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

The effect of ethanol on recovery of neural conduction after spinal cord compression was evaluated in an isolated rat spinal cord preparation. Controlled compression of 50 to 75 percent of the cord cross-section was delivered using a piezoelectric translator. Postcompression compound action potential (CAP) amplitude, latency, and refractory periods were measured relative to pre-compression values. Recovery of CAP's was compared for spinal cords exposed to ethanol in vitro (100 mg/dl bath concentration, started one hour prior to compression) versus those maintained in normal artificial CSF. The in vitro effects of ethanol were evaluated on spinal cords from rats maintained on a normal diet and from those repeatedly intoxicated with ethanol for 15 days prior to the acute experiment. Compression of the cord resulted in an immediate 68% decrease in CAP peak amplitude and an increase in latency (171%) and refractory period (256%). In normal bathing medium, CAP amplitude recovered to 83% of pre-compression values 180 minutes after compression. The addition of ethanol to the artificial CSF did not directly affect CAP parameters, but combined with compression, CAP amplitude recovered to only 42% of pre-compression values 180 minutes after impact (p less than .01). Recovery was less affected by acute ethanol exposure in cords from ethanol pretreated animals. CAP amplitude recovered to 83% of pre-compression levels and was not different from compression-only recovery (p less than 0.10). The data suggest that direct effects of ethanol on axonal membranes may affect the sensitivity of axons to mechanical trauma or their capacity to recover normal function. Since spinal cords from repeatedly exposed animals are less sensitive to the acute effects of ethanol, ethanol may be acting to "fluidize" the axonal membrane.

We have attempted to address some of the current issues and new trends in the urologic management of SCI patients. Although tremendous progress has been made with these patients, resulting in a significant lowering of renal morbidity and mortality, there is still room for improvement. Newer methods of bladder management and refinements of older techniques are being sought. Progress in treating urinary infections should occur through development of new antibacterials and through improved understanding of host-bacterial interactions. Research into these problems and the general management of the neurologic dysfunction in SCI offers the hope of an even brighter future for these severely disabled patients.

Rehabilitation Indicators (RI) form a multipart system for assessing the macrofunctioning of patients in medical rehabilitation. The RI system was designed to provide a holistic view of the patient as a means of integrating the diverse data sets that are obtained at present. The computerization of the RI system creates an easily accessible database to optimize intrateam communication and the sharing of information with patients and families, as well as to optimize the service provider's response to increasing demands for accountability.

We document here microvascular alterations occurring in models of mild, moderate, and severe cerebral ischemic injury. The relationship of the vascular abnormalities to the generation of hemodynamic alterations was also evaluated. Following periods of severe incomplete ischemia, scanning electron microscopic analysis of cerebral microvessels revealed the widespread production of cerebral endothelial microvilli. These microvilli increased in frequency as the ischemic insult was prolonged and remained prominent during periods of recirculation. Although these luminal projections would not be expected to inhibit reperfusion completely, they might increase microvascular resistance, leading to moderate hemodynamic impediments extending into the post-ischemic period. Similar periods of complete ischemia resulted in more severe microvascular alterations. Light and electron microscopic studies revealed a high frequency of compressed capillary lumina with vascular stasis. These compressed vessels were consistently surrounded by swollen astrocytic foot processes. When recirculation was instituted for 1 hr following 1 hr of complete ischemia, regions of non-perfusion were detected autoradiographically within brain regions destined to undergo ischemic infarction. Finally, in an attempt to determine the consequences of a primary microvascular insult on brain structure and function, the endothelial layer of microvessels in the cerebral cortex was injured using a noninvasive photochemical method. Endothelial damage led to platelet aggregation in both pial and intraparenchymal vessels. Occlusive thrombi were frequently detected with perivascular edema associated with vascular compression and severe focal ischemia. Ultrastructural blood-brain barrier studies using the horseradish peroxidase tracer demonstrated that protein leakage at the site of primary vascular injury resulted in tracer material in brain regions remote from the pathological lesion. The widespread leakage of protein tracer was associated with decreased blood flow in remote brain regions at several postirradiation periods. These data emphasize the importance of injury-induced microvascular dysfunction in the generation of brain lesions and hemodynamic abnormalities.

