Article Figures & Data
Figures
Figure. (A) Diffusion-weighted MRI sequence shows acute infarction of the cerebral peduncles. (B) Intracranial MRA. The basilar artery and posterior cerebral arteries (PCAs) appear occluded on the reconstructed image, but source images suggest sluggish PCA flow from posterior communicating arteries.
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Files in this Data Supplement:
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- Tarek Zakaria, MD and
- Matthew L. Flaherty, MD
- Address correspondence and reprint requests to Dr. Matthew L. Flaherty, 231 Albert Sabin Way, MSB Room 5161B, University of Cincinnati Medical Center, Cincinnati, OH 45267-0525; e-mail: matthew.flaherty{at}uc.edu
A 71-year-old man had acute onset of ataxia, dysarthria, and visual blurring, which progressed in a stuttering fashion to a locked-in syndrome. Only pupillary reflexes and extraocular movements (both vertical and lateral) were ultimately preserved. MRI showed bilateral infarctions of the cerebral peduncles with sparing of the thalami and occipital lobes (figure). The basilar terminus and posterior cerebral arteries (PCAs) appeared occluded on the reconstructed MRA, but source images suggested sluggish PCA flow via small posterior communicating arteries, potentially explaining the limited distribution of infarction. Locked-in syndrome usually results from ischemic, traumatic, toxic, or demyelinating lesions of the ventral pons. It is rarely caused by infarction of the cerebral peduncles, which are supplied by multiple perforating arteries originating from the PCAs.1,2
Figure. (A) Diffusion-weighted MRI sequence shows acute infarction of the cerebral peduncles. (B) Intracranial MRA. The basilar artery and posterior cerebral arteries (PCAs) appear occluded on the reconstructed image, but source images suggest sluggish PCA flow from posterior communicating arteries.
Footnotes
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Disclosure: The authors report no conflicts of interest.
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