Botulinum toxin modulates the blink reflex via the trigeminal afferent system in hemifacial spasm: an early and late-term effect.

BACKGROUND

There is growing evidence that botulinum neurotoxin (BoNT) can mediate changes at the central level through peripheral mechanisms, leading to alterations in central sensorimotor integration. However, the effect of BoNT on brainstem excitability in patients with hemifacial spasm(HFS) is not yet fully understood, and its long-term effects remain unknown.

OBJECTIVE

This study aims to investigate the impact of BoNT on the excitability of the facial nucleus in patients with idiopathic HFS.

METHODS

In order to evaluate the peripheral effect of the toxin, the amplitude of compound muscle action potential (CMAP) of orbicularis oculi (OOc) muscles was evaluated. To investigate the effects of locally injected BoNT on the brainstem, particularly the facial motor nucleus, we evaluated the amplitude and latency of the blink reflex (BR), the synkinetic responses (SR) and the ratio of contralateral R2 (cR2) amplitude of BR/CMAP amplitude in 16 patients with HFS. These measurements were performed before and after the 1 and 4 month BoNT injection.

RESULTS

Following BoNT therapy there was a significant amplitude reduction and latency prolongation of R1, iR2, cR2 and SR elicited by the stimulation of the side of BoNT injection. The mean CMAP amplitude of OOc muscle was significantly lower after BoNT injection. The ratio of cR2 amplitude/CMAP amplitude of OOc showed a significant decline after BoNT therapy.

CONCLUSION

Our study demonstrated that BoNT suppresses the excitability of facial motor neurons in idiopathic HFS via the trigeminal afferent mechanism. These effects persisted during the fourth month, despite BoNT's diminished activity.