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

Cossu, Giovanni; Valls‐Solé, Josep; Valldeoriola, Francesc; Muñoz, Esteban; Benítez, Pedro; Aguilar, Francina

doi:10.1002/(sici)1097-4598(199905)22:5<614::aid-mus10>3.0.co;2-g

Cited by 49 publications

(31 citation statements)

References 26 publications

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“…The facial muscles share the subcutaneous musculoaponeurotic system (10), in place of the fascia, which enables the axon to sprout across the muscle. However, some researchers suggested ''myofiber conduction'' or ''motonucleus hyperexcitability'' to explain the phenomenon (9,11,12). In this study, we could observe contralateral reinnervation in far lateral muscles such as the zygomaticus and orbicularis oculi, which cannot be explained by ''myofiber conduction.''…”

Section: Discussioncontrasting

confidence: 51%

Contralateral Reinnervation in Patients With Facial Nerve Palsy

Jeong

Kim

et al. 2014

Otology &Amp; Neurotology

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Although contralateral reinnervation after facial nerve palsy is a common observation, it has not gained appropriate attention. Without recognition of this phenomenon, misinterpretation of the electromyography may mislead the proper timing of nerve repair or reanimation procedure. Therefore, routine examination of motor action potential by contralateral stimulation during electromyography, especially in patients with moderate-to-severe palsy, would provide accurate assessment of the injured nerves and would help in appropriate decision making for further treatment.

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Section: Discussioncontrasting

confidence: 51%

Contralateral Reinnervation in Patients With Facial Nerve Palsy

Jeong

Kim

et al. 2014

Otology &Amp; Neurotology

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“…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).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2013

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“…Evidence of the increased responsiveness of orbicularis oculi motoneurons surviving facial nerve damage is the appearance of an R1 response evoked by contralateral SO stimulation (Bratzlavsky and vander Eecken, 1977;Nacimiento et al, 1992). In addition, Cossu et al (1999) present electrophysiological evidence of hyperexcitability of orbicularis oculi motoneurons recovering from facial palsy. Thus, the long duration and intensity of a unilateral reduction in lid motility produced by facial nerve palsy amplifies both modes of adaptation engendered by lid restraint.…”

Section: Facial Nerve Palsy and Lid Restraint Produce The Same Blink mentioning

confidence: 96%

Lid Restraint Evokes Two Types of Motor Adaptation

Schicatano

Mantzouranis²,

Peshori³

et al. 2002

J. Neurosci.

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Unilateral reduction in eyelid motility produced two modes of blink adaptation in humans. The first adaptive modification affected both eyelids. Stimulation of the supraorbital branch of the trigeminal nerve (SO) ipsilateral to the upper eyelid with reduced motility evoked bilateral, hyperexcitable reflex blinks, whereas contralateral SO stimulation elicited normally excitable blinks bilaterally. The probability of blink oscillations evoked by stimulation of the ipsilateral SO also increased with a reduction in lid motility. The increased probability of blink oscillations correlated with the enhanced trigeminal reflex blink excitability. Thus, the trigeminal complex ipsilateral to the restrained eyelid coordinated an increase in excitability and blink oscillations independent of the eyelid experiencing reduced motility. The second type of modification appeared only in the eyelid experiencing reduced motility. When tested immediately after removing lid restraint, blink amplitude increased in this eyelid relative to the normal eyelid regardless of the stimulated SO. A patient with seventh nerve palsy exhibited the same two patterns of blink adaptation. These results were consistent with two forms of adaptation, presumably because unilateral lid restraint produced two error signals. The corneal irritation caused by reduced blink amplitude generated abnormal corneal inputs. The difference between proprioceptive feedback from the blink and expected blink magnitude signaled an error in blink amplitude. The corneal irritation appeared to drive an adaptive process organized through the trigeminal complex, whereas the proprioceptive error signal drove an adaptive process involving just the motoneurons controlling the restrained eyelid.

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

Cited by 49 publications

References 26 publications

Contralateral Reinnervation in Patients With Facial Nerve Palsy

Contralateral Reinnervation in Patients With Facial Nerve Palsy

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

Lid Restraint Evokes Two Types of Motor Adaptation

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