Treatment Of Spinal Cord Trauma Research Articles

The application of artificial intelligence in prehospital treatment of spinal cord trauma

The spinal cord trauma induced by production and accidents in the current society has the characteristics of complicated injuries and difficult treatment, which is an important cause of death and disability of the wounded. With the development of computer technology, artificial intelligence (AI) has been widely used in the field of trauma treatment. The application of AI to assist pre-hospital rescue personnel in rapid and accurate identification and emergency treatment of fatal concomitant injuries, the examination of spinal cord function, spinal stabilization, the transport and evacuation of wounded, and supportive treatment can improve the efficiency of spinal cord trauma treatment and reduce the rate of death and disability.

Enfermedades no degenerativas de la médula espinal

Myelopathy is a diagnostic priority. From his early treatment often depends patient recovery without sequelae. The urgent surgical treatment of spinal cord trauma is essential to prevent paraplegia or quadriplegia while in patients with cervical spondylotic myelopathy is reserved for patients with intractable pain, progressive disease and those associated weakness and neurological symptoms/signs. Transverse myelitis is a focal inflammatory disease. It can be caused by infectious agents, systemic diseases, connective tissue and paraneoplastic, or be the initial manifestation of MS or NMO. Its diagnosis is challenging today. Vascular diseases should be considered in patients with symptoms of acute onset, the most frequent complication of myocardial surgery of thoracoabdominal aneurysm causes. The primary spinal tumors (ependymoma, astrocytoma) or metastatic are infrequent and usually debut of subacute or chronic.

4(α-l-Rhamnosyloxy)-benzyl isothiocyanate, a bioactive phytochemical that attenuates secondary damage in an experimental model of spinal cord injury

4(α-l-Rhamnosyloxy)-benzyl isothiocyanate (glucomoringin isothiocyanate; GMG-ITC) is released from the precursor 4(α-l-rhamnosyloxy)-benzyl glucosinolate (glucomoringin; GMG) by myrosinase (β-thioglucoside glucohydrolase; E.C. 3.2.1.147) catalyzed hydrolysis. GMG is an uncommon member of the glucosinolate group as it presents a unique characteristic consisting in a second glycosidic residue within the side chain. It is a typical glucosinolate found in large amounts in the seeds of Moringa oleifera Lam., the most widely distributed plant of the Moringaceae family. GMG was purified from seed-cake of M. oleifera and was hydrolyzed by myrosinase at neutral pH in order to form the corresponding GMG-ITC. This bioactive phytochemical can play a key role in counteracting the inflammatory response connected to the oxidative-related mechanisms as well as in the control of the neuronal cell death process, preserving spinal cord tissues after injury in mice. Spinal cord trauma was induced in mice by the application of vascular clips (force of 24g) for 1min., via four-level T5–T8 after laminectomy. In particular, the purpose of this study was to investigate the dynamic changes occurring in the spinal cord after ip treatment with bioactive GMG-ITC produced 15min before use from myrosinase-catalyzed hydrolysis of GMG (10mg/kg body weight+5μl Myr mouse/day). The following parameters, such as histological damage, distribution of reticular fibers in connective tissue, nuclear factor (NF)-κB translocation and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκB-α) degradation, expression of inducible Nitric Oxide Synthases (iNOS), as well as apoptosis, were evaluated. In conclusion, our results show a protective effect of bioactive GMG-ITC on the secondary damage, following spinal cord injury, through an antioxidant mechanism of neuroprotection. Therefore, the bioactive phytochemical GMG-ITC freshly produced before use by myrosinase-catalyzed hydrolysis of pure GMG, could prove to be useful in the treatment of spinal cord trauma.

