Abnormal gating of somatosensory inputs in essential tremor (original) (raw)
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Cortical Involvement in the Generation of Essential Tremor
Journal of Neurophysiology, 2007
Conflicting results on the existence of tremor-related cortical activity in essential tremor (ET) have raised questions on the role of the cortex in tremor generation. Here we attempt to address these issues. We recorded 64 channel surface EEGs and EMGs from forearm muscles in 15 patients with definite ET. EEG and EMG power spectra, relative power of the rhythmic EMG activity, relative EEG power at the tremor frequency, and EEG-EMG and EEG-EEG coherence were calculated and their dynamics over time explored. Corticomuscular delay was studied using a new method for narrow-band coherent signals. Corticomuscular coherence in the contralateral central region at the tremor frequency was present in all patients in recordings with a relative tremor EMG power exceeding a certain level. However, the coherence was lost intermittently even with tremors far above this level. Physiological 15-to 30-Hz coherence was found consistently in 11 patients with significantly weaker EMG activity in this frequency range. A more frontal (mesial) hot spot was also intermittently coupled with the tremor and the central hot spot in five patients. Corticomuscular delays were compatible with transmission in fast corticospinal pathways and feedback of the tremor signal. Thus the tremor rhythm is intermittently relayed only in different cortical motor areas. We hypothesize that tremor oscillations build up in different subcortical and subcortico-cortical circuits only temporarily entraining each other. Baker SN, Kilner JM, Pinches EM, Lemon RN. The role of synchrony and oscillations in the motor output. Exp Brain Res 128: 109 -117, 1999. Baker SN, Pinches EM, Lemon RN. Synchronization in monkey motor cortex during a precision grip task. II. Effect of oscillatory activity on corticospinal output. CD. "Resetting" of postural tremors at the wrist with mechanical stretches in Parkinson's disease, essential tremor, and normal subjects mimicking tremor. Ann Neurol 31: 507-514, 1992. Brown P, Salenius S, Rothwell JC, Hari R. Cortical correlate of the Piper rhythm in humans. J Neurophysiol 80: 2911-2917, 1998. Bucher SF, Seelos KC, Dodel RC, Reiser M, Oertel WH. Activation mapping in essential tremor with functional magnetic resonance imaging. Ann Neurol 41: 32-40, 1997. Carter GC. Coherence and time delay estimation. Proc IEEE 75: 236 -255, 1987. Cerri G, Shimazu H, Maier MA, Lemon RN. Facilitation from ventral premotor cortex of primary motor cortex outputs to macaque hand muscles. J Neurophysiol 90: 832-842, 2003. Colebatch JG, Findley LJ, Frackowiak RS, Marsden CD, Brooks DJ. Preliminary report: activation of the cerebellum in essential tremor. Lancet 336: 1028 -1030, 1990. Conway BA, Halliday DM, Farmer SF, Shahani U, Maas P, Weir AI, Rosenberg JR. Synchronization between motor cortex and spinal motoneuronal pool during the performance of a maintained motor task in man. Govindan RB, Raethjen J, Arning K, Kopper F, Deuschl G. Time delay and partial coherence analyses to identify cortical connectivities. Biol Cybern 94: 262-275, 2006. Govindan RB, Raethjen J, Kopper F, Deuschl G. Estimation of time delay by coherence analysis (Abstract). Physica A 350: 277, 2005. Gross J, Tass PA, Salenius S, Hari R, Freund HJ, Schnitzler A. Corticomuscular synchronization during isometric muscle contraction in humans as revealed by magnetoencephalography. J Physiol 527: 623-631, 2000. Halliday DM, Conway BA, Farmer SF, Rosenberg JR. Using electroencephalography to study functional coupling between cortical activity and electromyograms during voluntary contractions in humans. Neurosci Lett 241: 5-8, 1998.
Intermittent cortical involvement in the preservation of tremor in essential tremor
Journal of Neurophysiology, 2017
Cortical involvement in essential tremor, an involuntary action tremor supposedly of subcortical origin, is uncertain. Conflicting results of corticomuscular coherence studies in essential tremor suggest an intermittent corticomuscular coupling. On the basis of the literature, we hypothesized that corticomuscular coupling is influenced by bilateral motor synchronization and “cognitive states” such as awareness of tremor. In the present study, we investigated 1) the existence of intermittent corticomuscular coherence (CMC) in essential tremor and 2) factors that influence CMC strength. In 18 essential tremor patients and 18 healthy controls, who mimicked tremor, we simultaneously recorded 64-channel EEG and 6-channel bipolar surface EMG from right and left wrist extensors and flexors. Right-sided (mimicked) hand tremor was recorded with and without a cognitive arithmetic task and with left-sided (mimicked) hand tremor. CMC values per task were compared within and between groups. Chan...
