Brain Imaging Findings in Enteroviral Rhombencephalitis and Autoimmune Encephalitis
In enteroviral rhombencephalitis, MRI demonstrates hyperintense T2 and FLAIR lesions localized to the midbrain, pons, and medulla (the brainstem/rhombencephalon), while autoimmune encephalitis most commonly shows limbic system involvement with T2 FLAIR hyperintensity, though 39-61% of cases may have completely normal MRI findings. 1
Enteroviral Rhombencephalitis - Specific Imaging Pattern
The imaging pattern for enterovirus 71 encephalitis is relatively specific and characteristic:
- Primary location: Dorsal pons and medulla oblongata (brainstem structures)
- Secondary involvement: May extend to cerebellar dentate nuclei, midbrain, or thalamus 2
- Signal characteristics:
- T1-weighted: Isointense or hypointense
- T2-weighted and FLAIR: Hyperintense lesions
- May show enhancement on contrast-enhanced sequences, particularly in early disease (within 7-8 days of onset) 2
Critical timing consideration: Enhanced MRI scans performed earlier in the disease course (mean 7.67 days) are more likely to show enhancement compared to later scans (mean 11.95 days), and can identify lesions missed on plain sequences 2. Diffusion-weighted imaging is superior to conventional MRI for detecting early signal abnormalities in enteroviral encephalitis 1.
The presence of abducens nerve palsy clinically should heighten suspicion for enteroviral rhombencephalitis and prompt immediate imaging 3.
Autoimmune Encephalitis - Variable Imaging Patterns
Autoimmune encephalitis presents a more heterogeneous imaging picture that varies by antibody subtype:
General Features Across AE Subtypes:
- Normal MRI in 39-61% of cases - particularly common in anti-NMDAR encephalitis where 61% have normal imaging 4
- Most common location: Limbic system (33% of cases) 4
- Typical signal characteristics:
Antibody-Specific Patterns:
Anti-LGI1 encephalitis: Unilateral or bilateral hippocampus OR basal ganglia involvement 5
Anti-NMDAR encephalitis: Low rate of imaging abnormalities; when present, shows diffuse, unfixed cortical or subcortical T2 FLAIR hyperintensity 5
Anti-GABABR encephalitis: Primarily temporal lobe or hippocampus 5
Anti-GFAP astrocytopathy: Characteristic radial perivascular enhancement 6, 7
MOG antibody cortical encephalitis: Cortical swelling with T2 FLAIR hyperintensity in unilateral or bilateral hemispheres, particularly frontal lobe 5
Anti-GAD65 encephalitis: Temporal lobe/hippocampus OR pontocerebellar regions 5
Prognostic Imaging Markers:
ADC values within lesions correlate with disease severity and prognosis - higher ADC values indicate worse outcomes and serve as a risk factor for poor prognosis 5. This quantitative measure can guide treatment intensity decisions.
Key Diagnostic Algorithm
- Obtain MRI with diffusion-weighted imaging within 24-48 hours of admission 8
- If brainstem/rhombencephalon involvement: Consider enteroviral rhombencephalitis, particularly if dorsal pons and medulla are affected
- If limbic system involvement: Consider autoimmune encephalitis, check specific antibody panels
- If MRI is normal but clinical suspicion remains high:
- AE is still possible (39-61% have normal MRI)
- Consider brain FDG-PET to confirm focal/multifocal abnormality 6
- Proceed with CSF antibody testing regardless
Critical Pitfalls to Avoid
- Do not rely on CT scanning - it misses early changes in 75% of viral encephalitis cases 8, 9
- Do not exclude AE based on normal MRI - over one-third of cases have normal imaging 4
- Do not wait for imaging results to start treatment - if clinical suspicion is high for HSV or enteroviral encephalitis, empiric acyclovir should be started within 6 hours 9
- Consider overlapping conditions - viral infection and autoimmune antibodies can coexist within 72 hours of symptom onset, requiring both antiviral and immunomodulatory therapy 10
The extent of brain involvement on MRI correlates with clinical symptom severity in both conditions 2, making imaging essential for prognostication and treatment planning.