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PubMed1992

Spinal cord injury: preventing secondary injury.

Spinal cord injury is devastating to the victim, as well as being costly in terms of medical expenses, lost wages, and lost independence. The initial damage to the spinal cord results from several mechanisms of injury--flexion, extension, compression, penetration, rotation, and the disease process. When the spinal cord is injured and there is necrosis of the nervous tissue, no regeneration of that tissue occurs. Unlike in the peripheral nervous system, where regeneration is possible, the spinal cord is part of the central nervous system, as is the brain. The spinal cord extends from the base of the skull to the L1 vertebrae: the cervical levels innervate the diaphragm and muscles of the arms; the thoracic levels innervate the muscles of the chest and abdomen; and the lumbar and sacral levels innervate the muscles of the legs. In addition, the sacral levels are responsible for bowel, bladder, and sexual function. The higher the level of injury, the more severe the loss of function because, not only is the level of injury affected, but also the levels below. Injury occurs by initial trauma to the surrounding ligaments, bones, and muscles, which then affect the spinal cord. There may be total loss of function with damage completely across the cord or partial loss of function with damage affecting only part of the cord. No current treatment can reverse this initial injury, which causes irreversible damage within minutes of injury. Secondary damage occurs as the injury spreads over several hours. Treatment can help prevent this secondary damage.

Biomechanical Phenomena↗
PubMed1985

Changes in substance P and somatostatin in the spinal cord after traumatic spinal injury in the rat.

Immunoreactive substance P (SPI) and somatostatin (SOMI) are found in spinal cord but their physiological roles remain speculative. Several classes of neuropeptides, including endogenous opioids and thyrotropin-releasing hormone (TRH), have been implicated in the pathogenesis or recovery from spinal cord injury. In the present studies, changes in SPI and SOMI were examined in the spinal cord after traumatic injury in the rat. Both peptides showed time-dependent, localized decreases at the injury site, which were statistically related to the degree of post-traumatic neurological dysfunction. Such changes differ from those of a number of other peptides after spinal injury and suggest that substance P and/or somatostatin may play a role in the secondary pathophysiological responses which follow trauma to the spinal cord.

Animals↗
PubMed1999

Spinal injuries in the Plateau State, Nigeria.

OBJECTIVE: To highlight the epidemiology, management and outcome of spinal cord injuries (SCI) in the Plateau State of Nigeria. DESIGN: A retrospective study involving case note analysis of all patients with SCI admitted into the hospital. SETTING: The study was carried out at the Jos University Teaching Hospital to cover January 1984 and December, 1997. SUBJECTS: Sixty eight cases of SCI were studied. INTERVENTIONS: Patients were managed by conservative and operative interventions especially in cervical subluxations involving C5 on C6. MAIN OUTCOME MEASURES: Neurological function was assessed employing Frankel scale. RESULTS: There was an increased hospital incidence for SCI between 1994 and 1997. Means age of presentation was 30 years and sex ratio M:F was 10:1. Vehicular accidents accounting for 49 per cent of SCIs and collapsed tunnels (26 per cent) were the two common causes. Fracture dislocation of the spine (unstable) occurred in 52 per cent and flexion wedge fractures (stable) in 14 per cent. Ten per cent of patients had no neural deficits at presentation, 21 per cent had partial cord lesions and 69 per cent complete cord lesions. Hospital mortality was 26 per cent. The four patients subjected to posterior spinal fusion, (Frankel A to E) including 8 other patients that were conservatively managed. CONCLUSION: Centres for spinal injuries should be established incorporating hospital wards, theatres, gymnasia, nursing units, occupational therapy units, activity centres and workshops. These centres will generate comprehensive data on morbidity and morality needed for future planning.

Adolescent↗
PubMedDate not supplied

Etiological and functional evaluation of the pediatric population with spinal cord injuries.

