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Meyers, S. P.

Publications and source records attributed to Meyers, S. P..

3 recordsLinked to original sources

Causal Lesion Evidence for Two Motor Speech Coordination Networks in the Brain

Speech production is supported by sensory-to-motor transformations to coordinate activity of the larynx and orofacial muscles. Here, we show that lesions to left temporal lobe areas involved in pitch processing cause reduced neural responses when repeating sentences and when humming piano melodies in a dorsal portion of the left precentral gyrus linked to laryngeal motor control. In contrast, lesions to left inferior parietal areas involved in somatosensory processing of speech cause reduced neural responses when repeating sentences but not when humming piano melodies in a ventral portion of the left precentral gyrus linked to orofacial motor control. Analyses in neurotypical participants converge in showing that the dorsal and ventral portions of the left precentral gyrus exhibit strong functional connectivity to left temporal and inferior parietal regions, respectively. These results provide causal lesion evidence that dissociable networks underlie distinct sensory-to-motor transformations supporting laryngeal and orofacial motor control for speech production.

neuroscience↗

Visual processing of manipulable objects in the ventral stream is modulated by inputs from parietal action systems

Functional object use requires the integration of visuomotor representations processed in the dorsal visual pathway with representations of surface texture and material composition of objects, processed in the ventral visual pathway. Do regions in the ventral visual pathway project outputs to dorsal visual pathway action systems, or are the outputs of the dorsal visual pathway communicated to the ventral visual pathway to modulate processing? And what are the white matter pathways that mediate structural connectivity in support of functional object use? Here we show that the left inferior parietal cortex, a region within the dorsal visual pathway, exerts a direct effect on neural responses in ventral occipital-temporal cortex during visual processing of manipulable objects. We studied a series of consecutively enrolled participants in the pre-operative phase of their neurosurgical care (N = 109) with lesions principally distributed throughout the left hemisphere. Participants completed an object processing category localizer functional MRI experiment in which they viewed images of manipulable objects, animals, faces, and places. We then used Voxel-based Lesion-Activity Mapping (VLAM), a technique in which functional responses in a region-of-interest are used to predict variance in voxel-wise lesion incidence throughout the brain. In the VLAM analyses performed here, we found that lesions to the left anterior intraparietal sulcus and left supramarginal gyrus, two inferior parietal regions known to support object-directed grasping and manipulation, respectively, cause reduced neural responses for manipulable objects (compared to faces, places and animals) in the fusiform gyrus. Parietal lesions do not affect neural responses during visual processing of places in the same region of the fusiform gyrus, even though places elicit stronger responses in the fusiform gyrus than manipulable objects. Seventy-five of 109 participants took part in a common diffusion MRI protocol, permitting a connectome-wide analyses relating white matter fiber integrity to the strength of functional responses for manipulable objects in the left fusiform gyrus. This analysis demonstrated that the descending portion of the left arcuate fasciculus mediates parietal-to-temporal lobe connectivity for manipulable objects, supporting the integration of action representations with conceptual and perceptual attributes of objects. By combining voxel-based and connectome-wide lesion-symptom mapping methods with functional MRI, we have demonstrated that structural connectivity to dorsal visual pathway areas supporting skilled manual action shape category-specific neural responses for manipulable objects within the ventral visual pathway.

neuroscience↗

Strain concentration drives the anatomical distribution of injury in acute and chronic traumatic brain injury

Brain tissue injury caused by mild traumatic brain injury (mTBI) disproportionately concentrates in the midbrain, cerebellum, mesial temporal lobe, and the interface between cortex and white matter at sulcal depths 1-12. The bio-mechanical principles that explain why physical impacts to different parts of the skull translate to common foci of injury concentrated in specific brain structures are unknown. A general and longstanding idea, which has not to date been directly tested in humans, is that different brain regions are differentially susceptible to strain loading11,13-15. We use Magnetic Resonance Elastography (MRE) in healthy participants to develop whole-brain bio-mechanical vulnerability maps that independently define which regions of the brain exhibit disproportionate strain concentration. We then validate those vulnerability maps in a prospective cohort of mTBI patients, using diffusion MRI data collected at three cross-sectional timepoints after injury: acute, sub-acute, chronic. We show that regions that exhibit high strain, measured with MRE, are also the sites of greatest injury, as measured with diffusion MR in mTBI patients. This was the case in acute, subacute, and chronic subgroups of the mTBI cohort. Follow-on analyses decomposed the biomechanical cause of increased strain by showing it is caused jointly by disproportionately higher levels of energy arriving to high-strain structures, as well as the inability of high strain structures to effectively disperse that energy. These findings establish a causal mechanism that explains the anatomy of injury in mTBI based on in vivo rheological properties of the human brain.

neuroscience↗