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PubMed2001

Intercostal nerve neurouma (PNS) implantation in spinal cord bridging spinal cord transection a functional internuncal pathway system result in recovery from paraplegia.

In these studies 76 mature female dogs were used. The spinal cord was transacted at T6 or T8. The intercostal nerve or nerves originating cephalic to the transaction were inserted into the distal isolated cord close to the transaction and plasma clot sutured to anchor the peripheral end of the nerve into the spinal cord. The transacted isolated spinal cord at the mid thoracic level results in paraplegia. 3, 4, 21 The isolated distal transacted spinal cord is capable of producing complex, detailed locomotor functions. The anatomical substrate is produced by systems of interconnected interneurons in the lumbar spinal cord that forms the central pattern generators (CPG). 3, 4, 21 The interneurons comprising (CPG) coordinates patterned movements of the rear limbs as flexion, extension, weight bearing, postural adjustments and alternating patterned limb movements. 3, 4, 21 In the case of implantation of a peripheral nerve distal stump into the transacted spinal cord the procedure enhances the function mediated by the central patterned generators (CPG) by training, conditioning and chemical and molecular treatments. 3, 4, 7, 8, 15, 1, 18, 19, 21.

Animals↗
PubMed2002

Neurogenic bladder model for spinal cord injury: spinal cord microdialysis and chronic urodynamics.

We describe an animal model to study neurotransmitter changes in parallel with urodynamic testing following Spinal Cord Injury (SCI). Urodynamic access was achieved using a subcutaneously placed 7 French dual lumen portacatheter. Spinal cord injury was induced by weight drop technique onto exposed dura at T8. The L6-S1 detrusor nuclei were localized stereotactically and microdialysis probe placement was confirmed through histologic methods. Chronic urodynamics revealed detrusor hyperreflexia (DH) 14 days following SCI. In vivo microdialysis of spinal cord amino acids was performed using CMA 11 (240 uM) probes in halothane-anesthetized rats at baseline and intervals of 20-30 min following spinal cord injury. Significant increases in the excitatory amino acid glutamate, and the inhibitory amino acids, glycine and taurine, were seen following spinal cord injury. Amino acid levels peaked at approximately 40 min following contusion injury with glycine demonstrating the highest levels of all amino acids measured. This neurogenic rat model provides a useful means of examining the effects of spinal cord injury on bladder function. By utilizing spinal cord microdialysis, one could intervene at the level of the detrusor nuclei to modulate bladder function.

Animals↗
PubMed2004

Suppression of detrusor-sphincter dyssynergia by immunoneutralization of nerve growth factor in lumbosacral spinal cord in spinal cord injured rats.

PURPOSE: We investigated the effects of intrathecal application of nerve growth factor (NGF) antibodies (NGF-Abs) and desensitization of C-fiber afferent pathways by capsaicin treatment on detrusor-sphincter dyssynergia (DSD) after spinal cord injury (SCI). MATERIALS AND METHODS: In adult female rats SCI was induced by complete transection of the spinal cord at Th8 to 9. Ten days after spinalization vehicle or NGF-Ab (10 microg daily) was continuously administered at the level of the L6-S1 spinal cord through an implanted intrathecal catheter connected to an osmotic pump for 2 weeks. Another group of spinalized rats was treated with capsaicin (125 mg/kg subcutaneously) 3 weeks after spinalization and 5 days before experiments. Simultaneous recordings of intravesical pressure and urethral perfusion pressure were then performed. NGF levels in the L6 spinal cord were measured in vehicle or NGF-Ab treated spinalized rats using enzyme-linked immunosorbent assay. RESULTS: DSD was observed in all vehicle treated spinalized rats. The average urethral pressure increase at the peak bladder contraction was significantly lower by 84% and 78% in NGF-Ab and capsaicin treated spinalized rats, respectively, than in vehicle treated rats. After NGF-Ab treatment NGF levels were significantly decreased by 38% in the L6 spinal cord compared with vehicle treated spinalized rats, in which NGF levels in the L6 spinal cord were 7 times higher than in spinal intact rats. CONCLUSIONS: Increased levels of NGF in the spinal cord could contribute to the emergence of DSD that is at least in part mediated by C-fiber bladder afferents after SCI. Thus suppression of NGF levels in afferent pathways could be useful for treating DSD following SCI.

Afferent Pathways↗
PubMed1984

Progressive cystic degeneration of the spinal cord following spinal cord injury.

