Opioid-induced toxic leukoencephalopathy in a child: A case report

In environments, where opioids are used increasingly for recreational purposes, children are more at risk for both accidental and non-accidental intoxications. In toxic doses, opioids can cause lethal leukoencephalopathy. Here, we report a case of an 8-year-old male child who presented with altered mental status following accidental morphine overdose and was managed with cardio respiratory support, naloxone, and supportive therapy.

Toxic leukoencephalopathy caused by chemotherapeutic drugs other than methotrexate

Background & Objective Chemotherapy-induced toxic leukoencephalopathy is clinically characterized by progressive cognitive loss, often resulting in sudden death. The objective of this study is to share distinctive clinicopathological features of chemotherapy-induced brain change.Methods The brains of a 64-year-old woman and a 63-year-old man who suffered from rapid deterioration of consciousness were autopsied. The initial clinical impressions were central nervous system (CNS) graft versus host disease (GVHD), infectious or autoimmune encephalitis. Both patients had been treated with multidrug chemotherapy, including cytarabine arabinoside, daunorubicin, fludarabine, azacitidine, and busulfan, and allogeneic peripheral blood stem cell transplantation because of hematological malignancy (acute myelogenous leukemia and myelodysplastic syndrome). Results The autopsies revealed a vacuolar change of the white matter with axonal spheroids, reactive gliosis, and foamy macrophage infiltration in the brain, predominantly in the visual pathway of the occipital and temporal lobes. There was no lymphocytic infiltration in the brain tissue, which is characteristic of CNS-GVHD or encephalitis, suggesting these syndromes were not the cause of brain illness. Conclusion The leukoencephalopathy found in our cases is often occur after methotrexate treatment, but our autopsy cases showed that it can also be caused by a regimen of chemotherapeutic drugs other than methotrexate.

Stroke-like leukopathy in children with acute lymphoblastic leukemia

There are considerable variations in the reported incidence methotrexate-induced neurotoxicity in children with malignancies. The etiology of acute neurological deficit in pediatric patients with malignancies during polychemotherapy can be diverse: cerebrovascular disease (arterial ischemic stroke, intracranial hemorrhage, venous sinus thrombosis, or their combination), stroke-like migraine attacks after radiation therapy (SMART), posterior reversible encephalopathy syndrome (PRES), thrombotic microangiopathy, toxic leukoencephalopathy (include strokelike leukoencephalopathy). The tactics of a neurologist largely depends on the reasons that caused the neurological deficit. The doctor needs knowledge not only of the clinical picture and the characteristics of the course of the underlying disease, but also of possible complications arising both as a result of the disease itself and due to the therapy being carried out. Timely diagnosis and correct interpretation of emerging neurological events make it possible to determine rational accompanying therapy. The article presents case histories of children with acute lymphoblastic leukemias and acute neurological deficits, with an analysis of their possible causes.

A Case Report of Toxic Leukoencephalopathy induced by metronidazole in a woman with suture infection

Metronidazole may rarely cause encephalopathy and neuropathy. In this study we report a 30-year-old post-partum, ex-addicted female with leukoencephalopathy due to metronidazole.

Treating the treatment: chemotherapy-induced multi-organ toxicity

A 40-year-old man presented to a local hospital with a 2-day history of dyspnoea having been started on adjuvant chemotherapy consisting of oxaliplatin and capecitabine for mucinous adenocarcinoma of the colon. During his admission, he develops chest pain, worsening shortness of breath, and intermittent dysarthria and disorientation. Investigations reveal severely impaired left ventricular function on echocardiogram, bilateral acute pulmonary embolisms on CT pulmonary angiogragraphy, and diffused subcortical and callosal white matter signal change and restricted diffusion consistent with a toxic leukoencephalopathy on MRI of brain. This case highlights the pivotal role of the multidisciplinary cardio-oncology approach which enabled these challenging diagnoses to be made and ensured optimal patient outcome.