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Study design :This is a case-control study., Objective: The objective of this study was to estimate the magnitude of association between spinal cord injury (SCI) and women's quality of sexual life and sexual function., Setting: This study was conducted in the Brain and Spinal Cord Injury Research Center, Tehran University of Medical Sciences, Tehran, Iran., Methods: From the referral university-based clinics, we used simple random sampling to recruit 62 women: 31 women with SCI and 31 women without SCI. Socio-demographic and reproductive traits questionnaire, Sexual Quality of life-Female (SQOL-F), Female Sexual Function Index (FSFI) and Spinal Cord Independence Measure (SCIM) were completed using telephone and face-to-face interviews in the cases and controls. After univariate analyses, multivariate linear and proportional odds regression models were conducted to investigate the relation between SCI and women's quality of sexual life, as well as sexual function., Results: The mean age of cases and controls was 35.42±6.51 and 33.77±4.02 years. Most women were high school-educated and housewives. Adjusting for probable confounders, the proportional odds regression model showed a significant relationship between the spinal cord injury (AOR=4.2, 95% CI: 1.8-9.2), non-college-educated (AOR=3.1, 95% CI: 1.2-5.9) and employed (AOR=1.8, 95% CI: 1.1-1.8) variables and being in one of the moderate or poor quality of life classes. Scores of SQOL-F and FSFI domains, except satisfaction, were significantly worse in cases versus controls (P<0.001)., Conclusion: Although our participants showed low sexual dysfunction, they tended to report moderate to poor quality of sexual life. Our findings support the implication that sexual rehabilitation must be provided for women with SCI soon after injury.

Study Design: An experimental study was conducted to evaluate the effects of methylprednisolone and MK-801 after the compressive injury of spinal cord in rats., Objectives: To investigate the effect of methylprednisolone and non-competitive NMDA antagonist MK-801 in long-term functional outcome after spinal cord injury (SCI)., Methods: A randomized group A of Sprague-Dawley rats were treated with MK-801 (1.0 mg/kg, n=10; Group A) after a compression injury. A group of methylprednisolone (MP)-treated (30 mg/kg, n=10; Group B) and non-treated animals (n=9; Group C) were included for comparison. The functional motor outcome such as inclined plane (IP), toe spreading reflex (TSR), and modified Tarlov scale (TS) were measured in each animal at regular time points up to 8 weeks post-treatment. Histologically the injury site was scored in four groups and immunohistochemically Wallerian Degeneration (WD), astrocytosis and expression of beta-amyloid protein was identified., Results: In examining the IP data, no significant difference was recognized between the group means (P-value>0.5). For the TSR, there were no differences in the group responses. For the TS, the differences were not statistically significant. Only group B showed significance in cavitation scores compared to group A (P>0.0094), WD was significantly different than group C (P>0.03), astrocytosis was significantly higher than group A (P>0.001) and modest presence of beta-amyloid protein., Conclusion: Our data indicate that one time bolus administration of MK-801 lacks any significant effect on axonal function in chronically injured rats. Daily bolus administration of MP at 30 mg/kg also did not ensure a better functional outcome. Immunohistochemically we have been able to show significant differences in WD, astrocytosis and small insignificant changes in beta-amyloid protein.

