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Functional Connections of the Rostral Nucleus of the Solitary Tract in Viscerosensory Integration of Ingestion Reflexes
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
From the preceding it is clear that feeding behavior is complex, requiring the activity of a number of motor nuclei.5,9,10 The trigeminal motor nucleus activates muscles involved in jaw opening, chewing, and the initial stage of swallowing (e.g., mylohyoid m.). The facial motor nucleus activates muscles controlling lip movements and ones ancillary to jaw movements and swallowing (e.g., stylohyoid m.). The hypoglossal nucleus is responsible for protrusion (genioglossus m.) and retrusion (styloglossus m.) of the tongue, as during licking, lateral movements of the tongue during chewing of a bolus, and elevation of the posterior tongue during swallowing. Nucleus ambiguus contains glossopharyngeal and vagal motoneurons that supply the striated muscles of the pharynx and esophagus that function during swallowing. The dorsal motor nucleus of the vagus nerve contributes parasympathetic innervation to the smooth musculature of the esophagus that is responsible for the “primary peristalsis” of swallowing. Motoneurons from the first through third cervical segments innervate muscles attached to the hyoid bone (e.g., geniohyoid m. and sternohyoid m.) that also function during swallowing.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
The seventh cranial nerve (see CRANIAL NERVES) composed of motor, sensory and AUTONOMIC fibres. The motor fibres arise in the facial motor nucleus in the rostral MEDULLA and supply superficial facial muscles that are important in facial expression. The sensory fibres are gustatory (see GUSTATION) and innervate TASTE BUDS on the anterior two-thirds of the tongue. These fibres comprise the CHORDA TYMPANI, and their cell bodies are located in the GENICULATE GANGLION in the temporal bone. The autonomic fibres in the facial nerve are involved in the secretion of saliva and tears. Their cell bodies are located in the superior salivatory nucleus in the medulla.
Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
The facial motor nucleus lies ventral and lateral to the abducens nucleus in the lower pons. From the facial nucleus, all the nerve fibers that innervate the ipsilateral facial muscles ascend posteriorly and medially to loop around the abducens nucleus (genu of the facial nerve) before travelling ventrally (immediately lateral to the corticospinal tract) to emerge from the ventrolateral aspect of the pons. The motor division of the facial nerve and the nervus intermedius (see below) then proceed laterally in the CPA along with CN VIII before entering the internal auditory canal of the temporal bone (with CN VIII). The nerve has four segments within the temporal bone:Meatal segment: this segment extends from the porus of the internal auditory canal to the meatal foramen. There are no major branches from this facial nerve segment.Labyrinthine segment: this segment extends from the meatal foramen to the geniculate ganglion. The labyrinthine segment is the narrowest part of the facial nerve and is susceptible to compression as a result of edema. In this section, which is 3–5 mm in length, the facial nerve changes direction to form the first genu and ends at the geniculate ganglion where the cell bodies of the general somatic and special visceral afferent neurons are located. The greater superficial petrosal nerve, which is the first major branch of the facial nerve, arises from the upper portion of the geniculate ganglion.Tympanic segment: this section is 10 mm in length and has no major nerve branches. It extends from the geniculate ganglion to the horizontal semicircular canal. The tympanic segment ends where the facial nerve makes its second genu.Mastoid segment: this is the final intracranial portion of the facial canal. The nerve proceeds vertically to the stylomastoid foramen where it exits the cranium. The nerve to the stapedius originates near the upper portion of this segment. The chorda tympani is another branch arising from this segment; it joins the lingual nerve and carries preganglionic parasympathetic fibers (from the superior salivatory nucleus), which innervate the submandibular and sublingual glands and afferent taste fibers from the anterior two-thirds of the tongue. A sensory branch exits the nerve immediately below the stylomastoid foramen and innervates the posterior wall of the external auditory canal and a portion of the tympanic membrane.
Two-dimensional structure analysis of hemifacial spasms and surgical outcomes of microvascular decompression
Published in Neurological Research, 2021
Shiyuan Han, Yongning Li, Zhimin Li, Xin Wang, Jun Gao
Hemifacial spasm (HFS) is characterized by paroxysmal unilateral contractions of facial muscles that are typically caused by ephaptic hyperactivation of the VII cranial nerve (CN). Primary HFS typically begins in the fifth and sixth decades of life with a female predilection, usually occurring in the left side [1].HFS often leads to social embarrassment, which leads to a diminished self-image and a reduced quality of life [2]. More importantly, HFS episodes may pose vital consequences in the work environment that cannot afford any mistakes such as driving a car or performing an operation. Thus, the problem of HFS must receive necessary attention and be treated properly. Neurovascular conflict (NVC) in the root exit zone (REZ) of VII CN is considered to be the leading cause of HFS [1,3]. The REZ of the VII CN is a transition area between central oligodendrocytes and peripheral Schwann cells, at which the facial nerve is susceptible to local demyelination [4,5]. Myelination serves as a natural inhibitor of ephaptic transmission. Eventually, local demyelinated areas impulsively compressed by vessels lead to excessive or abnormal firing of the VII CN either by neighboring neurons or by facial motor nuclei [6–9]. Although it is basically considered a vascular compression syndrome, primary HFS is reported to be absent in 10% to 20% individuals with NVC in the REZ according to imaging tests [10,11]. Obviously, the underlying pathogenesis of HFS still remains to be further illuminated.
Advances in the molecular biology and pathogenesis of congenital central hypoventilation syndrome—implications for new therapeutic targets
Published in Expert Opinion on Orphan Drugs, 2018
Simona Di Lascio, Roberta Benfante, Silvia Cardani, Diego Fornasari
Stornetta et al. (2006) [54] defined the RTN in rodents as a collection of glutamatergic neurons that express Phox2b and the vesicular glutamate transporter VGlut2 but not the catecholaminergic biosynthetic enzymes, and predominantly rise on the ventral surface of the medulla oblongata, below the facial motor nucleus. Rodent RTN neurons mediate a large portion of the ventilatory reflex to hypercapnia, and are more important in sustaining breathing during NREM than during REM sleep [83,84]. The human RTN has been tentatively identified by PHOX2B immunohistochemistry but not functionally defined [85,86], and recent post-mortem studies of CCHS brains have failed to identify any defect in any RTN-like structure, probably due to technical limitations [82]. Conditional mice obtained by selectively expressing the +7 alanine mutation in RTN neurons [79] showed a reduced ventilatory reflex to hypercapnia that is similar to that observed in the constitutive KI mice generated by Dubreuil et al. [7], but they survived and their response to CO2 subsequently partially recovered. This indicates that anatomical and functional disruption of the RTN is necessary to explain the lack of CO2 chemosensitivity in CCHS patients, particularly during NREM sleep, but it is not sufficient to provide a complete explanation of the respiratory deficits that some patients also experience during wakefulness.
Complete Horizontal Gaze Paresis Due to Medial Pontine Haemorrhage
Published in Neuro-Ophthalmology, 2023
Joan Pei Yun Sim, Jackie Jia Lin Sim, Sameer Saleem, Dennis Cordato
The haemorrhagic lesion had presumably damaged the facial motor nucleus and/or fascicle, which is anatomically located near the abducens nucleus, thereby explaining the lower motor neuron facial nerve palsy present. The corticospinal tracts were also involved, as is evidenced by the severe contralateral peripheral weakness.11 The overall findings are consistent with a Foville's ‘plus’ syndrome manifesting with crossed motor signs and bilateral horizontal ophthalmoplegia.