Treatment with botulinum toxin improves the hyperexcitability of the facial motoneuron in patients with hemifacial spasm

Ishikawa, Mami; Takashima, Koichi; Kamochi, Haruna; Kusaka, Gen; Shinoda, Souji; Watanabe, Eiju

doi:10.1179/174313209x431129

Cited by 13 publications

(7 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Collectively these results are consistent with a central hyperactivity mechanism contributing to the pathophysiology of hfS. an additional and intriguing contribution to facial nerve excitability in hfS is the role of the trigeminal nerve 30 . how trigeminal influences might affect facial Mep responses remains to be elucidated.…”

Section: Figure 1: Examples Of Facial Meps Elicited Using Single Pulssupporting

confidence: 76%

Facial Motor Neuron Excitability in Hemifacial Spasm: A Facial MEP Study

Wilkinson

Kaufmann

2014

Can. J. Neurol. Sci.

View full text Add to dashboard Cite

hemifacial spasm (hfS) is an involuntary and irregular spasm of the facial muscles innervated by the Vii cranial nerve that typically progresses in severity and extent over time. the etiology of hfS has been attributed to vascular compression of the facial nerve at the root exit zone (reZ) 1 . this led to the development of surgical microvascular decompression (MVd) of this cranial nerve by Jannetta and colleagues 2 for the treatment of hfS. this group also advocated the use of intraoperative neurophysiological monitoring to minimize iatrogenic injuries as well as an aid to the surgical procedure. Specifically, Moller and Janetta described the lateral spread (lS) response, an electromyographic hallmark specific to hfS [3][4][5] . this lS response is produced by electrical stimulation of one branch of the facial nerve and observing the electromyographic response in the facial musculature innervated by a different branch of the nerve.the neurophysiological mechanism of the lS response has been hotly debated between those that favor a peripheral mechanism 6,7 versus a centrally mediated hypothesis [3][4][5] . We sought to explore this debate by observing facial motor evoked potentials and lS responses during MVd surgeries for hfS 8 . We found that facial motor evoked potential (Mep) amplitude and duration became markedly reduced, coincident with the lS response, following the surgical microvascular decompression AbStRAct: Introduction: hemifacial spasm (hfS) may be due to peripheral axon ephapsis or central motor neuron hyperexcitability. low facial motor evoked potential (Mep) thresholds or Mep responses to single pulse stimulation (normally multipulse stimulation is needed) may support the central hypothesis. Methods: We retrospectively compared response thresholds for facial Meps in 65 patients undergoing surgical microvascular decompression (MVd) for hfS and 29 patients undergoing surgery for skull base tumors. Results: Single pulse stimulation elicited facial Mep in up to 87% of hfS patients whereas only 10% of tumor patients responded to single pulse stimulation. When comparing facial Mep thresholds using multi-pulse stimulus trains the voltage required in the hfS group were significantly lower then in skull base tumor patients (p < 0.001). the Mep latencies and amplitudes at threshold stimulation were similar between the two groups. Conclusions: these results suggest the facial corticobulbar pathway demonstrates enhanced excitability in hfS.RéSuMé: excitabilité du neurone moteur facial dans le spasme hémifacial : étude des PéM. Contexte : le spasme hémifacial (Shf) peut être dû à un éphapse au niveau d'axones périphériques ou à une hyperexcitabilité du neurone moteur central. le fondement de l'hypothèse centrale repose sur des seuils bas de potentiels évoqués moteurs (pÉM) faciaux ou des réponses pÉM à une impulsion unique (normalement, plusieurs impulsions sont nécessaires). Méthode : nous avons comparé rétrospectivement les seuils de réponse des pÉM faciaux chez 65 patients soumis à une chirurgie de décomp...

show abstract

Section: Figure 1: Examples Of Facial Meps Elicited Using Single Pulssupporting

confidence: 76%

Facial Motor Neuron Excitability in Hemifacial Spasm: A Facial MEP Study

Wilkinson

Kaufmann

2014

Can. J. Neurol. Sci.

View full text Add to dashboard Cite

show abstract

“…When injections are administered only into the orbicularis oculi muscle, the decrease in the spasms in lower facial muscles suggests that these injections may reduce the triggering of spasm activation, which is supported by some electrophysiological studies [7,16]. On the other hand, spasms can be reduced with the diffusion from orbicularis oculi to lower facial muscles as was shown in a study conducted by Eleopra et al [6].…”

Section: Discussionsupporting

confidence: 53%

“…It is also considered that there may be improvement in the spasms in lower facial muscles when the injections are made even only into the orbicularis oculi muscle. This is probably due to decreased triggering of spasm activation or local diffusion of toxin [6,7]. Thus, some of the investigators prefer to apply BTX to the orbicularis oculi without any injections to the perioral muscles [8,9,10].…”

