[Lumbosacral radiculoplexus neuropathy with a small intramedullary lesion in posterior spinal cord: a case report].

We present the unique case of a patient with lumbosacral radiculoplexus neuropathy (LRPN) and a small intramedullary lesion, probably an infarction, in the spinal cord. A previously healthy 58-year-old female developed acute severe pain involving the entire right lower limb, followed by weakness of the right lower limb a few hours later. The patient could not walk and was referred to our clinic. The patient reported no sphincter symptoms. Examination of the cranial nerves and upper limbs revealed no abnormalities. The strength in her right lower limb was reduced to Medical Research Council grade 1-2/5 with depressed tendon reflexes. The muscle power and tendon reflexes were normal in the left lower limb, whereas plantar responses were flexor on both sides. There was moderate sensory loss to light touch, pin-prick, vibration, cold temperature stimulation, and proprioception in the right lower limb. Routine laboratory tests and cerebrospinal fluid were unremarkable as were homocysteine, erythrocyte sedimentation rate, and antinuclear cytoplasmic antibody. The patient was diagnosed with LRPN, and treatment with intravenous immunoglobulin and methylprednisolone elicited favorable effects. After a four-week course of inpatient rehabilitation, the patient regained independent gait with a T-cane. Interestingly, thoracic MRI showed a small area of hyperintensity in the right posterior portion of the spinal cord at the level of T10 spine on diffusion-weighted images. The lesion showed slight hypointensity on the apparent diffusion coefficient map, suggesting acute infarction. Edema in the paraspinal muscles demonstrated by MRI suggested acute denervation caused by a lesion in the posterior rami or anterior roots. Somatosensory evoked potentials demonstrated prolonged N20 peak latency following right posterior tibial nerve stimulation, consistent with a lesion in right S1 and S2 roots. This case illustrates that microvasculitis, a keystone of the LRPN pathophysiology, could involve peripheral perforating arteries of the spinal cord.