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PubMed1993

Segmental recovery of amino acid neurotransmitters during posterior epidural stimulation after spinal cord injury.

Epidural spinal cord stimulation (SCS) has been used as an effective method for managing pain and spasticity for over two decades. However, the mechanisms of these beneficial effects are largely unknown. Since neurotransmitters are likely to be involved, we examined the relationship between SCS and local segmental amino acid release into the spinal cord extracellular space. Microdialysis was performed during continuous epidural SCS in animals subjected to ischemic spinal cord injury. Recovery of amino acid neurotransmitters from stimulated, injured animals was compared to that from a control group. Evoked potentials from the cortex and spinal cord were recorded to insure adequate stimulation and stable cord function. A significant increase in the concentrations of glycine and taurine was seen before, during, and after 90 minutes of continuous stimulation and was independent of the degree of injury. Levels of the other putative amino acid neurotransmitters were not significantly elevated. These results suggest that amelioration of pain or spasticity by epidural SCS may result from maintenance of post-injury elevation in baseline glycine and taurine levels.

Amino Acids↗
PubMed1994

Coagulation profile in persons with long-standing spinal cord injury.

Acute spinal cord injury (SCI) is associated with a marked propensity to thromboembolism and a variety of coagulation abnormalities. However, data on blood coagulation profiles in patients with uncomplicated long-standing SCI are limited. These data were studied here. Eight men with uncomplicated chronic SCI and nine able-bodied normal men were studied. Plasma activities and/or antigen concentrations of high molecular weight kininogen (HMWK) and of factors XII, XI, IX, VIII, VII, X, V, II and XIII as well as von Willebrand factor (vWF), fibrinogen and fibronectin were measured by appropriate functional and or immunological assays. The SCI group exhibited normal values for factors XII, IX, VIII, vWF, VII, X and V as well as HMWK, vWF and fibronectin concentration. However, they showed slight reductions in plasma factor XI activity, factor XIII antigen concentration and modest increases in fibrinogen and factor II concentrations. No correlation was found between the parameters studied and either the duration or the level of injury. In conclusion, in contrast to acute SCI, the coagulation profile in uncomplicated chronic SCI is noted to be largely normal with only a few minor alterations of questionable clinical significance.

Adult↗
PubMed2004

Na+,K+-ATPase concentration and fiber type distribution after spinal cord injury.

Complete spinal cord injury (SCI) is characterized, in part, by reduced fatigue-resistance of the paralyzed skeletal muscle during stimulated contractions, but the underlying mechanisms are not fully understood. The effects of complete SCI on skeletal muscle Na(+),K(+)-adenosine triphosphatase (ATPase) concentration, and fiber type distribution were therefore investigated. Six individuals (aged 32.0 +/- 5.3 years) with complete paraplegia (T4-T10; 1-19 years since injury) participated. There was a significantly lower Na(+),K(+)-ATPase concentration in the paralyzed vastus lateralis (VL) when compared to either the subjects' own unaffected deltoid or literature values (from our laboratory, utilizing the same methodology) of VL Na(+),K(+)-ATPase concentration for the healthy able-bodied (141.6 +/- 50.0, 213.4 +/- 23.9, 339 +/- 16 pmol/g wet wt., respectively; P < 0.05). There was also a significant negative correlation between the Na(+),K(+)-ATPase concentration in the paralyzed VL and years since injury (r = -0.75, P < 0.05). These findings are clinically relevant as they suggest that reductions in Na(+),K(+)-ATPase contribute to the fatigability of paralyzed muscle after SCI. Unexpectedly, the VL muscles of our subjects had a higher proportion of their area represented by type I fibers compared to literature values for the VL of the healthy able-bodied (52.6 +/- 25.3% vs. 36 +/- 11.3%, respectively; P < 0.05). As all our subjects had upper motor neuron injuries and, therefore, experienced muscle spasticity, our findings warrant further investigation into the relationship between muscle spasticity and fiber type expression after SCI.

Adult↗
PubMed1999

Pre-injury substance abuse among persons with brain injury and persons with spinal cord injury.

