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Results for “Peripheral Nerve Injuries”

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PubMed1990

[Early complex treatment of fractures of leg bones and peripheral nerve injuries].

A retrospective analysis of results of treatment of 104 patients with fractures of long tubular bones associated with injuries of peripheral nerves has shown complex therapy to be necessary. Main components of this treatment were biogenic stimulators, vitamin B12, spasmolytic and dehydration drugs in combination with electrophoresis with potassium iodide and thermal procedures. Rapid disturbance of conductivity of nerve trunks after trauma should be followed by revision of the given segment of the extremity in order to remove hematoma and make reposition of displaced fragments of the bone, which can provide recovery of the disturbed function of the nerve.

Adult↗
PubMed2003

Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal horn.

Using the blind whole cell patch-clamp recording technique, we investigated peripheral nerve injury-induced changes in excitatory synaptic transmission to neurones in lamina II of the dorsal horn. Partial (i.e. chronic constriction injury (CCI) and spared nerve injury (SNI)) and complete (i.e. sciatic nerve transection (SNT)) peripheral nerve injury altered the mean threshold intensity for eliciting A fibre-mediated EPSCs in lamina II neurones. Following SNT and CCI, EPSC threshold was significantly decreased, but following SNI, EPSC threshold was increased (naive: 32 +/- 2 mu A, SNT: 22 +/- 2 mu A, CCI: 23 +/- 2 mu A, SNI: 49 +/- 4 mu A; P < 0.01, Student's unpaired t test). Despite this disparity between models, dorsal root compound action potential recordings revealed no significant difference in the conduction velocity or activation threshold of A beta and A delta fibres in naive, SNT, CCI and SNI rats. In addition to the changes in EPSC threshold, we also observed a shift in the distribution of EPSCs. In spinal cord slices from naive rats, polysynaptic A beta fibre-evoked EPSCs were observed in 24 % of lamina II neurones, monosynaptic A delta fibre EPSCs were observed in 34 % and polysynaptic A delta fibre EPSCs were observed in 7 %. Following SNT and CCI, the percentage of neurones with polysynaptic A beta fibre EPSCs increased to > or = 65 % of the sampled population, while the percentage of neurones with monosynaptic A delta fibre EPSCs decreased to < 10 %. The percentage of neurones with polysynaptic A delta fibre EPSCs was unchanged. In contrast, following SNI, A beta fibre EPSCs decreased in incidence while the percentage of neurones with polysynaptic A delta fibre EPSCs increased to 44 %. Similar to the other injury models, however, monosynaptic A delta fibre EPSCs decreased in frequency following SNI. Thus, excitatory synaptic transmission is subject to divergent plasticity in different peripheral nerve injury models, reflecting the complexity of responses to different forms of deafferentation.

Action Potentials↗
PubMed1978

Transcutaneous electrical nerve stimulation in chronic pain after peripheral nerve injury.

Transcutaneous electrical stimulation was tested in 24 patients with chronic pain following a peripheral nerve injury in an extremity, in 10 patients with a good effect. All of these 10 patients displayed signs of increased sympathetic activity in addition to hyperalgesia. Sympathetic block gave complete freedeom from pain. In 14 patients with the same symptomatology but without an increased or with only very slightly increased sympathetic activity, no or an insignificant effect was obtained. Sympathetic block did not relieve the pain in this group. Transcutaneous electrical stimulation should be tried as an alternative to sympathectomy in causalgia major or minor.

Adult↗
PubMedDate not supplied

Peripheral nerve injury during anesthesia.

A case is presented where a peripheral nerve injury occurred due to the pressure of a restraint buckle causing a postoperative motor and sensory deficit. Because these are iatrogenic injuries it is useful to review the mechanism of injury and means of prevention.

Adult↗
PubMed2005

Emerging strategies to promote improved functional outcome after peripheral nerve injury.

