F76. Lumbosacral polyradiculopathy after intrathecal chemotherapy

Abstract

Introduction Intrathecal chemotherapy is commonly used in hematological malignancies, neurological toxicity is rare but it can have devastating effects. We report the case of a patient with B-cell diffuse lymphoma who developed severe pain in the legs, flaccid paraplegia and incontinence. We excluded neoplastic infiltration and concluded that it was the result of intrathecal toxicity. Methods We present the case of a 73 year old woman with a history of B cell lymphoma diagnosed 16 years ago, she received chemotherapy using CHOP regimen and radiotherapy and went into remission until 3 years ago when she had femur and fibula involvement for which she began treatment with rituximab, bendamustine and intrathecal metotrexate (MTX) and citarabine (Ara-C). One week after the second dose of Intrathecal chemotherapy she developed flaccid paraplegia with absent tendon reflexes, incontinence and severe pain in the legs, a few days later she developed lower limbs anesthesia. Cervical, thoracic and lumbosacral spine MRI images showed abnormal enhancement of the roots and medullary cone. Serial lumbar punctures didn’t reveal neoplastic infiltration or viral infection. Nerve conductions studies showed absent motor response in the peroneal and tibial nerves and low amplitudes in the superficial peroneal and sural nerves. High dose corticosteroids and piridoxine were initiated, there was not improvement. Results Intrathecal chemotherapy is a proven therapy and prophylaxis in leukemia and lymphomas,it reduces mortality and central nervous system infiltration. Neurological toxicity is a rare adverse effect; manifestations include arachnoiditis, myelopathy, leukoencephalopathy, cauda equina syndrome and polyradiculopathy. The onset of symptoms varies from days to weeks. Some of the risk factors for toxicity are: combined use of MTX, Ara-C, use of high doses, incorrect volume, pH and osmolality preparation and short time between chemotherapy cycles. There have been reports of toxicity due to contamination with traces of vincristine and aseptic meningitis incited by the preservative used in the diluent. The neurotoxicity may be caused by local depletion of folate with axonal loss. Treatments using corticosteroids, folinic acid rescue, cerebrospinal fluid exchange and dextromethorphan, have been proposed. Most patients with polyradiculopathy develop severe neurological sequelae. Conclusion Although toxicity is rare it should be kept in mind in patients with neurological complaints after intrathecal chemotherapy, its varied manifestations and time of presentation might be challenging. The correct preparation and dose calculation of chemoterapy might reduce the risk. Treatment with folinic acid and corticosteroids might be useful in some patients.