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A 76-year-old woman was admitted to our hospital with chorea in her left arm and leg. She also suffered from poorly controlled diabetes. Her arm and leg flexed and shook, and these movements were worsened by stress and disappeared during sleep. Neurological examinations were otherwise normal. The blood glucose level was 232 mg/dl and glycosylated hemoglobin A1c was 13.9%. Magnetic resonance (MR) showed high signal intensity on T1-weighted images (T1-WI) in the right striatum, and low signal intensity on T2-weighted images (T2-WI). T2*-weighted gradient-echo magnetic resonance imaging showed low signal intensity that gradually became even lower, suggesting petechial hemorrhage. SPECT showed normal blood flow in the right striatum under these conditions, and gradually decreased. The patient's diabetes was controlled with insulin, and the hemichorea improved on treatment with tiapride up to 75 mg per day, haloperidol up to 2.25 mg per day. Hemichorea with hyperglycemia is a disorder that is associated with poorly controlled diabetes, old age, and high signal intensity on T1-weighted MR imaging in the striatum contralateral to the hemichorea. The pathophysiology of the hemichorea is presumed to be ischemic changes in the striatum associated with hyperglycemia and hyperviscosity. The MR findings in our patient suggest petechial hemorrhage following ischemic change, although petechial hemorrhage has not been reported in similar cases in the recent literature. The striatal hyperactivity may be associated with the onset of hemichorea in our patient.
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PMID:[A case of hemichorea with hyperglycemia presenting with low signal intensity in the striatum on T2*-weighted gradient-echo magnetic resonance imaging]. 1519 55

We here report one case of hemichorea and Broca aphasia occurred with diabetic ketoacidosis. A 20-year-old woman with type 1 diabetes mellitus had experienced diabetic ketoacidosis fourth time after the onset of diabetes. At the third ketoacidotic episode, the patient was admitted to our hospital for the first time to show hemichorea of the left extremities. Brain computed tomography (CT) demonstrated a high-density area in the right caudate head and low-density area in the right putamen. Magnetic resonance angiography (MRA) demonstrated a stenosis at the root of the bilateral middle and anterior cerebral arteries. The hemichorea disappeared within 3 days. At the fourth ketoacidotic episode, not hemichorea but unconsciousness was there for 2 days even after ketoacidosis disappeared. After the unconscious state, Broca aphasia was demonstrated for 15 days. The cerebral angiography showed a finding compatible to Moyamoya disease. These findings support that chorea and Broca aphasia induced by diabetic ketoacidosis was developed in addition to blood vessel abnormalities such as Moyamoya disease. We suggest that poorly controlled diabetic patients with hemichorea should undergo cerebral angiography.
Diabetes Res Clin Pract 2005 Feb
PMID:Chorea and Broca aphasia induced by diabetic ketoacidosis in a type 1 diabetic patient diagnosed as Moyamoya disease. 1564 79

We report herein the case of a 28-year-old man presenting with hyperglycemic chorea-ballism (HCB) in addition to mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). He was admitted to a local hospital due to weight loss, general fatigue and thirst. The patient had diabetes mellitus, with a blood glucose level of 738 mg/dl and HbA1c of 19.8%. Although insulin therapy improved hyperglycemia, he noticed involuntary movements in the right upper and lower limbs, which subsequently extended to the left side. The patient was thus transferred to our hospital. He displayed short stature (154 cm) and emaciation, and a maternal family history of diabetes mellitus was elicited. He had no history of stroke-like episode, headache, vomiting and seizure. Neurological examination revealed low intelligence (IQ 57), mild sensorineural deafness, and chorea-ballism in the extremities and head without ptosis or eye movement disturbance. Brain computed tomography (CT) demonstrated areas of high density, while T1-weighted magnetic resonance imaging (MRI) revealed extreme hyperintensity and T2-weighted MRI showed hyperintensity in bilateral caudate nuclei, putamina and globi pallidus. HCB was diagnosed. In, CSF, lactate level was increased to 43.9 mg/dl (n, 4-16), pyruvate level was 1.65 mg/dl (n, 0.3-0.9) and total protein concentration was 59 mg/dl. Histological examination of a biopsy sample from the biceps brachii muscle demonstrated ragged-red fibers. An A3243G point mutation in the tRNA(Leu(UUR)) gene was detected, indicating the presence of MELAS. Involuntary movements improved on treatment with haloperidol up to 4.5 mg/day. HCB usually appears in elderly individuals, and cases less than 40-years-old are very rare. The mitochondrial dysfunction in MELAS may accelerate development of HCB.
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PMID:[A case of MELAS presenting juvenile-onset hyperglycemic chorea-ballism]. 1611 32

