Anatomical study of the variations in innervation of the orbicularis oculi by the facial nerve

Etienne, Ouattara Katinan; Vacher, C.; Vasconcellos, J.-J. Accioli de; Kassanyou, S; Gnanazan, G; N’guessan, BB

doi:10.1007/s00276-003-0168-0

Cited by 34 publications

(19 citation statements)

References 6 publications

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“…Interestingly enough, the three cases of lagophthalmos reported in the present paper primarily involved the medial part of the orbicularis oculi muscle of the upper eyelid (while surgery only took place at and below the medial canthal ligament). This is likely to be explained by a lesion of the quite recently described buccal and/or zygomatic branches of the facial nerve [8,9], also sometimes termed the "angular nerve" [10], that travels upward from the lower eyelid toward the medial canthal angle, to cross over, with the angular vessels, the medial canthal tendon to then eventually innervate the medial orbicularis oculi as well as the procerus and corrugator supercilii muscles. A damage to these fibers is more likely to explain the lagophthalmos observed rather than some local anesthetics-induced nerve toxicity (as it did not occur during numerous oculoplastic procedures performed during the same period of time of this study where the same type local anesthesia was performed), some cautery-induced damage (that was actually absent or minimal in all operated cases), or a trauma-induced damage to the orbicularis below the medial canthal ligament [11] (that could not satisfactorily explain the observed upper lid orbicularis muscle weakness).…”

mentioning

confidence: 99%

Temporary Medial Upper Eyelid Lagophthalmos after External Dacryocystorhinostomy

Haefliger

Meienberg

Figueiredo

2016

Klin Monatsbl Augenheilkd

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Background. Report of three cases of medial upper eyelid lagophthalmos as complication of external dacryocystorhinostomy. History and Signs. Shortly after dacryocystorhinostomy (skin incision on the side of the nose), three of ten consecutive patients (28 ± 4 years; mean ± standard deviation), presented with an ipsilateral lagophthalmos of 4 ± 1 mm in voluntary eyelid closure and 6 ± 1 mm in spontaneous blink. The lagophthalmos was due to a selective paresis of the medial part of the orbicularis oculi muscle of the upper eyelid. Patient 1 complained bitterly of dry eye symptoms and of her lagophthalmos. Patient 2 had mild symptoms but became very concerned after peers made her aware of her asymmetric blink. Patient 3 was asymptomatic and did not notice anything particular. Therapy and Outcome. Lagophthalmos resolved spontaneously within three months after surgery, first by improvement of voluntary eyelid closure and then of spontaneous blinking. Conclusions. Temporary lagophthalmos can occur as a complication of external dacryocystorhinostomy, most likely due to damage of the (only recently described) superficial buccal and/or zygomatic branches of the facial nerve that run upward to cross over the medial ligament and innervate the medial part of the orbicularis oculi muscle.

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mentioning

confidence: 99%

Temporary Medial Upper Eyelid Lagophthalmos after External Dacryocystorhinostomy

Haefliger

Meienberg

Figueiredo

2016

Klin Monatsbl Augenheilkd

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“…The OO muscle weakening is suggested to be about “30%” (Evinger, 2005), consistent with the fact that the OO muscle is innervated by the zygomatic and temporal branches of facial nerve (Ouattara et al, 2004) yet only the zygomatic branch is sectioned. As a result, the magnitude of the eyelid proprioceptive signal represented by somatosensory cortical input to the striatum should be reduced by 30% during eye blinks after the OO-weakening lesion, and the frequency of the blinks should be increased relative to the mean frequency of naturally occurring blinks.…”

Section: Computational Model Design Considerationsmentioning

confidence: 63%

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Peterson

Sejnowski

2017

Front. Comput. Neurosci.

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Blepharospasm (sometimes called “benign essential blepharospasm,” BEB) is one of the most common focal dystonias. It involves involuntary eyelid spasms, eye closure, and increased blinking. Despite the success of botulinum toxin injections and, in some cases, pharmacologic or surgical interventions, BEB treatments are not completely efficacious and only symptomatic. We could develop principled strategies for preventing and reversing the disease if we knew the pathogenesis of primary BEB. The objective of this study was to develop a conceptual framework and dynamic circuit hypothesis for the pathogenesis of BEB. The framework extends our overarching theory for the multifactorial pathogenesis of focal dystonias (Peterson et al., 2010) to incorporate a two-hit rodent model specifically of BEB (Schicatano et al., 1997). We incorporate in the framework three features critical to cranial motor control: (1) the joint influence of motor cortical regions and direct descending projections from one of the basal ganglia output nuclei, the substantia nigra pars reticulata, on brainstem motor nuclei, (2) nested loops composed of the trigeminal blink reflex arc and the long sensorimotor loop from trigeminal nucleus through thalamus to somatosensory cortex back through basal ganglia to the same brainstem nuclei modulating the reflex arc, and (3) abnormalities in the basal ganglia dopamine system that provide a sensorimotor learning substrate which, when combined with patterns of increased blinking, leads to abnormal sensorimotor mappings manifest as BEB. The framework explains experimental data on the trigeminal reflex blink excitability (TRBE) from Schicatano et al. and makes predictions that can be tested in new experimental animal models based on emerging genetics in dystonia, including the recently characterized striatal-specific D1R dopamine transduction alterations caused by the GNAL mutation. More broadly, the model will provide a guide for future efforts to mechanistically link multiple factors in the pathogenesis of BEB and facilitate simulations of how exogenous manipulations of the pathogenic factors could ultimately be used to prevent and reverse the disorder.

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“…An upper branch of the temporofacial division gives off terminal branches that form the temporal and zygomatic nerves. The OO is innervated by upper and lower nerve plexuses formed from these terminal branches that enter the muscle from its deep surface (Schmidt et al, 2001;Ouattara et al, 2004).…”

Section: Orbicularis Oculimentioning

confidence: 99%

Normal and abnormal lid function

Rucker

2011

Handbook of Clinical Neurology

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Anatomical study of the variations in innervation of the orbicularis oculi by the facial nerve

Cited by 34 publications

References 6 publications

Temporary Medial Upper Eyelid Lagophthalmos after External Dacryocystorhinostomy

Temporary Medial Upper Eyelid Lagophthalmos after External Dacryocystorhinostomy

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Normal and abnormal lid function

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