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At least 253 records · Page 14Linked to original sources
PubMed1993

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↗
PubMed2003

[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↗
PubMed1987

[Late results following treatment of peripheral nerve injuries of the upper extremity].

The authors re-examine cases of complete peripheral nerve injury of the upper extremity. Motor activity and sensibility assessment make use of Highet's scale. Some general principles of surgical treatment of peripheral nerve injuries are presented and individual factors which influence its results are worked out, e.g. moment of diagnosis, kind of nerve suture, moment of operation, age of patient, grade of injury, concomitant injuries, and length of graft. Conclusions are drawn for the concept of treatment.

Adolescent↗
PubMed2003

Yasargil-Phynox aneurysm clip: a simple and reliable device for making a peripheral nerve injury.

A great number of devices were used to make a peripheral nerve injury. In the scientific literature, experimental crush injuries have been usually created using forceps or hemostatic forceps, neither of which allows quantitative or standard application of compression. Therefore, we used a Yasargil-Phynox aneurysm clip to make a reliable and standardized peripheral nerve injury. The advantages and disadvantages of this clip were discussed. In particular, we think that standardization of the compression is necessary to compare interlaboratory results.

Animals↗
PubMed2001

H reflex restitution and facilitation after different types of peripheral nerve injury and repair.

This study addresses the restitution of monosynaptic H reflex after nerve injuries and their role in the recovery of walking. Adult rats were submitted to sciatic crush, complete section repaired by aligned or crossed fascicular suture, or an 8-mm resection repaired by autograft or tube repair. The sciatic nerve was stimulated proximal to the injury site and the M and H waves were recorded from gastrocnemius (GCm) and plantar (PLm) muscles at monthly intervals during 3 months postoperation. Walking track tests were also carried out and the sciatic functional index (SFI) calculated to assess gait recovery. The M and H waves reappeared in all the animals at the end of the follow-up. The H/M amplitude ratio increased during the first stages of regeneration and tended to decrease to control values as muscle reinnervation progressed. However, final values of the H/M ratio for the PLm remained significantly higher in all the groups except that with a nerve crush. The walking track pattern showed an appreciable recovery only after crush injury. Final SFI values correlated positively with the M wave amplitude and negatively with the H/M ratio. In conclusion, H reflex is facilitated after peripheral nerve injury and regeneration and tends to return to normal excitability with time. Changes in the H reflex circuitry and excitability correlated positively with the deficient recovery of walking pattern after severe nerve injury.

Animals↗
PubMed2004

Effects of peripheral nerve injury on delta opioid receptor (DOR) immunoreactivity in the rat spinal cord.

Morphine and other opioids have direct analgesic actions in the spinal cord and chronic spinal administration of opioid agonists is used clinically in patients suffering from severe, chronic pain. Neuropathic pain resulting from peripheral nerve injury is often less sensitive to opioid therapy than other forms of chronic pain in both humans and animal models. Changes in spinal mu-opioid receptor (MOR) expression have been demonstrated in animal models of neuropathic pain. However, these changes alone fail to account for the attenuation of opioid activity. Reduced expression of delta-opioid receptors (DOR) following peripheral nerve injury has been reported but most of these reports are limited to subjective observation. The magnitude and consistency of these changes is therefore unclear. In addition, previous studies did not evaluate the effects of nerve injury on behavioral measures to confirm induction of aberrant pain symptoms. We therefore performed quantitative image analysis to evaluate the effect of peripheral nerve injury on DOR-immunoreactivity in spinal cord sections from rats previously characterized for sensory responsiveness. We observed statistically significant decreases ipsilateral to nerve injury in all three models tested: sciatic nerve transection, chronic constriction injury of the sciatic nerve and L5/L6 spinal nerve ligation. These results suggest that decreases in the expression of DOR are a common feature of peripheral nerve injury.

Afferent Pathways↗
PubMed1954

Peripheral nerve injuries; early surgical treatment.

