Hemichorea Hemiballism Research Articles

Nonketotic Hyperglycemic Hemichorea Hemiballism as the Debut of Diabetes in An 80-Year-Old Woman: Case Report

Diabetes Mellitus is a chronic metabolic disease that constitutes one of the most serious public health problems worldwide. With the advent of new drugs and advances in the understanding of its etiopathogenesis, the quality of life of patients suffering diabetes mellitus has been improved. However, the large number of complications to which patients are exposed remains a challenge for health professionals, being the most frequent from cardiovascular nature, renal, retinal, peripheral nervous system and even increasing the risk of mortality. Not much has been documented about the consequent relationship of movement disorders as a result of metabolic alterations, although cases of glucotoxicity and hyperkinetic disorders such as chorea and ballism have been described. In the present article we describe the case of an 80-year-old woman with diabetes mellitus in poor metabolic control, associated with hemichorea and ballism.

Irreversible Hemichorea–Hemiballism in a Case of Nonketotic Hyperglycemia Presenting as the Initial Manifestation of Diabetes Mellitus

Irreversible Hemichorea–Hemiballism in a Case of Nonketotic Hyperglycemia Presenting as the Initial Manifestation of Diabetes Mellitus

Movement disorders and stroke

Stroke may be associated with different types of movement disorders, such as hyperkinetic syndromes (hemichorea–hemiballism, unilateral asterixis, limb-shaking, dystonia, tremor, myoclonus) and hypokinetic syndromes (especially vascular parkinsonism). However, movement disorders are rare and transient in acute stroke and, as a permanent consequence, are more often delayed. While ischemic and hemorrhagic strokes can happen at any level of the frontal–subcortical motor system, they can be explained most of the time by a dysfunction in the basal ganglia motor circuit. However, only brain MRI allows the involved structure(s) to be precisely located, and each syndrome is specific to the type of lesion. Treatment is above all symptomatic. Only limb-shaking syndrome requires urgent surgical treatment because of the low-perfusion hemodynamic state. The functional prognosis depends on the type of movement disorder.

Chorea associated with nonketotic hyperglycemia: An uncommon patient with bilateral movements

We report a 74-year-old woman who presented with bilateral chorea and no known history of diabetes. Movement disorders such as chorea can be observed in patients presenting with hyperglycemia. The occurrence of hemichorea–hemiballism has been increasingly associated with nonketotic hyperglycemia in the medical literature. The chorea disappeared completely after correction of the hyperglycemia.

Hemichorea–hemiballism: a case report

A 55-year-old woman with type 2 diabetes mellitus presented with abnormal left-sided movements of her arm and leg. Her initial CT scan of head showed a hyperintensity in the right...

Hyperglycemia-associated Hemichorea-hemiballism: The Spectrum of Clinical Presentation.

Hyperglycemia rarely manifests as hemichorea-hemiballism (HH), which is characterized by simple partial motor seizures. One of the difficulties in the management of hyperglycemia-induced HH is the failure to recognize this entity due to its relatively uncommon presentation. We herein present a case series of hyperglycemia-associated dyskinesias, highlighting the different possible clinical presentations of this entity. Both hyperglycemia and hyperosmolality are probable predisposing factors, while ketoacidosis has a protective role in preventing the dyskinesias. One of our patients had ketotic hyperglycemia leading to HH, a previously unreported finding. Early recognition of this entity is crucial as prompt glycemic control leads to the resolution of symptoms and signs.

Teaching Video NeuroImages: semiology and localization of ballistic movements.

Ballistic chorea (hemichorea–hemiballism) localizes to the subthalamic nucleus and its connections (video 1, figure, Aa) or the putamen (video 2, figure, Ab). Other large-amplitude hyperkinetic lesional movements can have similarly high localizing value. “Ballistic” tremor may develop months after recovering from ventrolateral thalamic strokes, in the thalamogeniculate vascular territory (video 3, figure, Ac and Ad).1 Similarly, “ballistic dystonia,” limb dystonia with superimposed arrhythmic and jerky movements often referred to as myoclonic dystonia, may develop months after recovering from combined vascular lesions in the striatum and posterior thalamus (video 4, figure, Ae and Af).2 These motor complications, delayed by hours to days (hemiballism) or weeks to months (ballistic dystonia and tremor), have relatively distinct localization value to a narrow “ballistic corridor” in the basal ganglia and thalamus (figure, B).

