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PubMed1994

Chronic peripheral nerve pain treated with direct electrical nerve stimulation.

Chronic somatic peripheral nerve pain was treated prospectively in 24 nonrandomized patients by a program of direct electrical nerve stimulation. Patients qualified for the program if anesthetic (lidocaine) nerve block of the involved cutaneous zone of the peripheral nerve relieved symptoms and transcutaneous electrical nerve stimulation transiently improved and did not exacerbate somatic pain. Results were judged according to a pain score. Patients noted improved sleep and complete absence of the need for narcotic pain medication. On the basis of subjective and objective criteria, 18 patients had good or excellent results and 6 had implant failures. Of the six patients with failures, three failed the trial period and did not have implantation, and three had no significant pain relief and were judged as treatment failures. Three patients had late equipment failure after initial good results. Most patients had some relief of pain, which increased their quality of life and eliminated the need for narcotic analgesia. Direct electrical nerve stimulation should be considered for somatic peripheral nerve pain that has not been ameliorated with other methods. It will reduce, although not necessarily eliminate, pain and pain behavior in most patients.

Adolescent↗
PubMed1995

4-Methylcatechol, an inducer of nerve growth factor synthesis, enhances peripheral nerve regeneration across nerve gaps.

The effect on peripheral nerve regeneration of 4-methylcatechol (MC), which is a potent inducer of nerve growth factor (NGF) synthesis in vitro and in vivo, was examined in a sciatic nerve-lesioned animal model. The sciatic nerve of adult male Wistar rats was transected and both of the cut ends were then inserted into sterile silicone tubes that were subsequently attached to an intervening silicone chamber. After surgery, the rats were injected i.p. every day for 2 weeks with MC. Two weeks after surgery, the density of nonmyelinated axons within the chamber was significantly increased in the MC-treated group compared with that in the control group. Five weeks after surgery, both the number and the diameter of myelinated axons within the chamber of the MC-treated group were significantly larger than those of the control group. When the chamber was filled with anti-NGF antibody solution, most of the MC effect was blocked. These results suggest that MC stimulates de novo synthesis of NGF (and/or NGF-related molecules), which results in the enhancement of sprouting and maturation of peripheral axons.

Animals↗
PubMed2002

Peripheral nerve blocks for postoperative analgesia.

Peripheral nerve blocks are used as part of a preemptive and multimodal analgesic technique to provide safe and effective postoperative pain management with minimal side effects. They are used for a variety of surgical procedures in both inpatient and outpatient settings. Peripheral nerve blocks have resulted in shorter recovery times, decreased anesthesia-related complications, and better postoperative pain management. Peripheral nerve blocks, as part of a multimodal analgesic regimen, have decreased recovery times by lessening side effects (e.g., nausea, vomiting, drowsiness). Nerve blocks have allowed procedures previously performed only in hospitals to be performed on an outpatient basis by providing extended surgical area analgesia. The use of peripheral nerve blocks, however, requires skilled and knowledgeable clinicians. This article discusses the mechanism of action and the role of peripheral nerve blocks in multimodal analgesia, as well as perioperative nursing implications and management for upper and lower extremity peripheral nerve blocks.

Analgesia↗
PubMed2003

Mesh electrode for peripheral nerve stimulation.

The implanted peripheral nerve stimulator has a role for pain relief in well-selected patients with pain in a peripheral nerve distribution. We describe an electrode to help simplify the surgical implantation of a peripheral nerve stimulator and also to reduce the possibility of electrode migration following implantation. Design details of the electrode are discussed, as are notes on surgical technique.

Electric Stimulation↗
PubMed2006

BDNF/TrkB signaling regulates HNK-1 carbohydrate expression in regenerating motor nerves and promotes functional recovery after peripheral nerve repair.

