The ability to recognize one's own inner speech is essential for a sense of self. The verbal self-monitoring model proposes that this process entails a communication from neural regions involved in speech production to areas of speech perception. According to the model, if the expected verbal feedback matches the perceived feedback, then there would be no change in activation in the lateral temporal cortices. We investigated the neural correlates of verbal self-monitoring in a functional magnetic resonance (fMRI) study. Thirteen healthy male volunteers read aloud presented adjectives and heard their auditory feedback which was experimentally modified. Decisions about the source of the feedback were made with a button-press response. We used a 'clustered' fMRI acquisition sequence, consisting of periods of relative silence in which subjects could speak aloud and hear the feedback in the absence of scanner noise, and an event-related design which allowed separate analysis of trials associated with correct attributions and misattributions. Subjects made more misattribution responses when the feedback was a distorted version of their voice. This condition showed increased superior temporal activation relative to the conditions of hearing their own voice undistorted and hearing another person's voice. Furthermore, correct attributions during this condition were associated with greater temporal activation than misattributions. These findings support the self-monitoring model as mismatches between expected and actual auditory feedback were associated with greater temporal activation.

The aim of this study was to identify the cerebral areas activated during kinematic processing of movement trajectories. We measured regional cerebral blood flow (rCBF) during learning, performance and imagery of right-hand writing in eight right-handed volunteers. Compared with viewing the writing space, increases in rCBF were observed in the left motor, premotor and frontomesial cortex, and in the right anterior cerebellum in all movement conditions, and the increases were related to mean tangential writing velocity. No rCBF increases occurred in these areas during imagery. Early learning of new ideomotor trajectories and deliberately exact writing of letters both induced rCBF increases in the cortex lining the right intraparietal sulcus. In contrast, during fast writing of overlearned trajectories and in the later phase of learning new ideograms the rCBF increased bilaterally in the posterior parietal cortex. Imagery of ideograms that had not been practised previously activated the anterior and posterior parietal areas simultaneously. Our results provide evidence suggesting that the kinematic representations of graphomotor trajectories are multiply represented in the human parietal cortex. It is concluded that different parietal subsystems may subserve attentive sensory movement control and whole-field visuospatial processing during automatic performance.

The authors' aim was to examine the regional anatomy of brain activation by cognitive tasks commonly used in hypoglycemia research and to assess the effect of acute hypoglycemia on these in healthy volunteers. Eight right-handed volunteers performed a set of cognitive tasks-finger tapping (FT), simple reaction time (SRT), and four-choice reaction time (4CRT)-twice during blood oxygen level-dependent (BOLD) functional magnetic resonance imaging of the brain on two occasions. In study 1 (n ‫؍‬ 6), plasma glucose was maintained at euglycemia (5 mmol/l) throughout. In study 2 (n ‫؍‬ 6), plasma glucose was reduced to 2.5 mmol/l for the second set. Performance of the tasks resulted in specific group brain activation maps. During hypoglycemia, FT slowed (P ‫؍‬ 0.026), with decreased BOLD activation in right premotor cortex and supplementary motor area and left hippocampus and with increased BOLD activation in left cerebellum and right frontal pole. Although there was no significant change in SRT, BOLD activation was reduced in right cerebellum and visual cortex. The 4CRT deteriorated (P ‫؍‬ 0.020), with reduction in BOLD activation in motor and visual systems but increased BOLD signal in a large area of the left parietal association cortex, a region involved in planning. Hypoglycemia impairs simple brain functions and is associated with task-specific localized reductions in brain activation. For a task with greater cognitive load, the increased BOLD signal in planning areas is compatible with recruitment of brain regions in an attempt to limit dysfunction. Further investigation of these mechanisms may help devise rational treatment strategies to limit cortical dysfunction during acute iatrogenic hypoglycemia. Diabetes 50:1618 -1626, 2001

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