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Results for “Peripheral Nerve Injuries”
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The modern treatment of peripheral nerve injuries.
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MANAGEMENT of acute peripheral nerve injuries.
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[Progressive clinical manifestations after peripheral nerve injury].
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Clinical evaluation and repair of peripheral nerve injuries.
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[Peripheral nerve injury as a complication from orthopedic operation].
Nerve injury following operation is one of the main causes of the iatrogenic peripheral nerve injury. In order to learn lessons from these cases, one hundred and seven cases of peripheral nerve injury complicated with the orthopedic operations were analyzed. Forty-four cases were cutting injury during operation, made up 41% of all cases and 27 cases were stretch and compression injury, made up 25%. The involved nerves included 41 radial nerves and 24 common peroneal nerves, composing 60.7% of all nerve injury. The operations responsible were mainly the bone and joint operations, which made up 81%. The cause, prophylaxis, diagnosis and treatment were discussed. The rich appropriate knowledge of anatomy and responsibility of the surgeon were emphasized in order to prevent the occurrence of complication. Once the injury was suspected, diagnosis should be made promptly and effective treatment should be performed in time.
[Effect of olfactory ensheathing cells transplantation on protecting spinal cord and neurons after peripheral nerve injury].
OBJECTIVE: To study the effect of olfactory ensheathing cells (OECs) transplantation on protecting spinal cord and neurons after peripheral nerve injury. METHODS: Fifty-five SD rats were randomly divided into blank group (n = 5), experimental group (n = 25) and control group (n = 25). The right sciatic nerves of all the rats were transected. The proximal end was embedded in muscle and treated with OECs (experimental group) and DMEM (control group). No treatment was given to the blank group. The rats were sacrificed 1, 2, 3, 7, and 14 days after the transplantation, the related neurons were observed with histological and TUNEL methods. RESULTS: After sciatic nerves were transected, death of neurons occurred in spinal cord and ganglion. One, 2, 3 days after treatment, the neuron survival rate in experimental group was 98.4% +/- 6.5%, 97.6% +/- 6.5%, 95.2% +/- 6.7% respectively. The neuron survival rate in control group was 97.8% +/- 6.7%, 97.4% +/- 6.4%, 94.3% +/- 6.8% 1, 2, and 3 days after treatment respectively. There was no significant difference between experimental group and control group. Seven and 14 days after treatment, the neuron survival rate in experimental group was 92.4% +/- 8.9%, 87.7% +/- 9.4% respectively. The neuron survival rate in control group was 87.4% +/- 8.6%, 83.4% +/- 8.5% 7 and 14 days after treatment respectively. There was significant difference between experimental group and control group. On 1st and 2nd day, no apoptosis was seen in spinal cord anterior horn of the rats in both experimental group and control group. On 3rd, 7th, and 14th day, the apoptosis index of spinal cord anterior horn motoneuron in experimental rats were lower (1.2+/-0.8, 1.4 +/- 0. 6, 4.1 +/- 1. 3) than that in the control group (2.1 +/- 1.1, 3.1 +/- 1.1, 6.1 +/- 1.8) (P < 0.05). One, 2, and 3 days after the operation, no ganglion neurons apoptosis was observed in all rats. On 7th day the apoptosis index of ganglion neurons in experimental group(2.10 +/- 0.32) were lower than that in control group (4.40+/-0.56) (P<0.05). On 14th day there was no significant difference in the apoptosis index of ganglion neurons between experimental group (4.30+/-1.80) and control group (6.70 +/- 2.50) (P<0.05). CONCLUSION: Apoptosis of neurons occur after peripheral nerve injury in spinal cord and ganglion. OECs transplantation is effective in preventing apoptosis.
Ultrastructural study of peripheral nerve injury induced by monopolar and bipolar diathermy.
The effect of unipolar and bipolar electrocoagulation on human and albino rat peripheral nerves was examined by transmission electron microscopy. The greater auricular nerve obtained from operated patients and the femoral nerve of an albino rat were chosen for this study. The nerves were divided into three groups: controls, segments of nerves spot-coagulated with unipolar instruments, and segments of nerves spot-coagulated with bipolar instruments. Significant cell injury, expressed by marked damage of the Schwann cells, was induced by unipolar coagulation in both myelinated and unmyelinated nerves, in humans as well as in the albino rat. However, in bipolar-treated nerves, the Schwann cell architecture remained well preserved in both types of nerves. The results are in favor of bipolar electrocoagulation when applied in areas rich in neurovascular supplies.
PERIPHERAL NERVE INJURIES ASSOCIATED WITH ANAESTHESIA.
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[Results of surgical treatment of peripheral nerve injuries in children].
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Role of spinal microglia in rat models of peripheral nerve injury and inflammation.
Mounting evidence supports the hypothesis that spinal microglia modulate the development and maintenance of some chronic pain states. Here we examined the role of spinal microglia following both peripheral inflammatory insult and peripheral nerve injury. We observed significant ipsilateral dorsal horn microglia activation 2 weeks after injury and bilateral activation 50 days following nerve injury as well as 24 h following intraplantar zymosan but not intraplantar complete Freund's adjuvant (CFA). Ipsilateral but not contralateral microglia activation was associated with hind paw mechanical hyperalgesia. Spinal injection of the glial metabolic inactivator fluorocitrate attenuated ipsilateral hyperalgesia and bilateral spinal microglia activation after peripheral nerve injury. Intrathecal fluorocitrate reversed hyperalgesia after intraplantar zymosan and produced no reversal of CFA-induced hyperalgesia. These data suggest a role for spinal glia in the persistence of mechanical hyperalgesia following peripheral nerve injury. However, activation of spinal microglia contralaterally did not correlate to nociception. Furthermore, it would appear that the time course of microglia activation and their contribution to inflammatory pain is dependent on the inflammatory stimulus administered.
