[Study of human speech function by magnetic stimulation].
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Biomedical subjects
Publications and source records attributed to H Tokimura.
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1. EMG responses evoked in hand muscles by transcranial stimulation over the motor cortex were conditioned by a single motor threshold electrical stimulus to the median nerve at the wrist in a total of ten healthy subjects and in five patients who had electrodes implanted chronically into the cervical epidural space. 2. The median nerve stimulus suppressed responses evoked by transcranial magnetic stimulation (TMS) in relaxed or active muscle. The minimum interval between the stimuli at which this occurred was 19 ms. A similar effect was seen if electrical stimulation was applied to the digital nerves of the first two fingers. 3. Median or digital nerve stimulation could suppress the responses evoked in active muscle by transcranial electrical stimulation over the motor cortex, but the effect was much less than with magnetic stimulation. 4. During contraction without TMS, both types of conditioning stimuli evoked a cutaneomuscular reflex that began with a short period of inhibition. This started about 5 ms after the inhibition of responses evoked by TMS. 5. Recordings in the patients showed that median nerve stimulation reduced the size and number of descending corticospinal volleys evoked by magnetic stimulation. 6. We conclude that mixed or cutaneous input from the hand can suppress the excitability of the motor cortex at short latency. This suppression may contribute to the initial inhibition of the cutaneomuscular reflex. Reduced spinal excitability in this period could account for the mild inhibition of responses to electrical brain stimulation.
The aim of the experiments was to investigate the effects of speech on the excitability of corticospinal pathways to human hand muscles. Single transcranial magnetic stimuli were given randomly over the hand area of either the left or right motor cortex of 10 right-handed and 3 left-handed normal volunteers. Electromyographic responses were recorded in the relaxed first dorsal interosseous muscle while the subjects (a) read aloud a piece of text, (b) read silently, (c) spoke spontaneously, or (d) made sounds without speaking. The only consistent effect across subjects occurred during task a, which significantly increased the size of responses evoked in the dominant hand of all subjects, but had either no effect (8 subjects) or a smaller effect in the nondominant hand. Tasks b and d had no reliable effect, whereas task c tended to increase response size in both hands. Control measurements suggest that the effects in task a were caused by changes in cortical rather than spinal excitability. This is the first demonstration of lateralized speech effects on the excitability of cortical arm areas. The results provide a useful adjunct to other tests of cerebral dominance, using only single- rather than repetitive-pulse cortical stimulation.
Pairs of threshold magnetic stimuli were applied over the motor cortex at interstimulus intervals of 1-6 ms, and EMG responses recorded from the relaxed or active first dorsal interosseous muscle of 7 normal subjects. In relaxed subjects, when the interval between the stimuli was around 1.0-1.5 ms, 2.5-3.0 ms or 4.5 ms or later, the size of the response to the pair of stimuli was much greater than the algebraic sum of the response to each stimulus alone. During contraction, fewer peaks of facilitation were observed. Facilitation was evident if the stimuli were 0.9-1.1 times threshold in the relaxed state, and 1.0-1.1 times threshold during voluntary contraction. Experiments using either magnetic followed by anodal electric stimulation, or pairs of anodal electric stimuli, suggested that the facilitation most likely occurred within the cerebral motor cortex. Given the timings at which facilitation is prominent, it seems likely that it reflects interactions between circuits normally responsible for production of I-waves.
Interfascicular neurolysis was performed in nine patients with spontaneous anterior interosseous nerve palsy. In eight of these patients, an hourglass-like constriction in the fascicles forming the anterior interosseous nerve was found within the main trunk of the median nerve at 2-7.5 cm above the medial epicondyle. The clinical signs and symptoms of these eight patients were similar to those that have been described to isolated neuritis. While the etiology remains unknown, when spontaneous anterior interosseous nerve palsy is suspected to be caused by isolated neuritis, interfascicular neurolysis should be performed to confirm the lesion and to discover whether fascicular constriction is present.