Directionality of corticomuscular coupling in essential tremor and cortical myoclonic tremor
Clinical Neurophysiology, 2021
h i g h l i g h t s Renormalized partial directed coherence is a suitable approach to investigate corticomuscular directionality in tremor. An efferent cortical drive is lacking in the majority of essential tremor (ET) patients; corticomuscular coupling in ET has predominantly an afferent direction. ET might be associated with a non-linear (rate-dependent) cortical transmission. a b s t r a c t Objective: A role of the motor cortex in tremor generation in essential tremor (ET) is assumed, yet the directionality of corticomuscular coupling is unknown. Our aim is to clarify the role of the motor cortex. To this end we also study 'familial cortical myoclonic tremor with epilepsy' (FCMTE) and slow repetitive voluntary movements with a known cortical drive. Methods: Directionality of corticomuscular coupling (EEG-EMG) was studied with renormalized partial directed coherence (rPDC) during tremor in 25 ET patients, 25 healthy controls (mimicked) and in seven FCMTE patients; and during a self-paced 2 Hz task in eight ET patients and seven healthy controls. Results: Efferent coupling around tremor frequency was seen in 33% of ET patients, 45.5% of healthy controls, all FCMTE patients, and, around 2 Hz, in all ET patients and all healthy controls. Ascending coupling, seen in the majority of all participants, was weaker in ET than in healthy controls around 5-6 Hz. Conclusions: Possible explanations are that tremor in ET results from faulty subcortical output bypassing the motor cortex; rate-dependent transmission similar to generation of rhythmic movements; and/or faulty feedforward mechanism resulting from decreased afferent (sensory) coupling. Significance: A linear cortical drive is lacking in the majority of ET patients.
Journal of Clinical Neurophysiology, 2004
The objective of the current study was to investigate the diagnostic potential of the routine tremor neurophysiologic analysis for the diagnosis of essential tremor (ET) in patients with postural tremor syndrome. Three hundred consecutive outpatients attending for postural tremor were included. Accelerometry and surface electromyography was performed between 1 and 4 weeks after the first clinical visit. A final clinical diagnosis (mean follow-up period, 53 months) of the postural tremor syndrome was made by two neurologists blind to the neurophysiologic results. Six neurophysiologic criteria for the diagnosis of ET were applied to define the neurophysiologic examination as compatible or not compatible with ET (all criteria must be present): (1) rhythmic burst of postural tremor on EMG; (2) tremor frequency greater than or equal to 4 Hz; (3) absence of rest tremor or, if present, frequency 1.5 Hz lower than the postural tremor; (4) absence of tremor latency from rest to postural position; (5) changes of the dominant frequency peak less or equal to 1 Hz after the weight load test; and (6) no changes in tremor amplitude after mental concentration. The neurophysiologic criteria for ET showed a sensitivity of 97.7%, a specificity of 82.3%, a positive predictive value of 95.1%, a negative predictive value of 91.1%, and positive probability ratio of 5.5. The odds ratio was 198.43 (95% CI, 66.03 to 596.35). For the diagnosis of ET in patients with postural tremor, routine neurophysiologic tests have high diagnostic and predictive value that justifies its practice in movement disorders clinics.
Essential tremors and TMS study
2019
Background: essential tremor (ET) is thought to emerge from activity in a distributed cerebello-thalamo-cortical network. It has been proposed that the network goes into oscillation because of some disorder of GABAergic inhibitory transmission. Objective: To test this idea by probing GABAergic circuitry in motor cortex using transcranial magnetic stimulation (TMS). Methods: Motor cortex excitability was examined using TMS in 21 patients with essential tremor and in 20 control subjects. Resting and active motor threshold (RMT, AMT) and input–output curves examined corticospinal excitability. Contralateral silent period (cSP) at a different range of stimulation intensities, and the ipsilateral silent period (iSP) using a stimulus intensity of 150% RMT were used as measures of GABAergic function. Results: RMT and AMT were significantly lower in patients than controls and patients had a steeper I/O curve. However, there were no significant differences in either cSP at different intensit...
