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Abstract Details

Unusual Etiology of Corpus Callosum Damage: A Case of Thallium Toxicity
Neuro Trauma and Critical Care
P3 - Poster Session 3 (11:45 AM-12:45 PM)
7-007

This case emphasizes the importance of recognizing thallium toxicity in patients with encephalopathy, corpus callosum lesions, and associated symptoms.

The splenium of the corpus callosum plays a crucial role in visuospatial processing and consciousness.  It is susceptible to damage from toxic and metabolic disorders due to its rich blood supply, high myelin content, and reliance on potassium channels and energy metabolism. Thallium toxicity can disrupt these factors, potentially leading to demyelination and axonal damage.

Not applicable

A 50-year-old Cantonese-speaking woman presented with encephalopathy, accompanied by acute peripheral neuropathy and gastrointestinal symptoms. Initial MRI revealed a non-enhancing hyperintense splenial lesion. Her condition worsened, requiring intubation due to acute hypoxic and hypercarbic respiratory failure.  Electrodiagnostic studies showed severe sensorimotor polyneuropathy with active denervation. Heavy metal screenings, metabolic work-up, CSF studies, and infectious work-up were unremarkable, and a definitive diagnosis remained elusive despite a broad toxicology work-up. A repeat MRI post-intubation showed an extension of the splenial lesion, resembling that seen in Marchiafava-Bignami Disease. After a month of hospitalization, the patient developed significant alopecia. This constellation of symptoms (encephalopathy, peripheral neuropathy, gastrointestinal issues, and alopecia) raised suspicion for thallium toxicity, which had not been tested for by our toxicology specialists given the uncommon occurrence of accidental exposure. Thallium toxicity was confirmed by elevated thallium levels in plasma (56 mcg/L). Additional specificity was confirmed through urine and hair samples.  Treatment with Prussian Blue was initiated, successfully reducing thallium levels. Follow-up MRI showed a progressive decrease in signal intensity in the corpus callosum without immediate improvement in the patient’s neurological status. Long-term follow-up is pending.

This case underscores the potential for severe and persistent neurological consequences from thallium poisoning, despite treatment, emphasizing the critical need for prompt diagnosis and management to mitigate long-term sequelae.

Authors/Disclosures
Zinat Annaev, MD
PRESENTER
Dr. Annaev has nothing to disclose.
Nabihah Kabir, MD (University of Illinois) Dr. Kabir has nothing to disclose.
Syeda B. Owais, MD Dr. Owais has nothing to disclose.
Sameera Khan, MD (University of Illinois at Chicago) Dr. Khan has nothing to disclose.
Gregory J. Heller Mr. Heller has received personal compensation for serving as an employee of University of Illinois, Chicago. The institution of Mr. Heller has received research support from NIH.
Faten El Ammar, MD (University of IL, Chicago) Dr. El Ammar has nothing to disclose.
Jared M. Davis, MD (University of Illinois, Chicago) Dr. Davis has nothing to disclose.
Mariyam Humayun, MD Dr. Humayun has nothing to disclose.
Ciro Ramos Estebanez, MD, PhD, MBA, FAAN (University of Illinois in Chicago) The institution of Dr. Ramos Estebanez has received research support from NIH. Dr. Ramos Estebanez has received intellectual property interests from a discovery or technology relating to health care.