From a group of 520 spinal cord injury patients treated at Rancho Los Amigos Hospital, two cases of progressive myelopathy secondary to cystic degeneration of the spinal cord have been identified. The cyst may dissect proximately to produce progressive neurologic deficit. Surgical treatment with shunting can allow stabilization and improvement with return of newly lost function.

Adult↗
PubMed2005

A simple technique for localizing consecutive fields for disector pairs in light microscopy: application to neuron counting in rabbit spinal cord following spinal cord injury.

Locating the same microscopic fields in consecutive sections is important in stereological analysis. The tools for achieving this requirement have limited number in practice. This paper presents a simple and inexpensive technique for localizing the same fields on disector pairs in conventional light microscopes equipped with widely available dial indicators. It is partly a modification of equipment previously described. The presented procedure requires two light microscopes equipped with dial indicators and modified slide clips. An application of the present system was shown in a model of spinal cord injury (SCI). A midthoracic laminectomy was performed leaving the dura intact. A contusion was done at the level of midthoracic spinal cord segments (T7-T8) by dropping a 10-g mass from a height of 30 cm. The subjects were randomly divided into three groups (10 animals in each): hypothermia group, methylprednisolone group, and traumatic spinal cord injury alone group. Present results show that treatment with hypothermia after spinal cord trauma has a neuroprotective effect on cell damage but not in the methylprednisolone treatment group.

Animals↗
PubMed1993

[Intraoperative monitoring for spinal cord tumor by spinal cord evoked potential following unilateral spinal cord stimulation].

We described our experiences with intraoperative spinal cord monitoring in 6 cases of spinal cord tumor. During the operation, spinal cord evoked potential following unilateral spinal cord stimulation was recorded from subdural monitoring electrodes. This series included two cases of intradural extramedullary tumor (one case each of neurinoma and of meningioma) and four cases of intramedullary tumor (2 cases of cavernous angioma, one case each of ependymoma, and of glioblastoma multiforme). Before the removal of the tumor, the spinal cord evoked potential showed lower amplitude or no response on the more affected side in all 6 cases. During the operation, the different intraoperative changes were shown on each side. The authors think that the detection of unilateral damage to the spinal cord is possible in spinal cord evoked potential using unilateral spinal cord stimulation.

Adult↗
PubMed2005

Synthes Award for Resident Research on Spinal Cord and Spinal Column Injury: granulocyte macrophage colony stimulating factor (GM-CSF) prevents apoptosis and improves functional outcome in experimental spinal cord contusion injury.

OBJECTIVE: Granulocyte macrophage colony stimulating factor (GM-CSF) is a potent hematopoietic cytokine, which stimulates stem cell proliferation in the bone marrow and inhibits apoptotic cell death in leukocytes. However, the effects of GM-CSF in the central nervous system are still unclear. The present study was undertaken to determine if GM-CSF can rescue neuronal cells from apoptosis and improve neurologic function in a spinal cord injury (SCI) model. METHODS: To study the effect of GM-CSF on apoptotic neuronal death, we used a staurosporine-induced neuronal death model in a Neuro 2A (N2A) cell line (in vitro) and in a rat SCI model (in vivo). N2A cells were preincubated with GM-CSF for 60 minutes before being exposed to staurosporine for 24 hours. To inhibit GM-CSF, we pretreated N2A cells with antibodies of the GM-CSF receptor for 60 minutes. SCI was made by clip compression. Rats were treated with daily GM-CSF (20 microg/d) for 5 days. The number of apoptotic cells in the spinal cord and neurologic improvements were checked. RESULTS: GM-CSF pretreatment was found to significantly protect N2A cells from apoptosis, and neutralizing antibodies for the GM-CSF receptors inhibited the rescuing effect of GM-CSF on apoptosis. In the rat SCI model, neurologic functions improved significantly in the GM-CSF-administered group versus the phosphate buffered saline (PBS)-treated control. TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeled) staining showed that GM-CSF administration reduced apoptosis in the injured spinal cord. CONCLUSION: Treatment of SCI with GM-CSF showed some beneficial effects. Neuronal protection against apoptosis is viewed as a likely mechanism underlying the therapeutic effect of GM-CSF in SCI.

Animals↗
PubMed1994

[Acute ischemic spinal cord disease. Spinal cord infarction. A clinical study and MRI in 8 cases].

