Lipomas are mostly located in the subcutaneous tissues and rarely cause symptoms. Occasionally, peripheral nerve compression by lipomas is reported. We describe a case of a 59-year-old man with a left-middle cerebral artery infarction who was newly diagnosed as right basal ganglia and thalamic intracranial hemorrhage. He had neuropathic pain in the left arm and leg that was suspected to be central post-stroke pain. The administration of pain medication brought only temporary symptom relief. Nerve conduction and electromyography studies revealed left L5 radiculopathy and he showed a positive ‘sign of the buttock’ in the left hip. Left-hip magnetic resonance imaging revealed an intermuscular lipoma compressing the sciatic nerve. After surgery, the range of motion in the left hip joint was significantly increased, and the patient's pain was relieved.
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Sciatic nerve injury after stretching exercise is uncommon. We report a case of an 18-year-old female trained dancer who developed sciatic neuropathy primarily involving the tibial division after routine stretching exercise. The patient presented with dysesthesia and weakness of the right foot during dorsiflexion and plantarflexion. The mechanism of sciatic nerve injury could be thought as hyperstretching alone, not caused by both hyperstretching and compression. Electrodiagnostic tests and magnetic resonance imaging revealed evidence of the right sciatic neuropathy from the gluteal fold to the distal tibial area, and partial tear of the left hamstring origin and fluid collection between the left hamstring and ischium without left sciatic nerve injury. Recovery of motor weakness was obtained by continuous rehabilitation therapy and some evidence of axonal regeneration was obtained by follow-up electrodiagnostic testing performed at 3, 5, and 12 months after injury.
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Method: Sciatic nerve of seventy rats was compressed with haemostatic forceps. The experimental group was divided into 4 subgroups according to the intensity and duration of injury: group 1, first degree compression for 5 seconds; group 2, first degree for 30 seconds; group 3, third degree for 5 seconds; and group 4, third degree for 30 seconds. Treadmill exercise was done for either 30 minutes or 2 hours a day, 5 days a week for 4 weeks. Histochemical study of soleus was done before nerve compression and 1 week, 4 weeks after compression.
Results: The fiber diameter of soleus was larger in the experimental group at 4 weeks (p＜0.05). The intensity of injury had greater impact on the recovery of fiber diameter than the duration. Thirty minute exercise was seen to have a earlier recovery of fiber diameter than 2 hours.
Conclusion: These results may provide the basic data to clarify the neurological recovery in relation to the severity of injury, and to help establishing adequate duration of exercise after nerve damage.
Method: 33 cases with elective operation for hallux valgus were prospectively investigated. All blocks were performed with the aid of a peripheral nerve stimulator, and 0.5% pucaine was injected in a dose of 1.5 mg/kg when minimal stimulator output still elicited a slight motor response of the foot. In evaluating the analgesics effects of the nerve block, the intensity of pain was assessed by using VAS before, immediately after, and at given time intervals during 36 hours. In the control group, the pain scores were assessed after immediate post-operation and at the given time intervals during 36 hours. The nerve block group rated their level of satisfaction at the first visit of out-patient clinic after discharge.
Results: There was significant pain-control effect at least during 24 hours after the nerve block. The patient's satisfaction was high and they had no severe complications.
Conclusion: Block of sciatic nerve in the popliteal fossa provides high satisfaction as the safe effective pain-control method after hallux valgus surgery, so it may be available method for postoperative analgesia after another foot surgery. (J Korean Acad Rehab Med 2003; 27: 102-105)
Objective: The purpose of this study was to develop a new neuropathic pain model in rat.
