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Focal and generalized peripheral nerve dysfunction in spinal cord-injured patients.

SUMMARY: The present study was undertaken to quantitate the incidence and clinical patterns of peripheral nerve dysfunction distal to the level of injury in patients with spinal cord injury (SCI). Through retrospective analysis, SCI patients were identified after referral for neurophysiologic investigation of new neuropathic symptoms. In total, peripheral nerve or nerve root lesions developed in 34 SCI patients, most commonly within the first year after SCI. Carpal tunnel syndrome was the most common upper-limb neuropathy (34%); sciatic neuropathy was the most common lower-limb abnormality (8.5%). A significant proportion of SCI patients had neurophysiological evidence of generalized peripheral nerve dysfunction, specifically axonal neuropathy (18%). Tetraplegic patients developed more frequent peripheral nerve lesions than paraplegics. Although most SCI patients presented within 4 years of their original injury, in a more chronic population of SCI patients that developed neuropathy 5 years after injury, 60% had evidence of coexistent syrinx formation. Maintenance of peripheral nerve function is a critical issue in all acute SCI and rehabilitation units, particularly in the context of spinal cord neuronal regeneration projects.

Action Potentials↗

Peripheral nerve injury after brief lithotomy for transurethral collagen injection.

Two patients with prior prostate surgery sustained peripheral nerve injuries after transurethral collagen injection for the treatment of urinary incontinence. In the first patient, brief lithotomy positioning caused a gluteal compartment syndrome and sciatic neuropathy. In the second patient, obturator neuropathy was due to leakage of collagen along the course of the obturator nerve. This is the first report of peripheral nerve injury in patients undergoing transurethral collagen injection.

Aged↗

Differential activation and block of peripheral nerve fibers by magnetic fields.

The ability to noninvasively and reversibly block conduction in peripheral nerves would have several clinical applications. As an initial step in this direction, we investigated the possibility of magnetically generating and differentially blocking activity in mammalian peripheral nerve fibers in vitro. Compound action potentials at each end of individual explanted phrenic nerves were recorded in response to currents induced at the midpoint of the nerve with an externally placed magnetic coil. Current in the coil was then reversed and the recordings repeated. In all cases, the area under the compound action potential on the virtual anode side of the magnetic stimulus was reduced (mean of 18.2 +/- 8.8%) in comparison to the area on the virtual cathode side. This indicates that peripheral nerve activity can be differentially induced by magnetic stimulation. Extension of this effect to the point of generating unidirectional action potentials in vivo may prove clinically useful in a number of contexts, such as reducing contractures secondary to spasticity and generating magnetically induced anesthesia in limbs. Further investigations of this effect seem warranted.

Action Potentials↗

Closed fractures complicated by peripheral nerve injury.

Closed fractures may be complicated by associated peripheral nerve injury. However, because clinical information is limited, determining the best course of treatment is difficult. Most patients with closed fractures have a local nerve injury without nerve division; their prognosis for recovery is favorable. In the acute setting, immediate surgery is usually unwarranted because of the difficulty in accurately defining the severity and extent of nerve injury. When débridement of an open fracture or repair is not required, peripheral nerve injuries are best observed and the extremity treated with splinting and exercise to prevent loss of joint motion. Patients who fail to demonstrate signs of recovery at 6 months, either clinically or with electrodiagnostic testing, should undergo exploration to maximize the likelihood for return of function. When, during exploration, the nerve is in continuity, intraoperative measurement of nerve action potentials should be done. Measuring nerve action potentials will determine whether nerve grafting, local neurolysis, or excision of the injured segment, accompanied by primary repair, is the most appropriate treatment.

Algorithms↗

Calcium-induced degeneration of the cytoskeleton in monkey and human peripheral nerves.

Biopsy specimens of human and monkey peripheral nerves, when incubated in calcium containing media, showed a loss of neurofilaments and microtubules with replacement by granular debris. Cytoskeletal structures remained intact when incubated in calcium-free media. Disruption of neurofilaments and microtubules in calcium containing media was inhibited by the thiol protease inhibitor, leupeptin. Similar incubations of excised Pacinian corpuscles revealed evidence of early terminal axon degeneration in the presence of calcium. These data substantiate the hypothesis that neural cytoskeletal degradation in primates and in man is calcium-mediated.

Animals↗

Pathology of ther peripheral nerves in leprosy: report of a case.

Peripheral nerve trunks were examined from a case of lepromatous leprosy. M. leprae was seen in the nerves in several types of cells. Isolated nerve fibre preparations showed demyelinating lesions due to Schwann cell damage and complete nerve fibre degeneration. The causes of this mixed pattern of damage may involve both a direct effect of the bacilli on nerve fibres and various epiphenomena.

