Functional movement ScreenTM--normative values in healthy distance runners.

Recreational runners have an estimated overuse injury incidence rate of up to 79% and 90% for marathoners. A pre-participation screening tool that can identify risk for injury may help reduce overuse injury in runners. The Functional Movement Screen (FMS(TM)) is a reliable clinical tool used with athletes to help predict injury. To date, the FMS(TM) has not been used with endurance athletes. The purpose of this article is to establish normative FMS(TM) values for distance runners. 45 healthy runners performed the FMS(TM). Descriptive statistics were calculated; independent t-tests were performed to examine the effect of gender, experience and injury on scores. A Chi-square test was used to evaluate whether significant differences in scores exist for any component of the FMS(TM). The mean FMS(TM) score was 13.13±1.8. No significant differences in FMS(TM) scores were found between novice and experienced runners (p=0.71) or runners with a history of injury and those without (p=0.20). While male and female runners did not differ significantly in their total FMS(TM) score (p=0.65), significant differences were found in the deep squat (p<0.05), trunk stability push-up (p<0.001) and active straight leg raise components (p=0.002). This study provides normative values for FMS(TM) scores when testing uninjured distance runners.

Safety versus efficacy of spinal cord stimulation for the generation of motor-evoked potentials in the rat.

The relative safety and efficacy of direct versus indirect methods of spinal cord stimulation for the production of descending motor-evoked responses was studied in pentobarbital-anesthetized rats (n = 39). Electrical stimuli were delivered for 1 h, either directly to the cord dorsum using silver ball electrodes or indirectly through jeweler's screws implanted in the intact laminae. Compound muscle action potentials (CMAPs) were recorded differentially in the quadriceps and evaluated for their morphology and reproducibility. The traumatic effects of stimulation were assessed using intraoperative somatosensory-evoked potentials, blinded neurological examinations for 2 weeks postoperatively, and histopathological and neurochemical analyses in postmortem spinal tissues. In separate experiments, the neural substrates of the muscle-evoked response to indirect cord stimulation were examined. Direct, epidural stimulation of the spinal cord at intensities sufficient to elicit reproducible CMAPs consistently resulted in mild behavioral deficits (13 of 18 animals) that were accompanied by postmortem changes in spinal histology and chemistry. Some of these behavioral deficits (5 of 13 animals) were resolved at 2 weeks. There was rarely an early sign of motor or sensory conduction derangement in these animals. In 2 animals with severe behavioral dysfunction, the somatosensory-evoked response was abolished immediately after spinal stimulation. However, CMAP responses were unaltered. Examination of the strength-duration relationship for the production of threshold responses to translaminar constant current stimulation, as well as experiments using selective transection of the dorsal columns, revealed the CMAP responses to be neurally mediated and conducted through the cord independent of the ascending sensory tracts that mediate the rat's somatosensory-evoked response. Data are discussed in terms of the potential experimental usefulness of CAMPs elicited by indirect dorsal spinal stimulation.

Comparison of a serotonin antagonist, opioid antagonist, and TRH analog for the acute treatment of experimental spinal trauma.

The therapeutic efficacies of a serotonin antagonist (mianserin), an opioid antagonist (nalmefene), and a TRH analog (YM-14673) were compared in a well-characterized model of experimental spinal trauma in the rat. Injury was produced by the weight-drop method at T10 and confirmed by the disappearance of the somatosensory evoked response during the subsequent 15 minutes. Drug or vehicle treatments were administered randomly as a single intravenous bolus 15 minutes after injury. Functional outcome was blindly assessed for 2 weeks postinjury using a modified Tarlov scale and the Rivlin-Tator angleboard test. The survival of descending raphe-spinal axons was determined by measurement of serotonin in postmortem spinal tissues located above and below the injury, and histopathologic studies were carried out at the site of injury. All agents displayed similar and significant efficacies with respect to Tarlov and Rivlin-Tator measures of motor recovery and preservation of raphe-spinal fibers below the lesion site. In contrast, none of the agents were effective for preserving the central gray matter or myelin staining in the white matter in slices of tissue from the site of injury. Results are discussed in terms of the early treatment of spinal cord injury and future clinical trials.

