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Colocalization of tenascin and sympathetic nerves in a canine model of nerve sprouting and sudden cardiac death.

INTRODUCTION: Sympathetic nerve sprouting after myocardial infarction (MI) may contribute significantly to the occurrence of ventricular arrhythmia and sudden cardiac death. Tenascin-X (TnX), a matrix protein known to be associated with nerve growth in central and peripheral nerves, also may play a role in cardiac nerve sprouting after MI. METHODS AND RESULTS: Immunocytochemical staining techniques were used to identify nerves in 5-microm serial sections from 6 normal dogs and 11 dogs with MI. Among the dogs with MI, 4 also received nerve growth factor infusion to the left stellate ganglion. The time between MI to tissue harvest averaged 35.7 +/- 14.4 days. Tyrosine hydroxylase (TH) stain was used to identify sympathetic nerves, and growth-associated protein-43 (GAP-43) was used to identify growing nerves. Polyclonal antibody was obtained for use in identifying TnX. Nerves were evident in both the infarcted and noninfarcted areas. Many nerves were found around blood vessels. A total of 181 nerves in 69 slides were examined: 89 were from noninfarcted myocardium, 4 from infarct, 13 from infarct border zone, and 75 from perivascular regions. Except in normal dogs, all nerves stained positive for TH also stained positive for GAP-43, indicating sympathetic nerve sprouting after MI. In all dogs, the nerves that stained positive for TH also stained positive for TnX. CONCLUSION: There is a colocalization of TnX, GAP-43, and TH in sprouted cardiac nerves. These results suggest that TnX is important not only in the existing normal myocardial nerve cells but also in cardiac sympathetic nerve sprouting after MI.

Animals↗

Effects of vascular endothelial growth factor on nerve regeneration in acellular nerve grafts.

The purpose of this study was to evaluate the effects of human recombinant vascular endothelial growth factor (VEGF-165) on peripheral nerve axonal sprouting and elongation following peripheral nerve injury and repair. Two-centimeter nerve gaps were created in rat peroneal nerves and repaired with either peripheral nerve autografts, acellular peripheral nerve isografts, or VEGF-165-treated acellular peripheral nerve isografts. Four months postoperatively, the peroneal nerves were harvested and histomorphometric analysis was performed. The reinnervated extensor digitorum longus (EDL) muscles were harvested and weighed. At the proximal nerve gap coaptation site, there was a statistically significant increase in the total number of axons and percent neural tissue in the VEGF-treated acellular nerve graft group, compared with the acellular peripheral nerve isograft and autograft groups. At the distal coaptation site, however, the total number of axons and percent neural tissue was similar in the acellular and VEGF-treated groups, which was significantly less than the autograft group. VEGF-165 treatment of acellular nerve grafts resulted in greater EDL muscle masses than acellular nerve grafts alone. VEGF treatment of acellular peripheral nerve isografts enhances axonal sprouting, resulting in an increased number of axons and percent neural tissue at the proximal nerve graft coaptation site. In the absence of any cellular elements, VEGF-impregnated acellular peripheral nerve grafts do not demonstrate enhanced axonal elongation, as noted by relatively few axons at the distal nerve graft coaptation site.

Animals↗

[Three essential elements of glaucomatous optic nerve damage and discrimination of optic nerve rim loss].

