Temporal features of magnetic resonance imaging and spectroscopy in non-ketotic hyperglycemic chorea-ballism patients

• Published in: European journal of neurology Vol. 17; no. 4; pp. 589 - 593
• Main Authors: Chang, K. -H., Tsou, J. -C., Chen, S. -T., Ro, L. -S., Lyu, R. -K., Chang, H. -S., Hsu, W. -C., Chen, C. -M., Wu, Y. -R., Chen, C. -J.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.04.2010; John Wiley & Sons, Inc
• Subjects: Acute Disease; Aged; Basal Ganglia - metabolism; Basal Ganglia - pathology; Choline - metabolism; chorea; Chorea - blood; Chorea - metabolism; Chorea - pathology; Creatine - metabolism; diabetes mellitus; Female; Follow-Up Studies; Functional Laterality; Humans; hyperglycemia; Hyperglycemia - blood; Hyperglycemia - metabolism; Hyperglycemia - pathology; Lactic Acid - metabolism; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Male; movement disorders; Osmolar Concentration; Time Factors
• ISSN: 1351-5101; 1468-1331
• DOI: 10.1111/j.1468-1331.2009.02867.x

Background:  Non‐ketotic hyperglycemic chorea‐ballism (NKHCB) had special reversible hyperintense on T1‐weighted imaging (T1WI) lesion in comparsion to gray matter. However, the mechanism accounts for these lesions is still unclear. Methods:  Patients diagnosed with NKHCB were recruited from 2002 to 2004. The demographic, clinical, magnetic resonance imaging (MRI), and spectroscopy (MRS) features were recorded at acute and remission phase. Results:  In 18 patients with NKHCB, the blood sugar level at onset was significantly higher than that after being free from chorea‐ballism (419.50 ± 257.33 vs. 198.22 ± 53.97 mg/dl, P = 0.001). The serum osmolality dropped from 318.33 ± 15.21 mOsm/kg at onset to 292.50 ± 7.85 mOsm/kg after recovery (P < 0.001). All patients displayed T1 hyperintense lesions at contralateral basal ganglia at acute phase. Eight patients receiving follow‐up MRI at remission phase, all T1 hyperintense lesions at the basal ganglia regressed. The ratios between choline‐containing compounds and creatine at acute and remission phases were significant higher in lesion than in normal side, respectively (acute phase: 1.12 ± 0.23 vs. 0.72 ± 0.28, P = 0.038; remission phase: 1.23 ± 0.47 vs. 0.68 ± 0.15, P = 0.013). The lactate peaks present at 1.3 ppm on the lesion side either in acute or in remission phase of most case. Conclusions:  The clinical, MRI, and MRS findings suggest that the mechanisms responsible for NKHCB may be a reversible ischaemia insult potentiated by hyperglycemia.