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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
Lesions in the medulla involving the nucleus ambiguus result in ipsilateral weakness of the palate, pharyngeal, and laryngeal muscles. This is often associated with involvement of other CN nuclei and descending/ascending tracts. Etiologies include infarcts, demyelinating lesions, tumors, infectious and inflammatory conditions, syringobulbia, and motor neuron disease.
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.
Vocal Motor Disorders *
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
The nucleus ambiguus receives rostral and caudal afferent impulses. It participates in the voluntary control of swallowing and phonation by innervating the striated muscles of the tongue, the intrinsic muscles of the larynx (constrictor), most of the striated muscles of the soft palate and pharynx, and the constrictor muscles of the pharynx (Brazis et al., 2001, p. 320; Martin, 1996, p. 400, Figure 13–10; p. 45). Cortical input arrives from cortical motor areas, particularly the precentral gyrus, and is bilateral and indirect (Hermanowicz & Truong, 1999). Bilateral corticobulbar fibers, which innervate CN nuclei, have axons that descend through the internal capsule to synapse on motor neurons in the nucleus ambiguus (Wilson-Pauwels et al., 1988, pp. 128–129). The nucleus ambiguus is in the special visceral motor column of the medulla and projects to the muscles that control facial expression, the jaw, the pharynx, and the larynx (i.e., nerves V, VII, IX, X, XI) (Martin, 1996, p. 45). Afferent input is received from receptors in the pharyngeal and laryngeal muscles, which convey reflexive impulses for coughing, swallowing, and vomiting.
Emerging evidence for noninvasive vagus nerve stimulation for the treatment of vestibular migraine
Published in Expert Review of Neurotherapeutics, 2020
Vagal afferents and efferents terminate in four medullary vagal nuclei: the nucleus tractus solitarius (NTS), nucleus ambiguus, trigeminal spinal nucleus, and dorsal motor vagus nucleus (DMX) [8]. The NTS is the first major relay station for vagal afferents, contains trigemino-vestibulo-vagal neurocircuitry, and plays an important role in motion sickness and migraine-related nausea [11–13]. It receives afferents from the ipsilateral medial vestibular nucleus (via the lateral pathway), the ipsilateral nucleus prepositus hypoglossi (via the medial pathway), and bilateral inferior vestibular nuclei [8]. The NTS receives vestibulo-cerebellar and vestibulo-hypothalamic afferents via the parabrachial and Kolliker-Fuse nuclei [14,15]. Indicating a role in migraine, neurons connecting the parabrachial nucleus and NTS express calcitonin gene-related peptide [16,17], and play a major role in conditioned taste aversion (the animal model for motion sickness) [18]. The DMX receives vestibular afferents [19,20], and projects to the cerebellar vermis, fastigial nucleus, and nucleus interpositus [21], structures that are important in ocular motor control [22]; these connections suggest a pathway by which nVNS modulates VM-associated vertigo and nystagmus. Other brainstem nuclei that host vestibulo-vagal connections, and thus provide a possible substrate for nVNS to act on VM episodes include the rostro-ventro-lateral medulla, reticular formation, locus coeruleus, and nucleus intercalatus [8,19,20].
Evaluation of ghrelin, nesfatin-1 and irisin levels of serum and brain after acute or chronic pentylenetetrazole administrations in rats using sodium valproate
Published in Neurological Research, 2018
Ozlem Ergul Erkec, Sermin Algul, Mehmet Kara
We also investigated the serum and brain FNDC5/irisin levels in a chronic PTZ kindling epilepsy model and acute PTZ-induced seizures for the first time. We found that serum and brain levels of FNDC5/irisin were significantly increased in APTZ, AVPA and PTZk groups compared to the control group. Chronic VPA treatment ameliorates serum and brain FNDC5/irisin levels in the KVPA group. Irisin is a newly discovered hormone [17] . Irisin levels were reported to increase with exercise [16] and physical activity is reported to decrease seizure frequency and improve cardiovascular and psychological health in epileptic patients [30]. Central irisin administration was reported to increase locomotion and metabolic activity [31]. In addition, it was reported that after irisin treatment, cytosolic Ca2+ concentration and neuronal depolarization was increased in nucleus ambiguus neurons in vitro [32]. Our results demonstrated that serum and brain levels of FNDC5/irisin significantly increased in all groups except KVPA compared to the control group. An important question is ‘Are excessive FNDC5/irisin levels a reason or a result of seizures’? Maybe excessive FNDC5/irisin is a way to cope with epileptic seizures, or FNDC5/irisin might contribute to the pathophysiology of epilepsy by increasing cytosolic Ca2+ concentration and neuronal depolarization in related neurons. The effects of irisin administration on epileptic seizures is unknown, therefore there is no answer, yet. Further studies are needed to answer these questions.
Predictive value of laryngeal adductor reflex testing in patients with dysphagia due to a cerebral vascular accident
Published in International Journal of Speech-Language Pathology, 2019
Megan E. Cuellar, Jennine Harvey
The LAR is a pre-patterned motoric response to sensory stimulation that provides the basis for a neurologically regulated framework of protection and support during swallowing (Ertekin & Aydogdu, 2003; Miller, 2002). Chemoreceptors and mechanoreceptors in the laryngopharyngeal mucosa are innervated by the ISLN (Ludlow, 2015). In response to chemical or mechanical stimulation that exceeds sensory thresholds, the ISLN transmits sensory information to the nucleus tractus solitarius, which sends the information through interneurons to the nucleus ambiguous (Ludlow, 2015). The nucleus ambiguous subsequently relays information to the efferent branch of the recurrent laryngeal nerve, which results in a brisk bilateral adduction of the vocal folds (Ludlow, 2015). In contrast, neuroimaging and lesion studies indicate that various levels of the central nervous system activate, typically bilaterally but asymmetrically, to modulate sensory processing during the pharyngeal phase of swallowing (Broussard & Altschuler, 2000; Ertekin & Aydogdu, 2003; Humbert & Suresh, 2011). The extensive cortical, subcortical and peripheral representations of swallowing may explain why various neurological disorders and lesion sites may result in similar sensorimotor symptoms and disorders of swallowing (Ertekin & Aydogdu, 2003; Hamdy, Mikulis, et al., 1999). Evidence of this diverse and complicated neural network also offers an explanation for the highly variable neurological aetiologies that may lead to dysphagia (Ertekin & Aydogdu, 2003; Zald and Pardo, 1999), and helps explain the relatively poor agreement between peripheral LAR test results and the clinical sensory findings in this study.