The role of the inferior parietal lobule in writer’s cramp

Abstract

Humans have a distinguishing ability for fine motor control that is subserved by a highly evolved cortico-motor neuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. Task-specific dystonia can be viewed as a corruption or loss of motor control confined to a single motor skill. Using a multimodal experimental approach combining neuroimaging and non-invasive brain stimulation, we explored interactions between the principal nodes of the fine motor control network in patients with writer’s cramp and healthy matched controls. Patients and healthy volunteers underwent clinical assessment, diffusion-weighted MRI for tractography, and functional MRI during a finger tapping task. Activation maps from the task-functional MRI scans were used for target selection and neuro-navigation of the transcranial magnetic stimulation. Single- and double-pulse TMS evaluation included measurement of the input-output recruitment curve, cortical silent period, and amplitude of the motor evoked potentials conditioned by cortico-cortical interactions between premotor ventral (PMv)-motor cortex (M1), anterior inferior parietal lobule (aIPL)-M1, and dorsal inferior parietal lobule (dIPL)-M1 before and after inducing a long term depression-like plastic change to dIPL node with continuous theta-burst transcranial magnetic stimulation in a randomized, sham-controlled design. Baseline dIPL-M1 and aIPL-M1 cortico-cortical interactions were facilitatory and inhibitory, respectively, in healthy volunteers, whereas the interactions were converse and significantly different in writer’s cramp. Baseline PMv-M1 interactions were inhibitory and similar between the groups. The dIPL-PMv resting state functional connectivity was increased in patients compared to controls, but no differences in structural connectivity between the nodes were observed. Cortical silent period was significantly prolonged in writer’s cramp. Making a long term depression-like plastic change to dIPL node transformed the aIPL-M1 interaction to inhibitory (similar to healthy volunteers) and cancelled the PMv-M1 inhibition only in the writer’s cramp group. These findings suggest that the parietal multimodal sensory association region could have an aberrant downstream influence on the fine motor control network in writer’s cramp, which could be artificially restored to its normal function.

Brain Structural Changes in Focal Dystonia—What About Task Specificity? A Multimodal MRI Study

“…In our TSD sample, structural alterations in cortical regions may be attributed to abnormal plastic remodeling processes or to primary pathophysiological processes, independent of the overuse that is typical of musician's dystonia but not of writer's cramp and spasmodic dysphonia 17,19,20 . Previous MRI studies suggested the presence of altered brain function (disrupted cortical representation, inhibitory function, and functional connectivity) in both musician's and non‐musician's TSD, which together with morphometric GM changes might be interpreted as consequences of maladaptive neuronal plasticity or as specific traits of the disease 2,8,17,21‐25 . Future combined functional/structural longitudinal MRI studies might at least partially disentangle this issue.…”

“…17,19,20 Previous MRI studies suggested the presence of altered brain function (disrupted cortical representation, inhibitory function, and functional connectivity) in both musician's and non-musician's TSD, which together with morphometric GM changes might be interpreted as consequences of maladaptive neuronal plasticity or as specific traits of the disease. 2,8,17,[21][22][23][24][25] Future combined functional/structural longitudinal MRI studies might at least partially disentangle this issue.…”

A microstructural neural network biomarker for dystonia diagnosis identified by a DystoniaNet deep learning platform

“…Different forms of dystonia have been characterized by similarities in largescale disorganization of gray and white matter architecture, including abnormal distribution of influential regions of information transfer (hubs) in prefrontal, parietal, occipital cortices and thalamus and reduced connectivity of the sensorimotor and frontoparietal regions (19)(20)(21)(22)(23). This knowledge critically shifted our understanding of dystonia pathophysiology from a basal ganglia disorder to a largescale neural network disorder and thrust the field toward probing these alterations as potential candidate markers for its diagnosis and treatment (24)(25)(26)(27)(28).…”

Sequential Finger-tapping Learning Mediated by the Primary Motor Cortex and Fronto-parietal Network: A Combined MRI-MRS Study

“…The dorsal part of the IPL (dIPL) is a multimodal sensory association region involved in the initial acquisition and learning of a motor task. The anterior parts of the IPL, PMv, and M1 consist of the ne motor control network [54][55][56][57] . The dorsal premotor cortex (PMd) is involved in movement selection 58 .…”