China
Africa
Explore chapters and articles related to this topic
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).
The salivary glands
Published in Rogan J Corbridge, Essential ENT, 2011
The submandibular and sublingual glands are supplied by the superior salivary nucleus. Fibres travel with the facial nerve, and then branch off as the chorda tympani. This leaves the VII cranial nerve within the middle ear cleft, to exit into the infratemporal fossa, where it joins the lingual nerve to reach the glands. The chorda tympani also supplies the sensation of taste to the anterior two-thirds of the tongue, but via different fibres.
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.
Dysautonomia in the pathogenesis of migraine
Published in Expert Review of Neurotherapeutics, 2018
Parisa Gazerani, Brian Edwin Cairns
ANS-related symptoms in migraine often include nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and ptosis [19]. In addition, the throbbing nature of the headache pain has been proposed to reflect sensitization of the trigeminovascular pain pathway, which monitors cerebral vascular tone and sends information to the central nervous system [8,20]. Activation of descending hypothalamic projections to, for example, the superior salivatory nucleus (SSN) and locus coeruleus, which are involved in changes in parasympathetic and sympathetic tone, respectively, may underlie the autonomic symptoms reported during migraine headache [8,21]. Functional connectivity studies that used functional magnetic resonance imaging have yielded evidence for hypothalamic-mediated autonomic symptoms that accompany or precede migraine attacks [21].