We describe an 81-year-old woman presenting with sudden onset of generalised chorea. She was unaware of suffering from diabetes. Laboratory screening revealed non-ketotic hyperglycaemia. Brain magnetic resonance imaging (MRI) failed to show basal ganglia abnormalities. Monotherapy with subcutaneous regular insulin induced a progressive normalisation of glycaemia as well as a parallel improvement of the abnormal involuntary movement scale on a nine-day sequential observation. This correlation strongly supports the hypothesis that non-ketotic hyperglycaemia itself might play a major pathogenetic role in chorea associated with non-ketotic hyperglycaemia. Diabetes mellitus should be suspected in patients who develop sudden onset of chorea even in the absence of putaminal abnormalities on MRI.
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PMID:Chorea induced by non-ketotic hyperglycaemia: a case report. 1619 55

Delusional parasitosis (DP) is a psychotic condition in which a person has the unshakeable and mistaken belief (delusion) and/or aberrant perception (hallucination) of being infested with parasites. The disorder will be usually classified in a primary DP-group without a detectable cause (so-called pure forms), while secondary DP-groups are associated with general organic conditions, psychiatric illnesses and drugs (substance induced). Etiology and pathophysiology of DP remain however unknown. In the present paper we hypothesize for the first time a decreased striatal dopamine transporter (DAT)-functioning (corresponding with an increased extracellular dopamine-level) as etiologic condition for DP (primary and secondary groups). The DAT as key regulator of the dopamine-reuptake in the human brain is well known (regulation of the extracellular dopamine concentration). It is a presynaptic plasma membrane protein highly dense represented in the striatum. The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP. Several other associated causes of secondary DP-groups (medications, parkinson, chorea huntington, multiple system atrophy, diabetes, cerebrovascular diseases, alcoholism, traumatic brain injury, hyperuricemia, human immunodeficiency virus, iron deficiency, schizophrenia, depression) suggest that the clinical expression of DP may be related to a decreased striatal DAT-functioning (blocking, reduced ligand binding, reduced density, reduced activity). Our examined DP-cases (2-females) show means of magnetic resonance imaging a structurally damaged striatum. Furthermore, we presume that by the primary DP-group, the physiologically age-related decline of the DAT-density is pathologically elevated. Based on this hypothesis we show in the present paper the relation between DP and decreased striatal DAT-functioning, trying to give a new insight into the pathophysiologically mechanism involved. The hypothesis provides supporting evidence that increased levels of extracellular dopamine in the striatum of DP-patients is likely to be the result of decreased DAT-functioning and not increased rates of release. The hypothesis can be investigated simply by dopamine transporter imaging in patients with DP.
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PMID:Delusional parasitosis and the dopamine transporter. A new insight of etiology? 1713 47

