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PubMed2007

Cdc2-mediated Schwann cell migration during peripheral nerve regeneration.

Schwann cell migration facilitates peripheral nerve regeneration after injury. We have recently found increased activation of Cdc2 kinase in regenerating sciatic nerves. Here we show that Cdc2 phosphorylation of caldesmon regulates Schwann cell migration and nerve regeneration. A robust but transient increase in Cdc2 expression was found in cultured Schwann cells prepared from the sciatic nerve in rats that had undergone crush injury for 7 days. These ;injury-preconditioned' Schwann cells exhibited enhanced migration compared with non-preconditioned control cells and treatment with the cdk inhibitor roscovitine prevented cell migration. After transduction with recombinant Cdc2 DNA adenoviral vectors, Schwann cells were implanted into sciatic nerves; those expressing wild-type Cdc2 migrated further in the distal direction than those expressing dominant-negative Cdc2. We identified caldesmon as a downstream substrate of Cdc2 in Schwann cells and its phosphorylation by Cdc2 changed its subcellular localization. Overexpression of dominant-negative caldesmon significantly counteracted the migration effect caused by Cdc2. Finally, neurite outgrowth of cultured DRG sensory neurons, facilitated by co-culture with injury-preconditioned Schwann cells, was suppressed by roscovitine treatment. The results indicate that activation of the Cdc2-caldesmon pathway is necessary for Schwann cell migration and suggest a role for this pathway in peripheral axonal growth.

Animals↗
PubMed1976

[Ganglions a rare cause of isolated peripheral nerve lesions].

Extra- and intraneural ganglionic cysts rarely involved peripheral nerves. They are found in the neighbourhood of large joints. The ulnar nerve is affected most often by extraneural cysts at the wrist. Intraneural cysts prefer the peroneal nerve at the tibiofibular joint. Ganglionic cysts as a cause of peripheral nerve damage are often overlooked, mainly because they are not considered as a cause of pain, paresis or sensory changes. Surgical treatment is recommended.

Cysts↗
PubMed1978

Benign fatty tumors of the peripheral nerves.

Fatty tumors of the peripheral nerves, although rare, occur with sufficient frequency to pose problems in diagnosis and treatment. Moreover, the nomenclature of these tumors has suffered from controversy over their morpological description. These factors have contributed to a misunderstanding about the treatment of these localized nerve abnormalities leading, in the past, to unnecessary radical nerve excisions with resultant total motor and sensory deficit. This paper reviews the various types of fatty tumors, describes the morphology and pathophysiology of one such lesion, and provides a basis for a rational surgical approach.

Adolescent↗
PubMed2006

[Tissue engineering of peripheral nerves].

BACKGROUND: In spite of considerable progress in microsurgical techniques, the treatment of long distance defects in peripheral nerves remains challenging for the surgeon. Autologous nerve grafting has been the only applicable procedure to overcome such defects in the past. Due to the known disadvantages of this procedure (neuroma formation and sensory deficits at the donor-site, limited availability of donor-material, etc.) and impaired regenerative results, different tubulisation techniques are discussed more frequently as alternatives to the autologous nerve grafts. AIM OF THE STUDY: In this work, the authors summarise their experiences and results with different synthetically developed materials, cellular and acellular tubes and venous conduits for the reconstruction of peripheral nerve defects. MATERIAL AND METHODS: To analyse peripheral nerve regeneration, we utilised a median nerve model in rats. In these studies nerve gaps up to 40 mm were induced. Guiding tubes of various materials (trimethylene carbonate-epsilon-caprolactone, polyethylene, veins, and collagen) were employed. Furthermore, we introduced Schwann cells as cellular elements into some of the trimethylene carbonate-epsilon-caprolactone tubes. The longest postoperative observation period was nine months. RESULTS: The results demonstrated that only in the case of cellular filled tubes (syngenic Schwann cells) did regeneration occur across the 20 mm gap. This regeneration was comparable to that induced after autologous grafting. Across a 40 mm gap the autologous graft demonstrated the best results.

Animals↗
PubMed2003

Tissue-engineered scaffolds are effective alternatives to autografts for bridging peripheral nerve gaps.

