Network localization of hemichorea-hemiballismus

Objective: To determine whether neuroanatomically heterogeneous strokes causing hemichorea-hemiballismus localize to a common functional network. Methods: We identified 29 cases of lesion-induced hemichorea-hemiballismus from the literature and mapped each lesion volume onto a reference brain. Using a recently validated technique termed lesion network mapping, we tested whether these lesions belonged to the same functional network. To accomplish this, the network of brain regions functionally connected to each lesion was identified using a connectome dataset from healthy participants. Network maps were overlapped to identify any region functionally connected to our set of lesions. Specificity was evaluated using a case-control design; control cohorts included a group of similar lesions randomized to different brain locations and a second group of lesions causing a separate movement disorder, asterixis. Reproducibility was evaluated using an independent cohort of 10 additional hemichorea-hemiballismus cases. Results: Lesions showed heterogeneity in anatomical location, consistent with prior reports. However, at least 90% of these lesions showed network overlap in the posterolateral putamen. This result was specific to lesions causing hemichorea-hemiballismus and reproducible in an independent cohort. The putaminal overlap site was itself connected to a broader motor network that predicted the distribution of lesions causing hemichorea-hemiballismus. Conclusions: Strokes causing hemichorea-hemiballismus, while anatomically heterogeneous, localize to a common functional network. Specifically, lesions occur in regions functionally connected to the posterolateral putamen, a region previously implicated in hyperkinetic movement disorders. Lesion network mapping may be useful in identifying the neuroanatomical substrates of heterogeneous lesion-based disorders.

[1]  J. P. Martin HEMICHOREA RESULTING FROM A LOCAL LESION OF THE BRAIN. (THE SYNDROME OF THE BODY OF LUYS , 1927 .

[2]  F. Mettler,et al.  Studies on the subthalamus of the rhesus monkey. II. Hyperkinesia and other physiologic effects of subthalamic lesions, with special reference to the subthalamic nucleus of Luys , 1949 .

[3]  L. Barrows,et al.  Hemiballism without involvement of Luys' body. , 1960, Archives of neurology.

[4]  C. Kase,et al.  Hemichorea‐hemiballism and lacunar infarction in the basal ganglia , 1981, Neurology.

[5]  C. Kase,et al.  Hemichorea‐hemiballism and lacunar infarction in the basal ganglia , 1981, Neurology.

[6]  G. E. Alexander,et al.  Parallel organization of functionally segregated circuits linking basal ganglia and cortex. , 1986, Annual review of neuroscience.

[7]  N. Takahashi,et al.  Hemichorea and its denial in a case of caudate infarction diagnosed by magnetic resonance imaging. , 1988, Journal of neurology, neurosurgery, and psychiatry.

[8]  M. Delong,et al.  Primate models of movement disorders of basal ganglia origin , 1990, Trends in Neurosciences.

[9]  V. Ibáñez,et al.  Presynaptic and postsynaptic striatal dopaminergic function in neuroacanthocytosis: A positron emission tomographic study , 1991, Annals of neurology.

[10]  B. Jenkins,et al.  Selective putaminal excitotoxic lesions in non-human primates model the movement disorder of Huntington disease , 1995, Neuroscience.

[11]  S. Lehéricy,et al.  Striatopallidal and thalamic dystonia. A magnetic resonance imaging anatomoclinical study. , 1996, Archives of neurology.

[12]  I. Wilkinson,et al.  Cranial MR imaging in Wilson's disease. , 1996, AJR. American journal of roentgenology.

[13]  Alan C. Evans,et al.  Dopamine transporters are markedly reduced in Lesch-Nyhan disease in vivo. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[14]  J. Bogousslavsky,et al.  Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry , 1997, Journal of the Neurological Sciences.

[15]  David C. Van Essen,et al.  Application of Information Technology: An Integrated Software Suite for Surface-based Analyses of Cerebral Cortex , 2001, J. Am. Medical Informatics Assoc..

[16]  Jong S. Kim Asterixis after unilateral stroke: Lesion location of 30 patients , 2001, Neurology.

[17]  Seung-Hun Oh,et al.  Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI study a meta-analysis of 53 cases including four present cases , 2002, Journal of the Neurological Sciences.

[18]  이경열 Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI study: a meta-analysis of 53 cases i , 2002 .

[19]  A. Lang,et al.  Hemiballism: revisiting a classic disorder , 2003, The Lancet Neurology.

[20]  S. Chung,et al.  Hemichorea after stroke: Clinical-radiological correlation , 2004, Journal of Neurology.

[21]  N. Swindale,et al.  Diffusion tensor fiber tracking shows distinct corticostriatal circuits in humans , 2004, Annals of neurology.

[22]  F. Alarcón,et al.  Post-stroke movement disorders: report of 56 patients , 2004, Journal of Neurology, Neurosurgery & Psychiatry.

[23]  D. Centonze,et al.  Improvement of choreic movements by 1Hz repetitive transcranial magnetic stimulation in Huntington's disease patients , 2005, Annals of neurology.

[24]  Chris Rorden,et al.  Improving Lesion-Symptom Mapping , 2007, Journal of Cognitive Neuroscience.

[25]  B. Biswal,et al.  Functional connectivity of human striatum: a resting state FMRI study. , 2008, Cerebral cortex.

[26]  J. Ghika Mouvements anormaux et accident vasculaire cérébral , 2008 .

[27]  [Movement disorders in stroke]. , 2008, Revue neurologique.

[28]  A. Handley,et al.  Movement disorders after stroke. , 2008, Age and ageing.

[29]  S. Tian Chorea associated with non-ketotic hyperglycemia , 2011 .

[30]  C. Tsai,et al.  Reversible abnormal functional neuroimaging presentations in polycythemia vera with chorea , 2011, Journal of Neurology.

[31]  Cathy J. Price,et al.  A comparison of VLSM and VBM in a cohort of patients with post-stroke aphasia☆ , 2012, NeuroImage: Clinical.

[32]  R. Buckner,et al.  Efficacy of Transcranial Magnetic Stimulation Targets for Depression Is Related to Intrinsic Functional Connectivity with the Subgenual Cingulate , 2012, Biological Psychiatry.

[33]  J. Hawley,et al.  Hemiballismus: current concepts and review. , 2012, Parkinsonism & related disorders.

[34]  Christopher A. Ross,et al.  Striatal Volume Contributes to the Prediction of Onset of Huntington Disease in Incident Cases , 2012, Biological Psychiatry.

[35]  Alvaro Pascual-Leone,et al.  Measuring and manipulating brain connectivity with resting state functional connectivity magnetic resonance imaging (fcMRI) and transcranial magnetic stimulation (TMS) , 2012, NeuroImage.

[36]  Michał Sobstyl,et al.  Right hemichorea treated successfully by surgical removal of a left putaminal cavernous angioma , 2013, Clinical Neurology and Neurosurgery.

[37]  R. Buckner,et al.  Resting-state networks link invasive and noninvasive brain stimulation across diverse psychiatric and neurological diseases , 2014, Proceedings of the National Academy of Sciences.

[38]  M. Hallett,et al.  Where does chorea come from? Cortical excitability findings challenge classic pathophysiological concepts , 2015, Movement disorders : official journal of the Movement Disorder Society.

[39]  Á. Pascual-Leone,et al.  Network localization of neurological symptoms from focal brain lesions. , 2015, Brain : a journal of neurology.

[40]  Bruce R. Rosen,et al.  Brain Genomics Superstruct Project initial data release with structural, functional, and behavioral measures , 2015, Scientific Data.