Abstract WP215: Role of Conventional Mri Brain for Basilar Artery Plaque Detection in Solitary Pontine Infarct
Background: Solitary pontine infarct is divided into paramedian pontine infarct (PPI) and small deep pontine infarct (SDPI). The novel high-resolution MRI is the current useful imaging method to characterize vessel walls and detect atherosclerotic plaques of the intracranial arteries. However, high-resolution MRI is not included in routine imaging protocol for patient with acute stroke. We intend to determine the role of conventional MRI and MRA of the brain in solitary pontine infarct.
Material and Method: Fifty patients with pontine infarct undergo imaging study of MRI of the brain on T1-weighted image, T2-weighted image and post-gadolinium T1-weighted image (if available) to assess the presence of atherosclerotic plaque, and MRA of the brain using 3-dimensional time-of-flight MRA (3D TOF MRA) to assess the basilar artery luminography. Basilar artery assesses by axial T2-weighted image was scored as “presence of plaque” or “absence of plaque” and 3D TOF MRA of basilar artery is scored as “normal”, “irregular” or “stenosis” ≥ 30%. Pontine infarction is divided into paramedian pontine infarction (PPI) and small deep pontine infarction (SDPI) groups.
Results: Fifty patients with pontine infarction are included, thirty-five with PPI and fifteen with SDPI. Conventional axial T2WI MRI of the brain detected basilar artery atherosclerotic plaques in about 50% of patients with pontine infarction: 51.4% (18 of 35 cases) in PPI and 46.7% (7 of 15 cases) in SDPI. No plaque is found in all cases of normal-appearing basilar luminography on 3D TOF MRA and plaque was identified in all patients with basilar artery stenosis on 3D TOF MRA.
Conclusion: Basilar artery atherosclerotic branch disease is frequently detected in both groups of solitary pontine infarct (PPI and SDPI). Conventional MRI and MRA of the brain are the useful imaging methods that may characterize intracranial vessel wall abnormalities and may be helpful in further study of intracranial arterial diseases and in comprehension of stroke mechanisms.
Author Disclosures: S. Muengtaweepongsa: None. W. Kantrakul: None. A. Watcharakorn: None. U. Chaumrattanakul: None.
- © 2016 by American Heart Association, Inc.