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Typical spinal nerves have six cutaneous branches which reach to the skin of the body wall in the thorax and abdomen. Each of these six cutaneous branches correlates to an acupuncture point. This communication describes acupuncture points found in the thoracic and abdominal walls using anatomic nomenclature relating to cutaneous branches of the spinal nerves.
The present study was carried out to investigate the permeability of normal spinal nerve root sheaths around dorsal and ventral roots in the rat. In vivo studies were performed using Evans blue-albumin and lanthanum chloride as tracers. The Evans blue-albumin complex is macromolecular in size and lanthanum ions are small and easily visible in the electron microscope. Both tracers were injected into the subarachnoid space and 15 min later samples were taken and further processed for detection of tracer. Postmortem studies with lanthanum was also performed. Following fixation by cardiac perfusion with fixative without tracer, lanthanum chloride was added to the fixative and applied directly to exposed spinal cord including the spinal nerve roots. Macroscopical examination showed Evans blue staining of the superficial blood vessels of the spinal cord, but no staining of the parenchyma of either spinal cord or nerve roots. Fluorescence microscopy revealed, in addition to a bright red fluorescence of root sheaths, a faint longitudinally orientated red fluorescence in the endoneurium of the nerve roots, indicating the presence of the dye-albumin complex. In both in vivo and post-mortem lanthanum studies, the tracer was detected between cell layers of the nerve root sheath and in invaginations of the plasma membrane of these cells, as well as inside the nerve root parenchyma. Some of the cells of the sheaths in post-mortem animals were diffusely marked with intracellular tracer. The endo-radicular lanthanum was most often seen superficially, but lanthanum could occasionally be detected deeper in the parenchyma in the post mortem studies.(ABSTRACT TRUNCATED AT 250 WORDS)
In spinal nerve ligated Lewis strain neuropathic rats, pain behaviors and the rate of ectopic discharges of injured sensory neurons were significantly reduced by systemic injection of phentolamine. A pharmacological study indicated that this adrenergic dependency was mediated by alpha(1)-adrenoceptors (alpha(1)-AR). The development of adrenergic sensitivity in injured sensory neurons might have resulted from changes in adrenoceptor expression as a consequence of changed expression of adrenoceptor genes. This possibility was examined by determining the changes in the mRNA expression of 3 subtypes of alpha(1)-ARs, alpha(1a)-, alpha(1b)-, and alpha(1d)-ARs, in the dorsal root ganglia (DRG) after spinal nerve ligation. The L4 and L5 spinal nerves were tightly ligated in Lewis rats. One week later, the L4 and L5 DRG were collected and RNase protection assay (RPA) and in situ hybridization were performed. In the DRG of unoperated rats, a moderate amount of alpha(1a)-AR mRNA was present while the amount of either alpha(1b)-AR or alpha(1d)-AR mRNA was small. After spinal nerve ligation, there was a significant increase in the amount of alpha(1b)-AR mRNA in the nerve ligated DRG as measured by RPA. The amount of alpha(1a)-AR mRNA was decreased to 20% of the normal level while that of alpha(1d)-AR mRNA did not change. The in situ hybridization study showed that the number of alpha(1b)-AR mRNA positive neurons increased in spinal nerve ligated DRG, confirming the results of RPA study. These data suggest that the up-regulated expression of alpha(1b)-AR mRNA in axotomized DRG neurons may play an important role in the development of adrenergic sensitivity in injured sensory neurons and thus contribute to the sympathetically maintained pain in spinal nerve ligated neuropathic Lewis rats.
Spinal nerve root compression occurs commonly in conditions such as herniated nucleus pulposus, spinal stenosis, and trauma. However, the pathophysiology of the symptoms and signs related to spinal nerve root compression is poorly understood. The purpose of the present study was to assess and compare effects of various pressures and durations of acute compression on spinal nerve root conduction in the pig cauda equina. Efferent conduction (compound motor action potentials) and afferent conduction (compound nerve action potentials) were monitored during compression for 2 or 4 hours with compression pressures of 0 (sham), 50, 100, or 200 mm Hg. Recovery from compression was monitored for 1.5 hours. No significant deficits in spinal nerve root conduction were observed with 0 or 50 mm Hg compression, compared to significant conduction deficits induced by 100 and 200 mm Hg compression. Three-way analysis of variance demonstrated significant effects of compression pressure and duration on conduction at the end of compression and recovery, with a significant difference between efferent and afferent conduction at the end of the recovery period. These observations suggest an interaction between biomechanical and microvascular mechanisms in the production of nerve root conduction deficits. Such information may relate to the motor and sensory dysfunction in clinical conditions associated with spinal nerve root compression.