Surgical repair of peripheral nerve injury.
Magnification, use of fine interfascicular grafts for repair, and development of intraoperative electrophysiologic measurements of function have had a substantial impact on this field in the last 10 to 20 years. Basic surgical principles established during and since World War II remain the foundation for surgical repair of peripheral nerve injury but have been complemented nicely by these more recent advances. Selection of patients for surgery, as well as the timing of such, has been reviewed with emphasis on the differences between suspected transections and lesions in continuity, as well as comments on serious peripheral entrapments and tumors affecting nerve. The importance of not only preoperative electromyographic studies but also the intraoperative use of stimulation and stimulation and recording of nerve action potentials (NAPs) for lesions in continuity has been stressed. Operative techniques such as neurolysis, NAP recordings, suture, split repair, and interfascicular graft repair have been reviewed and some commentary on results provided. There has been a gradual evolution of centers in this country and abroad for care of the more serious surgical nerve problems. It is anticipated that in the future, such centers will be able to provide improved data concerning results with civilian nerve injuries.
An experimental study about the incorrect electrophysiological evaluation following peripheral nerve injury and repair.
OBJECTIVE: This experiment was designed to explore the reasons of incorrect electrophysiological evaluation following peripheral nerve repair. METHODS: Twenty-four New Zealand white rabbits were used and divided into 2 groups. The first group of animals underwent severance of gastrocnemius muscle nerve and only the medial branch of the nerve was anastomosed. The second group of rabbits underwent severance of the muscle nerve as well as sural nerve, then the proximal end of the sural nerve was anastomosed to the distal end of the muscle nerve. Electrophysiological and morphological methods were used to study these models 3 months after the operations. RESULTS: Electrophysiologic comparison of muscle action potential for group A and B showed a significant difference in the values (p < 0.05). Morphologic studies showed that the muscle weights of group B were significantly lower than those of group A, but the myelin thickness failed to show any statistical difference between the two groups. CONCLUSION: Results suggested that one of the sources causing incorrect electrophysiological evaluation could be misdirected regeneration, resulting from a sensory fascicle anastomosing to a motor one or vice versa. The unfunctional regeneration showed low values of muscle action potentials (p < 0.05) as well as excessive fibrillation potentials, and marked atrophy of the muscles (p < 0.05).
Peripheral nerve injury.
Knowledge of the actions of conventional neurotrophic factors on peripheral neurons is accumulating rapidly, and growth factors that were discovered outside the nervous system have been found to have neurotrophic actions. The nature and initiation of proximal neuronal responses to nerve injury, the interactions of Schwann cells and growth cones, and the functions of macrophages in the peripheral nervous system are all areas of active investigation. Results of the surgical treatment of injuries to the brachial plexus and spinal accessory nerve are reported.
Fibrillation potential amplitude and muscle atrophy following peripheral nerve injury.
Maximum peak-to-peak fibrillation potential amplitude was measured in 69 subjects between 7 days and 10 1/2 years post complete or partial peripheral nerve injury. Mean amplitude during the first 2 months was 612 muV; third and fourth months 512 muV, fifth and sixth months 320 muV. After the first year, no population of fibrillation potentials greater than 100 muV was recorded. The sciatic nerve was sectioned in 13 guinea pigs and animals studied up to 17 weeks. Fibrillation potential amplitude in gastrocnemius muscles declined paralleling that in humans. By the end of the study, type I fibers had lost almost half of their initial diameter and type II fibers had atrophied more than twice this amount. Fibrillation potential amplitude may be useful in estimating the time post nerve injury and appears to correlate with the surface area and fiber diameter of a type I muscle fiber.
Plasticity of recurrent inhibitory reflexes in cat spinal motoneurons following peripheral nerve injury.
Chronic axotomy of a peripheral motor nerve in cat causes a gradual reduction in the number of intramedullary axon collaterals originating from the axotomized motoneurons (Havton and Kellerth 1984, 1989). This axon collateral elimination would be expected to reduce the amount of recurrent inhibitory reflex actions mediated by these cells. The aim of the present study was to investigate the recurrent inhibition originating from axotomized motoneurons and, also, to see whether the elimination of axon collaterals from the axotomized neurons might induce secondary compensatory changes in the recurrent inhibitory pathways originating from synergistic non-lesioned motoneurons. The results, which were obtained by means of intracellular recordings and monosynaptic reflex testing, indicate that postoperative enhancement of reflex actions may take place in the recurrent inhibitory pathways persisting in the axotomized motoneurons as well as in those originating from synergistic nonlesioned motoneurons. It is suggested that the site of compensatory enhancement is at the synaptic reflex contacts between the motoraxon collaterals and the inhibitory Renshaw interneurons.
[Post-traumatic rehabilitation of the hand with peripheral nerve injuries].
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