PPAR-α modulate the anti-inflammatory effect of glucocorticoids in the secondary damage in experimental spinal cord trauma

Glucocorticoids (GCs) are effective anti-inflammatory agents widely used in therapeutic approach to treatment of spinal cord trauma. Previous results suggest that peroxisome proliferator activated receptor alpha (PPAR-α), an intracellular transcription factor activated by fatty acids, plays a role in control of secondary inflammatory process associated with spinal cord injury (SCI). With the aim to characterize the role of PPAR-α in GC-mediated anti-inflammatory activity, we tested the efficacy of dexamethasone (DEX), a synthetic GC specific for glucocortioid receptor (GR), in an experimental model of spinal cord trauma induced in mice by the application of vascular clips (force of 24 g) to the dura via a four-level T5–T8 laminectomy, and comparing mice lacking PPAR-α (PPAR-αKO) with wild type (WT) mice. Results indicate that DEX-mediated anti-inflammatory activity is weakened in PPAR-αKO mice, as compared to WT controls. In particular, DEX was less effective in PPAR-αKO, compared to WT mice, as evaluated by inhibition of the degree of spinal cord inflammation and tissue injury, neutrophil infiltration, nitrotyrosine formation, pro-inflammmatory cytokine expression, NF-κB activation, inducible nitric-oxide synthase (iNOS) expression; and apoptosis. This study indicates that PPAR-α can contribute to the anti-inflammatory activity of GCs in SCI.

Combination of dexamethasone and etanercept reduces secondary damage in experimental spinal cord trauma

The aim of our study was to evaluate the therapeutic efficacy of combination therapy with etanercept and dexamethasone (DEX) in vivo in experimental murine model of spinal cord trauma, which was induced by the application of vascular clips (force of 24 g) to the dura via a four-level T5–T8 laminectomy. Spinal cord injury in mice resulted in severe trauma characterized by edema, neutrophil infiltration, and cytokine production followed by recruitment of other inflammatory cells, production of inflammation mediators, tissue damage, apoptosis and disease. Treatment of the mice with etanercept (1.25 mg/kg) and DEX (0.025 mg/kg) when administered as a combination therapy but not as a single treatment significantly reduced the degree of (1) spinal cord inflammation and tissue injury (histological score), (2) infiltration of neutrophils (MPO evaluation), (3) inducible nitric oxide synthase, nitrotyrosine, and cytokines expression (tumor necrosis factor-α and interleukin-1β), (4) and apoptosis (Terminal deoxynucleotidyltransferase-mediated UTP end labeling staining, Fas-ligand expression and Bax and Bcl-2 expression). In a separate set of experiments we have also clearly demonstrated that the combination therapy significantly ameliorated the recovery of limb function (evaluated by motor recovery score). Taken together, our results clearly demonstrate for the first time that strategies targeting multiple proinflammatory pathways may be more effective than a single effector molecule for the treatment of spinal cord trauma.

Chapter 14 Secondary injury mechanisms of spinal cord trauma: a novel therapeutic approach for the management of secondary pathophysiology with the sodium channel blocker riluzole

Traumatic spinal cord injury is a consequence of a primary mechanical insult and a sequence of progressive secondary pathophysiological events that confound efforts to mitigate neurological deficits. Pharmacotherapy aimed at reducing the secondary injury is limited by a narrow therapeutic window. Thus, novel drug strategies must target early pathological mechanisms in order to realize the promise of efficacy for this form of neurotrauma. Research has shown that an accumulation of intracellular sodium as a result of trauma-induced perturbation of voltage-sensitive sodium channel activity is a key early mechanism in the secondary injury cascade. As such, voltage-sensitive sodium channels are an important therapeutic target for the treatment of spinal cord trauma. This review describes the evolution of acute spinal cord injury and provides a rationale for the clinical utility of sodium channel blockers, particularly riluzole, in the management of spinal cord trauma.

Cytokine production in motor neurons by poliovirus replicon vector gene delivery.

Poliovirus replicon vectors transiently express foreign proteins selectively in motor neurons of the anterior horn of the spinal cord. Here we intraspinally inoculated mice transgenic for the poliovirus receptor (PVR) with replicons encoding murine tumor necrosis factor alpha (mTNF-alpha). We detected high-level expression of mTNF-alpha in the spinal cords of these animals at 8-12 h post inoculation; this returned to background by 72 h. The mice exhibited ataxia and tail atony, whereas animals given a replicon encoding green fluorescent protein (GFP) exhibited no neurological symptoms. Histology of spinal cords from mice given the replicon encoding mTNF-alpha revealed neuronal chromatolysis, reactive astrogliosis, decreased expression of myelin basic protein, and demyelination. These animals recovered with only slight residual damage. This study shows that replicon vectors have potential for targeted delivery of therapeutic proteins to the central nervous system and provide a new approach for treatment of spinal cord trauma and neurological disease.

