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At least 271 records · Page 15Linked to original sources
PubMed2000

Peripheral nerve injury leads to the establishment of a novel pattern of sympathetic fibre innervation in the rat skin.

Peripheral nerve injury has been shown to result in sympathetic fibre sprouting around dorsal root ganglia (DRG) neurons. It has been suggested that this anomalous sympathetic fibre innervation of the DRG plays a role in neuropathic pain. Other studies have suggested an interaction between sympathetic and sensory fibres more peripherally. To date, no anatomical study of these possible interactions in the terminal fields of sensory and sympathetic fibres has been performed; therefore, the authors set out to study them in the rat lower lip after bilateral lesions of a sensory nerve, the mental nerve (MN). Immunocytochemistry for both substance P (SP) and dopamine-beta-hydroxylase (DbetaH) was performed. Within the first week post-MN lesions, the SP-immunoreactive (IR) fibres had degenerated almost completely, whereas DbetaH-IR fibres were found in the upper dermis, an area from which they normally are absent. These DbetaH-IR fibres were present in the upper dermis at all postsurgery times studied (1, 2, 3, 4, 6, and 8 weeks). It is noteworthy that, although, by week 6 post-MN lesions, SP-IR fibre reinnervation of the lower lip was occurring, the DbetaH-IR fibres still were present in the upper dermis. Quantification revealed that the migration and branching of the DbetaH-IR fibres into the upper dermis occurred gradually and was most significant at 4 weeks post-MN lesions, as demonstrated by the fact that the DbetaH-IR fibres were found 169.6 +/- 91.4 microm away from the surface of the skin compared with 407.1 +/- 78.4 microm away in sham-operated animals. These findings suggest that the ectopic innervation of the upper dermis by sympathetic fibres may be important in the genesis of neuropathic pain through the interactions of sympathetic and SP-containing sensory fibres.

Animals↗
PubMed1993

Inhibitory effect of anisodamine on the neuropathic hyperalgesia following peripheral nerve injury (II).

A peripheral neuropathy with hyperalgesia and allodynia was produced by loosely tying constrictive ligature around the left sciatic nerve of rats, i.v. injection of anisodamine 20 mg/Kg abolished both neuropathic hyperalgesia responses to noxious radiant heat and ectopic discharges generated from the injured region of the nerve. Anisodanime applied either systemically or locally to the damaged area of the nerve not only ceased the spontaneous ectopic discharges recorded from A beta to C fibers but also blocked the afferent ectopic discharge elicited by K+ channel blocker, noradrenaline, Ca2+ or antidromic stimulation of sciatic nerve proximal to the injured nerve area. The experiments indicated that anisodamine probably possessed a calcium channel blocker-like activity and produced selective block of the new channels in the injured area. It is suggested that anisodamine may be a candidate therapeutic agent in relieving hyperalgesia and allodynia following nerve injury.

Animals↗
PubMed2006

[Peripheral nerve injury and male sexual dysfunction].

The genital organ is innervated by autonomic and somatic nerve. The former is both sympathetic and parasympathetic nerve and the later is comprised by sensory and motor fibers. The symptoms of male sexual dysfunction are sexopathy, erectile dysfunction, disorder of ejaculation and orgasm, and pianism. Not only different symptom but the same symptom can be induced by different injured nerve. The relationship between peripheral nerve injury and male sexual dysfunction should be understood correctly.

Erectile Dysfunction↗
PubMed1982

Chronic peripheral nerve injuries alter the somatotopic organization of the cuneate nucleus in kittens.

The effect of chronic peripheral nerve injuries on the somatotopic organization of the cuneate nucleus was examined in kittens, using electrophysiological techniques. In normal kittens, most cells in the dorsal part of the nucleus possessed small receptive fields on the ipsilateral front paw. Several weeks after paw denervation in young kittens, however, many cells in the corresponding dorsal part of the nucleus responded to tactile stimulation of the wrist, forearm, or trunk. Consistent with this change in receptive fields, the neurons in the dorsal part of the nucleus were more responsive to electrical stimulation of the medial cutaneous nerve, which innervates part of the forearm, in kittens after paw denervation than in control kittens. These somatotopic changes were not an artifact of severe atrophy of the dorsal part of the nucleus. This experiment confirms that after chronic peripheral nerve injuries, central somatosensory neurons can begin to respond to ascending afferent volleys originating from other undamaged peripheral axons, which were previously incapable of exciting the cells. Moreover, this change in functional connectivity is evident at the first synapse central to the injury site.

Animals↗
PubMed1988

Newer electrodiagnostic techniques in peripheral nerve injuries.