The use of autografts for "bridging" peripheral nerve gaps is limited by lack of suitable donor nerve grafts. Using a tissue-engineering approach, we have designed a three-dimensional scaffold that presents laminin 1 (LN-1) and nerve growth factor (NGF) in vivo. Semipermeable polysulfone tubes were used as carriers to introduce the tissue-engineered scaffolds to a 10-mm sciatic nerve gap in adult rats. Two months after implantation, the gross morphology of the regenerated nerve, the success rate of regeneration, and the total number and density of myelinated axons in the tissue-engineered scaffolds matched that observed in autografts. LN-1- and NGF-containing scaffolds performed comparably to autografts when functional measures that include the relative gastrocnemius muscle weight and the sciatic functional index were quantified. Our results demonstrate that tissue-engineered scaffolds match the performance of autografts in an in vivo model of peripheral nerve regeneration, raising the possibility of the scaffolds being used clinically instead of scarce autografts.

Animals↗
PubMed2006

[Perioperative analgesia with continuous peripheral nerve blocks in children].

Recently, regional anaesthesia in children has generated increasing interest. But single injection techniques have a limited duration of postoperative analgesia. Then, continuous peripheral nerve blocks have taken an important position in the anaesthetic arsenal, allowing an effective, safe and prolonged postoperative pain management. As adults, indications for continuous peripheral nerve blocks depend on the analysis of individual benefits/risks ratio. Main indications are intense postoperative pain surgical procedures, with or without postoperative rehabilitation, and complex regional pain syndrome. Contraindications to these procedures are rather similar to those in adults, plus parental and/or children refusal. Continuous peripheral nerve blocks are usually performed under general anaesthesia or sedation in children, and require appropriate equipment in order to decrease the risk of nerve injury. New techniques, such as transcutaneous nerve stimulation or ultrasound guidance, appeared to facilitate nerve and plexus approach identification in paediatric patients. Nevertheless, continuous peripheral nerve block may theoretically mask a compartment syndrome after trauma surgical procedures. Finally, ropivacaine appears to be the most appropriate drug for continuous peripheral nerve blocks in children, requiring low flow rates and concentrations of local anaesthetic. These techniques may facilitate early ambulation by an improved pain management or even postoperative analgesia at home with disposable pumps. One might infer from the current review that excellent pain relief coupled with a reduction of side effects would contribute to improve the quality of life and to decrease the frequency of disabling behavioural modifications in children, sometimes psychologically injured by hospital stay and postoperative pain.

Amides↗
PubMed1991

The relationship between sural nerve morphometric findings and measures of peripheral nerve function in mild diabetic neuropathy.

The morphological findings in sural nerve biopsy specimens from 15 diabetic patients with mild neuropathy were compared with control biopsies from eight non-neuropathic, non-diabetic subjects, and correlations were sought with electrophysiological studies and quantitative sensory tests for vibration, thermal, and current perception thresholds. Myelinated fibre density was reduced compared with control biopsies (4042 +/- 2090 (+/- SD) vs 6800 +/- 1100 mm-2; p less than 0.01). A strong correlation existed between myelinated fibre density and sural sensory conduction velocity (r = 0.84, p less than 0.001), sural action potential amplitude (r = 0.74, p less than 0.001), peroneal motor conduction velocity (r = 0.58, p less than 0.02), and median sensory amplitude (r = 0.64, p less than 0.01) but there was no correlation between myelinated fibre density and any quantitative sensory test. We conclude that conventional electrophysiological tests in the lower limb are reliable surrogate measures for structural abnormalities in early diabetic neuropathy.

Biopsy↗
PubMed1987

Effect of peripheral nerve on limb development.