Three essential elements of glaucomatous optic nerve damages are optic nerve rim loss, retinal nerve fiber layer defects (RNFLD) and optic disc linear hemorrhages. It's suggested that if there are two positive signs detected among the three elements, the diagnosis of the glaucomatous optic nerve damages can be established. There is no definitely described how to identify optic nerve rim loss in the previous textbooks, therefore it is important to know about the morphological features of the physical optic nerve rim and influence factors before discrimination of optic nerve rim loss. Most of physical optic nerve rim are in accordance with ISNT rule, physical large optic cups are also accord with ISNT rule. Exceptional cases exist in two patterns, optic nerve rim loss or normal optic nerve rim morphological variances. The latter includes part of small discs, horizontally oval optic discs, the position of the central retinal vessel trunk and the titled optic discs which affect the morphological feature of optic nerve rim as well. In some small discs, the width of inferior rim is narrower than that of superior rim, therefore, the inferior or the superior rim loss can be evaluated by comparison with nasal rim width. Concerning horizontal oval optic discs, the width of inferior rim and superior rim should be compared to evaluate whether there is the optic nerve rim loss. If those patterns of normal optic nerve rim variances can be recognized, it is not difficult to find the presence of the optic nerve rim loss. However, not all of the optic nerve rim loss is due to glaucomatous optic nerve damages, non-glaucomatous optic nerve damage should be distinguished.

Diagnosis, Differential↗

Denatured muscle grafts for nerve repair in an experimental model of nerve damage in leprosy. 1. A functional and morphometric study.

The effectiveness of denatured autologous muscle grafts for nerve repair in an experimental model of leprosy was assessed. Nerve damage resembling that caused by Mycobacterium leprae in humans was induced by the injection of cobalt-irradiated M. leprae into the tibial nerve of guinea pigs. At the time of maximum functional loss, caused by the formation of a granuloma within the nerve, the area of damage was excised and a denatured autologous muscle graft was used to repair the nerve. Assessment of nerve regeneration through the graft was made using clinical, electrophysiological and microscopic morphometric analysis at intervals up to 20 weeks. The results were compared with regeneration after grafting of a normal nerve. Clinically, some motor and sensory recovery occurred in all of the graft recipients in the normal nerve by 8 weeks, and by 11 weeks in the recipients of grafts in the granulomatous nerve. Full sensory recovery occurred in all but one animal by 20 weeks. Motor function recovered to near normal levels at 14 weeks after repair of the normal nerve but, at 20 weeks, there was variation in motor recovery after repair of the granulomatous nerve. Electrophysiology showed increased conduction velocity of the nerve fibers at each time-point. The conduction velocity at 8 weeks after grafting of the normal nerve was similar to that at 12 weeks after grafting of the granulomatous nerve. Morphometry showed an increasing number of myelinated fibers repopulating the distal nerve up to 20 weeks. Myelin fiber numbers, at this time, were one third of normal after repair of the granulomatous nerve and two thirds after repair of the normal nerve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Responses of cardiac vagus and sympathetic nerves to excitation of somatic and visceral nerves.

Somato-vagal and somato-sympathetic reflex responses were studied by recording simultaneously the activity of cardiac vagal and sympathetic efferents following excitation of various somatic (and 1 visceral) nerves in chloralose-anesthetized dogs. Stimulation of pure cutaneous (infraorbital, superficial radial, sural nerves), muscle (gastrocnemius, hamstring nerves) and mixed nerves (sciatic, brachial, intercostal, spinal) with short trains of pulses inhibited the activity of cardiac vagus nerve and excited that of cardiac sympathetic nerve after a latency of approximately 40-60 ms, depending on the nerve stimulated. These responses were followed by the opposite response, i.e. excitation of vagus and long-lasting inhibition ('silent period') of sympathetic nerve activity. These biphasic reflex responses recorded from both autonomic nerves had similar latencies so that a clear reciprocal relationship was observed. In addition to the above reflex responses which were observed in most instances, two peaks of excitation of short duration were recorded from the vagus nerve, in some instances, and an 'early (spinal) reflex' in sympathetic nerve was also observed. Both excitatory and inhibitory responses described above in either nerve were readily evoked by excitation of Group II (A beta), but not Group I (A alpha), afferent fibers and increased in magnitude when Group III (A delta) afferents were also excited. Group IV (C) afferent contributed insignificantly to the somato-vagal reflex. The vagus nerve discharge evoked by sinus nerve stimulation was inhibited during reflex inhibition produced by somatic nerve stimulation. The latency of such inhibition was less than 20 ms and lasted for 100 ms after sural nerve stimulation. We conclude that, as in case of the baroreceptor reflex and autonomic component of the 'defense reaction', the somato-vagal and somato-sympathetic reflex responses are reciprocal in nature.