1. Ephaptic transmission was observed between spontaneously active single nerve fibres in the spinal nerve roots of dystrophic mice. 2. In the five ephaptically interacting pairs of fibres studied in detail, the conduction velocities in the exciting fibres were < 1 m/sec and the conduction velocities in the excited fibres were 2-10 m/sec in the immediate vicinity of the ephapses at 26-28 degrees C. 3. Membrane current analysis suggested that conduction was continuous in the exciting fibres. In some cases conduction away from the ephapse in the excited fibre was saltatory in at least one and possibly in both directions of transmission. 4. It is concluded that in at least some cases the direction of ephaptic transmission is from bare axon to myelinated axon. 5. Transmission time across the ephapses, measured as the interval between peaks of inward membrane current in exciting and excited fibres, was less than or equal to microseconds-240 microseconds. 6. Ephaptic transmission is not necessarily contingent upon the direction of propagation of the impulse in the exciting fibre. 7. Ephaptic transmission between two fibres can remain stable at frequencies of at least 70 Hz. 8. There may be multiple sites of spontaneous ectopic excitation in single dystrophic mouse spinal root axons. An impulse traversing a site of ectopic excitation may incite a subsequent burst of impulses to arise from that site following a delay of more than 100 msec.
After 43 years of investigating the intervertebral disk, the long term results of the management of patients from the standpoint of pain are not significantly different than they were prior to the identification of the herniated disk nor do they seem to be significantly different than no treatment at all. This should at least suggest that the phenomena of low back pain is far more complex than can be accounted for on the basis of a simple mechanical-pressure theory of disk derangement. There is a significant volume of literature that would point to the neural tissues themselves as the most logical structures for future research that attempts to interfere with the natural history of this disease from the standpoint of pain. It seems most appropriate to attack lumbar disk disease from this standpoint because except in uncommon cases, the pathological process is benign and self limiting. It also seems logical that major advancements in the management of "diskogenic" back pain will depend upon an appreciation of the importance of controlling neural inflammation in the early phases of the disease rather than developing new techniques of managing irreversible neural lesions and their iatrogenetic or psychiatric sequelae.
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Corticosteroids have been used in the treatment of radiculopathy and postoperative pain after lumbar disc surgery. Although the effects of steroids are thought to be antiinflammatory, the underlying nature of action may be more complex and may involve a direct effect on pain mediators like substance P. A feline model of nerve root compression and decompression was used to study the effect of steroids on the expression of cytokine differentiation antigens 4 and 5, and substance P. Ten adult cats were used. The animals were divided equally into a steroid treatment group and a control group. The sixth lumbar nerve root was compressed surgically and subsequently decompressed followed by local application of betamethasone or saline. The cats then were perfused and the corresponding nerve root and dorsal root ganglion were removed and immunostained for cytokine differentiation antigens 4 and 5, and substance P, respectively. The relative absence of cytokine differentiation antigens 4- and 5-labeled lymphocytes at the compression site in the steroid treated group is consistent with an antiinflammatory effect of the steroid. Substance P expression at the dorsal root ganglion in the steroid treated group was decreased significantly. These findings may help explain clinical observations of efficacy of steroids after spinal nerve root decompression.
Schwannomas from cranial nerves and spinal roots are most often benign, malignant schwannomas being uncommon in this location. This report describes a unique case of multiple cellular and malignant schwannomas of the cranial and spinal nerves in a patient with features of neurofibromatosis 2. The tumors were arising from left optic, bilateral oculomotor, trochlear, abducent and vestibular nerves, the left facial and the spinal lumbar nerve roots. The tumor arising from the right trochlear nerve was seen excavating into the hippocampus and the left vestibular nerve into the medulla. In addition, the patient had nodular schwannomas adherent to the inferior surface of the optic chiasm and the cerebellum away from the cranial nerves. Hyperplastic schwannosis was noted in perivascular spaces of thalamus, cerebellum and hippocampus on both sides away from the main lesions. The immunohistochemical and ultrastructural profiles of the tumors suggest that neurofibromas and schwannomas are probably not distinct tumors but lie within a spectrum that differs histologically depending on the predominant cell type.