Anesthesia influences the outcome from experimental spinal cord injury.

The effect of anesthesia upon the functional outcome after experimental spinal cord injury (SCI) was studied in 221 rats subjected to graded weight drop contusion in the thoracic cord. Neurologic function was assessed in a blinded fashion for one week after injury using a modification of the method of Tarlov. The post-mortem concentrations of serotonin and its metabolite were measured in injured and surrounding spinal tissues in a subset of animals in order to estimate the survival of descending long-tract axons. In initial studies using non-ventilated animals where body temperature was not controlled (n = 130), halothane anesthesia was associated with significantly better neurologic scores at all levels of injury (50, 100 and 250 g.cm) in comparison to pentobarbital. In a second experiment under these conditions (n = 53) the effect of halothane was observed after a 50 g.cm injury in comparison to both pentobarbital and nitrous oxide. Improved neurologic recovery was accompanied by the preservation of normal serotonin and metabolite concentrations in spinal tissue caudal to the site of injury. These values did not differ from those measured in sham-operated animals. Separate experiments (n = 12) revealed halothane's preservation of somatosensory-evoked responses during the early postinjury period in animals showing improved neurologic recovery. Subsequent experiments (n = 12) were performed to assess the effect of oxygen supplementation and the control of rectal temperature and a separate series of acute experiments (n = 14) examined arterial blood pressure responses to injury in halothane- and pentobarbital-anesthetized animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Interleukin-1 beta enhances spinal cord blood flow after intrathecal administration in the normal rat.

The effects of acute intrathecal recombinant human interleukin-1 beta (rhIL-1 beta) administration on spinal cord blood flow (SCBF), volume, and velocity were determined by laser-Doppler flowmetry in normal anesthetized rats with the use of a randomized and blinded protocol. The intrathecal administration of rhIL-1 beta (0.16-16 ng) produced a dose-dependent increase in SCBF that was not related to changes in blood pressure; arterial pH, PO2, PCO2; or spinal cord temperature. The IL-1 beta-induced enhancement of SCBF was directly proportional to the resultant elevation of spinal cord rhIL-1 beta content and was significantly correlated with an elevated blood velocity. The IL-1 receptor antagonist (IL-1ra) in concentrations 50- and 200-fold higher than IL-1 beta completely blocked the IL-1 beta-induced increase in SCBF when both compounds were administered concomitantly, but when administered alone, IL-1ra did not affect SCBF or other parameters. This suggests that IL-1 beta action was mediated by a specific interaction with an IL-1 membrane receptor site. The results suggest a role of IL-1 beta in the regulation of spinal cord hemodynamics. A potential pharmacological approach using IL-1 agonists for the treatment of the delayed appearance of posttraumatic spinal ischemia is proposed.

Characterization of mianserin neuroprotection in experimental spinal trauma: dose/route response and late treatment.