Acute spinal cord infarction (ASCI) occurs infrequently and may have diverse causes. The diagnosis of ASCI, and particularly of an anterior spinal artery syndrome (ASAS) can be confirmed nowadays by MRI, whereas in the past only necropsy confirmation was possible. Pathophysiology and long-term prognosis may be better known at present and treatments more consistent. We present the longitudinal study and clinical features of 8 patients suffering from ASCI. All of them were personally studied and had MRI examinations, often with sequential studies. three groups must be considered: one included 4 cases of ASAS at cervical level, the second 2 cases of ASAS at thoracic level and the third group with infarction of the conus medullaris (ICM), one of them developed during surgical repair of an infrarenal aortic aneurysm. Motor and sensory sequelae were assessed in each case together with possible etiological factors. In conclusion, recovery after ASAS tends to be dependent on the severity of the initial deficit. At cervical level, clinical and morphological findings argue in favour of an extrinsic selective compression of the C7 right radiculo-medullary artery as responsible for the ASA. At thoracic level, the artery preferentially occluded seems to be the sulco-commisural artery as a consequence of disc compression. Finally, an underlying peculiarity of the pattern of arterial supply is a probable predisposing factor for ICM. Generally, the long-term prognosis of ASCI is not necessarily bad.

Adult↗
PubMed1977

The mechanism of spinal cord cavitation following spinal cord transection. Part 3: Delayed grafting with and without spinal cord retransection.

Cavitation adjacent to transection of spinal cords can be successfully eliminated by a second operation 1 week after the initial spinal cord transection. The second operation consists of removal of the necrotic spinal cord tissue, thus producing a gap. Segments of autogenous sciatic nerve are inserted into the gap between the spinal cord stumps. If the spinal cord is injured by retransection at the second operation, cavitation again occurs in the spinal cord stumps resulting in separation of the nerve grafts from the spinal cord. The results of the present experiments support the concept that lysosomal spinal cord autotomy, which causes spinal cord cavitation, is a self-limiting process and that once the spinal cord has completed the autotomy, the process will not occur again unless the spinal cord is agiain traumatized.

Animals↗
PubMed1998

High-resolution MRI of intact and transected rat spinal cord.

Spinal cord transection at midthoracic level leads to an immediate loss of hindlimb motor function as well as to a progressive degeneration of descending and ascending spinal cord pathways. Thoracic spinal cord in unlesioned control rats and in rats 2 to 6 months after complete midthoracic transection were imaged in vivo using an ultrahigh-field (4.7 T) magnetic resonance spectrometer. High-resolution spin-echo and inversion-recovery pulse sequences were employed. In addition, the apparent diffusion coefficients (ADCs) in longitudinal and transverse directions of the spinal cord were determined. Anatomical MRI findings were confirmed in histological spinal cord tissue preparations. In healthy spinal cord, gray and white matter were easily discerned in proton density-weighted images. An infield resolution of max. 76 micrometers per pixel was achieved. In animals with chronic spinal cord transection changes in gray-white matter structure and contrast were observed toward the cut end. The spinal cord stumps showed a tapering off. This coincided with changes in the longitudinal/transverse ADC ratio. Fluid-filled cysts were found in most cases at the distal end of the rostral stump. The gap between the stumps contained richly vascularized scar tissue. Additional pathologic changes included intramedullary microcysts, vertebral dislocations, and in one animal compression of the spinal cord. In conclusion, MRI was found to be a useful method for in vivo investigation of anatomical and physiological changes following spinal cord transection and to estimate the degree of neural degeneration. In addition, MRI allows the description of the accurate extension of fluid spaces (e.g., cysts) and of water diffusion characteristics which cannot be achieved by other means in vivo.

Animals↗
PubMed1975

[Morphologic and cytophotometric indices of the state of the neurons of the spinal cord and spinal cord ganglia following exposure to gravitational stress].

The work presents data on the state of the neurons of the spinal ganglia and the spinal cord of the lumbosacral part in 96 cats subjected to single stresses (10g) and repeated ones (6g). The material was stained with thionin after Nissl. RNA was detected after Einarson. Photometry of the sections was made in MUP.5. Morphological changes were shown to be more pronounced in sensory cells. The method of cytophotometry established the increase by 25% amount of RNA in their cytoplasm after single stresses. Repeated stresses resulted in depletion of RNA. The amount of RNA returned to the initial level within 2 days after single stresses and within 3 days after repeated rotations. The shifts were much less pronounced in motoneurons.

