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The Silent Period Induced by Transcranial Cranial Nerves

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The Silent Period Induced by Transcranial Cranial Nerves 5865tournal ofNeurology, Neurosurgery, and Psychiatry 1995;59:586-596 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.6.586 on 1 December 1995. Downloaded from The silent period induced by transcranial magnetic stimulation in muscles supplied by cranial nerves: normal data and changes in patients K J Werhahn, J Classen, R Benecke Abstract magnetic stimulation in limb muscles a period The silent period induced by transcranial of electromyographic (EMG) silence (silent magnetic stimulation of the sensorimotor period) lasting some 200 ms in small hand cortex (Magstim 200, figure of eight coil, muscles can be found if the target muscle is loop diameter 7 cm) in active muscles tonically active.'--8 The duration of the silent supplied by cranial nerves (mentalis, period follows a proximodistal gradient in the sternocleidomastoid, and genioglossus) upper limb muscles, being longer in small was studied in 14 control subjects and hand muscles than in proximal arm muscles. nine patients with localised lesions of the As to precisely what structures are involved sensorimotor cortex. In the patients, in the generation of the silent period there measurements of the silent period were is an increasing amount of data suggesting that also made in the first dorsal interosseus it is not due to changes in a motoneuron and tibialis anterior muscles. In the con- activity but to changes in pyramidal cell trols, there was a silent period in con- excitability.' 68-11 tralateral as weil as ipsilateral cranial Apart from the study of distal limb muscles, muscles and the duration of the silent several reports exist on activation of cortico- period increased with increasing stimulus nuclear fibres supplying cranial nerve intensities. The mean duration of the motoneurons using transcranial magnetic silent period was around 140 ms in con- stimulation.'2 13 With bilateral recordings two tralateral mentalis muscle and around types of responses can be seen in muscles sup- 90 ms in contralateral sternocleidomas- plied by cranial nerves: purely ipsilateral short toid muscle at 1-2 x threshold stimula- latency responses and bilateral responses of tion strengths. Whereas the duration of longer latency. On the basis of latency, ampli- the silent period in ipsilateral mentalis tude, configuration, and reaction to facilitatory muscle was shorter than on the contralat- manoeuvres, these two types were considered eral side it was similar on both sides in to originate from unilateral direct excitation of sternocleidomastoid muscle. In patients cranial nerves at proximal sites and the corti- with focal lesions of the face associated conuclear system respectively.'2 13 The bilateral primary motor cortex and corresponding (corticonuclear) long latency responses reflect http://jnnp.bmj.com/ central facial paresis, the silent period in the bilateral cortical input to the brainstem mentalis muscle was shortened whereas it nuclei of cranial nerves. was unchanged or prolonged in limb mus- The first aim of the present study was to cles (first dorsal interosseus, tibialis ante- describe the characteristics of the silent period rior) with stimulation over the affected induced by transcranial magnetic stimulation hemisphere. By contrast, in a patient with in facial, neck, and tongue muscles in normal a lesion within the parietal cortex, the subjects. If it is assumed that the silent period on September 23, 2021 by guest. Protected copyright. silent period in mentalis muscle was pro- in these muscles is also generated cortically, a longed with stimulation of the affected silent period should also exist in cranial mus- side. cles ipsilateral to the site of stimulation, given the bilateral corticonuclear projection. (3 Neurol Neurosurg Psychiatry 1995;59:586-596) Secondly, we wanted to examine changes in the duration of the silent period in muscles supplied by cranial nerves in patients with uni- Department of Keywords: transcranial magnetic stimulation, cranial lateral cortical lesions. Alterations of the silent Neurology, Heinrich- nerves, sensorimotor cortex, silent period period in distal limb muscles of Heine Universitat patients with Dusseldorf, Germany cortical and subcortical or thalamic lesions K J Werhahn Transcranial magnetic stimulation has been have been described.45 " In patients with J Classe widely used to study the function of the cor- lesions of the primary motor cortex itself the R Benecke ticospinal pathways in humans.' The silent period was shortened'4 or abolished'0 in Correspondence to: Professor Dr R Benecke, responses it evokes are thought to be gener- muscles contralateral to the hemispheric Department of Neurology, ated by excitation of corticomotoneuronal lesions. In patients with lesions in other motor Universitat Rostock, Gehlsheimer Strasse 20, pathways at the cortical or just subcortical competent cortical areas which are afferent to 18055 Rostock, Germany. level in the motor cortex and to be mediated the primary motor cortex a prolongation of the Received 7 October 1994 by fast conducting corticospinal pathways. 