The effect of peripheral nerve on limb growth and maturation has received little attention after the limb differentiation stage. This study used an amphibian model (Rana pipiens) to examine the effect of temporary denervation on the development of limb muscle and bone tissues. Quantitative microscopic techniques were employed to evaluate bone and muscle size and cellularity between denervated and control limbs. A 15% decrease in tibial length and a 17% decrease in cross-sectional area were found in the temporarily denervated limbs as compared with the control limbs during the growing period studied. A 26% increase in tibial osteocyte density was found in the denervated limbs, although total osteocyte number was the same. The same differences were found on comparing less and more mature limbs from normal animals. Gastrocnemius muscle from temporarily denervated limbs had a 46% lesser cross-sectional surface area and a 66% greater muscle fiber density as compared with control limbs. Total muscle fiber number was the same. Similar findings were observed comparing limbs of different maturities from normal unoperated animals. This study suggests that the absence of peripheral nerves decreases the rate of bone maturation, which effect may be responsible for the diminished size of denervated limbs. This work demonstrates a model for regional growth disturbances that may aid in understanding such disorders as idiopathic leg length discrepancy, hemihypertrophy, clubfoot, and the limb deformities created by paralytic diseases.

Animals↗
PubMed1984

Technical aspects of peripheral nerve repair.

This essay describes the internal topographical anatomy of peripheral nerves and outlines the use of this information in the specific steps of nerve suture. Repair is detailed in the context of overall wound management and those factors are emphasized which can be controlled by the surgeon and which have a definite effect on the functional outcome.

Humans↗
PubMed2001

The clinical application of peripheral nerve pathology.

The basic pathologic processes that can affect the peripheral nerve are discussed, with an emphasis on the basic findings seen on nerve biopsy. The indications and usefulness of nerve biopsy are discussed along with a review of the morphologic findings found with a variety of tissue preparation techniques. Advances, such as intradermal biopsies, which may prevent the need for standard nerve biopsies, are discussed.

Axons↗
PubMed1987

Peripheral nerve injury associated with fracture or fracture-dislocation of the pelvis in dogs and cats: 34 cases (1978-1982).

Peripheral nerve injury was associated with fracture or fracture-dislocation of the pelvis in 23 dogs and 11 cats. In most cases, peripheral nerve injury resulted from ilial fracture with craniomedial displacement of bone fragments, or from sacroiliac fracture-dislocation with cranial displacement of the ilium. Sciatic nerve injury was associated with fracture of the acetabulum in 2 dogs. A combination of sensory, voluntary motor, and reflex abnormalities were observed in the ipsilateral extremity of affected animals. Signs of severe pain were noticed in 4 of the dogs and in 1 cat. Eight of the animals died or were euthanatized for reasons not directly related to the severity of peripheral nerve injury. Of the remaining 26 animals, 21 (81%) had good or excellent limb function 16 weeks after peripheral nerve injury was sustained. Limb function was lost or self-mutilation occurred in 4 (15%) of the animals.

Animals↗
PubMed1991

Kinetics of anti-peripheral nerve myelin antibody in patients with Guillain-Barré syndrome treated and not treated with plasmapheresis.

Serial anti-peripheral nerve myelin antibody titers were determined in 28 consecutive patients with Guillain-Barré syndrome during the course of their illness. Eighteen patients were treated with plasmapheresis and 10 were not. Anti-peripheral nerve myelin antibody titers in the group treated with plasmapheresis declined significantly more rapidly than in the group not treated with plasmapheresis. Five patients treated with plasmapheresis who showed initial clinical improvement, with a concurrent decline in anti-peripheral nerve myelin antibody titer, had one or two recurrences of clinical symptoms during a 2- to 8-week period associated with an increase in anti-peripheral nerve myelin antibody titer. Recurrent weakness was severe enough to prompt additional courses of plasmapheresis. The data suggest that serial determinations of antiperipheral nerve myelin antibody in patients with Guillain-Barré syndrome may identify patients with antibody rebound associated with recurrence of clinical symptoms and prolonged recovery in whom further plasmapheresis should be considered.

Adolescent↗
PubMed2002

Effect of nerve growth factor on changes of myelin basic protein and functional repair of peripheral nerve following sciatic nerve injury in rats.

