title: Transcranial magnetic stimulation reduces masseter motoneuron pool excitability throughout the cortical silent period.
abstract: OBJECTIVE
  To evaluate the time-course of changes in masseter motoneuron pool excitability following transcranial magnetic stimulation of motor cortex, and relate this to the duration of the masseter cortical silent period (CSP).
  
  
  METHODS
  Surface EMG was recorded bilaterally from masseter and digastric muscles in 13 subjects. Focal TMS was applied at 1.3x active motor threshold (AMT) to motor cortex of one hemisphere to elicit a muscle evoked potential (MEP) and silent period bilaterally in masseter as subjects maintained an isometric bite at approximately 10% maximum. With jaw muscles relaxed, a servo-controlled stretcher evoked a stretch reflex in masseter which was conditioned by TMS (1.3x AMT) at 14 different conditioning-testing intervals. There were 20 trials at each interval, in random order. TMS evoked no MEP in resting masseter, but often produced a small MEP in digastric.
  
  
  RESULTS
  Mean (+/-SE) masseter CSP was 67+/-3ms. The masseter stretch reflex was facilitated when stretch preceded TMS by 8 and 10ms, which we attribute to spatial summation of corticobulbar and Ia-afferent excitatory inputs to masseter. Masseter stretch reflex amplitude was reduced when TMS was given up to 75ms before stretch, and for up to 2ms afterwards.
  
  
  CONCLUSIONS
  We conclude that descending corticobulbar activity evoked by TMS acts bilaterally on brainstem interneurons that either inhibit masseter motoneurons or increase pre-synaptic inhibition of Ia-afferent terminals for up to 75ms after TMS. The reduction of masseter motoneuron pool excitability following TMS has a similar time-course to the CSP.
  
  
  CONCLUSIONS
  In contrast to the situation for spinal and facial (CN VII) muscles, the masseter CSP appears to have no component that can be attributed exclusively to cortical mechanisms. Abnormalities in the masseter cortical silent period observed in neurological conditions may be due to pathophysiological changes at cortical and/or sub-cortical levels.
authors.affiliation: Discipline of Physiology, School of Molecular & Biomedical Sciences, Research Centre for Human Movement Control, The University of Adelaide, Adelaide SA 5005, Australia.
authors.forename: Paul F
authors.initials: PF
authors.lastname: Sowman
authors.forename: Stanley C
authors.initials: SC
authors.lastname: Flavel
authors.forename: Christie L
authors.initials: CL
authors.lastname: McShane
authors.forename: Timothy S
authors.initials: TS
authors.lastname: Miles
authors.forename: Michael A
authors.initials: MA
authors.lastname: Nordstrom
mesh_terms: D000328:Adult; D004525:Efferent Pathways / Q000502:physiology; D004576:Electromyography; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D008297:Male; D008406:Masseter Muscle / Q000294:innervation*; D009044:Motor Cortex / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology*; D012026:Reflex, Stretch / Q000502:physiology; D050781:Transcranial Magnetic Stimulation