Spinal cord lesions are the result of many etiological factors and are associated with motor, sensorial and autonomic dysfunctions. The subjects evaluated were a total of 217 paraplegics and quadriplegics who had been enrolled in a rehabilitation program during the last five years conducted by the Department of Physical Medicine and Rehabilitation of the Hacettepe University Faculty of Medicine. Forty-three of these patients were in the pediatric age group. In this clinical trial, the patients with spinal cord injuries were examined according to their age, sex, etiological factors and functional status. Frankel's scale was used for functional assessment. The mean age of patients was 9.19 +/- 4.19 years and varied between 1-16 years. The results of our classification according to etiological factors were as follows: Nineteen patients with tumors (44.1%), nine patients with infections (20.93%), five patients with congenital abnormalities (11.63%), five patients with vascular lesions (11.63%), four patients with trauma (9.30%), and one patient with a degenerative central nervous system disorder (2.32%). The effect of the rehabilitation program on the functional status of the patients is discussed.

Adolescent↗
PubMed1982

Gastrointestinal bleeding in patients with acute spinal injuries.

Twenty out of 365 patients (5.5 per cent) with acute spinal cord injuries referred to a spinal ward over a 91/2-year period bled from the gastrointestinal tract. A cause of the haemorrhage was found in 15 patients. Six patients were endoscoped. Most patients had gastroduodenal ulceration but we could not be certain whether this was due to stress or peptic ulceration. We did not confirm that cervical cord lesions were associated with a higher incidence of gastrointestinal bleeding. The 4 patients who died probably represent an "inevitable' mortality in severely ill patients. The role of endoscopy is outlined, the pathogenesis of gastrointestinal ulceration discussed and future management of these patients is suggested.

Gastrointestinal Hemorrhage↗
PubMed2004

Cardiovascular control after spinal cord injury.

Spinal cord injury (SCI) leads to profound haemodynamic changes. Constant outflows from the central autonomic pattern generators modulate the activity of the spinal sympathetic neurons. Sudden loss of communication between these centers and the sympathetic neurons in the intermediolateral thoracic and lumbar spinal cord leads to spinal shock. After high SCI, experimental data demonstrated a brief hypertensive peak followed by bradycardia with escape arrhythmias and marked hypotension. Total peripheral resistance and cardiac output decrease, while central venous pressure remains unchanged. The initial hypertensive peak is thought to result from direct sympathetic stimulation during SCI and its presence is anaesthetic agent dependent. Hypotension improves within days in most animal species because of reasons not totally understood, which may include synaptic reorganization or hyper responsiveness of alpha receptors. No convincing data has demonstrated that the deafferented spinal cord can generate significant basal sympathetic activity. However, with the spinal shock resolution, the deafferented spinal cord (in lesions above T6) will generate life-threatening hypertensive bouts with compensatory bradycardia, known as autonomic hyperreflexia (AH) after stimuli such as pain or bladder/colonic distension. AH results from the lack of supraspinal control of the sympathetic neurons and altered neurotransmission (e.g. glutamatergic) within the spinal cord. Despite significant progress in recent years, further research is necessary to fully understand the spectrum of haemodynamic changes after SCI.

Animals↗
PubMed1985

Data on spinal injuries--Part I. Collection and analysis of 352 consecutive admissions.

A prospective system of data collection, using computer storage, has been developed in the Spinal Injuries Unit, Austin Hospital. Three hundred and fifty-two consecutive admissions to the Unit between 1 July 1978 and 31 December 1982 are analysed, and this epidemiological data compared with other reports. Over 92% of the admissions were the result of spinal cord trauma and the balance due to a variety of non-traumatic causes. A high incidence of young males injured in road accidents, predominantly from motor cars, and lesser numbers from sporting, occupational and domestic accidents is noted. A high proportion of country accidents and a disproportionately high number of people who live in country areas indicates the need for greater concentration of preventative measures to rural areas. The study has confirmed the usefulness of such a sophisticated data collection system to collect, at relatively low cost, useful epidemiological data on a specific disability group. The system will help to plan treatment programmes, as well as preventative measures, for the future.

