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PubMed1991

[Electrophysiologic diagnosis of peripheral nerve lesions].

In the last two decades the surgical treatment of peripheral nerve lesions has improved considerably, mostly because of the introduction of the microsurgical technique. It was not until the introduction of microsurgery that the surgeon was able to achieve restoration at the level of the nerve fasciculi. The simultaneous use of electrophysiological techniques can improve the results of the reconstruction and especially the extent of functional outcome of nerve restoration. Electrophysiological methods allow detailed and objective assessment of the site, extent, and cause of the lesion and are therefore crucial for the decision upon the appropriate therapeutic procedure and for the success of the operation. The aim of the review is the demonstration of: 1. Today's understanding of peripheral nerve function/ 2. The neurophysiological mechanism of denervation and renervation/ 3. The different electrophysiological methods/ 4. The indications and 5. Application of these techniques in the context of reconstructive surgery.

Electrodiagnosis↗
PubMed2005

Neurofibroma, schwannoma or a hybrid tumor of the peripheral nerve sheath?

Classically, the different subtypes of the peripheral nerve sheets tumors display typical morphological features which differentiate them from the other nervous tumors. Either schwannoma or neurofibroma have characteristic histological and immunohistochemical features. We present a case of peripheral nerve sheets hybrid tumor which have had histological and immunohistochemical features of neurofibroma and schwannoma.

Humans↗
PubMed1996

Cellular migration and axonal outgrowth from adult mammalian peripheral nerves in vitro.

It is known that following peripheral nerve transections, sheath cells proliferate and migrate to form a bridge between nerve stumps, which may facilitate axonal regeneration. In the present investigations, cellular migration and axonal outgrowth from nerves of adult mice were studied in vitro using collagen gels. During the first 3 days in culture, profuse migration of fibroblasts and macrophages occurred from the ends of sciatic nerve segments, which had been lesioned in situ a few days prior to explantation, but not from segments of normal nerves. The mechanism of cellular activation in the lesioned nerves was not determined, but migration was blocked by suramin, which inhibits the actions of several growth factors. The migrating cells, which form the bridge tissue, may promote axonal regeneration in two ways. Firstly, axonal outgrowth from isolated intercostal nerves was significantly increased in co-cultures with bridges from lesioned sciatic nerves. This stimulatory effect was inhibited by antibodies to 2.5S nerve growth factor. Secondly, the segments of bridge tissue contracted when removed from animals. It is possible that fibroblasts within the bridge exert traction that would tend to pull the lesioned stumps of peripheral nerve together, as in the healing of skin wounds. The traction may also influence deposition of extracellular matrix materials, such as collagen fibrils, which could orient the growth of the regenerating axons toward the distal nerve stump.

Animals↗
PubMed1995

Modulation of NMDA receptor expression in the rat spinal cord by peripheral nerve injury and adrenal medullary grafting.

Excessive activation of N-methyl-D-aspartate (NMDA) receptors in the spinal cord consequent to peripheral injury has been implicated in the initiation of neuropathologic events leading to a state of chronic hyperexcitability and persistence of exaggerated sensory processing. In other CNS disease or injury states, NMDA-mediated neurotoxic damage is associated with a loss of NMDA receptors, and outcome may be improved by agents reducing NMDA activation. Previous findings in our laboratory have demonstrated that the transplantation of adrenal medullary tissue into the spinal subarachnoid space can alleviate sensory abnormalities and reduce the induction of a putative nitric oxide synthase consequent to peripheral nerve injury. In order to determine changes in NMDA receptor expression in the spinal cord following peripheral nerve injury and adrenal medullary grafting, NMDA receptor binding using a high-affinity competitive NMDA receptor antagonist, CGP-39653, and NMDAR1 subunit distribution using immunocytochemistry were investigated. Two weeks following peripheral nerve injury by loose ligation of the right sciatic nerve, either adrenal medullary or striated muscle (control) tissue pieces were implanted in the spinal subarachnoid space. Binding studies revealed a marked reduction in [3H]CGP-39653 binding at L4-L5 levels ipsilateral to peripheral nerve injury in control transplanted animals. In contrast, NMDA binding was normalized in adrenal medullary grafted animals. In addition, NMDAR1 immunoreactivity was reduced in both the dorsal horn neuropil and motor neurons of the ventral horn in animals with peripheral nerve injury, while levels in adrenal medullary grafted animals appeared similar to intact controls. These results suggest that adrenal medullary transplants reduce abnormal sensory processing resulting from peripheral injury by intervening in the spinal NMDA-excitotoxicity cascade.

