PMC3738334_01
(a) Axial trace diffusion-weighted image obtained 24 h after the onset of symptoms showed bilateral thalamic areas of high signal intensity (black arrows) suggesting acute paramedian thalamic infarcts. (b) Axial T1-weighted post-contrast image obtained after 20 days showed contrast enhancement in the bilateral thalamic infarcts (black arrows). (c) Axial flair-weighted image showed rounded areas (black arrows) of increased signal intensity in the medial thalamus. (d) Lateral T1-weighted image showed bilateral paramedian thalamic without anterior thalamus and midbrain area of low signal intensity (white arrow)
10.1258_arsr.2012.110004-fig1.jpg
PMC3738334_01_10.1258_arsr.2012.110004-fig1.jpg
ARSR-11-0004F1
Diffusion-weighted imaging (DWI) the next day showed symmetrical paramedian thalamic high signal intensity (Fig. 1). An MRI after three weeks showed symmetric enhanced signals in the paramedian thalamus (Fig. 1).
(a, b) DSA of the right vertebral injection, anteroposterior view (a) and lateral view (b) showed a stenotic AOP originating from the left P1 segment (white arrow). The P1 segment of the right PCA was absent (black double-arrow). (c) DSA of the right carotid artery injection showed the abnormally enlarged right PcomA could be the source of the right PCA (white arrow). (d) A schematic diagram represents a possible new variant of AOP. The P1 segment of the right PCA is absent while the AOP originates from the left
10.1258_arsr.2012.110004-fig2.jpg
PMC3738334_01_10.1258_arsr.2012.110004-fig2.jpg
ARSR-11-0004F2
A stenotic AOP originated from the left P1 segment was also visualized (Fig. 2).