Environmental enhancement of growth factor-mediated oligodendrocyte precursor proliferation

The timing of oligodendrogenesis depends on the specific location within the central nervous system, suggesting the local environment influences oligodendrocyte precursor proliferation. Spinal cord and optic nerve oligodendrocyte precursors both proliferate in response to platelet-derived growth factor (PDGF). Here we show that neurotrophin-3 (NT-3) enhanced PDGF-induced proliferation of optic nerve oligodendrocyte precursors, and these cells were labeled by an anti-trkC antibody. By contrast, NT-3 did not enhance PDGF-induced proliferation of spinal cord oligodendrocyte precursors, and these cells were not labeled by an anti-trkC antibody. Furthermore, PDGF-induced oligodendrocyte precursor proliferation was greater in spinal cord than in optic nerve cultures. The difference in NT-3 response between spinal cord and optic nerve oligodendrocyte precursors appears cell intrinsic, while the enhanced PDGF-induced proliferation of spinal cord oligodendrocyte precursors appears environmentally regulated. The spinal cord PDGF proliferation-enhancing activity may provide a mechanism to allow temporal and spatial regulation of gliogenesis.     

Failure of spinal cord oligodendrocyte development in mice lacking neuregulin

Oligodendrocytes develop from a subpopulation of precursor cells within the ventral ventricular zone of the spinal cord. The molecular cues that direct this spatially and temporally restricted event seem to originate in part from structures ventral to and within the spinal cord. Here, we present evidence that the family of ligands termed neuregulins are necessary for the normal generation of mouse spinal cord oligodendrocytes. Oligodendrocytes mature in spinal cord explants from wild-type mice and mice heterozygotic for a null mutation in the neuregulin gene (NRG +/-) in a temporal sequence of developmental events that replicates that observed in vivo. However, in spinal cord explants derived from mice lacking neuregulin (NRG -/-), oligodendrocytes fail to develop. Addition of recombinant neuregulin to spinal cord explants from NRG -/- mice rescues oligodendrocyte development. In wild-type spinal cord explants, inhibitors of neuregulin mimic the inhibition of oligodendrocyte development that occurs in NRG -/- explants. In embryonic mouse spinal cord, neuregulins are present in motor neurons and the ventral ventricular zone where they likely exert their influence on early oligodendrocyte precursor cells.     

Notochord is essential for oligodendrocyte development in Xenopus spinal cord

Oligodendrocyte precursors originate in the ventral ventricular zone of the developing spinal cord. To examine whether the notochord is essential for the development of oligodendrocytes in Xenopus spinal cord the notochord was prevented from forming, ablated, or transplanted during early stages of development. Differentiated oligodendrocytes did not appear in spinal cord regions lacking a notochord in animals in which notochord failed to develop after UV irradiation at the one-cell stage. Similarly, differentiated oligodendrocytes were not detected in the spinal cord adjacent to the site of segmental notochord ablation at embryonic or larval stages. Transplantation of an additional notochord dorsal to the spinal cord induced the premature appearance of differentiated oligodendrocytes in adjacent lateral and dorsal spinal cord white matter. These results indicate that the development of Xenopus spinal cord oligodendrocytes is dependent on local influences from the notochord and suggest that the notochord is essential for oligodendrocyte development in Xenopus spinal cord.     

The use micro-polarization in spinal cord lesions

Transdermal micropolarization of the spinal cord was made in patients with consequences of the spinal cord injury or tuberculous spondylitis. Changes in clinical and electrophysiologic status were evaluated. It was found that local direct current through dermal electrodes promotes an improvement of both motor and autonomic functions in such patients. This corresponded to a positive dynamics both of the spinal cord state and cardiac activity. Possible mechanisms of influence of the direct current on the spinal cord as well as perspectives of application of micropolarization in spinal cord's damage are outlined.     

