Abstract
Cervical dystonia is characterized by involuntary, abnormal movements and postures of the head and neck. Current views on its pathophysiology, such as faulty sensorimotor integration and impaired motor planning, are largely based on studies of focal hand dystonia. Using resting state fMRI, we explored whether cervical dystonia patients have altered functional brain connectivity compared to healthy controls, by investigating 10 resting state networks. Scans were repeated immediately before and some weeks after botulinum toxin injections to see whether connectivity abnormalities were restored. We here show that cervical dystonia patients have reduced connectivity in selected regions of the prefrontal cortex, premotor cortex and superior parietal lobule within a distributed network that comprises the premotor cortex, supplementary motor area, primary sensorimotor cortex, and secondary somatosensory cortex (sensorimotor network). With regard to a network originating from the occipital cortex (primary visual network), selected regions in the prefrontal and premotor cortex, superior parietal lobule, and middle temporal gyrus areas have reduced connectivity. In selected regions of the prefrontal, premotor, primary motor and early visual cortex increased connectivity was found within a network that comprises the prefrontal cortex including the anterior cingulate cortex and parietal cortex (executive control network). Botulinum toxin treatment resulted in a partial restoration of connectivity abnormalities in the sensorimotor and primary visual network. These findings demonstrate the involvement of multiple neural networks in cervical dystonia. The reduced connectivity within the sensorimotor and primary visual networks may provide the neural substrate to expect defective motor planning and disturbed spatial cognition. Increased connectivity within the executive control network suggests excessive attentional control and while this may be a primary trait, perhaps contributing to abnormal motor control, this may alternatively serve a compensatory function in order to reduce the consequences of the motor planning defect inflicted by the other network abnormalities.
Highlights
Cervical dystonia (CD) is the most common type of primary dystonia. [1] It is characterized by involuntary, abnormal movements and postures of the head
For CD patients, decreased connectivity within this network was found for regions in the bilateral prefrontal cortex (PFC), bilateral premotor cortex (PMC), and left superior parietal lobule (SPL). (Table 1, Figure 1A) At a less stringent inference (p#0.05 family-wise erros (FWE) corrected), SM1 and the extrastriate cortex demonstrated a similar decrease in connectivity. (Table S2, figure S1) In contrast to the sensorimotor network (SMN), CD patients exhibited increased connectivity with regard to the executive control network (ECN), which consists of functionally connected regions in the frontal cortex including the anterior cingulate and paracingulate, and parietal cortex
Several regions in the bilateral superior frontal and medial gyrus, bilateral middle frontal gyrus, bilateral paracingulate gyrus and rectal gyrus, and medial paracentral lobule, corresponding to the PFC, PMC and parts of the primary sensorimotor cortex [37], and regions in the early visual cortex demonstrated increased connectivity within the ECN. (Table 1, Figure 1B) At a less stringent inference (p#0.05 FWE corrected), an extension of SM1, the SPL, and the extrastriate cortex demonstrated a similar increase in connectivity. (Table S3, figure S1) No significant differences were found for the cerebellar network (CN) or default mode network (DMN)
Summary
Cervical dystonia (CD) is the most common type of primary dystonia. [1] It is characterized by involuntary, abnormal movements and postures of the head. Injecting the involved cervical muscles with botulinum toxin (BoNT) is an effective and evidence-based treatment of CD and leads to marked improvement in head posture and secondary symptoms such as pain. Patients with dystonia have abnormal motor system physiology, as for example shown by the loss of surround inhibition, that leads to unnecessary contractions of more muscles than required for given motor behaviour. Despite some clinical overlap and electrophysiological similarities, the pathophysiology of CD is likely to be, at least in part, different from that of WC, for example given the lack of task-specificity in CD. The few functional MRI and PET studies conducted in CD patients have mainly used event-related paradigms, which makes it difficult to conclude whether the observed effects represent the primary pathophysiological mechanism, a secondary (feedback) mechanism, or a compensatory effect to a specific task. The few functional MRI and PET studies conducted in CD patients have mainly used event-related paradigms, which makes it difficult to conclude whether the observed effects represent the primary pathophysiological mechanism, a secondary (feedback) mechanism, or a compensatory effect to a specific task. [5,6,13,14]
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