Contralateral early blink reflex in patients with facial nerve palsy: indication for synaptic reorganization in the facial nucleus during regeneration

Reflex excitability of facial motoneurons at onset of muscle reinnervation after facial nerve palsy

“…13,18,23 However, these mechanisms on their own cannot explain certain phenomena, such as the involvement of all hemifacial muscles after lesions of distal branches of the facial nerve, 16,17 or the occurrence of rhythmic myokymic discharges and the enhancement of reflex responses. 21,27 These findings suggest an abnormal enhancement of motoneuronal excitability. 7,28 Most studies on PFS have been carried out at a relatively long time after onset of the facial palsy, when neurophysiological identification of enhanced motoneuronal excitability may be masked by the simultaneous activity of many motor units and by peripheral nerve mechanisms such as lateral spread of excitability.…”

Deficient functional recovery after facial nerve crush in rats is associated with restricted rearrangements of synaptic terminals in the facial nucleus

“…In this scenario, restricted plasticity may account for residual functional defects after axonotmesis while the improvement of function after nerve crush compared with nerve transection may result from attenuated peripheral abnormalities like aberrant reinnervation and axonal deficits (small axon caliber and insufficient myelination). Alternatively or in addition, the persisting deafferentation of facial motoneurons after target reinnervation may be a compensatory mechanism aiming to reduce hyperexcitability observed after facial nerve injuries (Nacimiento et al, 1992;Cossu et al, 1999;Valls-Sole´and Montero, 2003;Valls-Sole´et al, 2011;Raslan et al, 2013).…”

Bell's palsy-induced blepharospasm

“…Syed et al [10] showed enhanced excitability of the blink reflex recovery function in patients with Bell's palsy when stimulating the supraorbital nerve on the paretic side. In addition, Nacimiento et al [11] reported that a contralateral early blink reflex response (R1) can be elicited by stimulation of the non-paralyzed side in patients with unilateral facial nerve palsy, and discussed the possibility that synaptic reorganization of the facial nucleus leads to functional unmasking of pre-existing crossed trigeminofacial reflex pathways during regeneration. These hitherto reported findings suggest that abnormal afferent input from the paralyzed side contributes to the abnormal sensitization of the blink reflex, thereby facilitating the induction of abnormal facial motor outputs such as blepharospasm.…”