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PubMed2000

Spinal nerve function in five volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia.

UNLABELLED: The etiology of transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia remains undetermined. Previous case reports have shown that patients acutely experiencing TNS have no abnormalities on neurologic examination or magnetic resonance imaging. The aim of our study was to determine whether volunteers with TNS would exhibit abnormalities in spinal nerve electrophysiology. Twelve volunteers with no history of back pain or neurologic disease underwent baseline electromyography (EMG), nerve conduction studies, and somatosensory-evoked potential (SSEP) testing. Then, the volunteers were administered 50 mg of 5% hyperbaric lidocaine spinal anesthesia and were placed in a low lithotomy position (legs on four pillows). The next day, all volunteers underwent follow-up EMG, nerve conduction, and SSEP testing and were questioned and examined for the presence of complications including TNS (defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of spinal anesthesia). Volunteers who had TNS underwent additional EMG testing 4-6 wk later. Five of the 12 volunteers reported TNS. No volunteer had an abnormal EMG, nerve conduction study, or SSEP at 24 h follow up, nor were there any changes in EMG studies at delayed testing in the five volunteers experiencing TNS. On statistical analysis, the right peroneal and the right tibial nerve differed significantly for all volunteers from pre- to postspinal testing. When comparing pre- and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right peroneal and left tibial nerve. There was no difference in measurements of F response, H reflex latency, amplitude, or velocity for either leg. Multivariate analysis of variance showed no significant difference between TNS and non-TNS volunteers for the changes in the nine nerve conduction tests when considered together (P = 0.4). We conclude that acute TNS after lidocaine spinal anesthesia did not result in consistent abnormalities detectable by EMG, nerve conduction studies, or SSEP in five volunteers. IMPLICATIONS: Electrophysiologic testing in volunteers experiencing transient neurologic symptoms is not abnormal.

Adult↗
PubMed2004

Spinal nerve injury increases the percentage of cold-responsive DRG neurons.

We tested the hypothesis that cold allodynia, observed following nerve injury reflects change(s) in the cold responsiveness of sensory neurons. To test this hypothesis we assessed the impact of the spinal nerve ligation (SNL) model of nerve injury on the responses of cutaneous sensory neurons to cooling in vitro. Nerve injury induced a significant increase in the incidence of cold responsive cutaneous neurons in uninjured but not injured ganglia. Because an increase in the percentage of cold responsive neurons in uninjured ganglia should increase the total neuronal response to cooling of peripheral tissue, these findings suggest that cold allodynia reflects, at least in part, a change in sensory neurons.

Animals↗
PubMed1995

Cryptorchidism and homeotic transformations of spinal nerves and vertebrae in Hoxa-10 mutant mice.

Homozygous mice mutated by homologous recombination for the AbdB-related Hoxa-10 gene are viable but display homeotic transformations of vertebrae and lumbar spinal nerves. Mutant males exhibit unilateral or bilateral criptorchidism due to developmental abnormalities of the gubernaculum, resulting in abnormal spermatogenesis and sterility. These results reveal an important role of Hoxa-10 in patterning posterior body regions and suggest that Hox genes are involved in specifying regional identity of both segmented and nonovertly segmented structures of the developing body.

Animals↗
PubMed1984

Von Hippel-Lindau syndrome with microscopic hemangioblastomas of the spinal nerve roots. Case report.

The authors describe a case of von Hippel-Lindau syndrome diagnosed at autopsy in a 49-year-old woman. She died suddenly following hemorrhage from a cerebellar hemangioblastoma. Other autopsy findings included a retinal hemangioblastoma, an adrenal pheochromocytoma, and a clear-cell renal tumor. The case was distinguished by the unexpected finding of multiple microscopic hemangioblastomas of the spinal nerve roots. The case is discussed with emphasis on the incidence of spinal hemangioblastomas in von Hippel-Lindau syndrome.

Adenoma↗
PubMed1995

Effects of potassium ions on action potential conduction in A- and C-fibers of rat spinal nerves.

