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A magnetic stimulator was used for direct transcutaneous stimulation of the intracranial portion of the facial nerve in 15 normal subjects and in patients with Bell's palsy, demyelinating neuropathy, traumatic facial palsy and pontine glioma. Compound muscle action potentials (CMAPs) thus elicited in the orbicularis oris muscle of controls were of similar amplitude but longer latency (1.3 SD 0.15 ms) compared with CMAPs produced by conventional electrical stimulation at the stylomastoid foramen. No response to magnetic stimulation could be recorded from the affected side in 15 of 16 patients with Bell's palsy. Serial studies in two patients demonstrated that the facial nerve remained inexcitable by magnetic stimulation despite marked improvement in clinical function. In the patient with a pontine glioma, the CMAP elicited by transcranial magnetic stimulation was of low amplitude but normal latency. In six of seven patients with demyelinating neuropathy, the response to intracranial magnetic stimulation was significantly delayed. Magnetic stimulation produced no response in either patient with traumatic facial palsy. Although the precise site of facial nerve stimulation is uncertain, evidence points to the labyrinthine segment of the facial canal as the most likely location. [ABSTRACT FROM AUTHOR]

Central motor conduction (CMC) to abductor digiti minimi (ADM) was evaluated in 22 patients with motor neurone disease (MND) using magnetic stimulation of the motor cortex and electrical stimulation at the C7/T1 interspace. CMC was abnormal in 14 patients; prolonged CMC time and absence of response to brain stimulation were more frequent abnormalities than low amplitude responses without prolonged CMC time. The technique can reveal subclinical upper motor neurone involvement and document central motor pathway dysfunction in MND. The patterns of abnormality are not specific to MND; all may occur in other neurological disorders including multiple sclerosis.

A conspicuous feature of rapid eye movement (REM) sleep is atonia of postural muscles due to a powerful brainstem inhibitory effect on spinal motoneurones. However, small myoclonic jerks occur during REM sleep and increased activity of cortical neurones is suggested by the EEG. Transcranial cortical stimulation with magnetic pulses has been used to investigate motor excitability during sleep in man. Motor responses were evoked during sleep using stimuli identical to those used in wakefulness. Response amplitudes were depressed during slow wave sleep (SWS) and enhanced or the same during REM sleep. These findings suggest that the susceptibility of the human motor cortex to stimulation is enhanced during REM sleep.

Central motor conduction (CMC) was evaluated in 32 normal subjects and 83 patients with multiple sclerosis, and the findings were correlated with clinical signs and evoked potential data. CMC time was obtained from the latency difference in responses from the abductor muscle of the little finger to magnetic stimulation of the motor cortex and electrical stimulation at the C-7/T-1 interspace. Mean CMC time in normal subjects was 6.2 msec (SD 0.86 msec), and amplitudes of responses to cortical stimuli were at least 18% of those obtained with stimuli at the wrist. CMC was abnormal in 60 patients with multiple sclerosis (72%); this correlated well with brisk finger flexor jerks (p less than 0.005). CMC was abnormal in 79% of patients with weakness of the abductor muscle of the little finger and in 54% with a normal muscle. Neurological examination was normal in 7 arms with abnormal CMC. Visual evoked potentials were abnormal in 67%, somatosensory evoked potentials in 59%, and brainstem auditory evoked potentials in 39% of those tested. For each procedure more subjects had abnormal CMC and normal evoked potentials than the reverse. The technique is of value for demonstrating and documenting central motor pathway lesions in multiple sclerosis, especially when physical signs are equivocal.