Perplexing Case of Aseptic Meningitis with Cytotoxic Lesions of the Corpus Callosum, Multifocal Cranial Nerve Enhancement, and Longitudinally Extensive Transverse Myelitis in an Unvaccinated Healthy Young Woman
Jason Gandhi1, Gurleen Kaur2, Thomas Scott3, James Valeriano4
1Allegheny Health Network, 2Allegheny General Hospital, 3Allegheny Neurological Assoc, 4Allegheny Neurological Associates
Background:
Cytotoxic lesions of the corpus callosum (CLOCC) are rare, often associated with infectious or inflammatory conditions, and can present with diverse neurological manifestations. By examining this case, we aim to elucidate the potential pathophysiological mechanisms underlying CLOCC and the clinical implications of its multifaceted neurological manifestations in young, immunocompetent individuals.
Results:
A 23-year-old woman presented with severe headache, strabismus, and a remote history of tick bites. Initial cerebrospinal fluid (CSF) analysis revealed elevated opening pressure (32 cm H₂O), high white cell count, and increased protein levels, suggestive of infectious or aseptic meningitis given history of being unvaccinated. Meningo-encephalitis CSF panel was negative. MRI demonstrated signal abnormalities in the splenium of the corpus callosum, extensive leptomeningeal enhancement, cranial nerve involvement, and extensive T2 hyperintense cord signal abnormality in the entire cervical-thoracic cord. Despite initial antibiotic therapy, her condition deteriorated with altered mentation and seizure-like activity, necessitating intubation.
She was treated with high-dose steroids and plasmapheresis were initiated, with a notable clinical response. Over the course of her hospitalization, repeat imaging showed gradual resolution of cranial nerve enhancement and improvement of spinal cord signal abnormalities. Post-hospitalization, she experienced significant deconditioning, generalized weakness, and vocal cord issues likely secondary to prolonged intubation.
Conclusions:
This case highlights the complexity of CLOCC in association with viral meningitis and multifocal neurological involvement. It underscores the importance of recognizing CLOCC as a potential syndrome with multifaceted cranial and spinal manifestations, particularly in young, immunocompetent individuals. Early recognition and treatment with immunomodulatory therapy can result in significant clinical improvement. Further studies are warranted to explore the underlying mechanisms of CLOCC and its associated neurological sequelae in viral infections.
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