Articles: brain-injuries.
-
A statistically significant elevation was observed in serum and CSF neuron-specific enolase (NSE) levels in patients with major head injury, relative to control individuals. No correlation was noted between serum NSE and either APACHE II, Injury Severity Score (ISS), Glasgow Outcome Score (GOS) or Glasgow Coma Scale (GCS). A significant correlation was noted between CSF NSE levels and GCS, but not between CSF NSE and APACHE II, ISS or GOS. ⋯ In nine patients with major head injury, changes in CSF levels reflected changes in serum NSE levels. In all nine patients, serum NSE decreased to reach normal values, regardless of the outcome as predicted by the GOS. Therefore, while NSE would appear to be a marker of neuronal cell damage, other markers are also essential.
-
Journal of neurochemistry · Oct 1996
mu-calpain activation and calpain-mediated cytoskeletal proteolysis following traumatic brain injury.
Increasing evidence suggests that excessive activation of the calcium-activated neutral protease mu-calpain could play a major role in calcium-mediated neuronal degeneration after acute brain injuries. To further investigate the changes of the in vivo activity of mu-calpain after unilateral cortical impact injury in vivo, the ratio of the 76-kDa activated isoform of mu-calpain to its 80-kDa precursor was measured by western blotting. This mu-calpain activation ratio increased to threefold in the pellet of cortical samples ipsilateral to the injury site at 15 min, 1 h, 3 h, and 6 h after injury and returned to control levels at 24-48 h after injury. ⋯ Although mu-calpain autolysis and cytoskeletal proteolysis occurred concurrently with early morphological alterations, evidence of calpain-mediated proteolysis preceded the full expression of evolutionary histopathological changes. Our results indicate that rapid and persistent mu-calpain activation plays an important role in cortical neuronal degeneration after traumatic brain injury. Our data also suggest that specific inhibitors of calpain could be potential therapeutic agents for the treatment of traumatic brain injury in vivo.
-
We have employed bedside multimodality methods to assess the influence of a slow (20 min) bolus of hypertonic mannitol on cerebral hemodynamics in comatose patients with head injuries. ⋯ Bedside multimodality monitoring may provide a useful means for assessing the effects of therapy in the comatose patient. The mechanisms by which mannitol reduces intracranial pressure in patients with head injuries are discussed.
-
To identify computed tomographic-detected intracranial hemorrhage (CTIH) risk factors and outcome in mild cognitive impairment (MCI) blunt trauma patients. ⋯ In mild cognitive impairment patients triaged directly to a Level I trauma center, age, arrival GCS score, and cranial soft tissue injury are risk factors for CT-detected intracranial hemorrhage. Neurologic deterioration and death are infrequent. These data strongly suggest that observation and discretionary brain CT imaging are a rational approach for blunt-injury mild cognitive impairment.
-
Critical care medicine · Oct 1996
Severe head injury in the United Kingdom and Ireland: a survey of practice and implications for management.
To study the current intensive care management of patients with severe head injury (defined as a Glasgow Coma Scale score of < or = 8) in neurosurgical referral centers in the United Kingdom (UK) and ireland. ⋯ We conclude that there are wide variations in the management of the severely head-injured patient in the UK and Ireland. Some of the therapies employed are not supported by available research findings. Rationalization (using rational management, i.e., based on good evidence) of the intensive care management of severe head injury with the development of widely accepted guidelines may result in an improvement in the quality of care of the head-injured patient.