Animals↗

Changes in median nerve somatosensory transmission and motor output following transient deafferentation of the radial nerve in humans.

OBJECTIVE: To determine if transient anaesthetic deafferentation of the radial nerve would lead to alterations in processing of early somatosensory evoked potentials (SEPs) from the median nerve or alter cortico-motor output to the median nerve innervated abductor pollicis brevis (APB) muscle. METHODS: Spinal, brainstem, and cortical SEPs to median nerve stimulation were recorded before, during and after ipsilateral radial nerve block with local anaesthesia. Motor evoked potentials (MEPs) and motor cortex output maps were recorded from the APB muscle. RESULTS: There were no significant changes to most early SEP peaks. The N30 peak, however, showed a significant increase in amplitude, which remained elevated throughout the anaesthetic period, returning to baseline once the anaesthetic had completely worn off. MEP amplitude of the median nerve innervated APB muscle was significantly decreased during the radial nerve blockade. There was also a significant alteration in the APB optimal site location, and a small but significant decrease in the silent period during the radial nerve blockade. CONCLUSIONS: Transient anaesthetic deafferentation of the radial nerve at the elbow leads to a rapid modulation of cortical processing of median nerve input and output. These changes suggest an overall decrease in motor cortex output to a median nerve innervated muscle not affected by the radial nerve block, occurring concomitantly with an increased amplitude of the median nerve generated N30 SEP peak, thought to represent processing in the supplementary motor area (SMA). Independent subcortical connections to the SMA are thought to contribute to the N30 response observed in this study. Unmasking of pre-existing but latent cortico-cortical and/or thalamo-cortical connections may be the mechanism underlying the cortical SEP increases observed following radial nerve deafferentation. SIGNIFICANCE: Transient deafferentation of the radial nerve, which supplies wrist and hand extensor muscles, has been shown to alter sensory processing from and motor output to the median nerve innervated thenar muscles.

Adult↗

Comparative morphometry of myelinated nerve fibres in the normal and pathologically altered human sural and tibial nerve.

To assess neuropathological changes in human nerves, biopsies are usually performed on the sural nerve or other nerves supplying only a small area of skin. It is not yet clearly understood to what extent the changes found in this sensory nerve correspond to the changes found in other distal sensomotory nerves. To answer this question, we made a comparative morphometric analysis of the sural and tibial nerve. In 39 autopsy cases (aged 22 - 90 years) the sural and the tibial nerve were subject of image analysis. The histological picture in this study group was clearly influenced by neuropathological changes as well as age-related changes. For each morphometric parameter in the sural and tibial nerve, we evaluated Pearson's correlation. The highest coefficient of correlation (r) was seen in those parameters that represented the condition of the myelin sheath area: the density of nerve fibre area (sum of measured nerve, fibre areas/analyzed endoneural area) (r = 0.86) and the density of myelin sheath area (sum of measured myelin areas/analyzed endoneural area) (r = 0.86). Similar correlations were obtained for the mean of axon diameter (r = 0.82), the numerical density of nerve fibre count (nerve fibre count/analyzed endoneural area) (r = 0.77), the mean of nerve fibre diameter (r = 0.77) and the mean of myelin sheath thickness (r = 0.72). Our results revealed a good or very good statistical correlation of morphometric parameters between the two examined nerves. They support the assumption that the sural nerve sufficiently reflects the histological changes in other distal sensomotoric nerves. This is valid at least in systemic neuropathological diseases and age-dependent processes.

Adult↗

Optic nerve regeneration after intravitreal peripheral nerve implants: trajectories of axons regrowing through the optic chiasm into the optic tracts.

