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. 2020 Dec 3;8(1):e924. doi: 10.1212/NXI.0000000000000924

Figure 1. The clinical, neurophysiological, and radiological characterization of PNS involvement in MOGAD.

Figure 1

(A) Clinical phenotyping of the number of CNS episodes in patients in this cohort. ON, inclusive of both BON and UON presentations, was the most frequent clinical phenotype, making up 39/47 (83%) episodes. (B) The right median nerve motor response (white) is smaller than the left (red) with a further reduction of amplitude at the elbow and with reduced persistence of median nerve F wave responses. These findings are consistent with right median neuropathy with conduction block at the elbow in a patient diagnosed with MMN. (C) Axial T1-weighted MRI with gadolinium showing enhancement of dorsal and ventral nerve roots (white arrows). (D) Sagittal T1-weighted MRI with gadolinium showing expansion of the conus (white arrow). (E) Axial fat-suppressed T1 with gadolinium showing enhancement of intradural right S1 nerve root (white arrow). (F) Proportion of the PNS syndromes identified in this cohort of patients with MOGAD. (G) A summary of the immunotherapy responsiveness of particular PNS syndromes—complete resolution occurred in 3/15 patients in whom immunotherapy was trialed (2 with myeloradiculitis and 1 with multifocal motor neuropathy), with 9/15 having only partial resolution and 3/15 being unresponsive to immunotherapy. AIDP = acute inflammatory demyelinating polyneuropathy; BON = bilateral optic neuritis; CIDP = chronic inflammatory demyelinating polyneuropathy; LETM = longitudinally extensive transverse myelitis; MMN = multifocal motor neuropathy; MOG = myelin oligodendrocyte glycoprotein; ON = optic neuritis; PNS = peripheral nervous system; sTM = short transverse myelitis; UON = unilateral optic neuritis.