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

Cervical spine injuries pose devastating potential problems for surgeon and patient alike. This review will stress the early diagnosis of cervical spine injuries, with emphasis on early suspicion of injury. This review will focus on the radiology and types of lesions found with cervical spine injury.

In the course of establishing a therapeutic model for experimental spinal cord injury in the rat, we determined the effects of trauma dose (20, 30, 40, 50, and 60 g-cm) on the mortality and motor deficit in the 4 weeks following injury. Mortality was dependent upon the trauma dose: 20 g-cm, 11%; 30 g-cm, 14%; 40 g-cm, 27%; 50 g-cm, 32%; 60 g-cm, 41%. Statistical analysis by linear regression is highly significant for increasing mortality with increasing trauma dose. The motor deficit determined by a modified Tarlov scale also was dependent upon trauma dose. A trauma dose-response curve based on this study indicates that a drug which reduces the motor deficit from that found at 40 g-cm to that at 30 g-cm may be detected at a significant level of 0.05 with a power of 0.8 if 30 rats are included in each of placebo and treated groups. The same sample size would detect a significant reduction of mortality from that of 40 g-cm to 30 g-cm.

Alterations in lumbar spinal cord white matter blood flow (SCBF) during the initial 4 hours following contusion injury were examined in cats anesthetized with either dial-urethane or sodium pentobarbital and correlated with changes in cardiovascular parameters (MAP, HR), blood gases (pCO2, pO2), and pH. In the dial-urethane anesthetized cats, the effect of a severe 500 g-cm contusion on SCBF was determined at the center of the injury site vs. an adjacent site 3 mm away. At the injury site, SCBF fell progressively from a pre-injury mean of 13.9 +/- 0.8 (S.E.) mg/100 g/min to a 4 hour value of 7.0 +/- 1.3 (-49.6%). In contrast, SCBF in the adjacent white matter tissue was dramatically increased to 22.4 +/- 1.9 ml/100 g/min (+61.2% over pre-injury; p less than 0.025), at 10 min post-injury falling gradually back to only slightly below the pre-injury level at 4 hours. The severe contusion resulted in prolonged hypotension and bradycardia that was significant by 10 min post-injury while arterial blood gases and pH did not change over the experimental course. A very similar post-traumatic hypoperfusion was observed at the injury site in pentobarbital anesthetized animals in regard to the time course and extent of the decline in SCBF (-55.6% at 4 hours). Although the decrease in SCBF over time was gradual, the MAP and HR were maximally depressed by 10 min post-injury. A more moderate contusion (300 g-cm) resulted in an initial hyperemia followed by a return of SCBF to the pre-injury level by 30 min with no significant change thereafter even though the MAP was depressed to nearly the same extent as in the more severely injured cats. These results demonstrate that post-traumatic spinal cord ischemia is a phenomenon localized to the spinal injury site and directly related to the injury force with moderate injury actually causing a temporary hyperemia. In addition, a significant difference in SCBF may exist between the injury site and adjacent spinal tissue only a few mm away. No correlation between the increase or decrease in SCBF and change in cardiovascular parameters or blood gases following injury is demonstrable nor does anesthetic choice seem to make a significant difference. Thus, post-traumatic changes in SCBF appear to be due to the elaboration of local mediators for the most part unrelated to concomitant alterations in spinal cord perfusion pressure.

A quantitative microassay method is described for brain tissue phosphates. Based on molybdate colorimetric measurements of inorganic phosphate in tissue solutions prepared by acid digestion and high temperature ashing, the method includes the use of calcium to precipitate inorganic phosphate in acid-digested tissues and a correction for contaminants released from porcelain crucibles during the ashing procedure. This method was used to measure the total tissue phosphate concentrations in regional microsamples of rat brain. Averaged values derived from these regional measurements were 100.1 +/- 10.2 mumol/gm wet tissue weight, corresponding closely to whole brain tissue phosphate values reported in the literature. Phosphate concentrations were remarkably uniform in different areas of the cortex and basal ganglia.

