On Reporting the Onset of the Intention to Move

In 1965, Hans Kornhuber and Luder Deecke made a discovery that greatly influenced the study of voluntary action. Using electroencephalography (EEG), they showed that when aligning some tens of trials to movement onset and averaging, a slowly decreasing electrical potential emerges over central regions of the brain. It starts 1 second ( s) or so before the onset of the voluntary action1 and continues until shortly after the action begins. They termed this the Bereitschaftspotential, or readiness potential (RP; Kornhuber & Deecke, 1965).2 This became the first well-established neural marker of voluntary action. In that, the RP allowed for more objective research on voluntary action rather than its previous dependence on subjective introspection. Two decades later, the RP captured the attention of the wider neuroscience community as well as of philosophers, legal scholars, and laypeople. This is because it was associated with a key question in the debate on free will: Is human voluntary action caused by the conscious intention to act? Or does the conscious experience only follow unconscious neural activity, which is the true origin of that action, and over which humans have only-limited immediate control?https://digitalcommons.chapman.edu/psychology_books/1019/thumbnail.jp

Functional recovery following traumatic spinal cord injury mediated by a unique polymer scaffold seeded with neural stem cells

To better direct repair following spinal cord injury (SCI), we designed an implant modeled after the intact spinal cord consisting of a multicomponent polymer scaffold seeded with neural stem cells. Implantation of the scaffold–neural stem cells unit into an adult rat hemisection model of SCI promoted long-term improvement in function (persistent for 1 year in some animals) relative to a lesion-control group. At 70 days postinjury, animals implanted with scaffold-plus-cells exhibited coordinated, weight-bearing hindlimb stepping. Histology and immunocytochemical analysis suggested that this recovery might be attributable partly to a reduction in tissue loss from secondary injury processes as well as in diminished glial scarring. Tract tracing demonstrated corticospinal tract fibers passing through the injury epicenter to the caudal cord, a phenomenon not present in untreated groups. Together with evidence of enhanced local GAP-43 expression not seen in controls, these findings suggest a possible regeneration component. These results may suggest a new approach to SCI and, more broadly, may serve as a prototype for multidisciplinary strategies against complex neurological problems