Potassium ions in dentifrices for treating 'hypersensitive' dentin are believed to act directly on intradental nerves by raising extracellular potassium ion concentration ([K+]o) sufficiently to prevent action potential generation by axonal accommodation. However, the [K+]o necessary to block nerve conduction is not precisely known, nor is it certain that K+ can diffuse from a dentifrice in sufficient amounts to inactivate intradental nerves. To establish more accurately the [K+]o required to block nerve conduction under controlled conditions, we studied the effects of increased [K+]o on the sizes of compound action potentials (CAP) recorded from rat spinal nerves in vitro. [K+]o was increased by the addition of either KCl or KNO3 to Krebs' solutions applied to the central portion of the nerves. CAP attenuation increased in a dose-dependent manner as [K+]o was raised in the 8 to 64 mmol/L range, and complete block was generally produced with solutions containing at least 32 mmol/L K+. CAP attenuation was reversible, and recovery times increased with increasing [K+]o. The effects of KCl and KNO3 solutions were the same for all [K+]o tested. Half-maximal (50%) reduction in the A beta-fiber component of the CAP occurred with 17.4 mmol/L K+, and with 17.8 mmol/L and 19.3 mmol/L K+, respectively, for the A delta- and C-fiber components. Control experiments with glucose and choline chloride confirmed that the conduction block observed with increased [K+]o was not due to increased solution osmolarity or ionic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1999

Expiratory muscle activation by functional magnetic stimulation of thoracic and lumbar spinal nerves.

OBJECTIVE: This study was conducted to stimulate respiratory muscles by functional magnetic stimulation (FMS) of the spinal nerves (T1-L5) to obtain maximum expiratory function. DESIGN: A prospective before and after trial. SETTING: Functional Magnetic Stimulation Laboratory, Spinal Cord Injury Service, VA Palo Alto Health Care System, Palo Alto, CA. PARTICIPANTS: Twelve normal able-bodied subjects. INTERVENTION: A commercially available magnetic stimulator with a round magnetic coil (MC) was used. Respiratory muscle activation was achieved by placing the MC at each spinous process ranging from T1 to L5 vertebral levels. MAIN OUTCOME MEASURE: The planned major outcome was to determine the optimal MC placement for producing maximal expiratory pressure (MEP) and expiratory reserve volume (ERV) by FMS. These measurements were compared with the subjects' voluntary maximal efforts. A profile with varying stimulation intensities was also obtained in select individuals for determining the highest expiratory pressure. RESULTS: Stimulation at the T9 spinal level resulted in the highest mean MEP and ERV. Stimulation between T8 and L5 produced similar MEP and ERV as obtained from the T9 MC placement. The mean maximum MEP and ERV produced by FMS were 76.8 +/- 6.4 cm H2O (7.52 +/- 0.62 kPa) and 1.28 +/- 0.15 L, which were 67% and 79% of the subjects' voluntary maximal efforts, respectively. A stimulation intensity of 80% resulted in the highest expiratory pressure. CONCLUSION: FMS of lower thoracic and lumbar regions produced significant expiratory pressures and volumes. FMS of the expiratory muscles may prove to be a valuable technique for restoring cough in patients with spinal cord injury or other neurologic diseases, and in critical care or perioperative settings.

Adult↗
PubMed1980

[Percutaneous electrocoagulation of posterior ramus of spinal nerves in pain relief treatment of spondylogenic low back pain (author's transl)].

The author presents his results on 70 patients under treatment of low back pain by means of electrocoagulation of the posterior ramus of spinal nerves. In many cases of disc hernia it was possible to attain good results that enabled us to abandon the operative procedure. The best results were achieved in cases of sciatalgic pains, which were diminished more considerably than the local lumbosacral ones. When conservative methods fail, and no absolute operative indications exist, coagulation may be helpful in pain relief.

Back Pain↗
PubMed2002

Intrathecal adenosine following spinal nerve ligation in rat: short residence time in cerebrospinal fluid and no change in A(1) receptor binding.

BACKGROUND: Intrathecal adenosine produces a remarkably prolonged effect to relieve mechanical hypersensitivity after peripheral nerve injury in animals. The purpose of the current study was to investigate whether this reflected an alteration in kinetics of adenosine in cerebrospinal fluid or in the number of spinal A1 adenosine receptors after nerve injury. METHODS: Male rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. Two weeks later, a lumbar intrathecal catheter and intrathecal space microdialysis catheter were inserted. Adenosine, 20 microg, was injected intrathecally in these and in normal rats, and microdialysates of the intrathecal space were obtained. Radioligand binding studies of adenosine A1 receptors were determined in spinal cord tissue from other normal and spinal nerve-ligated rats. RESULTS: Adenosine disappeared from rat cerebrospinal fluid within 30 min after intrathecal injection, with no difference between normal and spinal nerve-ligated animals. A1 adenosine receptor binding sites in the spinal cord were increased after spinal nerve ligation. This increase disappeared when adenosine deaminase was added to the membrane homogenates, suggestive of decreased endogenous adenosine in the membranes of nerve-ligated animals. CONCLUSION: These data show that prolonged alleviation of hypersensitivity observed with intrathecal adenosine in this animal model of neuropathic pain is not due to prolonged residence in cerebrospinal fluid, although pharmacokinetics in tissues are unknown. Similarly, there is no evidence for up-regulation in spinal A1 adenosine receptors after spinal nerve ligation, and the adenosine deaminase experiment is consistent with a depletion of adenosine in spinal cord tissue after spinal nerve ligation.

