Table 3 Summary of the studies reporting neuroimaging findings, electroencephalogram, and autoimmune panels associated with MPXV-associated neuroinflammatory disorders

Hammad et al. [12]

Long-segment hyperintense signals on T2-weighted and FLAIR sequences observed in the cervical and upper thoracic spinal cord, occupying more than two-thirds of the cross-sectional area. Mild cord swelling in the upper cervical spine. No enhancement observed in the spinal cord, but increased meningeal enhancement along the anterior and posterior margins.

Multiple hyperintense signals in the cortical and subcortical regions of both hemispheres on T2-weighted and FLAIR sequences. Hyperintense signals observed in the basal ganglia, thalamus, medial temporal lobe, insular cortex, and brainstem. Subtle enhancement noted in the brainstem, with no other significant findings.

Not Reported

Not Reported

Not reported

Money et al. [13]

Patient 1

Multifocal, longitudinally extensive, partially enhancing central thoracic lesions with a gray matter lesion in the conus medullaris

Partially enhancing T2/FLAIR hyperintense subcortical lesion in the right frontal lobe, with additional lesions in the bilateral medial thalami, basal ganglia, splenium, and pons.

Generalized rhythmic delta activity and slowing

Not reported

Negative for myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies

Patient 2

Multifocal, partially enhancing T2 hyperintense lesions in the cervical and thoracic spine with central cord and dorsal column involvement

Ill-defined T2/FLAIR hyperintensities in the cerebellum, pons, and medulla, with persistent DWI hyperintensities

Not Reported

Not reported

Positive for anti-smooth muscle antibodies, negative for aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

Patient 3

No abnormalities detected in cervical or thoracic spinal imaging.

Restricted diffusion in the central and lateral thalami and posterior globus pallidi, with subtle T2/FLAIR hyperintensity; no parenchymal or leptomeningeal enhancement.

Generalized rhythmic delta activity and generalized bifrontal slowing.

Not reported

Not reported

Moore et al. [14]

Longitudinally extensive, non-enhancing T2/FLAIR hyperintense lesion in the thoracic spinal cord, spanning T1 to T10 vertebral levels—slight swelling of the cord in the same distribution.

Lesion was central, predominantly involving gray matter

Multiple discrete, non-enhancing T2/FLAIR hyperintensities. Lesions located in the left external capsule, central pons, left cerebellar white matter, and right middle cerebellar peduncle

Not Reported

Negative

Negative

Cole et al. [15]

Longitudinally extensive transverse myelitis. T2 hyperintense signal along the entire spinal cord with both central gray and peripheral white matter involvement. Cord swelling observed in the cervicothoracic and lumbar regions. Post-contrast enhancement in the cauda equina nerve roots and patchy enhancement in the cervical spine

Diffuse T2 hyperintensities throughout the cerebral white matter. Hyperintensities in both thalami, middle cerebellar peduncle, and brainstem. New lesions in the posterior limb of the left internal capsule and splenium of the corpus callosum. Cortical swelling with early uncal herniation and brainstem mass effect

Not Reported

Negative for aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies, paraneoplastic autoantibodies, and autoantibodies to glial fibrillary acidic protein

Negative for aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies, antinuclear antibodies, extractable nuclear antigens, paraneoplastic autoantibodies, and autoantibodies to glial fibrillary acidic protein

Marín-Medina et al. [16]

T2/STIR hyper-intense longitudinally extensive transverse myelitis comprising levels T1 to T12, with no enhancement or compression

Extensive T2/FLAIR hyperintensities were observed, primarily affecting the white matter of the brain hemispheres, as well as the basal ganglia, anterior thalamus, internal capsules, frontal medial cortex, cerebral peduncles, and the entire pons. Some lesions exhibited restricted diffusion with mild contrast enhancement and no evidence of compression

Not Reported

Not reported

Negative aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

Pastula et al. [17]

Patient 1

Multifocal, longitudinally extensive, partially enhancing lesions in the central thoracic spinal cord.

Gray matter involvement in the conus medullaris. Chronic cervical spinal stenosis causing partial cord compression (presumed non-acute)

Partially enhancing lesions in the frontal lobes (consistent with demyelination).

Non-enhancing lesions in the bilateral basal ganglia, medial thalami, splenium, and pons

Not reported

Not reported

Negative aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

Patient 2

Multifocal, partially enhancing lesions in the central cervical and thoracic spinal cord. Gray matter involvement

Non-enhancing T2/FLAIR hyperintensities in the pons, cerebellum, and medulla.

No restricted diffusion noted

Not reported

Negative aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

Negative aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

Rodríguez et al. [18]

Longitudinally extensive intramedullary T2 hyperintensity from T1 to T8 and T11 suggestive of inflammation or demyelination

T2/FLAIR hyperintensities in the anterior right thalamus, bilateral lentiform nuclei, posterior insular regions, left frontal parasagittal area, pons, and midbrain, with no restricted diffusion or gadolinium enhancement

Not reported

Negative myelin oligodendrocyte glycoprotein antibodies and paraneoplastic antibodies (anti-Hu, Yo, Ri, Ma)

Not reported

Karin et al. [19]

Not reported

Bilateral symmetrical restricted diffusion in the cingulate gyrus, insula, and cortical regions

Generalized slow waves without epileptiform activity

Negative

Negative

Yadav et al. [20]

Not reported

Diffuse cerebral edema. Altered signal intensity with FLAIR hyperintensity and mild restricted diffusion. Lesions observed in bilateral cerebral cortical and subcortical regions, bilateral caudate nucleus, putamen, and posterior genu of the corpus callosum.

Generalized cerebral dysfunction

not reported

Not reported

Sejvar et al. [21]

Not reported

Diffuse cortical, thalamic, and brainstem edema, meningeal enhancement, and left thalamic and right parietal signal abnormality

Generalized slowing, consistent with diffuse cerebral dysfunction

Not reported

Not reported

Jezek et al [22]

Not reported

Not reported

Not reported

Not reported

Not reported

Ogoina et al. [23]

Not reported

Not reported

Not reported

Not reported

Not reported

Reuters (Faus) [24]

Not reported

Not reported

Not reported

Not reported

Not reported