Topographical distribution and functional properties of cortically induced rhythmical jaw movements in the monkey (Macaca fascicularis)

1989 ◽  
Vol 61 (3) ◽  
pp. 635-650 ◽  
Author(s):  
C. S. Huang ◽  
H. Hiraba ◽  
G. M. Murray ◽  
B. J. Sessle

1. The lateral part of the pericentral cortex of both hemispheres in three awake monkeys was explored with intracortical microstimulation (ICMS) using short trains (T/S; 200-microseconds pulses at 333 Hz for 35 ms, less than or equal to microA) and long trains (C/S; 200-microseconds pulses at 50 Hz for 3 s, less than or equal to 60 microA). In both hemispheres of one of these monkeys, the responsiveness of single cortical neurons to stimulation of the orofacial region was tested at the same intracortical sites where ICMS was applied. 2. Movements were evoked from four physiologically defined cortical regions: the primary face motor cortex (MI), the primary face somatosensory cortex (SI), the principal part of the cortical masticatory area (CMAp) which was located in the precentral gyrus lateral to MI, and a deep part of the cortical masticatory area (CMAd) which was located in the inferior face of the frontal operculum. 3. Two types of cortically induced movements were observed: a single twitch movement and EMG activity of the orofacial muscles that was evoked by T/S at a short latency (10–45 ms) and rhythmical jaw movements (RJMs) which were only evoked by C/S. 4. RJMs were evoked at C/S frequencies ranging from 20 to 300 Hz. At movement threshold, the frequency of the cortically induced RJMs varied from 0.7 to 1.5 Hz and usually increased with the increase of C/S intensity up to 2 times movement threshold. The vertical amplitude of RJMs was also stimulus dependent, and at movement threshold it ranged from 3 to 9 mm. 5. The movement patterns of the cortically induced RJMs remained constant during the course of C/S but could be differentiated in the frontal plane into ipsilateral- (RJMi), vertical-(RJMv), and contralateral- (RJMc) directed movements. These three different patterns of RJMs were associated with different patterns of masticatory muscle activity. 6. Each cortical region contained many sites from which RJMs could be induced (so-called RJM sites). The RJMi sites were more numerous than RJMc sites in all regions except SI and were located anterolateral or lateral to the RJMc sites in each region; the RJMv sites were scattered throughout each cortical region. 7. In MI, C/S elicited RJMs from 94 intracortical sites from which short-latency twitch movements could also be evoked by T/S.(ABSTRACT TRUNCATED AT 400 WORDS)

1988 ◽  
Vol 59 (3) ◽  
pp. 819-832 ◽  
Author(s):  
S. H. Chandler ◽  
L. J. Goldberg

1. In the ketamine-anesthetized guinea pig, electromyographic (EMG) responses of the digastric muscle and vertical and horizontal movements of the mandible were studied when loci within the caudal pontine and rostral medullary reticular formation were stimulated during rhythmic jaw movements (RJMs) evoked by stimulation of the masticatory area of the cortex. 2. Within these regions electrical brain stem stimulation of the pontis nucleus caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation completely blocked RJMs at stimulus intensities as low as 10 microA while suppressing the short-latency digastric EMG response that was time locked to each cortical stimulus in the train. PnC-Gi stimulation did not, however, reduce the excitability of the short-latency corticotrigeminal excitatory pathway to digastric motoneurons when tested by short pulse train stimulation at 2 Hz (3 pulses, 500 Hz, 0.3 ms) in the absence of RJMs. 3. Short trains (80 ms) of PnC-Gi stimuli delivered at various phases of the RJM cycle produced a permanent phase shift of the RJM rhythm. If the stimulus train was delivered at an early phase of the cycle (8-40%) the next cycle onset was advanced; if the train was delivered later in the cycle (60-80%) the next cycle onset was delayed. Long trains of PnC-Gi stimuli (100, 200, 300, and 400 ms) increased the time of onset of the next cycle by an amount directly proportional to the duration of the stimulus train. 4. Digastric EMG activity occurring during cortically evoked RJMs occupied nearly 50% of the cycle. If a short train of PnC-Gi stimuli was delivered between approximately 5 and 125 ms after the onset of the burst, the duration of the burst was significantly shortened. 5. These results demonstrate that the suppression of cortically evoked RJMs resulting from PnC-Gi stimulation is due to direct effects on central circuits responsible for the production of the RJM behavior and not on the motoneurons themselves. The evidence presented is consistent with our previously presented hypothesis that the neurons involved in mediating the short-latency corticotrigeminal pathway to digastric motoneurons are separate and distinct from those neurons comprising the central networks responsible for the production of the fundamental jaw oscillation during RJMs.


