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At least 19 recordsLinked to original sources
PubMed1991

Treatment of traumatic peripheral nerve injury.

Peripheral nerve injuries are caused by traction, laceration and missile injury. Primary surgical repair is recommended for clean, sharp injuries that cause transection of a nerve. In compressed, stretched or contused nerves, surgical repair at three months is indicated if functional recovery has not occurred. Electromyography and nerve conduction studies are helpful in deciding which patients need secondary repair. Recovery is possible for 18 months following injury. Since nerve regeneration occurs at a rate of one inch per month, the distance from the nerve injury to the innervated muscle must be less than 18 inches. Therefore, the outcome is generally better in distal lesions than in proximal ones.

Action Potentials↗
PubMedDate not supplied

Sports and peripheral nerve injury.

Peripheral nerve injury is one of the serious complications of athletic injuries; however, they have rarely been reported. According to the report by Takazawa et al., there were only 28 cases of peripheral nerve injury among 9,550 cases of sports injuries which had been treated in the previous 5 years at the clinic of the Japanese Athletic Association. The authors have encountered 1,167 cases of peripheral nerve injury during the past 18 years. Sixty-six of these cases were related to sports (5.7%). The nerves most frequently involved were: brachial plexus, radial nerve, ulnar, peroneal, and axillary nerves (in their order of frequency). The most common causes of such injuries were mountain climbing, gymnastics, and baseball. More often, peripheral nerve injury seemed to be caused by continuous compression and repeated trauma to the involved nerve. Usually it appeared as an entrapment neuropathy and the symptoms could be improved by conservative treatment. Some of the cases were complicated by fractures and surgical exploration became necessary. Results of treatment produced excellent to good improvement in 87.9% of the cases. With regard to compartment syndrome, the authors stress the importance of early and precise diagnosis and a fasciotomy.

Adolescent↗
PubMed2004

Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury.

Peripheral nerve injury is known to upregulate the rapidly repriming Na(v)1.3 sodium channel within first-order spinal sensory neurons. In this study, we hypothesized that (1) after peripheral nerve injury, second-order dorsal horn neurons abnormally express Na(v)1.3, which (2) contributes to the responsiveness of these dorsal horn neurons and to pain-related behaviors. To test these hypotheses, adult rats underwent chronic constriction injury (CCI) of the sciatic nerve. Ten days after CCI, allodynia and hyperalgesia were evident. In situ hybridization, quantitative reverse transcription-PCR, and immunocytochemical analysis revealed upregulation of Na(v)1.3 in dorsal horn nociceptive neurons but not in astrocytes or microglia, and unit recordings demonstrated hyperresponsiveness of dorsal horn sensory neurons. Intrathecal antisense oligodeoxynucleotides targeting Na(v)1.3 decreased the expression of Na(v)1.3 mRNA and protein, reduced the hyperresponsiveness of dorsal horn neurons, and attenuated pain-related behaviors after CCI, all of which returned after cessation of antisense delivery. These results demonstrate for the first time that sodium channel expression is altered within higher-order spinal sensory neurons after peripheral nerve injury and suggest a link between misexpression of the Na(v)1.3 sodium channel and central mechanisms that contribute to neuropathic pain after peripheral nerve injury.

Animals↗
PubMed1997

Growth-associated protein 43 immunoreactivity in the superficial dorsal horn of the rat spinal cord is localized in atrophic C-fiber, and not in sprouted A-fiber, central terminals after peripheral nerve injury.

Peripheral nerve injury induces the up-regulation in dorsal root ganglion cells of growth-associated protein 43 (GAP-43) and its transport to the superficial laminae of the dorsal horn of the spinal cord, where it is located primarily in unmyelinated axons and growth-cone like structures. Peripheral nerve injury also induces the central terminals of axotomized myelinated axons to sprout and form novel synaptic contacts in lamina II of the dorsal horn. To investigate whether the sprouting of A-fiber central terminals into lamina II is the consequence of GAP-43 incorporation into their terminal membranes, we have used an ultrastructural analysis with double labelling to identify the localization of GAP-43 immunoreactivity. Transganglionic transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) was used to identify C-fiber terminals. Transganglionic transport of the B fragment of cholera toxin conjugated to horseradish peroxidase (B-HRP) was used to label A-fiber sciatic nerve central terminals in combination with GAP-43 immunocytochemistry. GAP-43 was found to colocalize only with WGA-HRP- and not with B-HRP-labelled synapses or axons. In addition, many single-labelled GAP-43 synapses were observed. Many of the WGA-HRP-labelled terminals that were characterized by degenerative changes were GAP-43 immunoreactive. Our results indicate that peripheral nerve injury induces novel synapse formation of A fibers in lamina II but that up-regulated levels of GAP-43 are present mainly in other axon projections to the superficial dorsal horn.