The neuroprotective action of the 5-hydroxytryptamine (5-HT2/5-HT1C) antagonist mianserin was examined with respect to optimal dosage, route of administration and time of treatment after a moderate spinal impact trauma (50 g.cm by the weight-drop method) to the thoracic region of the rat. In a previous study (Salzman et al., 1991b) a single 1-mg/kg i.v. dose of mianserin improved multiple measures of functional outcome when given 15 min after injury, whereas higher doses (5 and 10 mg/kg i.v.) displayed lesser therapeutic actions as well as pulmonary depressant effects. In these studies, lower dosages of minanserin (0.5 and 0.1 mg/kg i.v.) also were not associated with neuroprotection. Although the 1-mg/kg i.v. dosage again displayed significant efficacy when administered at 15 min delaying treatment to 30 min resulted in only marginal therapeutic actions. Nonetheless, i.p. dosage of 10 mg/kg (but not 2.5 mg/kg) at 15 min retained therapeutic efficacy, suggesting a pharmacodynamic influence. In support of this conclusion, the intrathecal administration of a 50-fold lower dose of minanserin (0.006 mg) at 15 min after injury resulted in neuroprotection that was superior to that of peripheral doses and was retained when this intrathecal dosage was administered at 1 hr after trauma. These results suggest a central mechanism of action for mianserin. Consistent with this was the lack of effect of mianserin (1 mg/kg i.v. at 15 min) upon post-traumatic spinal edema but its ability to reverse the decrease in central 5-HT oxidative metabolism after injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Halothane anesthesia is neuroprotective in experimental spinal cord injury: early hemodynamic mechanisms of action.

The neuroprotective potential of halothane anesthesia was explored in a weight-drop model of spinal trauma in the rat (N = 252). In initial experiments, animals were subjected to 25, 50 or 100 g cm impact injuries at T10 during pentobarbital or halothane anesthesia and their outcomes determined using somatosensory-evoked potentials, blinded neurologic evaluations for two weeks, and post-mortem analysis of spinal serotonin levels. Subsequently, halothane anesthesia was combined with either pentobarbital or nitrous oxide or given as a late treatment to pentobarbital anesthetized rats subjected to 50 g cm injuries. A series of acute studies were then performed in order to assess the hemodynamic and respiratory concomitants of halothane vs. pentobarbital, as well as the effect of mechanical ventilation and bicarbonate treatment upon halothane neuroprotection. Finally, the effect of a 50 g cm impact upon local white matter spinal cord blood flow was measured during halothane or pentobarbital anesthesia using laser-Doppler flowmetry. Results demonstrate an active neuroprotective action for halothane anesthesia that is not altered by the presence of other anesthetics and is most prominent at severe injury levels. The data suggest the importance of immediate injury responses in this action. Late halothane treatment was ineffective when given as early as 10 minutes postinjury while both the electrophysiological and hemodynamic effects of halothane vs. pentobarbital were apparent during this 10 minute period. Thus, halothane was associated with the prevention of spinal ischemia during the first 10 minutes after trauma in comparison to pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

The serotonin antagonist mianserin improves functional recovery following experimental spinal trauma.

The ability of the serotonin antagonist mianserin to improve neurological recovery after graded impact trauma to the thoracic region of the spinal cord was compared to that of cyproheptadine and ketanserin in pentobarbital-anesthetized rats. Spinal cord injury was produced at T-10 by the weight-drop method and confirmed by the disappearance of the somatosensory-evoked response during the subsequent 15 minutes. In all experiments, drug or vehicle treatments were randomly administered as a single intravenous bolus 15 minutes after injury. Functional outcome was blindly assessed for 2 weeks after injury using a modified Tarlov scale, and in some cases, the Rivlin-Tator angleboard test. The survival of descending raphe-spinal axons was determined by the measurement of serotonin in postmortem spinal tissues located above and below the site of injury. In separate acute experiments, the physiological and hemodynamic correlates of a 50 gm cm injury and either mianserin or vehicle injection were examined, as were the effects on serotonin content and metabolism in spinal tissues harvested 30 minutes after injury. All doses of mianserin were associated with some index of improved recovery following a 50 gm cm injury, with a 1-mg/kg dose being clearly superior. Both ketanserin (0.1 mg/kg) and cyproheptadine (2 mg/kg) displayed marginal therapeutic actions for 50 gm cm injuries. In acute studies, mianserin at 1 mg/kg was associated with the preservation of posttraumatic spinal cord blood flow at T-12 as well as a pronounced alteration in postmortem spinal serotonin content and metabolism, in contrast to vehicle control treatments.(ABSTRACT TRUNCATED AT 250 WORDS)