2-Amino-5-phosphonovalerate↗
PubMed1983

Effect of blood glucose control on peripheral nerve function in diabetic patients.

A prospective, stratified, randomized 3-year clinical trial was conducted on the effect of rigorous versus conventional glucose control on peripheral nerve function in 33 insulin-treated diabetic patients with a duration of diabetes of less than 2 years. The goals for conventional glucose control were the mean of fasting and 80-minute postprandial plasma glucose of 150 mg/dl for non-insulin-dependent diabetes and 200 mg/dl for insulin-dependent diabetes. The goal of rigorous glucose control was an approximation of nondiabetic glucose control. No significant difference in glucose control or peripheral nerve function was observed between the rigorously and the conventionally controlled groups. Eight patients in the conventional-control group spontaneously achieved glucose control in the range that was the objective for the rigorous-control group, and five patients in the rigorous-control group never achieved the desired glucose control. In the remaining 20 patients, with similar baseline glucose control and peripheral nerve function characteristics, observed over a median of 2 years, improved blood glucose control (P less than 0.01) was not associated with any significant improvement in peripheral nerve function. Nevertheless, a significant (P less than 0.05) correlation was found between the degree of abnormal nerve function at entry into the study and change in nerve function during the study. If control of hyperglycemia benefits peripheral nerve function of diabetic patients, its demonstration may require a closer approximation of normoglycemia, a larger difference in glucose control between the two study groups, a longer duration of treatment, and the use of patients with more advanced peripheral nerve function abnormalities than those in this study.

Adult↗
PubMed1999

[Peripheral nerve stimulation for pain relief in CRPS II and phantom-limb pain].

OBJECTIVES: We performed 52 peripheral nerve stimulation procedures since 1991. In addition to 48 patients with CRPS II, 4 patients with phantom-limb pain were treated. Incomplete or complete lesion of the stimulated peripheral nerves was determined in all patients. Surgically treatment failed in all cases. All patients had been given extensive conservative pain therapy. MATERIAL AND METHOD: The aim was to define a standardised method, which would be as objective as possible, to verify the success of treatment, by measuring the pain-related disability assessment, the subjective intensity of pain and the subjective perception of pain. Long-term follow-up was arranged in addition to determine social and occupational re-integration. The implantation of the stimulating electrode, proximal to the lesion, was performed after microsurgical neurolysis of the peripheral nerves. The patient carried out a stimulation trial after the operation. At the conclusion of the trial stimulation phase, a stimulator unit was permanently implanted in 47 cases, with a marked reduction in pain. Only in 5 cases, the success of the trial stimulation was unsatisfactory. RESULTS: After implanting the stimulator unit an average pain-related disability of 10% was achieved by the 47 patients fitted with a permanent implant. 43 patients have used the permanent stimulator implants with lasting, excellent to good success. The stimulator system was removed in only 4 cases, due to the need for stimulation having passed, or due to a lack of lasting success with stimulation. CONCLUSION: Neurostimulation of peripheral nerves should be considered as an established concept to treat surgically failed peripheral nerve lesions.

English Abstract↗
PubMed2005

Peripheral nerves: a target for the action of neuroactive steroids.