We have studied axon regeneration through the optic chiasm of adult rats 30 days after prechiasmatic intracranial optic nerve crush and serial intravitreal sciatic nerve grafting on day 0 and 14 post-lesion. The experiments comprised three groups of treated rats and three groups of controls. All treated animals received intravitreal grafts either into the left eye after both left sided (unilateral) and bilateral optic nerve transection, or into both eyes after bilateral optic nerve transection. Control eyes were all sham grafted on day 0 and 14 post-lesion, and the optic nerves either unlesioned, or crushed unilaterally or bilaterally. No regeneration through the chiasm was seen in any of the lesioned control optic nerves. In all experimental groups, large numbers of axons regenerated across the optic nerve lesions ipsilateral to the grafted eyes, traversed the short distal segment of the optic nerve and invaded the chiasm without deflection. Regeneration was correlated with the absence of the mesodermal components in the scar. In all cases, axon regrowth through the chiasm appeared to establish a major crossed and a minor uncrossed projection into both optic tracts, with some aberrant growth into the contralateral optic nerve. Axons preferentially regenerated within the degenerating trajectories from their own eye, through fragmented myelin and axonal debris, and reactive astrocytes, oligodendrocytes, microglia and macrophages. In bilaterally lesioned animals, no regeneration was detected in the optic nerve of the unimplanted eye. Although astrocytes became reactive and their processes proliferated, the architecture of their intrafascicular processes was little perturbed after optic nerve transection within either the distal optic nerve segment or the chiasm. The re-establishment of a comparatively normal pattern of passage through the chiasm by regenerating axons in the adult might therefore be organised by this relatively immutable scaffold of astrocyte processes. Binocular interactions between regenerating axons from both nerves (after bilateral optic nerve transection and intravitreal grafting), and between regenerating axons and the intact transchiasmatic projections from the unlesioned eye (after unilateral optic nerve lesions and after ipsilateral grafting) may not be important in establishing the divergent trajectories, since regenerating axons behave similarly in the presence and absence of an intact projection from the other eye.

Age Factors↗

Anatomical basis for nerve-sparing radical hysterectomy: immunohistochemical study of the pelvic autonomic nerves.

BACKGROUND: Autonomic nerve damage plays a crucial role in the etiology of bladder dysfunction, sexual dysfunction, and colorectal motility disorders that occur after radical hysterectomy. We investigated the extent and nature of nerve damage in conventional and nerve-sparing radical hysterectomy. METHODS: Macroscopical disruption of nerves was assessed through anatomical dissection after conventional and nerve-sparing surgery on five fixed and one fresh cadaver. Immunohistochemical analysis of surgical margins was performed to confirm nerve damage using a general nerve marker (S100) and a sympathetic nerve marker (anti-tyrosine hydroxylase) within sections of biopsies. RESULTS: Macroscopical dissection showed that in the conventional procedure, transsection of the uterosacral ligaments resulted in disruption of the major part of the hypogastric nerve. After nerve-sparing surgery, only the medial branches of the hypogastric nerve appeared disrupted. Division of the cardinal ligaments in the conventional procedure identified the inferior hypogastric plexus running into the most posterior border of the surgical margin. The anterior part of the plexus was disrupted. Dissection of the nerves after the nerve-sparing procedure showed that this anterior part of the plexus was not involved in the surgical dissection line. Dissection of the vesicouterine ligament disrupted only small nerves on the medial border of the inferior hypogastric plexus in both techniques. Microscopical evaluation of the surgical margins confirmed the macroscopical findings. CONCLUSION: Conventional radical hysterectomy results in disruption of a substantial part of the pelvic autonomic nerves. The nerve-sparing modification leads to macroscopic reduction in nerve disruption which is substantiated by microscopical evaluation of surgical margins.

Antibodies, Monoclonal↗

The difference in E-cadherin expression between nonvascularized and vascularized nerve grafts: study in the rat sciatic nerve model.

