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PubMed2006

Clinical outcome of peripheral nerve decompression in diabetic and nondiabetic peripheral neuropathy.

Surgical decompression of peripheral nerves in patients with diabetes was reported to restore sensation and improve function. In this study, a retrospective review of 12 diabetic and 20 nondiabetic patients with lower-extremity peripheral neuropathy who underwent surgical decompression was performed. Clinical evaluation by Tinel test, muscle power examination, and 2-point discrimination were performed preoperatively, at 6 months, and between 9 and 15 months postdecompression. Clinical outcomes were classified into excellent, good, or fair based on improvement in symptoms and return of function. Thirty-two patients underwent 36 surgeries, in which 99 lower-extremity nerves were decompressed. There was a statistically significant improvement in muscle function (P < 0.001) and 2-point discrimination for the small toe (P = 0.008) and big toe (P = 0.038). At a mean of 7.7 months, 90% of patients showed significant improvement in pain and function. It is concluded that surgical decompression was associated with significant improvement in clinical outcome in patients with diabetic and idiopathic neuropathy with evidence of superimposed compression.

Decompression, Surgical↗
PubMed1988

Biosynthesis of membrane cholesterol during peripheral nerve development, degeneration and regeneration.

Biosynthesis of peripheral nerve cholesterol was investigated by the in vivo and in vitro incorporation of [1-14C]-acetate into sciatic endoneurium of normal rats during development, degeneration and regeneration. Labeled sterols were rapidly formed (less than 10 min) within the endoneurial portion of sciatic nerve after [1-14C]acetate administration by intraneural injection. The majority of labeled sterols were initially found in lanosterol and desmosterol. After six hr, the 14C-labeling in both precursors was decreased to minimum, whereas cholesterol became the major labeled product of sterol. As myelination proceeded, the incorporation of [1-14C]acetate into endoneurial cholesterol decreased rapidly and reached a minimum after six mo. In mature adult nerve, an increased proportion of biosynthesis of lanosterol and desmosterol also was demonstrated. The in vitro incorporation of [1-14C]acetate into cholesterol was inhibited during Wallerian degeneration. Instead, cholesteryl esters were labeled as the major sterol product. Such inhibition, however, was not observed in the adult Trembler nerve (Brain Res. 325, 21-27, 1985), which is presumed to be due to a primary metabolic disorder of Schwann cells. The cholesterol biosynthesis was gradually resumed in degenerated nerve by either regeneration of crush-injured nerve or reattachment of the transected nerve. These results suggest that cholesterol biosynthesis in peripheral nerve relies on the axon to provide necessary substrates. De novo synthesis appears to be one of the major sources of endoneurial cholesterol that forms and maintains peripheral nerve myelin.

Animals↗
PubMed2001

[Analysis of unusual late responses of peripheral nerves].

F-waves are routinely evaluated in nerve conduction studies on proximal peripheral nerves. However, unusual late responses other than F-waves that show variation in latency and configuration sometimes confound evaluation of the F-waves. The unusual late responses were analyzed in this study. In two patients with cervical radiculopathy, two patients with brachial plexus injury and 9 patients with polyneuropathy, A-waves showing constant latency and configuration were recorded in addition to temporally dispersed F-waves. The A-waves in these patients persisted after supramaximal stimulation of the peripheral nerves, although the A-waves should normally disappear in response to supramaximal stimulation. The supramaximally stimulated A-waves were prominent in polyneuropathy and nerve lesions with demyelinating pathology. A patient with Guillain-Barré syndrome showed unusual repetitive discharges that might be important electrodiagnostic findings in the early stage of illness. In patients with myotonic dystrophy, electrical stimulation elicited repetitive discharges that continued from the M-waves. Recordings with a concentric needle electrode showed characteristics similar to those of myotonic discharges recorded during needle electrode insertion. When the repetitive discharges were mild, the F-waves were recorded. Absence of the F-waves in myotonic dystrophy might be related to the myotonic discharges elicited by electrical stimulation, and may not imply impaired conduction of the peripheral nerves. A patient with myokymia showed repetitive discharges with constant configuration but variable latency, although the F-waves were normal. These repetitive discharges may be evoked by ephaptic transmission resulting from abnormal excitability of the peripheral nerves or muscles of different etiologies.

Adolescent↗
PubMed1986

Trapped immunoglobulins on peripheral nerve myelin from patients with diabetes mellitus.

