Central nervous system trauma : journal of the American Paralysis Association最新文献

Experimental fluid percussion brain injury in anesthetized cats causes vascular injury characterized by sustained arteriolar dilation, abnormal reactivity to vasoconstrictor and vasodilator interventions, focal endothelial lesions, and reduction of the oxygen consumption of the vessel wall. These abnormalities are minimized or completely inhibited by pretreatment with cyclooxygenase inhibitors or with oxygen radical scavengers. They were therefore ascribed to oxygen radicals generated in the course of accelerated arachidonate metabolism via cyclooxygenase. Following this type of brain injury, there is an increase in the activity of phospholipase c in the brain and a transient increase in brain concentration of prostaglandins. Superoxide anion radical was detected in the extracellular space of the brain both immediately following brain injury as well as one hour afterwards as the superoxide dismutase inhibitable portion of nitroblue tetrazolium reduction. The sustained dilation and abnormal reactivity of cerebral arterioles following brain injury were also reversed by superoxide dismutase and catalase applied on the brain surface 30 minutes after injury. These results suggest that treatment with oxygen radical scavengers might be effective in inhibiting or reversing some of the effects of brain injury, even though the intervention with the therapeutic agents occurs sometime after the injury has taken place.

The evolving techniques of motor evoked potential (MEP) monitoring are reviewed here with reference to their application in clinical and experimental CNS trauma, and with particular relevance to spinal cord injury. Transcutaneous electrical stimulation of the motor cortex for analysis of descending pathways has been developed over the past 6 years in a number of centers. It has now been greatly augmented by the introduction of magnetic stimulation technology. The MEP offers a valuable insight into the physiological status of motor tracts within the spinal cord and is applicable to conscious patients, intraoperative monitoring, and animal studies. It is seen as complementary to somatosensory evoked potential monitoring rather than an alternative or replacement for it. The chief limitations of the technique, common to all evoked potential methods, are the restricted information content, and the need for rigorous electrophysiological interpretation of the resulting signals, if meaningful diagnostic data are to be extracted.

Irregularities in vital sign (pulse, blood pressure, cardiac rhythm) recordings are commonly observed following acute spinal cord injury. These abnormalities have been generally attributed to autonomic instability. However, there have been no clinical reports that evaluate these problems in a large group of acutely injured patients. Therefore, this study was performed on 45 patients with acute cervical spinal cord injuries to evaluate the incidence, severity, and risk factors for cardiovascular instability. This investigation revealed that there is a direct correlation between the severity of the cord injury and the incidence and severity of cardiovascular problems. Endotracheal suctioning with or without documented hypoxia are major causes of severe bradycardia and cardiac arrest within the first 2 weeks after trauma. Careful monitoring of severely injured patients and attention to the warning signs of cardiovascular instability can reduce the risk of life-threatening emergencies.

The neurophysiologic monitoring of interventional neuroradiologic procedures is a new field of intraoperative monitoring. Interventional neuroradiology makes use of different diagnostic or therapeutic catheterization techniques in both cerebral and spinal cord arteries. Both procedures can be made more secure by monitoring of EEG or evoked potentials. Using the advantages of the different catheter techniques, such as series of balloon occlusions or injections of drugs or contrast dye, the neuroradiologist and the neurophysiologist are able to plan and test the next steps of an interventional maneuver. The results and implications of neuromonitoring during occluding maneuvers of the internal carotid artery, during local fibrinolytic therapy, during embolization procedures of cerebral or spinal arteries, malformations, or tumors, and during drug application are discussed and illustrated.

