Popliteal entrapment syndrome caused by isolated popliteus muscle enlargement is very rare, although its occurrence has been reported after discrete trauma. However, popliteal artery stenosis with combined peroneal and proximal tibial neuropathy caused by popliteus muscle enlargement without preceding trauma has not been reported. A 57-year-old man presented with a tingling sensation and pain in his left calf. He had no previous history of an injury. The symptoms were similar to those of lumbosacral radiculopathy. Calf pain became worse despite treatment, and the inability to flex his toes progressed. Computed tomography angiography and magnetic resonance imaging of the lower extremity showed popliteal artery stenosis caused by popliteus muscle enlargement and surrounding edema. An electrodiagnostic study confirmed combined peroneal and proximal tibial neuropathy at the popliteal fossa. Urgent surgical decompression was performed because of the progressive neurologic deficit and increasing neuropathic pain. The calf pain disappeared immediately after surgery, and he was discharged after the neurologic functions improved.
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Intestinal entrapment between two vertebral bodies is very rare. In all previous cases, it occurred by major trauma. However, the bowel entrapment between two vertebral bodies without trauma has never been reported, not to mention as the cause of lower extremity radicular pain. We describe the case of an 82-year-old female patient with right lower extremity radicular pain without recent trauma history. The patient was diagnosed sigmoid colon entrapment between the L5 and S1 vertebrae by lumbar spinal computerized tomography and magnetic resonance imaging, and showed improvement in radicular pain after manual reduction of interpositioned colon during surgery. Intestinal entrapment between two vertebrae without trauma is caused by degenerative and vacuum changes of the intervertebral disc combined with the anterior longitudinal ligament injury.
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To evaluate the analgesic effect of intrathecal gabapentin therapy on secondary hyperalgesia in a rat model of persistent muscle pain.
Intrathecal catheters were implanted into rats. Mechanical secondary hyperalgesia was induced by repeated intramuscular injections of acidic solution into the gastrocnemius muscle. Gabapentin was administrated intrathecally. Rats were allocated to control and experimental (gabapentin 30, 100, 300, and 1,000 µg) group. After gabapentin administration, mechanical withdrawal threshold was measured every 15 minutes and the motor function was measured 30 minutes later.
Mechanical hyperalgesia was evoked after the second acidic buffer injection. There was a significant improvement on the mechanical threshold after administration of 100, 300, and 1,000 µg gabapentin compared to pre-injection and the control group. The analgesic effect continued for 105, 135, and 210 minutes, respectively. To discern side effects, motor function was measured. Motor function was preserved in both groups after gabapentin administration, except for rats who received 1,000 µg gabapentin.
Intrathecal gabapentin administration produces dose-dependent improvements in mechanical hyperalgesia in a persistent muscle pain rat model. This implicates the central nervous system as having a strong influence on the development of persistent mechanical hyperalgesia. These results are helpful in understanding the pathophysiology of secondary hyperalgesia and in the treatment of patients with chronic muscle pain.
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