1991 ◽  
Vol 66 (4) ◽  
pp. 1156-1165 ◽  
Author(s):  
V. L. Smith-Swintosky ◽  
C. R. Plata-Salaman ◽  
T. R. Scott

1. Extracellular action potentials were recorded from 50 single neurons in the insular-opercular cortex of two alert cynomolgus monkeys during gustatory stimulation of the tongue and palate. 2. Sixteen stimuli, including salts, sugars, acids, alkaloids, monosodium glutamate, and aspartame, were chosen to represent a wide range of taste qualities. Concentrations were selected to elicit a moderate gustatory response, as determined by reference to previous electrophysiological data or to the human psychophysical literature. 3. The cortical region over which taste-evoked activity could be recorded included the frontal operculum and anterior insula, an area of approximately 75 mm3. Taste-responsive cells constituted 50 (2.7%) of the 1,863 neurons tested. Nongustatory cells responded to mouth movement (20.7%), somatosensory stimulation of the tongue (9.6%), stimulus approach or anticipation (1.7%), and tongue extension (0.6%). The sensitivities of 64.6% of these cortical neurons could not be identified by our stimulation techniques. 4. Taste cells had low spontaneous activity levels (3.7 +/- 3.0 spikes/s, mean +/- SD) and showed little inhibition. They were moderately broadly tuned, with a mean entropy coefficient of 0.76 +/- 0.17. Excitatory responses were typically not robust. 5. Hierarchical cluster analysis was used to determine whether neurons could be divided into discrete types, as defined by their response profiles to the entire stimulus array. There was an apparent division of response profiles into four general categories, with primary sensitivities to sodium (n = 18), glucose (n = 15), quinine (n = 12), and acid (n = 5). However, these categories were not statistically independent. Therefore the notion of functionally distinct neuron types was not supported by an analysis of the distribution of response profiles. It was the case, however, that neurons in the sodium category could be distinguished from other neurons by their relative specificity. 6. The similarity among the taste qualities represented by this stimulus array was assessed by calculating correlations between the activity profiles they elicited from these 50 neurons. The results generally confirmed expectations derived from human psychophysical studies. In a multidimensional representation of stimulus similarity, there were groups that contained acids, sodium salts, and chemicals that humans label bitter and sweet. 7. The small proportion of insular-opercular neurons that are taste sensitive and the low discharge rates that taste stimuli are able to evoke from them suggest a wider role for this cortical area than just gustatory coding.(ABSTRACT TRUNCATED AT 400 WORDS)


Author(s):  
Jordan A. Borrell ◽  
Dora Krizsan-Agbas ◽  
Randolph J. Nudo ◽  
Shawn B. Frost

