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Swallowing traditionally occurs in three phases. In the oral preparatory phase, food is inserted into the mouth mixed with saliva and broken down to form a bolus, this bolus is then transferred to the pharynx initiating the swallowing reflex. While the preparatory phase is completely voluntary, the latter two phases, once initiated, are involuntary and irreversible. The pharyngeal phase is the shortest but most complex of the phases. In the pharyngeal phase, the following series of movements occur to ensure successful deglutition of the bolus: the tongue blocks entry to oral cavity, the soft palate blocks entry to the nasal cavity, the vocal folds close to protect the airway to the lungs, the epiglottis covers entry to the trachea and the upper esophageal sphincter opens to allow passage of the bolus to the esophagus. Finally, in the esophageal phase, the bolus is directed via primary and secondary peristalsis toward the stomach. Dysphagia is a swallowing disorder characterised by unsuccessful or incomplete deglutition during any phase of eating, from the detection of food in the buccal cavity to manipulation and swallowing of food in every consistency (Papadopolou et al. 2013). Dysphagia is most common in the pharyngeal phase, but can occur during any of the three phases (Chaw et al. 2012).

Dysphagia occurs in a variety of clinical populations (Khan et al. 2014, Martino et al. 2005, Suttrup & Warnecke, 2016). In SCI, dysphagia is most often present in the oropharyngeal type, seen in those with an injury to the cervical spine nerves (Chaw et al. 2012). Damage along the cervical spine impedes the pathways of the glossopharyngeal, vagus and hypoglossal cranial nerves, all of which are fundamental in swallowing (Finsterer and Grisold, 2015). The glossopharyngeal cranial nerve provides efferent motor fibers to the stylopharyngeus muscle which controls the elevation of the larynx and pharynx, and is involved in parasympathetic control of the salivary gland (Ong and Chong, 2010). The vagus cranial nerve innervates the palatoglossus muscle which is involved in the initiation of swallowing, the palatopharyngeal muscle which controls the movement of the food bolus, and the pharyngeal constrictor muscles which pushes food into the esophagus and allows for shortening and widening of the pharynx during swallowing (Ong and Chong, 2010). Finally, the hypoglossal nerve innervates nearly all the muscles of the tongue (Papadopolou et al. 2013). Location of the injury is often a primary determinant of dysphagia severity; injuries to C1-C2 vertebrae may result in no sensory awareness of swallowing whilst damage at C4-C6 has a tendency to cause poor laryngeal movement and reduced cricopharyngeal opening (Logemann, 1998).

The prevalence of dysphagia varies considerably with studies reporting incidences of 16-30% among SCI patients (Shin et al. 2011; Seidl et al. 2010; Stinneford et al. 1993) whilst other articles have reported rates of 36-60% (Gordan et al. 2009). Dysphagia was reported in one study to be most prevalent among injuries within the mid-cervical level (C3-C5) with 40% of dysphagic patients exhibiting an injury to the C4 vertebrae (Seidl et al. 2010).

For the majority of SCI patients who present with dysphagia during acute care, the problem tends to be transient and a natural recovery usually occurs as rehabilitation progresses (Shin et al. 2011). However, for patients with persistent dysphagia, complications may result including malnutrition, dehydration, aspiration, and increased hospitalization (Papadopolou 2013). Aspiration is the greatest clinical concern; it occurs in the pharyngeal phase of swallowing, and is defined as the movement of the bolus from the oropharynx moves past the vocal folds into the trachea and respiratory tract, as a result of a dysfunctional epiglottis inversion during the swallowing reflex. Aspiration can lead to life threatening complications including pneumonia, chemical pneumonitis, respiratory insufficiency, transient hypoxemia, atelectasis, bronchospasm and death (Chaw 2012, Shem et al. 2012b).

Due to the nature of dysphagia, there is a varied symptomology amongst SCI patients including: coughing, choking, repeated clearing of the throat after swallowing, drooling, watery-eyes or runny nose during or after feeding, audible swallowing, regurgitation, and aspiration (Chaw et al. 2012). Logemann (1998) also adds that SCI patients can also experience a number of oral-motor deficits such as reduced tongue motion, delayed pharyngeal swallowing, and unilateral or bilateral pharyngeal wall dysfunction. Symptoms can be observed via a plethora of measures including bedside swallowing evaluation (BSE) assessments, Videofluoroscopy Swallow Study (VFSS), Fiberoptic Endoscopic Evaluation of Swallowing (FEES), and barium swallow tests (Papadopoulou et al. 2013).