Method: Twenty Sprague-Dawley adult male rats, 10 for control and 10 for experimental, were anesthetized and their sciatic nerves were exposed. In an experimental group, exposed nerve was injured with 10 volts electrical current for 10 seconds. The mechanical and thermal allodynia and pain behavior were evaluated in pre-electrical injury and post-injury 1, 2, 3 days, 1, 2, 3, 4, 6 and 8 weeks. The mechanical allodynia was evaluated by the frequency of response to 5 stimulations of von Frey hairs (4.31 and 4.56) and the thermal allodynia was tested by withdrawal latency to stimulation with radiant heat. Spontaneous pain behavior (paw shaking, paw elevation) was observed for 5 minutes in the cage.
Results: The experimental group exhibited significantly higher withdrawal frequency to mechanical stimulation: from post-injury 3 days to 6 weeks for von Frey hair 4.31 and from 2 days to 4 weeks for von Frey hair 4.56 (p＜0.05). There was no difference between two groups in withdrawal latency to radiant heat stimulation. The experimental group showed spontaneous pain behavior but control group did not. In electron microscopic finding, prominent myelin destruction and axonal sprouting were observed in experimental group.
Conclusion: These results suggest that a new neuropathic pain model can be made by 10 volts electrical injury for 10 seconds to rat sciatic nerve.
Objective: To investigate the effects of treadmill running and swimming exercise for the functional and electrophysiological recovery in rats with sciatic nerve damage, and to evaluate the patterns of recovery according to various degree of intensity and duration of injury.
Method: Sixty male Sprague-Dawley rats (200∼250 g) were used, and divided into the control and the experimental groups. Crushing injuries to the sciatic nerve at the sciatic notch was manipulated using a hemostatic forcep, treadmill and swimming exercise programs were performed for 30 minutes on a daily basis, 5 days a week during the 4 week period. The experimental group was divided into 2 sub-groups in correlation with the intensity of injury, and into 5 and 30 seconds group in correlation with the duration of injury. The test results were analysed by sciatic nerve functional index (SFI) that was obtained through walking tract analysis, and by the amplitude of compound muscle action potentials in calf muscles through the sciatic motor nerve conduction study.
Results: 1) After 4 weeks following sciatic nerve injuries, the SFI were 21.8⁑10.8, 23.1⁑7.0, 32.5⁑9.1 in treadmill, swimming, and control groups, respectively. Treadmill and swimming groups showed markedly improved function compared to the control group. Amplitudes of sciatic nerve compound muscle action potentials in calf muscle were 21.2⁑6.5, 15.9⁑5.8, 12.5⁑2.0 mV in treadmill, swimming, and control groups respectively, and revealed marked electrophysiological improvement in treadmill group. 2) The results concerning the intensity and the duration of injury, nerve recovery patterns showed the most significant improvement in the first degree-5 seconds group in both treadmill and swimming exercise programs.
Conclusion: These findings suggest that the treadmill and swimming exercises have significantly better effect in the regeneration of damaged sciatic nerve than that of control, and the intensity of injury was a more important factor in the recovery of nerves compared to the duration of injury.
Objective: The purpose of this study is to develop a new neuropathic pain model in the rat.
Method: Each male adult rat was anesthetized and the sciatic nerve was exposed. Each exposed nerve was injected with 0.03 cc of 1% phenol solution. Normal saline 0.03 cc was injected to the placebo group. Rats were tested for the presence of mechanical allodynia by von Frey hair. Spontaneous pain behavior (paw shaking, paw elevation) was examined for 5 minutes in the cage.
Results: Phenol injected group developed allodynia after the second post-injection day for up to 1 month. Allodynia was also observed in the contralateral legs of phenol injected group. The control group did not develop allodynia. Spontaneous pain behavior was not observed in either group.
Conclusion: Neuropathic pain model was developed by 1% phenol solution injection to the rat sciatic nerve. This study suggests an easier method for making the neuropathic pain model. Key_words: 페놀, 신경병증성 통증 모형, 좌골 신경, Phenol, Neuropathic pain model, Sciatic nerve
Objective: To identify the precise locations of the motor branches and motor points of hamstring and triceps surae muscles to the bony landmarks.