Diabetic peripheral neuropathy is characterized by endoneurial capillary closure and by segmental demyelination and axonal degeneration in a spatial pattern consistent with ischemic damage. The increased permeability of human diabetic endoneurial capillaries to plasma proteins may contribute to the pathogenesis of these structural changes in peripheral nerve by further accelerating the rate at which plasma proteins are trapped by reactive nonenzymatic glycosylation products on long-lived proteins such as myelin. We have measured trapped immunoglobins (Ig) G and M on peripheral nerve myelin from diabetic and nondiabetic patients by an enzyme-linked immunosorbent assay to determine whether plasma proteins accumulate on nerves as they do in the glomerular matrix of diabetics. The amount of trapped IgG on brain myelin from these subjects was also determined. Peripheral nerve myelin from diabetics had on average greater than 14 times the amount of trapped IgM found in identically prepared samples from nondiabetics (0.90 +/- 0.2 vs. 0.06 +/- 0.004 OD/micrograms myelin protein) and greater than 4 times the amount of trapped IgG (6.40 +/- 1.92 vs. 1.5 +/- 0.25 OD/micrograms myelin protein). In contrast, no significant trapping of IgG was detected in any samples of brain myelin. This most likely reflects effective exclusion of IgG by the blood-brain barrier. These data suggest that excessive trapping of Igs and other plasma proteins by diabetic peripheral nerve myelin may contribute to the development of peripheral nerve damage, whereas the lack of such trapping by brain myelin may partly explain the rarity of diabetic central neuropathy.

Adult↗
PubMed1990

A nerve cuff technique for selective excitation of peripheral nerve trunk regions.

Numerical modeling and experimental testing of a nerve cuff technique for selective stimulation of superficial peripheral nerve trunk regions is presented. Two basic electrode configurations ("snug" cuff monopolar and tripolar longitudinally aligned dots) have been considered. In addition, the feasibility of "steering" excitation into superficial nerve trunk regions using subthreshold levels of current flow from an electrode dot located on the opposite side of the nerve has been tested. Modeling objectives were to solve for the electric field that would be generated within a representative nerve trunk by each electrode configuration; and to use a simple nerve cable model to predict the effectiveness of each configuration in producing localized excitation. In three acute experiments on cat sciatic nerve the objective was to characterize the effectiveness of each electrode configuration in selectively activating only the medial gastrocnemius muscle. Modeling and experimentation both suggest that longitudinally aligned tripolar dot electrodes on the surface of a nerve trunk, and bounded by a layer of insulation (such as a nerve cuff), will restrict excitation to superficial nerve trunk regions more successfully than will monopolar dot electrodes. Excitation "steering" will improve the spatial selectivity of both monopolar and tripolar electrode configurations.

Animals↗
PubMed1999

Evaluation and surgical management of peripheral nerve problems.

OBJECTIVE: To illustrate how an understanding of the basic biological responses of peripheral nerves to injury is important in formulating a rational treatment plan. METHODS: Peripheral nerve anatomy and physiology are described in a context that is relevant to understanding the different grades of peripheral nerve injury. Methods of evaluating and treating peripheral nerve injuries both medically and surgically are reviewed. Relevant scientific studies with potential clinical impact are also discussed. RESULTS: The clinical symptoms, physical findings, and electrodiagnostic and imaging test results relevant to the diagnosis of peripheral nerve problems are reviewed. Conventional and new medical or surgical strategies in the management of peripheral nerve injuries and mass lesions are described. CONCLUSION: The diagnosis and treatment of peripheral nerve injuries follow logically from an understanding of the biological responses of peripheral nerves after injury and during recovery.

Action Potentials↗
PubMed2003

[Transplantation in peripheral nerve injuries].

Autologous nerve grafting is the most commocommnlynly used operative technique in delayed primary, or secondary nerve repair after the peripheral nerve injuries. The aim of this procedure is to overcome nerve gaps that results from the injury itself, fibrous and elastic retraction forces, resection of the damaged parts of the nerve, position of the articulations and mobilisation of the nerve. In this study we analyse the results of operated patients with transections and lacerations of the peripheral nerves from 1979 to 2000 year. Gunshot injuries have not been analyzed in this study. The majority of the injuries were in the upper extremity (more than 87% of cases). Donor for nerve transplantation had usually been sural nerve, and only occasionally medial cutaneous nerve of the forearm was used. In about 93% of cases we used interfascicular nerve grafting, and cable nerve grafting was performed in the rest of them. Most of the grafts were 1 do 5 cm long (70% of cases). Functional recovery was achieved in more than 86% of cases, which is similar to the results of the other authors. Follow up period was minimum 2 years. We analyzed the influence of different factors on nerve recovery after the operation: patient's age, location and the extent (total or partial) of nerve injury, the length of the nerve graft, type of the nerve, timing of surgery, presence of multiple nerve injuries and associated osseal and soft tissue injuries of the upper and lower extremities.