The demyelination process is an important factor contributing to long term sensory and motor impairments after spinal cord injury (SCI). Exposure of axonal K+ channels after demyelination may contribute to blockage of action potentials across the injury site. A K+ channel blocker, 4-aminopyridine (4-AP), has been effective in restoring some sensory and motor impairment in incomplete SCI patients. The long-term effect of this compound in chronic model of SCI is not known. In this study, after a compression injury of 50 grams in rats, a randomized treatment was initiated 3 weeks after the initial injury which was followed by daily administration of 4-AP at 2 mg/kg (n = 8), 4 mg/kg (n = 8), and 6 mg/kg (n = 8) for 4 weeks. A group of methylprednisolone (MP)-treated (30 mg/kg, n = 8) and non-treated animals (n = 8) were included for comparison. The functional motor outcome was measured in each animal at regular time points up to 4 weeks post-treatment. All animals receiving 6 mg/kg developed generalized seizure and were excluded from the study. In the other animal groups, analysis of the behavioral outcome and neuro-pathological changes were essentially similar and did not show any significant effect of treatment. Our data indicate that daily administration of 4-AP, over 4 weeks of treatment period, lacks any significant effect on axonal function in chronically injured rats. This could be due to (a) lack of significant numbers of demyelinated axons which could improve the functional outcome and (b) a treatment regimen that was not adequate to contribute to a better functional outcome. One time bolus-administration of MP at 30 mg/kg also did not ensure a better functional outcome.

Nine subjects (seven male, two female) underwent transcranial magnetic stimulation (TMS) toward the evaluation of spinal cord injury (SCI). The evaluation of SCI with TMS tended to support clinical findings. Those subjects with clinically complete injuries demonstrated no evoked muscle response below the level of injury. Those subjects with clinically incomplete injuries showed trends toward prolonged evoked muscle latencies on the weaker side. Facilitation tended to enhance distal muscle responses. With incomplete spinal injury, the facilitation maneuver allowed the recording of weak muscle responses as well as those otherwise not present at rest. Maximum anal sphincter contraction also helped facilitate muscle responses and tended to impart less noise in the recordings. Facilitation failed, however to produce a response in those subjects with clinically complete injuries. No subject experienced adverse effects during the study. TMS promises to be an effective tool for the evaluation of SCI.

The post-traumatic release of excitatory amino acids (EAA) and their actions on N-methyl-D-aspartate (NMDA) receptors plays a major role in the spinal cord secondary injury process. The neuronal damage caused by the release of EAA may be reduced by NMDA-receptor channel blockers. To investigate the involvement of NMDA receptors in spinal cord injury (SCI), we pretreated animals with the noncompetitive NMDA antagonist MK801 (1.0 mg kg-1) before a compressive acute SCI. Pretreated animals with MK801 significantly (p = 0.038) improved the recovery of function as measured by evoked potential activities. Morphologically, specimens from rats treated with MK801 were characterized by milder and more localized hemorrhage in the gray matter. Immunohistochemical staining for glial fibrillary acidic protein (GFAP) and neurofilament (NF) histochemistry showed leakage of these antigens in traumatized cord while characteristic staining of astrocytes and neurons and their processes was observed in morphologically preserved tissue. The loss of NF immunoreactivity was reduced by MK801 treatment.

Background: Taxol is a diterpene alkaloid that stimulates tubulin production in cells. It may be effective in preserving the cytoskeleton of spinal cord axons after injury., Methods: Thirty-nine rats were submitted to spinal cord compression. The animals were divided into three groups that received taxol (18.75 mg/m2), methylprednisolone (30 mg/kg), or 4-aminopyridine (1 mg/kg). Taxol was administered as one dose immediately after injury and two additional doses on days 14 and 21. Methylprednisolone was given as a single injection immediately postinjury. Four-aminopyridine was administered on days 25, 26, and 27. A group of nine injured animals served as a control without any treatment. Evoked potentials were recorded before, during, and 4 weeks postinjury. Behavioral tests were measured to evaluate recovery of motor function., Results: The taxol and methylprednisolone-treated animals demonstrated a significant improvement in comparison with the control group. No functional improvement was found at 1 mg/kg treatment of 4-aminopyridine in rats., Conclusions: We conclude that taxol and methylprednisolone given shortly after the compression injury improve functional outcome after an incomplete spinal cord injury.

