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At least 289 records · Page 16Linked to original sources
PubMed1994

Dermatome mapping in the rat hindlimb by electrical stimulation of the spinal nerves.

In rats treated with Evans blue (i.v.), electrical stimulation of the lumbar spinal nerves produced an extravasation zone in the skin. Stimulation of L1 produced extravasation in the lower abdomen; that of L2, in the cranial region of the hindlimb; that of L3, in the ventral region of the hindlimb and the medial paw; that of L4, in the lateral region of the hindlimb and the middle paw; that of L5, in the caudal region of the hindlimb and the lateral paw; and that of L6, in the caudal region of the hindlimb and the scrotum. Since the substance P antagonist FK224 inhibited the extravasation caused by stimulation of the sciatic nerve, the extravasation zones appeared to be related to antidromic activation of afferent C-fibers. Thus, a dermatome of afferent C-fibers was revealed in rats.

Afferent Pathways↗
PubMed2004

Pharmacological evaluation of the selective spinal nerve ligation model of neuropathic pain in the rat.

Rodent models of neuropathic pain are used to investigate the underlying mechanisms of pain associated with damage to peripheral nerves and to evaluate the efficacy of novel compounds. However, few models have been adequately characterized and the validity of many models remains unclear. The present experiment examined the activity of known anti-allodynic compounds in the L5 spinal nerve ligation (SNL) model of peripheral mononeuropathy in the rat, a modified version of the L5/L6 SNL model [S.H. Kim, J.M. Chung, An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat, Pain 50 (1992) 355-363]. Tactile sensitivity was measured 7-21 days post-surgery using von Frey monofilaments before and following treatment with gabapentin (30, 60 and 120 mg/kg), morphine (1, 3 and 6 mg/kg), amitriptyline (1.5, 3 and 10 mg/kg), fluoxetine (3, 10 and 30 mg/kg), WIN55,212-2 (0.5, 1 and 2.5 mg/kg), indomethacin (1 and 5 mg/kg) or U-50,488H (3 and 6 mg/kg). Compared to sham-operated control animals, L5 SNL animals displayed significant tactile allodynia in the ipsilateral hindpaw that was completely reversed by treatment with gabapentin, morphine, and WIN55,212-2, partially reversed by amitriptyline and fluoxetine, and unaffected by U-50,488H or indomethacin. The robust effects of the non-selective cannabinoid receptor agonist WIN55,212-2 and morphine support reports in the literature that systemic cannabinoid receptor agonists and opioids are active in neuropathic pain. These results suggest that the L5 SNL model can be utilized to determine the anti-allodynic activity of novel compounds.

Analgesics↗
PubMed1992

Determination of the segmental sensory and motor innervation of the lumbosacral spinal nerves. An electrophysiological study.

The knowledge of the segmental innervation of the skin and muscles of the lower limb in man is inadequate. For this reason, sensory and motor segmental innervation of the lower extremities was examined by electrophysiological methods in 27 normal subjects, one patient with possible L5 radiculopathy and one with possible lumbosacral plexus affection. Needle electrodes were placed at root levels from L3 to S2 using bony landmarks. The electrode was then placed close to the spinal nerve as indicated by a low (less than or equal to 1 mA) threshold necessary to stimulate motor fibres. The position was controlled by X-ray in 10 subjects. Sensory innervation was determined by recording the sensory action potential evoked by stimulating the saphenous nerve at the medial epicondyle (mainly L3 and L4) and at the medial malleolus (mainly L4 and in some L3), the medial plantar nerve at the first plantar interstice (mainly S1, some L5 and S2), the deep peroneal nerve at the first dorsal interstice (mainly L5, some S1), the sural nerve at the dorsolateral aspect of the foot (mainly S1, some L5 and S2) and at the lateral malleolus (mainly S1, some L5 and S2), and the superficial peroneal nerve at the superior extensor retinaculum (mainly L5, S1). The motor innervation was determined by stimulating the spinal nerves supramaximally and recording the evoked responses from the medial and lateral vastus (mainly L3, L4), the anterior tibial (mainly L5), the peroneus longus (L5, S1), the extensor digitorum brevis (mainly S1), the gastrocnemius (mainly S1), the abductor hallucis (mainly S2) and the biceps femoris (mainly L5, S1). Sensory and motor conduction velocity measurements along the leg and across the lumbosacral plexus indicated that there was no difference in a disto-proximal direction, except for a 10% reduction along the most distal part of the sural nerve which, however, might be explained by utilization time. There was therefore no evidence of gradual tapering of nerve fibres in a distal direction. The proximal motor conduction velocity to the most distally placed muscle (abductor hallucis) was about 20% lower than to the proximally placed muscles (gastrocnemius and biceps femoris) suggesting a general difference in fibre calibre.

