Biomarker |
Pros |
Cons |
Autoantibodies (e.g., anti-NMDAR, anti-LGI1, anti-CASPR2) |
High specificity for AE subtypes. Directly linked to pathogenesis. Can guide treatment decisions. |
Not all patients with AE have detectable antibodies (seronegative cases). Testing can be time-consuming and may not correlate well with disease severity or prognosis in all cases. |
CSF analysis (pleocytosis, protein levels, oligoclonal bands) |
Widely available and can support the diagnosis of the inflammatory process |
Low specificity for AE. Can be normal in some AE cases. Requires invasive lumbar puncture |
MRI findings |
Non-invasive and can exclude other pathologies. Specific patterns can suggest AE. |
Can be normal in early stages or some AE subtypes. Findings can be non-specific Limited sensitivity in some AE cases. |
EEG changes |
Can detect subclinical seizures. Specific patterns (e.g., extreme delta brush in anti-NMDAR encephalitis) can be suggestive. |
Low specificity for AE. Requires expertise for interpretation. Findings can be variable and non-specific. |
Inflammatory markers (e.g., IL-6, TNF-α) |
Can indicate ongoing inflammation and may correlate with disease activity |
Low specificity for AE. Can be elevated in various inflammatory conditions. Limited availability of testing in some settings |
FDG-PET |
Can show abnormalities before structural MRI changes and may help in monitoring the treatment response |
Limited availability and high-cost exposure to radiation. Patterns can overlap with other conditions. |