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At least 343 records · Page 19Linked to original sources
PubMed2006

Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury.

Spinal cord injuries above mid-thoracic levels can lead to a potentially life-threatening hypertensive condition termed autonomic dysreflexia that is often triggered by distension of pelvic viscera (bladder or bowel). This syndrome is characterized by episodic hypertension due to sudden, massive discharge of sympathetic preganglionic neurons in the thoracolumbar spinal cord. This hypertension is usually accompanied by bradycardia, particularly if the injury is caudal to the 2nd to 4th thoracic spinal segments. The development of autonomic dysreflexia is correlated with aberrant sprouting of peptidergic afferent fibers into the spinal cord below the injury. In particular, sprouting of nerve growth factor-responsive afferent fibers has been shown to have a major influence on dysreflexia, perhaps by amplifying the activation of disinhibited sympathetic neurons. Using a model of noxious bowel distension after complete thoracic spinal transection at the 4th thoracic segment in rats, we selectively altered C-fiber sprouting, at specified spinal levels caudal to the injury, with microinjections of adenovirus encoding the growth-promoting nerve growth factor or the growth-inhibitory semaphorin 3A. This was followed by assessment of physiological responses to colorectal distension and subsequent histology. Additionally, anterograde tract tracers were injected into the lumbosacral region to compare the extent of labeled propriospinal rostral projections in uninjured cords to those in cords after complete 4th thoracic transection. In summary, overexpression of chemorepulsive semaphorin 3A impeded C-fiber sprouting in lumbosacral segments and mitigated hypertensive autonomic dysreflexia, whereas the opposite results were obtained with nerve growth factor overexpression. Furthermore, compared to naïve rats, there were significantly more labeled lumbosacral propriospinal projections rostrally after thoracic injury. Collectively, our findings suggest that distension of pelvic viscera increases the excitation of expanded afferent terminals in the disinhibited lumbosacral spinal cord. This, in turn, triggers excitation and sprouting of local propriospinal neurons to relay visceral sensory stimuli and amplify the activation of sympathetic preganglionic neurons in the thoracolumbar cord, to enhance transmission in the spinal viscero-sympathetic reflex pathway. These responses are manifested as autonomic dysreflexia.

Adrenergic Fibers↗
PubMed1997

Increased calpain content and progressive degradation of neurofilament protein in spinal cord injury.

Spinal cord injury was induced in rat by weight drop. The extent of degradation of neurofilament proteins in the lesion following trauma was examined and served as a measure of calpain activity. Calpain was identified in the samples by myelin mcalpain antibody and the content was estimated from the immunoblot. There was progressive degradation of both 68 kDa and 200 kDa neurofilament proteins in the cord lesion at intervals after injury. At 30 min after injury there was 20% degradation of both neurofilament proteins while the breakdown of 68 kDa and 200 kDa NFPs amounted to more than 60% at 24 h and beyond. Calpain content progressively increased in the lesion by 22% at 30 min to 91% at 4 h after trauma compared to control and then decreased but remained elevated for up to 72 h following injury. These results suggest that calpain is a primary responder synthesized early in injury and involved initially in the breakdown of cytoskeletal proteins in spinal cord trauma. Later in the injury cascade, increased calpain activity is derived from inflammatory as well as endogenous cells supporting a pivotal role for calpain throughout the process of secondary and evolving tissue damage in spinal cord trauma.

Animals↗
PubMed1983

[Computer tomographic diagnosis of spinal injuries].

The examination of patients with spinal trauma by computed tomography offers a direct view into the spinal canal. A stenosis of the spinal canal by fragments of a fracture or haematoma is recognized easily; myelography has become redundant. For the injured patient computed tomography is connected with only a minimal risk.

Fractures, Bone↗
PubMed1980

Orthopedic management of the patient with a spinal injury.

I have tried to make clear that there are no absolute principles in the orthopedic management of patients with a spinal cord injury. Although debate continues regarding the approach to the problem, the goals remain optimal patient care, free of complications, and preparation for a smooth transition of the patient into a new life with handicaps. Most strides in spinal cord injury care have been made in improvement of internal fixation and immobilization, advances in rehabilitation techniques and marked shortening of hospitalization. Active research continues to investigate the pathophysiology of the injury and a means of reversing or impeding the damage to neural tissue. Currently, certain spinal cord injuries are considered irreversible despite treatment with spinal cord hypothermia, reanastomosis of spinal cords or administration of enzyme injections. The person with a spinal cord injury and paralysis rarely loses the hope that a cure might be the next great discovery of medical science and active spinal cord injury research centers have the same goal.

Adult↗
PubMed2004

Variation in urological practice amongst spinal injuries units in the UK and Eire.

