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Clinical Neuroanatomy
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
The VIIth nerve is primarily motor to the muscles of facial expression. It also carries the important taste fibres from the anterior two-thirds of the tongue via the chorda tympani and taste from the palate via the nerve of the pterygoid canal (Figure 111.10). A small but clinically important cutaneous supply to the skin of the external ear is mediated in fibres carried from the nerve via the vagus. These sensory fibres are contained in a separate trunk, the nervus intermedius, which runs with the VIIIth nerve rather than the VIIth nerve in the subarachnoid space. The cell bodies of the sensory root lie in the geniculate ganglion. The nervus intermedius also carries preganglionic, parasympathetic secretomotor fibres to the lacrimal, submandibular and sublingual salivary glands. These fibres originate in the lacrimatory nucleus and superior salivatory nucleus.
Specific Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Superior salivatory nucleus4 (C&S, p. 388) Superior salivatory nucleus and lacrimal nucleus (B&K, p. 133)See, also, D: Nucleus vs. subnucleus vs. nuclear complex.
Trigeminal Autonomic Cephalalgias
Published in Gary W. Jay, Clinician’s Guide to Chronic Headache and Facial Pain, 2016
Two key aspects characterizing the pathophysiology of PH and other TACs are the source and trigeminal distribution of pain, and the ipsilateral cranial and facial autonomic features. The trigeminal—autonomic reflex involves the trigeminal afferents and the brain stem connections between nucleus caudalis and superior salivary nucleus. Activation of the superior salivary nucleus is responsible for the cranial and facial parasympathetic outflow via the facial nerve. Given the anatomical connections, trigeminal efferent activation also results in pain in the distribution of the trigeminal and upper cervical nerves in addition to stimulating the facial nerve parasympathetic outflow (1,35,62). Due to the anatomical extension of the nucleus caudalis to upper cervical nerves (1), PH pain may also involve the neck and occiput (22). It has also been reported that neurotransmitters such as calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) released by sensitized trigeminal neurons are elevated during PH attacks and return to normal after treatment (1) implicating involvement of trigeminal afferents. This is supported by experimental studies whereby stimulation of the trigeminal ganglion results in local release of CGRP, substance P, and VIP from parasympathetic nerves mimicking the occurrence during PH attacks (63).
A review of dry eye disease therapies: exploring the qualities of varenicline solution nasal spray
Published in Expert Review of Ophthalmology, 2023
Siddharth Bhargava, Ranjani Panda, Asma M Azam, John D Sheppard
The maintenance of the ocular surface by LFU’s nerve pathways can be divided into a sensory afferent and a parasympathetic efferent system. Changes in homeostasis and new environmental stressors are sensed by the afferent branch, which is composed of the nasal mucosa, ocular surface, and the skin [16]. The ophthalmic division of the trigeminal nerve (V1), including its nasociliary branch, receives sensory innervation from the eyelids, conjunctiva, and cornea [14]. In the nasal cavity, the sensory afferent stimulus originates from the nasociliary branch of V1 and branches of the maxillary branch of the trigeminal nerve (V2) [14,57–59]. The afferent signals from the ocular surface and nasal mucosa synapse onto the superior salivatory nucleus in the brainstem and enact an efferent parasympathetic response that stimulates aqueous tear production from goblet cells, meibomian glands, and lacrimal glands with the goal of restoring homeostasis of the ocular surface [14,57,60]. The reflexive production of tears in response to a stimulus is referred to as nasolacrimal reflex. An approach to promote parasympathetic nervous system activity through the nasolacrimal reflex (NLR) could be utilized to treat dry eye disease [14,61].
Congenital alacrima
Published in Orbit, 2022
Zhenyang Zhao, Richard C. Allen
The neural regulation of lacrimal gland secretion comprises an afferent sensory arm and a parasympathetic dominant efferent arm. The afferent arm receives input from the nasal mucosa and ocular surface sensory fibers, which are composed of the polymodal nociceptors of the cornea.4 The stimulatory signal is processed in the spinal trigeminal nucleus and relayed to the superior salivary nucleus.5 The efferent arm originates from the superior salivary nucleus projecting to the pterygopalatine ganglion, initially through the greater superficial petrosal nerve, which later joins the deep petrosal nerve to form the vidian nerve before synapsing. The postganglionic fibers from the pterygopalatine ganglion provide parasympathetic innervation for the lacrimal gland.6 The same process regulates both reflex and basal tear secretion despite being different clinical concepts. This is supported by the observation that minimal basal tear secretion occurs without stimuli during sleep and under local or general anesthesia.7 Any interruptions along this pathway can lead to decreased tear production and alacrima.
The enigma of headaches associated with electromagnetic hyperfrequencies: Hypotheses supporting non-psychogenic algogenic processes
Published in Electromagnetic Biology and Medicine, 2020
Considering HF biophysical properties, the trigemino-thalamo-cortical terminal activation, including a microvascular releasing of inflammatory mediators, seems to be the main process that can be triggered by such irradiation. Without prejudice to etiology, trigeminal-vascular activation begins with the activation of the superior salivary nucleus (SSN) and its vegetative pathways. The relay is carried out in the sphenopalatine ganglion (SPG). Post-ganglionic fibers then release mediators (VIP, NO and ACh) that alter perfusion and capillary permeability in the middle meningeal vessels (Charles and Brennan 2010; Moskowitz and Buzzi 2010). This results in extravasation of plasma and local influx of inflammatory cells. Mediators such as CGRP, NKA A and MS are then released: it is the neurogenic inflammation (Charles and Brennan 2010; Edvinsson and Uddman 2005; Zeller et al. 2008). These substances sensitize and then activate the trigeminal sensory endings. Finally, painful information is transferred to the cortex via the trigeminal nucleus caudalis (TNC) and the thalamus. Trigemino-vascular activation is mainly associated with the genesis of migraine (Figure 1). For this model, migraine induction involves the activation of the trigeminal nucleus. This may be due to dysfunction of truncular nucleus (Charles and Brennan 2010; Moskowitz and Buzzi 2010), or may follow cortical spreading depression (Dalkara et al. 2010; Denuelle et al. 2008). However, the involvement of the trigeminal-vascular system may be involved in other types of headache.