Adenosine↗
PubMedDate not supplied

Alar transverse process impingement of the L5 spinal nerve: the far-out syndrome.

This syndrome occurs in two types of patients: (1) the elderly person with degenerative scoliosis and (2) a somewhat younger adult population with isthmic spondylolisthesis and at least 20% slip. On plain radiograph, the Ferguson view (25 degrees caudocephalic) is best for visualizing the condition, however, CT is by far the best diagnostic tool. To show this far laterally, the "window" on the CT scanner must be opened wider than usual. Both coronal and parasagittal views will demonstrate the condition, but the coronal is the most valuable. Symptoms are classical spinal nerve compression. Usually it is the L5/S1 level that is involved, but other levels can be. At surgery, it is most important that nerve decompression be carried far enough laterally. This can mean sacrificing the lower half of the pedicle and the entire transverse process. Part of the body of S1 and of the sacral ala can be removed if the surgeon prefers. Because so much bone is removed, instability is a factor to be seriously considered. How to decompress adequately and still maintain stability often poses a most difficult problem.

Adult↗
PubMed1994

Behavioral manifestations of an experimental model for peripheral neuropathy produced by spinal nerve ligation in the primate.

A goal of the present study was to document the behavioral changes observed in a model of painful neuropathy in the primate (Macaca fascicularis). A neuropathic state was induced by tight ligation of the L7 spinal nerve, just distal to the L7 dorsal root ganglion. Sensory testing was done on the ventral surface of the foot, a region that includes the L7 dermatome. Within 1 week following surgery, all monkeys (n = 3) developed a marked sensitivity to mechanical stimulation (with a camel hair brush and von Frey hairs), indicating the presence of mechanical allodynia. In 2 animals, the increased sensitivity to mechanical stimulation was also observed on the contralateral side. The threshold for withdrawal to a heat stimulus decreased, indicating the presence of heat hyperalgesia. Presentation of various cooling stimuli, such as acetone and cold water baths, suggested that cold allodynia had also developed. These behavioral phenomena are similar to those seen in humans diagnosed with peripheral neuropathic pain. The behavioral abnormalities are discussed in relation to the responses of spinothalamic tract cells recorded from primates with the same peripheral nerve injury (Palecek et al. 1992).

Animals↗
PubMed1995

Spinal nerve root injuries in brachial plexus lesions: basic science and clinical application of new surgical strategies. A review.

This paper reviews studies aimed at developing novel surgical means to correct functional deficits after spinal nerve root injuries in brachial plexus lesions. In a long series of animal experiments it has been possible to demonstrate re-established connectivity between severed roots and the damaged spinal cord segment. This encouraging functional recovery by a new surgical strategy of managing ventral root avulsion injuries prompted clinical application, with restoration of activity.

Animals↗
PubMed1994

Relationship between the intervertebral foramina and the spinal nerves at the level of C4-T2 of the human fetal vertebral column.

In 80 human fetuses of both sexes, aged 4 to 7 months the spatiality of the intervertebral foramina and the area of the cross-section of the spinal nerves at the level of C4-T2 of the vertebral column were investigated. It was found that the narrowness of the intervertebral foramen is not related to the sex of fetus. The most probable places for such narrowness are intervertebral foramina C4-C5 and T1-T2 on the right side and C7-T1 on the left side.

Embryonic and Fetal Development↗
PubMed1989

Changes in lectin binding of lumbar dorsal root ganglia neurons and peripheral axons after sciatic and spinal nerve injury in the rat.

The effects of chronic lesions of rat lumbar spinal or sciatic nerves on the binding of Glycine max (soybean) agglutinin to galacto-conjugates, in small- and medium-size primary sensory neurons of the L4 and L5 dorsal root ganglia, were examined over a 580-day period. Spinal nerve section resulted in a marked decrease in the population of stained neurons within 7 days. However, despite some retrograde morphological changes triggered by axonal injury, the proportion of stained nerve cells was normalized 180 days postoperatively. This temporary decrease in perikaryal lectin reactivity was initially associated with a marked accumulation of stained material in the nerve, proximal and distal to the site of section, with similar accumulations also being noticeable at each level of injury in sciatic nerves subjected to double ligature. This may reflect the presence of glycocompounds linked to the autolysis of nerve fibers during the phase of retrograde dying-back and Wallerian degeneration. At later stages, stained deposits could be seen scattered along central and peripheral axonal processes of the dorsal root ganglion neurons in the vicinity of the cell body. They may indicate a disturbance in the peripheral turnover of glycoproteins in chronically-transected nerves, with piling up of neuronal products. Sciatic nerve injury caused similar but less severe effects which, except for the L4 ganglion cells, were rapidly reversible.