Chorea, Hyperglycemia, Basal Ganglia Syndrome (C-H-BG) in an uncontrolled diabetic patient with normal glucose levels on presentation.

Patient: Female, 66Final Diagnosis: Chorea • hyperglycemia • Basal Ganglia Syndrome (C-H-BG)Symptoms: Hemibalism • hemichoreaMedication: —Clinical Procedure: —Specialty: Endocrinology and MetabolicObjective:Challenging differential diagnosisBackground:Hemichorea-hemiballism (HCHB) is a spectrum of involuntary, continuous non-patterned movement involving 1 side of the body. Possible causes of HCHB include hemorrhagic or ischemic stroke, neoplasm, systemic lupus erythematosus, HHNK, Wilson’s disease, and thyrotoxicosis. This case illustrates the need to be aware of hyperglycemia as a cause of hemiballism/hemichorea, which is now referred to in the medical literature as C-H-BG (chorea, hyperglycemia, basal ganglia) syndrome.Case Report:A 66-year-old Hispanic woman presented to our care with hemiballism/hemichorea of the right arm and leg of 1 week duration. She had been admitted 3 months prior with toxic metabolic encephalopathy secondary to hyperosmolar hyperglycemic non-ketotic syndrome with a blood glucose level of 984 mg/dL. Her blood glucose level was normal but hemoglobin A1C was 12.2%. A brain MRI revealed an asymmetric T1 hyperintensity of the left putamen. This specific finding was compatible with hyperglycemia-induced hemichorea hemiballism syndrome. The hemiballism/hemichorea slowly improved over the course of the hospitalization with strict glycemic control. At the 3-month follow-up visit she had no involuntary movements of her extremities, and she had well controlled blood glucose levels and a hemoglobin A1C of 9.0.Conclusions:In a patient with normal glycemic levels but a history of uncontrolled diabetes, C-H-BG syndrome should be on the top of the differential list when the characteristic MRI findings of a hyperintensity in the basal ganglia are observed. This is a rare disease that deserves attention because it is reversible with correction of hyperglycemia. Thus, prompt recognition and treatment is essential to avoid adverse outcomes.

Resolution of Acute Onset Hemichorea–Hemiballismus After Treatment With Intravenous Tissue Plasminogen Activator

Hyperkinetic movement disorders are uncommon after acute ischemic stroke. Since these movement disorders are rarely the initial manifestation of acute cerebral ischemia, their presence may result in diagnostic uncertainty or it may inappropriately delay intravenous thrombolytic therapy for ischemic stroke. Hemichorea-hemiballism (HC-HB) is one of the more frequently encountered hyperkinetic movement disorders occurring in conjunction with stroke. Although HC-HB may result from a stroke mimic, the acute onset should prompt rapid evaluation and consideration for the presence of stroke along with its time-dependent therapies including recombinant tissue plasminogen activator (rtPA). In this article, we describe a case of a patient with acute cerebral ischemia presenting clinically with HC-HB, who was given intravenous rtPA therapy despite an initially negative, early diffusion-weighted magnetic resonance imaging (MRI). Follow-up brain MRI performed 24 hours after the initiation of thrombolytic therapy confirmed acute infarction in the contralateral striatum. The patient had near-complete resolution of her HC-HB on discharge and had no complications related to the administration of intravenous rtPA.

Diabetic hemichorea–hemiballism – Case report of a patient with enduring striatal lesion

This report describes a case of sudden onset of hyperglycaemic hemichorea–hemiballism as first manifestation of diabetes mellitus in a patient with previous history of Whipple’s surgery. Initial cranial computed tomography scanning and magnetic resonance imaging showed characteristic striatal lesions contralateral to the affected body side. A treatment with insulin led to an improvement of diabetic laboratory parameters but hyperkinesia still persisted and follow-up imaging revealed an enduring lesion in the posterior part of the caudate nucleus head.