Method: Twenty-eight limbs of 14 adult cadavers were anatomically dissected. The adult cadavers were selected randomly without regard to gender and age. The cadravers which were unable to obtain a neutral position or which received a trauma to the posterior thighs or the lower legs were excluded from the study. The number and location of the motor branches and motor points from sciatic nerve to each hamstirng muscles and from tibial nerve to each triceps surae muscles were identified related to the bony landmarks. Bony landmarks were ischial tuberosity, medial and lateral epicondyles of femur, and medial and lateral malleolli of tibia. The length of femur was defined as the distance from the ischial tuberosity to the intercondylar line of femur and the length of lower leg was defined as the distance from the intercondylar line of femur to the intermalleolar line of tibia. The locations of the muscular branches and the motor points were expressed as the percentage of the length of femur and lower leg.
Results: One muscular branch from the sciatic nerve to the semimembranosus muscle and from the posterior tibial nerve to the soleus muscle, and one or two muscular branches to the biceps femoris, semitendinosus, and semimembranosus, medial gastrocnemius, lateral gastrocnemius and soleus muscle were located at 23.0⁑5.7%, 21.0⁑10.5%, 25.0⁑10.3% of the femur from the ischial tuberosity and 2.0⁑6.2%, 4.0⁑3.3% and 10.0⁑3.3% of the lower leg from the intercondylar line of femur. There were one to four motor points in the hamstring and triceps surae muscles. The motor points of biceps femoris, semitendinosus and semimembranosus were located at 33.0⁑7.8%, 28.0⁑14.5% and 48.0⁑19.0% of the femur. The motor points of the medial gastrocnemius, lateral gastrocnemius and soleus were located in 5.0⁑0.6%, 10.0⁑3.0% and 18.0⁑4.3% of the lower leg below the intercondylar line of femur.
Conclusion: The identification of the locations of muscular branches and motor points related to the bony landmarks from this study would increase the accuracy of the motor branch blocks or motor point blocks to the hamstrings and triceps surae muscles.
Objective: To investigate the electrophysiologic and histopathologic changes of the prheral nerve from hyperthermal nerve injury and to observe the difference of these changes according to the level of temperature and the duration of heat application.
Method: The experimental rats (Sprague-Dawley) were divided into four groups according to the degree of temperature and the duration of heat application : Group 1, 43oC for 15 min; Group 2, 43oC for 30 min; Group 3, 45oC for 15 min; Group 4, 45oC for 30 min. A segment of 5 mm of the sciatic nerve was exposed and treated in vivo with local hyperthermia using a thermostatically controlled heating unit.
For the electrophysiologic examination, both sciatic nerve conduction study and needle electromyographic examination were performed immediately before, and at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hyperthermia. For the histopathologic study, a sciatic nerve biopsy was performed at 1 day, 1 week, 2 weeks, and 4 weeks after the hyperthermia and the changes were investigated under the light microscopic and electronmicroscopic examinations.
Results: In experimental groups, the compound muscle action potentials (CMAPs) showed a significant reduction compared to the control group (p＜0.05). Amplitudes of CMAPs following the heat application to the nerve were inversely related with the degree and duration of hyperthermia. A significant recovery of CMAPs was observed at 4 weeks after the hyperthermia in all experimental groups. The motor conduction latencies, however, did not show any significant changes. The needle electromyography of the gastrocnemius began to reveal fibrillation potentials on the 3rd day after the hyperthermia and continued to appear until the second week and then completely disappeared at 4 weeks after the hyperthermia. The histopathologic findings began to show the degeneration of axon and myelin within 24 hours and a remarkable regeneration at 4 weeks after the hyperthermia.
Conclusion: The results revealed that the hyperthermia of peripheral nerve within the range of 43∼45oC for 15∼30 min is likely to cause a significant acute, but not necessarily permanent nerve injury, and the severity of nerve injuries is related to the temperature and duration of heat applications. Whether the results can be clinically applied to human beings would require further exploration.
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