Anti-N-methyl-D-aspartate receptor-associated encephalitis: A review of clinicopathologic hallmarks and multimodal imaging manifestations

Table 1 Magnetic resonance imaging differential diagnosis for anti-N-methyl-D-aspartate receptor-associated encephalitis

Condition	Classic imaging manifestations
NMDARE	T2/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 encephalomyelitis	Areas 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/PACNS	Foci 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 disease	Symmetric T2/FLAIR hyperintensity involving the pulvinar and dorsomedial thalamic nuclei
	Diffusion restriction with concomitant T2 shine through is often present
Heroin inhalational leukoencephalopathy	Symmetric 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 encephalitis	Asymmetric 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 poisoning	Symmetric 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 sclerosis	Periventricular, 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 optica	Optic 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

GRE: Gradient echo; NMDARE: Anti-N-methyl-D-aspartate receptor-associated encephalitis; PACNS: Primary angiitis of the central nervous system; SWI: Susceptibility weighted imaging.