Functional recovery after peripheral nerve injury is often poor despite high regenerative capacity of peripheral neurons. In search for novel treatments, brief electrical stimulation of the acutely lesioned nerve has recently been identified as a clinically feasible approach increasing precision of axonal regrowth. The effects of this stimulation appear to be mediated by BDNF and its receptor, TrkB, but the down-stream effectors are unknown. A potential candidate is the HNK-1 carbohydrate known to be selectively reexpressed in motor but not sensory nerve branches of the mouse femoral nerve and to enhance growth of motor but not sensory axons in vitro. Here, we show that short-term low-frequency electrical stimulation (1 h, 20 Hz) of the lesioned and surgically repaired femoral nerve in wild-type mice causes a motor nerve-specific enhancement of HNK-1 expression correlating with previously reported acceleration of muscle reinnervation. Such enhanced HNK-1 expression was not observed after electrical stimulation in heterozygous BDNF or TrkB-deficient mice. Accordingly, the degree of proper reinnervation of the quadriceps muscle, as indicated by retrograde labeling of motoneurons, was reduced in TrkB+/- mice compared to wild-type littermates. Also, recovery of quadriceps muscle function, evaluated by a novel single-frame motion analysis approach, and axonal regrowth into the distal nerve stump, assessed morphologically, were considerably delayed in TrkB+/- mice. These findings indicate that BDNF/TrkB signaling is important for functional recovery after nerve repair and suggest that up-regulation of the HNK-1 glycan is linked to this phenomenon.

Animals↗
PubMed1980

Funicular orientation by electrical stimulation and internal neurolysis in peripheral nerve suture.

Eleven peripheral nerve lacerations around the wrists of ten patients were treated with funicular suture or nerve graft. In three freshly lacerated nerves funicular orientation could be made only by electrical stimulation to both cut ends. The electrophysiological method was also utilised to obtain funicular orientation of a proximal stump in eight old nerve lacerations. However, funicular orientation of the distal stump of old lacerations, which was not responsive to electrical stimulation, was performed anatomically by internal neurolysis from a terminal branching area up to a distal stump. By six months after the operation, motor and sensory functions of the patients with funicular suture had recovered to an excellent degree with rapid reinnervation.

Adolescent↗
PubMed2001

Clinical grading of peripheral nerve problems.

To treat peripheral nerve problems appropriately, and to evaluate outcomes of peripheral nerve surgery, it is necessary to be able to stage the degree of nerve impairment. This article describes quantitative sensory testing that permits the necessary measurements for clinical grading of peripheral nerve functions.

Cubital Tunnel Syndrome↗
PubMed1988

Imaging of peripheral nerve lesions.

The imaging of peripheral nerve lesions remains limited to the radiographic demonstration of secondary skeletal lesions in birth trauma, reflex sympathetic dystrophy, neuropathic arthropathy, leprosy, and congenital indifference to pain. Nerve root avulsions can be imaged directly and the newer imaging modalities now allow delineation of lesions that previously could not be studied using conventional radiography. The ability of ultrasound, CT, and MRI to differentiate soft tissue structures makes it possible, in many instances, to study the primary abnormality in trauma, nerve entrapment syndromes, and tumors. With fractures, the possibility of trauma to adjacent nerves can only be inferred on the radiographs, while the role that peripheral nerve injury plays remains controversial in other entities, such as amputation with replantation. Imaging of peripheral nerve lesions remains in its infancy. With further refinement in the signal-to-noise ratio made possible by advances in MRI technology, we may be optimistic about future imaging of peripheral nerve pathology.

Arthropathy, Neurogenic↗
PubMed1990

Nerve sprouting induced by a piece of peripheral nerve placed over a normally innervated frog muscle.

