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- When to Scan Again: MRI Patterns at MUO Relapse Guide Diagnosis and Treatment
When to Scan Again: MRI Patterns at MUO Relapse Guide Diagnosis and Treatment
Journal of Veterinary Internal Medicine 2025
Obi Veterinary Education
January 12, 2026
Carole Soulé, Laurent Blond, Robin Cavalerie, Stéphanie Piazza, Clément Baudin-Tréhiou
Background:
Meningoencephalomyelitis of unknown origin (MUO) is an immune-mediated, non-infectious inflammatory central nervous system disease in dogs, comprising granulomatous meningoencephalomyelitis (GME) and necrotizing encephalitis subtypes. Despite treatment, relapses are common, but the evolution of MRI lesions between initial diagnosis and relapse has not been described. This study aimed to characterize changes in MRI findings over time and determine the diagnostic and clinical utility of repeat MRI at relapse.
Methods:
This retrospective, descriptive longitudinal case series included 18 small-breed dogs diagnosed with MUO who underwent MRI at initial diagnosis and at clinical relapse. Eight of these dogs also had intermediate (control) MRI during treatment. MRIs were reviewed for lesion number, size, location, and features including contrast enhancement, perilesional edema, and intracranial hypertension. Relapse timing was categorized as early (<157 days) or late (>233 days) based on a median interval of 259 days between MRIs.
Results:
Early relapsing dogs had stable or fewer lesions with no new lesion development; residual lesions often enlarged with signs of activity (contrast enhancement and edema), indicating persistent disease. In contrast, all late relapsing dogs developed new lesions. Half had persistent or enlarged residual lesions, while the other half showed resolution or shrinkage of original lesions, suggesting remission followed by relapse in a new brain region. Lesions in the parietal lobe increased markedly at relapse. T2-FLAIR signal suppression (indicative of necrosis) increased from 28% to 44% of dogs. Control MRIs showed lesion resolution and improved imaging features during immunosuppressive treatment in most dogs. Clinical signs did not always correspond with imaging changes, emphasizing the value of MRI for detecting subclinical disease.
Limitations:
The study was limited by its retrospective design and small sample size. All imaging was performed on a low-field MRI scanner, potentially reducing sensitivity for certain lesion types. The MUO subtype was presumptively diagnosed without histopathologic confirmation, and treatment protocols were not standardized across cases.
Conclusions:
MRI lesion evolution in MUO follows a time-dependent pattern. Before 6 months, residual lesions may remain active without new lesions; thus, repeat MRI adds limited diagnostic value. After 6 months, new lesion development is common—whether the original lesions resolve or not—and repeat MRI is valuable for detecting relapse and guiding management. These findings support a tailored approach to follow-up imaging, with timing based on relapse risk and clinical evolution.
Example of MUO lesion evolution between initial, control, and relapse MRI of multifocal MUO lesions with a relapse delay exceeding 6 months, characterized by a good lesional response to immunosuppressive therapy with resolution of the initial lesions and/or cicatricial gliosis of the residual lesions associated with new lesion development. Transverse T2W (A, E, I), T2W-FLAIR (B, F, J), T1W (C, G, K), T1W + C (D, H, L) sequences of the brain of a 1-year-old female Pomeranian at the level of the fronto-parieto-temporal lobe junction at the time of initial (A–D) (T0), control (E–H) (T0 + 105d), and relapse (I–L) (T0 + 446d) MRI. (A–D) Initially, there was a T2W hyperintense lesion without a necrotic area (no T2W-FLAIR signal suppression) at the left fronto-temporal lobe junction, with heterogeneous peripheral contrast enhancement (arrowheads) surrounded by perilesional edema and associated with suspected intracranial hypertension (mass effect on the cerebral falx and attenuation of the cerebral sulci). (E–H) On control MRI, after immunosuppressive treatment, the lesion decreased in size (first arrowheads) without evidence of lesional contrast enhancement or intracranial hypertension (midline position of the cerebral falx, visible cerebral sulci). (I–L) At relapse, the initial lesion had almost disappeared (first arrowheads), and a new T2W hyperintense lesion without evidence of necrosis and discretely enhancing at the right fronto-parieto-temporal lobe junction (second arrowheads), with perilesional edema and intracranial hypertension (attenuation of cerebral sulci) was present. d, day, MRI, magnetic resonance imaging; MUO, meningoencephalomyelitis of unknown origin; T1W, T1-weighted; T1W + C, T1-weighted after contrast media injection; T2W, T2-weighted; T2W-FLAIR, T2-weighted fluid-attenuated inversion recovery.
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