Peripheral nervous system possesses both classical and non-classical steroid receptors and consequently may represent a target for the action of neuroactive steroids. The present review summarizes the state of art of this intriguing field of research reporting data which indicate that neuroactive steroids, like for instance progesterone, dihydroprogesterone, tetrahydroprogesterone, dihydrotestosterone and 3alpha-diol, stimulate the expression of two important proteins of the myelin of peripheral nerves, the glycoprotein P0 (P0) and the peripheral myelin protein 22 (PMP22). Interestingly, the mechanisms by which neuroactive steroids exert their effects involve classical steroid receptors, like for instance progesterone and androgen receptors, in case of P0 and non-classical steroid receptors, like GABA(A) receptor, in case of PMP22. Moreover, neuroactive steroids not only control the expression of these specific myelin proteins, but also influence the morphology of myelin sheaths and axons suggesting that these molecules may represent an interesting new therapeutic approach to maintain peripheral nerve integrity during neurodegenerative events.

Animals↗
PubMed1985

Injured neurons in the olfactory bulb of the adult rat grow axons along grafts of peripheral nerve.

Certain neurons in the central nervous system (CNS) of adult mammals extend axons for several cm along peripheral nerve grafts inserted into the brain or spinal cord. It is not clear, however, if these nerve cells constitute a special population or are examples of a general capacity of the injured mammalian CNS to regrow processes under these experimental conditions. Furthermore, because the new axons could originate by collateral sprouting from uninjured neurons, it is important to prove that the interruption of a central axonal projection can be followed by extensive fiber regrowth from the damaged neurons. In this anatomical study, we examined whether: (1) nerve cell type; and (2) axotomy, influence CNS axon regrowth along peripheral nerve grafts. For this purpose, we grafted segments of sciatic nerve into the olfactory bulb (OB) of adult rats and used combinations of neuroanatomical tracers (horseradish peroxidase and the fluorescent dyes True Blue and Nuclear Yellow) to investigate axonal regrowth from the different neurons that normally populate the OB. We demonstrate that OB axons extending along peripheral nerve grafts originate from mitral and tufted cells near the graft tip, rather than from the smaller OB neurons (periglomerular, short axon, and granule cells). Most of the mitral and tufted cells that extend new axons in grafted peripheral nerve segments lose their normal projections through the lateral olfactory tract because of axotomy at the time of grafting. Neuronal type, damage, and proximity to the graft appear to be prerequisites of this regenerative response from the OB.

Animals↗
PubMed1997

Genetic mediation of the correlation between peripheral nerve conduction velocity and IQ.

Variation in peripheral nerve conduction velocity (PNCV) and intelligence was studied in 18-year-old Dutch twins. It has been suggested that both brain nerve conduction velocity and PNCV are positively correlated with intelligence (Reed, 1984) and that heritable differences in nerve conduction velocity may explain part of the well-established heritability of intelligence. The relationship among IQ, obtained with the Wechsler Adult Intelligence Scale, and median nerve PNCV was examined in 159 twin pairs. Genetic analyses showed a heritability of 81% for IQ and 66% for onset PNCV. The small but significant phenotypic correlation between IQ and onset PNCV (.15) was entirely mediated by common genetic factors. Analyses of differences scores for PNCV of this study and PNCV from the same subjects collected at age 16 suggest that there might still be development in PNCV in this age interval. This maturation is highly controlled by genetic factors. It is suggested that variation in IQ that is associated with nerve conduction velocity becomes apparent only after the developmental processes in peripheral nerves are completed. This is in line with the suggestion of increasing heritability of IQ in adulthood.

Adolescent↗
PubMed2004

DNA ploidy and chromosome (FISH) pattern analysis of peripheral nerve sheath tumors.