A figure-8 coil was designed that was capable of generating currents over a relatively limited area. In this study, we used the figure-8 coil to localize human cerebral motor cortex by transcranial magnetic stimulation and assessed its value as a diagnostic tool for neurosurgical disease. The subjects were 10 normal volunteers and 12 neurosurgical patients. The points obtaining a response were plotted and the response area was delineated for each stimulus output. Rectangular coordinates were subsequently determined for the C3-Cz-C4 line with the stimulation sites set 1.0 cm apart. Then amplitude and latency maps were displayed by a computer wave map program. In normal volunteers, the posterior margin of the site where a threshold +5% stimulus obtained a response from the THE or ADM muscles almost coincided with the central sulcus. The optimal areas were relatively narrow on the amplitude and latency maps. In the patient with a left frontal convexity meningioma, the left threshold +5% area for the THE and ADM muscles showed marked anterolateral shift. No threshold map could be obtained on the affected side in patients with metastatic tumor and astrocytoma. Low perfusion areas caused by moyamoya disease and arteriovenous malformations produced narrowing of the optimal zone on the threshold map of the affected side. Hyperexcitability of the motor cortex was recognized in the arteriovenous malformation patients. Transcranial focal magnetic stimulation is a useful noninvasive diagnostic method for identification of the human cerebral motor cortex. It provides important information about changes in the localization and excitability of the motor cortex in neurosurgical patients and should be helpful for treatment planning.
The actual site of excitation of the facial nerve by transcranial magnetic stimulation was investigated in five patients with hemifacial spasm who underwent microvascular decompression. The facial nerve was stimulated preoperatively and intraoperatively by transcranial magnetic stimulation and intraoperatively by electrical stimulation at its root exit zone with a minimum of surgical invasion of the facial nerves. The onset latency of compound muscle action potentials recorded from the nasalis muscle was 5.06 +/- 0.44 ms by magnetic stimulation and 5.08 +/- 0.43 ms by electrical stimulation. The latency difference was 0.06 +/- 0.08 ms. Therefore, transcranial magnetic stimulation was basically the same as electrical stimulation in onset latency. From this study, it appears that the root exit zone of the facial nerves is stimulated by transcranial magnetic stimulation.
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A rare case of extracranial internal carotid artery (ICA) aneurysm coexisting with intracranial multiple aneurysms in a 64-year-old female is reported. The three intracranial aneurysms were clipped uneventfully by two-stage craniotomies. The extracranial ICA aneurysm at the infratemporal region was excised through a high cervical route and ICA was reconstructed by an end-to-end direct anastomosis. Ours is the first case reported of extra- and intracranial aneurysms surgically treated successfully.
It was the object of the present study to determine whether transcranial facial nerve stimulation using a magnetic coil can be clinically applicable, and to find the site where the facial nerve is best stimulated. A magnetic coil was placed over the parieto-occipital skull of the subjects for stimulation, and the facial nerve was electrically stimulated in its intracranial and peripheral courses. Then an electromyogram was recorded from the nasalis muscle of the face on the stimulated side. In 9 healthy volunteers, 18 facial nerves received magnetic and electric stimuli in the peripheral region, and the actual site of stimulation was estimated from the conduction velocity of the nerve. The conduction velocity was 56.6 +/- 4.8 m/s, and the latency between CMAPs for electric at the magnetic stimuli to the posterior tragus was 1.23 +/- 0.21 ms. Therefore, the position stimulated by magnetic coil was estimated to be 70.0 +/- 11.4 mm central to the posterior tragus, i.e., near the root exit zone. In two patients undergoing surgery in the cerebellopontine angle, transcranial magnetic stimulation and electrical stimulation of the intracranial facial nerve were compared intraoperatively. The CMAP produced by transcranial magnetic stimulation coincided closely with that produced by direct electrical stimulation of the root exit zone. Thus, the facial nerve was stimulated at the root exit zone, and this method could be expected to be useful for evaluation of disorders of the intracranial facial nerve.
Five patients with aneurysms in the cavernous sinus were treated by direct surgical approach. Two small aneurysms were located in the C3 segment, one small aneurysm was on the primitive trigeminal artery (PTA), and the last two aneurysms were giant ones. The three small aneurysms were discovered incidentally by angiography and the two giant aneurysms presented oculomotor palsy. After ordinary fronto-temporal craniotomy, the two C3 aneurysms were treated through an intradural approach, and the PTA aneurysm and the two giant aneurysms were treated through combined epi- and subdural approach. The three small aneurysms were clipped and the two giant aneurysms were trapped with the reconstruction of ICA by saphenous veins. In all cases the aneurysms were excluded postoperatively, but in one giant-aneurysm case (Case 5) the bypass was occluded postoperatively, but the patient had no permanent neurological deficit. The four patients developed third nerve palsy and one developed fourth nerve palsy which resolved within 3 to 6 months. In one C3-aneurysm case (case i) the patient had loss of vision due to much packing in the medial side of the ICA. All patients were discharged and returned to their usual life. Three cases (case 2, 4, 6) are presented here and the problems of direct surgical management of aneurysms in the cavernous sinus are discussed with the related literature.