Difference of disability between electrophysiologic subgroups of essential tremor
Canadian Journal of Neurological Sciences, 2000
The aim of the study was to test the validity of the controversial subdivision of essential tremor (ET) patients into electrophysiological subgroups. We evaluated a hundred patients with ET using surface electromyographic (EMG) recordings of antagonists forearm muscles and distinguished three groups: the first group showed synchronous activity of antagonistic muscles, the second showed alternating activity of antagonist muscles; and the third group consisted of patients whose EMG recordings were not compatible with the other two groups. We compared patients with synchronous and alternating activity in terms of sex, age at onset, duration of illness, family history of tremor, symmetry and frequency of tremor, and the scores of a disability scale. The only significant difference between the patients with synchronous and alternating activity was that the patients with synchronous activity were more disabled. This result adds to the evidence for distinct electrophysiological subgroups o...
Annals of Neurology, 1993
The origin of essential tremor is unknown. Animal models have suggested that the inferior olivary nucleus may act as a tremor generator. We used positron emission tomography to study changes in regional cerebral blood flow associated with involuntary postural tremor and passive wrist oscillation in patients with essential tremor. Activation due to voluntary wrist oscillation and arm extension without tremor was studied in normal control subjects. The essential tremor group had bilaterally increased cerebellar blood flow at rest (without tremor) compared with the control group. Involuntary postural tremor was associated with further bilateral cerebellar activation, and also contralateral striatal, thalamic, and sensorimotor cortex activation. Voluntary wrist oscillation, maintained arm extension without tremor, and passive wrist oscillation were all associated with significant ipsilateral rather than bilateral cerebellar activation. We conclude that essential tremor is asociated with increased bilateral cerebellar activity both at rest and during tremor. Jenkins IH, Bain I'G, Colebatch JG, Thompson PI), Findley IJ, Frackowiak RSJ, Marsden CD, Brooks DJ. A positron emission tomography smdy of essential tremor: evidence for overactivity of cerelxllar connections. Ann Neurol 1933;34:82-30 Essential tremor (ET) is considered to be the most common movement disorder. Various studies have reported an overall population prevalence of between 0.3 and 1.794, and up to 5.5% in the over-40 age group [I}. The variation in these figures may in part reflect differences both in the diagnostic criteria used and in the genetic makeup of the communities studied. The pathological bais of ET is not understood; no consistent lesions have been found at postmortem examinations [2-6]. The existence of a possible central generator for the tremor has been hotly debated. Ipsilateral hemiparesis { 7 ] , cerebellar stroke LS}, and stereotactic lesions of the contralateral nucleus ventralis intermedius (Vim) of the thalamus 197 can all abolish ET in humans, lending support to a central origin for El-. The pharmacology of ET fails to clarify the issue of central or peripheral tremor origin; patients with ET gain variable relief from centrally acting agents (alcohol, benzodiazepines, and the anticonvulsant primidone) {10-12}, while useful P-blockers, such as propranolol and sotalol, have peripheral Pz-antagonist action {I 31. Consequently, the mechanisms by which alcohol, P-blockers, and primidone reduce the amplitude of tremor are likely to be variable, involving the suppression of either central o r peripheral neural activity. Centrally acting agents that induce postural tremor in humans include cholinergic and monoaminergic agonists, the anticonvulsant (and y-;uninobutyric acid [GAUA} agonist) sodium valproate, heavy metals, metal chelators, and carbon tetrachloride 1141.
Journal of Neurophysiology
Pathological tremor is an oscillation of body parts at 3-10 Hz, determined by the output of spinal motor neurons (MNs), which receive synaptic inputs from supraspinal centres and muscle afferents. The behaviour of spinal MNs during tremor is not well understood, especially in relation to the activation of the multiple muscles involved. Recent studies on essential tremor patients have shown that antagonist MN pools receive shared input at the tremor frequency. Here, we investigate the synaptic inputs related to tremor and voluntary movement, and their coordination across antagonist muscles. We analysed the spike trains of motor units identified from high-density surface electromyography from the forearm extensor and flexor muscles in 15 essential tremor patients during postural tremor. The shared synaptic input was quantified by coherence and phase difference analysis of the spike trains. All pairs of spike trains in each muscle showed coherence peaks at the voluntary drive frequency...