Representation of head-centric flow in the human motion complex.

Contains fulltext : 50364.pdf (publisher's version ) (Open Access)Recent neuroimaging studies have identified putative homologs of macaque middle temporal area (area MT) and medial superior temporal area (area MST) in humans. Little is known about the integration of visual and nonvisual signals in human motion areas compared with monkeys. Through extra-retinal signals, the brain can factor out the components of visual flow on the retina that are induced by eye-in-head and head-in-space rotations and achieve a representation of flow relative to the head (head-centric flow) or body (body-centric flow). Here, we used functional magnetic resonance imaging to test whether extra-retinal eye-movement signals modulate responses to visual flow in the human MT+ complex. We distinguished between MT and MST and tested whether subdivisions of these areas may transform the retinal flow into head-centric flow. We report that interactions between eye-movement signals and visual flow are not evenly distributed across MT+. Pursuit hardly influenced the response of MT to flow, whereas the responses in MST to the same retinal stimuli were stronger during pursuit than during fixation. We also identified two subregions in which the flow-related responses were boosted significantly by pursuit, one overlapping part of MST. In addition, we found evidence of a metric relation between rotational flow relative to the head and fMRI signals in a subregion of MST. The latter findings provide an important advance over published single-cell recordings in monkey MST. A visual representation of the rotation of the head in the world derived from head-centric flow may supplement semicircular canals signals and is appropriate for cross-calibrating vestibular and visual signals

Neuroprosthetic baroreflex controls haemodynamics after spinal cord injury.

Spinal cord injury (SCI) induces haemodynamic instability that threatens survival <sup>1-3</sup> , impairs neurological recovery <sup>4,5</sup> , increases the risk of cardiovascular disease <sup>6,7</sup> , and reduces quality of life <sup>8,9</sup> . Haemodynamic instability in this context is due to the interruption of supraspinal efferent commands to sympathetic circuits located in the spinal cord <sup>10</sup> , which prevents the natural baroreflex from controlling these circuits to adjust peripheral vascular resistance. Epidural electrical stimulation (EES) of the spinal cord has been shown to compensate for interrupted supraspinal commands to motor circuits below the injury <sup>11</sup> , and restored walking after paralysis <sup>12</sup> . Here, we leveraged these concepts to develop EES protocols that restored haemodynamic stability after SCI. We established a preclinical model that enabled us to dissect the topology and dynamics of the sympathetic circuits, and to understand how EES can engage these circuits. We incorporated these spatial and temporal features into stimulation protocols to conceive a clinical-grade biomimetic haemodynamic regulator that operates in a closed loop. This 'neuroprosthetic baroreflex' controlled haemodynamics for extended periods of time in rodents, non-human primates and humans, after both acute and chronic SCI. We will now conduct clinical trials to turn the neuroprosthetic baroreflex into a commonly available therapy for people with SCI