Early neurosurgical intervention of spinal cord contusion: an analysis of 30 cases / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The incidence of spinal injury with spinal cord contusion is high in developed countries and is now growing in China. Furthermore, spinal cord injury happens mostly in young people who have a long life expectance. A large number of patients thus are wheelchair bound for the rest of their lives. Therefore, spinal cord injury has aroused great concern worldwide. Despite great efforts, recovery from spinal cord injury remains unsatisfactory. Based on the pathology of spinal cord contusion, an idea of early neurosurgical intervention has been formulated in this study.</p><p><b>METHODS</b>A total of 30 patients with "complete" spinal cord injury or classified as American Spinal Injury Association (ASIA)-A were studied. Orthopedic treatment of the injured vertebra (e), internal fixation of the vertebral column, and bilateral laminectomy for epidural decompression were followed directly by neurosurgical management, including separation of the arachnoid adhesion to restore cerebrospinal fluid flow and debridement of the spinal cord necrotic tissue with concomitant intramedullary decompression. Rehabilitation started 17 days after the operation. The final outcome was evaluated after 3 months of rehabilitation. Pearson chi-square analysis was used for statistical analysis.</p><p><b>RESULTS</b>All the patients recovered some ability to walk. The least recovered patients were able to walk with a wheeled weight support and help in stabilizing the weight bearing knee joint (12 cases, 40%). Thirteen patients (43%) were able to walk with a pair of crutches, a stick or without any support. The timing of the operation after injury was important. An optimal operation time window was identified at 4 - 14 days after injury.</p><p><b>CONCLUSIONS</b>Early neurosurgical intervention of spinal cord contusion followed by rehabilitation can significantly improve the locomotion of the patients. It is a new idea of a therapeutic approach for spinal cord contusion and has been proven to be very successful.</p>

Glutamine Synthetase Induced Spinal Seizures in Rats

Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. It is responsible for converting glutamate to glutamine, consuming one ATP and NH3 in the process. Glutamate is neurotoxic when it accumulates in extracellular fluids. We investigated the effects of GS in both a spinal cord injury (SCI) model and normal rats. 0.1-ml of low (2-microM) and high (55-microM) concentrations of GS were applied, intrathecally, to the spinal cord of rats under pentobarbital anesthesia. Immediately after an intrathecal injection into the L1-L3 space, the rats developed convulsive movements. These movements initially consisted of myoclonic twitches of the paravertebral muscles close to the injection site, repeated tonic and clonic contractions and extensions of the hind limbs (hind limb seizures) that spread to the fore limbs, and finally rotational axial movements of the body. An EMG of the paravertebral muscles, fore and hind limbs, showed the extent of the muscle activities. GS (2-microM) caused spinal seizures in the rats after the SCI, and GS (6-microM) produced seizures in the uninjured anesthetized rats. Denatured GS (70 degrees C, 1 hour) also produced spinal seizures, although higher concentrations were required. We suggest that GS may be directly blocking the release of GABA, or the receptors, in the spinal cord.

Therapeutic time window for methylprednisolone in spinal cord injured rat

Recent clinical trials have reported that methylprednisolone sodium succinate administered within 8 hours improves neurological recovery in human spinal cord injury (SCI). Methylprednisolone, however, was ineffective and possibly even deleterious when given more than 8 hours after injury. This finding suggests that a therapeutic time window exists in spinal cord injury. In order to determine the doses, durations and timing of methylprednisolone treatment for optimal neuroprotection, a single or two bolus dose of methylprednisolone (30 mg/kg) was administered at 10, 30, 120, 150 and 240 min. after three graded spinal cord injury. The primary outcome measure was 24-hour spinal cord lesion volumes estimated from spinal cord Na+ and K+ shifts. A single 30 mg/kg dose of methylprednisolone at 10 min. after injury significantly reduced 24-hour lesion volumes in injured rat spinal cords. However, any other methylprednisolone treatment starting 30 min. or more after injury had no effect on 24-hour lesion volumes compared to the vehicle control group. Moreover, delayed treatment increased lesion volumes in some cases. These results suggest that the NYU SCI model has a very short therapeutic window.

Pre-injury Treatment of Methylprednisolone in Experimental Spinal Cord Injury

The purpose of this study was to establish whether pre-injury administration of the methylprednisolone sodium succinate(MP) is effective for the treatment of acute spinal cord injury in rat, as it has ben demonstrated that high dose of MP is effective in the treatment of acute spinal cord injury. Spinal cord injury was made by dropping a rod weighing 10 gm from a height of 1.25, 2.5, and 5.0cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. In order to determine the effectiveness, single dose of 5, 15 and 30mg/kg of MP was administrated at 10 minute before injury. The primary outcome was 24-hour spinal cord lesion volume estimated from spinal cord Na+ and K+ shifts. Surprisingly, we failed to find any statistically significant preventive effect compare to control vehicle. Until this result is clearfied, we recommend that acute pre-injury MP therapy be cautiously applied in operating room. The possible causes of this unexpected result are discussed.

Serotonin 1A Receptor Agonist(8 OH DPAT) Reduces Tissue Lesion Volume in the Rat Middle Cerebral Artery Occlusion Model of Ischemia

We studied the effectiveness of serotonin 1a agonist(8 OH DPAT) on the 24 hour ionic lesion volume produced by permanent occlusion of the middle cerebral artery(MCAo) in rats. A 4-hour intravenous infusion of 30 micro mg/kg/hr of 8 OH DPAT were given starting at 10 minutes after occlusion. Tissue concentrations of Na, K, and water at infarct and peri-infarct zone were measured by atomic absorption spectroscopy and by wet-dry weight measurements 24 hours after occlusion. Compared with vehicle treatment, 8 OH DPAT treatment reduced tissue water accumulation by 10% and 55% in the frontopyriform cortex(L1) and frontoparietal cortex(L2), sodium accumulation by 20% at L1 and 47% at L2, potassium loss by 24% at L1 and 44% at L2, cell volume fraction loss by 24% at L1 and 47% at L2. Finally the treatment reduced overall lesion volume by about 37%. All these changes were statistically significant at p<0.05. Our findings suggest strongly that 8 OH DPAT is neuroprotective in the rat MCAo model of focal cerebral ischemia.