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      Encephalopathy, Hypoglycemia, and Flailing Extremities: A Case of Bilateral Chorea–Ballism Associated with Diabetic Ketoacidosis

      case-report

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          Abstract

          Background

          Hypo/hyperglycemia is a known cause of chorea and hemiballism. The temporallobes, hippocampus, basal ganglia, and substantia nigra are most susceptible to hypoglycemic changes.

          Methods

          We present a caseof bilateral chorea and bi-ballism accompanied by encephalopathyin the setting of severe hypoglycemia and diabetic ketoacidosis. The patient had brain MRI changes involving both caudate nuclei, temporal lobes, and hippocampi.

          Discussion

          This case demonstrates the basal ganglia's vulnerability to hypoglycemia and the need for cautious evaluation of involuntary movements when they occur in the setting of encephalopathy.

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          Most cited references21

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          Hemichorea-hemiballism: an explanation for MR signal changes.

          Some cases of hemichorea-hemiballism (HCHB) are associated with a hyperintense putamen on T1-weighted MR images, the cause of which remains unclear. Our purpose was to determine the cause and significance of these MR signal changes. We analyzed the clinical and neuroimaging findings in 10 patients with HCHB, focusing on locations of the hyperintense lesions on T1-weighted images, comparing them with those on CT scans, and evaluating their changes after years of follow-up. A biopsy was performed in one patient. Seven patients had hyperglycemia and two had cortical infarcts. HCHB recurred in four patients. A hyperintense putamen preceded the occurrence of HCHB in two patients. T1-weighted MR images revealed hyperintense lesions limited to the ventral striatum in six patients. Hyperintense lesions extended to the level of the midbrain in one patient and persisted for as long as 6 years in another patient. T2-weighted MR images revealed slit-shaped cystic lesions in the lateral part of the putamina 2 to 6 years after the onset of symptoms in two patients. A biopsy specimen from the hyperintense putamen in one patient revealed a fragment of gliotic brain tissue with abundant gemistocytes. Proton MR spectroscopy of the specimen showed an increase in lactic acid, acetate, and lipids, and a decrease in N-acetylaspartate and creatine, suggesting the presence of pronounced energy depletion and neuronal dysfunction. Gemistocytes are sufficient to explain the shortening of T1 relaxation time. Our investigation suggests that neurons in the ventral striatum and striatonigral pathway may play a critical role in generating ballism.
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            Specific changes in human brain after hypoglycemic injury.

            Very few reports are available on serial changes in the human brain after severe hypoglycemic injury. The aim of this study was to investigate sequential neuroradiological changes in brains of patients after hypoglycemic coma compared with those after cardiac arrest previously studied with the same methods. We repeatedly studied CT scans and MR images obtained at 1.5 T in four vegetative patients after profound hypoglycemia associated with diabetes mellitus. In all patients, consecutive CT scans showed symmetrical, persistent low-density lesions with transient enhancement in the caudate and lenticular nuclei and transient enhancement in the cerebral cortex 7 to 14 days after onset. Serial MR images consistently revealed symmetrical lesions of persistent hyperintensity and hypointensity on T1- and T2-weighted images, respectively, in the caudate and lenticular nuclei, cerebral cortex, substantia nigra, and/or hippocampus from 8 days to 12 months after onset. Repeated MR images revealed specific lesions in the bilateral basal ganglia, cerebral cortex, substantia nigra, and hippocampus, which suggests the particular vulnerability of these areas to hypoglycemia in the human brain. We speculate that the localized lesions represent tissue degeneration, including some combination of selective neuronal death, proliferation of astrocytic glial cells, paramagnetic substance deposition, and/or lipid accumulation. The absence of localized hemorrhages on MR images in hypoglycemic encephalopathy is in marked contrast to the presence of regional minor hemorrhages in postischemic-anoxic encephalopathy.
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              Diabetic striatal disease: clinical presentation, neuroimaging, and pathology.

              Unilateral movement disorders and contralateral neuroimaging abnormalities of the striatum have been sporadically reported as a rare syndrome associated with diabetes mellitus. Despite characteristic imaging findings and clinical manifestations, the mechanism underlying this syndrome is still unclear. Six patients with this syndrome were studied clinically and subjected to MRI neuroimaging; one underwent biopsy of the striatum, and another underwent additional MR spectroscopy at 3.0T and FDG-PET. Neuroimaging findings were characterized by a T1-hyperintense unilateral lesion restricted to the striatum, contralateral to the symptomatic limbs. The biopsied striatum contained patchy necrotic tissue, severe thickening of all layers of arterioles, and marked narrowing of vessel lumens. Hyaline degeneration of the arteriolar walls, extravasation of erythrocytes, and prominent capillary proliferation were also notable, together with lymphocytic infiltration and macrophage invasion. In one patient, PET examination revealed decreased accumulation of FDG in the lesion. The MR spectrum for the diseased striatum revealed a decrease in the NAA/Cr ratio (1.35), normal Cho/Cr ratio (1.22), and a peak for myoinositol, while the spectrum on the contralateral site revealed a decrease in the NAA/Cr ratio (1.48), increase in Cho/Cr (1.32), but no peak for myoinositol. The constellation of signs and symptoms and neuroimaging characteristics in previous reports and the six additional cases described here with neuropathological data and findings of MR spectroscopy appears unique enough to be termed "diabetic striatopathy." This syndrome appears in poorly controlled diabetics due to obliterative vasculopathy with prominent vascular proliferation, vulnerability to which is restricted to the striatum.
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                Author and article information

                Journal
                Tremor Other Hyperkinet Mov (N Y)
                Tremor Other Hyperkinet Mov (N Y)
                TOHM
                Tremor and Other Hyperkinetic Movements
                Columbia University Libraries/Information Services
                2160-8288
                2012
                27 June 2012
                : 2
                : tre-02-58-235-1
                Affiliations
                [1 ]University of Florida, Department of Neurology, Center for Movement Disorders & Neurorestoration, Gainesville, Florida, United States of America
                Columbia University, United States of America
                Author notes
                *To whom correspondence should be addressed. E-mail: nikolaus.mcfarland@ 123456neurology.ufl.edu
                Article
                tre-58-235-1
                3569973
                23439397
                af935512-c9ed-4745-a156-e407afbc4a31
                Copyright @ 2012

                This is an open-access article distributed under the terms of the Creative Commons Attribution–Noncommerical–No Derivatives License, which permits the user to copy, distribute, and transmit the work provided that the original author and source are credited; that no commercial use is made of the work; and that the work is not altered or transformed.

                History
                : 22 August 2011
                : 28 October 2011
                Page count
                Pages: 4
                Categories
                Case Report

                encephalopathy,hypoglycemia,chorea,ballism,diabetic ketoacidosis,hyperglycemia

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