Alcohol and drug use at the time of injury have been strongly implicated as causal factors of spinal cord injury (SCI) and traumatic brain injury (TBI). Researchers have only begun their efforts to investigate the pre-injury incidence of substance abuse in an effort to identify persons at risk for traumatic injury. No studies have compared brain and spinal cord injury populations. This investigation was based in an urban, level one trauma center federally designated as a model system of comprehensive rehabilitative services for persons with TBI and persons with SCI. Pre-injury patterns of alcohol and illicit drug use were compared among patients with SCI and patients with TBI, matched for age, gender, race, and mechanism of injury (n= 52). In accordance with previous research, participants were primarily young, unmarried, males with at least a high school education. Eighty-one percent of patients with TBI and 96% of patients with SCI reported pre-injury alcohol use. The rate of pre-injury heavy drinking for both groups was alarmingly high. Fifty-seven percent of persons with SCI and 42% of persons with TBI were heavy drinkers. Implications for risk identification, treatment, and future research are discussed.

Adult↗
PubMed2003

Spinal cord injury medicine.

Spinal cord injury/spinal cord rehabilitation provides comprehensive rehabilitation care to reach the patient's functional goals in an acute inpatient, subacute, home, and/or outpatient rehabilitation setting. Spinal cord injury/spinal cord medical specialists are trained specifically on the evaluation and management of the unique medical and surgical conditions among those following SCI. They are trained in the care and rehabilitation of persons with SC dysfunction resulting from traumatic or non-traumatic spinal cord injuries and work in coordination both in clinical care and research with a variety of other medical and surgical specialists, for the care and optimum functional recovery for patients with SCI. These specialists work within a comprehensive rehab team including nursing staff and physician extenders, therapists, psychologists, respiratory staff, nutritionists, case managers, social workers, and vocational rehabilitation counselors for patients with SCI. There are a number of resources, clinics, and inpatient rehabilitation units in the Maryland area that provide this subspecialty care.

Cardiovascular Diseases↗
PubMed1998

Assessment of lower urinary tract functional deficit in rats with contusive spinal cord injury.

Traumatic spinal cord injury (SCI) produces lower urinary tract (LUT) dysfunction that has been studied in surgical transection models. Our aim was to assess LUT functional deficit in a clinically relevant model of incomplete SCI to investigate how partial preservation of supraspinal connections might affect LUT dysfunction. Standardized weight-drop contusion (10 g x 2.5 cm) or complete transection, was produced at T8 in female Sprague-Dawley rats. Behavioral tests were used to assess hind limb sensorimotor function at Day 1 after surgery and weekly thereafter. The urometric experiments were conducted on groups (n = 7) of uninjured rats and on injured rats during Weeks 1 and 2 after SCI (before and after spontaneous voiding was established) as well as Week 2 after a complete transection (n = 3). Under anesthesia, the bladder was continuously perfused with saline. Changes in bladder pressure and external urethral sphincter (EUS) electrical activity were monitored. The bladder was then dissected and weighed and both the bladder and spinal cord were fixed for pathoanatomical analyses. Our results indicate that several aspects of LUT dysfunction after contusive SCI were similar to transection, e.g., reduction of voiding efficiency (approximately 5% of normal value), decrease in inter-contraction interval (47%), increase in bladder capacity (8-fold), and weight (4.6-fold). One aspect appeared different from transection--partial recovery from acute bladder/sphincter dyssynergia. Because the coordination of bladder and EUS function is mediated by brainstem pathways, partial recovery of synergy after SCI was likely due to sparing of some relevant bulbospinal projections as was confirmed by retrograde transneuronal viral tracing.

Animals↗
PubMed1983

Neuronophagia by leukocytes in experimental spinal cord injury.

Experimental spinal cord injury was produced in cats by compression trauma. The major histologic features in the first 24 hours following injury included hemorrhagic necrosis, edema, and acute inflammation of gray and white matter. Neutrophilic leukocytes (NL) were apparent in the walls of and adjacent to veins and venules within four hours of injury, but large numbers of NL were not observed in tissue until eight to 24 hours. Acute inflammation was especially prominent in gray matter, and NL frequently surrounded and phagocytized neuronal somata. Large numbers of NL and neuronophagia by leukocytes were evident only in areas of hemorrhage. The role of blood in producing the acute inflammatory response and in generating chemotactic factors responsible for neuronophagia is incompletely understood. Neutrophilic leukocytes, in addition to their response as phagocytes, release histolytic enzymes, reactive species of oxygen, and proinflammatory factors which lead to further tissue necrosis and inflammation.

Animals↗
PubMed2006

Remodeling of synaptic structures in the motor cortex following spinal cord injury.

