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S Rona

Publications and source records attributed to S Rona.

10 recordsLinked to original sources
PubMed2006

[Suggestion for a new, patient-oriented epilepsy classification].

The recent proposal by the ILAE Task Force for Epilepsy Classification is a multiaxial, syndrome-oriented approach. Epilepsy syndromes--at least as defined by the ILAE Task Force--group patients according to multiple, usually poorly defined parameters. As a result, these syndromes frequently show significant overlap and may change with patient age. We propose a five-dimensional and patient-oriented approach to epilepsy classification. This approach shifts away from syndrome orientation, using independent criteria in each of the five dimensions similarly to the diagnostic process in general neurology. The main dimensions of this new classification consist of (1) localizing the epileptogenic zone, (2) semiology of the seizure, (3) etiology, (4) seizure frequency, and (5) related medical conditions. These dimensions characterize all information necessary for patient management, are independent parameters, and include information more pertinent than the ILAE axes with regard to patient management. All cases can be classified according to this five-dimensional system, even at initial encounter when no detailed test results are available. Information from clinical tests such as MRI and EEG are translated into the best possible working hypothesis at the time of classification, allowing increased precision of the classification as additional information becomes available.

Epilepsy↗
PubMed2000

Spinal and cortical inhibition in Huntington's chorea.

In this article we studied spinal and cortical inhibitory mechanisms in patients with Huntington's disease. To evaluate spinal cord inhibitory circuitries, we assessed reciprocal inhibition between antagonist forearm muscles and the recovery cycle of the H reflex in the flexor carpi radialis. Patients showed a significant decrease in the presynaptic phase of reciprocal inhibition reaching a minimum at the conditioning-test interval of 20 msec and an abnormal facilitation of the test H reflex at the conditioning test interval of 40 to 60 msec. Throughout its time course (10-200 msec), the H reflex recovery cycle showed a more prominent facilitation in patients than in control subjects. To assess whether the observed pathophysiological abnormalities might have arisen from an abnormal motor cortical excitability, we examined the recovery cycle of the motor potentials evoked by paired transcranial magnetic stimuli. We found that the inhibitory mechanisms controlling motor cortical excitability were normal. An interpretation of the spinal cord abnormalities is that the intrinsically normal but deafferentated motor cortex in Huntington's disease partly loses its inhibitory control, thus disinhibiting spinal cord circuitry. Our findings from paired transcranial magnetic stimulation suggest that cortical motor areas are not hyperexcitable in Huntington's disease. Hence, the postulated thalamocortical overactivity in experimental models of Huntington's disease needs to be reappraised.

Adult↗
PubMed1998

Polarization of the human motor cortex through the scalp.

Direct currents (DC) applied directly to central nervous system structures produce substantial and long-lasting effects in animal experiments. We tested the functional effects of very weak scalp DC (< 0.5 mA, 7 s) on the human motor cortex by assessing the changes in motor potentials evoked by transcranial magnetic brain stimulation. We performed four different experiments in 15 healthy volunteers. Our findings led to the conclusion that such weak (< 0.5 mA) anodal scalp DC, alternated with a cathodal DC, significantly depresses the excitability of the human motor cortex, providing evidence that a small electric field crosses the skull and influences the brain. A possible mechanism of action of scalp DC is the hyperpolarization of the superficial excitatory interneurones in the human motor cortex.

Adult↗
PubMed1998

Alterations of motor cortical inhibition in patients with dystonia.

Cortical inhibitory mechanisms were investigated with the technique of paired transcranial magnetic stimulation in 10 patients with dystonia of the right arm: six patients had focal, task-specific dystonia (writer's cramp) and three had segmental and one had generalized dystonia. Paired stimuli were delivered in a conditioning-test design during slight voluntary activation of the target muscle, with subthreshold conditioning stimuli at short intervals (3-20 ms) and suprathreshold conditioning stimuli at long intervals (100-250 ms). The amount of inhibition at short interstimulus intervals did not differ significantly between patients and normal subjects. With long interstimulus intervals, patients showed more inhibition of the test response, which was significant at the 150-ms interval. The cortical silent period following a single suprathreshold magnetic stimulus was slightly shorter in patients. No significant difference was detected between the affected side and the unaffected side in patients with unilateral task-specific dystonia, neither in the duration of the silent period nor in the response to paired magnetic stimuli. These results indicate that the different types of motor cortical inhibition are produced by different inhibitory circuits. We propose that the alterations observed in patients with dystonia are the result of impaired feedback from the basal ganglia to motor cortical areas, with the ultimate effect of a flattening of the excitability curve of the cortical motoneuron pool during voluntary muscle activation.

Adult↗
PubMed1996

Cortical inhibition in Parkinson's disease. A study with paired magnetic stimulation.

The activity of motor cortical inhibitory circuits was studied with paired transcranial magnetic stimuli in 16 patients with Parkinson's disease 'off' therapy, five patients 'off' and 'on' therapy, and 11 normal subjects. Paired stimuli were delivered at short (3-20 ms) as well as long (100-250 ms) intervals during slight voluntary contraction. The intensity of the conditioning stimulus was subthreshold (80%) at short, and suprathreshold (150%) at long intervals. In addition, the silent period following a single magnetic shock given at 150% of threshold was measured. With short interstimulus intervals, no significant difference between patients and normal subjects could be detected. With long interstimulus intervals, the test response was significantly more inhibited in patients than in normal subjects. Although the cortical silent period was found to be slightly shorter, the recovery of motor evoked potentials was incomplete in patients with Parkinson's disease. This alteration could be partially reverted in dopaminergic therapy. In conclusion, the responsiveness of motor cortices to suprathreshold magnetic stimuli delivered after the end of the silent period is impaired in patients with Parkinson's disease, possibly due to prolonged activity in intracortical inhibitory circuits. The positive effect of L-dopa suggests that dopaminergic modulation of cortical activity, most probably at basal ganglia level, is involved in the pathogenesis of this phenomenon.

Adult↗