Temporal features of magnetic resonance imaging and spectroscopy in non-ketotic hyperglycemic chorea-ballism patients
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...
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| Published in | European journal of neurology Vol. 17; no. 4; pp. 589 - 593 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.04.2010
John Wiley & Sons, Inc |
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| Online Access | Get full text |
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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. |
|---|---|
| AbstractList | BACKGROUNDNon-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.METHODSPatients 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.RESULTSIn 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.CONCLUSIONSThe 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. 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 c 257.33 vs. 198.22 c 53.97 mg-dl, P = 0.001). The serum osmolality dropped from 318.33 c 15.21 mOsm-kg at onset to 292.50 c 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 c 0.23 vs. 0.72 c 0.28, P = 0.038; remission phase: 1.23 c 0.47 vs. 0.68 c 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. 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. 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. 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. 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. 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. |
| Author | Chen, C. -J. Hsu, W. -C. Chang, H. -S. Chen, C. -M. Chen, S. -T. Lyu, R. -K. Tsou, J. -C. Chang, K. -H. Ro, L. -S. Wu, Y. -R. |
| Author_xml | – sequence: 1 givenname: K. -H. surname: Chang fullname: Chang, K. -H. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 2 givenname: J. -C. surname: Tsou fullname: Tsou, J. -C. organization: Department of Neurology, E-Da Hospital, I-Shou University, Kaohsiung – sequence: 3 givenname: S. -T. surname: Chen fullname: Chen, S. -T. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 4 givenname: L. -S. surname: Ro fullname: Ro, L. -S. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 5 givenname: R. -K. surname: Lyu fullname: Lyu, R. -K. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 6 givenname: H. -S. surname: Chang fullname: Chang, H. -S. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 7 givenname: W. -C. surname: Hsu fullname: Hsu, W. -C. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 8 givenname: C. -M. surname: Chen fullname: Chen, C. -M. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 9 givenname: Y. -R. surname: Wu fullname: Wu, Y. -R. organization: Department of Neurology, Chang Gung Memorial Hospital and University College of Medicine, Taipei – sequence: 10 givenname: C. -J. surname: Chen fullname: Chen, C. -J. organization: Department of Radiology, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan |
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| References_xml | – volume: 16 start-page: 1243 year: 1995 end-page: 1246 article-title: Hyperintense putamen on T1‐weighted MR images in a case of chorea with hyperglycemia publication-title: AJNR Am J Neuroradiol – volume: 23 start-page: 564 year: 2006 end-page: 568 article-title: Radiological and pathological changes in hemiballism‐hemichorea with striatal hyperintensity publication-title: J Magn Reson Imaging – volume: 251 start-page: 1486 year: 2004 end-page: 1490 article-title: Hyperglycemia‐induced unilateral basal ganglion lesions with and without hemichorea. A PET study publication-title: J Neurol – volume: 77 start-page: 853 year: 1972 end-page: 860 article-title: Serum viscosity and hyperviscosity syndrome in IgG multiple myeloma. Report on 10 patients and a review of the literature publication-title: Ann Intern Med – volume: 60 start-page: 428 year: 1996 end-page: 430 article-title: Non‐ketotic hyperglycaemic chorea: a SPECT study publication-title: J Neurol Neurosurg Psychiatry – volume: 54 start-page: 682 year: 1973 end-page: 688 article-title: Hyperviscosity syndrome in multiple myeloma. A reversible, concentration‐dependent aggregation of the myeloma protein publication-title: Am J Med – volume: 25 start-page: 1977 year: 1994 end-page: 1984 article-title: Stroke in patients with diabetes. The Copenhagen stroke study publication-title: Stroke – volume: 200 start-page: 57 year: 2002 end-page: 62 article-title: Chorea associated with non‐ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1‐weighted