Articles: brain-injuries.
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Journal of neurotrauma · Jul 2001
Case ReportsDelayed hemispheric neuronal loss in severely head-injured patients.
Recent experimental studies have revealed that traumatic brain injury as well as ischemic brain injury can cause chronic progressive neuronal damage. In the present study, we demonstrate previously unreported delayed cerebral atrophy on computerized tomography (CT) scans in severely head-injured patients. Seventeen severely head-injured patients who required mild hypothermia to control intracranial hypertension after the failure of conventional therapies were retrospectively analyzed. ⋯ Six of these eight patients with DNL achieved functional recovery despite progressive atrophic changes demonstrated on CT scans. On CT scans, DNL was characterized by (1) the sudden appearance at several months postinjury of a low-density area in the hemisphere ipsilateral to the injury; (2) the preservation of essential cortical structure although related white matter structures showed severe atrophic changes; and (3) no spread of the low-density area to the contiguous territory of the other main cerebral artery. It is concluded that focal primary injury to underlying brain, if severe enough, can result in delayed hemispheric atrophy.
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To determine the epidemiology of pediatric traumatic brain injury (TBI) in a midwestern state and to examine differences between metropolitan and nonmetropolitan residents. ⋯ This study reports the lowest incidence of pediatric TBI that results in death or hospitalization to date. One half of severely injured patients suffered poor outcomes. A greater proportion of nonmetropolitan than metropolitan residents suffered severe TBI and had higher mortality and case-fatality rates.
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Pediatr. Clin. North Am. · Jun 2001
ReviewCerebral resuscitation after traumatic brain injury and cardiopulmonary arrest in infants and children in the new millennium.
As outlined in Figure 1, it is likely that a series of interventions beginning in the field and continuing through the emergency department, ICU, rehabilitation center, and possibly beyond, will be needed to optimize clinical outcome after severe TBI or asphyxial CA in infants and children. Despite the many differences between these two important pediatric insults, it is likely that many of the therapies targeting neuronal death, in either condition, will need to be administered early after the insult, possibly at the injury scene. Even cerebral swelling, a pathophysiologic derangement routinely treated in the PICU, almost certainly is better prevented rather than treated. ⋯ Further research is needed to define better the pathobiology of these two important conditions at the bedside, to understand the optimal application of contemporary therapies, and to develop and apply novel therapies. The tools necessary to carry out these studies are materializing, although the obstacles are great. This difficult but important challenge awaits further investigation by clinician-scientists in pediatric neurointensive care.
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Alcohol. Clin. Exp. Res. · Jun 2001
Effects of ethanol and naltrexone in a model of traumatic brain injury with hemorrhagic shock.
Ethanol predisposes to traumatic injury and causes respiratory depression and cardiovascular compromise in models of traumatic brain injury (TBI) and hemorrhagic shock (HS). Endogenous opioids may play a role in ethanol intoxication and TBI. We studied the effects of ethanol and the opiate antagonist agent naltrexone (NTX) in a TBI/HS model. ⋯ In this TBI/HS model, NTX reverses ethanol-induced depression of hypercapnic ventilatory response but does not improve MAP, CPP, or metabolic acidosis. This suggests that the respiratory effects of ethanol in TBI, but not the hemodynamic effects, may be mediated by opiate receptor activation.
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Rigid collars are routinely used to immobilise the cervical spine during early management of trauma victims until spinal injury is excluded. Spinal injuries commonly coexist in patients with severe head injury, and there is still uncertainty as to whether application of a rigid collar may adversely affect intracranial pressure. The aim of this study was to examine this effect by applying rigid collars to patients with traumatic head injury. ⋯ The mean rise in intracranial pressure was greater in those patients with a baseline intracranial pressure > 15 mmHg compared to those with a baseline intracranial pressure < 15 mmHg (p < 0.05). Since there was no significant change in cardiorespiratory parameters during this time, venous compression in the neck seems a likely explanation for the effect observed. These findings suggest that in head-injured patients, rigid collars should be removed as soon as cervical spine injury has been excluded or, if this is delayed, an alternative method of spinal stabilisation considered.