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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
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Spinal Abnormalities
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in Dysphagia
Derrick R. Randall
INTRODUCTION
The cervical spine is a feature of all organisms belonging to the phylum chordata and affords multiple differ­ent ranges of neck motion: flexion, extension, rotation, lateral flexion, and translation. In hominids and some pri­mates, it is held in a primarily vertical orientation responsible for maintaining the head upright and at an appropri­ate plane for vision while supporting and protecting the spinal cord along with its spinal nerves, which affords a number of functional advantages but also anatomic challenges. The chronic strain from the weight of the head and high joint mobility cause strain on the musculoskeletal supports and translate to anatomic derangements over time in many people. Deeper understanding of the interplay of these alterations with normal swallowing and adaptation forms a complex and largely unan­swered area of dysphagia research. The
importance of swallowing disorders and dysphagia in the context of cervical spine anomalies is underscored by their frequency, and the lack of scientific evaluation and hypothesis-based test­ing needed to guide recommendations is an avenue for future research inves­tigations. Multiple medical subspecial­ties and allied health fields encounter patients with cervical anomalies, result­ing in further confusion and disagree­ment on the contribution of the spine to these disorders.
Dysphagia can develop from cranial
neuropathies, physical obstruction, degenerative disease, traumatic injury, or any combination of the above. The interplay between cervical and cranial nerves is an important element in the severity of dysphagia, and contribu­tions from the cervical nerves are often overlooked — granted, they may be more involved with structural support than the mechanics of deglutition, since most sensory and functional input to
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swallowing is mediated by the cranial nerves. Cervical structural support is thought to be primarily attributed to muscle function from the long muscles with attachments to multiple cervical levels, particularly longus colli and lon­gus capitis through the cervical plexus (Mann et al., 1999). It has been observed that less than half of patients with quad­riplegia have dysphagia despite no cer­vical nerve contribution (Shem et al.,
2012). The most likely explanation for the degree of cervical and cranial nerve roles in dysphagia is a continuum of various contributions from each com­ponent that is highly dependent on the specific pathology.
ANATOMIC CONSIDERATIONS
Congenital Anomalies
Congenital cervical spine anomalies are commonly associated with dys­phagia in young children. However, many of these patients are affected by global developmental delay or other anatomic deformities that make it diffi­cult to rigorously evaluate and attribute dysphagia to the cervical changes. Not surprisingly, these complexities repre­sent a serious challenge for identifying appropriate therapies for dysphagia management. Although congenital anomalies can persist throughout life, it is uncommon for dysphagia to pres­ent as a new symptom among adults with congenital anomalies. When a congenital anomaly contributes to a swallowing disorder in a delayed fash­ion, this is usually through progressive worsening of cranial neuropathies, particularly those at the level of the craniocervical junction that affect the
vagus, glossopharyngeal, and hypo­glossal nerves (Kang & Moon, 2016; Kotil et al., 2007; Song et al., 1996). One particular, uncommon congenital issue that sometimes presents in adulthood is the aberrant right subclavian artery (lusorian artery). On detailed history, dysphagia has usually been present for many years but either unrecognized in the face of more problematic symptoms or not appreciated by the patient since they did not recognize it was abnormal (Figure 19–1).
Scoliosis
Scoliosis is abnormal curvature of the spine in the lateral plane (seen on anteroposterior view) of greater than 10 degrees as measured by Cobb angle. Scoliosis most commonly affects the lumbar and thoracic spine, but the cer­vical spine can be involved. Compres­sion of the esophagus in the thorax or the pharyngoesophageal segment (PES) can cause dysphagia by extralu­minal narrowing (Bar-On et al., 1998; Papadopoulou et al., 2013). In some instances, patients who have suffered a stroke leading to persistent hemiplegia may develop cervical scoliosis due to lateral neck flexion toward the strong side with muscle contracture. A similar outcome may arise from chronic mus­cle spasticity or contraction in cerebral palsy or Parkinson’s disease.
Kyphosis and Lordosis
Measurement of cervical kyphosis or lordosis is accomplished through Cobb angles of either the occipital to second cervical planes (O–C2) or C2–C7 planes.
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Figure 19–1. Dysphagia lusoria (Latin for natural anomaly) was described in
1787 and is the consequence of abnormal development of the pharyngeal arch arteries. An AP image from a barium esophagram (A) shows the indenta­tion of the esophagus from the aberrant right subclavian artery in the upper mediastinum, while the vessel’s takeoff from the aorta is shown in the axial CT scan image in (B) with posterior compression of the esophagus in (C).
