Acute disseminated encephalomyelitis and Guillain-Barré syndrome represent distinct demyelinating diseases that share an autoimmune pathogenesis. A history of viral infection or vaccination are essential for the diagnosis[1],[2],[3].
A 26-month-old boy presented with fever 10 days after vaccination (inactivated polio vaccine and tetravalent), progressive drowsiness, lower limb strength/sensory loss and urinary retention. The cerebrospinal fluid showed mild pleocytosis and an elevated total protein concentration; it was negative for infections. The initial MRI study was compatible with acute disseminated encephalomyelitis, with no spine abnormalities ([Figure 1]).
Figure 1 Brain MRI revealed white matter hyperintensities lesions in T2/fluid- attenuated inversion recovery (FLAIR) (A, B) in the cerebral hemispheres and cerebellum, without restriction to water molecules diffusivity or gadolinium enhancement, suggestive of acute disseminated encephalomyelitis . Sagittal T1 SPIR post-gadolinium (C), without cauda equina root enhancement.
Ten days later, after therapy with corticosteroids, he experienced acute paraplegia. Follow-up brain and spine MRI scans demonstrated partial regression of brain lesions and nerve root thickening with intense enhancement extending along the cauda equina, compatible with Guillain-Barré syndrome. ([Figure 2]).
Figure 2 Follow-up MRI one week after steroids, showed partial recovery of the brain lesions; axial (A) and sagittal T1 SPIR post-gadolinium (B), enhancement of the cauda equina roots (white arrow), compatible with Guillain-Barré Syndrome.
