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At least 217 records · Page 12Linked to original sources
PubMed1995

Substance P induced by peripheral nerve injury in primary afferent sensory neurons and its effect on dorsal column nucleus neurons.

Using in situ hybridization and the retrograde tracer, Fluorogold, we examined the expression of preprotachykinin (PPT) mRNA in the rat dorsal root ganglion neurons projecting to the gracile nucleus. Seven days after unilateral sciatic nerve transection, some medium- to large-sized neurons in the rat dorsal root ganglia projecting to the gracile nucleus express PPT mRNA, whereas very few gracile nucleus-projecting neurons on the contralateral side express PPT mRNA. Immunohistochemistry revealed an increase in substance P (SP) immunoreactivity in the gracile nucleus and large myelinated fibers in the dorsal root 2 weeks after unilateral sciatic nerve transection. The results suggest that medium to large DRG cells that project to the gracile nucleus express PPT mRNA de novo in response to peripheral nerve injury, and increased SP is transported to the gracile nucleus through large myelinated fibers. To determine whether the increased SP might affect the excitability of the gracile nucleus neurons postsynaptically, Fos expression after electrical stimulation of the injured sciatic nerve was examined. Multiple injections of the NK-1 receptor antagonist, CP-96,345, suppressed stimulus-induced Fos expression in gracile nucleus neurons including thalamic relay neurons. The inactive enantiomer, CP-96,344, had no effect on stimulus-induced Fos expression. These data indicate that the de novo synthesized SP in the lesioned primary afferent neurons may be involved in an augmentation of excitability in the dorsal column-medial lemniscus sensory pathway. This hyperexcitability may play a role in the pathogenesis of abnormal neuropathic sensations following peripheral nerve injury.

Animals↗
PubMedDate not supplied

Peripheral nerve injuries and repair in the upper extremity.

Peripheral nerve injuries are commonly seen as a result of domestic, industrial, or military trauma. Sharp objects usually cause these nerve injuries. When assessing these injuries, it is important to evaluate each nerves' motor and sensory function. One must be cognizant of associated injuries such as fractures, vascular damage, and musculotendinous lacerations. The time since the injury, level of injury, and age of the patient are important prognosticators impacting the return of function. Intraoperatively, one must assess the vascularity of the soft tissue bed and the nerve itself, the nerve gap, conduction, and the topography of the fascicles to insure proper orientation. Application of the principles of nerve repair (magnification, minimal tension, meticulous soft tissue handling, experienced surgeon and staff) can enhance the chances for a successful result. Additionally, to maximize functional recovery following peripheral nerve repair, a carefully planned program of postoperative occupational therapy and rehabilitation must be instituted.

Arm Injuries↗
PubMed2006

Peripheral nerve injuries: a retrospective survey of 456 cases.

This 16-year retrospective study reports the data on 456 consecutive patients with 557 peripheral nerve injuries (PNIs) between 1989 and 2004. Most patients were men (74%) and the mean age was 32.4 years. In 83% of cases the PNIs were isolated; combined lesions most commonly involved the ulnar and median nerves. Upper-limb PNIs occurred in 73.5% of cases; the ulnar nerve was most often injured, either singly or in combination. Vehicle accidents affecting the brachial plexus or radial, sciatic, facial, and peroneal nerves were the most common cause of injury. Penetrating trauma commonly affected the ulnar and median nerves; falls and gunshot wounds frequently affected the ulnar, radial, and median nerves; and sports injuries, particularly soccer, affected mainly the peroneal and tibial nerves. More than half of the brachial plexus lesions after vehicular accidents were from motorcycle crashes.

Adolescent↗
PubMed1980

Clinical use of vibratory stimuli to evaluate peripheral nerve injury and compression neuropathy.