Adolescent↗
PubMed1998

Antibody to transforming growth factor beta reduces collagen production in injured peripheral nerve.

Epineurial scarring in peripheral nerve after injury inhibits normal axonal regeneration primarily due to fibroblast deposition of type I collagen. The transforming growth factor beta (TGF-beta) family is an important class of signaling molecules that has been shown to stimulate fibroblasts to produce collagen. The aim of this study was to design a prototypic therapeutic system in which the neutralization of TGF-beta in crushed rat sciatic nerve would decrease collagen formation. A total of 45 experimental Lewis rats were used. Group 1 animals (20 rats) sustained a unilateral crush injury to the sciatic nerve with injection of phosphate buffer solution. Group 2 animals (20 rats) sustained a unilateral crush injury to the sciatic nerve with injection of phosphate-buffered saline and goat, anti-rat, panspecific TGF-beta antibody. Group 3 control animals (five rats) underwent only exposure of sciatic nerve with injection of antibody. All animals were killed at 14 days and sciatic nerve specimens were harvested at that time. Slides of experimental tissue were processed using a 35S-labeled oligomer for procollagen alpha-1 mRNA, then dipped in photographic emulsion and examined by darkfield autoradiography. Morphometric analysis of pixel counts was then performed. A significant reduction in total pixel count per high-power field and in total number of fibroblasts per high-power field was found in crushed rat sciatic nerve treated with anti-TGF-beta antibody when compared with those treated only with phosphate-buffered saline. These findings are consistent with successful reduction in procollagen induction after a crush injury by topical administration of blocking antibody against transforming growth factor beta. The concept of growth factor blockade for therapeutic collagen reduction is attractive in the context of nerve injury, and the current article provides a model for future clinical application.

Animals↗
PubMed2002

Glutamine-, glutamine synthetase-, glutamate dehydrogenase- and pyruvate carboxylase-immunoreactivities in the rat dorsal root ganglion and peripheral nerve.

Supporting glial cells of the peripheral nervous system include satellite cells of dorsal root ganglia and Schwann cells of peripheral nerves. In the central nervous system, glial cells contain enzymes related to the tricarboxylic acid and glutamine cycles: pyruvate carboxylase, glutamate dehydrogenase, and glutamine synthetase. The present study used immunohistochemistry in the rat peripheral nervous system to determine the cellular distribution of these enzymes along with glutamine. In dorsal root ganglia and peripheral nerves, glutamine and glutamine related enzymes were enriched in satellite and Schwann cells. In the dorsal root ganglia, immunoreactive satellite cells surrounded neurons of all sizes. In peripheral nerve, immunoreactive Schwann cells were most easily observed surrounding large diameter, myelinated axons. These Schwann cells contained immunoreactivity in their cell bodies, nodes of Ranvier, and the rim of cytoplasm outside the myelin sheath. Myelin sheaths were non-immunoreactive. The peripheral glial tricarboxylic and glutamine cycles may be used to produce glutamine for neuronal cell uptake and conversion to glutamate for synaptic transmission. Alternatively, these cycles may function in peripheral glia similar to central nervous system astrocytes for supporting the energy demands of neurons.

Animals↗
PubMed1996

Peripheral nerve explants grafted into the vitreous body of the eye promote the regeneration of retinal ganglion cell axons severed in the optic nerve.

