Articles: brain-injuries.
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Mechanical ventilation is the potential therapeutic approach to traumatic brain lesion and acute adult respiratory distress syndrome (ARDS) in the wake of severe injury in an accident. Aggravating cerebral symptoms, such as non-targeted defence reactions in coma, hemiplegia, synergism of extension, convulsions, pontine respiratory disorders, and intracerebral pressure beyond 30 Torr are diagnostic criteria for immediate mechanical ventilation of patients with brain trauma. The same action is indicated for cases of ARDS exhibiting, on top of the typical constellation of causes, hypoxia below 60 Torr paO2 and vital capacity below 15 ml/kg body weight or respiratory rates in excess of 30/min.
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Review Case Reports
The autonomic dysfunction syndrome: aetiology and treatment.
Nine patients with autonomic dysfunction syndrome (ADS) characterised by sympathetic discharge and extensor posturing are presented. Morphine was given to three patients and in all cases consistently stopped the episodes. Dantrolene was given to one patient and reduced the severity of the extensor posturing without affecting the other components of the ADS. ⋯ The autonomic dysfunction syndrome appears to be related to both severe closed head injury and acute hydrocephalus. The clinical similarity of the two diverse etiologic groups and the absence of precipitating increased ICP in the former suggests the common theme is a release of the brain stem from higher control. The responses to morphine and bromocriptine suggest that the opiate and dopaminergic pathways play roles in the entity.
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Journal of neurotrauma · Jan 1988
Controlled cortical impact: a new experimental brain injury model.
A new experimental model of mechanical brain injury was produced in the laboratory ferret (Mustela putorius furo) using a stroke-constrained pneumatic impactor. Cortical impacts were made on vertex to the intact dura mater overlying the cerebral cortex with contact velocities ranging from 2.0 to 4.0 m/sec and with deformations of 2.0 to 5.0 mm. The dwell time of the impact and the stability of the skull during impact were verified with high speed (1000 to 3000 frames/sec) cineradiography. ⋯ The spectrum of anatomic injury and systemic physiologic responses closely resembled aspects of closed head injury seen clinically. This procedure complements and improves on existing techniques by allowing independent control of contact velocity and level of deformation of the brain to facilitate biomechanical and analytic modeling of brain trauma. Graded cortical contusions and subcortical injury are produced by precisely controlled brain deformations, thereby allowing questions to be addressed regarding the influence of contact velocity and level of deformation on the anatomic and functional severity of brain injury.
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Calorie and protein supplementation improves nutritional status. This support may improve outcome and decrease morbidity and mortality in acutely brain-injured patients. Investigators have observed a poor tolerance to enteral feedings after brain injury and have noted that this persists for approximately 14 days postinjury. ⋯ The authors conclude that patients with acute severe brain injury do not adequately tolerate feedings via the enteral route in the early postinjury period. Tolerance of enteral feeding is inversely related to increased ICP and severity of brain injury. It is suggested that parenteral nutritional support is required following brain injury until enteral nutrition can be tolerated.
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Journal of neurotrauma · Jan 1988
The effects of scopolamine and traumatic brain injury on central cholinergic neurons.
This study examined the effects of scopolamine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min, 4 h, and 24 h after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass fragmentography. ⋯ The responses of thalamic, hippocampal, and amygdaloid cholinergic neurons to TBI did not differ substantially in scopolamine-pretreated rats from those studied previously in untreated fluid-percussion-injured rats. However, cholinergic neurons in the cingulate-frontal cortex of rats receiving TBI did respond in a different manner to scopolamine than those of rats receiving sham injury, suggesting a disruption of regulation of cortical cholinergic neurons following this model of TBI.