Aged↗

Peripheral nerve injuries in athletes. Treatment and prevention.

Peripheral nerve lesions are uncommon but serious injuries which may delay or preclude an athlete's safe return to sports. Early, accurate anatomical diagnosis is essential. Nerve lesions may be due to acute injury (e.g. from a direct blow) or chronic injury secondary to repetitive microtrauma (entrapment). Accurate diagnosis is based upon physical examination and a knowledge of the relative anatomy. Palpation, neurological testing and provocative manoeuvres are mainstays of physical diagnosis. Diagnostic suspicion can be confirmed by electrophysiological testing, including electromyography and nerve conduction studies. Proper equipment, technique and conditioning are the keys to prevention. Rest, anti-inflammatories, physical therapy and appropriate splinting are the mainstays of treatment. In the shoulder, spinal accessory nerve injury is caused by a blow to the neck and results in trapezius paralysis with sparing of the sternocleidomastoid muscle. Scapular winging results from paralysis of the serratus anterior because of long thoracic nerve palsy. A lesion of the suprascapular nerve may mimic a rotator cuff tear with pain a weakness of the rotator cuff. Axillary nerve injury often follows anterior shoulder dislocation. In the elbow region, musculocutaneous nerve palsy is seen in weightlifters with weakness of the elbow flexors and dysesthesias of the lateral forearm. Pronator syndrome is a median nerve lesion occurring in the proximal forearm which is diagnosed by several provocative manoeuvres. Posterior interosseous nerve entrapment is common among tennis players and occurs at the Arcade of Froshe--it results in weakness of the wrist and metacarpophalangeal extensors. Ulnar neuritis at the elbow is common amongst baseball pitchers. Carpal tunnel syndrome is a common neuropathy seen in sport and is caused by median nerve compression in the carpal tunnel. Paralysis of the ulnar nerve at the wrist is seen among bicyclists resulting in weakness of grip and numbness of the ulnar 1.5 digits. Thigh injuries include lateral femoral cutaneous nerve palsy resulting in loss of sensation over the anterior thigh without power deficit. Femoral nerve injury occurs secondary to an iliopsoas haematoma from high energy sports. A lesion of the sciatic nerve may indicate a concomitant dislocated hip. Common peroneal nerve injury may be due to a direct blow or a traction injury and results in a foot drop and numbness of the dorsum of the foot. Deep and superficial peroneal nerve palsies could be secondary to an exertional compartment syndrome. Tarsal tunnel syndrome is a compressive lesion of the posterior tibial nerve caused by repetitive dorsiflexion of the ankle--it is common among runners and mountain climbers.(ABSTRACT TRUNCATED AT 400 WORDS)

Accessory Nerve Injuries↗

Peripheral nerve injury induces trans-synaptic modification of channels, receptors and signal pathways in rat dorsal spinal cord.

Peripheral tissue injury-induced central sensitization may result from the altered biochemical properties of spinal dorsal horn. However, peripheral nerve injury-induced modification of genes in the dorsal horn remains largely unknown. Here we identified strong changes of 14 channels, 25 receptors and 42 signal transduction related molecules in Sprague-Dawley rat dorsal spinal cord 14 days after peripheral axotomy by cDNA microarray. Twenty-nine genes were further confirmed by semiquantitative RT-PCR, Northern blotting, in situ hybridization and immunohistochemistry. These regulated genes included Ca2+ channel alpha1E and alpha2/delta1 subunits, alpha subunits for Na+ channel 1 and 6, Na+ channel beta subunit, AMAP receptor GluR3 and 4, GABAA receptor alpha5 subunit, nicotinic acetylcholine receptor alpha5 and beta2 subunits, PKC alpha, betaI and delta isozymes, JNK1-3, ERK2-3, p38 MAPK and BatK and Lyn tyrosine-protein kinases, indicating that several signal transduction pathways were activated in dorsal spinal cord by peripheral nerve injury. These results demonstrate that peripheral nerve injury causes phenotypic changes in spinal dorsal horn. Increases in Ca2+ channel alpha2/delta1 subunit, GABAA receptor alpha5 subunit, Na+ channels and nicotinic acetylcholine receptors in both dorsal spinal cord and dorsal root ganglia indicate their potential roles in neuropathic pain control.

Animals↗

[Peripheral nerves biopsies: analysis of 89 cases].

Results of 89 peripheral nerve biopsies studied only by paraffin sections are analysed to determine the abnormalities incidence, and in what extent a general pathology laboratory can help in final diagnosis of patients with peripheral nerve disorders. 37% normal nerve biopsies and 63% with some histological alteration were found; only in 22% the nosological diagnosis was possible. A discussion about the low incidence of nosological diagnosis is made, and a literature revision on routine nerve biopsies. It is concluded that nerve biopsies should be done only in special cases, particularly when other diagnostic methods failed, taking into account always the limitation of the method, and preferentially studying a clinically involved nerve.

