Abstract

Dear Sirs,Classical causes for camptocormia include amyotrophiclateral sclerosis (ALS), muscle diseases, parkinsonism, andidiopathic cases. We describe a patient who developedtypical camptocormia 7 years after having receivedextended-field radiotherapy.In 1982 a 78-year-old man was diagnosed with follicularlymphoma. He received CHOP (cyclophosphamide, hy-droxydaunorubicin, oncovin, and prednisone) chemother-apy to treat left supraclavicular adenopathy followed byextended-field mantle radiotherapy bilaterally to the axil-lary and subclavicular lymph node areas (40 Gray, 20fractions over 28 days at 5 MV photons). In 1987, relapseoccurred in the iliac area and the patient received a secondcourse of radiation treatment (mediastinal area, spleen,lumboaortic lymph nodes area, bilateral inguinal and iliaclymph nodes areas, 40 Gray, 25 fractions over 25 days). In2001, he relapsed again and received R-CHOP (Rituximab-CHOP). Since then, he has been in clinical remission.He came to our clinic in 2005, with 11 years of pro-gressive camptocormia and lower limb weakness thatinsidiously appeared in 1994; he was 63. He had no familyhistory of neuromuscular disease and had taken no partic-ular drugs (i.e., neuroleptics). Marked camptocormia(Fig. 1) was associated with atrophy and weakness in allparaspinal, cervical, and dorsolumbar muscles and in thebilateral and symmetrical proximodistal lower limbs. Therewere also fasciculations, distal hypoesthesia, and minimalstretch reflexes in the lower limbs. The last follow-up was

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