2 silent period occurred.14 and in final revised form 16 June 1995 After the early compound muscle action Some of the data from the present investiga- Accepted 18 August 1995 potential (CMAP) evoked by transcranial tion have appeared in abstract form .15 The silent period induced by transcranial magnetic stimulation in muscles supplied by cranial nerves: normal data and changes in patients 587 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.6.586 on 1 December 1995. Downloaded from Methods was established by MRI and CT performed Experiments were performed in 14 control during the stay in hospital. subjects and nine patients. All gave their informed consent for the study and the project STIMULATION PROCEDURE AND RECORDINGS IN was approved by the local ethics committee. MUSCLES SUPPLIED BY CRANIAL NERVES IN CONTROLS AND PATIENTS CONTROLS Subjects and patients were seated in a comfort- Fourteen control subjects (11 men, three able chair. Transcranial magnetic stimulation women, mean age 34-2 (range 19-52) years) was performed with a conventional Nova- were chosen from among the authors and metrix 200 stimulator (Fa Madaus, Magstim other members of the department. Subjects Company UK) with a maximum output of 2-0 with a history of hypertension, headache, a Tesla, connected to a figure of eight magnetic cerebrovascular event, or subjects over the age coil, each loop having a diameter of 7 cm. of 60 were excluded. This last criterion was Technical information about the stimulator used to reduce the possibility of subclinical can be found elsewhere.'1 16 cerebrovascular abnormalities. The coil was held over the skull with the maximum current in the coil flowing in an PATIENTS anteroposterior direction. The centre of the Table 1 lists the clinical details of the patients. coil was placed consecutively over both hemi- Patients (five men, four women, mean age spheres about 9 cm lateral and 3 cm anterior 59-1 (range 41-75) years were selected among to a line connecting the vertex and the external consecutive patients seen as inpatients in our auditory meatus. The precise coil position was department, who had a unilateral hemispheric then adjusted to give a response of maximum lesion due to vascular accident or tumour. size in the contralateral cranial muscle at a Patients unable to cooperate or confined to given stimulus intensity. The optimal position bed were excluded. Clinical data and results of of the coil was marked on the skull for better investigations were obtained from the patients' retrieval. Before each recording session the records. Two patients (3 and 5) reported pre- threshold for evoking cortical muscle vious cerebrovascular events. Patient 3 had responses was determined for each muscle had a left hemispheric infarct with global dys- with the subject or patient at rest and the coil phasia and right facial weakness one year held over the optimal spot. Threshold was before the study and patient 5 had had a left defined as the lowest stimulus intensity (as a hemispheric infarct with right sided hemipare- percentage of the maximal output of the sis, including the face, with complete remis- device) with which a defined cortically evoked sion after a few weeks, four years previously. response of at least 100 ,uV peak to peak The localisation of the lesions in the patients amplitude could be obtained on three consecu- Table 1 Clinical datafor patients CMCTIAmplitude Patient Age (y) Sex Localisation Type Interval Clinicalfindings Hand Leg http://jnnp.bmj.com/ 1 49 F Right parietal TU* 33 months CN normal, mild Normal Normal sensory deficits left arm, no dysphasia 2 61 M PMC Infarct 4 months Initially mild lower T CMCT Normal facial weakness, mono- left paresis left lower arm, no dysphasia 3 75 F Left fronto- Infarct 5 days CN normal, in 1992 4 Amp Normal parietal dysphasia and right facial right weakness, sensorimotor on September 23, 2021 by guest. Protected copyright. dysphasia, paresis right arm 4 65 F Right fronto- Infarct 4 years Minor hemiparesis left Normal Normal parietal arm > leg, predominant left facial weakness, no dysphasia, left hemi- neglect and sensory deficits 5 64 M Left postcentral Infarct 1 year CN normal, no dysphasia, 4 Amp Normal gyrus spastic monoparesis right right arm, transient right hemi- paresis (including face) in 1989 6 54 M Left PMC and Infarct 2 8 months Right facial weakness and No response 4 Amp striatocapsular minor motor aphasia, right t CMCT spastic hemiparesis right
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