Biopsy↗

Characterization of complement-fixing antibodies to peripheral nerve myelin in Guillain-Barré syndrome.

Complement-fixing antibodies to peripheral nerve myelin (anti-PNM Ab) can be detected in the serum of patients with Guillain-Barré syndrome (GBS). Kinetics of these antibodies can be correlated with the changing clinical course; the appearance of activation products of the terminal complement cascade in cerebrospinal fluid, serum, and peripheral nerve of patients with GBS; and the ability of GBS serum to mediate complement-dependent demyelination of myelinating cultures of rodent dorsal root ganglion. Some of the anti-PNM Ab in all GBS serum tested thus far bind a neutral glycolipid of human PNM and cross react with Forssman antigen, a cross-species antigen found in many infectious agents. Studies suggest that an IgM antibody in GBS patients that could be triggered by multiple infectious agents binds a surface determinant of a Forssman-like lipid of human PNM and participates in demyelination of peripheral nerve through the activation of complement.

Autoantibodies↗

Peripheral nerves in the rat exhibit localized heterogeneity of tensile properties during limb movement.

Peripheral nerves in the limbs stretch to accommodate changes in length during normal movement. The aim of this study was to determine how stretch is distributed along the nerve relative to local variations in mechanical properties. Deformation (strain) in joint and non-joint regions of rat median and sciatic nerves was measured in situ during limb movement using optical image analysis. In each nerve the strain was significantly greater in the joint rather than the non-joint regions (2-fold in the median nerve, 5- to 10-fold in the sciatic). In addition, this difference in strain was conserved in the median nerve ex vivo, demonstrating an in-built longitudinal heterogeneity of mechanical properties. Tensile testing of isolated samples of joint and non-joint regions of both nerves showed that joint regions were less stiff (more compliant) than their non-joint counterparts with joint: non-joint stiffness ratios of 0.5 +/- 0.07 in the median nerve, and 0.8 +/- 0.02 in the sciatic. However, no structural differences identified at the light microscope level in fascicular/non-fascicular tissue architecture between these two nerve regions could explain the observed tensile heterogeneity. This identification of localized functional heterogeneity in tensile properties is particularly important in understanding normal dynamic nerve physiology, provides clues to why peripheral nerve repair outcomes are variable, and suggests potential novel therapeutic targets.

Animals↗

Tubulation for peripheral nerve gap: its history and possibility.

A large gap in peripheral nerve will not allow effective regeneration unless a grafting conduit is used to bridge the defect. Conventionally, nerve tissue has been used as such a conduit in nerve reconstruction; however, results from techniques using these grafts are often unsatisfactory. A number of recent investigations have indicated that nerve fibers will regenerate through a non-neural tube. The purpose of this review is: 1) to provide an overview of the various tubulation techniques previously reported for peripheral nerve gap repair; 2) to investigate new possibilities for enhancing the regenerative capacity of nerves following these tubulation techniques by drawing from technical innovations in microsurgery and recent progress in immunology and neurobiology. The interposed graft thus may perform a more positive role, not merely as a pathway for deregenerating axons, but as a source for neuronotrophic factors and neurite-promoting factors, which would nurture and guide the neurons and axons. Such modifications in graft materials may lead to clinical applications of tubulation of nerve defects that would result in an improvement in clinical results.

Humans↗

Mast cell invasion of peripheral nerve in skin lesions of atopic dermatitis.

To ascertain whether or not a spatial relationship between mast cells and peripheral nerves is present in skin lesions of atopic dermatitis, 10 biopsy specimens of the skin lesions were examined with both semi-thin and ultrathin serial sections. Mast cell invasion of peripheral nerves was observed in 9 out of the 10 biopsy specimens (4 subacute lesions, 3 lichenified lesions, and 3 prurigo lesions). The mast cells within peripheral nerves often showed degranulation, and the nerve fiber bundle showed conspicuous edema. The degranulation of mast cells within peripheral nerve bundles and edema of the nerve bundle may pay a role in provoking or aggravating itchiness of atopic dermatitis.

Adolescent↗

The reduced responsiveness of neurones in nucleus reticularis gigantocellularis following their excitation by peripheral nerve stimulation.

