[RARE ELECTROMYOGRAPHIC PICTURES IN CASES OF PERIPHERAL FACIAL PARALYSIS WITH SPECIAL REFERENCE TO THE ORBICULARIS OCULI].
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Electromyography↗
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[Cystinuria-lysinuria with dwarfism, facial dysmorphy, muscle hypoplasia and psychomotor retardation].
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Abnormalities, Multiple↗
[Electromyographic approach to the facial skin muscles].
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Journal Article↗
[Clinical aspects of contracture of the mimic muscles innervated by the facial nerve].
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Adolescent↗
[A case of congenital myopathy with the pathologic transformation from fiber type disproportion to type 1 fiber predominance myopathy].
Many patients with a severe infantile form of congenital myopathies have respiratory and feeding difficulties from early infancy. We experienced a male patient who required an artificial ventilation soon after birth and showed marked generalized muscle weakness involving the facial muscles. He had skull deformity and mild mental retardation at the age of one year and 10 months. The first muscle biopsy at the age of 1 month showed small caliber fibers and an increase in the number of undifferentiated type 2C fibers, indicating muscle fiber immaturity. Since type 1 fibers were smaller than type 2 fibers, he was tentatively diagnosed as having congenital fiber type disproportion myopathy. The muscle biopsied findings improved significantly in the second biopsy at 1 year of age which showed type 1 fiber predominance but no cytoarchitectural abnormalities. Accordingly, he was diagnosed as having congenital myopathy with type 1 fiber predominance. A severe neonatal form of congenital myopathies may show striking muscle fiber immaturity in the early infancy. This may later develop into characteristic morphologic findings such as the formation of nemalines and cores, and abnormal fiber type distribution.
Biopsy↗
Quantitative analysis of facial motion components: anatomic and nonanatomic motion in normal persons and in patients with complete facial paralysis.
The maximal static response assay of facial motion, described in 1994, enables the simultaneous measurement of multiple facial motions by tracking the positions of specific facial points. While the maximal static response assay provides accurate measurement of facial motion, the analysis of these data lacks the simplicity of a single-number scale such as the House-Brackmann system, a subjective scale traditionally used to classify facial function. The purpose of this study was to develop a simplified numerical index capable of summarizing the data generated by the maximal static response assay in a clinically meaningful way. We also wanted to develop a method whereby only anatomic motion or nonanatomic motion in the paralyzed face could be quantitated. Anatomic motion is the motion of the specific facial points studied by the maximal static response assay that can be attributed solely to the pull of the regional facial muscles that govern the movement of those points. Nonanatomic motion is motion that is secondary to the pull of the unaffected contralateral muscles that is transmitted to the paralyzed hemiface. Thirty-four patients with complete facial paralysis were studied. The maximal static response assay was performed on all patients on presentation to the Facial Nerve Center at the University of Pittsburgh Medical Center or after development of complete facial palsy postoperatively. The data from these patients were compared with maximal static response assay data from 26 unaffected controls. The anatomic index of facial motion and the nonanatomic index of facial motion were calculated for all study participants. The anatomic index of facial motion measures anatomic facial motion, and the nonanatomic index of facial motion measures nonanatomic facial motion. To calculate the anatomic index of facial motion, the vector magnitudes of the supraorbital, infraorbital, and modiolar motions during brow lift, eye closure, and smile are summed. The anatomic index of facial motion represents a ratio of this sum on the affected side to the corresponding sum on the unaffected side using only anatomic motions. The nonanatomic index of facial motion is a similar ratio using nonanatomic motion only (i.e., motions in directions that cannot be produced by the ipsilateral muscles). The anatomic index of facial motion represents a single number that can be used to assess facial motion. The value of the anatomic index of facial motion for patients with complete facial paralysis is 0.07 +/- 0.08. The anatomic index of facial motion for normal individuals is 1.05 +/- 0.13 (p < 0.0001, Mann-Whitney rank-sum test). The nonanatomic index of facial motion in normal individuals is 0.05 +/- 0.08; in patients with complete facial paralysis, it is 0.34 +/- 0.32 (p < 0.0001, Mann-Whitney rank-sum test). During recovery from complete facial paralysis, the anatomic index of facial motion and the nonanatomic index of facial motion each revert steadily toward normal values. The anatomic index of facial motion and the nonanatomic index of facial motion are single numbers based on the maximal static response assay, which quantitatively describes anatomic motion and nonanatomic motion in patients with complete facial paralysis. Although patients with complete facial paralysis have motion on the paralyzed hemiface, the motion is primarily nonanatomic. Both indices can be used to track recovery from complete facial paralysis.
Adolescent↗
[Contribution of EMG to the diagnosis of facial nerve and muscle involvement in neurinoma of the VIIIth nerve].
