Risk factors for prolonged hemichorea-hemiballism caused by hyperglycemia

Su, Chen-San; Chang, Yung‐Yee; Liu, Kuan‐Ting; Lan, Min-Yu; Liu, Jiashou

doi:10.1016/j.parkreldis.2011.06.003

Cited by 8 publications

(7 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The age of chorea onset in C‐NKH patients (mean, 77 years) was significantly higher than in C‐URE patients (mean, 48 years), which is consistent with findings from previous studies . The underlying cause of this difference is unclear.…”

Section: Discussionsupporting

confidence: 90%

“…Chorea may occur as a neurological complication of systemic, toxic, or other medical diseases, including nonketotic hyperglycemia in patients with diabetes mellitus . Chorea associated with nonketotic hyperglycemia (C‐NKH) with basal ganglia lesions occurs predominantly in Asian countries, although C‐NKH also has been reported in patients of all ethnic backgrounds . Uremic patients also may develop chorea associated with reversible lesions in the basal ganglia .…”

mentioning

confidence: 99%

See 1 more Smart Citation

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

Kim

et al. 2015

Movement Disorders

View full text Add to dashboard Cite

This study was undertaken to describe the clinical and imaging characteristics of patients with chorea associated with nonketotic hyperglycemia (C-NKH) in comparison with patients with chorea associated with uremia (C-URE). We retrospectively analyzed the clinical data of consecutive 10 C-NKH and five C-URE patients who were treated between January 1, 2001 and January 31, 2013. Women were more frequently affected by C-NKH (70% vs. 30%) and C-URE (80% vs. 20%) compared with men. The C-NKH patients demonstrated T1-hyperintense and inhomogeneous lesions in the basal ganglia, whereas C-URE patients demonstrated T2-hyperintense and homogeneous lesions in the basal ganglia. The mean time for chorea resolution after treatment was significantly shorter in C-NKH patients than in C-URE patients (4.4 ± 2.6 d vs. 73.8 ± 14.2 d, respectively; P = 0.005). The clinical and imaging features are remarkably different between C-NKH and C-URE patients, suggesting distinct pathogenic mechanisms.

show abstract

Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

Kim

et al. 2015

Movement Disorders

View full text Add to dashboard Cite

show abstract

“…1 Extended lesions at MRI were associated with prolonged involuntary movements. 5 Our findings of focal atrophy strengthen these results, suggesting a role of the pathological disease severity, in-vivo assessed by MRI, to determine the persistence of the disorder. We hypothesize that a mild disorder, solved with anti-chorea treatment, might be associated with a lower degree of atrophy, unrecognized without a volumetric analysis.…”

supporting

confidence: 80%

Striatal Atrophy and Hypometabolism in Drug‐Resistant Non‐Ketotic Hyperglycemic Chorea‐Ballism

Scamarcia

Anzalone

Volontè

et al. 2021

Movement Disord Clin Pract

View full text Add to dashboard Cite

“…The protracted clinical course was not related to DM control. Delayed introduction of DRB and an extended lesion were suggested as risk factors for persistent CB, but were not applicable to our case 2 …”

mentioning

confidence: 58%

“…Delayed introduction of DRB and an extended lesion were suggested as risk factors for persistent CB, but were not applicable to our case. 2 Because dystonic movement was mixed with chorea in the early phase of the recurrence, post-stroke dystonia or pseudoathetosis related to the thalamic infarction is to be considered. Interestingly, the involuntary movements became purely choreic afterwards.…”

mentioning

confidence: 99%

Abolition of Hyperglycaemic Hemichorea and Recurrence after Medical Illness

Lee

Ahn

Hong

2016

Can. J. Neurol. Sci.

View full text Add to dashboard Cite

Choreoballism (CB) can develop as a complication of diabetes mellitus (DM). Although the recurrence of CB was reported, it was related to drug discontinuation or transient hyperglycaemia or was without evident provoking factors.1 Herein, we report a case of hyperglycaemic CB that persisted for longer than a year, was resolved by cerebral infarction, and then returned after medical illness.A 62-year-old woman with poorly controlled DM visited our department due to sudden-onset involuntary movements. Her neurological examination (NE) was normal, with the exception of involuntary movements consisting of continuous, irregular, mixed choreic and ballistic movements involving the left face, arm and leg. At admission, her serum glucose was 195 mg/dl and her glycated haemoglobin (HbA1c) 16.2%. MRI showed hypointensities on T2-weighted image, hyperintensities on T1-weighted image and normal diffusion-weighted image in the right putamen ( Figure 1A). 18F-fluorodeoxyglucose positron emission tomography ( 18 F-FDG-PET) showed hypometabolism in the right putamen ( Figure 1D).Serum glucose was controlled (HbA1c < 7 %). Various drugs including haloperidol and tetrabenazine were ineffective for CB. She showed postural instability after anti-dopaminergic drugs including clozapine. The second MRI showed no new lesions. 18F-fluorinated N-3-fluoropropyl-2-beta-carboxymethoxy-3-beta-(4-iodophenyl) nortropane ( 18 F-FPCIT) PET showed decreased uptake in the right putamen ( Figure 1B). Levodopa was effective. Both clozapine and levodopa were tapered, leaving CB as the lone symptom. She had been followed up for persistent CB for 15 months until sudden-onset left hemiparesis developed. The third MRI showed an acute infarction in the right thalamus (Th) and corona radiata (CR; Figure 1C). NE showed left hemiparesis without sensory deficit. After she recovered from hemiparesis, she remained free of CB. Three years later, she was hospitalized for coronary heart disease and an appendectomy (HbA1c < 7.5%). The hemichorea returned during hospitalization without any suspected drugs. Choreic movements of her left hand were temporarily mixed with dystonia in the early follow-up but became purely choreic later. No new lesion was demonstrated on the fourth MRI. 18F-FDG-PET was repeated and compared with the previous using voxel-based subtraction analysis, demonstrating decreased metabolism in the right subthalamic nucleus (STN), caudate nucleus (CN), putamen and Th ( Figure 1E-F).Because of multiple morbidities and mildly severe hemichorea, only clonazepam was added. Her hemichorea persisted for longer than a year.The patient's CB was present for 15 months before an infarction and persisted after recurrence. The protracted clinical course was not related to DM control. Delayed introduction of DRB and an extended lesion were suggested as risk factors for persistent CB, but were not applicable to our case. 2Because dystonic movement was mixed with chorea in the early phase of the recurrence, post-stroke dystonia or pseudoathetosis related to the th...

show abstract

Risk factors for prolonged hemichorea-hemiballism caused by hyperglycemia

Cited by 8 publications

References 5 publications

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

Chorea due to diabetic hyperglycemia and uremia: Distinct clinical and imaging features

Striatal Atrophy and Hypometabolism in Drug‐Resistant Non‐Ketotic Hyperglycemic Chorea‐Ballism

Abolition of Hyperglycaemic Hemichorea and Recurrence after Medical Illness

Contact Info

Product

Resources

About