BACKGROUND: We investigated the expression of E-cadherin during nerve regeneration after nonvascularized and vascularized nerve grafts. MATERIALS AND METHODS: We used the rat sciatic nerve model. E-cadherin expression was detected by Western blot analysis and immunofluorescent staining with anti E-cadherin monoclonal antibody. The level of E-cadherin expression was calculated as the amount relative to that of E-cadherin expression of normal control nerve. Furthermore, repair of the neural tissue structure was examined by toluidine blue staining. RESULTS: In both cases, the level of E-cadherin expression decreased at first, and then gradually increased. The maximum level was 1.61 +/- 0.066-fold in the nonvascularized nerve graft and 2.254 +/- 0.071-fold in the vascularized nerve graft. From the 1st to the 16th postoperative weeks, the level of E-cadherin expression in the vascularized nerve graft was significantly higher than that in the nonvascularized nerve graft. In the immunofluorescent staining, E-cadherin expression was almost negative or decreased immediately after the operation, but the degree of expression was gradually increased in Schwann cells. The degree of E-cadherin expression in the vascularized nerve graft was greater than that in the nonvascularized nerve graft. In toluidine blue staining, the velocity of tissue repair was more rapid in the vascularized nerve graft than in the nonvascularized graft. CONCLUSION: These results demonstrate that the E-cadherin expression of grafted nerve was increased during the nerve regeneration, and the expression was mainly observed in Schwann cells. Because the level of E-cadherin expression was significantly higher in the vascularized nerve graft than in the nonvascularized nerve graft, the level of E-cadherin expression may affect the rapidity of nerve regeneration.

Animals↗

Characteristics of cat skeletal muscles grafted with intact nerves or with anastomosed nerves.

Grafting of 3-g extensor digitorum longus (EDL) muscles of cats may be made with (i) severence of the nerve with spontaneous reinnervation, termed standard grafts (ii) severence of the nerve with reinnervation facilitated by anastomosis of the nerve, termed nerve-anastomosed grafts; and (iii) preservation of the nerve, termed nerve-intact grafts. In previous studies, standard grafts developed a maximum isometric tetanic tension (P0) that was 22% of the value for control EDL muscles. We hypothesized that the low values of P0 resulted from incomplete reinnervation of muscle fibers. To test this hypothesis, EDL muscles were grafted in cats with nerves intact and with nerves anastomosed. In standard grafts differences were observed in both structure and function at 120 compared with 240 days after grafting. Characteristics of the nerve-intact and nerve-anastomosed grafts did not change significantly between 120 and 240 days and the data were pooled for comparisons with control EDL muscles. Nerve-anastomosed and nerve-intact grafts developed P0 values that were 34 and 64% of the control values, respectively. Nerve-intact grafts had a mass and fiber cross-sectional area not different from control EDL muscles. Compared with control values, all grafts had fewer fibers, more connective tissue, lower absolute and normalized P0, reduced capillary density, and increased fatigability. The greater P0 of nerve-intact compared with standard and nerve-anastomosed grafts supported our hypothesis that the degree of reinnervation is a factor that limits graft development. The presence of a necrotic core and the low tension development of even the nerve-intact grafts suggested that revascularization is a significant limitation as well.

Animals↗

The anatomic relationship of the sciatic nerve to the lesser trochanter: implications for anterior sciatic nerve block.

