Transcranial magnetic stimulation of the motor cortex was performed in 10 normal subjects and 10 patients with radiographical abnormalities of the corpus callosum. Seven patients had a complete or partial agenesis or hypoplasia of the corpus callosum, two had a thin corpus callosum due to hydrocephalus or white matter degeneration and one had a circumscript contusion lesion of the corpus callosum. The patients served as a clinical model to investigate transcallosal influences on excitatory and inhibitory effects of motor cortex stimulation and to assess the potential diagnostic use of interhemispheric conduction studies and the contribution of interhemispheric interaction on transcranially elicited contralateral excitatory and inhibitory motor responses. Stimulation over one motor cortex suppressed tonic voluntary electromyographic activity in ipsilateral hand muscles in all subjects with preserved anterior half of the trunk of the corpus callosum. Since this suppression was lacking or had a delayed onset latency in patients with absence or abnormalities of the anterior half of the trunk of the corpus callosum it can be concluded that it is due to a transcallosal inhibition (Ti) of the opposite motor cortex mediated by fibres passing through this part of the corpus callosum. In normal subjects Ti had an mean onset latency of 36.1 +/- 3.5 ms (SD) and a duration of 24.5 +/- 3.9 ms. The calculated mean transcallosal conduction time was 13 ms. The threshold of Ti recorded in muscles ipsilateral to stimulation tended to be higher than the one for eliciting excitatory contralateral motor responses (56 +/- 6% versus 46 +/- 10% maximum stimulator output). Cortical thresholds (at rest) for contralateral excitatory hand motor responses were higher in patients with developmental abnormalities of the corpus callosum than in normals (66 +/- 17% versus 46 +/- 10% maximum stimulator output), which probably reflects also a facilitatory transcallosal interaction of both motor cortices in normals. In contrast, facilitation of cortically elicited motor responses in one hand by strong contraction of the other hand was the same in the patients with agenesis of the corpus callosum and normals, which suggests that this facilitatory spread takes place on a spinal rather than on a cortical level. Central motor latencies and amplitudes of contralateral hand motor responses were the same in patients with developmental abnormalities of the corpus callosum and normals (6.1 +/- 0.7 ms versus 6.3 +/- 0.7 ms and 6.7 +/- 2.4 mV versus 6.6 +/- 2.9 mV) so that callosal transfers do not seem to influence corticospinal conduction properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Bimanual motor coordination is essential for piano playing. The functional neuronal substrate for high-level bimanual performance achieved by professional pianists is unclear. We compared professional pianists to musically naïve controls while carrying out in-phase (mirror) and anti-phase (parallel) bimanual sequential finger movements during functional magnetic resonance imaging (fMRI). This task corresponds to bimanually playing scales practiced daily by pianists from the beginning of piano playing. Musicians and controls showed significantly different functional activation patterns. When comparing performance of parallel movements to rest, musically naïve controls showed stronger activations than did pianists within a network including anterior cingulate cortex, right dorsal premotor cortex, both cerebellar hemispheres, and right basal ganglia. The direct comparison of bimanual parallel to mirror movements between both groups revealed stronger signal increases in controls within mesial premotor cortex (SMA), bilateral cerebellar hemispheres and vermis, bilateral prefrontal cortex, left ventral premotor cortex, right anterior insula, and right basal ganglia. These findings suggest increased efficiency of cortical and subcortical systems for bimanual movement control in musicians. This may be fundamental to achieve high-level motor skills allowing the musician to focus on artistic aspects of musical performance.

Disturbances in recognizing facial expressions of disgust have been reported previously in pre-symptomatic and manifest Huntington's disease. Given the substantial role of the insula and basal ganglia in the perception of disgust as revealed by functional imaging, lesion studies and intracerebral recordings, we propose dysfunction within the insula and/or basal ganglia as the underlying neural substrate. Using functional MRI (fMRI), we studied a group of nine pre-symptomatic Huntington's disease gene carriers and nine healthy controls, matched for age, gender, intelligence and years of education, while they were viewing disgusted facial expressions. As control conditions, surprised and neutral expressions were presented. Compared with healthy controls, Huntington's disease gene carriers showed reduced responses within the left dorsal anterior insula during processing of disgusted facial expressions. Moreover, processing of disgust was associated with significant activation of the left dorsal anterior insula and putamen in healthy controls, but not in Huntington's disease gene carriers. Furthermore, behavioural assessment revealed a selective impairment in recognizing facial expressions displaying disgust in Huntington's disease gene carriers. Our finding of dysfunctional decreased insula activation in pre-symptomatic Huntington's disease provides an explanation for the clinical deficit in recognizing facial expression of disgust. Furthermore, it underscores the role of the insula in the emotion of disgust.