PURPOSE: To present a general review of experimental strategies used to improve functional outcome after peripheral nerve injury. In order to understand the mechanisms behind the strategies, the process of nerve healing after injury is described briefly and each strategy is described in its context. Since the functional outcome is not solely determined by nerve regeneration but by a number of different factors, we have also chosen to cover many other important topics. METHODS: Literature review. RESULTS: Review article. CONCLUSIONS: Functional outcome after peripheral nerve injury is often poor and sometimes associated with neuropathic pain. Therapeutic intervention can be carried out at different levels and we attempt to place the different strategies and target molecules, in the context of the nerve healing process. The most obvious interventions are perhaps to minimize cell death and enhance regeneration across the lesion gap. Others, which are more difficult, may be to limit neuropathic pain, improve target finding and cortical reorganization, counteract effects of prolonged denervation/axotomy, and reduce electrical conduction block at the scar formation. Although clinical outcome is often poor at present, recent preclinical research provides several promising approaches and new target molecules for therapeutic intervention, such as neurotrophic factor (GDNF and ARTN) treatment of neuropathic pain, manipulation of the small Rho GTPases (Rac, Rho, Cdc42, Tc10), lipid raft manipulation, gene silencing with DNA enzyme and siRNA. In addition, recent research involving high throughput screening of gene expression (microarray) after nerve injury encourages the discoveries of new possible target molecules.

Animals↗
PubMed2004

Detection of neuropathic pain in a rat model of peripheral nerve injury.

BACKGROUND: Behavioral criteria that confirm neuropathic pain in animal injury models are undefined. Therefore, the authors sought clinically relevant measures that distinguish pain behavior of rats with peripheral nerve injury from those with sham injury. METHODS: The authors examined mechanical and thermal sensory sensitivity, comparing responses at baseline to responses after spinal nerve ligation (SNL group), sham nerve injury (sham group), or skin incision alone (control group). RESULTS: Substantial variance was evident in all sensory tests at baseline. After surgery, tests using brush, cold, or heat stimulation showed minimal distinctions between surgical groups. Postsurgical thresholds for flexion withdrawal from mechanical stimulation with von Frey fibers were decreased bilaterally in SNL and sham groups. In contrast, the probability of a complex hyperalgesia-type response with prolonged elevation, shaking, or licking of the paw was selectively increased on the ipsilateral side in the SNL group. Nonetheless, the effect of SNL on behavior was inconsistent, regardless of the sensory test. The behavioral measure that best distinguishes between SNL and sham groups and thereby best identifies animals with successful SNL-induced neuropathic pain is increased ipsilateral postsurgical probability of a hyperalgesia-type response to noxious mechanical stimulation. Using receiver operating characteristics analysis, mechanical hyperalgesia identifies a local SNL effect in approximately 60% of animals when specificity is required to be 90% or higher. CONCLUSIONS: Simple withdrawal from von Frey tactile stimulation, although frequently used, is not a valid measure of peripheral nerve injury pain in rats, whereas a complex hyperalgesic-type response is a specific neuropathy-induced behavior.

Animals↗
PubMed1988

Peripheral nerve injuries in the adult with traumatic brain injury.

Fifty adult patients who sustained a traumatic brain injury (TBI) were screened for the presence of a peripheral nerve injury (PNI). All suspected patients had diagnostic electromyography performed in order to confirm the clinical findings. The incidence of PNI with TBI was 34%. A variety of nerve injuries were seen, the most frequent of which were ulnar nerve entrapment at the elbow (10%) and brachial plexus injuries (10%). No patient initiated a complaint that led to the diagnosis. In addition, all the neuropathies were missed prior to admission. The neuropathies commonly were found in the neurologically impaired extremity and associated with spasticity. The results of this study suggest that patients sustaining a TBI have a significant and higher incidence of PNI as a complication than previously reported.

Accidents, Traffic↗
PubMed1986

Evaluation and therapy after injury to peripheral nerves.

Peripheral nerve injuries from whatever cause should be classified according to the degree of axon, fascicle, and main nerve trunk damage. This approach is useful in assessing the chances for spontaneous recovery and planning for surgery directed at improving neural recovery. Evaluation over time may be required to better classify the degree of injury. Once recovery slows or ceases, the surgical approaches available include neurolysis, nerve repair, nerve transposition, autograft reconstruction, and various procedures directed at painful neuromata. With proper mobilization and protection of neural and vascular structures, even extensive orthopaedic reconstructive procedures may be performed. Ischemic neuritis and myopathies may be improved by such combined approaches.

Humans↗
PubMed2001

Transformation of synaptic vesicle phenotype in the intramedullary axonal arbors of cat spinal motoneurons following peripheral nerve injury.

