PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “NERVES, SPINAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

Spinal nerve segmentation in the chick embryo: analysis of distinct axon-repulsive systems.

In higher vertebrates, the segmental organization of peripheral spinal nerves is established by a repulsive mechanism whereby sensory and motor axons are excluded from the posterior half-somite. A number of candidate axon repellents have been suggested to mediate this barrier to axon growth, including Sema3A, Ephrin-B, and peanut agglutinin (PNA)-binding proteins. We have tested the candidacy of these factors in vitro by examining their contribution to the growth cone collapse-inducing activity of somite-derived protein extracts on sensory, motor, and retinal axons. We find that Sema3A is unlikely to play a role in the segmentation of sensory or motor axons and that Ephrin-B may contribute to motor but not sensory axon segmentation. We also provide evidence that the only candidate molecule(s) that induces the growth cone collapse of both sensory and motor axons binds to PNA and is not Sema3A or Ephrin-B. By grafting primary sensory, motor, and quail retinal neurons into the chick trunk in vivo, we provide further evidence that the posterior half-somite represents a universal barrier to growing axons. Taken together, these results suggest that the mechanisms of peripheral nerve segmentation should be considered in terms of repellent molecules in addition to the identified molecules.

Animals↗

Chronic spinal nerve ligation induces microvascular permeability disturbances, astrocytic reaction, and structural changes in the rat spinal cord.

The possibility that a chronic nerve ligation impairs the spinal cord cellular microenvironment was examined using leakage of endogenous albumin, reaction of astrocytes, and structural changes in a rat model. Rats subjected to 8 weeks of unilateral L4/L5 nerve ligation (a model of neuropathic pain) showed leakage of albumin, up-regulation of glial fibrillary acidic protein (GFAP) immunoreaction, and abnormal cell reaction. Distortion and loss of nerve cells as well as general sponginess of the gray matter was clearly evident. Cell changes were present in both dorsal and ventral horns and were most marked on the ipsilateral side compared to the contralateral cord. Nerve cell and glial cell changes are normally present in the regions showing intense albumin immunoreactivity, indicating disruption of the blood-spinal cord barrier (BSCB). Our observations indicate that a chronic nerve lesion has the capacity to induce selective breakdown of the BSCB that could be responsible for activation of astrocytes and abnormal cell reaction. These findings enhance our understanding of the pathophysiology of neuropathic pain and/or other spinal cord disorders.

Adaptation, Physiological↗

Compressive neuropathy of spinal nerve roots. A mechanical or biological problem?

Pathophysiologically, nerve root pain production is a complex issue. For many years, mechanical compression has been regarded as the sole cause for such pain. There are indications, however, that other factors, such as intraneural inflammation, may be of importance in this context. In this article, four cases are presented in which nerve root related pain gradually resolved without any proven change in the mechanical deformation of the involved nerve root. The data presented here suggest that mechanical compression, per se, may not always be the sole cause of radicular pain and dysfunction. These findings suggest that improvement is needed in our understanding of the pathophysiology of nerve root compression and inflammation.

Adult↗

[Anatomic considerations in relation to the importance of the external branch of the spinal nerve in surgery on the posterior cervical triangle].

The integrity of the spinal accessory nerve plays an important role in cervicofacial surgery since the majority of surgical approaches involve this structure. The resection of the spinal accessory nerve leads to the so-called < > mainly due to the denervation of the trapezius. This syndrome is characterised by the onset of regional pain, functional deficit and deformation of the shoulder joint. The anatomy of the accessory nerve is defined in the light of 93 functional neck dissections with particular regard to the following aspects: its relation with the internal jugular vein, its relation with the sternocleidomastoid muscle (ECM) and mastoid tip and its anastomoses with the cervical plexus.

Accessory Nerve↗

Ependymoma of the spinal nerve root: case report.

Ependymomas are the most common intramedullary tumor of the spinal cord. They are most common at the region of the cauda equina, accounting for up to 90% of primary tumors in that area. Extraspinal ependymomas are rare. We describe a case of an ependymoma arising in a spinal peripheral nerve root.

Adult↗

Effects of systemic carbamazepine and gabapentin on spinal neuronal responses in spinal nerve ligated rats.

