stable xenon computed tomography at variable times from admission to 9 days after TBI. In 12 patients, PaCO2 was manipulated an average of 8.4 torr (range 5-11 torr) and a second CBF study performed to determine CO2 vasoreactivity (CO2VR), defined as the percent change in CBF per torr change in PaCO2. ⋯ Younger age, low CBF in the early period after TBI, and a CO2VR of <2% was associated with a poor outcome in this subgroup of children. Young children (<24 months) may represent a particular high-risk group with early hypoperfusion after severe TBI. This finding may be a key factor in the pathophysiology and outcome in this age group, and may need to be addressed in our future therapeutic protocols.
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Journal of neurotrauma · Apr 1997
Comparative StudyEarly neuropathologic effects of mild or moderate hypoxemia after controlled cortical impact injury in rats.
Hypoxemia has detrimental effects after traumatic brain injury (TBI) in both experimental models and humans. The purpose of this study was to determine the effect of mild or moderate hypoxemia on early histologic and motor functional outcome after controlled cortical impact (CCI) in rats. Anesthetized rats underwent CCI and were randomized to receive mild (FiO2 = 13%, n = 6), moderate (FiO2 = 11%, n = 9), or no (FiO2 = 33%, n = 6) hypoxemia for 30 min after trauma. ⋯ TUNEL-positive neurons were seen in ipsilateral cortex and dentate gyrus at 6, 24, and 72 h after trauma, and in ipsilateral CA3 hippocampal neurons and thalamus at 24 and 72 h. Moderate hypoxemia augments CA3 neuronal death and early motor functional deficits after CCI. The pattern of DNA fragmentation in selectively vulnerable neurons suggests that apoptosis may play a role in the delayed neuronal death seen after TBI.