Many models have been developed to study spinal cord injury (SCI), such as cryogenic lesioning, hot water injury, scalpel lesioning, compressive trauma using clips, electromechanical devices, extradural cuffs, and weight-drop techniques. In this study, the radiofrequency (RF) lesion was used for inducing an experimental SCI in cats. The neuropathology was correlated with the MRI. In this model, 4 cats were injured at the thoracic spinal cord (T11-T12) with a lesion of 65 degrees C for 1 min using a micromanipulated penetrating RF electrode. The MRI of the lesions after 2, 3, 5, and 6 weeks post-injury as well as the correlative histological changes were obtained. The RF-induced lesion was discrete with little spreading across the spinal cord. There was a good correlation between the histopathology findings and the MRI. We conclude that experimental RF lesioning of the spinal cord can produce a consistent lesion with predictable histopathological changes in experimental animals. A 65 degree C injury for 1 min induced a clinical picture of an incomplete SCI. The RF lesioning should be considered as a new model to study SCI, particularly those with a penetrating component.

Fourteen cats were subjected to a moderate (100 gm-cm; n = 7) or a severe (600 gm-cm; n = 7) spinal cord injury at the C4-C5 level using a weight drop technique. Somatosensory evoked potentials (SSEPs) were recorded after stimulation of the median nerve in the forearm. The SSEPs were measured in each animal before and after the injury. Motor evoked potentials (MEPs) were recorded from forearm extensor muscles after transcranial magnetic stimulation of the motor cortex. The SSEPs and The MEPs were measured in each animal before and after the injury under ketamine-based anesthesia. After the moderate injury (n = 7), 83% of the animals (6/7) maintained the SSEPs and 100% (7/7) maintained the MEPs. Postoperatively, only one animal who lost the SSEPs post-injury became tetraplegic. The remainder were neurologically intact. In the severely injured animals (n = 7), 5/7 of animals lost SSEPs and subsequently became tetraplegic. The MEPS were maintained in 3/5 (60%) of these tetraplegic animals. Two of seven animals (40%) in this group did not lose SSEPs or MEPs and recovered with no clinical deficit. Our data show a good correlation between the presence of SSEPs and functional recovery in the injured groups. The presence of MEPs in 3/5 (60%) of the tetraplegic animals may imply the existence of functionally active motor fibers after severe spinal trauma.

Background: The demyelination process has been proven to be an important factor contributing to long-term sensory and motor impairments after spinal cord injury (SCI). The loss of myelin promotes exposure of K+ channels in internodal region of the damaged myelinated axons leading to K+ efflux into the neurons with subsequent blockage of action potentials. The potassium channel blocker 4-aminopyridine (4-AP) has been effective in restoring some sensory and motor impairment in incomplete SCI patients. The effect of this compound given immediately after an acute injury is not known. The objective of this study was to determine if blockage of K+ ions efflux immediately after an acute SCI would improve neuronal conduction in this model of injury., Methods: Cortical somatosensory evoked potentials (SSEPs) were recorded before and after a weight-induced compression injury of 120 grams, and were monitored up to 5 hours postinjury. A randomized treatment was initiated with administration of either vehicle or 4-AP. All 4-AP treatments were given as intravenous bolus injections of 1.0, 0.5, and 0.3 mg/kg at 1, 2, and 3 hours after the trauma., Results: The SSEPs were abolished immediately after the injury in all control and treated animals. Both groups showed spontaneous recovery of the SSEPs at the rate of 44.5% for the 4-AP treated and nontreated groups at the second hour postinjury. This recovery rate remained the same for both groups at the end of the experiments., Conclusions: Based on the recovery of the SSEPs, our data indicate that early administration of 4-AP lacks any beneficial effect on axonal function during acute stage of spinal cord injury.

