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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.
Physiology of Swallowing
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Joanne M. Patterson, Stephen McHanwell
The efferent pathways from the medulla and pons to the muscles involved in swallowing involve several cranial motor nuclei. The most important are the nucleus ambiguus for the muscles of the palate, pharynx and larynx, the hypoglossal nucleus for the muscles of the tongue, and the motor nuclei of the trigeminal and facial nerves for the muscles of the jaws and lips. In addition, motor neurons within the cervical spinal cord control the muscles of the neck including the infrahyoid muscles.
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 supranuclear innervation of the hypoglossal nucleus is usually bilateral but can be mainly contralateral, so that in some cerebrovascular accidents transient weakness of one side of the tongue may be found. The nerve is particularly vulnerable to surgical trauma in operations on the submandibular gland and ducts and during carotid endarterectomy.29 Paralysis following central venous catheterization has also been reported.30
Facial onset amyotrophic lateral sclerosis with K3E variant in the Cu/Zn superoxide dismutase gene
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Kazumoto Shibuya, Setsu Sawai, Atsuhiko Sugiyama, Mizuho Koide, Ayumi Nishiyama, Masashi Aoki, Satoshi Kuwabara
Facial onset ALS has rarely been described. Two case reports described two familial ALS patients with C6G variant in SOD1 gene, who had facial onset, experienced rapid progression of weakness and died after 2–3 months after onset, due to respiratory failure (7,8). Additionally, several studies disclosed patients with facial onset sensory and motor neuronopathy (FOSMN) syndrome as a rare type motor neuron diseases (9). Moreover, a case with heterozygous D90A variant in SOD1 gene has been reported as presenting FOSMN syndrome manifestations (10). Characteristics of FOSMN syndrome are entirely distinct from those of the present case, because FOSMN is characterized by initial development of sensory involvement in the trigeminal nerve territory, and subsequent slowly progressive bulbar and upper limb amyotrophy. However, a previous animal model study, utilizing mice with G93A variant in SOD1 gene, revealed decreased motor neuron population in the facial nucleus as well as the hypoglossal nucleus. As such, several ALS patients with variants in SOD1 gene may experience a facial onset manifestation. Nevertheless, it should be stressed that ALS with variants in SOD1 almost starts in the lower limb region. Moreover, other family members of the present case experienced limb onset.
TDP-43 pathology in primary lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Ian R. A. Mackenzie, Hannah Briemberg
Anatomical regions evaluated included primary motor cortex, prefrontal cortex, medulla at the level of the hypoglossal nucleus and multiple levels of spinal cord. Paraffin embedded tissue sections of formalin fixed material were stained using hematoxylin and eosin (HE) and HE combined with Luxol fast blue (HE/LFB). Immunohistochemistry (IHC) was performed on 5 µm thick sections using the Ventana BenchMark® XT automated staining system (Ventana, Tuscon, AZ) using primary antibodies against ubiquitin (Dako, 1:500), phosphorylation-independent TDP-43 (ProteinTech Group anti-TARDBP, 10782-2-AP, 1:1000), pathological TDP-43 phosphorylated at site S409/410 (pTDP-43 clone 1D3, dilution 1:1000), FUS (Sigma-Aldrich, 1:1000), misfolded SOD1 (DSE2-10E11C11, gift from Dr. N. Cashman; 1:500 dilution), hyperphosphorylated tau (Innogenetics AT-8, 1:2000), GFAP (Dako, 1:2000), and HLA-DR (Dako CR3/43, 1:1000).
Neuropathology of primary lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Five subsequent case reports included IHC for ubiquitin only (26–30). These also described degeneration of the motor cortex and CST with only one reporting loss of LMN that was restricted to the hypoglossal nucleus (26). In three of these cases, IHC was performed on the cerebrum and demonstrated abundant ubiquitin-ir NCI and neurites in the motor cortex (26,27,29). These same cases also had ubiquitin-ir pathology in the prefrontal and temporal neocortex and the hippocampus, consistent with FTLD-U, and one was thought to have become demented a year prior to death (29). IHC was performed on sections of spinal cord in all five cases and ubiquitin-ir NCI were found in LMN in three (26,29,30). Notably, in all three of these cases the inclusions were reported to be infrequent (described as “few”, “some”, or “mild”). A similar case report by Konagaya et al. (31), that is often cited as an example of PLS neuropathology, also showed widespread cortical ubiquitin-ir pathology and “occasional” inclusions in LMN; however, the disease duration was slightly less than the three year minimum required for a PLS clinical diagnosis.