Animals↗
PubMed2006

Sodium channel expression in the ventral posterolateral nucleus of the thalamus after peripheral nerve injury.

Peripheral nerve injury is known to up-regulate the expression of rapidly-repriming Nav1.3 sodium channel within first-order dorsal root ganglion neurons and second-order dorsal horn nociceptive neurons, but it is not known if pain-processing neurons higher along the neuraxis also undergo changes in sodium channel expression. In this study, we hypothesized that after peripheral nerve injury, third-order neurons in the ventral posterolateral (VPL) nucleus of the thalamus undergo changes in expression of sodium channels. To test this hypothesis, adult male Sprague-Dawley rats underwent chronic constriction injury (CCI) of the sciatic nerve. Ten days after CCI, when allodynia and hyperalgesia were evident, in situ hybridization and immunocytochemical analysis revealed up-regulation of Nav1.3 mRNA, but no changes in expression of Nav1.1, Nav1.2, or Nav1.6 in VPL neurons, and unit recordings demonstrated increased background firing, which persisted after spinal cord transection, and evoked hyperresponsiveness to peripheral stimuli. These results demonstrate that injury to the peripheral nervous system induces alterations in sodium channel expression within higher-order VPL neurons, and suggest that misexpression of the Nav1.3 sodium channel increases the excitability of VPL neurons injury, contributing to neuropathic pain.

Animals↗
PubMed1998

NT-3 modulates NPY expression in primary sensory neurons following peripheral nerve injury.

Peripheral nerve transection induces significant changes in neuropeptide expression and content in injured primary sensory neurons, possibly due to loss of target derived neurotrophic support. This study shows that neurotrophin-3 (NT-3) delivery to the injured nerve influences neuropeptide Y (NPY) expression within dorsal root ganglia (DRG) neurons. NT-3 was delivered by grafting impregnated fibronectin (500 ng/ml; NT group) in the axotomised sciatic nerve. Animals grafted with plain fibronectin mats (FN) or nerve grafts (NG) were used as controls. L4 and L5 DRG from operated and contralateral sides were harvested between 5 and 240 d. Using immunohistochemistry and computerised image analysis the percentage, diameter and optical density of neurons expressing calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP) and NPY were quantified. Sciatic nerve axotomy resulted in significant reduction in expression of CGRP and SP, and significant upregulation of VIP and NPY (P < 0.05 for ipsilateral vs contralateral DRG). By d 30, exogenous NT-3 and nerve graft attenuated the upregulation of NPY (P < 0.05 for NT and NG vs FN). However, NT-3 administration did not influence the expression of CGRP, SP or VIP. The mean cell diameter of NPY immunoreactive neurons was significantly smaller in the NT-3 group (P < 0.05 for NT vs FN and NG) suggesting a differential influence of NT-3 on larger neurons. The optical densities of NPY immunoreactive neurons of equal size were the same in each group at any time point, indicating that the neurons responding to NT-3 downregulate NPY expression to levels not detectable by immunohistochemistry. These results demonstrate that targeted administration of NT-3 regulates the phenotype of a NPY-immunoreactive neuronal subpopulation in the dorsal root ganglia, a further evidence of the trophic role of neurotrophins on primary sensory neurons.

Analysis of Variance↗
PubMed2006

Spatial and temporal relationship between monocyte chemoattractant protein-1 expression and spinal glial activation following peripheral nerve injury.

Peripheral nerve injury can induce spinal microglial/astrocyte activation. Substances released by activated glial cells excite spinal nociceptive neurons. Pharmacological disruption of glial activation or antagonism of substances released by activated glia prevent or reverse pain hypersensitivity. It is not known, however, what causes spinal cord glia to shift from a resting to an activated state. In an attempt to understand the potential role of monocyte chemoattractant protein-1 (MCP-1) in triggering spinal glial activation and its contribution to the development of neuropathic pain, we investigated the effect of peripheral nerve injury on MCP-1 expression in dorsal root ganglia (DRG) and the spinal cord, and established its temporal relationship with activation of spinal microglia and astrocytes. We observed that MCP-1 was induced by chronic constriction of the sciatic nerve in DRG sensory neurons, spinal cord motor neurons and in the superficial dorsal horn, ipsilateral to the injury. Neuronal MCP-1 induction was followed by surrounding microglial activation. After peaking at day 7 after injury, MCP-1 levels began to decline rapidly and had returned to baseline by day 150. In contrast, microglial activation peaked by day 14 and declined afterwards to reach a lower, yet significantly raised level beyond day 22 and remained increased until the end of the test period. Astrocyte activation became detectable later, progressed more slowly and also remained increased until the end of the test period, in parallel with a decreased nociceptive threshold. Our results suggest that neuronal MCP-1 may serve as a trigger for spinal microglial activation, which participates in the initiation of neuropathic pain. Delayed, sustained astrocyte activation may participate with microglia in the persistent phase of pain hypersensitivity.