Hemichorea–hemiballism syndrome following a thrombo-embolic striatal infarction

A 70-year-old man was admitted to our emergency department for sudden onset of abnormal involuntary movements involving his upper and lower left limbs. Hemichoreal movements were restricted to his left limbs, associated with rare episodes of hemiballism (video). There were no cranial nerve alterations, no sensory loss or limb weakness. The patient reported mild hypertension under treatment. There was no history of diabetes mellitus or epilepsy, no prior exposure to neuroleptics or recent change in therapy. He denied any similar previous episode or family history of movement disorders. Chest radiography, electrocardiography, and laboratory tests including glucose, glycated hemoglobin, coagulation parameters, and immunoglobulin electrophoresis were normal. Brain non-contrast CT scan on admission showed no signs of acute ischemia (Fig. 1a). A supra-aortic-trunk Doppler sonography revealed an irregular surface plaque, partly ulcerated, on the origin of the right internal carotid artery with stenosis of about 90 %, confirmed at CT angiography (Fig. 1b). Brain MRI examination, performed 3 days after onset of symptoms, showed a linear altered signal area in the right basal ganglia, mostly in globus pallidus, on diffusion weighted imaging (DWI) sequences (Fig. 1c). The area was also visualized on the apparent diffusion coefficient (ADC) map (Fig. 1d), and on fluid attenuated inversion recovery (FLAIR) sequences (Fig. 1e). T1-weighted sequences of the basal ganglia were unremarkable (Fig. 1f). MRI angiography did not reveal abnormalities in the intracranial circulation. Our patient was thus diagnosed having an acute left hemichorea–hemiballism (HCHB) syndrome, caused by a carotid-originating embolic stroke, which affected the right lenticular nucleus. Medical treatments included immediate unfractionated heparin infusion, followed by warfarin and atorvastatin, while waiting for surgical treatment of the right carotid artery stenosis. The movement disorder was symptomatically controlled by oral administrations of clonazepam. 2 months later, he underwent surgical revascularization of the internal right carotid stenosis by thromboendarterectomy. 3-month follow-up revealed considerable symptom reduction with minimally disabling residual movements.

Bilateral hemichorea–hemiballism caused by metastatic lung cancer

Bilateral hemichorea–hemiballism caused by metastatic lung cancer

A case report on pituitary macroadenoma presented as hemichorea hemiballism syndrome

A case report on pituitary macroadenoma presented as hemichorea hemiballism syndrome

Successful long-term deep brain stimulation for hemichorea—hemiballism in a patient with diabetes

The authors report a case of hemichorea-hemiballism (HC-HB) that was successfully treated using deep brain stimulation (DBS). A 65-year-old right-handed man exhibited a sudden onset of right HC-HB without a diabetic coma. At admission T1-weighted magnetic resonance (MR) images revealed a high-intensity signal in the left striatum, contralateral to the patient's involuntary movements. The HC-HB continued for 5 months after onset of the condition despite medical treatment and a decreased intensity of the signal on T1-weighted MR images. The patient underwent placement of a quadripolar DBS electrode in the left thalamus, including the left ventral oralis (VO) anterior and posterior nuclei (the VO complex). Postoperatively, the right-sided HC-HB disappeared rapidly during electrical stimulation and there were no neurological deficits. The authors demonstrate that DBS can be an effective treatment for medically refractory HC-HB. This is the first case of HC-HB that has been successfully treated with DBS.

Hemicorea inducida por cetoacidosis diabética e hiperdensidad estriatal en la tomografía axial computarizada

Hyperglycaemia, usually not ketotic, may cause hemichorea hemiballism. The mechanism of this physiopathological syndrome is still not clear. It usually occurs in elderly ladies and is associated with hyperdensity in the striate area contralateral to the affected side, on CT and MR potentiated in T1. Three days before hospital admission, and 86 year old woman presented with the acute onset of choreiform movements of her left limbs, particularly her left arm. She had not taken neuroleptic drugs and there was no family history of chorea. On neurological examination there were no other unusual findings. Laboratory tests showed hyperglycemia with metabolic acidosis and ketone bodies in the urine. On the CT scan there was a hyperdense lesion in the right striate area, but this did not act as a space occupying lesion. Treatment was started with intravenous insulin and the symptoms disappeared 48 hours later. We emphasize the rarity of the association of hemichorea and diabetic ketoacidosis. From the histological studies done in some of these patients, it seems that the hyperdensity of the striate area may be due to the proliferation of hypertrophic astrocytes secondary to small ischemic lesions. When the hyperglycaemia is treated, the chorea disappears within a few days and it is unusual for neuroleptic treatment to be required. In cases of hemichorea, hyperglycaemia should be ruled out, as should structural causes (tumors, infarcts, hematomas, traumatic lesions, etc.).

Do Striatal Petechial Hemorrhages Underlie Hyperglycemic Hemichorea-Hemiballism?

Hemichorea-hemiballism (HH) is typically caused by a vascular lesion in the contralateral basal ganglia structures, usually the striatum or the