Animals↗
PubMed1982

[Nuclear proteins and nucleic acids during differentiation of neurons in the spinal cord ganglia, spinal cord and tectum opticum in chickens. Cytophotometric study with computation programs].

By means of doublewave cytophotometry of the histological sections and smears performed with the device mtsfv-1 (lomo) it has been demonstrated that differentiation of some neurons of the spinal ganglia and the spinal cord is accompanied with hyperreplication of DNA amount exceeding the diploid contents, while the large neurons in layer III of the tectum opticum remain diploid. In the process of differentiation an increased amount of RNA and histones, and decreasing portion of histones sented for the microcalculator b3-21.

Animals↗
PubMed2001

Diffusion anisotropy MRI for quantitative assessment of recovery in injured rat spinal cord.

Spinal cord injury and its devastating consequences are the subject of intensive research aimed at reversing or at least minimizing functional loss. Research efforts focus on either attenuating the post-injury spread of damage (secondary degeneration) or inducing some regeneration. In most of these studies, as well as in clinical situations, evaluation of the state of the injured spinal cord poses a serious difficulty. To address this problem, we carried out a diffusion-weighted MRI experiment and developed an objective routine for quantifying anisotropy in injured rat spinal cords. Rats were subjected to a contusive injury of the spinal cord caused by a controlled weight drop. Untreated control rats were compared with rats treated with T cells specific to the central nervous system self-antigen myelin basic protein, a form of therapy recently shown to be neuroprotective. After the rats were killed their excised spinal cords were fixed in formalin and imaged by multislice spin echo MRI, using two orthogonal diffusion gradients. Apparent diffusion coefficient (ADC) values and anisotropy ratio (AI) maps were extracted on a pixel-by-pixel basis. The calculated sum of AI values (SAI) for each slice was defined as a parameter representing the total amount of anisotropy. The mean-AI and SAI values increased gradually with the distance from the site of the lesion. At the site itself, the mean-AI and SAI values were significantly higher in the spinal cords of the treated animals than in the controls (P = 0.047, P = 0.028, respectively). These values were consistent with the score of functional locomotion. The difference was also manifested in the AI maps, which revealed well-organized neural structure in the treated rats but not in the controls. The SAI values, AI histograms, and AI maps proved to be useful parameters for quantifying injury and recovery in an injured spinal cord. These results encourage the development of diffusion anisotropy MRI as a helpful approach for quantifying the extent of secondary degeneration and measuring recovery after spinal cord injury. Magn Reson Med 45:1-9, 2001.

Animals↗
PubMed2001

Developmental regulation of N-methyl-D-aspartate- and kainate-type glutamate receptor expression in the rat spinal cord.

Spinal motor neurons undergo experience-dependent development during a critical period in early postnatal life. It has been suggested that the repertoire of glutamate receptor subunits differs between young and mature motor neurons and contributes to this activity-dependent development. In the present study we examined the expression patterns of N-methyl-D-aspartate- and kainate-type glutamate receptor subunits during the postnatal maturation of the spinal cord. Young motor neurons express much higher levels of the N-methyl-D-aspartate receptor subunit NR1 than do adult motor neurons. Although there are eight potential splice variants of NR1, only a subgroup is expressed by motor neurons. With respect to NR2 receptor subunits, young motor neurons express NR2A and C, while adult motor neurons express only NR2A. Young motor neurons express kainate receptor subunits GluR5, 6 and KA2 but we are unable to detect these or any other kainate receptor subunits in the adult spinal cord. Other spinal cord regions display a distinct pattern of developmental regulation of N-methyl-D-aspartate and kainate receptor subunit expression in comparison to motor neurons. Our findings indicate a precise spatio-temporal regulation of individual subunit expression in the developing spinal cord. Specific combinations of subunits in developing neurons influence their excitable properties and could participate in the emergence of adult neuronal form and function.

Alternative Splicing↗
PubMed1990

A rapid procedure for the preparation of oligodendrocyte-enriched cultures from rat spinal cord.