Activating Transcription Factor 3↗
PubMed1990

[Dynamic changes in abnormal afferent activities following peripheral nerve injury].

Peripheral nerve injury by chronic compression caused a decrease in conductive velocity or a delay in the transmission of the action potential, later blocking it completely following demyelination of the damaged nerve region. Abnormal firing activities were recorded from the injured peripheral nerve fibers after the 6-7th postoperative day. There were different patterns of abnormal firing from fibers. Regular tonic ectopic firings with high frequency were always recorded from A beta fibers. A delta/C fibers, however, had burst or irregular spikes. A single antidromic shock to the damaged region sometimes induced ectopic spikes following the expected one. The demyelinated region of the damaged nerve was very sensitive to both tetraethylammonium, a K+ channel blocker, and noradrenaline. The authors suggest that new ion channels or receptors, absent in normal, form in the damaged region.

Action Potentials↗
PubMed2005

Differential pharmacological modulation of the spontaneous stimulus-independent activity in the rat spinal cord following peripheral nerve injury.

Peripheral nerve injury is a significant clinical problem that is often difficult to treat. The major clinical symptoms are numbness, tactile and cooling allodynia, hyperalgesias as well as ongoing pain. In animal models of neuropathy, abnormal responses to applied (or evoked) stimuli can be gauged, but spontaneous pain, a major clinical issue, has proved very difficult to assess. In neuropathic animals, spinal neuronal hyperexcitability indicative of peripheral and central changes with high levels of spontaneous neuronal firing has been reported. This latter stimulus-independent firing of sensory neurones may be a measure related to ongoing pain. Two weeks after L5/6 spinal nerve ligation, deep dorsal horn neurones were recorded in halothane-anesthetized rats. The majority of neurones in neuropathic rats showed increased levels of spontaneous firing with irregular firing patterns. We examined and compared the effects of 5 centrally acting pharmacological agents: morphine (i.t. or i.v.), gabapentin, ketamine, memantine and mepyramine on stimulus-independent neuronal firing. This ongoing activity showed high sensitivity to gabapentin (s.c.) and morphine (i.t.) administration, being significantly reduced in a dose-dependent manner. Morphine administered via the systemic route produced modest but non-significant reductions of spontaneous activity. The two NMDA receptor antagonists, ketamine and memantine, and the histamine H1 receptor antagonist, mepyramine, produced minor effects at doses known to be effective on stimulus evoked measures of deep dorsal horn neurones. This may form an electrophysiological basis for the efficacy of gabapentin and spinal morphine on ongoing pain in patients with peripheral neuropathy.

Action Potentials↗
PubMed1996

Fatty acid binding protein is induced in neurons of the dorsal root ganglia after peripheral nerve injury.

Peripheral nerve trauma induces the expression of genes presumed to be involved in the process of nerve degeneration and repair. In the present study, an in vivo paradigm was employed to identify molecules which may have important roles in these processes. A cDNA library was constructed with RNA extracted from rat dorsal root ganglia (DRG) 3 days after a sciatic nerve crush. After differential hybridization to this library, several cDNAs were identified that encoded mRNAs that were upregulated in the DRG ipsilateral to the crush injury, as opposed to the contralateral or naive DRG. Approximately 0.15% of all the clones screened were found to be induced. This report presents the types of induced sequences identified and characterizes one of them, DA11. The 0.7 kb DA11 full length cDNA clone contains a 405 nucleotide open reading frame that encodes a putative protein of 15.2 kDa (135 amino acid residues) and is a member of the family of fatty acid binding proteins (FABP). The DA11 protein differs by one amino acid residue from the sequence of the C-FAPB protein and by eight residues from the sequence of mal1, proteins found in rat and mouse skin, respectively. Northern and Western blot analyses showed that the DA11 mRNA and protein were induced in the injured DRG. Furthermore, studies using antibodies generated against DA11 found that the DA11-like immunoreactivity was more pronounced in the nuclei of neurons located in the DRG ipsilateral to the sciatic cut than those located in the contralateral DRG. The induction of DA11 mRNA and protein in DRG neurons suggests, for the first time, the involvement of a neuronal FABP in the process of degeneration and repair in the nervous system.

