Articles: brain-injuries.
-
Ann. N. Y. Acad. Sci. · Jan 1999
Clinical TrialAn open-label study of CP-101,606 in subjects with a severe traumatic head injury or spontaneous intracerebral hemorrhage.
CP-101,606 is a postsynaptic antagonist of N-methyl-D-aspartate (NMDA) receptors bearing the NR2B subunit. When administered intravenously (i.v.), it decreases the effects of traumatic brain injury (TBI) and focal ischemia in animal models. Therapeutic plasma concentrations (200 ng/ml) in animals, have been well tolerated in healthy human volunteers. ⋯ CSF concentrations were slightly higher than that in plasma by the end of infusion suggesting good penetration of CP-101,606 into the CSF. Outcome in the severe TBI patients, as measured by the Glasgow Outcome Score at six months, suggested that a two-hour infusion yielded a range of scores similar to contemporary patients with a severe TBI treated at our hospital while the outcomes of the patients treated with either a 24- or 72-hour infusion were better on average. Thus, these results indicate that CP-101,606 infused for up to 72 hours is well tolerated, penetrates the CSF and brain, and may improve outcome in the brain-injured patient.
-
Ann. N. Y. Acad. Sci. · Jan 1999
Randomized Controlled Trial Clinical TrialA double-blind, placebo-controlled study of the safety, tolerability and pharmacokinetics of CP-101,606 in patients with a mild or moderate traumatic brain injury.
CP-101,606 is a postsynaptic antagonist of the glutamate-mediated NR2B subunit of the N-methyl-D-aspartate (NMDA) receptor. When administered intravenously (i.v.) at the time of injury, CP-101,606 is neuroprotective in animal models of traumatic brain injury (TBI) and ischemia. Minimal adverse effects have been observed in normal human volunteers given i.v. doses of up to 3 mg/kg/hr for 72 hours. ⋯ A Neurobehavioral Rating Scale, used to detect personality changes and behavioral disturbances, indicated that all subjects showed an improvement from their postinjury, predosing baseline but did not significantly differ from each other with respect to type of head injury and/or treatment with drug or placebo. Modified Kurtzke Scoring also showed a similar pattern of improvement irrespective of type of head injury or drug/placebo treatment. This study suggests that CP-101,606, infused for up to 72 hours has no psychotropic effects and is well-tolerated in patients who have sustained a mild or moderate TBI or hemorrhagic stroke.
-
Arch Phys Med Rehabil · Jan 1999
Comparative Study Clinical Trial Controlled Clinical TrialLong-term continuously infused intrathecal baclofen for spastic-dystonic hypertonia in traumatic brain injury: 1-year experience.
To determine if the long-term use of continuously infused intrathecal baclofen (ITB) over a 1-year period will control spastic-dystonic hypertonia in patients with traumatic brain injury (TBI). ⋯ Continuous intrathecal infusion of baclofen is capable of maintaining a reduction in spasticity and dystonia in both the upper and lower extremities of TBI patients.
-
British medical bulletin · Jan 1999
ReviewCerebral protection in severe brain injury: physiological determinants of outcome and their optimisation.
The primary role of intensive care in acute head injury lies in the prevention, detection and reversal of secondary neuronal injury. The maintenance of optimal systemic and cerebrovascular physiology can substantially contribute to these aims. There is, however, a role for novel neuroprotective interventions, many of which are currently under investigation.
-
Acta Neurochir. Suppl. · Jan 1999
Case Reports Comparative StudyContinuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.
Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. ⋯ CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. Hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.