An examination of 5 cases of acoustic nerve neurinoma, and 3 cases where the diagnosis was suspected, showed that EMG signs of a possible facial nerve compression in the ponto-cerebellar angle were represented by abnormal activity at rest, sub-clinical signs of progressive neurogenic atrophy in the hemi-facial muscles, and a significant increase in the latency of the oligosynaptic R1 reflex response.
Cerebellopontine Angle↗
Neurophysiological monitoring of cranial nerves during posterior fossa surgery.
Intraoperative neurophysiological monitoring of cranial nerve functions in surgery for microvascular decompression and tumors of the posterior fossa is important for minimizing risk of permanent damage to the nerves. In particular, intraoperative BAEP and the EMG function of muscle innervated by trigeminal and facial muscle have been found useful. We report here our experiences with intraoperative monitoring of brainstem auditory evoked potentials (BAEP) and EMG recorded from muscles supplied by the trigeminal and facial nerves.
Blinking↗
Reanimation of early facial paralysis with hypoglossal/facial end-to-side neurorrhaphy: a new approach.
The classic hypoglossal transfer to the facial nerve invariably results in profound functional deficits in speech, mastication, and swallowing, and causes synkinesis and involuntary movements in the facial muscles despite good reanimation. Techniques such as a hypoglossal/facial nerve interpositional jump graft and splitting the hypoglossal nerve cause poor functional results in facial reanimation and mild-to-moderate hemiglossal atrophy, respectively. Direct hypoglossal/facial nerve cross-over through end-to-side coaptation without tension was done in three fresh cadavers and four patients. The patients had facial paralysis for less than 7 months. Complete mobilization of the facial nerve trunk and its main branches beyond the pes anserinus from the stylomastoid foramen, division of the frontal branch, if necessary, and superior elevation of the hypoglossal nerve after dividing the descendens hypoglossi, thyrohyoidal branches, occipital artery, and retromandibular veins were performed. The end of the facial nerve was hooked up through both a quarter of a partial oblique neurotomy and a perineurial window at the side of the hypoglossal nerve. Temporalis muscle transfer to the eyelids and the first stage of cross-facial nerve transfer were performed simultaneously. None of the patients experienced hemiglossal atrophy, synkinesis, and involuntary movements of the facial muscles. Regarding facial reanimation, one patient had excellent, one patient good, and the others fair and poor results after a follow-up of at least 1 year.
Adult↗
The facial tics.
The abnormal movements of the facial muscles are classified and the diagnosis and treatment considered in light of 22 cases of hemifacial spasm. Forms of treatment which give only temporary cessation of spasm and require complex and unpleasant treatment to be oft repeated are seldom tolerated for long by the patient. Permanent cure of spasm can only be obtained when the facial nerve or its branch to the muscle is permanently divided or the muscle itself excised. Neurotomy as practised by German (1942) and Scoville (1955) has not been found satisfactory in the present series. Neuro-anastomosis at different sites in the course of the 7th nerve is discussed and shown to be of value in patients with severe widespread spasm and in those in which the spasm is more localised. This method results in only temporary palsy of the facial muscles, the duration of the palsy depending on the site of the division of the facial nerve.
Blepharospasm↗
Facial asymmetry in superior oblique muscle palsy.
Facial asymmetry is an underrecognized association or sequela of torticollis in congenital or very early onset superior oblique muscle palsy, which when present in an adult, helps to confirm chronicity and prevent unnecessary neurologic evaluation. Nineteen cases of superior oblique muscle palsy were studied prospectively. Of 12 unilateral palsies presenting in adulthood, 9 were considered congenital by history and 7 (77%) of these had facial asymmetry. Large vertical fusional vergence amplitudes and torticollis, on review of childhood photographs, confirmed the early onset of the palsy in each facial asymmetry patient. In addition, two children presenting at age 18 months and 3 years of age with constant head tilting had facial asymmetry. If torticollis is corrected before maturation of the facial structure, resolution of the asymmetry may occur.
Adolescent↗
Anatomy of the SMAS revisited.
Despite the relevance of the superficial musculoaponeurotic system (SMAS) in facial rejuvenation a clear anatomic definition of the SMAS is still lacking. Therefore, the morphology of the SMAS in 18 cadavers was investigated using different macroscopic and microscopic techniques. The region-specific anatomy of the SMAS is described in the forehead, parotid, zygomatic, and infraorbital regions, the nasolabial fold, and the lower lip. The SMAS is one continuous, organized fibrous network connecting the facial muscles with the dermis. It consists of a three-dimensional scaffold of collagen fibers, elastic fibers, and fat cells. Two different types of SMAS morphology were demonstrated: type 1 SMAS architecture is located lateral to the nasolabial fold with relatively small fibrous septa enclosing lobules of fat cells, whereas type 2 architecture is located medial to the nasolabial fold, where the SMAS consists of a dense collagen-muscle fiber meshwork. Overall, it was demonstrated that different facial regions show specific morphological characteristics, and thus region-specific surgical interventions may be necessary in facial rejuvenation.