Amino Acid Sequence↗
PubMed1998

Anti-hyperalgesic and anti-allodynic effects of intrathecal nociceptin/orphanin FQ in rats after spinal cord injury, peripheral nerve injury and inflammation.

We examined the effects of intrathecal nociceptin, the endogenous ligand for the orphan opioid receptor-like receptor, on abnormal pain-related behaviors in rats after carrageenan-induced inflammation and photochemically-induced peripheral nerve or spinal cord ischemic injury. Intrathecal nociceptin dose-dependently alleviated mechanical and cold allodynia-like behavior in the two models of neuropathic pain. The heat hyperalgesia associated with peripheral inflammation was also significantly reduced, although the efficacy of the antihyperalgesic effect of nociceptin in the inflammation model was decreased. Intrathecal nociceptin also induced significant antinociception on the tail-flick test in all three groups of rats. However, the antinociceptive effect of nociceptin was significantly reduced in rats with peripheral nerve injury. These results indicated that spinally administered nociceptin has anti-allodynic and anti-hyperalgesic effects in animal models of tonic or chronic pain of different origins. Peripheral inflammation and nerve injury may induce spinal plasticity which leads to altered potency and efficacy of nociceptin.

Analgesics↗
PubMed1992

Response of the gustatory system to peripheral nerve injury.

Peripheral taste nerve damage occurs as a result of disease and surgery. The response depends on the taste field affected and the species. Nerve regeneration is robust after the nerve is crushed or after it is cut if the severed ends are anastomosed. Taste buds, which appear after nerve regeneration, may be derived from dormant stem cells outside of taste buds or from remnants of taste buds that persist following denervation. Sprouting by intact taste nerves into denervated fields apparently does not occur. Regenerated primary afferents have taste response specificity, but it is unknown if neural response types are retained peripherally or centrally. Recent behavioral studies show specific deficits following loss of restricted taste fields in rodents, but little is known about recovery after nerve regeneration. Specific deficits have not been demonstrated in humans, although taste sensitivity has been correlated with numbers of taste buds. Enigmas such as these may be solved once the response of the central nervous system to gustatory nerve injury is defined.

Animals↗
PubMed2000

Effects of endogenous neurotrophins on sympathetic sprouting in the dorsal root ganglia and allodynia following spinal nerve injury.

Peripheral nerve injury is often complicated by a chronic pain syndrome that is difficult to treat. In animal models of peripheral nerve injury, sympathetic nerve terminals in the dorsal root ganglia (DRG) sprout to form baskets around large diameter neurons, an anatomical change that has been implicated in the induction of neuropathic pain. In the present study, we have investigated whether neurotrophins derived from peripheral sources play any roles in sympathetic sprouting and neuropathic pain in a rat model of peripheral nerve injury. After transection of the left lumbar (L) 5 spinal nerve, antisera specific to neurotrophins were injected intraperitoneally twice a week for 2 weeks. The foot withdrawal response to von Frey hairs was examined on days 1, 3, 7, 10, and 14 postlesion. After completion of behavioral tests, sympathetic sprouting in DRG was examined by tyrosine hydroxylase (TH) immunohistochemistry. The number of TH-immunoreactive (ir) fibers and baskets around large neurons within the lesioned DRG was dramatically increased in the rats treated with control normal sheep serum. Antisera specific to nerve growth factor (NGF), neurotrophin-3 (NT3), and brain-derived neurotrophic factor (BDNF) significantly reduced the sympathetic sprouting and the formation of baskets. L5 spinal nerve lesion induced a significant increase in foot withdrawal responses to von Frey hair stimuli, which was attenuated by treatment of antisera to neurotrophins with a different time sequential. The effect of BDNF antiserum occurred earlier and lasted longer than those of NGF and NT3 antisera. These results implicate that peripherally derived neurotrophins are involved in the induction of sympathetic sprouting and neuropathic pain following peripheral nerve injury.

Animals↗
PubMed1996

Peripheral nerve injury.