AbstractObjectiveThe purpose of this study was to determine the effects of spinal cord injury (SCI) on spike activity evoked in the hindlimb spinal cord of the rat from cortical electrical stimulation.ApproachAdult, male, Sprague Dawley rats were randomly assigned to a Healthy or SCI group. SCI rats were given a 175 kDyn dorsal midline contusion injury at the level of the T8 vertebrae. At four weeks post-SCI, intracortical microstimulation (ICMS) was delivered at several sites in the hindlimb motor cortex of anesthetized rats, and evoked neural activity was recorded from corresponding sites throughout the dorsoventral depths of the spinal cord and EMG activity from hindlimb muscles.Main resultsIn healthy rats, post-ICMS spike histograms showed reliable, evoked spike activity during a short-latency epoch 10-12 ms after the initiation of the ICMS pulse train (short). Longer latency spikes occurred between ~20-60 ms, generally following a Gaussian distribution, rising above baseline at time LON, followed by a peak response (Lp), and then falling below baseline at time LOFF. EMG responses occurred between LON and Lp (25-27 ms). In SCI rats, short-latency responses were still present, long-latency responses were disrupted or eliminated, and EMG responses were never evoked. The retention of the short-latency responses indicates that spared descending spinal fibers, most likely via the cortico-reticulospinal pathway, can still depolarize spinal cord motor neurons after a dorsal midline contusion injury.SignificanceThis study provides novel insights into the role of alternate pathways for voluntary control of hindlimb movements after SCI that disrupts the corticospinal tract in the rat.


2012 ◽  
Vol 33 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Alicia Foster ◽  
Mark G. Blanchette ◽  
Yi-Chen Chou ◽  
Christopher M. Powers

Background: Wearing high heel shoes is thought to increase an individual's likelihood of experiencing a lateral ankle sprain. The purpose of this study was to evaluate the influence of heel height on frontal plane kinematics, kinetics, and electromyographic (EMG) activity of the ankle joint during walking. Methods: Eighteen healthy women participated. Three-dimensional kinematics, ground reaction forces, and EMG signals of the tibialis anterior (TA) and peroneus longus (PL) were recorded as subjects ambulated in high (9.5 cm) and low (1.3 cm) heel shoes at a self-selected walking velocity. Peak ankle plantarflexion, peak ankle inversion angle, and the peak ankle inversion moment during the stance phase of gait were evaluated. The EMG variables of interest consisted of the normalized average signal amplitude of the TA and PL during the first 50% of the stance phase. Paired t-tests were used to assess differences between the two shoe conditions. Results: When compared to the low heel condition, wearing high heels resulted in significantly greater peak ankle plantarflexion and inversion angles ( p < 0.001). In addition, the peak inversion moment and PL muscle activation was found to be significantly higher in the high heel condition ( p < 0.001). No difference in TA muscle activity was found between shoe conditions ( p = 0.30). Conclusion: The plantarflexed and inverted posture when wearing high heels may increase an individual's risk for experiencing a lateral ankle sprain. Clinical Relevance: Data obtained from this investigation highlights the need for increased awareness and proper education related to the wearing of high heel shoes.


1998 ◽  
Vol 80 (3) ◽  
pp. 1391-1406 ◽  
Author(s):  
S. N. Baker ◽  
R. N. Lemon

Baker, S. N. and R. N. Lemon. Computer simulation of post-spike facilitation in spike-triggered averages of rectified EMG. J. Neurophysiol. 80: 1391–1406, 1998. When the spikes of a motor cortical cell are used to compile a spike-triggered average (STA) of rectified electromyographic (EMG) activity, a post-spike facilitation (PSF) is sometimes seen. This is generally thought to be indicative of direct corticomotoneuronal (CM) connections. However, it has been claimed that a PSF could be caused by synchronization between CM and non-CM cells. This study investigates the generation of PSF using a computer model. A population of cortical cells was simulated, some of which made CM connections to a pool of 103 motoneurons. Motoneurons were simulated using a biophysically realistic model. A subpopulation of the cortical cells was synchronized together. After a motoneuron discharge, a motor unit action potential was generated; these were summed to produce an EMG output. Realistic values were used for the corticospinal and peripheral nerve conduction velocity distribution, for slowing of impulse conduction in CM terminal axons, and for the amount of cortical synchrony. STA of the rectified EMG from all cortical neurons showed PSF; however, these were qualitatively different for CM versus non-CM cells. Using an epoch analysis to determine reliability in a quantitative manner, it was shown that the onset latency of PSF did not distinguish the two classes of cells after 10,000 spikes because of high noise in the averages. The time of the PSF peak and the peak width at half-maximum (PWHM) could separate CM from synchrony effects. However, only PWHM was robust against changes in motor unit action-potential shape and duration and against changes in the width of cortical synchrony. The amplitude of PSF from a CM cell could be doubled by the presence of synchrony. It is proposed that, if a PSF has PWHM <7 ms, this reliably indicates that the trigger is a CM cell projecting to the muscle whose EMG is averaged. In an analysis of experimental data where macaque motor cortical cells facilitated hand and forearm muscle EMG, 74% of PSFs fulfilled this criterion. The PWHM criterion could be applied to other STA studies in which it is important to exclude the effects of synchrony.