After spinal cord injury (SCI), structural reorganization occurs at multiple levels of the motor system including the motor cortex, and this remodeling may underlie recovery of motor function. The present study determined whether SCI leads to a remodeling of synaptic structures in the motor cortex. Dendritic spines in the rat motor cortex were visualized by confocal microscopy in fixed slices, and their density and morphology were analyzed after an overhemisection injury at C4 level. Spine density decreased at 7 days and partially recovered by 28 days. Spine head diameter significantly increased in a layer-specific manner. SCI led to a higher proportion of longer spines especially at 28 days, resulting in a roughly 10% increase in mean spine length. In addition, filopodium-like long dendritic protrusions were more frequently observed after SCI, suggesting an increase in synaptogenic events. This spine remodeling was accompanied by increased expression of polysialylated neural cell adhesion molecule, which attenuates adhesion between the pre- and postsynaptic membranes, in the motor cortex from as early as 3 days to 2 weeks after injury, suggesting a decrease in synaptic adhesion during the remodeling process. These results demonstrate time-dependent changes in spine density and morphology in the motor cortex following SCI. This synaptic remodeling seems to proceed with a time scale ranging from days to weeks. Elongation of dendritic spines may indicate a more immature and modifiable pattern of synaptic connectivity in the motor cortex being reorganized following SCI.

Amino Acids↗
PubMed1994

Bronchial hyperresponsiveness after cervical spinal cord injury.

Cervical spinal cord injury results in interruption of sympathetic airway innervation, which originates from the upper thoracic spine, whereas parasympathetic nerve supply, arising in the vagal nuclei of the brainstem, remains intact. To assess the effect of such an altered neural environment on airway reactivity, bronchoprovocation testing was performed on eight subjects with nonacute traumatic lesions of the cervical spine, all of whom were lifetime nonsmokers without history of respiratory symptoms prior to their injury. Bronchial challenge was subsequently repeated after pretreatment with the anticholinergic agent, ipratropium bromide, an inhibitor of airway muscarinic receptors. All subjects demonstrated hyperresponsiveness to methacholine (the concentration of methacholine producing a fall in FEV1 of 20 percent from baseline [PC20] = 1.42 +/- 1.61 [SD] mg/ml). Airway hyperreactivity was completely blocked by pretreatment with inhaled ipratropium bromide (mean PC20 > 25 mg/ml [p < 0.0001]). The bronchial hyperresponsiveness observed in this population most likely reflects the loss of sympathetic airway innervation and resultant unopposed cholinergic bronchoconstrictor tone which results from transection of the cervical spine. Blockade of methacholine hyperresponsiveness with ipratropium bromide suggests a muscarinic receptor-mediated phenomenon.

Administration, Inhalation↗
PubMed2002

Upregulation of Kv 1.4 protein and gene expression after chronic spinal cord injury.

After spinal cord injury (SCI), white matter tracts are characterized by demyelination and increased sensitivity to the K(+) channel blocker 4-aminopyridine (4-AP). These effects appear to contribute to neurological impairment after SCI, although the molecular changes in K(+) channel subunit expression remain poorly understood. We examined changes in gene expression of the 4-AP-sensitive voltage-gated K(+) channel Kv 1.4 after chronic SCI in the rat. Quantitative immunoblotting showed that Kv 1.4 protein was significantly increased at 6 weeks, but not at 1 week, after SCI in spinal cord white matter. Kv 1.4 was localized to astrocytes, oligodendrocytes, and oligodendrocyte progenitor cells but not to axons in both the normal and the injured spinal cord white matter. Because glial cells proliferate after SCI, we used immunogold electron microscopy to quantify Kv 1.4 protein in individual glial cells and found a sixfold increase of Kv 1.4 in cells of the oligodendrocyte lineage after chronic injury. Finally, quantitative in situ hybridization showed that Kv 1.4 mRNA was significantly upregulated in spinal cord white matter, but not gray matter, after SCI. In summary, we show that Kv 1.4 is expressed in glial cells and not in axons in the rat spinal cord white matter and that its expression is markedly increased in cells of the oligodendrocyte lineage after chronic SCI. Given that K(+) channels play a role in glial cell proliferation, cells exhibiting changes in Kv 1.4 expression may represent proliferating oligodendroglia in the chronically injured spinal cord.

Animals↗
PubMed2005

Incomplete Freund's adjuvant enhances locomotor performance following spinal cord injury.

