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1100213
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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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
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,
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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) (Figure19–4). 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.
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