Paired Magnetic Stimuli Research Articles

Simulation of cough in man by magnetic stimulation of the thoracic nerve roots.

Normal cough requires abdominal muscle contraction. We have previously reported contraction of the abdominal muscles elicited by a single percutaneous magnetic stimulation of the thoracic nerve roots. We hypothesized that paired magnetic twitches could generate sufficient tension in the abdominal muscles to simulate cough. Therefore, six normal subjects were stimulated at the T10 intervertebral level in the seated position. We measured the gastric pressure elicited by paired magnetic stimuli (pTw Pga) with interstimulus intervals in the range of 10 ms (100 Hz) to 999 ms (1 Hz). In the second part of the study we evaluated paired stimuli (at the frequency found to produce the greatest response) using a valve to simulate the function of the glottis; the valve was arranged such that it opened once mouth pressure exceeded a predetermined threshold. Mean pTw Pga during stimulation for the 6 subjects was 74 cm H2O (range, 30-109), and mean peak flow was 209 L/min (range, 128-345 L/min). These values were increased if the subject took a prior inspiration or had previously made a vigorous expiratory effort. Comparable values for a maximal natural cough were 212 cm H2O and 649 L/min. We conclude that paired magnetic thoracic nerve root stimulation produces gastric pressure and expiratory flow of an order of magnitude comparable to a natural cough.

Frequency-dependent conduction delay of motor-evoked potentials in multiple sclerosis.

Paired transcranial magnetic stimulation was applied in 33 multiple sclerosis (MS) patients and in 21 healthy controls. A major abnormality was found in latency of the second motor-evoked potential in MS patients. At interstimulus intervals of 75, 100, and 150 ms the central motor conduction time (CMCT) was significantly prolonged in MS patients to 139%, 150%, and 125% of the CMCT of a single magnetic stimulation (P=0.02, P=0.004, P=0.03), respectively. Voluntary contraction of the target muscle abolished the difference in latency independent of the degree of contraction. Stimulation intensity influenced the length of the interstimulus interval during which the maximal conduction delay was obtained. In MS patients there was no correlation between prolonged CMCT to a single magnetic stimulus and the frequency-dependent conduction delay to paired magnetic stimuli. It is hypothesized that the conduction delay of the conditioned response of paired magnetic stimuli in MS is of cortical origin and induced by abnormalities of the ascending volley to the neocortex.

The effect of lorazepam on the motor cortical excitability in man.

The effect of the short-acting benzodiazepine lorazepam on motor cortex excitability was investigated in 11 healthy volunteers using the technique of focal transcranial magnetic stimulation. The threshold intensity for evoking an electromyographic response in the resting and active abductor digiti minimi muscle, the size of the motor evoked potential, the duration of the cortical and peripheral silent periods, the corticocortical inhibition and facilitation after paired magnetic stimuli, and the transcallosal inhibition were used as parameters to assess various aspects of motor system excitability. Baseline values were compared with data obtained 2, 5 and 24 h after a single oral dose of 2.5 mg lorazepam. Resting and active motor thresholds and the size of the motor evoked potential remained unchanged. The duration of the cortical silent period was prolonged with a maximum effect 5 h after drug intake, while the peripheral silent period did not show any lengthening at that time. The corticocortical inhibition showed a tendency toward more inhibition, while the corticocortical facilitation was almost completely suppressed. The transcallosal inhibition showed an inconsistent trend to less inhibition. In parallel to the pharmacokinetics of lorazepam, all effects peaked at 2 h and 5 h, and were (partially) reversible after 24 h. It is hypothesized that most of these findings are due to the reinforcement of GABA action by lorazepam at the level of the motor cortex. The lack of effect on motor threshold and on the size of the motor evoked potential may indicate that these parameters are physiologically distinct from corticocortical excitability and the cortical silent period. The relevance of the present data in clinical epileptology is discussed.

PS-10-7 Short latency facilitation of responses to paired threshold magnetic stimuli of the human motor cortex

PS-10-7 Short latency facilitation of responses to paired threshold magnetic stimuli of the human motor cortex