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The aim of this study was to use time-resolved functional magnetic resonance imaging (fMRI) to investigate temporal differences in the activation of the supplementary motor area (SMA) and the primary motor cortex (M1). We report data from eight human volunteers who underwent fMRI examinations in a 1.5T Philips Gyroscan ACS-NT MRI scanner. While wearing a contact glove, subjects executed a complex automated sequence of finger movements either spontaneously or in response to external auditory cues. Based on the result of a functional scout scan, a single slice that included the M1 and the SMA was selected for image acquisition (echo planar imaging, repetition time 100 ms, echo time 50 ms, 64 x 64 matrix, 1,000 images). Data were analyzed with a shifting cross-correlation approach using the STIMULATE program and in-house programs written in Interactive Data Language (IDL(TM)). Time-course data were generated for regions of interest in the M1 as well as in the rostral and caudal SMA. Mean time between onset of the finger movement sequence and half-maximum of the signal change in M1 was 3.6 s for the externally cued execution (SD 0.5) and 3.5 s for the spontaneous execution (SD 0.6). Activation in the rostral section of the SMA occurred 0.7 s earlier than it did in the M1 during the externally cued execution and 2.0 s earlier during the spontaneous execution, a difference significant at the P < 0.01 level. Our results indicate that rostral SMA activation precedes M1 activation by varying time intervals in the sub-second range that are determined by the mode of movement initialization. By applying a paradigm that exerts a differential influence on temporal activation, we could ensure that the observed timing differences were not the result of differences in hemodynamic response function.

Background-Diffusion-weighted imaging (DWI) has been established to diagnose acute cerebral ischemia. Signal intensity changes occur not only in patients with definite stroke but also in up to 67% of transient ischemic attack (TIA) patients. We investigated the predictive value of DWI signal intensity changes to distinguish between TIA and stroke. Methods-Clinical data, conventional magnetic resonance imaging (MRI), and DWI were collected in 60 consecutive patients with TIA and 37 consecutive patients with stroke. DWI was performed within 24 hours after symptom onset.Using an image analyzing system, we calculated the ratio of the lesion and corresponding contralateral normal tissue average signal intensity (rAI). Results-Eighteen of 60 TIA patients (30%) revealed focal abnormalities on DWI. The mean duration of symptoms was 5.3 hours in TIA patients with DWI lesions and 5.2 hours in patients without lesions. The time to DWI was comparable in TIA and stroke patients. Even within 6 hours after symptom onset, the signal intensity was significantly higher (Pϭ0.03) in stroke patients (nϭ13, rAIϭ1.26) as compared with TIA patients with DWI lesions (nϭ9, rAIϭ1.16). Conclusions-Our data indicate that already within 6 hours after symptom onset, TIA and stroke might be differentiated by analyzing the signal intensity of the lesions.

DWI is a sensitive method of demonstrating ischemic events after CEA. The number and volume of DWI lesions after CEA are highly predictive of brain infarction.

We report intrathecal use of gadolinium DTPA for MRI of the cerebrospinal fluid (CSF). In two patients with leptomeningeal carcinomatosis, we injected 0.01 mmol gadolinium DTPA into the lateral ventricle via an Ommaya device. Coronal T1-weighted images of the head were obtained at 0.2 T prior to and after injection. There was pronounced enhancement of CSF close to the injection site, allowing good delineation of CSF and surrounding brain tissue. No side effects occurred. MRI with intrathecal administration of highly diluted gadolinium DTPA may be a promising alternative to conventional investigation of CSF-filled cavities using iodinated X-ray contrast media or radionuclides.