Table 7

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

ImagingPatternsPredictive value for poor outcome
Posterior reversible encephalopathy
CTHypodensities 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 distributionNo clear evidence
  • ▸ 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
CTUsually normalNo clear evidence
  • ▸ 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
CTUsually normalNo clear evidence
  • ▸ 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
PETPET may reveal increased metabolism mesial temporalNo clear evidence
Autoimmune limbic encephalitis
CTUsually normalNo clear evidence
  • ▸ 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
  • ▸ 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
CTUsually normal, but can characteristically show reduced attenuation in the temporal lobes after the first week of the diseaseLesions on CT are predictive of prolonged course of disease
  • ▸ 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
SPECTIncreased tracer accumulation which reflects hyperperfusion possibly earlier than pathological signals appear on MRINo clear evidence
Susac's syndrome
CTDoes not reveal any of the specific structural abnormalities, but can demonstrate foci of subtle low attenuation in the corpus callosumNo clear evidence
  • ▸ 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
PETMarked hypometabolism in the frontal, parietal and temporal lobes—an unspecific pattern that can be mistaken as ADEMNo clear evidence
Creutzfeldt-Jakob disease
CTNon-specific generalised cortical and subcortical atrophy in the later phases of diseaseNo clear evidence
  • ▸ 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
PETHypometabolism in the cerebral cortex and the basal gangliaNo clear evidence
SPECTHypoperfusion in the cerebral cortexNo 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.