AIMS: To investigate variations in common urological practice between the Spinal Injuries Units (SIU) of UK and Eire. METHODS: In December 2002, each of the 12 SIU in the UK and Eire were sent a questionnaire addressing basic practice relating to urological outpatient follow-up, management of urinary tract infection, upper tract surveillance, and urodynamic studies. RESULTS: Regarding frequency of urological review, two units only saw patients when specifically required. One unit reviewed patients every 6 months and six centres reviewed patients annually. The remaining three units had a patient-specific follow-up protocol. Regarding urinary tract infection, only five units had a unified departmental management protocol. Four units advocated antibiotic prophylaxis for recurrent UTI. Only one unit would routinely treat asymptomatic UTI in individuals using catheters. The range of recommended duration of treatment for symptomatic UTI was 3-14 days (mean 6.3). All units performed routine upper tract screening, ranging from annually to every 3 years. Six units did not perform routine urodynamic studies; in other units the range of frequency of urodynamics was from annually to every 3 years. CONCLUSIONS: The variation in urological practice amongst SIU in the UK and Eire is considerable. This finding supports the need for an increase in the level of collaboration and research.

Follow-Up Studies↗
PubMed1997

Audit of a British Centre for spinal injury.

The aim of this study was to determine the benefits of patients admitted early to the specialist spinal injuries centre. The results show a significant reduction in the incidence of pressure sores in the early admitted patients and demonstrate the lowered incidence of both preventable and non preventable complications, as well as reduction of hospitalisation time.

Adult↗
PubMed1986

Unilateral chest wall paradoxical motion mimicking a flail chest in a patient with hemilateral C7 spinal injury.

After a lower hemi-cervical spinal cord injury, a patient presented with a left hemiplegia and on the same side a unilateral chest wall paradoxical motion mimicking a flail chest. X-rays demonstrated a left hemilateral C6 injury but no rib fractures. We demonstrated that the paradoxical motion was due to the action of the diaphragm acting on the rib cage with intercostal respiratory paralysis on the side of hemiplegia.

Diagnosis, Differential↗
PubMed2002

T cell-based therapeutic vaccination for spinal cord injury.

Spinal cord injury results in a massive loss of neurons, due not only to the direct effects of the primary injury but also to self-destructive processes triggered by the insult. Our group has recently reported that traumatic injury of the central nervous system (CNS) spontaneously evokes a purposeful T cell-mediated autoimmune response that reduces the injury-induced degeneration in the CNS; in its absence, the outcome of the injury is worse. Using a rat model of spinal cord contusion, we show here that this autoimmune protection can be induced and/or boosted by post-traumatic immunization with CNS myelin-associated self antigens such as myelin basic protein (MBP). In an attempt to reduce the risk of pathogenic autoimmunity while retaining the benefit of the immunization, we immunized spinally injured rats with MBP-derived peptides with attenuated pathogenic properties created by replacement of one amino acid in the T cell receptor-binding site. Immunization with these altered peptide ligands immediately after spinal cord contusion resulted in a significant improvement in recovery, assessed by locomotor activity in an open field. The feasibility of T cell-based vaccination, as opposed to vaccination mediated by antibodies for the treatment of nerve trauma, is further suggested by the relatively rapid onset of the T cell response following immunization. Such cell-mediated therapy is not only a way to evoke and boost a physiological remedy; it also has the advantage of being mediated by mobile cells, which can produce a variety of neurotrophic factors and cytokines in accordance with the tissue needs. T cells can also regulate other immune cells in a way that favors tissue maintenance and repair.

Animals↗
PubMed2006

Neutralization of the chemokine CXCL10 reduces apoptosis and increases axon sprouting after spinal cord injury.

Spinal cord injury (SCI) is followed by a secondary degenerative process that includes cell death. We have previously demonstrated that the chemokine CXCL10 is up-regulated following SCI and plays a critical role in T-lymphocyte recruitment to sites of injury and inhibition of angiogenesis; antibody-mediated functional blockade of CXCL10 reduced inflammation while enhancing angiogenesis. We hypothesized, based on these findings, that the injury environment established by anti-CXCL10 antibody treatment would support greater survival of neurons and enhance axon sprouting compared with the untreated, injured spinal cord. Here, we document gene array and histopathological data to support our hypothesis. Gene array analysis of treated and untreated tissue from spinal cord-injured animals revealed eight apoptosis-related genes with significant expression changes at 3 days postinjury. In support of these data, quantification of TUNEL-positive cells at 3 days postinjury indicated a 75% reduction in the number of dying cells in treated animals compared with untreated animals. Gene array analysis of treated and untreated tissue also revealed six central nervous system growth-related genes with significant expression changes in the brainstem at 14 days postinjury. In support of these data, quantification of anterograde-labeled corticospinal tract fibers indicated a 60-70% increase in axon sprouting caudal to the injury site in treated animals compared with untreated animals. These findings indicate that anti-CXCL10 antibody treatment provides an environment that reduces apoptosis and increases axon sprouting following injury to the adult spinal cord.

Animals↗
PubMedDate not supplied

Characteristics of patients with cervical spinal injury requiring permanent pacemaker implantation.

