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Jousmaki, V.

Publications and source records attributed to Jousmaki, V..

4 recordsLinked to original sources

Large-Scale Motor Dynamics Associated with Reaching are Altered in Essential Tremor

Essential Tremor (ET) is a very common neurological disorder characterised by involuntary rhythmic movements attributable to pathological synchronization within corticothalamic circuits. Previous work has focused on tremor in isolation, overlooking broader disturbances to motor control during naturalistic movements such as reaching. We hypothesised that ET disrupts the sequential engagement of large-scale rhythmic brain networks, leading to both tremor and deficits in motor planning and execution. To test this, we performed whole-head neuroimaging during an upper-limb reaching task using high-density electroencephalography in ET patients and healthy controls, alongside optically pumped magnetoencephalography in a smaller cohort. Key motor regions--including the supplementary motor area, premotor cortex, posterior parietal cortex, and motor cerebellum--were synchronized to tremor rhythms. Patients exhibited a 15% increase in low beta (14-21 Hz) desynchronization over the supplementary motor area during movement, which strongly correlating with tremor severity (R2 = 0.85). A novel dimensionality reduction technique revealed four distinct networks accounting for 97% of the variance in motor-related brain-wide oscillations, with ET altering their sequential engagement. Consistent with our hypothesis, the frontoparietal beta network- normally involved in motor planning-exhibited additional desynchronization during movement execution in ET patients. This altered engagement correlated with slower movement velocities, suggesting an adaptation towards feedback-driven motor control. These findings reveal fundamental disruptions in distributed motor control networks in ET and identify novel biomarkers as targets for next-generation brain stimulation therapies.

neuroscience↗

Temporally stable beta sensorimotor oscillations and cortico-muscular coupling underlie force steadiness

As humans, we seamlessly hold objects in our hands, and may even lose consciousness of these objects. This phenomenon raises the unsettled question of the involvement of the cerebral cortex, the core area for voluntary motor control, in dynamically maintaining steady muscle force. To address this issue, we measured magnetoencephalographic brain activity from healthy adults who maintained a steady pinch grip. Using a novel analysis approach, we uncovered fine-grained temporal modulations in the [~]20-Hz sensorimotor brain rhythm and its coupling with muscle activity, with respect to several aspects of muscle force (rate of increase/decrease or plateauing high/low). These modulations preceded changes in force features by [~]40 ms and possessed behavioral relevance, as less salient or absent modulation predicted a more stable force output. These findings have consequences for the existing theories regarding the functional role of cortico-muscular coupling, and suggest that steady muscle contractions are characterized by a stable rather than fluttering involvement of the sensorimotor cortex.

neuroscience↗

Neocortical activity tracks syllable and phrasal structure of self-produced speech

To gain novel insights into how the human brain processes self-produced auditory information during reading aloud, we investigated the coupling between neuromagnetic activity and the temporal envelope of the heard speech sounds (i.e., speech brain tracking) in a group of adults who 1) read a text aloud, 2) listened to a recording of their own speech (i.e., playback), and 3) listened to another speech recording. Coherence analyses revealed that, during reading aloud, the readers brain tracked the slow temporal fluctuations of the speech output. Specifically, auditory cortices tracked phrasal structure (<1 Hz) but to a lesser extent than during the two speech listening conditions. Also, the tracking of syllable structure (4-8 Hz) occurred at parietal opercula during reading aloud and at auditory cortices during listening. Directionality analyses based on renormalized partial directed coherence revealed that speech brain tracking at <1 Hz and 4-8 Hz is dominated by speech-to-brain directional coupling during both reading aloud and listening, meaning that speech brain tracking mainly entails auditory feedback processing. Nevertheless, brain-to-speech directional coupling at 4- 8 Hz was enhanced during reading aloud compared with listening, likely reflecting speech monitoring before production. Altogether, these data bring novel insights into how auditory verbal information is tracked by the human brain during perception and self-generation of connected speech.\n\nHighlightsO_LIThe brain tracks phrasal and syllabic rhythmicity of self-produced (read) speech.\nC_LIO_LITracking of phrasal structures is attenuated during reading compared with listening.\nC_LIO_LISpeech rhythmicity mainly drives brain activity during reading and listening.\nC_LIO_LIBrain activity drives syllabic rhythmicity more during reading than listening.\nC_LI

neuroscience↗

Attenuated post-movement beta rebound in Parkinson’s disease to proprioceptive afferent feedback

Motor symptoms are defining traits in the diagnosis of Parkinsons disease (PD). A crucial component in motor function and control of movements is the integration of efferent signals from the motor network to the peripheral motor system, and afferent proprioceptive sensory feedback. Previous studies have indicated abnormal movement-related cortical oscillatory activity in PD, but the role of the proprioceptive afference on abnormal oscillatory activity in PD has not been elucidated. In the present study, we examine the role of proprioception by studying the cortical processing of proprioceptive stimulation in PD patients, ON/OFF levodopa medication, as compared to that of healthy controls (HC). We used a proprioceptive stimulator that generated precisely controlled passive movements of the index finger and measured the induced cortical oscillatory responses following the proprioceptive stimulation using magnetoencephalography (MEG). Both PD patients and HC showed a typical initial mu/beta-band (8-30 Hz) desynchronization during the passive movement. However, the subsequent beta rebound after the passive movement that was apparent in HC was much attenuated and almost absent in PD patients. Furthermore, we found no difference in the degree of beta rebound attenuation between patients ON and OFF levodopa medication. Our results hence demonstrate a disease-related deterioration in cortical processing of proprioceptive afference in PD, and further suggest that such disease-related loss of proprioceptive function is due to processes outside the dopaminergic system affected by levodopa medication.

neuroscience↗