Figure 1 Lesion locations causing cervical dystonia

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Figure 1 Lesion locations causing cervical dystonia Figure 1 Lesion locations causing cervical dystonia. A systematic literature search identified 25 cases of cervical ... Figure 1 Lesion locations causing cervical dystonia. A systematic literature search identified 25 cases of cervical dystonia with an identifiable lesion location that could be traced onto a standard brain atlas. Case numbers correspond to those in Table 1 and Supplementary Table 1, which provides additional clinical details of cases listed in Table 1. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 2 Lesion network mapping technique Figure 2 Lesion network mapping technique. In step one, lesions causing cervical dystonia were traced onto a standard ... Figure 2 Lesion network mapping technique. In step one, lesions causing cervical dystonia were traced onto a standard atlas. In step two, connectivity between each lesion location and the rest of the brain was computed using a normative dataset of resting state functional connectivity scans from 1000 healthy individuals, and a standard seed-based approach. In step three, functional connectivity maps were thresholded, binarized (functionally connected or not), and overlapped to identify voxels connected to the greatest number of lesion locations. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 3 Lesion network mapping of cervical dystonia Figure 3 Lesion network mapping of cervical dystonia. (A) Regions positively correlated (orange/yellow) or negatively ... Figure 3 Lesion network mapping of cervical dystonia. (A) Regions positively correlated (orange/yellow) or negatively correlated (blue/green) to lesion locations causing cervical dystonia (thresholded at 90% or 23/25 cases). From left to right: thalamus (z = 10); globus pallidus (z = −2); midbrain (z = −13); cerebellum (z = −32), and somatosensory cortex (projected onto the brain surface). (B) Regions that are both sensitive and specific to lesions causing cervical dystonia, with significantly greater (positive or negative) functional connectivity to lesion locations causing cervical dystonia compared to control lesion locations (conjunction across four separate specificity analyses). Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 4 Lesions causing cervical dystonia are part of a commonly connected brain network. The combination of positive ... Figure 4 Lesions causing cervical dystonia are part of a commonly connected brain network. The combination of positive connectivity to our cerebellum region of interest and negative connectivity to our somatosensory region of interest defines a network of regions (blue) that encompasses 24 of 25 lesion locations causing cervical dystonia (red). Case 8 lesion location falls immediately adjacent to this network. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 5 Relevance to idiopathic cervical dystonia Figure 5 Relevance to idiopathic cervical dystonia. Connectivity with our lesion-derived cerebellar region of interest ... Figure 5 Relevance to idiopathic cervical dystonia. Connectivity with our lesion-derived cerebellar region of interest (A, red) and somatosensory region of interest (B, blue) is abnormal in patients with idiopathic cervical dystonia. Patients with idiopathic cervical dystonia had a loss of negative functional connectivity from our cerebellar region of interest to the right sensorimotor cortex (z = 38) (orange/yellow) (A). Patients with idiopathic cervical dystonia also had loss of negative connectivity from our somatosensory region of interest to regions in the thalamus/basal ganglia and anterior cingulate (z = 12) (orange/yellow), and loss of positive connectivity to the sensorimotor and occipital cortex (z = 27) (blue/green) (B). All images were corrected with threshold-free cluster enhancement P<sub>FWE</sub> < 0.05. Corresponding average (SEM) Fischer z transformed correlation coefficients (Fz) are shown in box and whisker plots. Middle line within plot represents median, and cross shows mean. CD = idiopathic cervical dystonia patients; HV = healthy volunteers. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 6 Relevance to deep brain stimulation Figure 6 Relevance to deep brain stimulation. Lesions causing cervical dystonia are negatively connected to the ... Figure 6 Relevance to deep brain stimulation. Lesions causing cervical dystonia are negatively connected to the somatosensory cortex and positively to the cerebellum (A). Globus pallidus interna DBS locations associated with good clinical response in cervical dystonia (B) and all dystonia patients (C) also show negative functional connectivity to the somatosensory cortex and positive functional connectivity to the cerebellum. Voxels associated with good response also show similar connectivity profile when controlling for voxels associated with poor response (D). Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.comThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Brain, awz112, https://doi.org/10.1093/brain/awz112 The content of this slide may be subject to copyright: please see the slide notes for details.