Action Potentials↗
PubMed1996

Treatment of refractory urge urinary incontinence with sacral spinal nerve stimulation in multiple sclerosis patients.

BACKGROUND: Urge urinary incontinence in multiple sclerosis patients is usually due to detrusor hyperreflexia. Patients who do not respond to conservative measures such as anticholinergics, with or without clean intermittent catheterisation, are difficult to manage. METHODS: We applied electrical stimulation to the S3 sacral spinal nerves with the aim of activating afferent somatic nerve fibres. Stimulation of these fibres can inhibit the micturition reflex. An S3 electrode coupled to a subcutaneously placed pulse generator was implanted in four women who had shown a good response during temporary stimulation via a percutaneously placed wire electrode. All patients were followed for at least 2 years. FINDINGS: The number of leakage episodes decreased from a mean of 4 to 0.3 per 24 h. Two patients were completely dry. The hyperreflexia disappeared in one, improved in two, and got worse in one patient. The urodynamic result in the last patient may be explained by clinical progression of the multiple sclerosis. INTERPRETATION: Chronic stimulation of the S3 sacral spinal nerve by an implantable neuroprosthesis is a promising treatment option for selected multiple sclerosis patients with refractory urge incontinence.

Adult↗
PubMed1999

The anatomic relation of lateral mass screws to the spinal nerves. A comparison of the Magerl, Anderson, and An techniques.

STUDY DESIGN: Analysis of the anatomic relation of the Magerl, Anderson, and An screws to the spinal nerve. OBJECTIVES: To compare the potential incidence of nerve root (ventral and dorsal ramus) injury caused by the Magerl, Anderson, and An techniques. SUMMARY OF BACKGROUND DATA: Posterior plating with lateral mass screw fixation is a common procedure for managing an unstable cervical spine. Comparative study of the Roy-Camille and Magerl techniques has been reported. However, the risk of nerve root injury for the Anderson and An techniques is not known. METHODS: Three lateral mass screw insertion techniques were performed in this study: Magerl, Anderson, and An. Each technique involved two specimens and 20 screws inserted from C3 through C7. A 20-mm-long screw was used to overpenetrate the ventral cortex. The anterolateral aspect of the cervical spine was carefully dissected to allow observation of the screw-ramus relationship. RESULTS: The overall percentage of nerve violation was significantly higher with the Magerl (95%) and Anderson (90%) techniques than with the An (60%) technique (P < 0.05). The largest percentages of nerve violation for the Magerl, Anderson, and An screws were found at the dorsal ramus (50%), the bifurcation of the ventral dorsal ramus (45%), and the ventral ramus (55%), respectively. CONCLUSIONS: The results of this study indicate that the potential risk of nerve root violation is higher with the Magerl and Anderson techniques than with the An technique.

Aged↗
PubMed2005

Unilateral spinal nerve ligation leads to an asymmetrical distribution of mast cells in the thalamus of female but not male mice.

Mast cells are restricted to the leptomeninges and thalamus of healthy mice. These populations are increased by stress and highly sensitive to reproductive hormones. To examine the influence of nociception, a form of stress, on thalamic mast cells, we ligated the left fifth lumbar spinal nerve of male and female mice to induce hyperalgesia. Two, 7 and 14 days later, mice were killed and thalami examined histologically using toluidine blue stain. The total number of thalamic mast cells was not influenced by ligation of the spinal nerve compared to sham-operation in either female or male mice. However, in females, the percent of thalamic mast cells located on the side of the thalamus contralateral to the ligation was greater on days 2 and 7, coincident with mechanical hyperalgesia. At these times, areas in which mast cells were most dense contralateral to nerve-injury included the posterior (Po) and lateral geniculate (LG) nuclei compared to their symmetrical distribution in sham-operated mice. These data suggest that local nociceptive signals to each side of the thalamus rather than stress hormones influence the location of mast cells during the development of allodynia and hyperalgesia. In addition, both hyperalgesia and mast cell distribution induced by nerve-ligation differ in females compared to males, reflecting a novel neuroimmune response to pain within the CNS.

Animals↗
PubMed1981

An ultrastructural study of spinal nerve roots and dorsal root ganglia in aging rats with spontaneous radiculoneuropathy.