The accuracy of reinnervation in peripheral nerves following second degree injuries, which do not disrupt the longitudinal continuity of the endoneurial sheaths, has been studied in rats. The sciatic nerve or lumbar spinal nerves (that is the extraspinal nerves before their fusion in the sciatic plexus) were crushed with fine watchmakers' forceps in neonatal and adult rats. In addition, the lumbar spinal nerves were frozen in a group of 5 adult rats. After allowing reinnervation to occur for 5 to 9 weeks, the motoneurons whose axons ran in the plantar nerve were labelled retrogradely with horseradish peroxidase. Their positions in the grey matter of the lumbar spinal cord were recorded and compared with those labelled from the contralateral unoperated plantar nerve. Very few errors of projection occurred after a crush lesion of the adult sciatic nerve but all the other lesions produced significant numbers of errors. The order, starting with the preparations with fewest errors was as follows (numbers in brackets = percentage of neurons misplaced): sciatic crush in adult (3%), sciatic crush in neonate (23%), spinal nerve freeze in adult (23%), spinal nerve crush in adult (35%), and spinal nerve crush in neonate (72%). It seems that a significant number of axonal growth cones cross endoneurial sheaths after crush or cryoinjuries. Explanations for the difference in observed reinnervation accuracy between young and old rats and between lesions in peripheral nerves and spinal nerves are discussed. The first is that axons in peripheral nerves in older rats have a less penetrable endoneurial membrane encasing them. The second is that the amount of misrouting is the same at all lesion sites but is much less easily detectable after sciatic lesions than spinal nerve lesions. This is because axons are organized in a 'musculotopic' manner in peripheral nerves and exchange of axon positions will occur largely between axons destined for the same peripheral target. In contrast, exchange of positions of axons in spinal nerves will lead to more overt errors because at this site axons destined for particular muscles do not lie side by side but are intermingled with axons innervating other peripheral targets.
The purpose of this study was to measure the changes in levels of nerve growth factor (NGF) in dorsal root ganglia (DRG) and spinal nerves with the aim of investigating the role of NGF in a rat neuropathic pain model. Nerve injuries were made by tight ligation of the left L5 and L6 spinal nerves using 6-0 silk thread in male Sprague-Dawley rats. Before surgery and 1, 3, 5, 7, and 14 days after surgery, tissue samples collected included the L3-6 DRGs bilaterally, segments of the ipsilateral L5-6 spinal nerves proximal and distal to ligation sites, and corresponding sites of the contralateral L3-6 and the ipsilateral L3-4 spinal nerves. NGF levels in the DRGs of the injured spinal nerves (the left L5 and L6) did not change significantly from control values. The spinal nerve segments distal to ligation sites had higher levels of NGF than the control values. Unlesioned sites did not show any significant changes in NGF levels. The increase of NGF in distal segments of injured spinal nerves may be due to an accumulation of retrogradely transported NGF. The maintenance of NGF levels in the DRGs that had lost peripheral connections may reflect local synthesis after nerve injury.
The L5 spinal nerve ligation model of neuropathic pain in rats has been proposed as a model for sympathetically maintained pain (SMP) based on the effects of surgical or chemical sympathectomy on nerve injury induced behavior. In an attempt to confirm that the lesion produces an animal model of SMP, surgical sympathectomies were independently conducted in two different laboratories (Johns Hopkins and University Kiel) using male Sprague-Dawley (n = 30) or Wistar rats (n = 14). The L5 spinal nerve was ligated or cut and ligated. Using von Frey hairs, paw withdrawal threshold and incidence of paw withdrawal were tested concurrently before and after the sympathectomy. The sympathectomy was either verified by (a) glyoxylic acid staining of peripheral blood vessels of the hindpaw or (b) skin temperature measurements of the hindpaws. To blind the experimenter, surgeries and behavioral tests were performed by two different investigators and a sham sympathectomy was performed at Johns Hopkins. Decreased paw withdrawal thresholds and increased frequencies of paw withdrawal on the lesioned side were observed after the L5 lesion. Thus, the L5 spinal nerve ligation resulted in behavioral signs of allodynia and hyperalgesia to mechanical stimuli. Lumbar surgical sympathectomy 1-3 weeks after the lesion or prior to lesion with bilateral removal of the sympathetic ganglia L2-L4, however, did not reverse or prevent the behavioral changes induced by the nerve injury. The lack of effect of the sympathectomies was independent of the testing paradigm used. Experiments in Wistar and Sprague-Dawley rats yielded the same results. Potential reasons for the discrepancies between the present study and earlier reports are discussed. These results indicate that an L5 spinal nerve injury rat model is not a reliable model for SMP.
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The possible basal differences in lipid class and fatty acid composition between a cranial nerve (the trigeminal nerve) and two spinal nerves (the ulnar and sciatic nerves) as well as the effects of dietary lipids on the same nerves were studied. A basal (BD) and four experimental diets containing respectively hydrogenated coconut oil (HCO), grapestone oil (GSO), olive oil (OO) and linseed oil (LSO) were used. Trigeminal lipids fatty acid composition differs significantly from sciatic and ulnar ones in the percentages of 16:0, 16:1, 18:0, 18:2 n-6, 20:0, 20:1, 20:4 n-6, 24:0, 24:1 and 22:6 n-3. Also the proportions of triacylglycerols and free cholesterol strongly differ in trigeminal and spinal nerves whereas no significant difference was detected between ulnar and sciatic nerve lipids. Following the administration of the four experimental diets for 60 days, no significant change was observed in the fatty acid pattern of trigeminal lipids while the spinal ones showed a significant increase in the proportions of the fatty acids present in large quantities in the dietary oils used (i.e.: oleic acid in the OO samples). These changes are probably linked with the rapid metabolic turnover of triacylglycerols, present in larger amounts in spinal nerve lipids.
