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Coordination of Emesis Several brainstem nuclei—including the nucleus tractus solitarius, dorsal vagal and phrenic nuclei, medullary nuclei that regulate respiration, and nuclei that control pharyngeal, facial, and tongue movements—coordinate the initiation of emesis. Neurotransmitters involved in this coordination are uncertain; however, roles for neurokinin NK1, serotonin 5-HT3, and vasopressin pathways are postulated. Somatic and visceral muscles exhibit stereotypic responses during emesis. Inspiratory thoracic and abdominal wall muscles contract, producing high intrathoracic and intraabdominal pressures that facilitate expulsion of gastric contents.

38 Differential Diagnosis . . . . . . . . . . . . . . . . 38 ■ Further Readings . . . . . . . . . . . . . . . . . 41 This is supported by electroencephalographic studies showing activation of temporofrontal cortical regions during nausea. Nausea is the subjective feeling of a need to vomit. Vomiting is contrasted with regurgitation, the effortless passage of gastric contents into the mouth. Rumination is the repeated regurgitation of stomach contents, which may be rechewed and reswallowed.

Myositis (polymyositis, dermatomyositis, sarcoidosis) B. Metabolic myopathy (mitochondrial myopathy, thyroid myopathy) C. Primary myopathies (myotonic dystrophy, oculopharyngeal myopathy) Dysphagia I. Wall defects A. Congenital 1. Cleft lip, cleft palate 2. Laryngeal clefts B. Post surgical II. Intrinsic narrowing A. Inflammatory 1. Viral (herpes simplex, varicella-zoster, cytomegalovirus) 2. Bacterial (peritonsillar abscess) 3. Fungal (Candida) 4. Mucocutaneous bullous diseases 5. Caustic, chemical, thermal injury B.

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