OBJECTIVE: To investigate the therapeutic effect of nerve growth factor (NGF) on changes of myelin basic protein (MBP) and functional repair of sensory and motor nerve following sciatic nerve injury. METHODS: The sciatic nerves of rats were injured by sectioning with shaver,and divided into 3 groups: NGF group (Group A), group of normal saline solution (Group B), untreated group (Group C). The time point of observation was at the 4th week after operation. Sensory evoked potential (SEP) and motor evoked potential (MEP) were detected by Model WD-4000 nerve potential working diagnosis system. Immunohistochemical analysis was used for identification of MBP. RESULTS: The latency of SEP in the Group A at the 4th week after operation was shorter than that in the Group B (P<0.05). The MEP was elicited in 76% of the Group A and was higher than that in the Group B. Results of immunohistochemistry showed that there were less MBP-positive cells in the Group A than in the Group B in one and four weeks respectively. CONCLUSIONS: NGF can improve the conductive function of injured peripheral nerve and facilitate regeneration of nerve.

Animals↗
PubMed1983

IgM paraproteins with immunological specificity for a Schwann cell component and peripheral nerve myelin in patients with polyneuropathy.

The sera of 9 patients with benign IgM paraproteinaemia and chronic sensorimotor neuropathy were tested for reactivity to human peripheral nerves by the indirect immunoperoxidase method. They reacted in very high titre (10(-3)-10(-6) with a cytoplasmic Schwann cell component, and to lesser degree, with peripheral nerve myelin (10(0)-10(-3). The Schwann cell staining was in the form of perinuclear cytoplasmic granules and was only seen with adult nerve. The distribution of the antigen was similar to that of the metachromatically staining Pi-granules of Reich, which accumulate in the peripheral nerves with age. Specific activity was present in the IgM and F(ab)2 fractions and could be absorbed out with peripheral nerve tissue, but not with liver. Reactivity is not a simple function of the IgM level, since many IgM paraproteins do not react. The antibody is species specific and binds to human, but not to any component of rabbit, rat or guinea pig sciatic nerves. Antigenicity is removed by pretreatment of the nerve with chloroform-methanol or periodate, but not protease or trypsin. Reactivity is restored, after periodate treatment, by exposure to sodium borohydride. It is suggested that some IgM paraproteins have a specificity for a myelin glycolipid or glycoprotein, which normally accumulates in the Pi-granules of the Schwann cell cytoplasm as a function of age.

Humans↗
PubMed1995

Inhibition of hand muscle motoneurones by peripheral nerve stimulation in the relaxed human subject. Antidromic versus orthodromic input.

In active muscle, a supramaximal conditioning stimulus to peripheral nerve produces a classic silent period in the EMG. The present experiments examined the effect of this type of conditioning stimulus on motoneurone excitability in relaxed muscle. EMG responses evoked by transcranial magnetic stimulation of the brain were recorded from the first dorsal interosseus muscle (FDI) in 10 healthy subjects and 5 patients with sensory neuropathy. These responses (motor evoked potentials) were conditioned by supramaximal peripheral nerve stimuli given 0-150 msec beforehand. In the normal subjects, the classic silent period in the FDI lasted about 100 msec. The same conditioning stimulus only abolished motor evoked potentials when the conditioning-test interval was so short that the antidromic peripheral nerve volley collided with the orthodromic volley set up by magnetic brain stimulation. At longer conditioning-test intervals, although remarkably inhibited (65% mean suppression between 10 and 40 msec), the test motor potential was never completely abolished and gradually recovered by 100 msec. Inhibition of cortically evoked motor potentials did not depend upon activity set up by the conditioning stimulus in peripheral nerve sensory fibres. The patients with complete peripheral sensory neuropathy had the same extent and time-course of inhibition as the normal subjects. We conclude that in relaxed subjects the inhibitory effect of peripheral conditioning results almost exclusively from the motoneuronal inhibitory mechanisms consequent to antidromic invasion.

Adult↗
PubMed2001

Reinnervation of the biceps brachii muscle following cotransplantation of fetal spinal cord and autologous peripheral nerve into the injured cervical spinal cord of the adult rat.

