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

K. H. Chang, J. C. Tsou, S. T. Chen, L. S. Ro, R. K. Lyu, H. S. Chang, W. C. Hsu, C. M. Chen, Y. R. Wu, C. J. Chen

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)589-593
Number of pages5
JournalEuropean Journal of Neurology
Volume17
Issue number4
DOIs
Publication statusPublished - Apr 2010

Fingerprint

Chorea
Magnetic Resonance Spectroscopy
Magnetic Resonance Imaging
Basal Ganglia
Creatine
Choline
Hyperglycemia
Osmolar Concentration
Blood Glucose
Lactic Acid
Ischemia
Demography
Serum

Keywords

  • Chorea
  • Diabetes mellitus
  • Hyperglycemia
  • Movement disorders

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

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

In: European Journal of Neurology, Vol. 17, No. 4, 04.2010, p. 589-593.

Research output: Contribution to journalArticle

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. / Temporal features of magnetic resonance imaging and spectroscopy in non-ketotic hyperglycemic chorea-ballism patients. In: European Journal of Neurology. 2010 ; Vol. 17, No. 4. pp. 589-593.
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abstract = "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.",
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AU - Chang, K. H.

AU - Tsou, J. C.

AU - Chen, S. T.

AU - Ro, L. S.

AU - Lyu, R. K.

AU - Chang, H. S.

AU - Hsu, W. C.

AU - Chen, C. M.

AU - Wu, Y. R.

AU - Chen, C. J.

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N2 - 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.

AB - 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.

KW - Chorea

KW - Diabetes mellitus

KW - Hyperglycemia

KW - Movement disorders

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