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Copyright ©The Author(s) 2024.
World J Radiol. Jan 28, 2024; 16(1): 1-8
Published online Jan 28, 2024. doi: 10.4329/wjr.v16.i1.1
Table 1 Magnetic resonance imaging differential diagnosis for anti-N-methyl-D-aspartate receptor-associated encephalitis
Condition
Classic imaging manifestations
NMDARET2/FLAIR hyperintense lesions that frequently involve the hippocampus or bilateral hippocampi
Lesions within the infratentorial brain parenchyma and spinal cord are uncommon
Leptomeningeal enhancement is occasionally present
Acute disseminated encephalomyelitisAreas of high T2/FLAIR signal, predominantly within the subcortical white matter
An “open ring” pattern of enhancement, similar to multiple sclerosis
Lesions with peripheral diffusion restriction
Central nervous system vasculitis/PACNSFoci of T2/FLAIR hyperintensity within the periventricular white matter or along watershed zones
Parenchymal microhemorrhages may be present on GRE/SWI sequences
Evidence of acute, subacute, or chronic stroke within a discrete vascular territory is present in some individuals
Creutzfeldt-Jakob diseaseSymmetric T2/FLAIR hyperintensity involving the pulvinar and dorsomedial thalamic nuclei
Diffusion restriction with concomitant T2 shine through is often present
Heroin inhalational leukoencephalopathySymmetric T2/FLAIR hyperintensity within the posterior limb of the internal capsules, which may extend inferiorly to the pontine corticospinal tracts
Symmetric T2/FLAIR hyperintensity within the cerebellar white matter with sparing of the dentate nuclei
Herpes simplex encephalitisAsymmetric T1 hypointense/T2 hyperintense edema involving the bilateral medial temporal lobes and insular cortex
Gyral or leptomeningeal enhancement may be present
Diffusion restriction is sometimes present
Blooming on GRE/SWI sequences may be present in the setting of hemorrhage
Methanol poisoningSymmetric or asymmetric T1 hyperintensity within the putamina, indicative of necrosis
Asymmetric blooming within the putamina on GRE/SWI sequences in the setting of hemorrhage
Multiple sclerosisPeriventricular, cortical, or juxtacortical T2/FLAIR hyperintense lesions disseminated in space and time
Infratentorial and spinal cord T2/FLAIR hyperintense lesions may develop in some individuals
An “open ring” pattern of enhancement is present in active disease
Neuromyelitis opticaOptic nerve edema with T2/FLAIR hyperintense signal and, in some patients, optic nerve enhancement
High T2/FLAIR signal within the spinal cord spanning at least three contiguous vertebral segments
Brain parenchymal lesions are often absent
Table 2 Cerebral metabolic patterns of autoimmune encephalopathies[18-20]
Autoantibody
Metabolic pattern
Anti-NMDA receptorBifrontal hypermetabolism or normal frontal lobe metabolism
Marked bilateral parieto-occipital hypometabolism
Anti-LGI-1 Bitemporal hypermetabolism
Bilateral fronto-occipital hypometabolism
Anti-CASPR2 Bifrontal hypermetabolism
Basal ganglia hypermetabolism
Bilateral temporo-parietal hypometabolism
Anti-GAD-65 Bilateral basal ganglia hypometabolism
Bitemporal hypometabolism
Anti-Hu Bitemporal hypermetabolism
Table 3 Multimodal imaging of anti-N-methyl-D-aspartate receptor-associated encephalitis[12-24]
UltrasoundPelvic or scrotal ultrasound may be used to identify an underlying teratoma in the appropriate patient population
Ultrasound-guided lymph node biopsy may be required in the setting of metastatic disease with no known primary
MRIA normal brain MRI is present in half of patients with NMDARE
T2/FLAIR hyperintense lesions are most commonly present within the supratentorial brain parenchyma and may correlate with prognosis:
   Type 1: Normal brain MRI; favorable prognosis
   Type 2: Hippocampal lesions only; poor prognosis
   Type 3: Lesions involving structures other than the hippocampus; intermediate prognosis
   Type 4: Lesions involving both the hippocampus and other brain structures; poor prognosis
Infratentorial, spinal cord, and cranial nerve lesions are less common, but may occur in some individuals
Leptomeningeal enhancement is rare, but has been described
MRSReduced NAA peak
Decreased NAA/creatine ratio
Increased choline peak
FDG PETBrain FDG PET classically shows bifrontal hypermetabolism with parieto-occipital hypometabolism
The frontal-to-parietooccipital metabolic gradient may correlate with prognosis, with an increased gradient portending a worse outcome
Whole-body FDG PET may be of value to identify a primary neoplasm and/or localize a lesion for image-guided biopsy
SPECTHMPAO and I-123-IMP SPECT may be useful for metabolic evaluation in patients with clinical features of NMDARE and a normal brain MRI and FDG PET