There are few pharmacological studies of central neuronal measures in animal models of neuropathic pain. In the present study we have compared the effects of two anticonvulsants, carbamazepine and gabapentin, on spinal neuronal responses of nerve injured rats (selective ligation of spinal nerves L5 and L6, SNL) and sham-operated rats. The development and maintenance of cooling and mechanical allodynia of the lesioned hindlimb of SNL rats was followed with behavioural indices. The contralateral hindlimb of SNL rats and the ipsilateral hindlimb of sham-operated rats did not develop allodynia. Electrophysiological studies of SNL rats were then performed at two post-operative (PO) time points (PO days 7-10 and PO days 14-17). Spinal neurones of SNL rats, but not sham-operated rats, exhibited spontaneous activity at both PO days 7-10 and 14-17 (1 +/- 0.4 and 3 +/- 1 Hz, respectively). Paradoxically, the magnitude of electrical (C-fibre) and natural (mechanical and thermal) evoked neuronal responses of SNL rats at PO days 14-17 were smaller than the evoked neuronal responses of SNL rats at PO days 7-10 and sham-operated rats. The electrical evoked A-fibre responses of neurones were comparable for the three groups of rats. Both subcutaneous carbamazepine (0.5-22.5 mg/kg) and gabapentin (10-100 mg/kg) significantly reduced the spontaneous activity of spinal neurones of SNL rats at both PO time points. Carbamazepine had inhibitory effects on electrical C- and A-fibre and mechanical punctate (9 and 50 g) evoked neuronal responses of SNL rats which were significantly different to the lack of effect of carbamazepine on these measures in sham-operated rats. Gabapentin had comparable effects as carbamazepine on the electrical C-and A-fibre and mechanical punctate (9 and 50 g) evoked neuronal responses of SNL rats. In contrast to carbamazepine, gabapentin also reduced evoked neuronal responses of sham-operated rats and there was no difference between the effects of gabapentin in SNL and sham-operated rats. Robust behavioural changes in the SNL model of neuropathy are paralleled by a temporal increase in spontaneous activity and a paradoxical decrease in evoked spinal neuronal responses. The peripheral nerve dysfunction reveals an effect of carbamazepine which is maintained throughout the observation period, validating this experimental approach. Gabapentin, a novel treatment for neuropathic pain states, also reduced neuronal responses, but the actions of the drug were not dependent on nerve injury. Further studies at the spinal level may shed light on the physiology and pharmacology of the aberrant processes associated with neuropathic pain.

Acetates↗

Ultrastructural alterations of the rabbit sciatic nerve, spinal cord and cerebellum, following methionine sulphoximine administration.

Methionine sulphoximine (MSO) is a centrally acting neurotoxin which inhibits the glutamate metabolism enzymes and has convulsive properties. Small doses of MSO were administered to rabbits, either intravenously (i.v.) or intracerebroventricularly (ICV), and electron microscopic examination of the cerebellum, the spinal cord and the sciatic nerve was performed on the first day of rabbit hind leg rigid paralysis (myopathy with histological findings resembling myositis), which set in by the 2nd to 4th day after MSO administration. In the cerebellum focal minor alterations were found in the astrocytes (swelling and lucidity, diminution of glycogen granules) and sparsely in the presynaptic terminals (lucidity and clumping), whereas most of the neuron presented a normal appearance. In the spinal cord and in the sciatic nerve a dissociation of the axon from the myelin sheath was evident in a small number of myelinated nerve fibres, along with the appearance of vacuolated spaces. Mitochondrial disorganisation in the axons, as well as glial cell alterations, were also seen. The ultrastructural alterations were non specific, and since they were induced 2 to 4 days after the administration of either minimum doses (i.v.) or of extremely low doses (ICV) of MSO, they may be attributed to the inordinate increase of metabolism during the period of convulsions.

Animals↗

Plasticity of spinal nicotinic acetylcholine receptors following spinal nerve ligation.

The nicotinic cholinergic system is known to be important in the processing of nociceptive information. In the spinal cord, nicotinic receptors are expressed on primary afferent terminals, inhibitory interneurons and descending noradrenergic and serotoninergic fibers. Following peripheral nerve injury, the expression of numerous receptors involved in nociceptive processing is altered in the superficial dorsal horn of the spinal cord. However, the expression of nicotinic acetylcholine receptor subunits in the lumbar spinal cord following peripheral nerve injury has not been investigated. We examined the expression of the alpha3, alpha4, alpha5, alpha7, beta2, beta3 and beta4 nicotinic subunits in the spinal cord of normal and spinal nerve ligated rats using immunocytochemistry. Two nicotinic subunits were found to have an increased expression following spinal nerve ligation. The number of cells expressing the alpha3 subunit in the dorsal horn increased bilaterally following spinal nerve injury. Also, the number of alpha5 immunoreactive fibers increased significantly ipsilateral to ligation. The expression of the alpha4, alpha7, beta2, beta3 and beta4 subunits was unchanged. We propose that the increased expression of the alpha3 and alpha5 nicotinic subunits may contribute to the mechanical hypersensitivity observed following spinal nerve ligation.

Animals↗

Intercostolumbar spinal nerve anastomosis. An experimental study in dogs.

End-to-end anastomoses were done between the motor roots of T12 and T13 intercostal nerves and the ipsilateral transsected L1 lumbar nerve in four dogs. In three of the dogs, the clinical and electrophysiologic findings showed functional viability of the intercostolumbar anastomosis 3.5 months after the anastomosis was done. The method may be practical for reinnervating an injured lumbar nerve with two intercostal nerves or to bypass a spinal cord lesion.

Abdominal Muscles↗