Accidents, Traffic↗
PubMed1997

Transplant therapy: recovery of function after spinal cord injury.

Spinal cord injuries (SCI) result in devastating loss of function and altered sensation. Presently, victims of SCI have few remedies for the loss of motor function and the altered sensation often experienced subsequent to the injury. A goal in SCI research is to improve function in both acute and chronic injuries. Among the most successful interventions is the utilization of transplanted tissues toward improved recovery. The theory is that the transplanted tissue could (1) bridge the spinal lesion and provide chemical and/or mechanical guidance for host neurons to grow across the lesion, (2) bridge the spinal lesion and provide additional cellular elements to repair the damaged circuitry, (3) provide factors that would rescue neurons that would otherwise die and/or modulate neural circuits to improve function. A variety of tissues and cells have been added to the adult mammalian spinal cord to encourage restoration of function. These include Schwann cells, motor neurons, dorsal root ganglia, adrenal tissue, hybridomas, peripheral nerves, and fetal spinal cord (FSC) tissue en bloc or as disassociated cells. It is postulated that these tissues would rescue or replace injured adult neurons, which would then integrate or promote the regeneration of the spinal cord circuitry and restore function. In some instances, host-appropriate circuitry is supplied by the transplant and functional improvement is demonstrated. In this presentation, specific examples of recent work with transplanted tissue and cells that demonstrate improved behavioral outcome are presented. New recent work describing the in vitro propagation and characterization of human fetal spinal cord multipotential progenitor cells are also described in the context of a potential resource for transplantable cells. Additionally, data from transplantation experiments of human FSC cells into nonimmunosuppressed rat spinal cord are described, and the resultant improvements in behavioral outcome reported. Lastly, directions for future SCI research are proposed.

Animals↗
PubMedDate not supplied

Enoxaparin for thromboembolism prophylaxis in spinal injury: preliminary report on experience with 105 patients.

Venous thromboembolism continues to be a major cause of morbidity and mortality in patients with spinal injury (SI). Recently, we reported on the effectiveness and safety of a low molecular weight heparin (LMWH), tinzaparin, in preventing deep vein thrombosis in motor-complete SI patients. Recently, another LMWH, enoxaparin, was approved by the United States Food and Drug Administration for prevention of thromboembolism in hip and knee replacement surgery. Since its approval, we have used 30 mg of enoxaparin subcutaneously every 12 h as routine prophylaxis in all hospitalized SI patients. In this retrospective study, we present an analysis of safety and efficacy of the first six months experience, during which 105 patients received the drug. No patient developed clinical evidence of thromboembolism, and none of the 60 venous ultrasound examinations showed a deep vein thrombus. Eleven patients had evidence of hemorrhage, but the LMWH was considered to have contributed to the bleeding in only three. This additional experience with enoxaparin reinforces our previous conclusion that LMWHs are safe and effective thromboprophylactic agents in SI patients.

Adolescent↗
PubMed2005

Neural plasticity after spinal cord injury.

Spinal cord injury (SCI) has devastating physical and socioeconomical impact. However, some degree of functional recovery is frequently observed in patients after SCI. There is considerable evidence that functional plasticity occurs in cerebral cortical maps of the body, which may account for functional recovery after injury. Additionally, these plasticity changes also occur at multiple levels including the brainstem, spinal cord, and peripheral nervous system. Although the interaction of plasticity changes at each level has been less well studied, it is likely that changes in subcortical levels contribute to cortical reorganization. Since the permeability of the blood-brain barrier (BBB) is changed, SCI-induced factors, such as cytokines and growth factors, can be involved in the plasticity events, thus affecting the final functional recovery after SCI. The mechanism of plasticity probably differs depending on the time frame. The reorganization that is rapidly induced by acute injury is likely based on unmasking of latent synapses resulting from modulation of neurotransmitters, while the long-term changes after chronic injury involve changes of synaptic efficacy modulated by long-term potentiation and axonal regeneration and sprouting. The functional significance of neural plasticity after SCI remains unclear. It indicates that in some situations plasticity changes can result in functional improvement, while in other situations they may have harmful consequences. Thus, further understanding of the mechanisms of plasticity could lead to better ways of promoting useful reorganization and preventing undesirable consequences.