The spinal nerve roots and dorsal ganglia of 104- to 135-week-old rats with spontaneous radiculoneuropathy were examined by light and electron microscopy. Demyelination was common in myelinated fibers of various diameters of both ventral and dorsal roots. The most striking alteration was wide distention of myelin sheaths, which extended throughout the entire internode. The spaces formed between separated lamellae frequently were invaded by macrophages. Subsequent vesicular degeneration of myelin seemed to be mediated by invading macrophages. These processes caused complete myelin destruction, but most axons showed no degenerative changes except for obvious reduction in diameter. Occasionally, there were clumping and partial degradation of neurofilaments and ruptured axolemma in the severely demyelinated axons. A few fibers also were undergoing wallerian-type degeneration, perhaps secondary to the severe demyelinative changes. Remyelinating fibers in various phases of repair were coexistent with markedly demyelinated ones. Demyelinative changes described above also developed within some of these remyelinated internodes. There were no remarkable changes in neurons of the dorsal root ganglia, though accumulation of lipofuscin was common. Our findings suggest that the changes in the nerve roots are essentially a primary segmental demyelination in aging rats with radiculoneuropathy.

Aging↗
PubMed2005

Distinct membrane effects of spinal nerve ligation on injured and adjacent dorsal root ganglion neurons in rats.

BACKGROUND: Painful peripheral nerve injury results in disordered sensory neuron function that contributes to the pathogenesis of neuropathic pain. However, the relative roles of neurons with transected axons versus intact adjacent neurons have not been resolved. An essential first step is identification of electrophysiologic changes in these two neuronal populations after partial nerve damage. METHODS: Twenty days after spinal nerve ligation (SNL), intracellular recordings were obtained from axotomized fifth lumbar (L5) dorsal root ganglion neurons and adjacent, intact L4 neurons, as well as from control neurons and others subjected to sham-SNL surgery. RESULTS: Pronounced electrophysiologic changes were seen only in L5 neurons after SNL. Both Aalpha/beta and Adelta neuron types showed increased action potential duration, decreased afterhyperpolarization amplitude and duration, and decreased current threshold for action potential initiation. Aalpha/beta neurons showed resting membrane potential depolarization, and increased repetitive firing during sustained depolarization developed in Adelta neurons. The afterhyperpolarization duration in neurons with C fibers shortened after axotomy. In contrast to the axotomized L5 neurons, neighboring L4 neurons showed no changes in action potential duration, afterhyperpolarization dimensions, or excitability after SNL. Depolarization rate (dV/dt) increased after SNL in L4 Aalpha/beta and Adelta neurons but decreased in L5 neurons. Time-dependent rectification during hyperpolarizing current injection (sag) was greater after SNL in Aalpha/beta L4 neurons compared with L5. Sham-SNL surgery produced only a decreased input resistance in Aalpha/beta neurons and a decreased conduction velocity in medium-sized cells. In the L5 ganglion after axotomy, a novel set of neurons, consisting of 24% of the myelinated population, exhibited long action potential durations despite myelinated neuron conduction velocities, particularly depolarized resting membrane potential, low depolarization rate, and absence of sag. CONCLUSIONS: These findings indicate that nerve injury-induced electrical instability is restricted to axotomized neurons and is absent in adjacent intact neurons.

Action Potentials↗
PubMed1989

Age changes in axon number along the cervical ventral spinal nerve roots in rats.

Axon counts were made at two standardised levels of C7 ventral spinal nerve roots from 46 female rats representing nine ages between birth and 500 days. The objective was to provide a definitive account of proximodistal changes in axon numbers and of age changes in axon numbers both during postnatal development and at several stages during maturity. At each age there is a proximodistal increase in the numbers of axons in all categories examined (myelinated, promyelin, transitional, and fetal) between levels midway along the subarachnoid course of the root and where it is apposed to but separate from the dorsal root ganglion. During maturation and throughout maturity axon totals change similarly at both levels: After a slight increase immediately postnatum, they decline sharply between 4 and 20 days due to a marked loss of unmyelinated axons. A gradual decline in myelinated axon numbers continues to 500 days. While these changes are occurring, axon numbers in all categories show a proximodistal increase throughout. The magnitude of this increase lessens with age for all but the transitional category due to a preferential decrease in numbers distally. Though these observations do not differentiate between axon branching and looping of sensory axons into the ventral root as a cause of the proximodistal increase in numbers, they tend to support the former. At each age during maturation axon proportions at proximal and distal levels correspond well for each animal, indicating that axon segregation proceeds at related rates within each root. Age changes in axon proportions within the transitional and fetal categories indicate that the postnatal stage of axon segregation results from axon loss, rather than Schwann cell proliferation.

Aging↗
PubMedDate not supplied

Glial outgrowth and central-type myelination of regenerating axons in spinal nerve roots following transection and suture: light and electron microscopic study in the pig.

