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PubMed1998

[Analytical study of the treatment of facial paralysis by hypoglossal-facial anastomosis. Apropos of 25 cases].

Hypoglosso-facial anastomosis (HFA) is an already old alternative for the surgical treatment of facial paralysis. 25 patients, 17 men and 8 women, with complete facial paralysis were operated according to this technique, 6 to 12 months after onset of the paralysis. Based on analysis of the results, the authors describe the advantages and disadvantages of this technique. The advantages are: facial symmetry at rest, protection of the cornea, voluntary movements of facial muscles. The disadvantages are: paralysis and atrophy of one side of the tongue, absence of expression of emotional and involuntary states on one half of the face, synkinesia, disorders of mastication. Disorders of deglutition improve with time. In this series of 25 patients, the authors never observed eyelid movements independent of movements of the labial commissure. By comparing these advantages and disadvantages, the authors consider that HFA should no longer be proposed for the treatment of facial paralysis. In the current state of microsurgery, if the facial nerve cannot be repaired by direct suture or graft, the authors recommend revascularized, reinnervated muscle transfer onto the facial nerve of the healthy side.

Adult↗
PubMed2003

Free perforator flap for the treatment of defects after resection of huge arteriovenous malformations in the head and neck regions.

The authors report two cases of huge arteriovenous malformations in the head and neck regions treated successfully with preoperative superselective transarterial embolization and resection followed by a free perforator flap transfer. Based on the authors' previous cases, en block mass resection of the malformation was possible with bleeding of less than 150 ml. The massive defects could be repaired with free perforator flaps using an anterolateral thigh flap and a deep inferior epigastric artery perforator flap. One patient who lost facial muscle underwent reconstruction by simultaneous muscle transfer, and both patients regained acceptable cosmetic appearance and dynamic facial function. Now, more than 4 to 7 years after surgery, the patients have shown no reexpansion of the malformation. The important points of this treatment are complete embolization to accomplish total resection with minimal bleeding, free flap transfer to prevent postoperative reexpansion or recurrence of arteriovenous malformations, and the selection of recipient vessels because of arterial embolization in part of the lesion.

Adult↗
PubMed1990

Localization of motoneurons innervating the stylohyoid muscle in the monkey, cat, rabbit, rat and shrew.

The distribution of motoneurons innervating the stylohyoid muscle was examined in the Japanese monkey (Macaca juscata), cat, rabbit, rat and house musk shrew (Suncus murinus) using the retrograde tracing method of horseradish peroxidase. The enzyme was injected into the stylohyoid muscle after ligating the central cut ends of the main peripheral branches of the facial nerve supplying the superficial facial muscles, or the trunk of the glossopharyngeal nerve supplying the pharyngeal muscles. In the monkey, cat and rabbit, stylohyoid motoneurons were identified in the reticular formation dorsomedial, dorsal or rostrodorsal to the main facial nucleus, and in the dorsomedial or dorsal border region, central part and ventral border region of the main facial nucleus. On the other hand, in the rat and shrew, stylohyoid motoneurons were found in the reticular formation dorsal or dorsomedial to the main facial nucleus and in the dorsal or dorsomedial border region of the main facial nucleus, but not in the central part and ventral border region of the main facial nucleus.

Animals↗
PubMed1998

The effect of unilateral partial facial paralysis and muscle ablation on craniofacial growth and development: an experimental study in the rabbit.

