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UNILATERAL SCIATIC NEUROPATHY OF THE TERMINAL BRANCHES, WITH ABNORMAL MRI OF THE NERVE AT THE THIGH
Author(s) -
Lori S.,
Briccoli M.,
Zanfranceschi G.,
Fusi I.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000.00513-33.x
Subject(s) - medicine , sciatic nerve , thigh , anatomy , posterior compartment of thigh , popliteal fossa , denervation , obturator nerve , paralysis , sensory loss , muscle belly , sural nerve , surgery , tendon
A 52‐year‐old woman had a subarachnoid haemorrhage in 1996. No cause of bleeding was detected. After a hospital stay of 2 months, the patient fully recovered, except for a persistent distal paralysis of her right lower limb. The patient is currently undergoing a reevaluation. The knee jerks are slightly asymmetric dx > sn, whereas the right Achilles tendon reflex is lost. Atrophic hypotonic paralysis of the muscles of the right leg is a prominent feature, with sparing of the thigh. Sensory loss is distributed in leg's sciatic area. Some tenderness is consistently appreciated with deep palpation of the posterior aspect of the thigh. EMG shows severe denervation of TA and calf muscles on right, whereas ischio‐crural muscles are bilaterally normal. The latencies of MAPs from TA and gastrocnemius, evoked by nerve stimulation at the knee, are prolonged (>20 msec). Sural nerve antidromic SAP is undetectable. An MRI comparative study of the thighs has been performed (1.5 TESLA, SPIR suppression of fat tissue technique, and MIP reconstructions for the nerve). The sciatic nerve imaging is sharply asymmetric. The left nerve is barely visible, as expected. On the right, one can see normal fascicular structure and no evidence of either extrinsic compression or hypertrophy. The unusual ease of imaging is ascribed to increased water content, suggesting persistent edema and/or inflammation. The hypothesis of ongoing activity of disease is consistent with the neurographic findings, but the cause and mechanism of nerve damage are not clear. The hypothesis of a compartment syndrome may be suggested by the history of coma, but the selective distal damage is not easily explained on this basis.