Glial bundles growing out of the spinal cord were observed in spinal nerve roots in the pig after their section and surgical repair. The heterotopic occurrence of glial cells, most of which were identified as astrocytes, was more frequent and more pronounced in dorsal than in ventral roots. Several of the glial bundles contained regenerated myelinated axons. These were probably myelinated by cells which showed the typical cytological criteria for oligodendrocytes and the mode of myelination was clearly of central type. It was concluded that the glial outgrowth is induced by degeneration and regeneration of axons passing the central-peripheral transition zone.

Animals↗
PubMed1999

Endogenous noradrenergic tone controls symptoms of allodynia in the spinal nerve ligation model of neuropathic pain.

Endogenous inhibitory controls were studied in the spinal nerve ligation model of neuropathic pain. Atipamezole, a selective alpha2-adrenoceptor antagonist, produced both mechanical and cold allodynia in those rats which had not developed clear neuropathic symptoms. The same doses (50 microg i.t. or 1 mg/kg s.c.) did not increase the severity of symptoms in rats which had developed them. The opioid receptor antagonist naloxone (20 microg i.t. or 1 mg/kg s.c.) had no effect on the neuropathic symptoms. These results indicate that mechanical and cold allodynia are under endogenous noradrenergic rather than opioidergic control in this model of neuropathic pain.

Adrenergic alpha-Antagonists↗
PubMed1998

Clinical evaluation of C7 spinal nerve transection: 21 patients with at least 2 years' follow-up.

We have performed C7 spinal nerve transfer to treat root injury of the brachial plexus since 1989. Out of a total of 43 patients, 21 have been followed up for at least 2 years. Evaluation of the effect of C7 transection included clinical examination, intraoperative C7 stimulation, LIDO Workset machine and electrophysiological studies to test C7 innervated muscles, and histochemical analysis of the anterior and posterior division of the upper trunk using acetylcholinesterase stain. Nearly half of the study group (48%) reported no significant sensory changes and most patients (81%) did not notice any weakness of the limb following C7 transection. Some patients did experience sensory and motor abnormalities which were most frequent during the first postoperative month, improved during the 2nd month and in most cases resolved in the 3rd postoperative month. The only longer persistent abnormality was the triceps reflex, which becomes weak or absent. We also found that intraoperative C7 stimulation was a useful predictor of possible post-transection morbidity. Subclinical deficits, detected by the LIDO workset machine and by electro-physiological studies, were quite common. Histochemical analysis revealed that the posterior division of C7 had more motor fibres than the anterior division.

Adolescent↗
PubMed2000

Downregulation of TrkA expression in primary sensory neurons after unilateral lumbar spinal nerve transection and some rescuing effects of nerve growth factor infusion.

Peripheral nerve injury results in sprouting of sympathetic and sensory nerve terminals around large diameter neurons in the dorsal root ganglia (DRG), but the underlying mechanism is not clear. Current study sought to examine changes of the nerve growth factor (NGF) receptor TrkA in DRG and spinal cord after a spinal nerve transection by an immunohistochemical technique and to investigate effects of NGF on the expression of TrkA protein in the same animal model. In the control rat, TrkA immunoreactivity was localized to about 55 +/ -1% of total neurons in DRG and to laminae I and II of the spinal cord. The percentage of TrkA immunoreactive neurons in DRG and TrkA staining intensity of spinal cord were reduced 1 week after the nerve lesion. The changes became maximal 2 weeks, but recovered partially 4 weeks after the lesion. The size of TrkA immunoreactive neurons dramatically shifted to smaller sizes, becoming more remarkable 4 weeks after the lesion. In the contralateral DRG, the percentage of TrkA immunoreactive neurons also decreased significantly. Exogenous NGF delivered to DRG for 2 weeks partially reversed the reduction of TrkA expression as well as atrophy of TrkA immunoreactive neurons. No TrkA immunoreactive basket was found around neuronal somata. Our data show that unilateral peripheral nerve injury results in dynamic downregulation of TrkA in sensory neurons in bilateral DRG and spinal cord, and that TrkA expression in sensory neurons is partially regulated by target-derived NGF.

Animals↗
PubMed2005

Glutamate uptake is attenuated in spinal deep dorsal and ventral horn in the rat spinal nerve ligation model.

