Ifosfamide-induced encephalopathy: the EEG with frontal intermittent delta activity, and rapid resolution with methylene
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(2020) 10:25 Hamilton et al. Clin Sarcoma Res https://doi.org/10.1186/s13569-020-00147-3
Open Access
CASE REPORT
Ifosfamide‑induced encephalopathy: the EEG with frontal intermittent delta activity, and rapid resolution with methylene blue: A case report Juliette E. Hamilton1* , Michael Alexander2 and Fergal C. Kelleher1
Abstract Background: Encephalopathy is an established side effect of the chemotherapeutic agent, ifosfamide, occurring in 10–30% of cases. The EEG commonly shows non-specific features of encephalopathy, and rarely shows frontal intermittent rhythmic delta activity (FIRDA). Case presentation: This is a case report of a 71 year old woman with pleomorphic sarcoma, who developed ifosfamide-induced encephalopathy with her second dose of ifosfamide. It shows the characteristic EEG findings that have been described previously with ifosfamide-induced encephalopathy and additionally the unusual and rare finding of FIRDA. This was followed up by a further EEG showing resolution of the encephalopathy, after administration of methylene blue, coinciding with rapid and complete resolution of her symptoms. Conclusion: The rapid resolution of the encephalopathy on the EEG after administration of methylene blue adds further evidence to its effectiveness as a treatment for the disorder. Keywords: Ifosfamide, Encephalopathy, Methylene blue, Frontal rhythmic intermittent delta activity FIRDA Background Ifosfamide (3-[2-chloroethyl]-2-[(2-chloroethyl)-amino] tetrahydro-2H-1, 3,2-oxazaphosphorin-2-oxide) is a chemotherapeutic agent used for a variety of solid organ and haematological malignancies, including in the management of sarcomas [1, 2]. It is a prodrug that is metabolized in the liver into the active alkylating agents by cytochrome P450 enzymes [3]. The alkylating agents produced are 4-hydroxy-ifosfamide and ifosfamide mustard with other resultant products including chloroacetaldehyde and chlorothylamine. Chloroacetaldehyde and chlorothylamine are thought likely to be the major *Correspondence: [email protected] 1 Department of Medical Oncology, Trinity College Dublin, St James’s Hospital, Dublin 8, Ireland Full list of author information is available at the end of the article
contributing factors in the development of encephalopathy, as they are known to be neurotoxic and are able to penetrate the blood–brain barrier [3, 4]. These metabolites are excreted predominantly by the kidneys [2]. Neurotoxicity can manifest in several ways, including lethargy, agitation, disorientation, confusion, hallucinations, extra-pyramidal signs and seizures [1, 5]. In rare cases, the symptoms can progress to coma, irreversible brain damage and death [1]. These symptoms are thought to develop due to glutaric acid accumulation, which may inhibit mitochondrial respiration [4]. This specific pathway was identified after glutaric acid was found in the urine of patients with congenital glutaric aciduria, a congenital metabolic disorder which results in a lack of the flavoproteins for electron transfer in mitochondri
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