Spinal cords and cerebra from 7-day-old rat pups were compared as tissue sources for the isolation of oligodendrocytes and for studies on the development of these cells in culture. After 1 day in culture the serum-containing medium was replaced by a chemically-defined medium, which contained a cocktail of hormones that stimulated oligodendrocyte development. The cultures were characterized with various immunocytochemical markers; monoclonal A2B5 for bipotential glial progenitor cells, anti-galactocerebroside (GC) serum for oligodendrocytes, and anti-glial fibrillary acidic protein (GFAP) serum for astrocytes. The number of positive cells was counted and expressed as a percentage of total cells. At 1 day in culture the cell cultures from spinal cord contained 30% GC+ cells, increasing to 90% after 7 days in culture. In cultures derived from cerebra the percentage of GC+ cells was always lower than in cultures from spinal cord. In cerebral cultures GFAP+ cells increased from 15% at 1 day in culture to 30% at 7 days in culture, whereas it remained low in spinal cord cultures. The activity of oligodendroglial marker enzyme 2',3'-cyclic-nucleotide 3'-phosphodiesterase was followed during development in culture. The specific activity increased rapidly in both types of culture but was more than threefold higher in cultures derived from spinal cord. This procedure yields, within one week and without subculture, primary glial cultures from rat spinal cord, that are highly enriched in oligodendrocytes (greater than or equal to 90%; 3.10(5) oligodendrocytes per rat pup).

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed2001

Autonomic dysreflexia and primary afferent sprouting after clip-compression injury of the rat spinal cord.

Spinal cord injury leads to many forms of autonomic dysfunction including autonomic dysreflexia, a condition involving recurrent episodes of paroxysmal hypertension and associated bradycardia. This hypertension may reach intensities that are life-threatening. We investigated autonomic dysreflexia and the sprouting of central processes of primary afferent neurons (a potential mechanism for autonomic dysreflexia) in a clinically-relevant calibrated clip-compression model of spinal cord injury in the rat. Autonomic dysreflexia was induced by colon distension in the conscious rats 2 weeks after severe (50-g) clip compression injury of the spinal cord at the 4th thoracic segment. The central arbor of small-diameter primary afferent fibers in laminae III-VII of the spinal cord dorsal horn was also assessed at 2 weeks after cord injury by quantitative morphometry, using calcitonin gene-related peptide as a marker. In response to colon distension, arterial pressure increased by 41 +/- 3 mmHg from a resting value of 109 +/- 4 mmHg, and heart rate decreased by 124 +/- 13 beats/min from a value of 515 +/- 16 beats/min (n = 7). Minimal locomotor function was recovered by these rats: by 2 weeks after injury they attained scores of only 3.1 +/- 1.3 on the Basso, Beattie and Bresnahan scale. Histopathology of the clip-compression lesion site in the cord consisted of extensive central necrosis extending several segments rostral and caudal to the lesion. Quantitative measures of the small-diameter afferent arbors revealed significant increases in area ranging from 20-27% in thoracolumbar segments caudal to the injury (n = 5) in comparison to sham-injured rats (n = 6). A second study was done to assess the impact of severity of injury on the relationship between the size of the primary afferent arbors and autonomic dysreflexia. At 2 weeks after milder (20-g) clip injury at T4, rats exhibited responses to colon distension that were not those associated with autonomic dysreflexia (n = 5). Arterial pressure increased by only 16 +/- 3 mmHg and heart rate tended to increase (+19 +/- 12 beats/min). These rats attained a locomotor score of 7.1 +/- 0.4 by 2 weeks. The lesions at the injury site also contained necrosis and mild cavitation within the gray matter. No change in the small-diameter afferent arbor was detected at 2 weeks after the 20-g clip injury at T4 (n = 6 rats). These findings suggest that after severe but not mild clip compression injury of the spinal cord, sprouting of the afferent component of the spinal reflex are contributes to the development of autonomic dysreflexia. Neither dysreflexia, nor changes in the afferent arbor size occurred after mild cord injury. This clinically relevant clip compression cord injury model, studied more frequently for locomotor function, is excellent for investigating mechanisms for the development of autonomic dysreflexia and strategies for its prevention.

Animals↗
PubMedDate not supplied

[Subarachnoid hemorrhages in primary tumors of the spinal cord].

Spinal subarachnoid hemorrhages and multiple hemorrhages into the tissue of the tumor were diagnosed in 11 (5%) of 221 patients with primary tumors of the spinal cord. The clinical picture was characterized by sudden sharp pain in the spine corresponding in localization to the level of the spinal cord tumor. The stroke-like development of the neurological symptoms alters the classical course of spinal cord tumors considerably and makes it difficult to recognize the pathological process. Vascular disorders predominate in patients with meningiomas of the spinal cord in the upper and middle thoracic segments. The pathogenesis of spinal subarachnoid hemorrhages and hemorrhages into the tumor tissue in primary tumors of the spinal cord is discussed.

Cauda Equina↗