Acute cervical spinal cord injury frequently results in bradydysrhythmia, which may lead to hypotension and asystole. Such symptoms are more common in the first 2 weeks after the injury. Treatment modalities include atropine, epinephrine, aminophylline, and pacemaker insertion. The criteria for pacemaker use in this population are not well defined. We describe characteristics of 3 patients who required permanent, transvenous pacemaker implantation for recurrent symptoms. In 2 of the 3 patients, transcutaneous pacing failed to provide adequate protection. Transcutaneous pacemakers are not reliable, as was the case of these patients, and early consideration for transvenous pacemaker insertion may be indicated, especially in hemodynamically unstable patients. In this report, all 3 patients required permanent pacemaker implantation.

Adult↗
PubMed2006

[Labor management using epidural anesthesia in a gravida patient with high spinal injury].

Since autonomic hyperreflexia (AH) is a serious complication during labor in a gravida with spinal cord injury, anesthetic measures should be taken for the suppression of AH even in a sensory-loss condition. Several reports have described various methods for the suppression of AH, in which epidural anesthesia has been advocated as a useful means for the prevention or amelioration of AH. However, it is difficult to evaluate the efficacy of epidural anesthesia due to the lack of sensory and motor functions. We report a primipara who had spinal cord injury below the T 3 level at the age of 17 due to a traffic accident and underwent successful vaginal delivery twice under epidural anesthesia at the ages of 30 and 32. For the first delivery, we placed two epidural catheters. We controlled the rate and the content of epidural infusion through the two different injection sites so as to meet delivery process. For the second delivery we did epidural anesthesia in the same way. Tubal-ligation was also performed under epidural anesthesia after the second delivery. No major obstetric complication including AH occurred in either of delivery. The woman with high spinal injury could have two healthy children without major complications during labor by the cooperation of gynecologists and anesthesiologists.

Adult↗
PubMed1998

Graded thoracolumbar spinal injuries: development of multidirectional instability.

Injuries of the thoracolumbar spine are serious, disabling, and costly to society. These injuries vary from mild ligament tears to severe bony fractures. Increased range of motion (ROM) and neutral zone (NZ) have been suggested as indicators of the resulting clinical instability. The purpose of the present study was to investigate the relative sensitivities and merits of the ROM and NZ in relation to spinal injuries of the thoracolumbar junction. A graded spinal trauma experiment was designed, in which the threshold of injury and injury progression were examined. Ten thoracolumbar human spine specimens (T11-L1) were traumatized using a high-speed incremental trauma model. The ROM and NZ, which indicate altered mechanical properties, were determined for three physiological motions: flexion/extension (FE), lateral bending (LB), and axial rotation (AR). The injury threshold was found to be 84 J (or 84 Nm) by examining both ROM and NZ for all motion types (P < 0.05), but the NZ was more sensitive. At the injury threshold, the NZ showed an overall average increase of 566% above that of the intact, while the equivalent increase in the ROM was only 94%. The NZ was also a more sensitive parameter documenting the progression of the injury beyond the injury threshold. After the maximum trauma of 137 J, the NZs for the three motions (FE, LB, and AR) increased by 700%, 1700%, and 3000% above their respective intact values. Corresponding increases in the ROM were much smaller: 115%, 184%, and 425% respectively. Direct extrapolation of the in vitro experimental findings to the clinical situation, as always, should be done with care. Our findings, however, suggest that the ROM, as measured from functional radiographs of a traumatized patient, may underestimate the true injury to the spinal column.

Adult↗
PubMed2000

Induction of VEGF and VEGF receptors in the spinal cord after mechanical spinal injury and prostaglandin administration.

Vascular endothelial growth factor (VEGF) is an angiogenetic factor that promotes endothelial cell proliferation during development and after injury to various types of tissue, including the central nervous system (CNS). Using immunohistochemical and in situ hybridization methods we have here demonstrated that VEGF and its receptors Flk-1, Flt-1 and Neuropilin-1 mRNAs and proteins are induced after incisions in the rat spinal cord. The inducible enzyme for prostaglandin synthesis cyclooxygenase-2 (COX-2) is known to be upregulated after spinal injury, cerebral ischemia and to stimulate angiogenesis. To test the hypothesis that prostaglandins may be involved in the VEGF response after lesion we investigated whether intraspinal microinjections of prostaglandin F2alpha (PGF2alpha) alters VEGF expression in the spinal cord. Such treatment was followed by a strong upregulation of VEGF mRNA and protein in the injection area. Finally, by use of an in vitro model with cell cultures of meningeal fibroblast and astrocyte origin, resembling the lesion area cellular content after spinal cord injury but devoid of inflammatory cells, we showed that VEGF is expressed in this in vitro model cell system after treatment with PGF2alpha and prostaglandin E2 (PGE2). These data suggest that cells within a lesion area in the spinal cord are capable of expressing VEGF and its receptors in response to mechanical injury and that prostaglandins may induce VEGF expression in such cells, even in the absence of inflammatory cells.

Animals↗