PMC6852355_01
Before spine surgery (day 0) showing loss of flow void with elevated T2 signal within
the left vertebral artery from the level of C2-C3 (A) to T1 (B) within the left
vertebral artery (arrowhead).
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In addition, there was loss of flow void in the left vertebral artery concerning for possible thrombosis/dissection (see Figure 1).
Magnetic resonance imaging (MRI) after spine surgery (day 1) showing persistent
unchanged absence of T2 flow void of the left vertebral artery (arrowheads) in sagittal
view (A), and axial view (B) including the intracranial vertebral artery segment. B,
Reduced flow void in the intracranial segment on the left vertebral artery (arrowhead)
compared with the right vertebral artery. Also, loss of flow signal seen on magnetic
resonance angiography (MRA) sequence (C) in the left vertebral artery (arrowhead) with
present flow in the right vertebral artery (arrow).
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Important to mention that the brain MRI was limited in part due to orthodontic braces, but otherwise was normal (see Figure 2).
Magnetic resonance imaging (MRI) 2 days after surgery showing interval development of
T2/fluid-attenuated inversion recovery signal abnormality within the left lateral aspect
of the medulla, left dentate nucleus, and inferior medial portion of the left cerebellum
(A and B). The cerebellar abnormality is correlated with a posterior inferior cerebellar
artery (PICA) distribution while the medullary finding likely relates to the known
vertebral artery thrombosis. Unfortunately, due to artifact created by dental hardware
there is obscuration of this area on the diffusion-weighted imaging (C) and apparent
diffusion coefficient "ADC" (not shown); only the most inferior medial aspect of the
posterior cerebellum is spared of the artifact and demonstrates restricted diffusion in
keeping with an infarction (arrowhead).
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His brain MRI at day 2 (post neurological symptoms showed interval development of T2W/fluid-attenuated inversion recovery signal abnormality within the left lateral medulla and inferomedial aspect of the cerebellum in keeping with infarcts secondary to the left vertebral artery thrombosis and occlusion of the left posterior inferior cerebellar artery (see Figure 3).