Articles: brain-injuries.
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Journal of neurotrauma · Feb 2001
Age-dependency of 45calcium accumulation following lateral fluid percussion: acute and delayed patterns.
This study was designed to determine the regional and temporal profile of 45calcium (45Ca2+) accumulation following mild lateral fluid percussion (LFP) injury and how this profile differs when traumatic brain injury occurs early in life. Thirty-six postnatal day (P) 17, thirty-four P28, and 17 adult rats were subjected to a mild (approximately 2.75 atm) LFP or sham injury and processed for 45Ca2+ autoradiography immediately, 6 h, and 1, 2, 4, 7, and 14 days after injury. Optical densities were measured bilaterally within 16 regions of interest. 45Ca2+ accumulation was evident diffusely within the ipsilateral cerebral cortex immediately after injury (18-64% increase) in all ages, returning to sham levels by 2-4 days in P17s, 1 day in P28s, and 4 days in adults. ⋯ Histological analysis of cresyl violet-stained, fresh frozen tissue indicated little evidence of neuronal loss acutely (in all ages), but considerable delayed cell death in the ipsilateral thalamus of the P28 and adult animals. These data suggest that two temporal patterns of 45Ca2+ accumulation exist following LFP: acute, diffuse calcium flux associated with the injury-induced ionic cascade and blood brain barrier breakdown and delayed, focal calcium accumulation associated with secondary cell death. The age-dependency of posttraumatic 45Ca2+ accumulation may be attributed to differential biomechanical consequences of the LFP injury and/or the presence or lack of secondary cell death.
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Journal of neurotrauma · Feb 2001
The relation between acute physiological variables and outcome on the Glasgow Outcome Scale and Disability Rating Scale following severe traumatic brain injury.
The relation between outcome and duration of adverse physiological events was studied, using suggested critical physiological values. Subjects were 184 patients with severe traumatic brain injury who received continuous monitoring of intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and jugular venous oxygen saturation. ⋯ When analyses excluded patients who died, the relation between adverse physiological events and GOS was nonsignificant; however, duration of ICP, MAP, and CPP still accounted for a significant portion of the variance in DRS scalres. The relative sensitivity of the GOS and DRS is discussed.
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Brain injury : [BI] · Feb 2001
ReviewDiagnostic criteria and differential diagnosis of mild traumatic brain injury.
Brain injury is classified clinically as severe, moderate or mild brain injury characteristics, including admission Glasgow coma score, duration of unconsciousness and post-traumatic amnesia and any focal neurological findings. Most traumatic brain injuries are classified as mild traumatic brain injury (MTBI). Headache, nausea and dizziness are frequent symptoms after MTBI and may continue for weeks to months after the trauma. ⋯ Computed tomography of the brain seems to be the best way to exclude the development of relevant intracranial lesions. MTBI has a good clinical outcome, although a substantial group of patients develop post-concussional complaints (PCC). There is little information on the effectiveness of various methods suggested for reducing the frequency of PCC.
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Ann Fr Anesth Reanim · Feb 2001
Review[Hyponatremia in neurologic intensive care: cerebral salt wasting syndrome and inappropriate antidiuretic hormone secretion].
Hyponatraemia is a frequent complication in neurologically injured patients; it is a secondary cerebral injury. Hyponatraemia leads to consciousness problems, convulsions, worsening of the neurological status and thus the neurological evaluation. Hyponatraemia is secondary to free water retention (inappropriate ADH secretion) or to renal salt loss. ⋯ The diagnostic approach and monitoring are based on the assessment of sodium and water losses. Therapy is based on correction of the circulating volume and natraemia. Speed of correction is a matter of debate: slow correction presents the risk of further neurological injury whereas rapid correction presents the risk of central pontine myelinosis.