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POSTIRRADIATION LUMBOSACRAL RADICULOPLEXOPATHY: IMPROVEMENT AFTER IMMUNE THERAPY
Author(s) -
Bersano A.,
Carpo M.,
Di Troia A.,
Scarlato G.,
NobileOrazio E.
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.1529-8027.2000.00513-4.x
Subject(s) - medicine , lumbosacral joint , radiation therapy , weakness , lumbosacral plexus , complication , surgery , lumbar , brachial plexopathy , muscle weakness , proximal muscle weakness , brachial plexus , biopsy , muscle biopsy
A delayed progressive impairment of peripheral nervous system including brachial and lumbosacral radiculoplexopathy is a well‐known complication of local radiotherapy. No treatment for this infrequent complication is currently available. Recently, improvement after treatment with high dose immunoglobulin (IVIg) has been reported in some patients, suggesting either an immune‐mediated inflammatory nerve damage induced by irradiation or a dysimmune neuropathy (CIDP‐like) misdiagnosed as a postirradiation disease. We report on two patients who developed motor lumbosacral radiculoplexopathy several years after local radiotherapy. The first patient (ZA) is a 49 y.o. man developing a progressive proximal>distal weakness and hypotrophy of lower limbs, 20 years after radiotherapy of lumbosacral region for seminoma. Electrophysiological studies showed markedly reduced motor conduction velocities (CV) and prolonged F‐wave latencies in lower limb nerves. The second patient (BF), is a 52 y.o. woman who developed progressive left brachial plexopathy and distal>proximal weakness and hypotrophy of lower limbs 12 years after a first course of toracoascellar and lumbar irradiation for Hodgkin lymphoma followed by a second course of cervicoclavicular irradiation for tumor recurrence 7 years later. Electrophysiological studies showed markedly reduced CMAP amplitudes and proportionally reduced CV in motor nerves. No sensory impairment was detected in both patients. CSF protein was elevated in both patients while cells were normal. On the assumption of a possible dysimmune origin of the disease, patient ZA underwent high dose intravenous steroid treatment, while patient BF, who had previously deteriorated after steroids, was treated with IVIg. After treatment, patient ZA became able to walk with less waddling, to rise from the floor and climb stairs without support, and to run. Improvement was less consistent in patient BF, whose right leg strength improved even if she still needed bilateral support to walk. The improvement observed in both patients supports the hypothesis that, at least in some patients, an immune‐mediated mechanism may underlie postirradiation radiculoplexopathy.