Nonketotic Hyperglycemia Hemichorea: the Initial Presenting Symptom of Diabetes Mellitus
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MEDICINE
Nonketotic Hyperglycemia Hemichorea: the Initial Presenting Symptom of Diabetes Mellitus Ibrahim Labbad 1
&
Yaser A. Saleh 1
Accepted: 10 August 2020 / Published online: 13 August 2020 # Springer Nature Switzerland AG 2020
Abstract Diabetes mellitus is a common disease, but sometimes it presents with unusual manifestations. In our case, we describe a 53-yearold female patient with a rare movement disorder, which is hemichorea as a complication of nonketotic hyperglycemia. The hyperkinesia was the initial presenting symptom of diabetes mellitus. Diagnosis was made by the presence of the classic triad: unilateral involuntary movements, contralateral striatal abnormalities on neuroimaging, and nonketotic hyperglycemia. Although it is a well-recognized syndrome, this is the first case report from Syria. Keywords Chorea . Hyperglycemia . Nonketotic . Movement disorder
Introduction Chorea is a movement disorder that contains involuntary, irregular, and random movements [1]. It can be an isolated symptom or associated with behavioral and cognitive symptoms or other neurologic symptoms. The presence of hemichorea suggests a focal structural brain lesion secondary to a vascular event, metabolic disorder such nonketotic hyperglycemia, or an infection [2].
Case Presentation A 53-year-old woman presented to our hospital with a 2month history of right-sided hemiballistic movements. The movements disappeared during sleep. On physical examination, her muscle tone and strength were normal bilaterally. There was no evidence of sensory impairment, and cranial nerves were normal. The deep tendon reflexes were hypoactive. She had a first-degree family history of diabetes mellitus, but her previous medical history was unremarkable.
Serum glucose level was 441 mg/dl with no ketones present either in blood or urine. The percentage of glycated hemoglobin (HbA1C) was 12.9%. Electrolyte and hormone panel were normal. Measured serum osmolality was 320 mOsm/l. Peripheral blood cell counts and renal and hepatic functions were normal. Ceruloplasmine in blood was 31 mg/dl. At admission, unenhanced computed tomography (CT) of the brain showed hyperattenuation of the left putamen and the head of left caudate nucleus (Fig. 1), and magnetic resonance imaging (MRI) demonstrated abnormal hyperintense signals in the left caudate nucleus, left putamen, and globus pallidus on T1-weighted images (Fig. 2) and isointensity on T2weighted images. No enhancement was noticed after contrast injection. Diffusion-weighted images and T2* gradient echo images revealed normal signal intensity in the left putamen (Fig. 3). There was no evidence of mass effect. After admission, the patient’s blood sugar was controlled with insulin; this led to a steady correction of hyperglycemia in the subsequent days. The involuntary movements progressively decreased over the next few days until they disappeared on the tenth day. Two months later, follow up showed no recurrence of the involuntary movements.
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