We have conducted experiments in the adult rat visual system to assess the relative importance of an absence of trophic factors versus the presence of putative growth inhibitory molecules for the failure of regeneration of CNS axons after injury. The experiments comprised three groups of animals in which all optic nerves were crushed intra-orbitally: an optic nerve crush group had a sham implant-operation on the eye; the other two groups had peripheral nerve tissue introduced into the vitreous body; in an acellular peripheral nerve group, a frozen/thawed teased sciatic nerve segment was grafted, and in a cellular peripheral nerve group, a predegenerate teased segment of sciatic nerve was implanted. The rats were left for 20 days and their optic nerves and retinae prepared for immunohistochemical examination of both the reaction to injury of axons and glia in the nerve and also the viability of Schwann cells in the grafts. Anterograde axon tracing with rhodamine-B provided unequivocal qualitative evidence of regeneration in each group, and retrograde HRP tracing gave a measure of the numbers of axons growing across the lesion by counting HRP filled retinal ganglion cells in retinal whole mounts after HRP injection into the optic nerve distal to the lesion. No fibres crossed the lesion in the optic nerve crush group and dense scar tissue was formed in the wound site. GAP-43-positive and rhodamine-B filled axons in the acellular peripheral nerve and cellular peripheral nerve groups traversed the lesion and grew distally. There were greater numbers of regenerating fibres in the cellular peripheral nerve compared to the acellular peripheral nerve group. In the former, 0.6-10% of the retinal ganglion cell population regenerated axons at least 3-4 mm into the distal segment. In both the acellular peripheral nerve and cellular peripheral nerve groups, no basal lamina was deposited in the wound. Thus, although astrocyte processes were stacked around the lesion edge, a glia limitans was not formed. These observations suggest that regenerating fibres may interfere with scarring. Viable Schwann cells were found in the vitreal grafts in the cellular peripheral nerve group only, supporting the proposition that Schwann cell derived trophic molecules secreted into the vitreous stimulated retinal ganglion cell axon growth in the severed optic nerve. The regenerative response of acellular peripheral nerve-transplanted animals was probably promoted by residual amounts of these molecules present in the transplants after freezing and thawing. In the optic nerves of all groups the astrocyte, microglia and macrophage reactions were similar. Moreover, oligodendrocytes and myelin debris were also uniformly distributed throughout all nerves. Our results suggest either that none of the above elements inhibit CNS regeneration after perineuronal neurotrophin delivery, or that the latter, in addition to mobilising and maintaining regeneration, also down regulates the expression of axonal growth cone-located receptors, which normally mediate growth arrest by engaging putative growth inhibitory molecules of the CNS neuropil.

Animals↗
PubMed1993

The role of focal nerve ischemia and Wallerian degeneration in peripheral nerve injury producing hyperesthesia.

BACKGROUND: A new model of pain associated with an experimental peripheral mononeuropathy has stimulated interest in mechanisms of pain and their structural correlates in peripheral nerve, the site of the experimental lesion. METHODS: The pathology of the neuropathy was studied and the results correlated with alterations in nerve blood flow and with the behavioral response to heat applied to the foot. The focal neuropathy was created by loosely tying several ligatures around rat sciatic nerve, which produces hyperesthesia in the ligated limb in 3-5 days. The neuropathology was striking with epineurial and endoneurial vascular stasis, edema, and extensive nerve fiber injury in the ligated segment noted at 1 week after ligation. RESULTS: Nerve blood flow was reduced significantly in the ligated segment during the development of the hyperesthesia response, suggesting that changes in nerve blood flow caused by the ligature compression of the epineurial vessels contributes to the nerve fiber injury and pathophysiology of the model. To further test this hypothesis, the epineurial vasculature was removed from 1-cm lengths of rat sciatic nerve, which reduces nerve blood flow by 58%, and by ligation of the ipsilateral femoral artery, which focally reduces nerve blood flow by 70%, and the behavioral response to heating of the paw was evaluated at 1 week. Crush injury was used as a positive control creating Wallerian degeneration without a substantial reduction in nerve blood flow. CONCLUSIONS: The results suggest that ischemia is an important initial pathogenic mechanism in the hyperesthesia associated with the loose ligature pain model, in so far as it produces Wallerian degeneration and axonal injury. Modest degrees of ischemia producing only demyelination did not produce significant hyperesthesia.

Animals↗
PubMed1996

Receptor-mediated phosphoinositide metabolism in peripheral nerve and cultured Schwann cells.

Peripheral nerve possesses muscarinic cholinergic receptors, predominantly of the M3 subtype, that stimulate phosphoinositide metabolism. Evidence suggests that one site of this response is the myelin sheath. Purified peripheral nerve myelin contains several heterotrimeric GTP-binding proteins. Furthermore, carbachol and guanosine-5'-(3-O-thio)triphosphate-stimulated hydrolysis of exogenous phosphatidylinositol-4,5-bis-phosphate that is blocked by atropine can be reconstituted in a purified peripheral myelin-rich fraction. Nerve phosphoinositide turnover is also stimulated by adenosine analogs and blocked by adenosine receptor antagonists in a pattern consistent with the presence of adenosine A2 receptors in the tissue. Receptor-mediated phosphoinositide metabolism has also been studied in a human tumor-derived Schwann cell line (NF1T) derived from a neurofibromatosis-1 patient. By the same experimental criteria, NF1T cells also appear to contain adenosine A2 receptors which upon activation stimulate phosphoinositide turnover. However, phosphoinositide metabolism in these cells is not increased by either carbachol or ATP. Our findings taken together with other reports suggest that Schwann cells may possess a variety of receptors which regulate phosphoinositide metabolism.

Cells, Cultured↗
PubMed2005

The origin and development of glial cells in peripheral nerves.