The effect of unilateral partial facial nerve ablation and unilateral partial midface muscle ablation on craniofacial growth and development was investigated. New Zealand White rabbits (12 days old) were randomly assigned to three experimental groups: control group, to study normal craniofacial growth and development (n = 15); nerve ablation group, surgically induced unilateral paralysis of the buccal branches of the facial nerve (n = 15); and muscle ablation group, surgical unilateral ablation of the facial muscles innervated by the buccal branches of the facial nerve (n = 12). All animals were operated on at the age of 12 days; follow-up evaluations were performed at the ages of 2 months and 6 months. The age of 2 months represents the endpoint of the prepubertal craniofacial growth and development. At the age of 6 months, the animals are fully grown; therefore, the time period between 2 and 6 months is regarded as the pubertal growth period. Computerized dorsoventral roentgencephalometric (measurement of distances and angles) and computer tomographic (three-dimensional volumetric measurements) investigations were performed at both ages. Additional dry skull measurements were performed to determine more precisely the bone segments involved in the craniofacial growth alterations studied. The obtained results indicated the following. Unilateral partial facial paralysis involving the midface resulted in growth alterations analogous to those seen after unilateral total facial paralysis. The growth alterations were not to be seen as a growth restriction (reduction in bony volume) but as growth misdirections (alterations in shape). Major growth alterations were present in those regions closely related to the facial musculature, namely the nasal, maxillary, and premaxillary regions, resulting in a snout deviation toward the operated side. The growth alterations occurred during prepuberty and remained rather stable during puberty. Morphologic signs of muscle denervation were related to the craniofacial growth disturbances. The growth alterations after unilateral partial facial paralysis were mainly biomechanically induced, as they were analogous to those observed after unilateral midfacial muscle ablation. The fact that after unilateral midfacial muscle ablation at the age of 6 months the severity of the alterations had increased was attributed to the scar formation inherent to the surgical procedure.

Anesthesia↗
PubMed1991

Facial pain and muscle atrophy secondary to an intracranial tumour.

Orofacial pain rarely arises from a distant site. It is unusual for orofacial pain to be associated with wasting of the facial musculature and diminished sensation. This case report describes a patient who presented with temporomandibular joint pain dysfunction syndrome which was initially successfully managed with splint therapy. She re-presented later with unilateral wasting of the muscles of mastication, facial pain and diminished sensation ipsilaterally. An intracranial meningioma was diagnosed following an extensive series of investigations.

Adult↗
PubMed1997

Clinical outcome of continuous facial nerve monitoring during primary parotidectomy.

OBJECTIVES: To assess whether continuous facial nerve monitoring during parotidectomy is associated with a lower incidence of facial nerve paresis or paralysis compared with parotidectomy without monitoring and to assess the cost of such monitoring. DESIGN: A retrospective analysis of outcomes for patients who underwent parotidectomy with or without continuous facial nerve monitoring. SETTING: University medical center. PATIENTS: Fifty-six patients undergoing parotidectomy in whom continuous electromyographic monitoring was used and 61 patients in whom it was not used. MAIN OUTCOME MEASURES: (1) The incidence of early and persistent facial nerve paresis or paralysis and (2) the cost associated with facial nerve monitoring. RESULTS: Early, unintentional facial weakness was significantly lower in the group monitored by electromyograpy (43.6%) than in the unmonitored group (62.3%) (P=.04). In the subgroup of patients without comorbid conditions or surgeries, early weakness in the monitored group (33.3%) remained statistically lower than the rate of early weakness in the unmonitored group (57.5%) (P=.03). There was no statistical difference in the final facial nerve function or incidence of permanent nerve injury between the groups or subgroups. After multivariate analysis, nonmonitored status (odds ratio [OR], 3.22), advancing age (OR, 1.47 per 10 years), and longer operative times (OR, 1.3 per hour) were the only significant independent predictive variables significantly associated with early postoperative facial weakness. The incremental cost of facial nerve monitoring was $379. CONCLUSIONS: The results suggest that continuous electromyographic monitoring of facial muscle during primary parotidectomy reduces the incidence of short-term postoperative facial paresis. Advantages and disadvantages of this technique need to be considered together with the additional costs in deciding whether routine use of continuous monitoring is a useful, cost-effective adjunct to parotid surgery.

Cost-Benefit Analysis↗
PubMed1995

Facial reconstruction after a burn injury using two circumferential radial forearm flaps, and a dorsalis pedis flap for the nose.

A 21-year-old man is reported in whom flap tissue was required to reconstruct the face and nose following burns. The whole of both forearms were used as radial forearm flaps for both cheeks, both lower eyelids, the right upper eyelid, upper and lower lips and chin. A Tagliacozzi arm flap and a dorsalis pedis flap were used for the nose. The ears were resurfaced using grafted skin along the line of the superficial temporal arteries. No thinning of the flaps was required and some facial muscle attachments to the forearm deep fascia led to more recovery of facial movement than might be expected with a flap reconstruction.

