Unilateral injection of botulinum toxin in blepharospasm: Single fiber electromyography and blink reflex study

Abstract

We studied six patients affected with blepharospasm (BSP). We injected botulinum toxin (BTX) around only one eye and saline solution around the other. Clinical rating of BSP was performed. Single fiber electromyography (SFEMG), compound motor action potential (cMAP) at the orbicularis oculi muscle by stimulation of the facial nerve, blink reflex, and blink reflex recovery curve were recorded. All clinical and electrophysiological investigations were carried out before, and 1, 2, and 4 weeks after treatment. Evidence of bilateral clinical benefit was provided. Following therapy, facial cMAP decreased bilaterally and SFEMG revealed statistically significant changes on both sides while the excitability curve of blink reflex remained unmodified. The results confirm that BTX affects merely the neuromuscular junctions. The clinical and neurophysiological effects are present on both sides also for unilateral injection probably because of toxin spreading.

Enhanced Long-Term Potentiation-Like Plasticity of the Trigeminal Blink Reflex Circuit in Blepharospasm

“…At first sight, this normalization of blink "plasticity" seems at odds with previous work showing that BTX fails to reduce the heightened excitability of the blink in BEB as reflected in reduced prepulse inhibition and the enhanced recovery cycle of the R2 component (Girlanda et al, 1996). However, this may be related to the fact that two types of adaptation occur in the blink reflex circuit.…”

The blink reflex recovery cycle differs between essential and presumed psychogenic blepharospasm

“…However, this is unlikely to have affected the results since botulinum toxin injections have no effect on blink reflex recovery curves in BEB. 24,25 There was also no difference in the latency and duration of the responses nor in the recovery curve of the R1 component.…”

Neurophysiological effects of botulinum toxin type a

“…Whereas BoNT-A usually induces no changes in EMG activity or MVC in non injected muscles, it can reduce the contralateral CMAP in the orbicularis oculi muscle possibly because of toxin spreading (Girlanda et al, 1996). Repeated treatments may lead to functional weakening (decrease in turns/amplitude) of non injected muscles in dystonic patients (Erdal et al, 1999).…”