1. The effects of a segment of peripheral nerve on the innervation of a skeletal muscle were investigated in the cutaneous pectoris muscle of the frog Rana esculenta. An explant of the sciatic nerve was placed in an aneural region of the muscle at a distance of 1-3 mm from the zone of neuromuscular junctions. The muscles were examined morphologically and electrophysiologically at different post-operative times. 2. After the first month nerve sprouts were seen arising from both nerve terminals and intramuscular nodes of Ranvier. Both the number of sites of sprouting and the relative distance to the explant tip increased with time (up to 5 months), suggesting spread of a nerve sprouting-promoting stimulus. 3. Most neurites resulting from sprouting were seen growing towards the nerve explant, in the vicinity of which active neurite proliferation occurred. Some of them entered the explant as observed in semi-thin and thin sections which revealed the presence of both myelinated and unmyelinated nerve fibres. 4. Electrical stimulation of the nerve explant in preparations autografted for more than 2 months resulted in the contraction of bundles of muscle fibres. Endplate potentials of similar amplitudes were recorded intracellularly in some muscle fibres of such preparations when stimulating either the nerve explant or the cutaneous pectoris nerve. When two stimuli were paired by gradually reducing the interval of time between them, the second response was gradually facilitated. This confirmed that nerve fibres stimulated through the explant corresponded to new neuritic processes resulting from motor nerve sprouting. 5. Pieces of perineural tissue and segments of peripheral nerve killed by alcohol treatment or by repeated freezing and thawing were used as controls. They did not induce any nerve sprouting. 6. The results indicate that cells surviving in a segment of peripheral nerve trunk actively induce intact axons to sprout both from their terminals and intramuscular nodes of Ranvier; moreover these cells promote attraction and proliferation of growing neurites. The possibility of release of a diffusible factor by glial cells is discussed.

Animals↗
PubMed1992

Endoneurial blood supply to peripheral nerves is not uniform.

Peripheral nerves are not uniformly susceptible to the effects of ischemia in human and experimental ischemic neuropathies. Since endoneurial blood flow is directly proportional to the number of endoneurial capillaries, we studied endoneurial capillary density at multiple levels of the peripheral nerves of normal rats. Capillary density was lowest in the sciatic and proximal tibial nerves and significantly higher in dorsal and ventral roots and distal tibial and plantar nerves. Endoneurial capillary density corresponds to the hierarchy of susceptibility to ischemic nerve damage in human and experimental ischemic neuropathies. These findings suggest that susceptibility of peripheral nerves to ischemia is determined, at least in part, by the density of endoneurial capillaries.

Animals↗
PubMed1986

Beta 2-adrenergic receptors on peripheral nerves.

We report that peripheral nerves have a functional adenylate cyclase-coupled beta-adrenergic receptor. The pharmacological specificity of this receptor is shown to be of the beta 2 subtype. Two peripheral nerves, the sciatic from the frog and rat and the vagus from the rat, responded to beta 2-agonists with 10-50-fold increases in intracellular cyclic AMP level. This increase was inhibited by the beta-adrenergic antagonist propranolol. In contrast, a central nerve tract, the corpus callosum, responded to isoproterenol with only a minimal one- to twofold increase in cyclic AMP level. These studies demonstrate that peripheral nerves have beta 2-adrenergic receptors that are responsive to exogenously applied catecholamines and suggest a role for these ligands in the previously described modulation of axonal conduction.

Animals↗
PubMed1989

Spinal cord and peripheral nerve pathology in AIDS: the roles of cytomegalovirus and human immunodeficiency virus.

We examined spinal cords, nerve roots, or peripheral nerves of 27 patients who died with acquired immunodeficiency syndrome (AIDS) for the presence of cytomegalovirus (CMV) and human immunodeficiency virus (HIV) by immunoperoxidase techniques in paraffin-embedded tissue. Vacuolar myelopathy was seen in 8 of 26 spinal cords (31%) and microglial nodules were seen in 13 (50%). All of the patients with lateral column vacuolar myelopathy showed severe brain pathology. HIV antigens had been detected in the brains of 15 (55%) of the 27 patients but were detected in only 3 (11%) of 26 spinal cords and were not localized to regions of vacuolar myelopathy. This suggests that the vacuolar myelopathy may be due to a remote or indirect effect of HIV or other infectious agent. CMV antigens were detected in none of the patients who showed vacuolar myelopathy but were detected in 2 of the 13 with microglial nodules. Focal nerve root or peripheral nerve inflammation was seen in 7 patients; 4 had CMV antigens and none had HIV antigens. CMV appears to be an important cause of inflammatory peripheral neuropathy in AIDS patients.