The classical approach to evaluating the hand with impaired sensibility is unsatisfactory and frequently incorrect. Since the perception of vibratory stimuli is mediated through the same neural pathways as moving touch, we investigated the clinical use of the tuning fork in 101 patients with peripheral nerve injury and compression neuropathy. In potential nerve lacerations, the preoperative tuning fork evaluations accurately predicted the intraoperative findings: diminished perception of vibratory stimuli correlated with a neural conduction block, due usually to complete nerve division. Furthermore, this study suggests that diminished vibratory perception may be the earliest indication for surgical intervention in the acute compartment syndrome. We concluded that the clinical use of vibratory stimuli to evaluate peripheral nerve injury and compression neuropathy is valid, reliable, expeditious, and a test with high patient acceptability.

Adolescent↗
PubMed2005

Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury.

We show that transsynaptic apoptosis is induced in the superficial dorsal horn (laminas I-III) of the spinal cord by three distinct partial peripheral nerve lesions: spared nerve injury, chronic constriction, and spinal nerve ligation. Ongoing activity in primary afferents of the injured nerve and glutamatergic transmission cause a caspase-dependent degeneration of dorsal horn neurons that is slow in onset and persists for several weeks. Four weeks after spared nerve injury, the cumulative loss of dorsal horn neurons, determined by stereological analysis, is >20%. GABAergic inhibitory interneurons are among the neurons lost, and a marked decrease in inhibitory postsynaptic currents of lamina II neurons coincides with the induction of apoptosis. Blocking apoptosis with the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) prevents the loss of GABAergic interneurons and the reduction of inhibitory currents. Partial peripheral nerve injury results in pain-like behavioral changes characterized by hypersensitivity to tactile or cold stimuli. Treatment with zVAD, which has no intrinsic analgesic properties, attenuates this neuropathic pain-like syndrome. Preventing nerve injury-induced apoptosis of dorsal horn neurons by blocking caspase activity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity.

Afferent Pathways↗
PubMed2000

Melatonin attenuates neuronal NADPH-d/NOS expression in the hypoglossal nucleus of adult rats following peripheral nerve injury.

Oxidative stress and massive production of nitric oxide (NO) have been implicated in the neuropathogenesis following peripheral nerve injury. This study was aimed to ascertain whether melatonin would exert its neuroprotective effect on the lesioned hypoglossal neurons after peripheral axotomy, since it is known to reduce the oxidative damage in a variety of experimental neuropathologies in which NO is involved. Right-sided hypoglossal nerve transection was performed in adult rats following which the animals were given two different doses of melatonin administered intraperitoneally for 3, 7, 14, 21 and 30 successive days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were carried out to detect the neuronal NADPH-d/NOS expression in the hypoglossal nucleus (HN). At various time intervals following axotomy, the neurons in the affected HN were induced to express NADPH-d/NOS reactivity on the lesioned side peaking at 14 days. However, the enzyme expression was markedly depressed by melatonin treatment in a dose-dependent manner in terms of frequency of labelled neurons and staining intensity. It is suggested that the suppressive effect of melatonin on NADPH-d/NOS expression may be attributed to its antioxidant properties. Hence, in consideration of therapeutic strategies for reducing the oxidative stress following peripheral nerve injury, melatonin may prove to be beneficial.

Animals↗
PubMed1998

[The protective effects of nerve growth factor on peripheral nerve injury].

The protective effects of nerve growth factor (NGF) on peripheral nerve injury and sensory neuron growth were studied in three models: peripheral sympathetic nerve injury induced by intraperitoneal injection of 6-hydrodopamine (6-OHDA), mechanically injured ulnar nerve and cultured dorsal root ganglion (DRG) of newborn rats in vitro. The results indicate that NGF dose-dependently increased norepinephrine content in mouse submandibular gland and cell numbers of C7 (seventh cervical vertebra), T1 (first thoracic vertebra) dorsal root ganglion in rabbits, and also dramatically promoted the growth of neuronal projections in cultured DRG. These results suggest that NGF has significant neuroprotective action in peripheral nerve injury and a strong neuronutrition on sensory neuron.

