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Around 1741, composer Johann Sebastian Bach published a long and complicated keyboard piece, calling it Aria with diverse variations for a harpsichord with two manuals. It was the capstone of a publication project called German Clavier-Übung (Keyboard Practice) where Bach wanted to show what was possible at the keyboard in terms of technical development, virtuosic finesse and compositional sophistication. The music is meticulously patterned, beginning with a highly ornamented Aria, the bass line of which fuels the 30 variations that follow. The piece is clearly divided into two parts with the second half beginning with an overture with a fanfare opening, in variation 16. The piece ends as it begins, with the return of the Aria. Here, we present an investigation into activation and connectivity in the brain of a pianist, who listened to her own recording of the "Goldberg" variation while undergoing a fMRI examination. Similarity of brain connectivity is quantified and compared with the subjective scores provided by the subject.
This article was published in the following journal.
Name: Medical problems of performing artists
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A neurobehavioral syndrome associated with bilateral medial temporal lobe dysfunction. Clinical manifestations include oral exploratory behavior; tactile exploratory behavior; hypersexuality; BULIMIA; MEMORY DISORDERS; placidity; and an inability to recognize objects or faces. This disorder may result from a variety of conditions, including CRANIOCEREBRAL TRAUMA; infections; ALZHEIMER DISEASE; PICK DISEASE OF THE BRAIN; and CEREBROVASCULAR DISORDERS.
Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.
Volume of circulating blood in a region of the brain. It is a functional measure of the brain perfusion status which relates changes in this to changes in CEREBROVASULAR CIRCULATION that are often seen in brain diseases.
The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.