Facial Nerve Injuries: Traumatic injuries to the facial nerve. This may result in FACIAL PARALYSIS, decreased lacrimation and salivation, and loss of taste sensation in the anterior tongue. The nerve may regenerate and reform its original pattern of innervation, or regenerate aberrantly, resulting in inappropriate lacrimation in response to gustatory stimuli (e.g., "crocodile tears") and other syndromes.Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.Facial Paralysis: Severe or complete loss of facial muscle motor function. This condition may result from central or peripheral lesions. Damage to CNS motor pathways from the cerebral cortex to the facial nuclei in the pons leads to facial weakness that generally spares the forehead muscles. FACIAL NERVE DISEASES generally results in generalized hemifacial weakness. NEUROMUSCULAR JUNCTION DISEASES and MUSCULAR DISEASES may also cause facial paralysis or paresis.Facial Nerve Diseases: Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.Peripheral Nerve Injuries: Injuries to the PERIPHERAL NERVES.Facial Muscles: Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)Sciatic Nerve: A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.Cranial Nerve Neoplasms: Benign and malignant neoplasms that arise from one or more of the twelve cranial nerves.Cranial Nerve Injuries: Dysfunction of one or more cranial nerves causally related to a traumatic injury. Penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA; NECK INJURIES; and trauma to the facial region are conditions associated with cranial nerve injuries.Hypoglossal Nerve Injuries: Traumatic injuries to the HYPOGLOSSAL NERVE.Nerve Regeneration: Renewal or physiological repair of damaged nerve tissue.Optic Nerve Injuries: Injuries to the optic nerve induced by a trauma to the face or head. These may occur with closed or penetrating injuries. Relatively minor compression of the superior aspect of orbit may also result in trauma to the optic nerve. Clinical manifestations may include visual loss, PAPILLEDEMA, and an afferent pupillary defect.Neuroma, Acoustic: A benign SCHWANNOMA of the eighth cranial nerve (VESTIBULOCOCHLEAR NERVE), mostly arising from the vestibular branch (VESTIBULAR NERVE) during the fifth or sixth decade of life. Clinical manifestations include HEARING LOSS; HEADACHE; VERTIGO; TINNITUS; and FACIAL PAIN. Bilateral acoustic neuromas are associated with NEUROFIBROMATOSIS 2. (From Adams et al., Principles of Neurology, 6th ed, p673)Wounds and Injuries: Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.Facial Expression: Observable changes of expression in the face in response to emotional stimuli.
Electroneuronography: Electroneuronography or electroneurography (ENoG) is a neurological non-invasive test that was first described by Esslen and Fisch in 1979 and is used to examine the integrity and conductivity of a peripheral nerve. It consists of a brief electrical stimulation of the nerve in one point underneath the skin, and at the same time recording the electrical activity (compound action potentials) at another point of the nerve's trajectory in the body.Facial nerve paralysisNeurotmesis: Neurotmesis (in Greek tmesis signifies "to cut") is part of Seddon's classification scheme used to classify nerve damage. It is the most serious nerve injury in the scheme.Facial muscles: The facial muscles are a group of striated skeletal muscles innervated by the facial nerve (cranial nerve VII) that, among other things, control facial expression. These muscles are also called mimetic muscles.Sciatic nerve: The sciatic nerve (; also called ischiadic nerve, ischiatic nerve) is a large nerve in humans and other animals. It begins in the lower back and runs through the buttock and down the lower limb.Neuroregeneration: Neuroregeneration refers to the regrowth or repair of nervous tissues, cells or cell products. Such mechanisms may include generation of new neurons, glia, axons, myelin, or synapses.Vestibular schwannomaNational Center for Injury Prevention and Control: The U.S.Endoneurium: The endoneurium (also called endoneurial channel, endoneurial sheath, endoneurial tube, or Henle's sheath) is a layer of delicate connective tissue around the myelin sheath of each myelinated nerve fiber. Its component cells are called endoneurial cells.Emotional responsivity: Emotional responsivity refers to the ability to acknowledge an affective stimuli by exhibiting emotion. Any response, whether it is appropriate or not, would showcase the presence of this phenomena.
(1/71) Parotid neoplasms: a report of 250 cases and review of the literature.
A 25-year experience with parotid tumors was reviewed. From a total of 250 neoplasms, 173 were histologically benign and 77 were malignant. Benign mixed tumors accounted for 59% of all lesions. Clinical parameters used to diagnose parotid neoplasms were found to be unreliable in determining whether a given tumor was benign or malignant. The mean age for malignant lesions was 10 years greater than for benign lesions. The phenomenon of malignant transformation of a benign tumor was considered in four patients. Complete surgical excision is the safest and preferred method for diagnosis. Preoperative needle or incisional biopsy are associated with a high degree of local recurrence. The appropriate management of any parotid tumor is predicated on special histological type. Local excision or enucleation no longer have a place in the surgical management of benign parotid tumors. Postoperative tumor recurrence and morbidity are directly related to awareness of surgical anatomy and pursuit of correct surgical techniques for adequate resection. The five-year recurrence rate for 102 benign mixed tumors was 6%. Recurrence in malignant tumors varied with specific histological types but was generally high. Five-year survival for all malignant parotid tumors was 48%. (+info)
(2/71) Exacerbation of facial motoneuron loss after facial nerve transection in severe combined immunodeficient (scid) mice.