The acute abdomen in spinal cord injury individuals

A review of 1300 patients with spinal cord injury (SCI), over a period of 14 years, revealed 12 patients with an 'acute abdomen'. Seven events occurred during the initial admission, ranging from 10 days to 9 months from injury, and five during readmission of 'chronic' SCI patients. Four were in the acute stage 10-30 days from injury, all with peptic ulcer perforations. The remainder had either an intestinal obstruction, appendicitis or peritonitis. All of the neurological levels were above T6 except for one patient who had a low level paraplegia. The classical signs of an 'acute abdomen' may be missing in such patients thus delaying diagnosis by 1-4 days. The most important signs were autonomic dysreflexia, referred shoulder tip pain, abdominal pain, abdominal distension, increased spasticity and abdominal pain with nausea and vomiting. Less importance was given to the classical signs of abdominal tenderness, abdominal muscle rigidity, rebound, fever and of leukocytosis. Prompt diagnosis and treatment will minimise morbidity and mortality.     

Cellular delivery of neurotrophin-3 promotes corticospinal axonal growth and partial functional recovery after spinal cord injury

The injured adult mammalian spinal cord shows little spontaneous recovery after injury. In the present study, the contribution of projections in the dorsal half of the spinal cord to functional loss after adult spinal cord injury was examined, together with the effects of transgenic cellular delivery of neurotrophin-3 (NT-3) on morphological and functional disturbances. Adult rats underwent bilateral dorsal column spinal cord lesions that remove the dorsal corticospinal projections or underwent more extensive resections of the entire dorsal spinal cord bilaterally that remove corticospinal, rubrospinal, and cerulospinal projections. Long-lasting functional deficits were observed on a motor grid task requiring detailed integration of sensorimotor skills, but only in animals with dorsal hemisection lesions as opposed to dorsal column lesions. Syngenic primary rat fibroblasts genetically modified to produce NT-3 were then grafted to acute spinal cord dorsal hemisection lesion cavities. Up to 3 months later, significant partial functional recovery occurred in NT-3-grafted animals together with a significant increase in corticospinal axon growth at and distal to the injury site. These findings indicate that (1) several spinal pathways contribute to loss of motor function after spinal cord injury, (2) NT-3 is a neurotrophic factor for the injured corticospinal projection, and (3) functional deficits are partially ameliorated by local cellular delivery of NT-3. Lesions of the corticospinal projection may be necessary, but insufficient in isolation, to cause sensorimotor dysfunction after spinal cord injury in the rat.     

The neurogenic bladder in spinal cord injury--pattern and management

This study describes the various types of neurogenic bladder in spinal cord injury in relation to the level of lesion, defines the aims of bladder management, and discusses the importance of highly individualised management strategies and long-term follow-up. Urodynamic studies were done on 47 new patients with traumatic spinal cord injury when they had return of reflexic bladder activity. This study was conducted over a one-year period. Fifty-five per cent (n = 26) sustained cervical injuries (38.5% complete, 61.5% incomplete), 12.8% (n = 6) had thoracic injuries, 29.8% (n = 14) had lumbar injuries, and 2.1% (n = 1) had sacral injury. The urodynamic patterns according to injury level are shown in Table I. In patients with complete cervical injuries, 80% had detrusor sphincter dyssynergia (DSD), and areflexia was seen in 20% (n = 2). Of those with incomplete cervical injury, 7 (43.8%) had DSD, 5 (31.3%) had detrusor hyperrflexia without DSD, and 2 (12.5%) had areflexia or hyporeflexia. Normal urodynamic studies were only found in patients with incomplete cervical injury (n = 2). Of the 6 patients with thoracic injury, 4 (66.6%) had detrusor areflexia and 2 had DSD. The 2 patients with DSD had injury levels at T4/T6 and T5 respectively. Eleven (78.6%) patients with lumbar injury had detrusor areflexia, one (7.1%) had detrusor hyperreflexia (without DSD), and 2 (14.3%) had a normal urodynamic study. The various patterns of bladder management are shown in Table II. In total, there were 17 patients with DSD. Of these, 9 (52.9%) elected for intermittent catheterisation together with pharmacological therapy, 5 (29.4%) passed urine via spontaneous voiding/tapping, one (5.9%) had an in-dwelling catheter by virtue of his lack of manual dexterity and no care-giver, and 2 (11.8%) patients opted for sacral anterior root stimulator (SARS) or the Brindley device. Of the 6 patients with detrusor hyperreflexia, 4 (66.7%) passed urine spontaneously and 2 (33.3%) patients choose intermittent catheterisation together with pharmacologic therapy. There were 20 patients with detrusor areflexia/hyporeflexia; 15 (75%) were on clean intermittent catheterisation, 4 (20%) voided via straining and 1 (5%) had a suprapubic catheter inserted. The re-discovery of intermittent self-catheterisation, improved medical care, bladder training and surgical advances have enabled the goals of bladder management to be realised; namely safe bladder pressures, low residual urine volume and the attainment of continence.     