Inadequate peripheral nerve regeneration as a result of trauma contributes greatly to the morbidity of surgical patients. Animals admitted as an emergency often have concurrent orthopaedic injuries that impair mobility and may mask peripheral nerve dysfunction if a thorough neurological examination is not performed. This article reviews the pertinent anatomy of the peripheral nervous system as well as the degenerative and regenerative responses that occur in traumatized nerves. Physical examination and electrodiagnostic techniques that characterize the extent of nerve impairment are described. The management of peripheral nerve lacerations for open and closed wounds is detailed, as well as the presenting clinical signs and prognosis for brachial plexus avulsions, sciatic nerve damage, and sacrococcygeal injury.

Animals↗
PubMed2002

Acute reductions in GABAA receptor binding in layer IV of adult primate somatosensory cortex after peripheral nerve injury.

Following peripheral nerve transection, reorganizational plasticity has been reported to occur in two phases, one immediate and one more protracted. GABA (gamma-aminobutyric acid) has been implicated in the immediate "unmasking" phase of reorganization. We have used quantitative autoradiography to assess potential changes in GABA(A) and GABA(B) receptor binding in primate somatosensory cortex following peripheral nerve injury. Here we report reductions in GABA(A) receptor binding in layer IV of primate somatosensory cortex deprived of its normal activating inputs for 2-5 h by peripheral nerve transection.

Animals↗
PubMed1996

Peripheral neuropathy and peripheral nerve injury.

The peripheral nerves to the bladder can be altered by several disease processes. Voiding symptoms alone are not reliable in predicting the exact neurogenic bladder dysfunction. Urodynamic evaluation is crucial to optimize therapy and to rule out concomitant pathology.

Diabetes Complications↗
PubMed1996

Adrenal medullary implants reduce transsynaptic degeneration in the spinal cord of rats following chronic constriction nerve injury.

Peripheral nerve injury causes abnormal sensory processing, possibly due in part to neuroplastic changes in the CNS. Following chronic constriction injury of the sciatic nerve, transsynaptic degeneration is suggested by the presence of "dark neurons" found in superficial laminae of spinal cord. Previous studies in our laboratory have shown that grafts of adrenal medullary cells into the spinal subarachnoid space can reduce abnormal pain due to peripheral nerve injury. A possible mechanism for these beneficial effects is the reduction or interruption of excitotoxic events that lead to pathological CNS changes. In order to examine this, 2 weeks after unilateral sciatic nerve ligation using a chronic constriction injury model, animals received either adrenal medullary or control striated muscle tissue implanted in the lumbar subarachnoid space. Control striated muscle-transplanted animals with nerve injury displayed thermal hyperalgesia and elevated numbers of dark neurons in the superficial dorsal horn, compared to intact animals. These dark neurons were increased bilaterally, but predominantly ipsilaterally, to nerve injury. In contrast, in animals with adrenal medullary transplants, reduced numbers of dark neurons were found in parallel with reduced hyperalgesia. The low numbers of dark neurons in these animals were similar to age-matched unoperated controls. Two months after nerve ligation, dark neurons were not found in animals with nerve injury, although abnormal ruffled-appearing neurons were still present in untransplanted animals, suggesting partial recovery of damaged spinal neurons. The results of this study suggest that spinal adrenal medullary transplants can attenuate the neuropathological events perpetuating nerve-injury-induced pain by enhancing recovery of spinal neurons from excitotoxic insult.

Adrenal Medulla↗
PubMed1982

Results of untreated peripheral nerve injuries.

Closed injuries involving peripheral nerves are likely to occur in a severely comminuted fracture, a dislocated or stretched joint, or a fracture adjacent to a joint. Peripheral neuropathy associated with fractures are usually neurapraxia lesions and have an excellent prognosis for spontaneous recovery. Peripheral neuropathy associated with open injuries has a prognosis related to the etiology; lacerations are usually neurotmesis lesions and should be completely examined, explored, and sutured; shotgun wounds demand debridement and visualization of involved peripheral nerves; high-velocity missile wounds often create axonotmesis lesions, and involved peripheral nerves have a better prognosis for spontaneous recovery than peripheral neuropathy associated with low-velocity missile wounds. Complete and precise physical examination of peripheral nerve function at the time of injury is the best baseline for management. Electrodiagnostic studies should be initiated after one month and recorded periodically to evaluate the course of clinical recovery. It is appropriate to explore at three to four months the total nerve lesion associated with missile and shotgun wounds above the elbow or knee, stretch injuries from dislocated joints, and fractures that are severely comminuted or adjacent to joints. Many of these nerves will have a neuroma-in-continuity, and precise techniques for evaluation of nerve conduction must be utilized.

Electromyography↗