Animals↗
PubMed1977

Open reduction of unstable thoracolumbar spinal injuries and fixation with Harrington rods.

The results of treatment of sixteen patients with unstable thoracolumbar spinal injuries are recorded. Early open reduction, stabilization with Harrington rods, spine fusion, application of a plaster jacket until consolidation, and early mobilization was the treatment. Distraction rods were used in twelve patients and compression rods, in four. Nine patients with incomplete paraplegia showed marked neurological recovery, while five with complete paraplegia regained only some sensation. Two patients had no neurological involvement. Solid fusion was achieved in fifteen patients after a minimum of three months of plaster-cast immobilization. In one patient stabilization failed. There was a loss of 5 degrees on average (range, 2 to 23 degrees) in the correction of the kyphosis. Lateral angulation after surgery did not occur. The treatment allowed easier postoperative nursing and early mobilization of the patient.

Adolescent↗
PubMed1988

[Classification and prognosis of spinal injuries].

ABCD-0123-CLASSIFICATION: Taking into consideration the known classifications, a new scale of spiral injuries has been developed in which the three osteoligamentous columns (= three column spine) of the axial organ are designated by the letters A, B, and C. The letter D denotes the discoligamentous structures. This classification includes constriction of the spinal canal, whereby constriction of 1/3 is given the number 1, 2/3 the number 2, 3/3 the number 3, and no constriction 0. The prognosis of spinal injuries depends on many factors, especially the following: 1. Severeness of injury, 2. Time of operation, 3. Operation team, 4. Result of reconstruction and degree of stability, 5. Fusion distance, 6. Other diseases, and 7. Postoperative care. A good reconstruction of the spinal canal and good stability by short fusion in the injured part of the spine are very important for prognosis.

Humans↗
PubMed2003

Dual diagnoses: the person with a spinal cord injury and a concomitant brain injury.

Spinal cord injury (SCI) alone is a devastating event that often results in physical disability. When the SCI is combined with a brain injury, the degree of disability can be magnified and the patient's rehabilitation becomes further complicated. It is not unusual for the head injury to be overlooked or undetected during the emergent and acute phases of treatment. The brain injury may first appear when the client demonstrates an inability or resistance to carry out functional activities appropriate to his/her level of injury. Cognitive deficits can limit or complicate the client's ability to adapt to his/her physical limitations, learn compensatory skills, and achieve the maximal level of independence. These patients require a wide base of physical, psychological, educational, and medical support. Because they are at a high risk for developing complications, they will require lifelong interventions and involvement from an interdisciplinary team to provide a safety net. The following article examines the patient with dual diagnoses of SCI and brain injury. A comprehensive review of commonly encountered problematic scenarios and interventions is presented.

Autonomic Nervous System Diseases↗
PubMed1996

Mechanical and thermal allodynia in chronic central pain following spinal cord injury.

