Introduction

The objective of this study was to describe facial myokymia in experimental animals accompanying kainic acid affects on facial motor neurons.

Material & methods

Anesthetized cats were injected with kainic acid into the pons adjacent to the facial nucleus. Facial movements appeared shortly after the injections and facial electromyographic potentials were recorded. Cats were killed up to 4 weeks later, the brainstems were processed histologically, and the number of neurons in the facial nucleus counted.

Results

Cats receiving injection of kainic acid adjacent to facial nucleus all developed spontaneous writhing movements of the face ipsilateral to the injection site, clinically resembling facial myokymia in humans. Transient facial paresis, lasting several weeks, appeared in some of the cats. Facial myokymia occurred independent of histological evidence of neuronal loss in facial nucleus, whereas facial paresis occurred in all but one of the animals with significant neuronal loss in the facial nucleus. Placing a needle into the superior olive without injecting kainic acid or injections of kainic acid into cochlear nucleus was not accompanied by facial myokymia or subsequent facial paresis.

Conclusion

Facial movements in cats similar to myokymia in humans accompanies kainic acid injections adjacent to the nucleus of the facial nerve.

AIMS OF THE STUDY:The time course of motor excitability during a task-related unilateral right thumb movement was studied using sub-threshold transcranial magnetic stimulation (TMS) to the contralateral left motor cortex. The level of stimulation evoked a motor evoked potential (MEP) in the thumb when the subject was at rest in approximately 10% of the trials. METHODS:Subjects made a brief right thumb movement to the predictable omission of regularly presented tone bursts allowing experimental definition of TMS relative to the cue to move. Motor cortical excitability was characterized by amplitude and/or probability of eliciting MEPs. RESULTS:There were four periods of altered motor excitability during task performance compared to a control resting state: a first period of weak facilitation before movement between -500 to -200 ms, a second period without increased excitability approximately 150 ms before movement onset when MEPs amplitude was below that seen in rest, a third period of strong facilitation between -100 ms before movement and +200 ms after facilitation and a fourth period of weak facilitation between +200 to +500 ms. CONCLUSION:These results show that during performance of a task requiring a motor response, motor cortical excitability is increased above resting for hundreds of millisecond before and after the response, except for a transient period between 75 and 150 ms prior to movement onset. The temporal pattern of these excitability changes is compatible with multiple excitatory and inhibitory inputs interacting on motor cortex.

Objective

The time course of the right motor cortex excitability in relation to a task-related voluntary right thumb twitch was studied using sub-threshold transcranial magnetic stimulation (TMS) to the right motor cortex.

Methods

Motor excitability was studied in 8 adult subjects who made a brief right thumb twitch to the predictable omission of every fifth tone in a series of tones 2.5 s apart. This paradigm avoided an overt sensory cue, while allowing experimental control of TMS timing relative to both movement and the cue to move. Motor excitability was characterized by several measures of motor evoked potentials (MEPs) recorded from the left thenar eminence in response to TMS over the right scalp with a 9 cm coil: probability of eliciting MEPs, incidence of MEPs and amplitude of MEPs.

Results

All subjects showed suppression of motor excitability immediately following a voluntary right thumb twitch (ipsilateral response), and up to 1 s after it. However, two distinctly different effects on motor excitability were observed before the response: two subjects showed excitation, beginning about 500 ms before response until 300 ms after it, followed by the post-movement suppression; 6 subjects displayed pre-movement suppression, beginning about 600 ms before the response and persisting for the duration.

Conclusions

The net effect of an ipsilateral response on motor cortex can be either inhibitory or excitatory, changing with time relative to the response. These findings are compatible with two separate processes, inhibitory and excitatory, which interact to determine motor excitability ipsilateral to the responding hand.

Auditory brainstem evoked potentials (ABEP) were recorded from 16 awake cats to obtain 3-Channel Lissajous' Trajectories (3CLTs) using three orthogonal differential electrode configurations (nasion-midline nuchal ridge, left-right mastoids, vertex-midline under the mandible). Potentials, evoked by monaural 80 dBnHL (re, human threshold) clicks, were studied before, and up to 7 weeks after inducing neuronal lesions localized to the cochlear nucleus (CN) or the superior olivary complex (SOC), or myelin lesions localized to the fibers of the trapezoid body connecting these two structures. Neuronal lesions were induced by injection of kainic acid (KA), while myelin lesions were induced by injection of L-alpha-lysophosphatidylcholine (LPC). With CN neuronal lesions the major changes in 3CLT were in the time domain of 'b', 'c' and 'd' (components P2, P3 and P4 of single-channel ABEP). With SOC neuronal lesions the major changes were in 'c' and 'd' of 3CLT (P3 and P4 of ABEP). With trapezoid body lesions the major change was in 'c' (P3 of ABEP). The results are compatible with the peripheral generation of the first ABEP components (P1a and P1b). The second component (P2) is generated by ipsilateral CN neurones and their outputs. The third component (P3) is generated primarily by ipsilateral SOC neurones and their outputs, with the ipsilateral CN providing input. The The fourth component (P4) is generated bilaterally by the SOC neurones and their outputs, receiving their inputs from ipsilateral CN. The fifth ABEP component (P5) is generated by structures central to the SOCs and their immediate outputs. Neither focal neuronal nor myelin lesions were sufficient to produce obliteration of any component, consistent with a set of generators for each of the ABEP components, consisting of both cell bodies and their output fibers, that is distributed spatially in the brainstem.

The power spectrum of the feline auditory brain-stem evoked potentials (ABEPs) consists of 3 frequency bands, similar to the human wave form, but differing in range. The frequency bands in the feline spectra were separated by notches at 326 Hz and 732 Hz. Click-evoked ABEP from 15 cats were digitally filtered in 3 passbands: (1) below 326 Hz ('slow filter'), (2) between 326 and 732 Hz ('medium filter'); and (3) between 732 and 1790 Hz ('fast filter'). Filtering in each of these bands differentially affected the ABEP components. The vertex positive components are labeled by their order of appearance, i.e., 1, 2, ... 5. Peak 1 is subdivided into 2 subcomponents labeled 1a and 1b. The slow filter was associated with the loss of all components leaving a slow potential shift, i.e., the 'pedestal' peaking at the latency of peak 4. The medium filter was associated with the loss of components 1a, 1b and 2, sparing 3 and 4. The fast filter was associated with the loss of 1b and a diminution of 2. Comparing cat and human ABEP, feline components 2, 3 and 4 behaved precisely the same as the human II, III and V. In contrast to the human I, the feline first component (1a) was not detected with the medium filter. No feline component, following peak 1 in the unfiltered wave form, disappeared with the slow and medium filters, and reemerged with the fast filter (as human IV does).(ABSTRACT TRUNCATED AT 250 WORDS)