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Cytotoxic Lesion in the Splenium of Corpus Callosum Secondary to Subacute Methotrexate Neurotoxicity
Ahmad A Al-Awwad1, Ahmed Koriesh2
1Department of Neurology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.
Abstract:
Methotrexate neurotoxicity can present with a wide spectrum of neurologic symptoms and brain magnetic resonance imaging (MRI) typically demonstrates cerebral edema, demyelination, multifocal white matter necrosis, and atrophy relatively selective for the deep cerebral white matter. Here, we report a case of subacute methotrexate neurotoxicity in a 40-year-old man with B cell acute lymphoblastic leukemia. Brain MRI showed cytotoxic lesion in the splenium of corpus callosum and left middle cerebellar peduncle. Patient significantly improved 24 hours after receiving oral dextromethorphan. Methotrexate neurotoxicity should be suspected in any symptomatic patient receiving high dose of methotrexate or intrathecal methotrexate therapy. Dextromethorphan should be considered in these patients as it can modulate the excitatory responses to homocysteine and its metabolite which are usually elevated in such patients.
Insights
Subacute methotrexate neurotoxicity, a serious neurological complication, can be effectively treated with dextromethorphan. This intervention targets elevated homocysteine levels, offering rapid symptom improvement in patients with leukemia.
Area of Science:
- Neuroscience
- Oncology
- Radiology
Background:
- Methotrexate (MTX) is a crucial chemotherapeutic agent used in treating various cancers, including acute lymphoblastic leukemia.
- Neurotoxicity is a significant dose-limiting side effect of MTX therapy, manifesting with diverse neurological symptoms.
- Typical MTX neurotoxicity on brain MRI includes cerebral edema, demyelination, and white matter necrosis.
Observation:
- A 40-year-old male with B cell acute lymphoblastic leukemia developed subacute MTX neurotoxicity.
- Brain MRI revealed cytotoxic lesions in the splenium of the corpus callosum and left middle cerebellar peduncle.
- The patient experienced significant neurological symptom improvement within 24 hours of receiving oral dextromethorphan.
Findings:
- Dextromethorphan modulated excitatory responses potentially linked to elevated homocysteine and its metabolites, which are implicated in MTX neurotoxicity.
- This case highlights a novel therapeutic approach for MTX-induced neurological damage.
Implications:
- Methotrexate neurotoxicity should be considered in patients receiving high-dose or intrathecal MTX.
- Dextromethorphan presents a promising therapeutic option for managing MTX neurotoxicity.
- Further research into dextromethorphan's neuroprotective mechanisms in MTX toxicity is warranted.
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