The immune system functions to protect an organism against microbial infections and may be involved in the reparative response to nerve injury. The goal of this study was to determine whether the immune system plays a role in regulating motoneuron survival after a peripheral nerve injury. After a right facial nerve axotomy, facial motoneuron (FMN) survival in C.B-17 (+/+) wild-type mice was found to be 87 +/- 3.0% of the unaxotomized left side control. In contrast, facial nerve axotomy in C.B-17 (-/-) severe combined immunodeficient (scid) mice, lacking functional T and B lymphocytes, resulted in an average FMN survival of 55 +/- 3.5% relative to the unaxotomized left side control. This represented an approximately 40% decrease in FMN survival compared with wild-type controls. The reconstitution of scid mice with wild-type splenocytes containing T and B lymphocytes restored FMN survival in these mice to the level of the wild-type controls. These results suggest that immune cells associated with acquired immunity play a role in regulating motoneuron survival after a peripheral nerve injury. (+info)
(3/71) Impaired axonal regeneration in alpha7 integrin-deficient mice.
The interplay between growing axons and the extracellular substrate is pivotal for directing axonal outgrowth during development and regeneration. Here we show an important role for the neuronal cell adhesion molecule alpha7beta1 integrin during peripheral nerve regeneration. Axotomy led to a strong increase of this integrin on regenerating motor and sensory neurons, but not on the normally nonregenerating CNS neurons. alpha7 and beta1 subunits were present on the axons and their growth cones in the regenerating facial nerve. Transgenic deletion of the alpha7 subunit caused a significant reduction of axonal elongation. The associated delay in the reinnervation of the whiskerpad, a peripheral target of the facial motor neurons, points to an important role for this integrin in the successful execution of axonal regeneration. (+info)
(4/71) Spatial relationship between vestibular schwannoma and facial nerve on three-dimensional T2-weighted fast spin-echo MR images.
BACKGROUND AND PURPOSE: During surgical removal of a vestibular schwannoma, correct identification of the facial nerve is necessary for its preservation and continuing function. We prospectively analyzed the spatial relationship between vestibular schwannomas and the facial nerve using 3D T2-weighted and postcontrast T1-weighted spin-echo (SE) MR imaging. METHODS: Twenty-two patients with a unilateral vestibular schwannoma were examined with MR imaging. The position and spatial relationship of the facial nerve to adjacent tumor within the internal auditory canal (IAC) and cerebellopontine angle cistern (CPA) were assessed on multiplanar reformatted 3D T2-weighted fast spin-echo (FSE) images and on postcontrast transverse and coronal T1-weighted SE images. The entrance of the nerve into the bony canal at the meatal foramen and the nerve root exit zone along the brain stem were used as landmarks to follow the nerve course proximally and distally on all images. RESULTS: The spatial relationship between vestibular schwannoma and facial nerve could not be detected on postcontrast T1-weighted SE images. In 86% of the patients, the position of the nerve in relation to the tumor was discernible on multiplanar reformatted 3D T2-weighted FSE images. In tumors with a maximal diameter up to 10 mm, the entire nerve course was visible; in tumors with a diameter of 11 to 24 mm, only segments of the facial nerve were visible; and in tumors larger than 25 mm, the facial nerve could not be seen, owing to focal nerve thinning and obliteration of landmarks within the IAC and CPA. CONCLUSION: Identification of the facial nerve and its position relative to an adjacent vestibular schwannoma is possible on multiplanar reformatted 3D T2-weighted FSE images but not on postcontrast T1-weighted SE images. Detection of this spatial relationship depends on the tumor's size and location. (+info)
(5/71) Complete and long-term rescue of lesioned adult motoneurons by lentiviral-mediated expression of glial cell line-derived neurotrophic factor in the facial nucleus.