Intraoperative auditory brainstem response (ABR) monitoring was performed in 27 patients undergoing C-P angle surgery (12: hemifacial spasm, 10: trigeminal neuralgia, 2: glossopharyngeal neuralgia, 3: C-P angle tumor, 2 epidermoid, 1 meningioma). Because of the introduction of this method, no patient suffered from postoperative hearing disturbance in this series. During C-P angle surgery, the wave V of ABR changes according to the retraction of the cerebellum and the manipulation of the eighth cranial nerve. Many authors have discussed this change, however the timing and the mechanism of disappearance of wave V is unclear. Accordingly, the authors discussed the correlation between the prolongation of wave V latency and its amplitude. The wave V amplitude was measured from the positive peak of wave V to the next negative peak. Then, the correlation between the prolongation of wave V latency and its reduction ratio (%) of amplitude was represented as a parabola. The wave V reduces its amplitude when the prolongation of the latency is from 1.5 ms to 2.0 ms. Once the prolongation of the latency is over 1.5 ms, the amplitude of wave V seems to be reduced suddenly, because it takes over 1'30'' to finish each record. But the authors demonstrated the gradual reduction of the amplitude of wave V in Figure 3. As mentioned above, the prolongation of wave V latency must be less than 1.5 ms, and the neurosurgeon must recognize this turning point during C-P angle surgery.
Two cases of trigeminal neuralgia associated with the primitive trigeminal artery are reported. From 1981, the authors have treated 131 trigeminal neuralgia patients with microvascular decompression. Among them, we encountered two rare cases of trigeminal neuralgia associated with the primitive trigeminal artery (PTA) and its variant (PTAV). Case 1 is a 74-year-old woman who was admitted to our hospital due to pain of maxilla and mandible. We diagnosed her pain as trigeminal neuralgia. Preoperative angiogram showed the primitive trigeminal artery arising from the cavernous portion of the right internal carotid artery (ICA). She underwent a microvascular decompression operation. We found that her right trigeminal nerve was compressed by the right superior cerebellar artery (SCA) and the right anterior inferior cerebellar artery (AICA). We transferred the offending arteries, and her pain disappeared. Case 2 is a 48-year-old man who was admitted to our hospital due to severe mandibular pain. We diagnosed his pain as trigeminal neuralgia, and he underwent a microvascular decompression operation. His left trigeminal nerve was found compressed by the left SCA and the AICA, and the AICA was arising from the direction of Meckel's cave. His severe pain disappeared completely after operation. Postoperative angiogram of his left ICA showed an aberrant artery arising from the cavernous portion of the ICA, to the region of the left AICA. This aberrant artery is a variant of PTA (PTAV). PTA and PTAV, the so called persistent congenital arteries, are said to accompany aneurysms and other vascular lesions, and affect hemodynamic stress.(ABSTRACT TRUNCATED AT 250 WORDS)
A case of cerebellar AVM onset with hemifacial spasm was reported. The patient, a 47 year old woman, had been suffering from lt. hemifacial spasm for 10 years, and she visited our hospital for operation. Preoperative angiography revealed that there was an AVM in the lt. cerebellar hemisphere fed by the lt. SCA and the lt. PICA. In addition, a non-ruptured saccular aneurysm was observed on the feeding SCA. The microvascular decompression was performed and the AVM was removed, since the lt. facial nerve had been compressed by this elongated and redundant PICA. After the operation, lt. hemifacial spasm disappeared. Two months after the operation, the aneurysm disappeared angiographically. These findings indicated that the hemodynamic stress due to the presence of AVM seemed to have resulted in ectasia or redundancy of the PICA and in the development of the aneurysm. Such a case was quite rare and it may be the first time to be reported in literatures.