Acquired Immunodeficiency Syndrome↗
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↗
PubMed2001

Molecular mechanisms of cellular interactions in peripheral nerve regeneration.

The peripheral nervous system, as opposed to the central nervous system, has the intrinsic capacity to regenerate. It was recognized long ago that this can be achieved only after an extensive clean-up procedure, the so-called Wallerian degeneration, in which myelin debris is removed and a suitable environment for growing axons is generated. Wallerian degeneration and the regeneration process itself both depend on direct cellular interactions as well as on long-range signals between all participating cell types. Elucidating the nature and functional consequences of these signals is a main goal in understanding peripheral nerve repair.

Animals↗
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↗
PubMed1981

The protein antigens of peripheral nerve myelin.

Peripheral nervous system (PNS) tissue contains a variety of proteins, lipids, and carbohydrates that may serve as immunogens in proving immune responses, as antigens participating in immunological reactions, or as both types of agents. Three proteins P0, P1, and P2, account for approximately 70% of PNS myelin proteins. P0 is the major PNS myelin protein and is restricted to the PNS. P1 is similar to, if not identical with, myelin basic protein, the component of central nervous system myelin which induces experimental allergic encephalomyelitis. P2 has neuritogenic properties for inducing experimental allergic neuritis and may be involved in immune-mediated PNS myelin injury in humans. The complete amino acid sequence for P2 has recently been delineated, and its neuritogenic, immunogenic, and antigenic features can now be further characterized.

Amino Acid Sequence↗
PubMed1996

Peripheral nerve regeneration through short- and long-term degenerated nerve transplants.

The present study was designed to compare regenerative potential of normal and degenerated nerve grafts. Peripheral nerves in rats were induced to undergo in situ degeneration for a period of 6 weeks, 3, 6 and 12 months. During early phase of denervation the myelin and axons degenerated and were absorbed. With prolonged denervation (i.e. 12 months), such nerves were reduced in size and exhibited extensive fibrosis. A 2 cm long segment of the degenerated nerve was transplanted in an surgically created gap in the host peroneal nerve to evaluate their regeneration supporting ability. Regeneration of host axons occurred rapidly through nerves degenerated for a period up to 3 months. The extent of regeneration was compromised in 6-month degenerated nerve group, and was significantly reduced in the 12-month degenerated nerve grafts. These results show that with extended degeneration interval, the regeneration supporting ability of nerves is compromised. It is concluded that nerve repair should not be excessively delayed in order to compromise recovery.

Animals↗
PubMed2004

Altered neurotrophism in diabetic neuropathy: spelunking the caves of peripheral nerve.

Diabetic peripheral neuropathy (DPN) is a frequent and potentially traumatic complication in diabetic individuals. The chronic nature of diabetes and its associated hyperglycemic episodes initiate a complex and inter-related series of metabolic and vascular insults that contribute to the polygenic etiology of DPN. One contributing factor in DPN is an altered neurotrophism that results from changes in the synthesis and expression of neurotrophins, insulin-like growth factor, and various cytokine-like growth factors that can directly act upon distinct subpopulations of sensory and motor neurons. Although considerable effort has focused upon examining growth factor signaling in hyperglycemically stressed neurons, myelin-forming Schwann cells also undergo substantial degenerative changes in DPN. However, scant attention has been devoted to understanding the effect of hyperglycemia on the response of Schwann cells to growth factors critical to their function. Neuregulins are gliotrophic growth factors that signal through members of the Erb B receptor-tyrosine kinase family. The neuregulin/Erb B ligand-receptor cassette can differentially influence the response of Schwann cells throughout their development by regulating cell survival, mitogenesis, and differentiation. The activity of Erb B receptors may also be affected by their interaction with caveolin-1, a protein marker of caveolae ("little caves"). However, whether neuregulin signaling may be directly or indirectly altered under conditions of hyperglycemic stress and contribute to the physiological progression of DPN is unknown. This brief review will provide a perspective on a putative role of changes in the caveolar proteome of Schwann cells in contributing to an "altered neuregulinism" in DPN.

Animals↗