Veronica Birca, Christine Saint-Martin and
Kenneth A. Myers
From the Department of
Pediatrics (V.B., K.A.M.), Division of Child
Neurology, and Department of Medical Imaging
(C.S.-M.), Montreal Children's Hospital;
Department of Neurology & Neurosurgery
(K.A.M.), and Research Institute of the McGill
University Health Centre (K.A.M.), McGill
University Health Centre, Montreal,
Canada.
A 15-year-old boy had acute-onset
encephalopathy following a viral prodrome,
associated with frequent, dramatic yawning
without EEG change (video). There were no focal
deficits on examination. CSF protein elevation
(1.72 g/L) without pleocytosis, brain MRI, and
significant improvement following
methylprednisolone were consistent with acute
disseminated encephalomyelitis (ADEM).
Pathologic yawning is described in other
demyelinating diseases, neuromyelitis optica
spectrum disorder and multiple sclerosis, but is
rarely reported with ADEM. Although prior
reports postulated that brainstem and
hypothalamic lesions are responsible, yawning is
a complex reflex mediated by both supratentorial
and infratentorial structures; its precise
localization is not yet defined.
Axial views show normal T1 (A), asymmetric
T2 (B), and fluid-attenuated inversion recovery
(FLAIR) (C) hyperintensity of the dorsal
brainstem involving the reticular formation
(arrowheads) at the level of cranial nerves V,
VI, and VII nuclei, and T2 and FLAIR
hyperintensity of the bilateral, left more than
right, insula (arrows).