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Pancreatic ascites due to rupture of a mucinous cystic neoplasm

of the CSF during an episode of dysarthria but both patients declined consent to a lumbar puncture. In contradiction with this hypothesis is the finding that no CNS-toxicity is reported in over 140 irinotecantreated patients with brain tumours, despite the presence of a clearly disrupted blood-brain barrier in these patients [11 13]. Cytotoxic oedema is unlikely to play an important role in irinotecan induced CNS toxicity since normal diffusion-weighted MR images of the brain were found in one of our patients while experiencing dysarthria. It is also unlikely that irinotecan-mediated CNS toxicity occurs in the context of ACS. Dysarthria can occur in patients without ACS, while administration of atropine does not appear to prevent its (re-)occurrence whereas it effectively deals with ACS. Of importance, pre-clinical toxicology never revealed any CNS-toxicity (Pfizer, data on file) rendering it difficult if not impossible to further study this side effect in animal models. In conclusion, the exact cause of irinotecaninduced CNS toxicity remains unravelled and plasma pharmacokinetics also do not provide an explanation. Therefore, a specific treatment cannot be recommended. Most importantly, since in all cases CNS toxicity was fully reversible, was not exaggerated by rechallenge with irinotecan, and can even decline in severity at repeated exposure; CNS toxicity is not a reason to discontinue irinotecan treatment despite its sometimes impressive and threatening appearance.