The effect of prolonged spinal cord compression on the extent of morphological changes in experimental spinal cord injury in rabbits

The analysis of early spinal cord decompression influence on the extent of morphological and microvascular changes after traumatic cord injury was the subject of this study, carried out on Polish-breed rabbits divided into two groups. Microvascular changes were evaluated in the first group of 20 animals and morphological changes in the second group of 36 rabbits. The injury causing paraplegia was performed at D9-D10 level by Allen method modified. Every group was subdivided into 4 subgroups depending on the duration of cord compression 2, 4, 6 and 12 hours. Fragments of cord were taken for examination 12 hours after decompression, from sites 0.5, 1.0 and 1.5 cm distant from the injury level. Histopathological analysis was performed by light and electron microscopy and for the analysis of microcirculation with microangiography the Górkiewicz method was used. Great changes were found in nerve fibres, vascular endothelium and microcirculation. The most pronounced lesions were found in the subgroup with 6-hour compression, in the form of haemorrhage, central necrosis and oedema within and around axona as well as destruction of myelin sheaths. Early decompression (within 6 hours) can reduce the extent of morphological and vascular changes.     

The diagnosis and natural history of spinal cord arteriovenous malformations

The present study of 71 patients shows that the initial symptoms often cannot differentiate spinal cord arteriovenous malformation from other lesions causing cord dysfunction, but the picture at the time of presentation may suggest the diagnosis. Most patients are males with neurologic findings referable to the thoracolumbar area who present with gradually progressive pain, weadness, sensory distubance, and disturbance of micturition. Early impairment of micturition may help suggest this lesion because it is less likely to be an early complaint in patients with disk disease or tumor affecting the spinal cord. Symptoms occasionally vary with posture and exercise and menses. Most commonly there are combined upper motor neuron and lower motor neuron manifestations with nonradicular sensory deficit. The cerebrospinal fluid is abnormal in more than 75% of cases. The myelogram is positivie in 75 to 90% of cases and the angiogram is almost always diagnostic.     

The positive by-products of spinal cord injury and their correlates.

Objective: To assess positive by-products from the struggles with traumatic spinal cord injury and to explore their correlates. Study Design: Forty-two participants and nominated proxy informants were interviewed 18-36 months post spinal cord injury. Main Outcome Measures: The Perceived Benefit Scales (J. C. McMillen & R. Fisher, 1998) and Symptom Checklist 90-Revised (L. R. Derogatis, 1994). Results: Increased compassion and family closeness and decreased alcohol consumption were commonly reported following injury. Correlations between self- and proxy ratings of positive by-products were low. Positive by-products were not related to psychopathology and had different correlates. Conclusion: Positive by-products are different from other kinds of outcomes, but because loved ones do not necessarily notice these benefits, their validity remains in doubt. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

脊髓拴系综合症的手术治疗体会

我院自2005年8月～2009年8月共手术治疗30例脊髓拴系综合症的病人.本文总结我院30例脊髓拴系综合症的手术治疗体会.     