A large amount of biochemical, physiological, and pharmacological data has been obtained which supports a mechanistic role of oxygen free radical-induced lipid peroxidation (LP) in post-traumatic spinal cord degeneration. Biochemical evidence of early and progressive lipid peroxidative reactions occurring in the injured spinal cord includes: an increase in polyunsaturated fatty acid peroxidation products (e.g., malonyldialdehyde), a decrease in cholesterol and the appearance of cholesterol oxidation products, an increase in cyclic GMP presumably due to free radical activation of guanylate cyclase, a decrease in tissue anti-oxidant levels (e.g., alpha tocopherol, reduced ascorbate), and inhibition of membrane-bound enzymes such as Na+ + K+-ATPase. In vitro CNS tissue studies have provided support for the possibility that LP may contribute to other early post-traumatic events including intracellular calcium accumulation and arachidonic acid release. Moreover, spinal tissue lactic acidosis, which occurs early after injury, can exacerbate LP reactions. The involvement of LP in the development of progressive post-traumatic spinal white matter ischemia has been strongly inferred from pharmacological studies in cats with known inhibitors of LP. For example, the dose-response curves for the ability of the glucocorticoid methylprednisolone (MP) to inhibit post-traumatic LP and to retard ischemia development are identical. This relationship between LP and post-traumatic ischemia is more directly implied from studies showing that pretreatment of cats with high doses of anti-oxidants (e.g., d-alpha tocopherol plus selenium p.o. or 1-ascorbic acid i.v.) can also significantly antagonize the progressive decrease in spinal cord blood flow that follows severe blunt injury. However, a similar efficacy of certain calcium and prostaglandin antagonists suggests an interrelationship between aberrant calcium fluxes, vasoconstrictor/platelet aggregating prostanoids, and LP in the post-traumatic ischemic phenomenon. In addition to a role of LP in ischemia development, the action of intensive d-alpha tocopherol and selenium pretreatment to retard anterograde cat motor nerve fiber degeneration after nerve section suggests that LP may also be a fundamental mechanism of "Wallerian" axonal degeneration after neural injury. Finally, a critical role of LP in the acute pathophysiology of CNS injury in general has been supported by the finding of an excellent correlation, in terms of efficacy and potency, between the action of glucocorticoid and nonglucocorticoid steroids to inhibit neural tissue LP in vitro and to promote early neurological recovery in severely head-injured mice.

Functional neuromuscular stimulation (FNS) has been demonstrated to restore purposeful movement to muscles paralyzed by spinal cord injury (SCI). It is hoped that this technique will ultimately improve rehabilitation by enabling skilled activities for paraplegics (e.g., walking) and quadriplegics (e.g., feeding oneself) to be accomplished regularly with safety and reliability. It is also expected that FNS exercise programs will lead to higher levels of health and fitness for SCI individuals. However, high fatigability of electrically stimulated paralyzed muscles may severely limit FNS applications. This fatigability is related to numerous factors, including the deteriorated condition of the paralyzed muscles and cardiopulmonary system, the nonphysiologic way in which these muscles are activated with FNS, and the probability that organ system adjustments that normally accompany voluntary exercise do not occur to the same extent with this peripherally induced exercise. More research is necessary to determine the mechanisms of fatigue for FNS exercise so that methods could be devised to increase resistance to fatigue. In addition, more research is necessary to substantiate the potential health and fitness benefits that have been stated for FNS exercise training.

Based upon evidence that opioid antagonists improve neurological outcome following either traumatic or ischemic spinal cord injury, endogenous opioids have been implicated in the pathophysiology of these disorders. Naloxone improved both spinal cord perfusion and neurological function following traumatic spinal cord injury in cats, and was subsequently observed to improve neurological outcome following ischemic spinal cord injury in rabbits. Using several opioid antagonists with varied selectivities for different types of opioid receptors, it was suggested that kappa opioid receptors are involved in both these models of spinal cord injury. In addition, spinal cord trauma in rats is associated with increased concentrations of the endogenous kappa agonist dynorphin A, and increased kappa opioid receptor binding capacity localized to the injury site. Furthermore, dynorphin A induces hindlimb and tail flaccidity following intrathecal injection in rats. Thus, the pathophysiological effects of endogenous opioids in spinal cord injury have been proposed to involve dynorphin A interactions with kappa opioid receptors. However, disparities between the actions of intrathecally injected dynorphin A in rats and the presumed actions of endogenous dynorphin A in cat and rabbit spinal cord injury have been revealed in recent experiments. Paralysis resulting from intrathecal dynorphin A is not altered by opioid receptor antagonists or TRH, produced by non-opioid dynorphin A fragments but not by other selective kappa opioid agonists, and associated with non-opioid mediated reductions in spinal cord blood flow. Furthermore, despite reports of endogenous opioid changes following rat spinal cord trauma, in contrast to cats and rabbits, naloxone failed to improve neurological outcome following traumatic rat spinal cord injury. Thus, the specific endogenous opioids and opioid receptor types involved in spinal cord injury remain to be resolved, and do not appear to be universal among different models of spinal cord injury in different species. Additionally, dynorphin A may participate in spinal cord injury mechanisms in the rat through non-opioid actions.

The efficacy of visually displayed EMG feedback in treating hemiplegic upper limb motor disorders was investigated in 5 patients (0.5-4 years poststroke). A single case experimental method "multiple-baseline across target behaviors" was used to compare performance during the feedback phase to that occurring in the monitored baseline phase. The nonfeedback baseline phase was followed by the staggered introduction of audiovisual feedback for each of the targeted pairs of muscles. EMG feedback obtained from muscle pairs (shoulder: anterior deltoid and upper trapezius; elbow: brachial triceps and biceps; digits: extensor digitorum communis and digit flexors) was displayed as two distinct waveforms on a videomonitor during therapy. Nonfeedback assessment of each of the three pairs was performed during each session. The effects of feedback were not uniformly distributed. Elbow control responded best, and statistical tests confirmed the effects of intervention observed clinically in all 5 patients. Clinical improvements in shoulder flexion were observed in 4 patients but could be statistically attributed to EMG gains in just 1. Improvement in finger extension observed clinically in 3 patients was statistically attributable to EMG gains in 2. All patients regained control of at least one target activity. EMG gains were accompanied by increases in active range of motion and by varying functional improvement. Marked functional gains in 3 patients were obtained with recovery of finger control.