Injuries to the major nerves of the extremities are common.Surgical treatment should be undertaken soon after injury that completely or partly severs a peripheral nerve, because permanent changes appear in muscles that are deprived of nerve supply for more than a few months. The muscular changes may prevent restoration of normal function even though actual nerve regeneration is adequate. Injuries which do not completely sever a nerve may be hard to diagnose but special methods such as electromyography are helpful.

Electromyography↗
PubMed2001

Effect of peripheral nerve injury on dorsal root ganglion neurons in the C57 BL/6J mouse: marked changes both in cell numbers and neuropeptide expression.

Several types of changes have been reported to occur in dorsal root ganglia following peripheral nerve injury, including loss of neurons and increases and decreases in peptide expression. However, with regard to loss of neurons, results have not been consistent, presumably due to different quantitative methodologies employed and species analyzed. So far, most studies have been conducted on rats; however, with the fast development of the transgenic techniques, the mouse has become a standard model animal in primary sensory research. Therefore we used stereological methods to determine the number of neurons, as well as the expression of galanin message-associated peptide, a marker for galanin-expressing neurons, neuropeptide Y, and calcitonin gene-related peptide in lumbar 5 dorsal root ganglia of both control C57 BL/6J mice and in mice subjected to a 'mid-thigh' sciatic nerve transection (axotomy). In control animals the total number of lumbar 5 dorsal root ganglion neurons was about 12000. Seven days after axotomy, 24% of the dorsal root ganglion neurons were lost (P<0.001), and 54% were lost 28 days after axotomy (P<0.001). With regard to the percentage of peptide-expressing neurons, the results obtained showed that both galanin message-associated peptide (from <1% to about 21%) and neuropeptide Y (from <1% to about 16%) are upregulated, whereas calcitonin gene-related peptide is downregulated (from about 41% to about 14%) following axotomy. Results obtained with retrograde labeling of the axotomized dorsal root ganglion neurons indicate that the neuropeptide regulations may be even more pronounced, if the analysis is confined to the axotomized dorsal root ganglion neurons rather than including the entire neuron population. We also applied conventional profile-based counting methods to compare with the stereological data and, although the results were comparable considering the trends of changes following axotomy, the actual percentage obtained with the two methods differed markedly, both for neuropeptide Y- and, especially, for galanin message-associated peptide-positive neurons. These present results demonstrate that marked species differences exist with regard to the effect of nerve injury on dorsal root ganglion neurons. Thus, whereas no neuron loss is seen in rat up to 4 weeks after a 'mid-thigh' transection [Tandrup et al. (2000) J. Comp. Neurol. 422, 172-180], the present results indicate a dramatic loss already after 1 week in mouse. It is suggested that the proximity in physical distance of the lesion to the cell body is a critical factor for the survival of the target-deprived neurons. Finally, stereological methodology seems warranted when assessing the total number of neurons as well as changes in peptide regulations after axotomy in mouse.

Animals↗
PubMed2001

Effect of aging on the substance P receptor, NK-1, in the spinal cord of rats with peripheral nerve injury.

Substance P (SP) levels in the spinal cords of very old rats are less than the levels in younger rats (Bergman et al., 1996). After injury to a peripheral nerve in young rats, immunoreactivity (ir) to the SP receptor, NK-1 (neurokinin-1), increases in the spinal cord ipsilateral to the injury and the increases are correlated with the development of thermal hyperalgesia (Goff et al., 1998). Thus we postulated that aged rats might display an increased sensitivity to thermal stimulation before peripheral nerve injury and that they might respond differently to injury than do younger rats. To test this hypothesis, we used the Bennett and Xie model (1988) of chronic constriction injury (CCI) to the sciatic nerve to induce a neuropathic pain condition. We investigated the effect of age on changes in NK-1 ir in superficial layers of the dorsal horn and on numbers of NK ir cells in deeper laminae at the L4-L5 levels of the spinal cord after CCI. NK-1 receptors were tagged immunohistochemically and their distribution quantified by use of computer-assisted image analysis. NK-1 ir changes were related to alterations in thermal and tactile sensitivity that developed after CCI in young, mature and aged (4-6, 14-16, and 24-26 months) Fischer F344 BNF1 hybrid rats. No differences in thermal or tactile sensitivity of young and aged rats were seen in the absence of nerve injury. After injury, aged rats developed thermal hyperalgesia and tactile allodynia more slowly than did the younger rats. NK-1 receptor ir and numbers of NK-1 ir cells in the dorsal horn increased with time post-injury in all three groups. NK-1 ir increases were correlated with the development of thermal hyperalgesia in those rats that displayed hyperalgesia. However, some rats developed an increased threshold to thermal stimuli (analgesia) and that also was correlated with increases in NK-1 ir. Thus NK-1 ir extent, while correlated with thermal sensitivity in the absence of injury, is not a specific marker for disturbances in one particular sensory modality; rather it increases with peripheral nerve injury per se.