Animals↗
PubMed2004

Further development of reconstructive and cell tissue-engineering technology for treatment of complete peripheral nerve injury in rats.

UNLABELLED: In this work we evaluated the efficacy of biodegradable composite co-polymer guiding neurotube, based on tissue-engineering technology, for the treatment of complete peripheral nerve injury where the nerve defect is significant. The right sciatic nerve of 12 three-month-old rats was completely transected and peripheral nerve segment was removed. A 2.2-cm biodegradable co-polymer neurotube containing viscous gel (NVR-N-Gel) with survival factors, neuroprotective agents and Schwann cells was placed between the proximal and the distal parts of the transected nerve for reconnection a 2-cm nerve defect. The proximal and distal parts of the nerve were fixed into the neurotube using 10-0 sutures. Ultrasound observation showed growth of the axons into the composite neurotube 2 months after the surgery. Electrophysiological study indicated compound muscle action potentials in nine out of 12 rats, 2-4 months after peripheral nerve reconstructive surgery. The postoperative follow-up (up to 4 months) on the operated rats that underwent peripheral nerve reconstruction using composite co-polymer neurotube, showed beginning of re-establishment of active foot movements. The tube was dissolved and nerve showed complete reconnection. Histological observation of the nerve showed growth of myelinated axons into the site where a 2-cm nerve defect replaced by composite co-polymer neurotube and into the distal part of the nerve. IN CONCLUSION: (1) an innovative composite neurotube for reconstruction of significant loss of peripheral nerve segment is described; (2) a viscous gel, containing survival factors, neuroprotective agents and Schwann cells served as a regenerative environment for repair. Further investigations of this reconstructive procedure are being conducted.

Animals↗
PubMed1994

Peripheral nerve injury induces Schwann cells to express two macrophage phenotypes: phagocytosis and the galactose-specific lectin MAC-2.

In N mice, peripheral nerve injury is followed by the normal rapid progression of Wallerian degeneration: Schwann cells proliferate and lose their myelin, which is phagocytized and metabolized by blood-borne macrophages. The role of Schwann cells in myelin phagocytosis is debated. Additionally, the molecular mechanisms underlying myelin phagocytosis by the two cell types are not well understood. To elucidate the role of Schwann cells as phagocytes we studied, electron microscopically, in vivo and in vitro degenerating, frozen, and neuroma nerve segments. The major cell types composing these tissues differed: Schwann and macrophages in in vivo degenerating; Schwann in in vitro degenerating; macrophages in frozen; Schwann, macrophages, and fibroblasts in neuroma nerve segments. Both macrophages and Schwann cells phagocytized myelin. We further studied, by immunocytochemistry and immunoblot analysis, the expression of molecules that are characteristically displayed by inflammatory and mature murine macrophages: MAC-1 (the C3b complement receptor), MAC-2 (a galactose-specific lectin), the Fc receptor, and the F4/80 antigen. All were detected in the macrophage-rich, in vivo degenerating, frozen, and neuroma nerve segments. Surprisingly, MAC-2 was also expressed in the macrophage-scarce, Schwann-rich, in vitro degenerating nerve. Immunocytochemistry and immunoblot analysis of isolated non-neuronal cells revealed that both macrophages and Schwann cells displayed MAC-2 on their surface and in their cytoplasm. Morphometry unveiled that galactose and lactose specifically inhibited myelin phagocytosis, as predicted if MAC-2 was mediating myelin phagocytosis by lectinophagocytosis (lectin-mediated phagocytosis). The role of MAC-2 in mediating myelin phagocytosis was further supported by two observations made in W mice that display very slow progression of Wallerian degeneration. First, the failure to degenerate in vivo was associated with deficient MAC-2 production. Second, degeneration that occurred in vitro was associated with MAC-2 production. Furthermore, a strong positive correlation between levels of MAC-2 expression and the extent of myelin destruction by phagocytosis was observed over a wide range of values.

Animals↗