We investigated the probability of survival of mouse spinal neurons in monolayer cultures after transection lesions of dendrites made within 400 microns of the perikarya. Based on a total of 650 lesioned neurons, the following observations were made. First, neuronal survival is a function of lesion distance from the perikaryon and of process diameter at the lesion site. For an average lesion diameter of 3 microns, dendrite transections at 50 microns, 100 microns, and 150 microns were associated with survival probabilities of 30%, 53%, and 70%, respectively. Second, the fate of the injured cells was definitely established 24 hours after injury and very likely was determined as early as 2 hours. Third, early stages of deterioration leading to cell death were associated with cytoplasmic phase brightness on light microscopy, correlating with an appearance of numerous, small, electron-lucent vacuoles and swollen mitochondria on electron microscopy. The cytoplasm of these moribund cells stained darkly and contained no visible microtubules or neurofilaments. Fourth, the magnitude and time course of injury potentials recorded at the somata were a function of the lesion distance and did not return to prelesion levels within 30 minutes after transection. Fifth, at 24 hours after injury, the average membrane potential of lesioned neurons was 8% below that of control neurons. Sixth, at a lesion distance of approximately 300 microns both the injury potential and the probability of cell death approach zero. We conclude that, in the model system used, neuronal survival after dendrite amputation depends on physical parameters of the lesion that determine the magnitude of the injury current reaching the soma. Survival is not assured if the injury is inflicted within 250 microns of the cell body, and cell death is likely for lesions within 50 microns of the soma. The below-normal membrane potentials at 24 hours after injury suggest a possible greater vulnerability of recovering neurons to secondary insults. The characteristic mitochondrial disruption and loss of microtubules implies that the calcium component of the injury current contributes to cell death.

The direct effects of lipid peroxidation on axonal conduction were investigated by application of tertiary-butyl hydroperoxide (t-BOOH) to the isolated common peroneal nerve of the frog (Rana catesbeiana). The powerful oxidizing agent t-BOOH caused a concentration-related (0.03-3.0%) block of action potential conduction. This effect, presumably due to axonal lipid peroxidation, was progressive, with the time required for the conduction impairment to occur also being a function of t-BOOH concentration. In contrast, tertiary butyl alcohol had no effect even at a 3.0% concentration. The gamma-fibers in the nerve were the most sensitive to t-BOOH conduction block, followed in order by the larger diameter beta-fibers and the even larger alpha-fibers. The rate of decrease in conduction was faster in nerves that were stimulated continuously (1 Hz) than in those that were activated only at specific measurement times, indicating an association between axonal depolarization and susceptibility to peroxidative conduction block. Recovery of conduction was observed particularly in alpha- and beta-fibers. The rate and extent of recovery were inversely proportional to the concentration of t-BOOH, suggesting that moderate peroxidative damage is potentially reversible. The possible relationship of these results to lipid peroxidative axonal damage in acute central nervous system injury is discussed.

Confusion about the risk of seizures following head trauma might in part reflect methodologic limitations of reported studies. This epidemiologic review emphasizes four methodologic issues: selection of cases, selection of controls, definition and ascertain of seizures, and definition, of seizures, and definition, classification, and ascertainment of trauma. Although the focus of this review is a set of reports of civilian injuries, the relevance of war studies to civilian injuries is also discussed.

Compression trauma of the cat spinal cord induces a very rapid alteration in the lipid metabolism of cellular membranes, including lipid hydrolysis with release of fatty acids including arachidonate, production of biologically active eicosanoids, and loss of cholesterol. This disturbance of cellular membranes can directly damage cells and can lead to the secondary development of tissue ionic imbalance, ischemia, edema, and inflammation with neuronophagia. Pretreatment with either the synthetic glucocorticoid methylprednisolone sodium succinate (MPSS) or the antioxidants vitamin E and selenium (Se) completely prevented the loss of cholesterol and partially inhibited lipolysis and prostanoid production. Treatment with MPSS significantly reduced the postinjury tissue necrosis and paralysis. Preliminary evidence indicates that pretreatment with vitamin E and Se also protected against the effects of spinal cord injury (SCI). We speculate that the ability of these agents to preserve function after SCI may, in part, reside in their capacity to limit the trauma-induced changes in lipid metabolism.