Aging↗
PubMed2006

Use of a static magnetic field to promote recovery after peripheral nerve injury.

OBJECT: While pulsed electromagnetic stimulation has been shown to enhance peripheral nerve regeneration, the effect of a static magnetic field on nerve repair is less clear. The aim of this study was to establish what effect an imposed exogenous static magnetic field has on peripheral nerve regeneration after transection and repair. METHODS: Three groups of six adult sheep were used. The first group acted as normal controls. In the second group, the median nerve was divided and immediately repaired by entubulation within a "controlled-release" biodegradable glass tube. In the third group, small magnets were applied to the sides of the biodegradable glass tubes before the median nerve was repaired using these magnetic tubes. The sheep were allowed to recover and were reexamined 10 months later. The animals underwent comprehensive morphometric (cross-sectional morphometry and measurement of internodal lengths), electrophysiological (determinations of stimulated jitter, maximum conduction velocity, refractory period, and F waves), and isometric tension (isometric twitch and tetanic tension) assessments. CONCLUSIONS: Exogenously applied static electromagnetic fields do not enhance peripheral nerve regeneration.

Anastomosis, Surgical↗
PubMed1991

The electrophysiology of peripheral nerve injuries.

Neurophysiologic tests currently used in the diagnosis and treatment of peripheral nerve trauma include EMG, NCV, late responses, SEPs, and intraoperative NAPs. The physiologic basis of these tests has been reviewed. Examples of typical applications have been provided. The interested reader is referred to the listed references for more detailed information.

Adult↗
PubMed2003

Plasticity in action of intrathecal clonidine to mechanical but not thermal nociception after peripheral nerve injury.

BACKGROUND: Intrathecal clonidine reduces tactile allodynia in animal models of neuropathic pain, and this effect is blocked by atropine. However, the role of tonic spinal cholinergic activity and its interaction with alpha2-adrenergic systems in normal and neuropathic conditions and to different sensory methods has not been systematically examined. The authors examined cholinergic receptor involvement in thermal and mechanical sensitivity in normal and neuropathic animals and its interaction with intrathecal clonidine. METHODS: Normal rats and rats that received L5/L6 spinal nerve ligation were tested with acute radiant heat, paw pressure, and punctate mechanical stimulation before and after the intrathecal administration of saline, the muscarinic receptor antagonist, atropine, or a toxin to destroy cholinergic neurons, and then after intrathecal clonidine. RESULTS: Atropine, the cholinergic neuronal toxin, and saline did not alter baseline withdrawal thresholds. In nerve-injured rats, neither saline nor atropine altered antinociception from clonidine to a thermal stimulus, but atropine reduced the effect of clonidine to von Frey filament withdrawal threshold (34 +/- 5.6 vs. 14 +/- 5.8 g [mean +/- SEM], saline vs. atropine; P < 0.05) and to withdrawal threshold to paw pressure after clonidine (174 +/- 18 g vs. 137 +/- 16 g, saline vs. atropine; P < 0.05). CONCLUSIONS: These data suggest that after nerve injury, mechanical but not thermal antinociception from intrathecal clonidine relies on a muscarinic interaction, because only mechanical antinociception was antagonized by atropine. These results do not favor a regulation of nociceptive transmission by a tonic release of acetylcholine in nerve-injured rats.

Acetylcholine↗