Section: Introductionmentioning

confidence: 99%

Is It Always Necessary to Apply Botulinum Toxin into the Lower Facial Muscles in Hemifacial Spasm? A Randomized, Single-Blind, Crossover Trial

2011

View full text Add to dashboard Cite

Background: Botulinum toxin (BTX) injections are accepted as safe and efficacious in the treatment of hemifacial spasm (HFS), but it is still debated whether BTX treatment of lower facial muscles should be performed or not. Objective: The study aims to evaluate the necessity of BTX administration into lower facial muscles in patients with HFS. Methods: A randomized, single-blind, crossover, clinical trial was conducted. Twenty-three HFS patients were randomly allocated to two different application methods. The patients were administered BTX type A into both the orbicularis oculi and perioral muscles in the first method and BTX type A into the orbicularis oculi but placebo into the perioral muscles in the second method. Subjects were crossed over to the alternate method when they needed BTX injection with a minimum of 3 months’ duration. All the patients underwent both methods with no change in the total dose of BTX. Results: All the patients benefited from BTX treatment regardless of the methods. However, in the patients with severe lower facial muscle involvement, the application of BTX into both orbicularis oculi and lower facial muscles led to better results. Conclusion: Our data suggest that BTX application to lower facial muscles might not be necessary in patients with mild lower facial involvement.

show abstract

“…Several clinical observations are difficult to explain only by local peripheral action of BoNT/A: Distant effects in non‐injected muscles and limbs. A reduction of motor neuronal excitability was reported in the hand muscle of patients treated in the neck muscles for spasmodic torticollis (Wohlfarth, Schubert, Rothe, Elek, & Dengler, ) and in the lower facial muscles of patients treated in the orbicularis oris for hemifacial spasm (Ishikawa et al, ). In spastic patients, the observed reduction of recurrent inhibition of distant non‐injected muscles cannot be explained by the peripheral actions of BoNT/A on either local or distant neuromuscular junction or muscle spindles (Aymard, Giboin, Lackmy‐Vallée, & Marchand‐Pauvert, ; Marchand‐Pauvert et al, ).…”

Section: Discussionmentioning

confidence: 95%

Evidence for central antispastic effect of botulinum toxin type A

Matak

2019

British J Pharmacology

View full text Add to dashboard Cite

Background and Purpose Botulinum toxin type A (BoNT/A) injections into hyperactive muscles provide effective treatment for spasticity and dystonias, presumably due to its local effects on extrafusal and intrafusal motor fibres. A recent discovery of toxin's retrograde axonal transport to CNS might suggest additional action sites. However, in comparison to cholinergic peripheral terminals, functional consequences of BoNT/A direct central action on abnormally increased muscle tone are presently unknown. To address this question, the central effects of BoNT/A were assessed in experimental local spastic paralysis. Experimental Approach Local spastic paralysis was induced by injection of tetanus toxin (1.5 ng) into rat gastrocnemius. Subsequently, BoNT/A (5 U·kg−1) was applied i.m. into the spastic muscle or intraneurally (i.n.) into the sciatic nerve to mimic the action of axonally transported toxin. Functional role of BoNT/A transcytosis in spinal cord was evaluated by lumbar i.t. application of BoNT/A‐neutralizing antitoxin. BoNT/A effects were studied by behavioural motor assessment and cleaved synaptosomal‐associated protein 25 (SNAP‐25) immunohistochemistry. Key Results Tetanus toxin evoked muscular spasm (sustained rigid hind paw extension and resistance to passive ankle flexion). Subsequent injections of BoNT/A, i.m. or i.n, reduced tetanus toxin‐evoked spastic paralysis. Beneficial effects of i.n. BoNT/A and occurrence of cleaved SNAP‐25 in ventral horn were prevented by i.t. antitoxin. Conclusions and Implications Axonally transported BoNT/A relieves muscle hypertonia induced by tetanus toxin, following the trans‐synaptic movement of BoNT/A in the CNS. These results suggest that such direct, centrally mediated reduction of abnormal muscle tone might contribute to the effectiveness of BoNT/A in spasticity and hyperkinetic movement disorders.

show abstract

Treatment with botulinum toxin improves the hyperexcitability of the facial motoneuron in patients with hemifacial spasm

Cited by 13 publications

References 14 publications

Facial Motor Neuron Excitability in Hemifacial Spasm: A Facial MEP Study

Facial Motor Neuron Excitability in Hemifacial Spasm: A Facial MEP Study

Is It Always Necessary to Apply Botulinum Toxin into the Lower Facial Muscles in Hemifacial Spasm? A Randomized, Single-Blind, Crossover Trial

Evidence for central antispastic effect of botulinum toxin type A

Contact Info

Product

Resources

About