Careful attention to technique is essential for the accurate evaluation of peripheral nerve function using conventional EMG and nerve conduction studies. Numerous technical, anatomic, and physiologic pitfalls must be avoided. The amplitudes of the M wave and SNAP contain useful diagnostic information and should be evaluated carefully in addition to conduction velocity and distal latency. Newer techniques using the F wave, H reflex, SEP, dermatomal SEP, and quantitative EMG may be helpful in evaluation of selected peripheral nerve problems. Comparative nerve conduction studies using "inching" technique permit evaluation of short nerve segments. Comparisons with parallel nerves improve diagnostic sensitivity.

Diagnostic Errors↗
PubMed2004

Peripheral nerve injury induces trans-synaptic modification of channels, receptors and signal pathways in rat dorsal spinal cord.

Peripheral tissue injury-induced central sensitization may result from the altered biochemical properties of spinal dorsal horn. However, peripheral nerve injury-induced modification of genes in the dorsal horn remains largely unknown. Here we identified strong changes of 14 channels, 25 receptors and 42 signal transduction related molecules in Sprague-Dawley rat dorsal spinal cord 14 days after peripheral axotomy by cDNA microarray. Twenty-nine genes were further confirmed by semiquantitative RT-PCR, Northern blotting, in situ hybridization and immunohistochemistry. These regulated genes included Ca2+ channel alpha1E and alpha2/delta1 subunits, alpha subunits for Na+ channel 1 and 6, Na+ channel beta subunit, AMAP receptor GluR3 and 4, GABAA receptor alpha5 subunit, nicotinic acetylcholine receptor alpha5 and beta2 subunits, PKC alpha, betaI and delta isozymes, JNK1-3, ERK2-3, p38 MAPK and BatK and Lyn tyrosine-protein kinases, indicating that several signal transduction pathways were activated in dorsal spinal cord by peripheral nerve injury. These results demonstrate that peripheral nerve injury causes phenotypic changes in spinal dorsal horn. Increases in Ca2+ channel alpha2/delta1 subunit, GABAA receptor alpha5 subunit, Na+ channels and nicotinic acetylcholine receptors in both dorsal spinal cord and dorsal root ganglia indicate their potential roles in neuropathic pain control.

Animals↗
PubMed2005

Intrathecal morphine reduces allodynia after peripheral nerve injury in rats via activation of a spinal A1 adenosine receptor.

BACKGROUND: The degree to which intrathecally administered morphine can alleviate hypersensitivity in animals after peripheral nerve injury is controversial, and the mechanisms by which morphine works in these circumstances are uncertain. In normal animals, morphine induces adenosine release, and in vitro data suggest that this link is disrupted after peripheral nerve injury. Therefore, using a controlled, blinded study design, the authors tested intrathecal morphine efficacy in rats with peripheral nerve injury and the role of spinal A1 adenosine receptors in the action of morphine. METHODS: Male rats underwent intrathecal catheter implantation and lumbar spinal nerve ligation, resulting in hypersensitivity to tactile stimulation of the paw. Intrathecal morphine alone or with naloxone or the specific A1 adenosine receptor antagonist, 1,3-dipropyl-8-cyclopentyxanthine (DPCPX), was administered, and withdrawal threshold to von Frey filament application to the hind paw was determined. RESULTS: Intrathecal morphine (0.25-30 microg) dose-dependently reversed mechanical hypersensitivity after spinal nerve ligation, with an ED50 of 0.79 microg. The effect of morphine was blocked by intrathecal naloxone. Intrathecal DPCPX alone had no effect on withdrawal threshold after spinal nerve ligation but completely reversed the effect of morphine, with an ID50 of 5.6 microg. CONCLUSIONS: This study is in accord with two recent reports that support short-term efficacy of intrathecal morphine to reverse hypersensitivity to mechanical stimuli in animal models of neuropathic pain. Despite previous studies demonstrating that morphine releases less adenosine after peripheral nerve injury, the current study suggests that the antihypersensitivity effect of morphine in these conditions is totally reliant on A1 adenosine receptor activation.

Animals↗
PubMed1996

Altered connexin expression after peripheral nerve injury.