BACKGROUND AND METHODS: 44 peripheral nerve sheath tumors (PNST) (27 schwannomas, 9 neurofibromas and 8 malignant peripheral nerve sheath tumors (MPNST)) were analyzed to determine DNA ploidy pattern and to clarify the conflicting data in the literature concerning this topic (whether benign PNSTs are aneuploid or not). For further insight we analyzed 6 schwannomas, one atypical neurofibroma and five MPNSTs by fluorescence in situ hybridization (FISH) technique using centromeric chromosome probes (7, 17 and 18) and automatic image analysis station, Metafer 4. RESULTS: Benign schwannomas (including the problematic variants as ancient, cellular, neuroblastoma like and multiplex schwannomas) could be characterized by euploid-polyploidisation and by their 4c peak height value which was usually more than 10% of total cell number measured. These characters were not found among neurofibromas and MPNST-s. FISH analysis revealed and confirmed that the 'normal' euploid-polyploid cells are mainly eusomic-polysomic containing two, four, eight or sixteen signals for each chromosomes examined, but in a small proportion aneusomy was found among tumor cells of benign schwannomas (average: 2.58; range 1.33-3.44). In contrast, the atypical neurofibroma displayed marked aneusomy (18.44%) but it contained normal eusomic and polysomic cells too. Two diploid MPNSTs proved to be clearly aneusomic with trisomy of chromosome 17 and monosomy of chromosome 18. CONCLUSIONS: All these data suggest that ploidy pattern determination combined with FISH analysis may be a very useful supplementary tool for making a right diagnosis (to differentiate benign versus malignant schwannomas in problematic variants) and to understand better the malignant transformation in PNSTs.

Adolescent↗
PubMed1958

Electron microscopy of peripheral nerves and neuromuscular junctions in the wasp leg.

The peripheral nerve branch innervating the femoral muscles of the common yellow jacket (Vespula carolina) has been found to possess a thick lemnoblast basement membrane and a complex mesaxon. The term "tunicated nerve" is proposed to designate the type of peripheral nerve in which one or several axons are loosely mantled by meandering, cytoplasm-enclosing membranes of the lemnoblast. The peripheral axon courses longitudinally in a groove in the muscle fiber between the plasma membrane of the muscle fiber and a cap formed by lemnoblast and tracheoblast. The junction is characterized by apposition of plasma membranes of axon and muscle fiber, abundant mitochondria, and synaptic vesicles in the axon, and aggregates of "aposynaptic granules" plus mitochondria and endoplasmic reticulum on the muscle side of the synapse. Unlike the vertebrate striated muscle fiber, no complex infolding of the synapsing plasma membrane of the muscle fiber occurs. The "connecting tissue" of the insect is formed by tracheoblasts, their basement membranes, and the basement membranes of other cells. Further mechanical support is given by the ramifying tracheoles. The physiologic roles of the specialized structures are considered.

Animals↗
PubMed2000

Tonic blocking action of meperidine on Na+ and K+ channels in amphibian peripheral nerves.

BACKGROUND: Among opioids, meperidine (pethidine) also shows local anesthetic activity when applied locally to peripheral nerve fibers and has been used for this effect in the clinical setting for regional anesthesia. This study investigated the blocking effects of meperidine on different ion channels in peripheral nerves. METHODS: Experiments were conducted using the outside-out configuration of the patch-clamp method applied to enzymatically prepared peripheral nerve fibers of Xenopus laevis. Half-maximal inhibiting concentrations were determined for Na+ channels and different K+ channels by nonlinear least-squares fitting of concentration-inhibition curves, assuming a one-to-one reaction. RESULTS: Externally applied meperidine reversibly blocked all investigated channels in a concentration-dependent manner, i.e., voltage-activated Na+ channel (half-maximal inhibiting concentration, 164 microM), delayed rectifier K+ channels (half-maximal inhibiting concentration, 194 microM), the calcium-activated K+ channel (half-maximal inhibiting concentration, 161 microM), and the voltage-independent flicker K+ channel (half-maximal inhibiting concentration, 139 microM). Maximal block in high concentrations of meperidine reached 83% for delayed rectifier K+ channels and 100% for all other channels. Meperidine blocks the Na+ channel in the same concentration range as the local anesthetic agent lidocaine (half-maximal inhibiting concentration, 172 microM) but did not compete for the same binding site as evaluated by competition experiments. Low concentrations of meperidine (1 nM to 1 microM) showed no effects on Na+ channels. The blockade of Na+ and delayed rectifier K+ channels could not be antagonized by the addition of naloxone. CONCLUSIONS: It is concluded that meperidine has a nonselective inhibitory action on Na+ and K+ channels of amphibian peripheral nerve. For tonic Na+ channel block, neither an opioid receptor nor the the local anesthetic agent binding site is the target site for meperidine block.

