Articles: brain-injuries.
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Scand. J. Clin. Lab. Invest. Suppl. · Jan 1999
ReviewNeurochemical monitoring of the acutely injured human brain.
The main goal of modern neurointensive care (NIC) of patients with acute brain injury (traumatic brain injury, neurovascular disease) is to prevent additional loss of viable brain tissue due to secondary injury processes. It is generally held that secondary injury, mediated by, for example, cerebral hypoxia/ischemia and destructive molecular cascades on the cellular level, contributes significantly to the extent of brain damage after head injury and stroke. ⋯ This paper describes intracerebral microdialysis as a novel approach to neurochemical monitoring of the human brain. The main objectives are (i) to monitor cortical energy metabolism in order to detect secondary ischemia and (ii) to monitor secondary injury processes, such as glutamate receptor overactivation and increased free radical production, in NIC patients.
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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.
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BACKGROUND AND PURPOSE--Endothelin-1, in concentrations similar to that present in cerebrospinal fluid after fluid percussion brain injury (FPI), increases superoxide anion (O2-) production. Endothelin-1 also contributes to altered cerebral hemodynamics after FPI through impairment of ATP-sensitive K+ (KATP) channel function through protein kinase C (PKC) activation. Generation of O2- additionally occurs after FPI. ⋯ CONCLUSIONS--These data show that PKC activation increases O2- production and contributes to such production observed after FPI. These data also show that an activated system that generates an amount of O2- similar to that observed with FPI blunted pial artery dilation to KATP channel agonists and nitric oxide/cGMP. These data suggest, therefore, that O2- generation links PKC activation to impaired KATP channel function after FPI.
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J. Neurol. Neurosurg. Psychiatr. · Jan 1999
Randomized Controlled Trial Clinical TrialAdding insult to injury: the prognostic value of early secondary insults for survival after traumatic brain injury.
To assess the prognostic value of summary measures of secondary physiological insult in addition to baseline clinical variables for patients with traumatic brain injury. ⋯ Early intracranial hypertension is confirmed as a sign of poor prognosis in patients with traumatic brain injury, even after controlling for baseline clinical variables. The value or otherwise of treating such secondary insults, however, can only be definitively established in the context of prospective randomised controlled trials. The specific pathophysiological evolution of secondary insults is still the subject of much research, and a clear understanding will be necessary before the development of specific treatments is feasible.