Permanent transection of a peripheral motor nerve induces a gradual elimination of whole axon collateral systems in the axotomized spinal motoneurons. There is also an initial concurrent decrease in the amount of recurrent inhibition exerted by these arbors in the spinal cord for up to 6 weeks after the injury, whereas the same reflex action returns to normal by the 12-week postoperative state. The aim of the present investigation was to study the fine structure of the intramedullary axonal arbors of axotomized alpha-motoneurons in the adult cat spinal cord following a permanent peripheral motor nerve lesion. For this purpose, single axotomized alpha-motoneurons were labeled intracellularly with horseradish peroxidase at 12 weeks after permanent transection of their peripheral motor nerve. The intramedullary portions of their motor axon and axon collateral arbors were first reconstructed at the light microscopic level and subsequently studied ultrastructurally. This study shows that the synaptic contacts made by the intramedullary axon collateral arbors of axotomized motoneurons have undergone a change in synaptic vesicle ultrastructure from spherical and clear vesicles to spherical and dense-cored vesicles at 12 weeks after the transection of their peripheral axons. We suggest that the present transformation in synaptic vesicle fine structure may also correspond to a change in the contents of these boutons. This may, in turn, be responsible for the strengthening and recovery of the recurrent inhibitory reflex action exerted by the axotomized spinal motoneurons following a prolonged permanent motor nerve injury.

Animals↗
PubMed1985

The reaction of primary sensory neurons to peripheral nerve injury with particular emphasis on transganglionic changes.

This paper reviews light- and electron microscopic, histochemical and physiological evidence which demonstrate that peripheral nerve injury in mammals is followed by profound structural and functional changes in the central terminals of the affected primary sensory neurons. Available evidence indicates that at least some of these so-called transganglionic changes are the result of ganglion cell degeneration and death, although other mechanisms are probably in effect as well. Existing data suggest that this ganglion cell death does not effect all types of ganglion cells equally, but do not permit a clearcut answer to the question of which kinds of ganglion cells are affected more than others. Results from studies with microtubule inhibitors and antibodies to nerve growth factor are compatible with the notion that depletion of retrogradely transported trophic factors is involved in the production of certain transganglionic changes. This issue needs further examination, however. Physiological studies indicate marked alterations in certain primary afferent synaptic connections after peripheral nerve lesions. So far, these changes have not been satisfactorily correlated with the structural changes induced by similar lesions. Further studies on the structural and functional response of primary sensory neurons to peripheral nerve injury are likely to contribute to the understanding of the frequent failure to regain normal sensory functions after peripheral nerve lesions in man, as well as of the basic aspects of lesion-induced changes in general in the peripheral and central nervous system.

Acid Phosphatase↗
PubMed2005

Central glucocorticoid receptors modulate the expression and function of spinal NMDA receptors after peripheral nerve injury.

Central glucocorticoid receptors (GRs) and NMDA receptors (NMDARs) have been shown to play a significant role in the mechanisms of neuropathic pain after peripheral nerve injury; however, how central GRs and NMDARs interact in this process remains unknown. Here we show that the expression and function of spinal NMDARs after peripheral nerve injury were modulated by central GRs. Chronic constriction nerve injury (CCI) in rats induced a time-dependent upregulation of NR1 and NR2 subunits of the NMDAR within the spinal cord dorsal horn ipsilateral to CCI. The upregulation of NMDARs was significantly diminished by intrathecal administration (twice daily for postoperative days 1-6) of either the GR antagonist RU38486 or an antisense oligonucleotide against GRs. Moreover, this CCI-induced expression of NMDARs was significantly attenuated in rats receiving intrathecal treatment with an interleukin-6 (IL-6) antiserum and in mice with protein kinase Cgamma (PKCgamma) knock-out. Because IL-6 and PKCgamma mediated the upregulation of central GRs after CCI as demonstrated previously, the results suggest that IL-6 and PKCgamma served as cellular mediators contributing to the GR-mediated expression of NMDARs after CCI. Functionally, nociceptive behaviors induced by NMDAR activation and CCI were reversed by a single intrathecal administration of the GR antagonist RU38486. Conversely, a single intrathecal injection with the noncompetitive NMDAR antagonist MK-801 reversed neuropathic pain behaviors exacerbated by the GR agonist dexamethasone in CCI rats. These data suggest that interactions between central GRs and NMDARs through genomic and nongenomic regulation may be an important mechanism critical to neuropathic pain behaviors in rats.

Animals↗