Accidents, Traffic↗
PubMed1996

Botulinum toxin induces nitric oxide synthase activity in motoneurons.

Intramuscular injections of botulinum toxin A were made into the snout of 3-month- and 3-week-old rats, resulting in transient paralysis of the facial muscles. Nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry, which is a marker of nitric oxide synthase activity in fixed tissue and, in particular, in injured motoneurons, was studied in the facial nucleus. At variance with control injections of saline, the histochemical staining was found to be induced in facial motoneurons after botulinum toxin injection. The occurrence and persistence of the histochemical positivity in facial motoneurons paralleled that of muscle paralysis. These findings indicate that the enzyme of synthesis of the free radical nitric oxide can be induced in motoneurons after a functional disconnection from the target, which spares the axon and is associated with cell survival.

Animals↗
PubMed2005

Peripheral primitive neuroectodermal tumor of the cerebellopontine angle.

Peripheral primitive neuroectodermal tumors are highly malignant small cell neoplasms. A 27-year-old female presented with a 6-month history of right-sided facial pain and progressive weakness of the facial muscles. She had non-pulsative tinnitus, progressive right hearing loss and facial palsy. T2-weighted MRI showed a heterogeneous hyperintense lesion invading the right internal auditory canal. Surgical removal was performed. Pathological examination showed sheets of small cells with irregular nuclei. Immunohistochemical studies demonstrated positive immunoreactivity for neuron-specific enolase, synaptophysin, chromogranin, vimentin, S-100 protein and p30-32 MIC-2 gene product. The patient was treated with chemotherapy (etoposide, vincristine, adriamycin, ifosfamide and actinomycin D) and radiotherapy. After 65 months of follow-up, the patient presented with cervical metastasis. Radical cervical dissection was performed and the patient was treated with a second course of chemotherapy. At control MRI after 29 months of follow-up the patient showed no signs of local recurrence or distant metastasis.

Adult↗
PubMed2004

Temporary management of upper lid ptosis, lid malposition, and eyelid fissure asymmetry with botulinum toxin type A.

During the past 10 years the primary focus for the aesthetic use of botulinum toxin has been directed to the treatment of dynamic facial lines. This agent has been shown to be very effective for the improvement of facial shape. The use of botulinum toxin type A for the correction of a variety of presentations of facial asymmetry has also been well established. The general principles regarding the counter-effects of facial muscle protagonists and antagonists and their potential effects on the position of facial soft-tissue regions apply here as well. Twenty-two patients received botulinum toxin type A for the temporary treatment of mild to moderate unilateral upper eyelid ptosis and aesthetic improvement of lower eyelid position, with favorable results. Although commonly related to a rare yet feared adverse consequence from the inappropriate application of botulinum toxin, its application for the treatment of upper eyelid ptosis, eyelid position, and other lid fissure asymmetries for aesthetic improvement is presented.

Adult↗
PubMed1998

Defective peroxisome biogenesis with a neuromuscular disorder resembling Werdnig-Hoffmann disease.