Following spinal cord injury (SCI), the pathological sequelae which ensue through the secondary mechanisms of degeneration produce myelin deposits which are potent inhibitors of endogenous neuroregeneration. We have enhanced the immune-mediated response following a hemisection lesion by immunizing adult C57Bl/6 female mice against the inhibitor of neurite outgrowth Nogo-A(623-640) peptide. Moderate anti-Nogo-A(623-640) antibody titre levels were obtained by using Montanide as the adjuvant. However, this antibody response was not obtained using incomplete Freund's adjuvant (IFA). Significant benefit in locomotor performance was demonstrated only in animals which were vaccinated with IFA and not with Montanide. No further benefit could be demonstrated with the Nogo-A(623-640) peptide beyond that seen for adjuvant alone. These data imply that generating antibodies against Nogo-A(623-640) in vivo alone is not sufficient to enhance locomotor recovery and that subcutaneous injection of IFA prior to SCI can enhance locomotor performance.

Adjuvants, Immunologic↗
PubMed1998

Pathophysiological mechanisms of central neuropathic pain after spinal cord injury.

After spinal cord injury (SCI), between 10% and 20% of the patients may develop central neuropathic pain. This type of chronic pain usually is a very bothersome sequel and represents a major therapeutic challenge since conventional medical and surgical pain therapies generally are ineffective. This review focuses on recent advances in the understanding of the pathophysiology of this pain syndrome. Important clinical features of central neuropathic pain after SCI include loss of sensations mediated by spinothalamic pathways combined with development of abnormal pain perception (spontaneous continuous pain and abnormally evoked pain). Up-regulation of neuronal activity leading to spontaneous and evoked neuronal hyperactivity/hyperexcitability, may be the neurophysiological substrate for development of abnormal pain perception. This paper describes some neurochemical changes that may be important for the induction and maintenance of neuronal hyperactivity and abnormal pain perception: Increased excitatory glutaminergic activity involving N-methyl-D-aspartate (NMDA) receptor activation, may trigger the intracellular cascade reaction leading to upregulation of neuronal activity/excitability. Changes in voltage-sensitive Na+ channels may contribute to changes in nerve membrane excitability. Other important mechanisms may be loss of endogenous inhibition, including reduced gamma-amino-butyric acid (GABA)ergic, opioid and monoaminergic inhibition. These various mechanisms may provide new targets for treatment of a pain syndrome that traditionally has been so difficult to handle.

Animals↗
PubMed2003

Case for gait analysis as part of the management of incomplete spinal cord injury.

Incomplete spinal cord injury at ASIA (D) level often leads to major gait re-education attempts for patients and staff. Walking prognosis usually depends upon muscle power loss, degree of spasticity present, type of lower limb joint deformity developing and availability of treatment. As an adjunct to physical examination and observation, instrumented gait analysis can inform treatment, since three-dimensional dynamic joint range motion (kinematics) and estimation of joint forces occurring at the hip, knee and especially ankle/foot (kinetics) can be combined with walking EMG and energy cost tests to understand fully a gait deficit. This should then assist the clinical decision-making process. Knowledge of the effects of any dynamic contracture on the available redundancy within ipsilateral limb joints, and information about muscle actions obtained by calculating joint forces (including moments and powers) improves overall knowledge of gait cycle abnormality. Such gait analysis has revolutionised the management of spasticity in walking cerebral palsy children by guiding surgical and other treatments. Similar improvements could be looked for in incomplete SCI patients whose gait pattern is not ideal. Dynamic energy cost estimations could also be used as an outcome measure to study improvements after treatment: whether this is orthotic, pharmacological or following physiotherapy or surgical techniques.

Biomechanical Phenomena↗
PubMed1997

Psychological investigation of spinal cord injury patients.

Spinal cord injuries (SCI) often have psychological consequences, primarily anxiety and depression, which may interfere with rehabilitation possibilities, with adjustment to the impairment and therefore with the possibility of returning to previous familiar social life and work. To assess the degree of anxiety and depression in SCI patients, and to study the factors contributing to their genesis, 100 SCI in- and out-patients were administered questionnaires for self-rating anxiety and depression. A group of newly injured patients was followed up for a year after their discharge to study the evolution of the two psychological syndromes. These two psychological pathologies in SCI patients were respectively 13% (anxiety) and 16% (depression). Some characteristics were significantly associated with a higher risk of developing psychological distress: the presence of severe complications, the lack of autonomy, and low educational level. We did not observe any modification of the psychological picture over time. The lack of reduction in anxiety and depression over time could mean that the two pathologies are maintained by the obstacles SCI patients meet every day resulting from their neurological deficit. Our data justify the provision of psychological services for SCI patients in the rehabilitation centres; these services should still be available to the patients even after discharge.