Analgesics, Opioid↗
PubMed2003

Regeneration of ganglion cell axons into a peripheral nerve graft alters retinal expression of glial markers and decreases vulnerability to re-axotomy.

PURPOSE: To compare the effect of cutting the optic nerve versus replacing the cut optic nerve with a peripheral nerve (PN) graft on retinal glial markers, and to determine whether the PN graft can stabilize regenerating retinal ganglion cells (RGCs), thus preventing their death following re-axotomy. METHODS: Retinas harvested after ganglion cell regeneration into a sciatic nerve graft were compared to untreated control retinas and retinas obtained following optic nerve axotomy. Glial-specific proteins such as glial fibrillary acidic protein (GFAP), Bcl-2 and complement-3 receptor (Ox-42) were examined using immunohistochemistry. Ganglion cells that survived the second axotomy were quantified on retinal flat mounts by retrograde labeling from the graft. RESULTS: GFAP expression in astrocytes and Muller cells was elevated in axotomized retinas when compared to controls, and an additional up-regulation in Muller cells was found in retinas following ganglion cell regeneration. Increased GFAP expression in retinas containing regenerated neurons was accompanied by increased Bcl-2 expression with latter being confined to Muller cells. Moreover, re-axotomy of the regenerated axons within the graft did not result in significant retrograde degeneration of RGCs within 28 days. CONCLUSIONS: The data suggest that the graft stabilizes the regenerating RGCs to an extent reminiscent of peripheral neurons, a process that may involve the interaction between neuronal and glial elements.

Animals↗
PubMed2003

On the mechanism by which epinephrine potentiates lidocaine's peripheral nerve block.

BACKGROUND: Adding epinephrine to lidocaine solutions for peripheral nerve block potentiates and prolongs the action, but by incompletely understood mechanisms. In an effort to discriminate the pharmacokinetic from the pharmacodynamic effects of epinephrine, the authors measured the lidocaine content of peripheral nerve over the course of block produced by 0.5% lidocaine, with and without epinephrine, and correlated it with the degree of analgesia. METHODS: Percutaneous sciatic nerve blocks were performed in 18 groups of rats (10 in each) with 0.1 ml of either 0.5% lidocaine or 0.5% lidocaine with epinephrine (1:100,000). Over the full course of nerve block, the authors regularly measured analgesia to toe pinch and then rapidly removed nerves to assay intraneural lidocaine content at 2-120 min after injection. RESULTS: The kinetics of lidocaine's clearance from nerve was composed of a fast-decaying transient superimposed on a very slowly decaying component. The effect of epinephrine on the intraneural lidocaine content was to increase the amount of lidocaine in the slow-decaying component by threefold to fourfold, although the total neural content was not altered by epinephrine for the first 10 min after injection. Epinephrine prolonged blockade by almost fourfold and enhanced the intensity of peak analgesia, as well as the fraction of rats with complete block, almost throughout the 2-120-min period of behavioral observation. CONCLUSIONS: Adding epinephrine to lidocaine solutions increases the intensity and duration of sciatic nerve block in the rat. The early increase in intensity is not matched with an increase in intraneural lidocaine content at these early times, although the prolonged duration of block by epinephrine appears to correspond to an enlarged lidocaine content in nerve at later times, as if a very slowly emptying "effector compartment" received a larger share of the dose. The increase in early analgesia without increased lidocaine content may be explained by a pharmacodynamic action of epinephrine that transiently enhances lidocaine's potency, but also by a pharmacokinetic effect that alters the distribution of the same net content of lidocaine within the nerve.

Algorithms↗
PubMed2004

Clinical application of axonal repair technique for treatment of peripheral nerve injury.