UNLABELLED: Classic descriptions of the anterior sciatic nerve block suggest needle placement at the level of the lesser trochanter of the femur. Recently, investigators have reported that the sciatic nerve is not accessible at this level. To define more accurately the anatomic relationship of the sciatic nerve to the lesser trochanter, we analyzed magnetic resonance scans performed on 20 patients in the supine position. After IRB approval, magnetic resonance scans of the hip and proximal femur were reviewed in 20 supine patients in the neutral position. Images from five axial levels were studied, specifically, at the level of the lesser trochanter and at 1-cm intervals inferior to the lesser trochanter for 4 cm. In each axial image, the medial or lateral distance was measured from the sciatic nerve to a sagittal plane at the medial border of the femur. If the sciatic nerve was lateral to this sagittal plane (inaccessible), the distance was assigned a negative value, and if the sciatic nerve was medial to the sagittal plane (accessible), the distance was assigned a positive value. The distance between the coronal plane at the anterior border of the femur and the coronal plane through the sciatic nerve was also recorded for each level. At the level of the lesser trochanter, the sciatic nerve was lateral to the femoral border (inaccessible) in 13 of 20 patients with a mean distance of -4.0 +/- 7.7 mm. At 4 cm below the lesser trochanter, the sciatic nerve was medial to the femoral border (accessible) in 19 of 20 patients with a mean distance 7.8 +/- 5.8 mm. The distance from the anterior border of the femur to the sciatic nerve was 42.9 +/- 5.8 mm at the level of the lesser trochanter and 45.7 +/- 9.5 mm at 4 cm below the lesser trochanter. The classic description of the anterior approach to the sciatic nerve suggests that the needle be walked off medially at the level of the lesser trochanter. Our data are consistent with recent reports suggesting that in the majority of subjects, the position of the sciatic nerve relative to lesser trochanter made it inaccessible from an anterior approach at this level. In contrast, at 4 cm below the lesser trochanter, the sciatic nerve was medial to the femur in 19 of 20 subjects. We conclude that needle insertion medial to the proximal femur, 4 cm below the lesser trochanter, is a more direct anatomical approach to the anterior sciatic nerve block. IMPLICATIONS: Magnetic resonance images suggest that in the majority of supine subjects, the sciatic nerve is lateral to the lesser trochanter of the femur and therefore not accessible using the classic anterior approach. By contrast, 4 cm below the lesser trochanter, the sciatic nerve is consistently medial to the femoral shaft and therefore may be more accessible using an anterior approach.

Adult↗

Restoration of shoulder abduction by nerve transfer in avulsed brachial plexus injury: evaluation of 99 patients with various nerve transfers.

During the 5-year period between 1987 and 1991, 99 patients with total root or upper root (C5, C6, or C7) injuries were treated by nerve transfer to obtain shoulder abduction. More than eight different combinations of coaptation between donor nerves (intercostal nerves, phrenic nerve, spinal accessory nerve, ipsilateral C7, or cervical motor nerves) and recipient nerves (suprascapular nerve, axillary nerve, and upper trunk or C5) were applied. All patients had at least 2 years of follow-up. Different results were obtained in each category. Simultaneous neurotization of the suprascapular and axillary nerves with the phrenic and spinal accessory nerves obtained much better and more reliable shoulder abduction. Neurotization of the C5 spinal nerve by multiple nerve transfers was another good option that yielded good shoulder abduction in a single patient. If the phrenic nerve was traumatized, neurotization of the suprascapular nerve solely with the spinal accessory nerve was still capable of achieving an acceptable range of shoulder abduction.

Adolescent↗

[An effect of the omental wrapping on revascularization and nerve regeneration of the artificial nerve graft].

OBJECTIVE: To explore an effect of the artificial nerve graft wrapped in the pedicled greater omentum on the early revascularization and an effect of the increased blood supply to the artificial nerve graft on the nerve regeneration. METHODS: Seventy-five rabbits were randomized into 3 groups, in which there were 2 experimental groups where the rabbits were made to abridge respectively with the artificial nerve grafts wrapped in the pedicled greater omentum (Group A) and with the artificial nerve grafts only (Group B), and the control group where the rabbits were abridged with the autologous nerve (Group C). On the 3rd, 7th and 14th days after operation, the evans blue bound to albumin (EBA) was injected into the vessels in all the grafts to show their revascularization. Twelve weeks after operation the nerve regeneration was evaluated with the electrophysiological and histological observations on the serial sections, and was evaluated also with the transmission electron microscope. RESULTS: The artificial nerve grafts wrapped in the pedicled greater omentum in Group A and the autologous nerve grafts in Group C showed a beginning of revascularization on the 3rd day after operation, and the revascularization was increased on the 7th and 14th days. Compared with Groups A and C, the artificial nerve grafts in Group B showed a delayed revascularization on the 7th day after operation. At 12 weeks after operation, there were no significant differences in the motor never conduction velocity, density of the regenerated myelinated nerve fibers, myelin sheath thickness, and diameter between Group A and Group C (P > 0.05). However, both Group A and Group C were superior to Group B in the above variables, with significant differences (P < 0.05). CONCLUSION: Utilization of the pedicled greater omentum to wrap the artificial nerve grafts can promote an early revascularization of the artificial nerve graft and an early nerve regeneration of the artificial nerve graft because of an enhanced blood supply to the nerve graft.