Adipose Tissue↗
Electrophysiological determination of the site involved in generating abnormal muscle responses in hemifacial spasm.
In patients with hemifacial spasm (HFS), abnormal muscle responses due to abnormal cross-transmission are observed in facial muscles. However, the site in the facial nerve responsible for the cross-transmission remains a matter of controversy. We have developed a model in which by considering the electrophysiological parameters involved in producing the abnormal muscle response, we can determine the site of the abnormal cross-transmission within the facial nerve. This model was applied to HFS patients with three different etiologies: idiopathic, post-Bell's palsy, and post-XII-VII anastomosis. Our data show that: in idiopathic HFS, the cross-transmission may occur in the facial nerve at the level of the pontocerebellar angle; in post-Bell's palsy, it is inside the petrous bone; and in XII-VII anastomosis, it must be in the extracranial part of the facial nerve. The possible mechanisms for this cross talk are discussed in terms of ephaptic transmission or of a central hyperexcitability in the facial motor nucleus.
Adult↗
Current status of muscle biopsy in facial paralysis.
The six abnormalities found in pathologic muscle biopsies are described and discussed. Those changes which are indicative of nerve denervation or muscle regeneration are tabulated. Muscle biopsy, as it related to facial paralysis, must still be considered, for the most part, an experimental tool. In certain puzzling situations, eg, neonatal facial paralysis, it can be of value as an adjunct to nerve excitability and electromyographic tests.
Atrophy↗
Facial paralysis rehabilitation: retraining selective muscle control.
Traumatic facial paralysis can be improved with surgical techniques but alone will not restore full function. EMG sensory (bio) feedback can, however, facilitate rehabilitation. Four cases are described using a combined treatment technique of EMG, behavioural modification and specific action exercises. Retraining of eyelid control was also accomplished. Standardized evaluation methods are described. All four patients showed improvement, despite the failure of traditional retraining methods.
Adult↗
Pain-only decompression sickness affecting the orbicularis oculi.
A case is reported of a diver who experienced the onset of pain in the left orbicularis oculi muscle approximately 20 min after surfacing from an experimental dive. A careful neurologic examination disclosed no abnormality. The response of the orbicularis oculi muscle to stimulation of the facial nerve and the blink reflex were both normal as recorded with a clinical neurophysiologic recording system (Nicolet CA 1000). The pain resolved quickly with recompression, supporting a diagnosis of pain-only decompression sickness in this small facial muscle.
Adult↗
Facial rehabilitation with temporal muscle. New concepts.
Facial rehabilitation, utilizing the transposed temporalis muscle, was performed. Three new innovations of this technique include: (1) The whole muscle is transposed into the face to accomplish augmentation, support, protection for the eye, and movement. (2) Following transposition of the temporalis muscle, its nerve supply is lysed at the foramen ovale. Nerve substitution by a free, autogenous graft from the proximal segment of the ipsilateral facial nerve or crossfacial sural nerve is accomplished. This technique substitutes the facial nerve axons and nuclei for the trigeminal nerve in this muscle and thus eliminates movement on mastication and facilitates the possibility for expression. (3) This muscle may be transposed with a portion of the temporal and parietal bones to add bony architecture to the cheek and orbit.
Facial Muscles↗
Cortical mechanisms mediating the inhibitory period after magnetic stimulation of the facial motor area.
We studied the silent period (SP) that interrupts voluntary electromyographic activity (EMG) in facial muscles, after transcranial magnetic stimulation (TMS), in normal subjects. High-intensity magnetic stimulation with a 12-cm round coil centered at the vertex induced a long-lasting SP (215 ms), whereas supramaximal stimulation of the facial nerve only induced a short (< 20 ms) and incomplete EMG suppression, and cutaneous stimuli had no inhibitory effect at all. Cutaneous trigeminal stimulation delivered after TMS evoked blink-like reflexes, showing that facial motoneurons were not inhibited during the SP. Simultaneous recordings from perioral muscles (large cortical representation) and from orbicularis oculi and masseter muscles (small cortical representation) showed SPs of identical duration. Focal stimuli with a figure-of-eight coil showed that positioning of the coil was critical and that the optimal scalp sites for evoking the largest motor potentials and longest SPs coincided. Low-intensity stimulation occasionally elicited short SPs without a preceding motor potential. We conclude that the SP induced in facial muscles by TMS results from the excitation of cortical inhibitory interneurons surrounding the upper motoneurons.
Adult↗