Animals↗
PubMed2002

Subthreshold oscillations induced by spinal nerve injury in dissociated muscle and cutaneous afferents of mouse DRG.

Whole cell patch-clamp recordings were obtained from dissociated mouse lumbar dorsal root ganglion (DRG) neurons. Recordings were made from control neurons and neurons axotomized by transection of the corresponding spinal nerve 1-2 days prior to dissociation. Medium to large muscle and cutaneous afferent neurons were identified by retrograde transport of True Blue or Fluoro-Gold injected into the corresponding peripheral tissue. Action potentials were classified as non-inflected spikes (A(0)) and inflected spikes (A(inf)). High-frequency, low-amplitude subthreshold membrane potential oscillations were observed in 8% of control A(0) neurons, but their incidence increased to 31% in the nerve injury group. Fifty percent of axotomized muscle afferent A(0) cells displayed oscillations, while 26% of axotomized cutaneous afferents exhibited oscillations. Lower-frequency oscillations were also observed in a small fraction (4%) of A(inf) neurons on strong depolarization. Their numbers were increased after the nerve injury, but the difference was not statistically significant. The oscillations often triggered burst firing in distinct patterns of action potential activity. These results indicate that injury-induced membrane oscillations of DRG neurons, previously observed in whole DRG of rats, are present in dissociated DRG neurons of the adult mouse. Moreover, these observations indicate that both muscle and cutaneous afferents in the A(beta) size range give rise to injury-induced membrane oscillations, with muscle afferents being more prone to develop oscillations.

Action Potentials↗
PubMed2003

Changes in the gene expression of six subtypes of P2X receptors in rat dorsal root ganglion after spinal nerve ligation.

Increased purinergic sensitivity of injured sensory neurons suggests the possible involvement of purinoceptors for the generation of pain after nerve injury. To identify the purinoceptors that are involved, the changes in mRNA levels of 6 subtype purinoceptors were examined in the dorsal root ganglia (DRG) of the normal rat and after spinal nerve ligation, using RNase protection assay (RPA). In addition, the P2X(2) containing neurons were examined in the L5 DRG, using an immunohistochemical method. The relative amounts of mRNAs for the six purinoceptor subtypes were in the order of P2X(3)>>P2X(4)>P2X(6)>P2X(5) approximately P2X(2)>P2X(1) in the normal lumbar DRG. After nerve injury, the mRNA of P2X(5) was increased, those of P2X(3) and P2X(6) were decreased, and those of P2X(2) and P2X(4) were unchanged. Immunohistochemical studies, however, showed 23% of the total DRG neurons are P2X(2) positive in the normal L5 DRG, but that increased to 73% after nerve ligation. These data suggest that not only transcriptional but also posttranscriptional changes of multiple purinoceptors might be involved in the enhancement of purinergic sensitivity in injured sensory neurons.

Animals↗
PubMed2002

VR1, but not P2X(3), increases in the spared L4 DRG in rats with L5 spinal nerve ligation.

We investigated the expression of two candidate transducers of noxious stimuli in peripheral tissues, the vanilloid receptor subtype 1 (VR1) and the P2X(3), a subunit of the ionotropic P2X receptor for ATP, in spared L4 DRG neurons following L5 spinal nerve ligation, a neuropathic pain model. VR1 mRNA expression increased in the small- and medium-sized DRG neurons from the first to 28th day after injury, and this up-regulation corresponded well with the development and maintenance of thermal hyperalgesia of the hind paw. The increase in VR1-immunoreactive (ir) neurons was confirmed at the third day after surgery. In contrast, there was no change in expression of P2X(3) mRNA over 4 weeks after ligation, or in the percentage of P2X(3)-ir neurons observed 3 days after surgery. Our data suggests that increased VR1 in the spared L4 DRG may contribute to the exaggerated heat response observed in this neuropathic pain model. Taken together with the previous reports that P2X(3) expression increases in the spared DRG neurons in other neuropathic pain models, there appears to be differences in the phenotypic changes and pathomechanisms of the various neuropathic pain models.

Animals↗