During the development of peripheral nerves, neural crest cells generate myelinating and non-myelinating glial cells in a process that parallels gliogenesis from the germinal layers of the CNS. Unlike central gliogenesis, neural crest development involves a protracted embryonic phase devoted to the generation of, first, the Schwann cell precursor and then the immature Schwann cell, a cell whose fate as a myelinating or non-myelinating cell has yet to be determined. Embryonic nerves therefore offer a particular opportunity to analyse the early steps of gliogenesis from transient multipotent stem cells, and to understand how this process is integrated with organogenesis of peripheral nerves.

Animals↗
PubMed2001

Examination of postoperative peripheral nerve lesions with high-resolution sonography.

OBJECTIVE: Peripheral nerve lesions after surgery are common and are related either to direct compromise of the nerve by the surgical procedure (iatrogenic lesions) or to postoperative events such as scar formation. Despite a high sensitivity, electrodiagnosis may not reveal the exact location and cause of a nerve lesion. We hypothesized that high-resolution sonography could be helpful in diagnosing postoperative peripheral nerve lesions by direct visualization of the nerve and surrounding tissues. SUBJECTS AND METHODS: Eighteen patients with postoperative peripheral nerve lesions that were confirmed with clinical examination and electrodiagnosis were examined on sonography. Eight patients had lesions caused by direct nerve surgery, and 10 patients had undergone a previous orthopedic operation or open biopsy. Sonographic diagnoses were correlated with neurologic examinations and surgical findings. RESULTS: Reliable visualization of injured nerves on sonography was feasible in all patients. Axonal swelling of a nerve was diagnosed in three patients, direct compromise of a nerve by surrounding scar tissue or surgical implants was diagnosed in 10 patients, a neuroma was diagnosed in three, and insufficient surgical repair, in two. Sonographic findings were confirmed during surgery in all except one patient. CONCLUSION: In contrast to electrophysiologic tests, high-resolution sonography can show the exact location, extent, and type of a postoperative peripheral nerve lesion and the concurrent disease of surrounding tissues. Because the latter can often be the causative agent for the development of a lesion or the lack of improvement with conservative treatment, sonography yields important information that may not be obtained with other diagnostic modalities.

Adult↗
PubMed2005

Detection of neuropathy due to Mycobacterium leprae using noninvasive neurosensory testing of susceptible peripheral nerves.

The prevalence of disability in patients with Hansen disease is related to peripheral nerve dysfunction. This dysfunction, which is due to chronic nerve compression, is the result of invasion of the peripheral nerve by Mycobacteria leprae. This suggests that early identification of M. leprae would be aided by detection of early stages of peripheral nerve compression. Traditional evaluation of peripheral nerve function with monofilaments, electrodiagnostic testing, or by observing motor palsy or digital ulcers unfortunately identifies only late sequelae of peripheral nerve dysfunction. The cutaneous pressure threshold required to identify 1 from 2 static-touch stimuli was obtained with the Pressure-Specified Sensory Device in upper and lower extremities of 51 patients who completed multidrug therapy for Hansen disease. Abnormal peripheral nerve function was identified in each patient and in each of the 120 bilateral nerves that were evaluated. The degree of nerve dysfunction included the range from early to late stages of nerve compression, suggesting that this method of neurosensory testing offers the possibility for early detection of peripheral nerve problems in Hansen disease.

Adult↗
PubMed2003

Selective reactions of cutaneous and muscle afferent neurons to peripheral nerve transection in rats.

To determine whether peripheral nerve injury has similar effects on all functional types of afferent neuron, we retrogradely labeled populations of neurons projecting to skin and to muscle with FluoroGold and lesioned various peripheral nerves in the rat. Labeled neurons were counted after different periods and related to immunohistochemically identified ectopic terminals and satellite cells in lumbar dorsal root ganglia. After 10 weeks, 30% of cutaneous afferent somata labeled from transected sural nerves had disappeared but, if all other branches of the sciatic nerve had also been cut, 60% of cutaneous neurons were lost. Small-diameter sural neurons preferentially disappeared. In contrast, the number of muscle afferent somata was not affected by transection of various nerves. p75 was downregulated in axotomized cutaneous neurons but in not axotomized muscle neurons. Conversely, p75 was upregulated in satellite cells around cutaneous but not muscle neurons. Consistent with this, perineuronal rings containing tyrosine hydroxylase, calcitonin gene-related peptide, galanin, or synaptophysin were formed preferentially around cutaneous neurons. Selective lesions of predominantly cutaneous nerves triggered the formation of rings, but none were detected after selective lesions of muscle nerves. We conclude that cutaneous neurons are both more vulnerable and more associated with ectopic nerve terminals than muscle neurons in dorsal root ganglia after transection and ligation of peripheral nerves.

Animals↗