The identification of connexin32 (Cx32) in myelinating Schwann cells and the association of Cx32 mutations with peripheral neuropathies suggest a functional role for gap junction proteins in the nerve. However, after nerve crush injury, Cx32 expression dramatically decreases in Schwann cells in the degenerating region, returning to control levels at newly formed nodes of Ranvier and Schmidt-Lantermann incisures by 30 days. The present study examined increases in expression of other connexins that occur after peripheral nerve injury. A 56/58-kDa connexin46 (Cx46) protein species was detected in adult rat sciatic nerve, along with very low levels of Cx46 mRNA. However, by 3 days after crush injury, coincident with changes in Schwann cell phenotype, Cx46 mRNA rapidly increased in the degenerating regions. Additionally, the 56/58-kDa Cx46 protein species present in adult nerve decreased and a 53-kDa Cx46 species, which was also present in cultured Schwann cells, became apparent. Connexin43 (Cx43) mRNA and protein, which was localized to perineurial cells in adult nerve, dramatically increased in endoneurial fibroblasts in the crush and distal regions by 3 days, coincident with macrophage infiltration. By 12 days after injury, Cx43 decreased and was comparable to normal nerve. These results suggest that enhanced expression of Cx46 and Cx43, by nonneuronal cells, may be important for the injury and regenerative responses of peripheral nerves.

Animals↗
PubMed2000

Peripheral nerve injury after brief lithotomy for transurethral collagen injection.

Two patients with prior prostate surgery sustained peripheral nerve injuries after transurethral collagen injection for the treatment of urinary incontinence. In the first patient, brief lithotomy positioning caused a gluteal compartment syndrome and sciatic neuropathy. In the second patient, obturator neuropathy was due to leakage of collagen along the course of the obturator nerve. This is the first report of peripheral nerve injury in patients undergoing transurethral collagen injection.

Aged↗
PubMed2002

Changes in content of macrophage migration inhibitory factor secreted by Schwann cells after peripheral nerve injury.

OBJECTIVE: To investigate whether Schwann cells can secrete macrophage migration inhibitory factor (MIF) after peripheral nerve injury. METHODS: Two kinds of infant rat Schwann cells(which were derived from intact and injured nerves respectively) were cultured in 10% newborn calf serum (NCS) DMEM/F12 medium for 72 h. Then the level of MIF in the conditioned media was determined by an enzyme-linked immunoadsordent assay (ELISA). As control,MIF level was also determined in 10% NCS DMEM/F12 medium without any cells. RESULTS: The concentration of MIF in the conditioned medium of Schwann cells derived from injured nerves was significantly higher than that of control samples (P<0.05), while the concentration of MIF in the conditioned medium of Schwann cells from intact nerves was not elevated. CONCLUSION: After peripheral nerve injury, Schwann cells can secrete MIF which may play an important role as an immunomodulatory cytokine for macrophage activation, inflammatory reactions and immune responses.

Animals↗
PubMed1997

Delay of CNTF decrease following peripheral nerve injury in C57BL/Wld mice.

In peripheral nerves, ciliary neurotrophic factor (CNTF) is localized to a subset of Schwann cells and is decreased in synthesis during Wallerian degeneration. This pattern of expression is similar to that of myelin protein genes. In the present study, C57BL/Wld mice, which exhibit delayed Wallerian degeneration, were used to determine the role of axonal contact on the regulation of CNTF synthesis. Western blot analysis showed that CNTF immunoreactivity in Wld nerves remained almost normal even 10 days after ligation when it was almost undetectable in control mice. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that 4 days after ligation, concentrations of CNTF mRNA in Wld mice had decreased much less than in control mice, but that at 10 days CNTF mRNA concentrations in Wld and control mice were comparably low. These observations suggest that maintenance of axonal contact in the absence of axonal transport from the cell body delays the decrease of CNTF mRNA normally seen after injury. Also, during Wallerian degeneration in Wld mice, the decrease of CNTF protein is delayed for many days longer than the decrease in CNTF mRNA.

Animals↗
PubMedDate not supplied

1999 Marmara earthquake; peripheral nerve injuries--electrophysiologic evaluation.

This study evaluated the clinical, demographic and electromyographic (EMG) findings of 75 patients referred to our EMG laboratory with the preliminary diagnosis of peripheral nerve injury (PNI) during the 1999 Marmara earthquake. Forty-two patients had single and 33 had serial EMGs. Seventy-nine percent of the patients were found to have PNI. Eighty-six percent of these had PNI of the extremities and 23.7% had brachial plexus injury. PNI were detected in the upper extremities in 39% of patients, in the lower extremities in 47.5% of patients and in both extremities in 13.5% of patients. It was observed that brachial plexus degeneration was at a higher rate in patients with compartment and crush syndromes (35.70% and 42.9%) and peripheral nerve (PN) degeneration was higher in patients remaining under the debris (37%). In control EMG examinations, regeneration findings were observed at a rate of 79.2% in the upper extremities and 55.3% in the lower extremities (mean 64.5%) in the patients with PNI of the extremities and 90.9% in the patients with brachial plexus injury. In conclusion, after a mean EMG follow-up of 4 months in 75 earthquake victims a reasonably high level of regeneration findings shows that prognosis will be good in the majority of patients.

Adolescent↗