1. Post-stimulus histograms of neuronal activity, constructed from extracellular recordings in decerebrate, decerebellate cats, have been used to investigate the responsiveness of neurons in nucleus reticularis gigantocellularis following their excitation by a peripheral nerve stimulus. 2. The response to a testing stimulus applied to a peripheral nerve was depressed following the response to a conditioning stimulus applied to the same or a different peripheral nerve. This reduction in responsiveness was maximal within 50 msec of the peak of the response to the conditioning stimulus. Response latencies to the testing stimulus were increased during the period of reduced responsiveness. 3. Responsiveness to a peripheral nerve stimulus was also reduced following a spontaneous or an antidromically evoked spike, but this effect was weaker and much shorter-lasting than that following a nerve-evoked spike. Thus, the reduced responsiveness cannot be solely due to phenomena which are an inevitable consequence of an action potential in the neurone. 4. In spontaneously firing neurones, the duration of the reduced responsiveness to a testing stimulus generally outlasted the depression of spontaneous activity which often followed an excitation evoked by a peripheral nerve conditioning stimulus. 5. The reduction in responsiveness to a testing stimulus applied to the same nerve as the conditioning stimulus was greater and longer-lasting than that to a testing stimulus applied to a different nerve. 6. When stimuli were applied to one nerve at a relatively high rate, the neurone became much less responsive to that input, but simultaneously became more responsive to low rate stimulation of other nerves. 7. It is concluded that the greater part of the reduced responsiveness is due to events occurring on the input pathway to a reticular neurone, or possibly in the region of the afferent endings on its dendrites. These processes may allow selective changes in responsiveness to different inputs, and enable the units to act as novelty detectors.

Action Potentials↗

Lidocaine and octanol have different modes of action at tetrodotoxin-resistant Na(+) channels of peripheral nerves.

UNLABELLED: Local anesthetics and alcohols block impulse conduction in peripheral nerves by inhibiting Na(+) currents. In small peripheral nerve fibers, tetrodotoxin-resistant (TTX-r) Na(+) channels play an important role in impulse generation. We investigated the effects of lidocaine and the alcohol octanol on TTX-r Na(+) channels. Currents were recorded with the whole-cell patch-clamp method from enzymatically isolated rat dorsal root ganglion cells (data evaluation: nonlinear least-squares fitting). Lidocaine and octanol blocked the TTX-r Na(+) current in a reversible and concentration-dependent manner (50% inhibitory concentration values: 177 +/- 25 and 455 +/- 25 microM, respectively). Lidocaine additionally produced a strong use-dependent block. Both drugs showed a strong dynamic block (i.e., block developed during the time course of current activation and inactivation). Double-pulse protocols showed a slow dissociation of lidocaine from the channel during repolarization (time constant: 1763 +/- 63 ms; 300 microM). The dissociation of octanol was too quick to be distinguished from normal current repriming kinetics of 2.2 ms. Lidocaine and octanol acted noncompetitively in the Na(+) channel. Lidocaine and octanol have different blocking properties on the TTX-r Na(+) current and bind to different channel sites. IMPLICATIONS: Lidocaine and octanol have different inhibitory effects on the function of tetrodotoxin-resistant Na(+) channels in rat dorsal root ganglion cells, as well as noncompetitive modes of action, as investigated by the whole-cell patch-clamp method, and therefore are likely to have different binding sites on the channel.

1-Octanol↗

Optic nerve regeneration with return of vision through an autologous peripheral nerve graft.

The optic fiber termination layer in the contralateral optic tectum was reinnervated and useful vision was recovered in the adult frog, after successful optic nerve regeneration through an autologous peripheral nerve-bridge used to replace the optic nerve and optic chiasma. During their course through the nerve-bridge, the optic fibers were associated with Schwann cells in the usual relationship observed in peripheral nerve.

Animals↗

Multiexponential T2 relaxation in degenerating peripheral nerve.

The multiexponential T2 relaxation spectrum of peripheral nerve undergoing Wallerian degeneration has been measured both in vivo and in vitro. Degeneration of the sciatic nerve of the amphibian Xenopus laevis was induced by crush injury, and T2 relaxation spectra of the nerve were measured at several times up to 35 days following injury. Histologic evidence verified that the nerve underwent Wallerian degeneration. Relaxation spectra were observed to undergo measurable changes as degeneration progressed, the most evident being a reduction from three well-resolved T2 components to one and a decline in the fraction of the spectra associated with the shortest T2 component. The former appears to reflect the collapse and loss of myelinated fibers, while the latter a combination of interstitial edema and myelin loss.

Animals↗

[Microsurgical treatment of peripheral nerve injuries--analysis of 25 years' experience].

Microsurgical procedures on injured peripheral nerves have been performed in Institute of neurosurgery in Belgrade for twenty-five years. During this period 1284 procedures, including 1029 on peripheral nerves, and 255 on brachial plexus were done. In this paper we analyze surgical results of individual procedures and the other factors influencing the outcome. Despite advances caused by introduction of the operating microscope, there are numerous controversies mainly in microsurgical technique that are discussed.

Humans↗