OBJECTIVE: Characterization of the defect in a patient presenting a peripheral neuropathy with atypical features of distal motor involvement mimicking Werdnig-Hoffmann disease. PATIENT: Clinical signs included generalized hypotonia and floppiness, absence of stretch reflexes, muscle wasting, lack of head control and lingual fasciculations associated with unaffected facial muscles, and normal intellectual development. RESULTS: Normal muscle histology ruled out Werdnig-Hoffmann disease. Elevated plasma concentrations of very long-chain fatty acids and bile acid intermediates combined with normal plasmalogen levels in erythrocytes suggested defective peroxisomal beta-oxidation directly demonstrated by deficient pristanic acid and partially deficient C26:0 was present oxidation in cultured fibroblasts. Severely impaired pipecolic acid oxidation in liver and phytanic acid oxidation in fibroblasts was present. On light and electron microscopy of the liver tissue, rare peroxisomal membrane ghosts and trilamellar inclusions but absence of peroxisomes was noted. Immunoblot analysis revealed absence of peroxisomal beta-oxidation enzymes in liver tissue but normal results in fibroblasts. Remarkably, expression of the peroxisomal defect in fibroblasts was indicated by the finding of mainly cytoplasmatic catalase, as in liver. Preliminary studies excluded classification of this patient within the large PEX1 complementation group. CONCLUSIONS: The results suggest a novel peroxisome biogenesis disorder involving peroxisomal beta-oxidation as well as phytanic and pipecolic acid oxidation rather than an isolated defect of peroxisomal beta-oxidation. The association of a clinical picture mimicking Werdnig-Hoffmann disease with a novel peroxisomal disorder raises the question of whether investigation for peroxisomal function should be considered in every patient with an enigmatic spinal muscular atrophy-like syndrome.

Bile Acids and Salts↗
PubMed2000

A novel de novo mutation in the desmin gene causes desmin myopathy with toxic aggregates.

OBJECTIVE: To determine the cause and pathogenic mechanisms of a 21-year-old patient's cardioskeletal myopathy. The patient's muscle atrophy and weakness began in distal parts of limbs; cardiac and facial muscles were later involved. BACKGROUND: Desmin myopathy is a skeletal myopathy often associated with cardiomyopathy, caused by mutations in the desmin gene and characterized by desmin accumulation in affected muscle fibers, a leading marker of myofibrillar myopathies. Two kinds of deletions and seven missense mutations in the desmin gene have been identified. METHODS: Clinical examination, electron microscopy of muscle tissue, two-dimensional gel electrophoresis, DNA sequencing, restriction enzyme analysis, and gene transfection were performed. RESULTS: Electron microscopy showed disruption of sarcomeres at Z discs and electron-dense aggregates in biopsied skeletal and heart muscle. Two-dimensional gel electrophoresis of the patient's skeletal muscle proteins showed massive accumulation of desmin. The authors identified a novel desmin mutation, L385P in one allele in the carboxyl end of the rod domain 2B in the patient's leukocytes and skeletal muscle; neither parent had the mutation. Serologic study and DNA markers confirmed the de novo mutation. A peptide harboring desmin rod domains 2A and 2B with L385P tagged with green fluorescent protein induced cytoplasmic aggregates, nuclear DNA condensation, and cell death. CONCLUSIONS: A novel de novo mutation, L385P, causes desmin myopathy. An expression study indicated the toxic effect of the L385P mutation.

Adult↗
PubMed2000

The expression of Myf5 in the developing mouse embryo is controlled by discrete and dispersed enhancers specific for particular populations of skeletal muscle precursors.

The development of skeletal muscle in vertebrate embryos is controlled by a transcriptional cascade that includes the four myogenic regulatory factors Myf5, Myogenin, MRF4 and MyoD. In the mouse embryo, Myf5 is the first of these factors to be expressed and mutational analyses suggest that this protein acts early in the process of commitment to the skeletal muscle fate. We have therefore analysed the regulation of Myf5 gene expression using transgenic technology and find that its control is markedly different from that of the other two myogenic regulatory factor genes previously analysed, Myogenin and MyoD. We show that Myf5 is regulated through a number of distinct and discrete enhancers, dispersed throughout 14 kb spanning the MRF4/Myf5 locus, each of which drives reporter gene expression in a particular subset of skeletal muscle precursors. This region includes four separate enhancers controlling expression in the epaxial muscle precursors of the body, some hypaxial precursors of the body, some facial muscles and the central nervous system. These elements separately or together are unable to drive expression in the cells that migrate to the limb buds and in some other muscle subsets and to correctly maintain expression at late times. We suggest that this complex mechanism of control has evolved because different inductive signals operate in each population of muscle precursors and thus distinct enhancers, and cognate transcription factors, are required to interpret them.

Animals↗
PubMed2003

[Merosin-positive congenital muscular dystrophy with early orthopaedic problems in relation to Ullrich's disease].