COLOR DOPPLER AND DOPPLER SPECTRAL ANALYSIS IN THE SPINAL CORD OF NORMAL DOGS

Doppler ultrasonography of the spinal cord was performed in 34 normal, anesthetized dogs following hemilaminectomy. This study was part of an investigation to evaluate the efficacy of a 21‐aminosteroid compound and high dose methylprednisolone for the treatment of spinal cord trauma. Grey‐scale images of the canine spinal cord were similar to those described for the spinal cord of people. Doppler waveforms of intraparenchymal spinal arteries exhibited high end diastolic blood flow velocities, indicating low resistance to flow. Doppler values (mean ± SD) for arteries immediately ventrolateral to the central canal were: Peak Systolic Velocity = 5.78 ± 2.5 cm/sec, Minimum Diastolic Velocity = 3.5 ± 1.62 cm/sec, Mean Velocity = 4.45 ± 1.96 cm/sec, Minimum Diastolic Velocity = 3.5 ± 1.62 cm/sec, Mean Velocity = 4.45 ± 1.96 cm/sec, Systolic/Diastolic ratio = 169 ± 0.19, Pulsatility Index = 0.53 ± 0.09, and Resistance Index = 0.4 ± 0.06.

Analysis of mortality of patients after cervical spine trauma

An analysis of 167 deaths occurring among 1000 patients with cervical spine trauma, treated in the early post-traumatic period in the Rehabilitation Institute at Konstancin, has been carried out in this report. The high percentage of deaths is caused by the great number of elderly patients suffering from other illnesses, a large group with complete spinal cord injury, many cases of high cervical trauma (above C5) and by injuries of other organs, in particular of the skull and chest. We believe that the improvement of general health care in the country taking place in Poland lately, together with the progress in treatment of spinal cord trauma, will bring about a considerable decrease in mortality in the immediate future.

Acute enhancement of spinal cord synaptosomal (Na + + K +)-ATPase activity in cats following intravenous methylprednisolone

The acute intravenous administration of high doses of methylprednisolone sodium succinate (15–90 mg/kg) to cats enhanced (Na + + K +)-ATPase activity as much as 2-fold in synaptosomes prepared from lumbar spinal cord removed following drug administration. The effect was apparent within 5 min and was statistically significant at 1 h following a single injection of methylprednisolone 90 mg/kg. (Na + + K +)-ATPase activity had returned to control levels by 24 h post-injection. The implication of these findings to the treatment of spinal cord trauma and the reported neurophysiological effects of glucocorticoids are discussed.

Study of functional recovery produced by delayed localized cooling after spinal cord injury in primates.

N SPITE of the sophisticated advances in modern surgical therapy, the present day management of spinal cord trauma generally remains unsatisfactory. 6,~,:3 Current methods used in the treatment of spinal cord trauma consist of immobilization with skeletal traction, surgical decompression with or without incision of dural coverings, and immediate or delayed bony fusion to provide stabilization. Controversy even exists as to the merits of conservative treatment versus surgical decompression. s,'~,1'-1:~,1~,~7,:~~ Even among those favoring early laminectomy in patients displaying sensory-motor paralysis associated with a spinal fluid block, there is no unanimity of opinion whether the dura should be opened or left intact. In reviewing other approaches to the problem of spinal cord injury, we were impressed with some of the work relating to the protective effect of cold on brain. It has been shown that hypothermia will decrease the cerebral metabolic demand, reduce brain volume, bring about a reduction in the inflammatory response to brain injury, and allow the brain to tolerate extended periods of circulatory arrest? 4,1a-2u24,~'~,~'J,33 It has also been demonstrated that total body cooling to 30~ will protect the spinal cord of the dog during occlusion of the thoracic aorta? 5,16 Because of the accessibility of the injured segment of the spinal cord during surgical laminectomy, an attempt has been made to assess the practical advantages of direct