Animals↗

Using the nerve stimulator for peripheral or plexus nerve blocks.

Conventional methodology for nerve location utilizes anatomical landmarks followed by invasive exploration with a needle to a suitable endpoint. An appropriate endpoint can be either anatomical in nature (e.g. transaterial technique) or functional (paresthesia or motor response to electrical stimulation). Ability to electrically stimulate a peripheral nerve or plexus depends upon many variables, including; 1) conductive area at the electrode, 2) electrical impedance, 3) electrode-to-nerve distance, 4) current flow (amperage), and 5) pulse duration. Electrode conductive area follows the equation R = rhoL/A, where R = electrical resistance, p = tissue resistivity, L = electrode-to-nerve distance, and A = electrode conductive area. Therefore resistance varies to the inverse of the electrode's conductive area. Tissue electrical impedance varies as a function of the tissue composition. In general, tissues with higher lipid content have higher impedances. Modern electrical nerve stimulators are designed to keep current constant, in spite of varying impedance. The electrode-to-nerve distance has the most influence on the ability to elicit a motor response to electrical stimulation. This is governed by Coulomb's law: E = K(Q/r2) where E = required stimulating charge, K= constant, Q = minimal required stimulating current, and r = electrode-to-nerve distance. Therefore, ability to stimulate the nerve at low amperage (e.g. < 0.5 mA), indicates an extremely close position to the nerve. Similarly, increasing current flow (amperage) increases the ability to stimulate the nerve at a distance. Increasing pulse duration increases the flow of electrons during a current pulse at any given amperage. Therefore, reducing pulse duration to very short times (e.g. 0.1 or 0.05 ms) diminishes current dispersion, requiring the needle tip to be extremely close to the nerve to elicit a motor response. The above parameters can be varied optimally to enhance successful nerve location and subsequent blockade. Unlike imaging modalities such as ultrasonography, electrical nerve stimulation depends upon nerve conduction. Similarly, percutaneous electrode guidance (PEG) makes use of the above variables to allow prelocation of the nerve by transcutaneous stimulation.

Electric Stimulation↗

[Stimulating effect of isolated nerve segments on the regeneration of peripheral nerves].

The present paper concerns observations in two series of experiments in which the effect of isolated nerve segments on nerve regeneration was studied. Bridging of a nerve defect with a tube was used as an experimental model--a model often used in studies on nerve regeneration today. In the first series of experiments performed on rats, 14 mm of the femoral nerve were removed and the gap bridged with the femoral vein. A 2-mm nerve segment was inserted at the center of the vein in one group of the animals. In the second experimental series performed on rabbits, 40-45 mm of the peroneal nerve was resected. Up to three segments were introduced into the lumen of the bridging vein. The experiments demonstrated the promoting effect of nerve segments on nerve regeneration and indicated the probable mode of their action: the nerve segments serve as an additional source of Schwann cells and of neurofibroblasts, contributing substantially to the formation of the guiding structures for the axons. The nerve segments are apparently able to develop a similar nerve structure to that formed by the distal nerve stump. However, this ability also appears to be limited to a distance of 10 mm as is the case with distal nerve stumps. These conclusions do not exclude a possible neurotropic action of the nerve segments.

Animals↗