The effect of bolus injections of 21-aminosteroid U74389F after an acute spinal cord compression trauma in rats was studied. Cortical somatosensory evoked potentials (CSEPs) were recorded before and after a weight-induced injury of 120 g and monitored up to five hours post-injury. All U74389F treatments were given as i.v. bolus injections of 15, 7.5, and 3.75 mg kg-1 at 1, 2, 3 h after the trauma, respectively. The CSEPs were abolished immediately after the injury in the control and treated animals. The majority of the treated animals (88.8%) demonstrated a return of the CSEPs within the second hour post-injury. In contrast, the animals in the control group showed only 44.4% recovery at this time period. At three hours post-injury, U74389F-treated animals (n = 18) showed a full recovery (100%) while the recovery rate remained at 44.4% for the control animals. We conclude that the bolus administration of U74389F one hour after injury facilitates the return of the spinal cord function as measured by the CSEPs in this compression model of acute spinal cord trauma.

The cortical somatosensory evoked potentials (CSEPs) were recorded to determine if the administration of nimodipine improves axonal function after spinal cord injury. Animals receiving a 52 g compression injury (a moderately severe injury) for 5 minutes were randomly allocated to one of five treatment groups. Each group was given an infusion of one of the following nimodipine regiments over 2 hours, commencing 1 hour before compression: placebo (n = 20), 0.5 micrograms/kg (n = 10), 0.25 micrograms/kg (n = 20), 0.125 micrograms/kg (n = 10), and 0.25 micrograms/kg + Hetstarch (n = 10). In the control group, 65% of animals lost the CSEPs immediately after the injury with almost all (95%) of these regaining the CSEPs within 15 minutes after decompression of the spinal cord. In the treated groups, the rate of the CSEP loss was highest in the 0.5 micrograms/kg group. This group also had the lowest CSEP recovery. The proportion of the CSEP loss was essentially the same for the other nimodipine-treated groups, although it seemed that there was an increasing number of nonresponses with increasing the nimodipine dose. Our data indicate lack of any beneficial effects of nimodipine on axonal function as measured by evoked activities in experimental spinal cord injury.

The effect of continuous infusion of lidocaine on acute spinal cord trauma in cats was studied. Intravenous and subarachnoid administration of lidocaine did not alter generation and conduction of the spinal evoked responses (SERs) in intact animals. The cortical somatosensory evoked responses and SERs were abolished after weight drop injuries of 120 and 400 g-cm. No return of the evoked responses occurred within 4 hours after trauma in either the lidocaine- or the saline-treated groups. Loss of SERs and appearance of an evoked injury potential were sensitive determinants of spinal cord injury. We concluded that lidocaine treatment did not facilitate the return of spinal cord function in this model of acute spinal cord injury.

Naloxone, an opiate antagonist, has been reported to improve spinal cord blood flow and restore the neurological function of spinal cord in experimental animals. The present study investigated the short term effect of naloxone infusions in acute preparations. An impact of a 20-g weight dropped from 6 cm high was used to traumatize the thoracolumbar spinal cord in cats. Treatment was started immediately after trauma. The naloxone-treated cats received intrathecal (2 mg in 0.5 ml) as well as systemic (2-mg/kg bolus, 2 mg/kg/hour for 4 hours) doses of naloxone. In the control group, equal volumes of saline were administered. The physiological integrity of the spinal cord as measured by averaged spinal evoked potentials (SEPs) ceased immediately after trauma in both groups. No recovery of the SEP in response to sciatic nerve stimulation occurred in either group during the 4 hours of treatment and monitoring in this study.

The effect of nimodipine on acute spinal cord trauma was studied in cats. Spinal evoked responses (SERs) were abolished after weight drop injury of 100 g-cm. All control animals showed spontaneous recovery of spinal cord function as measured by SERs. Treatment with a moderate intravenous dose of nimodipine resulted in a 32% drop in systemic blood pressure and delay in or failure of spinal cord recovery. We concluded that in this model, nimodipine treatment had deleterious effect on the spinal cord recovery due to the significant associated hypotension. It is likely that marked hypotension in the case of traumatic loss of autoregulation overrides the expected nimodipine-related increase in spinal cord blood flow with resultant additional ischemic damage.