Table 7

Most consistent and pathognomonic neuroimaging patterns in the literature and their predictive value (data from the online supplementary tables S1–S3)

Imaging	Patterns	Predictive value for poor outcome
Posterior reversible encephalopathy
CT	Hypodensities in the parieto-occipital subcortical white matter and cerebellum with increased cerebral blood volume, blood flow, and reduced time to peak mainly in the posterior vascular distribution	No clear evidence
MRI	▸ T2, FLAIR and DWI hyperintensities in the posterior circulation areas and, less frequent, in the anterior circulation structures. ADC values in areas of abnormal T2 signal are high ▸ Contrast enhancement, restrictions on DWI and ADC ▸ Decrease in N-acetyl-aspartate on MRS in patients with normal MRI or reversible MRI changes and only minimal elevation of choline	More extensive T2 signal abnormalities were seen with poor outcome
Acute disseminated encephalomyelitis
CT	Usually normal	No clear evidence
MRI	▸ T2 and FLAIR with multiple brain lesions in the deep and subcortical white matter and in 1/3 in the brainstem and spinal cord characteristic of demyelination with contrast enhancement ▸ In the first week (acute phase) DWI with restricted diffusion, and later (subacute phase) with increased diffusion ▸ Decreased N-acetyl-aspartate in regions with T2 hyperintensities in the subacute phase on MRS	No clear evidence
Paraneoplastic limbic encephalitis
CT	Usually normal	No clear evidence
MRI	▸ T2 and FLAIR hyperintensities with mesial temporal contrast enhancement in >50% and/or atrophy ▸ Subcortical regions, the cerebellum or brainstem may be involved	No clear evidence
PET	PET may reveal increased metabolism mesial temporal	No clear evidence
Autoimmune limbic encephalitis
CT	Usually normal	No clear evidence
MRI	▸ In NMDAR-antibody-mediated limbic encephalitis, MRI is mostly (>50%) normal but can show T2 and FLAIR hyperintensities temporal and rarely extratemporal. MRI is used to exclude other causes of encephalopathy ▸ In SREAT, T2 and FLAIR can rarely resemble acute demyelinating encephalomyelitis or show hippocampal or multifocal hyperintensities ▸ In SREAT, MRS shows decreased N-acetyl-aspartate, myoinositol peaks, elevations in lipid, lactate, glutamate/glutamine and choline peaks support inflammation	No clear evidence
SPECT	▸ In NMDAR-antibody-mediated limbic encephalitis, abnormal multifocal cerebral blood flow ▸ In SREAT, decreased tracer uptake in the striatum and global cortical hypoperfusion	No clear evidence
Herpes simplex encephalitis
CT	Usually normal, but can characteristically show reduced attenuation in the temporal lobes after the first week of the disease	Lesions on CT are predictive of prolonged course of disease
MRI	▸ T2, FLAIR and DWI hyperintensities in the medial temporal lobes, the orbital surface of the frontal lobes, the insular cortex, the angular gyrus and in the insulas early in the course ▸ Abnormal areas may show enhancement with gadolinium ▸ Midline shift may be present with large cerebral oedema	The extent of brain involvement is an independent risk factor for poor prognosis
SPECT	Increased tracer accumulation which reflects hyperperfusion possibly earlier than pathological signals appear on MRI	No clear evidence
Susac's syndrome
CT	Does not reveal any of the specific structural abnormalities, but can demonstrate foci of subtle low attenuation in the corpus callosum	No clear evidence
MRI	▸ T2 and FLAIR hyperintensities in the corpus callosum, which is always involved ▸ Any part of the corpus callosum can be involved, but predominately the central fibres are showing microinfarcts that are typically small but may sometimes be large ▸ Foci in the corpus callosum may enhance following gadolinium administration and there can be restricted diffusion with corresponding low-signal intensity on the ADC map ▸ Spinal cord involvement is rare but exists ▸ Subsequently, central callosal holes arise	No clear evidence
PET	Marked hypometabolism in the frontal, parietal and temporal lobes—an unspecific pattern that can be mistaken as ADEM	No clear evidence
Creutzfeldt-Jakob disease
CT	Non-specific generalised cortical and subcortical atrophy in the later phases of disease	No clear evidence
MRI	▸ T2 and FLAIR hyperintensities in the cerebral cortex and lesions in the putamen and caudate head isointense to cortex and lesions in the putamen and caudate head isointense to cortical grey ▸ Less frequently, hyperintensity can be detected in the globus pallidus, thalamus, the deep white matter, and the cerebral and cerebellar cortex. Laminar lesions may be observed in the cerebral cortex and cerebellum ▸ DWI is most sensitive in early stages uncovering the altered diffusion in the regions aforementioned ▸ In vCJD symmetrical hyperintensities of the pulvinar thalami (relative to the cortex and especially the anterior part of the putamen) are characteristic and known as the ‘pulvinar sign’ ▸ Decreased N-acetyl-aspartate and slightly increased levels of myoinositol in the striatum and the insular cortex on MRS	Patients with cortical plus basal ganglia hyperintensity have shorter interval from symptom onset to akinetic mutism than those with isolated cortical ribbon hyperintensity
PET	Hypometabolism in the cerebral cortex and the basal ganglia	No clear evidence
SPECT	Hypoperfusion in the cerebral cortex	No clear evidence

ADC, apparent diffusion coefficient; ADEM, acute disseminated encephalomyelitis; DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; MRS, MR spectroscopy; NMDAR, N-methyl-d-aspartate receptor; PET, positron emission tomography; SPECT, single-photon emission CT; SREAT, steroid-responsive encephalitis with autoimmune thyroiditis; vCJD, variant Creutzfeldt-Jakob disease.