PMC9315246_01
Computed tomography (CT) and MRI of brain at admission. Diabetic striatopathy (DS)-associated striatal abnormalities were marked by red arrows, while infarction focuses were marked by yellow arrows. Typical imaging manifestations of DS were found in the left striatum with T1 hyperintensity [(A,B), coronal images; (P,Q), sagittal images] on MRI and hyper-density on CT images (S,T). The hypointensity on T2 (D,E), fluid-attenuation inversion recovery (FLAIR) (G,H), and apparent diffusion coefficient (ADC) (M,N) images, as well as equal signal intensity on DWI images (J,K) were also observed in DS-associated striatal lesions. Subacute cerebral infarctions showed T1 hypointensity [(B,C) coronal images; (Q) sagittal image], T2 hyperintensity (E,F), FLAIR hyperintensity (H,I), DWI hyperintensity (K,L), and slight ADC hyperintensity (N,O) on MRI images, as well as hypo-density on CT images (T,U). MRA images disclosed obvious stenosis of the left middle cerebral artery [(R), green arrow]. There were several artifacts on ADC images [(J,K), blue arrows].
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F1
His brain MRI showed T1-hypointensity, T2-, and FLAIR- and DWI-hyperintensity in the left striatum and adjacent areas, suggesting acute cerebral infarction lesions (Figures 1B,C,E,F,H,I,K,L, yellow arrows). Besides, slight hyperintensity on apparent diffusion coefficient (ADC) images (Figures 1N,O, yellow arrows) and T1-hyperintensity around T1-hypointensity (Figures 1A,B, red arrows) were also observed. Consistently, MRA images also disclosed severe atherosclerosis and stenosis of the left middle cerebral artery (MCA) (Figure 1R, green arrow). CT was performed and showed an extensive hyper-density (Figures 1S,T, red arrows) and focal low-density (Figures 1T,U, yellow arrows). Combined with the patient's clinical data and neuroimaging findings, we thought that diabetes-related striatum lesions were responsible for clinical attack and progress.
Follow-up magnetic resonance imaging (MRI) of brain 2 months after onset. Diabetic striatopathy (DS)-associated striatal abnormalities were marked by red arrows, while infarction focuses were marked by yellow arrows. DS-associated T1 hyperintensity on the left striatum was obviously extended [(A), coronal image; (P,Q) (R): sagittal images). DS-associated T2 and FLAIR hypointensity changed to slight hyperintensity (D,G). The left striatum showed an equal signal intensity on DWI images (J). DS-associated initial ADC hypointensity changed to equal signal intensity (M). DWI hyperintensity on infarction lesions disappeared (K,L) and ADC hyperintensity increased (N,O). Abnormal T1 hypointensity (B,C), T2 hyperintensity (E,F), and FLAIR hypointensity on the infarction core (H,I), as well as FLAIR hyperintensity around the infarction core (H,I) suggested the formation of softening lesions and secondary gliosis.
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F2
However, hyperintensity on T1-weighted MRI images within the striatum was increased compared to that of the initial images (Figures 2A,P-R, red arrows). ADC hyperintensity increased (Figures 2N,O). Abnormal T1 hypointensity, T2 hyperintensity, and FLAIR hypointensity on the infarction core, as well as FLAIR hyperintensity around the infarction core, suggested the formation of softening lesions and secondary gliosis (Figures 2B-I, 3B-I, yellow arrows). Therefore, we finally diagnosed the patient with DS and AIS.
Follow-up magnetic resonance imaging (MRI) of brain 18 months after onset. Diabetic striatopathy (DS)-associated striatal hyperintensity on T1 and T2 and fluid-attenuation inversion recovery (FLAIR) images were disappeared (A,D,G,J), but atrophy of the left caudate nucleus with resultant dilatation of frontal horn of left lateral ventricle was noted [(B,E,H,K) red arrows]. Remote cerebral infarctions were observed on T1, T2, FLAIR and diffusion weighted imaging (DWI) images [(B,C,E,F,H,I,K,L), yellow arrows].
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F3
Moreover, a re-examination of brain MRI showed that the striatal hyperintensity on T1 images has disappeared (Figure 3A) and atrophy of the left caudate nucleus with resultant dilatation of the frontal horn of the left lateral ventricle was noted (Figures 3B,E,H,K, red arrows). T1 hypointensity, T2 hyperintensity, and FLAIR hypointensity on the infarction core, as well as FLAIR hyperintensity around the infarction core, suggested the formation of softening lesions and secondary gliosis (Figures 2B-I, 3B-I, yellow arrows). Therefore, we finally diagnosed the patient with DS and AIS.