We report three patients with sporadic merosin-positive congenital muscular dystrophy (CMD) with torticollis and/or developmental dislocation of the hip in early childhood. Diagnosis of merosin-positive CMD was based on their clinical and dystrophic muscle biopsy findings. At the age 13 months, patient 1 was found to have developmental dislocation of both hips, which was surgically treated at 5 years. Patient 2 had severe torticollis and contracture of both hip joints which had been present since the neonatal period, and underwent repair of the torticollis at 2 years. Patient 3 was found to have developmental dislocation of the left hip at one month of age. Although she had generalized muscle hypotonia she learned to walk at 23 months. She had no facial muscle involvement nor contracture of joints, but had hyperlaxity of distal joints. Her muscle biopsy showed complete collagen VI deficiency immunohistochemically. In contrast to merosin-deficient CMD, merosin-positive CMD appears to be a group of heterogeneous diseases. Since collagen VI was reported to be defective in Ullrich's disease, patient 3 may be diagnosed as having Ullrich's disease but had no typical clinical characteristics of the disease. Further study is needed to identify the pathogenetic mechanism of congenital muscular dystrophy with early joint abnormalities to determine whether there is a primary abnormality of the connective tissue including collagen VI.

Adolescent↗
PubMedDate not supplied

Distal muscular dystrophy. Case reports.

The distal muscular dystrophy has been described in 1902 by Gowers. Since then a lot of cases with different mode of inheritance, clinical involvement and morphological findings have been described. Obviously distal myopathies are not a single entity. We describe four new cases of distal myopathy. Although we suppose that they are from the adult-onset Welander's form, they are different in some points. Two cases were with onset in the lower limbs and autosomal dominant inheritance, the third one was sporadic with onset in the lower limbs and the last one was sporadic with onset in the upper limbs. The distal muscles were markedly, while the proximal were slightly involved. Sternocleidomastoid, neck or facial muscles wasting were also found in three cases. The serum creatine kinase in all patients was in nearly normal limits. The electromyographic findings were consistent with chronic myopathy, although fibrillation potentials and positive sharp waves were found in three cases. Muscle biopsy data confirm the myopathic involvement in all patients. We have described patients, which confirm the variability of distal myopathies, regarding the age of onset, initial symptoms, clinical picture, electromyographic and muscle biopsy findings.

Adult↗
PubMed1994

Chemomyectomy of the orbicularis oculi muscles for the treatment of localized hemifacial spasm.

OBJECTIVE: To report our experience with doxorubicin chemomyectomy as an alternative to other treatments for hemifacial spasm (HFS). DESIGN: A prospective, open study Phase I clinical trial of chemomyectomy. SETTING: A hospital-based, referral neuro-ophthalmology and oculoplastic service. PATIENTS AND METHODS: Repeated (1-6, median: 4) local injections of doxorubicin were given in the eyelids of 8 patients (5 men, 3 women, average age: 71). MAIN OUTCOME MEASURES: Eyelid strength, self-reported spasm, and duration of improvement without seeking additional or alternative treatments. RESULTS: Chemomyectomy resulted in permanent (> or = 2.5 years) orbicularis oculi weakness and relief from spasms in the treated areas in 5 patients, although 2 patients requested occasional supplementary botulinum toxin (BT) injections in the facial muscles over the cheek. One patient had a successful result for 3 years, after which spasm recurred. One patient maintains a successful result in the eyelid but had a failed microvascular decompression in the lower face. One incompletely treated patient required microvascular decompression following spread of spasms to the lower branches of the facial nerve and increased severity of the HFS. One patient required eyelid surgery because of concurrent spastic entropion. One patient treated with a higher concentration than currently used required closure of a skin ulcer. CONCLUSIONS: Doxorubicin chemomyectomy is an effective alternative to conventional therapy for properly selected patients affected by HFS, particularly older patients with relatively localized eyelid muscle spasms. The modified technique of doxorubicin chemomyectomy has developed to the point where its safety is demonstrated and its risks are known.

Aged↗