Clinical and imaging features of diabetic striatopathy: report of 6 cases and literature review

Abstract

Objective: To explore the clinical manifestations, diagnosis, treatment, and pathogenesis of diabetic striatopathy (DS) to improve the understanding of the disease and avoid misdiagnosis or underdiagnosis.

Methods: The clinical, laboratory, and imaging data of 6 patients (5 Asian females and 1 Asian male) with diabetic striatum were analyzed retrospectively, and the related literature was reviewed.

Results: All 6 patients showed hyperglycemia, 5 patients presented with involuntary movement of unilateral limbs, and 1 with unilateral limb numbness. Besides, 5 patients (except case 3) underwent MRI examinations that showed hyperintensity in unilateral caudate and lentiform nucleus on T1-weighted images. And all 6 patients who underwent brain CT examinations showed hyperdensity or isodensity in unilateral caudate and lentiform nucleus. None had a family history of similar abnormal movements. After blood glucose control and symptomatic support treatment, the symptoms of all patients improved to various degrees, and reexaminations showed that the lesions gradually disappeared.

Conclusion: Diabetic striatal disease is a rare complication of diabetes mellitus, the result of a combination of different pathogenesis. It is characterized by hyperglycemia, hemichorea, and contralateral striatal T1WI hyperintensity or CT hyperdensity. Both ketosis and nonketotic hyperglycemic hemichorea have typical imaging manifestations. The prognosis is excellent when this disease is detected early, and the lesions can be gradually absorbed and dissipated with glycemic control.

Keywords: Computed tomography; Diabetic striatopathy; Hemichorea; Hyperglycemia; Magnetic resonance image.

Fig. 1

Imaging examinations of case 1. Computed tomography (CT) of the brain on July 30, 2020 (a) and magnetic resonance imaging (MRI) of the brain on August 2, 2020 (b-e) and August 6, 2020 (f, g). (a) The unenhanced axial CT images showed hyperdensity in the right caudate and lentiform nucleus, and the CT values was about 56 Hu. (b) The right caudate and lentiform nucleus showed hyperintensity on T1-weighted images. (c) The right caudate and lentiform nucleus indicated hypointensity on T2-weighted images. (d) The right caudate and lentiform nucleus with hypointensity on fluid-attenuation inversion recovery (FLAIR) sequences. (e) The right caudate and lentiform nucleus showed hyperintensity by diffusion weighted imaging (DWI), and the ADC value of the abnormal lesion center was 0.641 × 10 − 3 mm2 /s. (f) The right caudate and lentiform nucleus with hypointensity on MRA source images. (g) The bilateral basal ganglia showed isointersity with punctate hypointersity on susceptibility weighted imaging (SWI)

Fig. 2

Imaging examinations of case 2. Computed tomography (CT) of the brain on October 08, 2021 (a) and magnetic resonance imaging (MRI) of the brain on October 05, 2021 (b,c), and October 10, 2021(d, e). (a) The unenhanced axial CT images showed hyperdensity in the left lentiform nucleus, and the CT values was about 43 Hu. (b) The left lentiform nucleus showed hyperintensity on T1-weighted images. (c) The left lentiform nucleus indicated hyperintensity on MRA source images. (d) SWI demomstrated isointensity in bilateral basal ganglia with punctate hypointensity in the left basal ganglia. (e) Magnetic resonance arterial spin labeling(ASL) showed hypoperfusion in the left basal ganglia with the CBF valus of 29.456 mL/(100 g × min), while the CBF values of contralateral region was 50.608 mL/(100 g × min)

Fig. 3

Fig. 3. Imaging examinations of case 3. Computed tomography (CT) of the brain on August 13, 14 and 20, 2020 (a-c) and September 05,2020 (d). (a-c) The unenhanced axial CT revealed hyperdensity in the right caudate and lentiform nucleus, and the CT value of the abnormal lesion center was about 59Hu, 54Hu, 51Hu. (d) The disappearance of the hyperdensity the right caudate and lentiform nucleus on CT scans, and the CT value of the abnormal lesion center was about 33 Hu

Fig. 4

Imaging examinations of case 4. Magnetic resonance imaging (MRI) of the brain on November 14, 2017 (a) and December 01, 2017 (b-e), and computed tomography (CT) of the brain on April 01, 2018 (f). (a) The left caudate and lentiform nucleus showed hyperintensity on T1-weighted images on November 14, 2017. (b) The left caudate and lentiform nucleus showed hyperintensity on T1-weighted images on December 01, 2017, but the range was extended. (c-e) The left caudate and lentiform nucleus showed isointensity on T2-weighted images, slightly hyperintensity on T2-FLAIR images, slightly hyperintensity on DWI images. (f) The unenhanced axial CT images showed isodensity in the left caudate and lentiform nucleus with the CT value of about 30 Hu

Fig. 5

Imaging examinations of case 5. Magnetic resonance imaging (MRI) of the brain on October 4, 2019 (a-d) and computed tomography (CT) of the brain on October 5, 2019 (e). (a) The left caudate and lentiform nucleus showed hyperintensity on T1-weighted images. (b-d) The left caudate and lentiform nucleus showed hypointensity on T2-weighted images, slightly hyperintensity on T2-FLAIR images, hyperintensity on MRA source images. (e) The unenhanced axial CT images showed slightly hyperdensity in the left caudate and lentiform nucleus with the CT value of about 37Hu

Fig. 6

Imaging examinations of case 6. Magnetic resonance imaging (MRI) of the brain on Setemper 19, 2015 and computed tomography (CT) of the brain on Setemper 19, 2015 and Setemper 28, 2015. (a-c) The left caudate and lentiform nucleus showed hyperintensity on T1-weighted images, hypointensity on T2-weighted images, hypointensity on T2-FLAIR images. (d)The left caudate and lentiform nucleus revealed hyperdensity on CT scan. (e) CT reexamination showed the density and range of lesions in the left basal ganglia decreased