2009 ◽  
Vol 101 (1) ◽  
pp. 234-245 ◽  
Author(s):  
Gang Chen ◽  
Laurentiu S. Popa ◽  
Xinming Wang ◽  
Wangcai Gao ◽  
Justin Barnes ◽  
...  

The tottering mouse is an autosomal recessive disorder involving a missense mutation in the gene encoding P/Q-type voltage-gated Ca2+channels. The tottering mouse has a characteristic phenotype consisting of transient attacks of dystonia triggered by stress, caffeine, or ethanol. The neural events underlying these episodes of dystonia are unknown. Flavoprotein autofluorescence optical imaging revealed transient, low-frequency oscillations in the cerebellar cortex of anesthetized and awake tottering mice but not in wild-type mice. Analysis of the frequencies, spatial extent, and power were used to characterize the oscillations. In anesthetized mice, the dominant frequencies of the oscillations are between 0.039 and 0.078 Hz. The spontaneous oscillations in the tottering mouse organize into high power domains that propagate to neighboring cerebellar cortical regions. In the tottering mouse, the spontaneous firing of 83% (73/88) of cerebellar cortical neurons exhibit oscillations at the same low frequencies. The oscillations are reduced by removing extracellular Ca2+and blocking L-type Ca2+channels. The oscillations are likely generated intrinsically in the cerebellar cortex because they are not affected by blocking AMPA receptors or by electrical stimulation of the parallel fiber–Purkinje cell circuit. Furthermore, local application of an L-type Ca2+agonist in the tottering mouse generates oscillations with similar properties. The beam-like response evoked by parallel fiber stimulation is reduced in the tottering mouse. In the awake tottering mouse, transcranial flavoprotein imaging revealed low-frequency oscillations that are accentuated during caffeine-induced attacks of dystonia. During dystonia, oscillations are also present in the face and hindlimb electromyographic (EMG) activity that become significantly coherent with the oscillations in the cerebellar cortex. These low-frequency oscillations and associated cerebellar cortical dysfunction demonstrate a novel abnormality in the tottering mouse. These oscillations are hypothesized to be involved in the episodic movement disorder in this mouse model of episodic ataxia type 2.


2004 ◽  
Vol 83 (7) ◽  
pp. 572-577 ◽  
Author(s):  
Y. Shibukawa ◽  
M. Shintani ◽  
T. Kumai ◽  
T. Suzuki ◽  
Y. Nakamura

Slow cortical potentials (readiness potentials, RPs) reflecting the central programming of voluntary jaw movements were reported to appear preceding the movements. However, the current source producing the RP has not yet been localized. This study aimed to determine the cortical regions involved in the central programming of bilaterally symmetrical voluntary jaw movements, by locating the current source of the neuromagnetic counterpart of the RP (readiness field, RF). The RFs were found in the fronto-lateral region bilaterally, starting around 860 and 600 ms prior to the onset of masseter and digastric electromyograms (EMGs), respectively, and gradually increasing in magnitude to the peak within 100 ms before the EMG onset. Thus, the RFs appeared long before the reported onset of the excitability increase of pyramidal tract neurons. The current sources producing the RFs were located in the precentral gyrus bilaterally, with no bilateral differences in strength. We conclude that the primary motor cortex is involved bilaterally in central programming as well as in execution of bilaterally symmetrical voluntary jaw movements.


