The importance of premotor cortex for supporting speech production after left capsular-putaminal damage.

The left putamen is known to be important for speech production, but some patients with left putamen damage can produce speech remarkably well. We investigated the neural mechanisms that support this recovery by using a combination of techniques to identify the neural regions and pathways that compensate for loss of the left putamen during speech production. First, we used fMRI to identify the brain regions that were activated during reading aloud and picture naming in a patient with left putamen damage. This revealed that the patient had abnormally high activity in the left premotor cortex. Second, we used dynamic causal modeling of the patient's fMRI data to understand how this premotor activity influenced other speech production regions and whether the same neural pathway was used by our 24 neurologically normal control subjects. Third, we validated the compensatory relationship between putamen and premotor cortex by showing, in the control subjects, that lower connectivity through the putamen increased connectivity through premotor cortex. Finally, in a lesion-deficit analysis, we demonstrate the explanatory power of our fMRI results in new patients who had damage to the left putamen, left premotor cortex, or both. Those with damage to both had worse reading and naming scores. The results of our four-pronged approach therefore have clinical implications for predicting which patients are more or less likely to recover their speech after left putaminal damage.

Experiencing your brain: neurofeedback as a new bridge between neuroscience and phenomenology.

Neurophenomenology is a scientific research program aimed to combine neuroscience with phenomenology in order to study human experience. Nevertheless, despite several explicit implementations, the integration of first-person data into the experimental protocols of cognitive neuroscience still faces a number of epistemological and methodological challenges. Notably, the difficulties to simultaneously acquire phenomenological and neuroscientific data have limited its implementation into research projects. In our paper, we propose that neurofeedback paradigms, in which subjects learn to self-regulate their own neural activity, may offer a pragmatic way to integrate first-person and third-person descriptions. Here, information from first- and third-person perspectives is braided together in the iterative causal closed loop, creating experimental situations in which they reciprocally constrain each other. In real-time, the subject is not only actively involved in the process of data acquisition, but also assisted to directly influence the neural data through conscious experience. Thus, neurofeedback may help to gain a deeper phenomenological-physiological understanding of downward causations whereby conscious activities have direct causal effects on neuronal patterns. We discuss possible mechanisms that could mediate such effects and indicate a number of directions for future research.

Single-unit activities during epileptic discharges in the human hippocampal formation.

Between seizures the brain of patients with epilepsy generates pathological patterns of synchronous activity, designated as interictal epileptiform discharges (ID). Using microelectrodes in the hippocampal formations of 8 patients with drug-resistant temporal lobe epilepsy, we studied ID by simultaneously analyzing action potentials from individual neurons and the local field potentials (LFPs) generated by the surrounding neuronal network. We found that ~30% of the units increased their firing rate during ID and 40% showed a decrease during the post-ID period. Surprisingly, 30% of units showed either an increase or decrease in firing rates several hundred of milliseconds before the ID. In 4 patients, this pre-ID neuronal firing was correlated with field high-frequency oscillations at 40-120 Hz. Finally, we observed that only a very small subset of cells showed significant coincident firing before or during ID. Taken together, we suggested that, in contrast to traditional views, ID are generated by a sparse neuronal network and followed a heterogeneous synchronization process initiated over several hundreds of milliseconds before the paroxysmal discharges.