Table 1

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
Hypoxic-ischaemic encephalopathy
CT	▸ Global cerebral oedema ▸ Decrease of putaminal, cortical and corticomedullary contrast	Global oedema false-positive rate 0%. Higher putaminal, cortical and corticomedullary contrast was associated with Cerebral Performance Category (CPC) 4–5
MRI	▸ Diffuse signal abnormalities in the cortex and subcortical areas or effacement of the sulci	All patients with these findings died
	▸ Lower whole-brain and regional median ADC	Patients with modified Rankin Scale (mRS) >3 have lower whole-brain and regional ADC
	▸ DWI and FLAIR cortical multilobar, or diffuse lesion pattern ▸ ADC <650×10⁶ mm²/s ▸ DWI with global ischaemia or focal ischaemia with lesion volume >20 mL ▸ T2 and DWI changes in the cerebral cortex and the deep grey matter	False-positive rate 0% for death, profound cognitive impairment, persistent vegetative state or severe physical impairment
PET	Hypometabolism frontal, parietal including the precuneus, in the posterior cingulate gyrus, and in the occipital areas. Hypermetabolism in the insulas, cerebellum and brainstem	No clear evidence
Sepsis-related encephalopathy
MRI	▸ Vasogenic oedema can be detected when autoregulation is disturbed ▸ With marked sepsis, there may be multiple lesions of cerebral white matter, and ischaemic strokes located in the centrum semiovale. The patchy white matter lesions are dynamic and change over time ▸ Periventricular contrast enhancement may often be demonstrate best on T1 ▸ Signs of ventriculitis with paraventricular ependymal hyperintensities can be present	No clear evidence
Uraemic encephalopathy
CT	Hypodense basal ganglia and capsules	No clear evidence
MRI	▸ T2, FLAIR and DWI hyperintense basal ganglia, capsules and inconsistently in cortical areas ▸ Additional involvement of white matter and cerebral peduncles, occipital lobes and thalami ▸ Decrease of N-acetyl-aspartate and the presence of lactate on MRS	No clear evidence
PET	Decreased glucose metabolism in basal ganglia	No clear evidence
Hyperammonaemic encephalopathy
MRI	▸ T2, FLAIR and DWI cortical hyperintensities of the insula and cingulum ▸ Increased glutamine and glutamate; low myoinositol and choline on MRS	No clear evidence
Hepatic encephalopathy
CT	Usually normal	No clear evidence
MRI	▸ T1 hyperintensities in the globus pallidus and, less frequent, in the substantia nigra and the midbrain tegmentum ▸ FLAIR and DWI hyperintense thalami, posterior limbs of the internal capsule, periventricular region, dorsal brain stem and diffuse cortical involvement in 1 study of 20 patients ▸ Connectivity: decreased in the caudate of the anterior/middle cingulate gyrus; increased in the caudate of the left motor cortex; reduced between the putamen and the anterior cingulate gyrus, right insular lobe, inferior frontal gyrus, left parahippocampal gyrus and the anterior lobe of the right cerebellum; increased between the putamen and right middle temporal gyrus ▸ Increased glutamate/glutamine ratio and low myoinositol and choline on MRS ▸ Diminished choline and elevated glutamate/glutamine ratio in the parieto-occipital cortex on MRS	Correlations between the corticostriatal connectivity and neuropsychological performances, but not between the striatal connectivity and globus pallidus signal intensity
SPECT	▸ High blood flow in the cerebellum, basal ganglia and cerebral cortex ▸ Alteration of striatal D2-receptor binding and dopamine reuptake	No clear evidence
PET	▸ Hypoperfusion of the superior and middle frontal gyri, and inferior parietal lobules ▸ Increased peripheral benzodiazepine binding sites prefrontal and striatal in patients with cirrhosis	No clear evidence
Wernicke's encephalopathy
CT	Hypodense paraventricular thalamic regions with or without contrast enhancement and, less frequent, hypodense periaqueductal regions, tectum of the midbrain and tegmentum of the pons	No clear evidence
MRI	▸ T2 and FLAIR hyperintense periaqueductal and medial thalamic regions. Less-frequent hyperintense mammillary bodies, periaqueductal regions, hypothalamus, tectum and cerebellum ▸ Minimised mammillary bodies ▸ Contrast-enhanced mammillary bodies is related to alcohol abuse ▸ Atrophic mammillary bodies and cerebellar vermis (chronic phase) ▸ Thalamic lactate increase and low N-acetyl-aspartate/creatine on MRS	No clear evidence
SPECT	Hypoperfusion frontoparietal and in the right basal ganglia	No clear evidence
Hypoglycaemic encephalopathy
CT	Enhancing, hypodense basal ganglia, cerebral cortex, hippocampus and substantia nigra	No clear evidence
MRI	▸ T2 and FLAIR hyperintensities in the caudate, lenticular nuclei, cerebral cortex, substantia nigra, hippocampus and internal capsules ▸ In few patients DWI hyperintense white and deep grey matter and splenium of the corpus callosum	Associated with vegetative state or severe disability in two case series
Hyperglycaemic encephalopathy
CT	Hyperdense putamen and/or caudate nucleus	No clear evidence
MRI	Unilateral or bilateral T1 hyperintensities in the striatum (mostly putamen)	No clear evidence
SPECT	Hypoperfusion of the basal ganglia	No clear evidence
Hyponatraemic/hypernatraemic encephalopathies (pontine or extrapontine myelinolysis)
CT	▸ Normal in a few patients and hypodense pontine lesions in the others	No clear evidence
MRI	▸ T2, FLAIR and DWI hyperintense lesions of the pons. Less frequent lesions of the thalamus, midbrain, cortical grey matter, hippocampus, caudate, putamen and middle cerebral peduncle ▸ T2 hyperintensities may be distributed along the crowns and sides of the cerebral gyri	No clear evidence
SPECT	Decreased striatal dopamine transporter binding and pontine hyperperfusion during recovery	No clear evidence

ADC, apparent diffusion coefficient; DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; MRS, MR spectroscopy; PET, positron emission tomography; SPECT, single-photon emission CT.