The Encephalophone: A Novel Musical Biofeedback Device using Conscious Control of Electroencephalogram (EEG).

A novel musical instrument and biofeedback device was created using electroencephalogram (EEG) posterior dominant rhythm (PDR) or mu rhythm to control a synthesized piano, which we call the Encephalophone. Alpha-frequency (8-12 Hz) signal power from PDR in the visual cortex or from mu rhythm in the motor cortex was used to create a power scale which was then converted into a musical scale, which could be manipulated by the individual in real time. Subjects could then generate different notes of the scale by activation (event-related synchronization) or de-activation (event-related desynchronization) of the PDR or mu rhythms in visual or motor cortex, respectively. Fifteen novice normal subjects were tested in their ability to hit target notes presented within a 5-min trial period. All 15 subjects were able to perform more accurately (average of 27.4 hits, 67.1% accuracy for visual cortex/PDR signaling; average of 20.6 hits, 57.1% accuracy for mu signaling) than a random note generation (19.03% accuracy). Moreover, PDR control was significantly more accurate than mu control. This shows that novice healthy individuals can control music with better accuracy than random, with no prior training on the device, and that PDR control is more accurate than mu control for these novices. Individuals with more years of musical training showed a moderate positive correlation with more PDR accuracy, but not mu accuracy. The Encephalophone may have potential applications both as a novel musical instrument without requiring movement, as well as a potential therapeutic biofeedback device for patients suffering from motor deficits (e.g., amyotrophic lateral sclerosis (ALS), brainstem stroke, traumatic amputation).

Genetic interactions between doublecortin and doublecortin-like kinase in neuronal migration and axon outgrowth.

Although mutations in the human doublecortin gene (DCX) cause profound defects in cortical neuronal migration, a genetic deletion of Dcx in mice produces a milder defect. A second locus, doublecortin-like kinase (Dclk), encodes a protein with similar "doublecortin domains" and microtubule stabilization properties that may compensate for Dcx. Here, we generate a mouse with a Dclk mutation that causes no obvious migrational abnormalities but show that mice mutant for both Dcx and Dclk demonstrate perinatal lethality, disorganized neocortical layering, and profound hippocampal cytoarchitectural disorganization. Surprisingly, Dcx(-/y);Dclk(-/-) mutants have widespread axonal defects, affecting the corpus callosum, anterior commissure, subcortical fiber tracts, and internal capsule. Dcx/Dclk-deficient dissociated neurons show abnormal axon outgrowth and dendritic structure, with defects in axonal transport of synaptic vesicle proteins. Dcx and Dclk may directly or indirectly regulate microtubule-based vesicle transport, a process critical to both neuronal migration and axon outgrowth.

Doublecortin is required in mice for lamination of the hippocampus but not the neocortex.

Doublecortin (DCX) is a microtubule-associated protein that is required for normal neocortical and hippocampal development in humans. Mutations in the X-linked human DCX gene cause gross neocortical disorganization (lissencephaly or "smooth brain") in hemizygous males, whereas heterozygous females show a mosaic phenotype with a normal cortex as well as a second band of misplaced (heterotopic) neurons beneath the cortex ("double cortex syndrome"). We created a mouse carrying a targeted mutation in the Dcx gene. Hemizygous male Dcx mice show severe postnatal lethality; the few that survive to adulthood are variably fertile. Dcx mutant mice show neocortical lamination that is largely indistinguishable from wild type and show normal patterns of neocortical neurogenesis and neuronal migration. In contrast, the hippocampus of both heterozygous females and hemizygous males shows disrupted lamination that is most severe in the CA3 region. Behavioral tests show defects in context and cued conditioned fear tests, suggesting that deficits in hippocampal learning accompany the abnormal cytoarchitecture.