Med Pediatr Oncol 2003;41:491–497 LETTERS TO THE EDITOR Severe Encephalopathy Caused by Intraparenchymal Methotrexate Instillation Due to the Design of the Catheter To the Editor: Intraventricular application of chemotherapy especially methotrexate via an intraventricular catheter is an acknowledged method for the treatment of malignant childhood brain tumors [1,3] and case records of accidental intrapar- enchymal chemotherapy instillations via misplaced catheters are rare [2,4]. It is considered to be a safe, easy to perform, and less stressful way to instill drugs into the cerebrospinal fluid than repetitive lumbar punctures. Those catheters are usually perforated along the last few centimeters and have a dead end (Fig. 1). They are constructed that way because catheters, with just one open end, were often found to be blocked by ingrowing structures of the choroid plexus. Because of the catheter design it is likely that some of the catheter’s holes are in the intraparenchymal part of the tube even if the catheter’s tip is correctly placed into the ventricle. This is no problem as long as the catheter is only used for aspiration of cerebrospinal fluid (for example to relieve pressure in the case of internal hydrocephalus). But when administering drugs through the catheter and especially when administering cytotoxic substances such as methotrexate, it is obvious that depending on the amount of pressure cytotoxic fluid can inadvertently be injected directly into the brain parenchyma. This happened to a 4-year-old boy with medulloblastoma who received multiple intraventricular methotrexate applica- tions via a Rickham-reservoir-catheter placed in the right side ventricle. For 9 months after starting chemotherapy, the boy was in good physical condition, but 10 days after he had the last intraventricular methotrexate application he was admitted to Fig. 1. The tip of the removed catheter. It shows the perforation of the last 2 centimeters and the catheter’s dead end. Fig. 2. Contrast enhanced MRI shows the massive brain edema around the catheter with midline shift. Fig. 3. Contrast enhanced MRI shows the big cystic defect 4 months after the removal of the catheter. —————— *Correspondence to: Dr. Sven Gottschling, Department of Paediatric Haematology and Oncology, University Children’s Hospital, 66424 Homburg/ Saar, Germany. Received 29 November 2001; Accepted 6 February 2002. ß 2003 Wiley-Liss, Inc. DOI 10.1002/mpo.10117