Adolescent↗
PubMed1996

Endoscopic management of urethral trauma in male spinal cord injury patients.

Spinal cord injury (SCI) patients with a neuropathic bladder are more prone to develop catheter-induced urethral trauma than occurs in the general population because many of the SCI patients are on indwelling urethral catheter drainage, or intermittent urethral catheterisation is performed either by them or by their carers. The presenting symptoms of improperly positioned Foley catheter in SCI patients may be at times, peculiar to the SCI patients and these include profuse sweating, bypassing of the catheter, increased spasms, or rarely, full fledged features of autonomic dysreflexia. With the availability of the flexible cystoscope, cystourethroscopy has been performed safely on SCI patients who had sustained catheter-induced urethral trauma, on the bedside, with an immediate, and accurate diagnosis of the extent of urethral trauma, and the presence of urethral false passage(s). Further, flexible cystoscopy has helped to treat the patients with urethral trauma by introducing a flexible tip guide wire under vision into the urinary bladder via the normal urethral channel and subsequently, passing a 12 Fr. Foley catheter over the guide wire, thus avoiding the false passage(s) in the urethra. With this technique, it was possible to avert the need for suprapubic urinary diversion in those SCI patients who had sustained acute urethral trauma. Such endoscopic management of acute urethral trauma in SCI patients is described with illustrative case reports of eight patients seen during a 15 month period.

Cystoscopy↗
PubMed1989

Resection of heterotopic ossification in patients with spinal cord injuries.

Nineteen spinal cord injury (SCI) patients were treated with resection of heterotopic ossification (HO) in 24 hips. The average follow-up period after surgery was 6.1 years. The mean time to surgery after injury was 50.6 months. The indication for surgery in all patients was improvement in hip motion to allow sitting. The average preoperative motion in flexion and extension was 11.5 degrees. The average intraoperative motion was 82.7 degrees. The average postoperative motion at the follow-up evaluation was 35.2 degrees. Fourteen of 19 patients (74%) had sufficient motion at the follow-up evaluation for sitting. Unlimited sitting tolerance was achieved in seven patients (37%), and seven patients (37%) had improved sitting posture with some time limitations. The average arc of motion in those patients able to sit at the follow-up evaluation was 41.5 degrees. Normal bone scans, alkaline phosphatase levels, and the mature roentgenographic appearance of HO were unreliable predictors of recurrence. The preoperative range of motion was the best predictor of improved postoperative range of motion since patients with retained motion did better than those with severe ankylosis. All six hips with severe recurrence had 0 degree of preoperative motion. The average degree of preoperative motion for all remaining hips was 15.3 degrees. The best predictor of recurrence was the roentgenographic grade of HO. Nineteen of 22 hips (86%) with a mild to severe recurrence had large amounts of bone preoperatively (Grades 3-5). Complications excluding recurrence occurred in 19 of 24 hips (79%) and included superficial wound infections in nine of 24 hips (38%) and deep persistent infections (osteomyelitis) in eight of 24 hips (33%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Skeletal muscle fibre type transformation following spinal cord injury.

Following spinal cord injury (SCI), upper motor neuron paralysed muscles lose the normal type I (slow) and II (fast) fibre mosaic pattern and become predominantly composed of type II (fast glycolytic) fibres). The majority of the research demonstrating this fibre type shift was based on pH sensitive myofibrillar ATPase staining techniques on muscle from longstanding paraplegics and quadriplegics. The purpose of this study was to describe muscle fibre type changes over a wide time spectrum post SCI using immunofluorescent techniques which may be more sensitive to change. A total of 19 vastus lateralis muscle biopsy specimens were obtained from 12 SCI subjects representing time points of 0.5-219 months post SCI. Fast and slow myosin heavy chain isoform distribution was determined on single muscle fibres for each of the biopsy specimens. Early post SCI (< 1 month) myosin heavy chain (MCH) isoform composition remained relatively stable. A transitional period was seen between 1 and 20 months post SCI wherein there was a progressive drop in the proportion of slow MHC isoform fibres and a rise in the proportion that co-expressed both the fast and slow MHC isoform. By approximately 70 months post SCI a new steady state had been reached characterized by almost exclusively fast MHC isoform expression. This research has demonstrated that post SCI muscle type II transformation occurs in stages and commences earlier than previously appreciated. Interventions aimed at preventing or minimizing the transformation would need to be instituted within weeks post SCI.

Adenosine Triphosphatases↗