The effects of spinal cord compression on conduction of dorsal column fibers at various stimulus frequencies were analyzed in pentobarbital anesthetized cats. The responses to L6 dorsal root stimulation at 1 to 500 Hz were recorded from the L2 cord dorsum. The L4 cord segment was compressed gradually until the compound action potential (CAP) at 1 Hz was flat. There was no significant change of CAP at any frequency during the first part of compression, but there was progressive conduction failure, which was more severe with increased stimulus frequency, at a later stage. After decompression, the CAPs at all frequencies recovered progressively for 1 hour but slowly thereafter. However, marked differences were observed in recovery rate at different stimulus frequencies. The recovery rate at 500 Hz was much slower than that at 1 Hz, whereas the recovery rate at 100 Hz exceeded those at 1 Hz. Serial analysis of a train of high frequency impulses revealed the following different response patterns with stimulus frequencies after decompression. At 333-500 Hz the amplitude of CAPs decreased progressively, whereas at 33-125 Hz it increased up to 110-134% of the first CAP and then reached an almost steady level. At 200-250 Hz the amplitude increased transiently and then decreased progressively. The latency increased with decreased amplitude, and decreased with increased amplitude. Conduction failure at a high stimulus frequency (500 Hz) was observed at the compression site. In contrast, augmentation of CAPs at moderately high stimulus frequency (100 Hz) was observed rostral to the compressing site. The conduction failure at high stimulus frequency indicates incomplete impairment of spike generation in axons injured by mechanical compression and that these axons can transmit impulses at a low stimulus frequency. High frequency stimulation may be useful for monitoring of the function of the CNS axons. The mechanism underlying the augmentation of CAPs at moderately high stimulus frequency is briefly discussed.

The incidence of spinal cord injury in the United States is between 50 and 55 million per year. The personal and societal costs have been an impetus for experimental studies that defined the posttraumatic pathological and biochemical changes from which the hypothesis has arisen that a portion of the resulting neurological deficit is caused by the response of the spinal cord to the injury. Alteration in this response has been a therapeutic goal. Clinical series over a number of years with varied treatment regimens have failed to show any significant difference in neurological outcome. A single randomized clinical trial of 'high dose' 'low dose' steroid treatment failed to support the secondary injury response hypothesis. The experimental studies and lack of therapeutic effectiveness of present treatment both support the concept of further experimental studies and further randomized clinical trials. It is important to test the hypothesis of secondary injury since, if it is a cause of a portion of the resultant loss of neurological function, the benefit of its control would extend beyond spinal cord injury to other central nervous system injuries.

A simple and reliable method of quantifying tissue damage is described. This method, based on atomic absorption spectroscopic determinations of Na, K, and Ca concentrations in small brain samples, was applied to the rat middle cerebral artery occlusion model (MCAo). At the infarct site by 24 hours, Na concentration more than doubled, Ca concentration increased by greater than 70%, and K concentration fell nearly 80%; these changes are consistent with a greater than 80% disruption of cells. A remarkable acceleration of ionic shifts occurred between 4 and 6 hours after MCAo. At 4 hours, only 20-30% of the ionic shifts found at 24 hours had occurred; by 6 hours, 80-100% of the ionic shifts found at 24 hours had taken place. Since the measurements reflect ionic movement into and out of the tissue, they are likely to represent irreversible tissue damage. Although blood brain barrier breakdown may have contributed to an increased rate of ionic shifts, large ionic gradients must have been present between the extracellular space and the vascular compartment at 4-6 hours to drive the ionic shifts. Our results suggest an upper time limit of 4 hours for treatments of acute ischemic tissue damage in the rat MCAo model. The methods and analytical approach described may be useful for determining the time window for therapeutic intervention in acute CNS injuries, as well as for evaluating treatment effects.

We sought neurophysiologic evidence that spinal cord stimulation could modify the behavior of spinal reflexes in 15 chronic SCI patients who showed the beneficial effect of SCS on spasticity. We studied the behavior of passive stretch, clonus, cutaneous touch, plantar reflex irradiation, and the response to the neck flexion reinforcement maneuver during spinal cord stimulation by use of surface PEMG recordings. Fifty-five percent of the responses were changed during spinal cord stimulation, but with widely varying patterns of response in individual patients. Exceptional patients showed changes in most or all responses; most showed changes in two or three. Thirty of seventy-five responses showed a reduction in motor unit activity in the recordings. Eleven of seventy-five responses were increased. Excessive stimulation strength enhanced spasticity in patients in whom another stimulus setting suppressed spasticity. We conclude that spinal cord stimulation could modify segmental reflexes but that the effects were selective, probably dependent on the preserved segmental structures and ascending and descending pathways.