brain MRI study: a meta‐analysis of 53 cases including four present cases publication-title: J Neurol Sci – volume: 38 start-page: 517 year: 1978 end-page: 530 article-title: Myelomatosis and the hyperviscosity syndrome publication-title: Br J Haematol – volume: 30 start-page: 1043 year: 1999 end-page: 1046 article-title: Novel brain ischemic change on MRI. Delayed ischemic hyperintensity on T1‐weighted images and selective neuronal death in the caudoputamen of rats after brief focal ischemia publication-title: Stroke – volume: 9 start-page: 100 year: 1986 end-page: 101 article-title: Alternating choreoathetosis associated with uncontrolled diabetes mellitus and basal ganglia calcification publication-title: Diabetes Care – volume: 31 start-page: 797 year: 2000 end-page: 798 article-title: Delayed ischemic hyperintensity of T1‐weighted MRI publication-title: Stroke – volume: 43 start-page: 525 year: 2001 end-page: 531 article-title: In vivo proton MR spectroscopy of chorea‐ballismus in diabetes mellitus publication-title: Neuroradiology – volume: 26 start-page: 905 year: 2002 end-page: 911 article-title: Hemichorea‐hemiballism in primary diabetic patients: MR correlation publication-title: J Comput Assist Tomogr – volume: 42 start-page: 941 year: 1977 end-page: 945 article-title: Effect of osmolality on red blood cell viscosity and transit through the lung publication-title: J Appl Physiol – volume: 59 start-page: 448 year: 2002 end-page: 452 article-title: Diffusion‐weighted and gradient echo magnetic resonance findings of hemichorea‐hemiballismus associated with diabetic hyperglycemia: a hyperviscosity syndrome? publication-title: Arch Neurol – volume: 165 start-page: 178 year: 1999 end-page: 181 article-title: Persistent hemiballism with striatal hyperintensity on T1‐weighted MRI in a diabetic patient: a 6‐year follow‐up study publication-title: J Neurol Sci – volume: 19 start-page: 863 year: 1998 end-page: 870 article-title: Hemichorea‐hemiballism: an explanation for MR signal changes publication-title: AJNR Am J Neuroradiol – ident: e_1_2_5_16_2 doi: 10.1152/jappl.1977.42.6.941 – volume: 16 start-page: 1243 year: 1995 ident: e_1_2_5_8_2 article-title: Hyperintense putamen on T1‐weighted MR images in a case of chorea with hyperglycemia publication-title: AJNR Am J Neuroradiol contributor: fullname: Nagai C – ident: e_1_2_5_6_2 doi: 10.1016/S0022-510X(02)00133-8 – ident: e_1_2_5_18_2 doi: 10.1111/j.1365-2141.1978.tb01077.x – ident: e_1_2_5_11_2 doi: 10.1161/01.STR.30.5.1043 – ident: e_1_2_5_15_2 doi: 10.1161/01.STR.25.10.1977 – ident: e_1_2_5_17_2 doi: 10.1016/0002-9343(73)90127-7 – volume: 19 start-page: 863 year: 1998 ident: e_1_2_5_7_2 article-title: Hemichorea‐hemiballism: an explanation for MR signal changes publication-title: AJNR Am J Neuroradiol contributor: fullname: Shan DE – ident: e_1_2_5_10_2 doi: 10.2337/diacare.9.1.100b – ident: e_1_2_5_2_2 doi: 10.1001/archneur.59.3.448 – ident: e_1_2_5_12_2 doi: 10.1161/01.STR.31.3.791-e – ident: e_1_2_5_14_2 doi: 10.1007/s00415-004-0571-4 – ident: e_1_2_5_5_2 doi: 10.1097/00004728-200211000-00009 – ident: e_1_2_5_4_2 doi: 10.1007/s002340100538 – ident: e_1_2_5_13_2 doi: 10.1136/jnnp.60.4.428 – ident: e_1_2_5_3_2 doi: 10.1016/S0022-510X(99)00081-7 – ident: e_1_2_5_19_2 doi: 10.7326/0003-4819-77-6-853 – ident: e_1_2_5_9_2 doi: 10.1002/jmri.20548 |
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| Snippet | Background: Non‐ketotic hyperglycemic chorea‐ballism (NKHCB) had special reversible hyperintense on T1‐weighted imaging (T1WI) lesion in comparsion to gray... Non-ketotic hyperglycemic chorea-ballism (NKHCB) had special reversible hyperintense on T1-weighted imaging (T1WI) lesion in comparsion to gray matter.... Background: Non‐ketotic hyperglycemic chorea‐ballism (NKHCB) had special reversible hyperintense on T1‐weighted imaging (T1WI) lesion in comparsion to gray... Background: Non-ketotic hyperglycemic chorea-ballism (NKHCB) had special reversible hyperintense on T1-weighted imaging (T1WI) lesion in comparsion to gray... BACKGROUNDNon-ketotic hyperglycemic chorea-ballism (NKHCB) had special reversible hyperintense on T1-weighted imaging (T1WI) lesion in comparsion to gray... |
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| SubjectTerms | 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 |
| Title | Temporal features of magnetic resonance imaging and spectroscopy in non-ketotic hyperglycemic chorea-ballism patients |
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