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.
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.