Alteration of glutamatergic (GLU) neurotransmission within the spinal cord contributes to hyperalgesic and allodynic responses following nerve injury. In particular, changes in expression and efficacy of glutamate transporters have been reported. Excitatory, pain transmitting primary afferent neurons utilizing glutamate as an excitatory neurotransmitter project to both superficial (I-II) and deep (III-V) laminae of the dorsal horn. These experiments were designed to examine changes in glutamate uptake occurring concomitantly within the spinal deep dorsal and ventral horn in situ after experimentally induced neuropathic pain. In vivo voltammetry, using microelectrode arrays configured for enzyme-based detection of GLU were employed. Sprague-Dawley rats had either sham surgery or tight ligation of L5 and L6 spinal nerves (SNL). Four to six weeks later, the L4-L6 spinal cord of chloral hydrate-anesthetized animals was exposed, and ceramic-based glutamate microelectrodes equipped with glass micropipettes 50 microm from the recording surfaces were placed stereotaxically at sites within the spinal cord. Pressure ejection of GLU into the ipsilateral L5-L6 spinal cord resulted in a 72% reduction of GLU uptake in SNL rats compared to sham controls in the ipsilateral L5-L6 deep dorsal horn and a 96% reduction in the ventral horn. In contrast, in the same animals, the contralateral L5-L6 or the ipsilateral L4 spinal cord showed no change in glutamate uptake. The data suggest that spinal nerve ligation produced attenuated glutamate uptake activity extending into the deep dorsal and ventral horn. The study suggests that plasticity related to spinal nerve injury produces widespread alteration in glutamate transporter function that may contribute to the pathophysiology of neuropathic pain.

Amino Acid Transport System X-AG↗
PubMed2005

Spinal nerve ligation increases alpha2-adrenergic receptor G-protein coupling in the spinal cord.

Intrathecal and epidural administration of the alpha2-adrenergic receptor agonist clonidine in humans results in analgesia to both acute nociceptive and chronic neuropathic pain. The potency of clonidine increases with hypersensitivity to mechanical stimuli after nerve injury, although the reasons for this change are unknown. In the present study, we tested the hypothesis that peripheral nerve injury alters either spinal alpha2-adrenergic receptor-mediated G-protein activity or alpha2-adrenergic receptor number. Rats were randomized to left spinal nerve ligation (SNL) or sham surgery. Tactile hypersensitivity in the hindpaw was confirmed and lumbar spinal cords were removed for binding assays. To examine agonist-induced G-protein coupling, [35S]GTP gamma S binding experiments were performed in spinal cord membranes and sections using norepinephrine as an alpha2-adrenergic agonist. SNL was associated with an increase in maximal efficacy, but not potency, of norepinephrine-stimulated [35S]GTP gamma S binding in dorsal horn. SNL had no effect on basal [35S]GTP gamma S binding or on muscarinic cholinergic-stimulated [35S]GTP gamma S binding. [35S]GTP gamma S autoradiography showed that this increase in alpha2-adrenergic-activated G-proteins occurred both ipsilateral and contralateral to SNL surgery. SNL did not alter total alpha2-adrenergic receptor number or affinity to [3H]-rauwolscine binding, and displacement studies with the alpha2A-adrenergic antagonist BRL44408 revealed that most of the binding was associated with the alpha2A-adrenergic subtype. These data suggest that the increased potency of clonidine in neuropathic pain could reflect increased efficiency of G-protein coupling from spinal alpha2-adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed1989

Blood supply of spinal nerve roots. An experimental study in the rat.

The blood supply of rat spinal nerve roots was investigated using a variety of methods, including preparation of vascular casts with Microfil, alkaline phosphatase histochemistry and Epon embedding for light and electron microscopy. Dorsal and ventral roots were sampled and portions from the spinal cord, dorsal root ganglia and peripheral nerve were taken for comparison. There were two different types of vessels in the roots; the large extrinsic (radicular) and the minute intrinsic vessels of the nerve root parenchyma. The radicular vessels follow a straight course along the longitudinal axis of both ventral and dorsal roots. Their diameter appears to vary in different topographical regions. They are united with the longitudinal spinal cord arteries and are a major source of arterial supply to the spinal cord. There are also many small communicants with the intrinsic root vasculature. The radicular vessels are located in the root sheath and are surrounded by cells and collagen fibers forming this sheath. The intrinsic vessels of the spinal roots form a plexus of minute vessels, chiefly capillaries. Most of them are longitudinally arranged along the roots but there are also many loops and twisted portions. There are many direct connections to neighbouring vascular networks. The microvessels are surrounded by a basement lamina and wide, collagen containing extracellular spaces. The intrinsic vascularization of the roots is similar to that in the endoneurium of peripheral nerves, i.e., chiefly a plexus of minute vessels. Many direct communicants exist between these intrinsic vessels and blood vessels in the spinal cord parenchyma, ganglia and nerve.

Alkaline Phosphatase↗