OBJECTIVE: To evaluate the efficacy of axonal repair technique for treatment of peripheral nerve injury clinically. METHODS: In 1998, the authors applied axonal repair technique to treat peripheral nerve injuries in 12 patients with 13 nerves. It consists of four steps, ie, stumps of the nerve being soaked in a modified Collins fluid, freezed, trimmed, and coapted with glue, making the injured nerve repaired at the axonal level. RESULTS: The patients were followed up for an average of 13 months. Results showed that in 4 cases of first-stage contralateral C7 transfer, regenerating axons reached to the sternoclavicular joint or axilla at 4 to 7 months, offering the timing for performing the second-stage contralateral C7 transfer. In 5 cases of accessory nerve transferred to the suprascapular nerve, the abduction of the shoulder was 40 degree on average. In the other 3 patients with four different nerves repaired, results were also satisfactory. CONCLUSIONS: This technique is promising in the treatment of peripheral nerve injury.

Adult↗
PubMed2000

Ultrasonography of peripheral nerves.

With recent improvements in ultrasound (US) imaging equipment and refinements in scanning technique, an increasing number of peripheral nerves and related pathologic conditions can be identified. US imaging can support clinical and electrophysiologic testing for detection of nerve abnormalities caused by trauma, tumors, and a variety of nonneoplastic conditions, including entrapment neuropathies. This article addresses the normal US appearance of peripheral nerves and discusses the potential role of US nerve imaging in specific clinical settings. A series of US images of diverse pathologic processes involving peripheral nerves is presented.

Carpal Tunnel Syndrome↗
PubMed2001

Bridging a peripheral nerve defect using collagen filaments.

We describe bridging a peripheral nerve defect using collagen filaments instead of a tube. Cords of collagen filaments were grafted to bridge 20-mm defects of rat sciatic nerves. Nerve autografts were grafted as the control. The mean number and the mean fiber diameter of regenerated myelinated axons were approximately 4,800 and 3.3 microm, respectively, in the distal end of the nerve autograft and approximately 5,500 and 2.3 microm, respectively, in the distal end of the collagen-filaments nerve guide 8 weeks after surgery. The mean number and the mean fiber diameter of regenerated myelinated axons were approximately 6,900 and 3.1 microm, respectively, in the distal end of the nerve autograft and approximately 6,300 and 3.3 microm, respectively, in the distal end of the collagen-filaments nerve guide 25 weeks after surgery. Histologic studies suggested that the collagen filaments guided regenerating axons effectively. This new procedure offers a possible solution for the need to sacrifice a healthy nerve and for the shortage of graft material available for the repair of severed nerves.

Animals↗
PubMed1989

[Study of conductivity of the motor fibers of the ulnar nerve with respect to intensity, localization and diagnosis of peripheral nerve disease. I. General and morphologic observations on the affected area of the ulnar nerve with emphasis on the elbow region and causes of the disease].

The introductory part deals with a great community impact of ulnar nerve damage and its high incidence. From peripheral nerves, this ulnar is the most frequently exposed to injuries and impresses. The impressory damage occurs mainly in elbow region. Anatomic peculiarities of ulnar nerve are scrutinized concerning with more connective tissue presence on its cutting section comparably to the other upper limb nerves. Frequent innervative deviations are referred to especially in ulnar and median nerve regions in the course of ulnar nerve branching. Also three types of anastomoses are listed between the both nerves which are important as to the clinical pattern in damages and for electrophysiologic diagnosing. From the clinical tests, those of rare use are emphasized (test of crossed fingers, palmaris brevis sign, Mumenthaler's sign, ulnar test). The last part deals in detail with anatomic, functional and clinical problems of ulnar nerve in elbow area. Its biomechanic relations in the cubital tunnel are elucidated as well as etiopathogenetic factors of neural damage in this area (traction and compressive theories and hypermobility of the nerve etc.). The most frequent causes of ulnar injuries are reviewed. The present work is of introductory value for those dealing mainly with electrophysiologic problems of both sensitive and motoric neural injuries varying in the intensity, location and diagnosis.

Humans↗