Reduction at the O–C2 level causes
Osteophytes
a relative mandible retrusion into the oropharynx, which limits the oropha­ryngeal inlet, and combined with the hyperlordosis can project the anterior cervical spine into the pharynx (Ota et al., 2011; Tian & Wu, 2013). The C2–C7 angle reflects lower cervical curvature, where excessive kyphosis (Figure 19–2) causes swallowing impairment (Mum­maneni et al., 2006; Randall et al., 2017). Though still unclear, dysphagia may be attributable to cervical myelopathy or progressive ligament and muscular lax­ity due to changes on the suspensory forces in these cases of more severe ana­tomic alteration.
Osteophytes are bony outgrowths from joint margins and can occur anywhere in the body, typically due to osteoar­thritis or degenerative joint disease. Approximately one third of the weight of the head and axial load is supported in the anterior column of the spine, with the remainder supported by the posterior column and facet joints; when muscle laxity and decreased joint stabil­ity develop, inflammation at the joint edges build and osteophytes grow as a physiologic response (Cho et al., 2019). In the cervical spine, posterior osteo­phytes arise from the articular processes
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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
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Figure 19–2. Severe scoliosis in a young adult male. A. AP radiographic indicating
degree of thoracic scoliosis. B. Axial CT scan showing relative position of epiglottis tip (arrow ) and vertebrae oriented perpendicular to each other. The spinal canal is indicated with an asterisk. C. Demonstration of compression of esophagus by lateral process of vertebrae (small black airspace marked by white arrow ventricle (white arrowhead
) and surrounding thyroid cartilage at the same height.
), with the laryngeal
and facets to impinge on the spinal roots, where they may cause radicu­lopathy or myopathy. Anterior osteo­phytes extend from the anterior margin of the upper and lower borders of the cervical vertebrae to appear as small or large bony protrusions that can cause external compression of the pharynx (Figure 19–3). As they are consequences of degenerative spine disease and insta­bility, these entities commonly coexist. The anterior and posterior surfaces of the vertebral bodies are lined with liga­ments called the anterior longitudinal
Figure 19–3. Cervical kyphosis with rever-
sal of normal cervical lordosis.
ligament and posterior longitudinal ligament, respectively. These ligaments, as well as the fibrous margins of the intervertebral discs (annulus fibrosus), can also ossify, which are termed enthe­sophytes in the former and syndesmo­phytes in the latter. Syndesmophytes represent the classic radiologic find­ing in the “bamboo spine” of ankylos­ing spondylosis. Pathophysiologically, osteophytes, enthesophytes, and syn­desmophytes all develop from similar pathways of inflammation and second­ary ossification.
Osteophytes are the most common
natural development in the cervical spine connected to dysphagia. Osteo­phytes with cervical degenerative disc disease are very prevalent radiographic findings in asymptomatic patients and have been found in 27% of people under the age of 50 and in 86% of those older than 50 in a Japanese population-based study, with C5/6 the most frequently affected level at all ages and genders (Teraguchi et al., 2014). Osteophytes may involve single or multiple levels,
19. SPINAL ABNORMALITIES IN DYSPHAGIA
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and if four or more contiguous levels are involved, then it is termed diffuse idiopathic skeletal hyperostosis (DISH). In the presence of DISH, dysphagia is reported in up to 28% of patients (Lam­bert et al., 1981) (Figure19–4). Mecha­nisms proposed to explain dysphagia resulting from osteophytes include narrowing of the oropharynx, reduced pharyngeal wall contraction, inflamma-
tory restriction of laryngeal elevation and tissue adhesion, impeded epiglot­tic inversion, bolus obstruction in the esophagus or PES, retained bolus and secondary aspiration or penetration, or deflection of material directly into the larynx (Carlson et al., 2011; Papa­dopoulou et al., 2013). There is poor correlation between osteophytes and dysphagia, with multiple small-scale
Figure 19–4. Examples of large osteophytes. A. Multiple large anterior cervical
spine osteophytes altering contour of posterior pharyngeal wall and imping­ing on upper esophageal sphincter opening. Since there are at least four contiguous levels involved, this is classified as diffuse idiopathic skeletal hyper­ostosis (DISH). B. Endoscopic appearance of a large osteophyte causing oblit­eration of the left hypopharyngeal inlet. Even with Valsalva, the hypopharynx was inaccessible. The same patient is shown in a videofluoroscopic swallow­ing study prior to (C) and during (D) a swallow. Note that in (D), a portion of the bolus passes to the side of the osteophyte and preferentially into the right hypopharynx.