In order to compensate the loss of motoneurons resulting from severe spinal cord injury and to reestablish peripheral motor connectivity, solid pieces of fetal spinal cord, taken from embryonic day 14 rat embryos, were transplanted into unilateral aspiration lesions of the cervical spinal cord of adult rats. Concomitantly, one end of a 3.5-cm autologous peripheral nerve graft was put in close contact with the embryonic graft; the other end was sutured to the distal stump of the musculocutaneous nerve which innervate the biceps brachii muscle. The animals were examined 3 and 6 months after surgery. Following intramuscular injection of horseradish peroxidase, retrograde axonal labeling studies indicated that both transplanted and host spinal neurons were able to extend axons all the way through the peripheral nerve graft and nerve stump, up to the reconnected muscles. The labeled cells in the transplant were generally observed close to the intraspinal tip of the peripheral nerve graft. Retrograde axonal tracing, as well as electrophysiological and histological data, demonstrated the sensory and motor reinnervation of the reconnected muscles. This muscular reinnervation was able to reverse the atrophic changes observed in the denervated muscle. In control experiments, the extraspinal end of the peripheral nerve graft was ligatured in order to compare the differentiation of the transplanted neurons and the survival of their growing axons with or without their muscular targets. Six months after both types of surgery, large-size grafted neurons, identified as motoneurons by immunocytochemistry for peripherine and calcitonin gene-related peptide, were only observed in fetal spinal cord transplants which were connected to denervated muscles, thus demonstrating the trophic influence of the muscle target on the survival and differentiation of the transplanted neurons and on the maintenance of the axons they had grown into the peripheral nerve graft.

Animals↗
PubMed2006

Bladder sensation in peripheral nerve lesions.

OBJECTIVE: To present bladder sensory data of three common peripheral nerve lesions (e.g., distal, intermediate/focal, and proximal). METHODS: We measured first sensation (FS) and bladder capacity (BC) (not exceeding 600 ml) in 71 patients with peripheral nerve lesions: 35 diabetic neuropathy (D group), 6 post-pelvic surgery (S), and 27 cauda equina syndrome due to lumbar spondylosis (L). We excluded those with detrusor overactivity or low compliance that might affect bladder sensation. RESULTS: The mean FS was 301.7 ml (D), 271.3 ml (S), and 189.4 ml (L), with the largest being in the D group (P < 0.05); the mean BC was 495.2, 475.4, and 391.4 ml, with the largest being in the D group (P < 0.05); who commonly had less frequent toileting. The mean post-void residual volume was 106.5, 29.0, and 42.0 ml; the values tended to increase along with BC. In the D group, the mean FS in patients with skin hypoalgesia as detected by pin prick and in those without it was 407.8 and 210.0 ml. The percentage of patients with FS < 100 ml was 5.7%, 0%, and 7.4%, respectively, who commonly had urinary urgency and frequency. CONCLUSIONS: Bladder sensation is affected in diabetic neuropathy more severely than in intermediate/proximal lesions, together with somatic sensory disturbance. Bladder sensory disturbance leads to less frequent toileting, resulting in bladder over-distension and large post-void residuals. A small proportion of patients with peripheral nerve lesions develop urinary urgency, presumably reflecting irritation of the afferent nerve fibers or the urothelium.

Aged↗
PubMed1991

Distribution of P0 protein and the myelin-associated glycoprotein in peripheral nerves from Trembler mice.

The Trembler mouse has a dysymelination of peripheral nerves that includes hypomyelination, failure of myelin compaction, and demyelination/remyelination. We have localized the myelin proteins P0 and myelin associated glycoprotein in Trembler peripheral nerve and correlated their distributions with the ultrastructure of myelin internodes. Immunocytochemically, myelin-associated glycoprotein was localized in Schwann cell periaxonal membranes, Schmidt-Lanterman incisures, paranodal loops, and internal and external mesaxons. P0 staining was located over compact myelin and regions of Schwann cell cytoplasm rich in Golgi membranes. An unusual abundance of small, P0-stained, Golgi-related vesicles was found in some Schwann cells. P0 protein was also detected in multiple spiral wraps of myelin-associated glycoprotein-positive mesaxon membranes. At some sites the periodicity of the myelin membranes was intermediate to that found in mesaxon membranes and compact myelin. The distance between apposing extracellular leaflets was similar to that found in mesaxon membranes, while the cytoplasmic leaflets were fused but twice as thick as normal major dense lines. These intermediate membranes were stained by P0 and myelin-associated glycoprotein antiserum. These studies suggest that altered transport and/or translocation of P0 and myelin-associated glycoprotein results in defective myelin compaction in Trembler peripheral nerve.

Animals↗