1985 ◽  
Vol 54 (5) ◽  
pp. 1194-1212 ◽  
Author(s):  
S. S. Palmer ◽  
E. E. Fetz

We examined the magnitude and extent of output effects elicited from focal cortical sites on the activity of individual motor units (MUs) by delivering single-pulse intracortical microstimuli (S-ICMS) (5-15 microA) during isometric wrist activity. Stimulation sites in the precentral gyrus (area 4) were chosen for study if stimulus-triggered averages (stimulus-TAs) of multiunit electromyograms (EMGs) revealed poststimulus facilitation (PStimF) of EMG activity in any of the coactivated wrist muscles. Single MUs were then isolated in the facilitated muscles with a remotely controlled tripolar microelectrode. MUs were identified by their signatures in their parent muscles (from MU-triggered averages of EMGs) and by their firing pattern during ramp-and-hold wrist responses. One objective was to quantify the magnitude and time course of the effects on single MUs by compiling peristimulus histograms of MU firing. The cross-correlation histograms between S-ICMS and MU action potentials showed peaks with onset latencies of 8.8 +/- 1.7 ms (mean +/- SD, n = 64) and durations of 1.8 +/- 1.2 ms (n = 104). The cumulative sums of the correlogram peaks resembled the rising phase of corticomotoneuronal excitatory postsynaptic potentials previously recorded in forelimb motoneurons. Comparison of correlogram peaks with stimulus-TAs of MU potentials suggests that the duration of PStimF of multiunit EMG can be accounted for, in approximately equal proportions, by l) the variation in firing time of single MUs (i.e., the width of the MU correlogram peaks), 2) the width of single MU potentials, and 3) the contribution of different MUs at different latencies. The sizes of the correlogram peaks relative to base line were larger than the PStimF of multiunit EMGs, and increased more rapidly with stimulus intensity, indicating appreciable cancellation in the multiunit records. A second objective was to determine whether S-ICMS affected all the MUs of a facilitated muscle, or only a particular subset. Of 104 MUs sampled in facilitated muscles, 99 (95%) were found to be individually facilitated (P less than 0.05). MU firing patterns during isometric ramp-and-hold torque responses were characterized as phasic, phasic-tonic, tonic, or decrementing; stimulation at a given cortical site was found to facilitate all four types of MUs. When more than one muscle showed PStimF from a site, MUs belonging to each of the facilitated muscles were facilitated individually by S-ICMS at that site.(ABSTRACT TRUNCATED AT 400 WORDS)


2021 ◽  
Author(s):  
Jaakko O. Nieminen ◽  
Heikki Sinisalo ◽  
Victor H. Souza ◽  
Mikko Malmi ◽  
Mikhail Yuryev ◽  
...  

Background: Transcranial magnetic stimulation (TMS) allows non-invasive stimulation of the cortex. In multi-locus TMS (mTMS), the stimulating electric field (E-field) is controlled electronically without coil movement by adjusting currents in the coils of a transducer. Objective: To develop an mTMS system that allows adjusting the location and orientation of the E-field maximum within a cortical region. Methods: We designed and manufactured a planar 5-coil mTMS transducer to allow controlling the maximum of the induced E-field within a cortical region approximately 30 mm in diameter. We developed electronics with a design consisting of independently controlled H-bridge circuits to drive up to six TMS coils. To control the hardware, we programmed software that runs on a field-programmable gate array and a computer. To induce the desired E-field in the cortex, we developed an optimization method to calculate the currents needed in the coils. We characterized the mTMS system and conducted a proof-of-concept motor-mapping experiment on a healthy volunteer. In the motor mapping, we kept the transducer placement fixed while electronically shifting the E-field maximum on the precentral gyrus and measuring electromyography from the contralateral hand. Results: The transducer consists of an oval coil, two figure-of-eight coils, and two four-leaf-clover coils stacked on top of each other. The technical characterization indicated that the mTMS system performs as designed. The measured motor evoked potential amplitudes varied consistently as a function of the location of the E-field maximum. Conclusion: The developed mTMS system enables electronically targeted brain stimulation within a cortical region.


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