CHEMOTHERAPY FOR ACUTE LYMPHOBLASTIC-LEUKEMIA MAY CAUSE SUBTLE CHANGES OF THE SPINAL-CORD DETECTABLE BY SOMATOSENSORY-EVOKED POTENTIALS

Intrathecal chemotherapy has been determined to cause transient or per manent paraparesis due to myelopathy in patients with leukemia or othe r malignancies. To systematically evaluate the effect of methotrexate on spinal cord function, somatosensory evoked potentials (SEP) were me asured in children with acute lymphoblastic leukemia (ALL). A prospect ive evaluation was performed in 38 consecutive children aged 1.4-15.3 years with newly diagnosed ALL during treatment. Intrathecal methotrex ate therapy was included in the therapy schedule of all patients as ce ntral nervous system (CNS) therapy in addition to intravenous chemothe rapy in 19 standard risk patients and intravenous chemotherapy with cr anial irradiation in 19 intermediate or high-risk patients. The measur ed conduction times were compared with those of 38 control children ma tched for age, height, and sex. A significant increase in the conducti on time of the tibial nerve SEP was found between the Th12 level and t he cortex in children with ALL after receiving intrathecal methotrexat e therapy during the induction and CNS therapy phases when compared wi th their controls. The difference of the mean latencies was 1.45 ms (9 5% CI 0.39-2.51;P < 0.01). There was no significant delay in the media n nerve SEP from the brain stem to the cortex, indicating that the con duction delay was in the area of the spinal cord exposed to intratheca l methotrexate. Moreover, the cortical amplitudes of the median nerve SEPs were significantly reduced when measured immediately after intrav enous and intrathecal methotrexate and compared to the amplitudes meas ured after induction therapy in standard risk patients (P = 0.001). In trathecal methotrexate with systemic chemotherapy causes a deteriorati on in the somatosensory pathways within the CNS, suggesting also spina l cord dysfunction in children with ALL in addition to the cerebral dy sfunction described earlier. (C) 1997 Wiley-Liss, Inc.