To date, delivery of neurotrophic factors has only allowed to transiently protect axotomized facial motoneurons against cell death. In the present report, long-term protection of these neurons was evaluated by continuously expressing the neurotrophic factor glial cell line-derived neurotrophic factor (GDNF) within the facial nucleus using a lentiviral vector system. The viral vector was injected unilaterally into the facial nucleus of 4-month-old Balb/C mice. In contrast to axotomy in other adult rodents, facial nerve lesion in these animals leads to a progressive and sustained loss and/or atrophy of >50% of the motoneurons. This model thus represents an attractive model to evaluate potential protective effects of neurotrophic factors for adult-onset motoneuron diseases, such as amyotrophic lateral sclerosis. One month after unilateral lentiviral vector injection, the facial nerve was sectioned, and the animals were killed 3 months later. Viral delivery of the GDNF gene led to long-term expression and extensive diffusion of GDNF within the brainstem. In addition, axotomized motoneurons were completely protected against cell death, because 95% of the motoneurons were present as demonstrated by both Nissl staining and choline acetyltransferase immunoreactivity. Furthermore, GDNF prevented lesion-induced neuronal atrophy and maintained proximal motoneuron axons, despite the absence of target cell reinnervation. This is the first evidence that viral-mediated delivery of GDNF close to the motoneuron cell bodies of the facial nucleus of adult mice can lead to complete and long-term protection against lesion-induced cell death. (+info)
(6/71) Conditional gene ablation of Stat3 reveals differential signaling requirements for survival of motoneurons during development and after nerve injury in the adult.
Members of the ciliary neurotrophic factor (CNTF)/leukemia inhibitory factor (LIF)/cardiotrophin gene family are potent survival factors for embryonic and lesioned motoneurons. These factors act via receptor complexes involving gp130 and LIFR-beta and ligand binding leads to activation of various signaling pathways, including phosphorylation of Stat3. The role of Stat3 in neuronal survival was investigated in mice by Cre-mediated gene ablation in motoneurons. Cre is expressed under the neurofilament light chain (NF-L) promoter, starting around E12 when these neurons become dependent on neurotrophic support. Loss of motoneurons during the embryonic period of naturally occurring cell death is not enhanced in NF-L-Cre; Stat3(flox/KO) mice although motoneurons isolated from these mice need higher concentrations of CNTF for maximal survival in culture. In contrast, motoneuron survival is significantly reduced after facial nerve lesion in the adult. These neurons, however, can be rescued by the addition of neurotrophic factors, including CNTF. Stat3 is essential for upregulation of Reg-2 and Bcl-xl expression in lesioned motoneurons. Our data show that Stat3 activation plays an essential role for motoneuron survival after nerve lesion in postnatal life but not during embryonic development, indicating that signaling requirements for motoneuron survival change during maturation. (+info)
(7/71) Local injection of botulinum toxin type A for hemifacial spasm.
The preliminary experience of botulinum toxin treatment for hemifacial spasm is reported in this study. Five patients were treated with 10 injections of botulinum toxin in total. Botulinum toxin had a good to excellent effect in all cases. Improvement was observed 2 weeks to 1 month after the injection. The duration of improvement was 0-9 months (mean 4.2 months). The peak rank tended to decrease and the duration of improvement increased after several treatments. Hemifacial spasm caused by the anterior inferior cerebellar artery tended to subside easily. In contrast, compression by the vertebral artery was more refractory. Continuous facial spasm caused by operative trauma subsided after the injection, but paroxysmal spasm still occurred when eating or laughing. Spasm caused by trauma disappeared 4.5 months after the injection. The complications, which were facial nerve paresis in two cases (3 injections, 30%) and diplopia in one case (1 injection, 10%), were transient and subsided in 2 weeks. (+info)
(8/71) Transplantation of olfactory mucosa minimizes axonal branching and promotes the recovery of vibrissae motor performance after facial nerve repair in rats.
The occurrence of abnormally associated movements is inevitable after facial nerve transection. The reason for this post-paralytic syndrome is poor guidance of regrowing axons, whereby a given muscle group is reinnervated by misrouted axonal branches. Olfactory ensheathing glia have been shown to reduce axonal sprouting and stimulate axonal regeneration after transplantation into the spinal cord. In the present study, we asked whether transplantation of olfactory mucosa (OM) would also reduce sprouting of a damaged peripheral pure motor nerve. The adult facial nerve was transected, and the effect of the OM placed at the lesion site was analyzed with regard to the accuracy of target reinnervation, axonal sprouting of motoneurons, and vibrissal motor performance. Accuracy of target reinnervation and axonal sprouting were studied using preoperative/postoperative labeling and triple retrograde labeling of facial motoneurons, respectively. The vibrissal motor performance was monitored using a video-based motion analysis. We show here that implantation of OM, compared with simple facial-facial anastomosis, (1) improved the protraction, amplitude, angular velocity, and acceleration of vibrissal movements up to 80% of the control values, (2) reduced the percentage of branching motoneurons from 76 to 39%, and (3) improved the accuracy of reinnervation from 22 to 49%. Moreover, we present evidence, that transplanted OM but not buccal mucous membrane induced a sustained upregulation of trophic factors at the lesion site. It is concluded that transplantation of OM to the transected facial nerve significantly improves nerve regeneration. (+info)