The importance of physical activity in the management of diabetes is well established. The effect of programmed exercise and measurable skeletal activities on diabetes has been variously studied. Chorea induces an increase in spontaneous movement. Its occurrence in a teenager with type 1 diabetes provides new insights into our knowledge of metabolic outcomes. In our patient, the reduction in daily insulin demand was linked to choreic movement: a 67% decrease in insulin supply was needed to avoid episodes of hypoglycaemia; moreover, improved metabolism (measured as glycated haemoglobin) was obtained. Since no dietary changes were made and clinical events (including fever, drugs, weight loss, voluntary physical activity, psychological opposition or refusal of treatment) interfering with metabolic control of diabetes occurred, it appeared that only increased physical movements due to chorea reduced the patient's insulin requirement. As spontaneous movements declined with healing, metabolic control was lost, requiring an increase in insulin dosage to restore it. This article sheds additional light on our current understanding of hypoglycaemia and the variability of exogenous insulin demand in childhood and adolescent diabetes, when there are spontaneous movements and play. This finding highlights the importance of movement in type 1 diabetes.
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PMID:Transient chorea in a patient with type 1 diabetes may induce a reduction in insulin demand through increased spontaneous movements. 1730 25

Chorea and ballism are movement disorders that result from a variety of conditions. Hyperglycemia is an unusual recognized cause of these movement disorders. We report 3 cases of new-onset chorea-ballism induced by nonketotic hyperglycemia in elderly patients, highlighting that chorea may be the first manifestation of undiagnosed decompensated diabetes mellitus.
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PMID:Chorea-ballism as a manifestation of decompensated type 2 diabetes mellitus. 1749 37

Woodhouse Sakati syndrome is a rare autosomal recessive neuroendocrine disorder characterized by the combination of alopecia, hypogonadism, diabetes mellitus, mental retardation, sensory neural deafness and extrapyramidal features. Movement disorders mainly consist of dystonia and chorea of the limbs with onset in adolescence. Facial muscles are usually spared, but dysarthria is common. Pyramidal features and peripheral abnormalities are inconsistent features. Most of the reported families are from the Middle Eastern countries although rarely Caucasian cases have been described. Here we present clinical details of two affected siblings from a new Middle East family and draw attention of movement disorder specialists to this entity. We summarize findings from pervious cases with particular focus on neurological and movement disorder features.
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PMID:Dystonia in the Woodhouse Sakati syndrome: A new family and literature review. 1817 54

Patients with vitamin B12 deficiency have protean neurological manifestations that are often insidious. Acute onset of cerebellar dysfunction and extrapyramidal manifestations like dystonia and chorea are rather uncommon in adults. We describe a patient who manifested with acute onset of language dysfunction, chorea and ataxia. There was no history of hypertension, diabetes or ischemic heart disease. He had low serum vitamin B12 and elevated serum homocystine levels. He improved dramatically following B12 replacement therapy. Our patient provides insight into the pathophysiological mechanism of this rare manifestation. Further the importance of considering vitamin B12 deficiency, in country like India, where vegetarian food practice is quite common, is being emphasized.
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PMID:Serum vitamin B12 deficiency and hyperhomocystinemia: a reversible cause of acute chorea, cerebellar ataxia in an adult with cerebral ischemia. 1867 79

Diabetic patients during hyperglycaemic crises may present a rare syndrome characterised by a typical triad: unilateral involuntary movements (hemichoreahemiballism), radiological contralateral striatal abnormality, and rapid resolution of symptoms after glycae - mic correction. This study reports a series of patients showing less usual aspects and also discusses the pathophysiology of this clinical-radiological syndrome. We included in this study four patients presenting choreic or ballic involuntary movements and in whom aetiological assessment revealed frank non-ketotic hyperglycaemia, without other abnormalities that could explain the movement disorder. All the patients underwent CT or MR brain imaging. The typical triad was present in only one case. Less classical aspects were more frequently found: movement disorders revealed diabetes in two patients and one patient had generalised chorea and strictly normal neuroimaging. Correction of blood glucose was not sufficient to improve symptoms in two cases. In one, abnormal movements persisted despite treatment with tetrabenazine. The clinical, radiological and outcome spectrum of the syndrome of chorea-ballismus induced by non-ketotic hyperglycaemia is heterogeneous and not restricted to a typical triad.
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PMID:Chorea-ballismus in acute non-ketotic hyperglycaemia. 2001 39


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