Spinal cord injury (SCI) results in variable motor recoveries and chronic central pain syndromes develop in the majority of SCI patients. To provide a basis for further studies, we report a new rodent model of chronic central pain following spinal cord trauma. Male Sprague-Dawley rats (N = 10) were hemisectioned at T13 and were tested both preoperatively and postoperatively and compared to sham-operated controls (N = 10) for locomotor function, and mechanical and thermal thresholds of both paw withdrawal and supraspinal responses. Results support the development and persistence of allodynia which persists for 160 days. Locomotor function was tested using the Basso, Beattie and Bresnahan (BBB) open field test and only the limb ipsilateral to the hemisection was affected, demonstrating acute flaccid paralysis with motor recovery which approached normal values by postoperative day (POD) 15. Prior to the hemisection, the rats showed little to no paw withdrawal response to von Frey stimulation of 4.41 mN or 9.41 mN in both forelimbs and hindlimbs. Postoperatively, responses in both ipsilateral and contralateral forelimbs and hindlimbs increased over time and the increase was statistically significant compared to intra-animal presurgical and sham control values (P < 0.05). There were no significant side-to-side differences in limb responses preoperatively or beyond POD 15. The forelimbs and hindlimbs responded to von Frey hair strengths of 122 mN preoperatively and postoperatively with similar withdrawal frequencies that were not statistically significant. Preoperatively, the paw withdrawal latency to heat stimuli was 22.9 +/- 3.0 (mean +/- SE) and 20.1 +/- 3.1 sec for the hindlimbs and forelimbs, respectively. Postoperatively, the mean hindlimb and forelimb latency of paw withdrawals decreased to 11.9 +/- 1.8 and 9.2 +/- 2.5 sec, respectively. This decrease in thermal thresholds is statistically significant when compared to intra-animal preoperative and sham control values (P < 0.05). These data indicate that somatosensory thresholds for non-noxious mechanical and radiant heat which elicit paw withdrawal (flexor reflex) are significantly lowered following SCI. To further support the development and persistence of chronic pain following hemisection, supraspinal responses such as paw lick, head turns, attacking the stimulus, and vocalizations were elicited in response to mechanical and thermal stimuli and were statistically significant compared to presurgical intra-animal or sham control values (P < 0.05). Hemisected animals vocalized to von Frey hair bending forces of 49.8 with a mean of 6.0 +/- 1.2 times out of 10 stimuli compared to intra-animal presurgical and sham control values of zero. Supraspinal responses of hemisected animals to thermal stimuli occurred at lower temperatures that were statistically significant compared to sham control or preoperative values (P < 0.05). These chronic changes in thresholds to both mechanical and thermal stimuli represent the development and persistence of mechanical and thermal allodynia after SCI.

Animals↗
PubMed2004

The 5-HT3 receptor facilitates at-level mechanical allodynia following spinal cord injury.

Spinal cord injury (SCI) results in the development of mechanical allodynia immediately rostral to the lesion site, within the dermatome border of normal sensation and sensory loss (at-level mechanical allodynia). We propose that an observed threefold increase in serotonergic fibre immunoreactivity within spinal segments corresponding to these allodynic dermatomes facilitates the maintenance of chronic neuropathic pain via activation of the 5-HT(3) receptor (5-HT(3)-R). Serotonin (5-HT), the non-selective 5-HT(1)/5-HT(2) receptor antagonist, methysergide, the 5-HT(3)-R agonist, m-chlorophenylbiguanide (m-CPBG) or the 5-HT(3)-R antagonist, ondansetron were intrathecally administered five weeks following SCI in rats. Ondansetron produced a robust, long-term reduction of at-level mechanical allodynia, while m-CPBG exacerbated allodynia. Exogenous 5-HT transiently reduced at-level mechanical allodynia. This effect was opposed by methysergide, which enhanced mechanical allodynia. Co-administration of 5-HT and ondansetron produced a short-lasting partial summation of effects, further decreasing mechanical allodynia while co-administration of methysergide attenuated the anti-allodynic effect of ondansetron. Depletion of spinal 5-HT via 5,7-dihydroxytryptamine (5,7-DHT) resulted in decreased at-level mechanical allodynia. The reduction of allodynia by ondansetron was lost following 5,7-DHT administration, suggesting that reduced allodynia following intrathecal ondansetron is via blockade of 5-HT-induced excitation of the 5-HT(3)-R. These results suggest that increased 5-HT fibre density immediately rostral to the SCI lesion site could have transient effects to reduce mechanical allodynia via actions at 5-HT(1) and/or 5-HT(2) receptors. However, the more long-lasting effects of this enhanced serotonergic input may facilitate chronic, at-level allodynia via the 5-HT(3)-R.

5,6-Dihydroxytryptamine↗