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Results for “Nerve Expansion”

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At least 19 recordsLinked to original sources
PubMed1997

Nerve expansion in nerve regeneration: effect of time on induction of ornithine decarboxylase and Schwann cell proliferation.

We studied the effect of initiation time of nerve expansion after nerve transection on the induction of ODC activity and Schwann cell proliferation in nerve tissue under Wallerian degeneration. The levels of ODC activity and Schwann cell proliferation decreased as the initiation time of nerve expansion was delayed after nerve transection, and peak levels of ODC activity following nerve expansion preceded peak levels of Schwann cell proliferation.

Animals↗
PubMed1996

Rapid intraoperative facial nerve expansion.

The repair of nerve length defect presents a reconstructive challenge after trauma and oncologic resection. This study examined rapid intraoperative nerve expansion as a method of repairing nerve length defects with the cat facial nerve model. We compared expanded nerves with grafted nerves and intact nerves 1 year after repair using the criteria of gross function (symmetry and blink reflex according to a modified House scale), electromyography thresholds, nerve-conduction velocity, morphology, and axon count. Three of the five expanded nerves regenerated, and all of the grafted nerves regenerated. Functional results were similar for the regenerated expanded and the grafted facial nerves, and both methods achieved an equivalent level of function. The facial nerves of the regenerated expanded group, grafted group, and intact group had mean electromyography thresholds of 132 mV, 98 mV, and 134 mV, respectively, and mean conduction velocities of 48.3 mg/second, 47.9 m/second, and 44.7 m/second, respectively. Morphologic examination of all five expanded nerves immediately after the expansion process revealed an intact fascicular structure. However, 1 year after excision of the expanded segment and repair, only three of the five nerves regenerated. Axon count at 1 year was as follows: 404 for the regenerated expanded nerves, 449 for the grafted nerves, and 403 for the intact nerves. The potential advantages of rapid intraoperative nerve expansion over nerve grafting for the repair of nerve gap defects include a single suture line and absence of donor site morbidity. This pilot study demonstrates that rapid intraoperative nerve expansion and regeneration is possible and can be used to repair a nerve length deficit. The development of a rapid and reliable method of intraoperative nerve expansion deserves further study.

Animals↗
PubMed1995

Nerve expansion. The optimal answer for the short nerve gap. Behavioral analysis.

Treatment of the short nerve gap remains a challenge for the reconstructive surgeon, but it is a clinical problem that can be addressed by nerve expansion. In the present study, the effects of slow nerve expansion on the walking behavior of the rat were examined. When expansion was applied on a normal sciatic nerve or on a transected nerve at either the proximal or the distal segments, permanent 30% elongation could be achieved. The recovered function from the expanded nerve stumps was compared with such classical methods of nerve reconstruction as nerve graft, coaptation under moderate tension, and tensionless repair. The results compared favorably between the expanded groups and the time-honored methods of nerve repair. Analysis of the behavioral data indicated that any amount of expansion affected the functional capabilities of the involved nerve. However, expansion of a normal nerve and/or proximal segment of a transected nerve was better tolerated than distal segment expansion, which suggests that the presence of an axon may have a beneficial effect in minimizing the deforming mechanical insult. Slow nerve expansion appears to have a definite role in the microsurgical management of the short nerve gap.

Animals↗
PubMed1997

A case of popliteal pterygium treated along with nerve expansion.

The presence of a short sciatic nerve in the free edge of a popliteal pterygium makes this syndrome a surgical challenge. We present a case of popliteal pterygium that was treated by nerve expansion. The range of motion of the patient's knee joint was between 30 and 120 degrees. A 75-cc tissue expander was placed under the sciatic nerve and filled with 5 cc of saline solution weekly. When a total of 60 cc was reached, wound dehiscence was observed, and the procedure had to be stopped. The maximum extension obtained was 160 degrees. Since the expansion process had to be stopped early, the elongation attained by expansion was less than expected. We conclude that the nerve expansion method can be used as a good alternative treatment modality for patients with popliteal pterygium.

Child, Preschool↗
PubMed1994

[Experimental study of peripheral nerve expansion with a tissue expander].

If a peripheral nerve could be elongated by a tissue expander (TE) without apparent damage, the length gained could be used to overcome a nerve gap without recourse to nerve graft. An experimental study was made to investigate whether this method for repairing a nerve gap is feasible. The tissue expander was designed by the authors and the median nerve of rabbits were stretched with TE at the rate of about 1 mm/day. The results showed that when the elongation rate was 18.4%, the motor nerve conduction velocity (MCV) was 67.8% and the myelinated nerve fibres (MNF) was 82.9% of the control nerves. In a further study nerve grafting and nerve expansion for repairing segmental nerve loss were compared with 10 mm defects. 4 months later the MCV, MNF, isometric contraction force (ICF) and muscle wet weight (MWW) were not significantly different between the 2 techniques. But with the 15 mm defects, elongated nerve were inferior to the nerve grafting method.

Animals↗
PubMed1998

Electroneurography during facial nerve expansion.

With the use of tissue-expansion techniques, it is possible to elongate the facial nerve without impairing its function. The rate of expansion is limited by ischemic events imposed by stretching of the nerve and by anatomic characteristics of the nerve segment. In this study, we used various electroneurography techniques to determine the first sign of facial dysfunction during expansion. The main objective of the study was to ascertain test-retest variability of electroneurography techniques. Facial nerves were expanded in 16 cats with the use of a tissue expander secured more deeply to the main trunk. We conducted electroneurography measurements with the use of surface electrodes, temporary needle electrodes, and permanently implanted electrodes. Technique-dependent variations encountered with the surface electrodes made this method unreliable. Using implanted electrodes, we noted gradual worsening of the compound-action potential amplitude with increasing expansion. During acute expansion, reduction in compound-action potential amplitude was correlated with clinically observed deterioration of facial-nerve function. In this study, electroneurography with implanted electrodes was found to be the most reliable predictor of the rate of successful facial nerve expansion.

Action Potentials↗
PubMed1991

Regulated plasmalemmal expansion in nerve growth cones.

To study the mechanisms underlying plasmalemmal expansion in the nerve growth cone, a cell-free assay was developed to quantify membrane addition, using ligand binding and sealed growth cone particles isolated by subcellular fractionation from fetal rat brain. Exposed versus total binding sites of 125I-wheat germ agglutinin were measured in the absence or presence of saponin, respectively, after incubation with various agents. Ca2(+)-ionophore A23187 in the presence of Ca2+ increases the number of binding sites (Bmax) but does not change their affinity (KD), indicating that new receptors appear on the plasma membrane. Similarly, membrane depolarization by high K+ or veratridine significantly induces, in a Ca2(+)-dependent manner, the externalization of lectin binding sites from an internal pool. Morphometric analysis of isolated growth cones indicates that A23187 and high K+ treatment cause a significant reduction in a specific cytoplasmic membrane compartment, thus confirming the lectin labeling results and identifying the plasmalemmal precursor. The isolated growth cones take up gamma-amino-butyric acid and serotonin, but show no evidence for Ca2(+)-dependent transmitter release so that transmitter exocytosis is dissociated from plasmalemmal expansion. The data demonstrate that plasmalemmal expansion in the growth cone is a regulated process and identify an internal pool of precursor membrane.

Animals↗