Relapsing MUO in Dogs: New MRI & CSF Clues Every Clinician Should Know

Relapsing Meningoencephalitis of Unknown Origin in Dogs Results in Changes in Neuroanatomical Localization, Magnetic Resonance Imaging, and Cerebrospinal Fluid

Ivona Orgonikova, Sumari Dancer, Josep Brocal, Steven De Decker, Cecilia-Gabriella Danciu, Lucia Martin, Rodrigo Gutierrez-Quintana, Rita Gonçalves, Kiterie M. E. Faller

Background

Meningoencephalitis of unknown origin (MUO) is a common noninfectious inflammatory CNS disease in dogs, presenting with diverse neurological signs and histopathologic subtypes. Diagnosis is typically based on neurological examination, MRI, and cerebrospinal fluid analysis. MRI has high specificity for inflammatory brain disease, while CSF often reveals mononuclear pleocytosis, though up to 22% of cases may show normal results. MUO is considered immune mediated and treated with immunosuppressive therapy, yet relapse rates remain high (28–65%), often leading to treatment adjustments, neurological decline, or euthanasia. This study investigates how clinical localization, MRI findings, and CSF profiles change between initial presentation and relapse.

Methods

This multicenter retrospective observational study included dogs with presumptive MUO diagnosed between April 2011 and August 2023. Inclusion required neurological signs of brain disease, exclusion of infectious etiologies, an initial positive response to immunosuppressive therapy for at least three weeks, relapse of neurological signs, and MRI at both initial presentation and relapse. CSF was evaluated when available. MRI studies were reanalyzed by a board-certified imaging specialist using standardized criteria, documenting lesion distribution, intensity, contrast enhancement, and anatomical location. Statistical analyses compared clinical, MRI, and CSF variables between timepoints.

Results

Thirty-nine dogs met inclusion criteria. Neuroanatomical localization differed between initial presentation and relapse in 56% of cases, and 77% developed new neurological deficits. Initial MRI abnormalities persisted in 92% of dogs at relapse, while 85% developed new lesions sharing similar imaging characteristics. New lesions most commonly appeared in the parietal cortex, whereas lesions in the brainstem showed the greatest likelihood of resolution. Gray matter involvement increased from 67% initially to 85% at relapse, and perilesional edema was more common at relapse. CSF total nucleated cell count was significantly lower at relapse, and lymphocyte predominance decreased from 72% to 50%, indicating a shift toward more mixed inflammatory profiles. Protein levels remained similar.

Limitations

The retrospective design, multicenter variability, and lack of histopathologic confirmation introduce potential diagnostic and treatment heterogeneity. Not all dogs had CSF analysis at both timepoints, and MRI protocols varied across institutions, though each dog’s follow-up imaging occurred at the same facility. Inclusion of dogs with normal MRI or CSF reflects clinical practice but may broaden case heterogeneity. Treatment regimens differed widely, limiting conclusions about therapeutic impact.

Conclusions

Relapsing MUO in dogs is associated with substantial changes in neuroanatomical localization, MRI lesion burden, and CSF characteristics. Persistence and development of new lesions—particularly in the parietal cortex—are common, whereas brainstem lesions are more likely to resolve. CSF findings show reduced inflammation at relapse, with lower nucleated cell counts and fewer lymphocyte-predominant samples. The study emphasizes the importance of repeat MRI and CSF analysis to optimize monitoring, guide therapeutic adjustments, and refine long-term management strategies for MUO.

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