Intradural spinal root lesions cannot be recognized by dissecting the brachial plexus and lead to ineffective surgery if they remain undetected. Therefore, patients need to undergo a diagnostic procedure to assess the intradural status of the spinal roots. Although motor recovery is the main goal of brachial plexus surgery, the techniques currently applied do not permit adequate evaluation of the anterior root. In search of an alternative, we performed intraoperative motor evoked potentials. Ninety spinal nerves in 19 patients suffering from brachial plexus lesions were dissected. Twenty-seven spinal nerves were avulsed; 8 nerves were disrupted and 17 were completely scarred, resulting in 25 stumps. Thirty-eight nerves appeared to be undamaged. On central stimulation, nerve compound action potentials were recorded from the exposed spinal nerves. Nerve compound action potentials could only be recorded from 21 stumps and from 32 apparently undamaged nerves. No recordings were obtained from 4 stumps and 7 spinal nerves in continuity. According to these findings, it is highly probable that surgery would have been insufficient in 10 spinal nerves if intraoperative motor evoked potentials had not been performed. We conclude that (1) intraoperative motor evoked potentials are an effective means for investigating the functional status of anterior motor roots and motor fibers in exposed spinal nerves, and (2) the use of motor evoked potentials should be considered during brachial plexus surgery to improve interventions.
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The influence of carbon monoxide (CO) on chronic spinal nerve lesion induced spinal cord neurodegeneration was examined using immunohistochemical expression of the constitutive isoform of its synthesising enzyme, hemeoxygenase-2 (HO-2) in a rat model. Spinal nerve lesion at L-5 and L-6 level was produced according to the Chung model of neuropathic pain and rats were allowed to survive for 8 weeks. Sham operated rats, in which the spinal nerves were exposed but not ligated, served as controls. Ligation of spinal nerves in rats resulted in an upregulation of HO-2 expression which was most pronounced in the ipsilateral gray matter of the spinal cord compared to the contralateral side. In these rats, morphological investigations showed distorted neurons, membrane disruption, synaptic damage and myelin vesiculation. Sham operated rats did not show an upregulation of HO-2 expression and the structural changes in the spinal cord were absent. These observations strongly suggest that spinal nerve lesion is associated with an increased production of CO which is somehow contributing to the neurodegenerative changes in the spinal cord, not reported earlier.
We studied whether a chronic neuropathy induced by unilateral spinal nerve ligation changes the response characteristics of spinal dorsal horn wide-dynamic range (WDR) neurons or their periaqueductal gray (PAG)-induced descending modulation. Experiments were performed in rats with behaviorally demonstrated allodynia induced by spinal nerve ligation and in a group of nonneuropathic control rats. The stimulus-response functions of WDR neurons for mechanical and thermal stimuli and the modulation of their peripherally evoked responses by electrical stimulation of the PAG were determined under pentobarbital anesthesia. The results showed that neuropathy caused a significant leftward shift in stimulus-response functions for mechanical stimuli. In contrast, stimulus-response functions for noxious heat stimuli in the neuropathic limb were, if anything, shifted rightward, although this shift was short of statistical significance. In neuropathic rats, PAG stimulation produced a significantly stronger attenuation of spinal neuronal responses induced by noxious heat in the unoperated than in the operated side. At the intensity that produced attenuation of noxious heat stimuli, PAG stimulation did not produce any significant change in spinal neuronal responses evoked by mechanical stimuli either from the operated or the nonoperated hindlimb of the neuropathic rats. Spontaneous activity of WDR neurons was higher in the operated side of neuropathic rats than in control rats. Afterdischarges evoked by peripheral stimuli were observed in 1/16 of the WDR neurons ipsilateral to spinal nerve ligation and not at all in other experimental groups. The WDR neurons studied were not activated by innocuous or noxious cold stimuli. The results indicate that spinal nerve ligation induces increased spontaneous activity and enhanced responses to mechanical stimuli in the spinal dorsal horn WDR neurons, whereas noxious heat-evoked responses are not significantly changed or if anything, attenuated. Moreover, the inhibition of noxious heat stimuli by PAG stimulation is attenuated in the neuropathic side. It is proposed that the observed changes in the response characteristics of the spinal dorsal horn WDR neurons and in their descending modulation may contribute to the neuropathic symptoms in these animals.