The significance of spinal cord compression as the initial manifestation of lymphoma

Sex hormones have profound effects on immune responses and may influence the outcome of autoimmune diseases such as rheumatoid arthritis (RA). We investigated the effect of gonadal steroids on the production of interleukin-1 (IL-1) and IL-6, cytokines believed to be important in the pathogenesis of RA. Peripheral blood mononuclear cells (PBMCs) were isolated from healthy male donors and male patients with RA, and were stimulated with lipopolysaccharide (LPS) in the presence of different concentrations of 17-beta-estradiol, progesterone or testosterone. In studies of cells from normal male donors, 17-beta-estradiol at pharmacological concentrations (> or = 10(-6) M) enhanced IL-1 and IL-6 secretion as well as the production of cell-associated IL-1. Progesterone and testosterone at similar concentrations inhibited IL-1 secretion but had no significant effect on IL-6 secretion or on the production of cell-associated IL-1. In studies of male RA donors, 17-beta-estradiol failed to enhance IL-1 or IL-6 secretion and progesterone failed to inhibit IL-1 secretion. The inhibitory effects of testosterone, however, appeared to be similar to that in normal donors. It is suggested that 17-beta-estradiol may promote IL-1 and IL-6 production and release, while gestation hormone, progesterone, and testosterone may inhibit IL-1 release in vivo. These data may partly explain the gender and age differences in the incidence of RA and the development of the disease in men with low and androgen levels.     

The skeleton after spinal cord injury. Part 1. Theoretical aspects

Sublesional osteoporosis occurs after acute spinal cord injury (SCI), preferentially weakening the skeleton below the level of the neurological lesion. Although its pathogenesis is unclear, it resembles post-menopausal, high turnover osteoporosis. Physical and pharmacologic therapies are currently being tested for their ability to prevent early loss and restore lost bone. Although treatment strategies hold promise, preservation of skeletal strength after injury may ultimately rest on lifestyle decisions made early in life. If skeletal strength is to be maintained after SCI, ways must be found to optimize skeletal strength prior to injury, arrest early losses, and stabilize, if not restore, lost bone over time.     

The cocoon syndrome: A coping mechanism of spinal cord injured persons.

Institutionalized spinal-cord-injured persons have been noted frequently to spend their bed rest and sleep time with their head covered with bed linens or pillows. The present study determined the prevalence of this behavior and its etiology. Comparison groups of 29 spinal-cord-injured and 80 non-spinal-cord-injured patients at 2 rehabilitation facilities were periodically observed during sleep and bedtimes. Following the observation periods, the Ss who manifested the behavior were interviewed to determine causal factors. Results establish a marked prevalence of the behavior in the spinal-cord-injured population compared to other physical disability types. Interview data suggest that head-covering fulfills a variety of functions related to the coping process, but the reason for its prevalence in the spinal-cord-injured population remains uncertain. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The Brief Symptom Inventory: Measuring psychological distress in spinal cord injury.

Explored the appropriateness of the Brief Symptom Inventory (BSI) as a measure of psychological distress among 79 traumatic spinal cord injured (SCI) patients (aged 18–70 yrs) and emphasized the limitations of using the BSI as a replacement for the SCL-90—Revised (SCL-90—R). Ss' BSI scores were compared with a nonpatient normative group (N?=?974). Ss were significantly more psychologically distressed in somatization, depression, and phobic anxiety than the normative group. However, several somatization symptoms endorsed by these Ss are common physical effects of SCI rather than psychosomatic complaints. When comparing BSI and SCL-90—R scores of the same Ss, significant statistical differences were found with respect to the level of psychological distress being reported by each test. The BSI may not represent an equivalent abbreviated form of the SCL-90—R for the SCI population. (PsycINFO Database Record (c) 2010 APA, all rights reserved)