Transcript Abnormal Swallowing #2

Pathophysiology of Swallowing
Impairments
Part 2: Disordered Behaviors
The Oral Preparatory Phase
In general, when the oral preparatory phase of swallow is
disturbed, drooling and leakage of liquids are observed, as
well as pocketing of more solid foods on the weaker side.
 These behaviors reflect deficits in facial and tongue
musculature.
 Some specific disorders include:



Reduced labial closure—food falls from the mouth
anteriorly;
Reduced mandibular range of motion—difficulty putting
mandible into proper occlusion for chewing, especially in
patients who have had lower jaw surgery; and
The Oral Preparatory Phase

Reduced buccal tension—food falls into the anterior or
lateral sulcus as the patient is chewing.
When there is reduced range and/or coordination of
tongue movement, difficulty may be exhibited in pulling
food back together into a cohesive bolus.
 Swallow may be initiated with food spread throughout
the oral cavity.
 Some specific problems may include:

 Reduced tongue
movement laterally; and
 Reduced tongue elevation.
The Oral Phase


Problems with the oral phase affect lingual propulsion of
the bolus through the oral cavity.
Some specific disorders include:
Reduced tongue range/coordination—food is not
maintained cohesively for anterior to posterior lingual
transport.
 Disturbed lingual peristalsis—somewhat random, nonproductive, disorganized motion.

The Oral Phase
 Repetitive lingual
rolling—repetitive upward and
backward movement of the anterior tongue and failure
of the posterior tongue to lower; bolus can only move
to midpalate before it rolls forward again.
 Reduced anterior to posterior tongue movement—the
tongue moves minimally in posterior direction so food
just sits on the tongue.
 Reduced ability to shape the tongue—liquid or paste
cannot be held in a cohesive bolus so material spreads
throughout the oral cavity and may fall into the anterior
lateral floor of the mouth during attempts at oral
transit.
The Oral Phase


Tongue thrust—food is pushed up against the anterior
teeth by forward protrusion of the tongue when the
swallow is initiated.
Other oral phase problems include:


Piecemeal deglutition--bolus is not swallowed in single,
cohesive mass; only a portion or piece of the bolus is
swallowed at a time. Repeated swallows are necessary to
clear the oral cavity;
Aspiration before the swallow—when unswallowed bolus
or portion thereof falls into the open airway and makes its
way into the pulmonary bronchi.
The Pharyngeal Phase
 Disorders
of the pharyngeal phase include dysfunctions of
the swallow programming mechanism in the brainstem to
organize and initiate the swallow response, or dysfunctions
of any of the neuromuscular components that actualize
the response behaviors.
 Problems may be seen at the level of the velum, the
pharynx, the larynx, and/or the PE segment.
 At the level of the velum, observed problems may include:
 Reduced or inadequate
velar elevation
 Material being refluxed through the nose.
The Pharyngeal Phase
 Since
velopharyngeal (VP) closure during swallow lasts
only a second or less, as the bolus passes the VP port,
nasal reflux occurring later in the swallow is a result of
dysfunction farther down the pharynx.
 If the bolus cannot pass through the pharynx into the
esophagus, it may be refluxed upward into the
nasopharynx when the VP port is normally open.
 Reduced pharyngeal peristalsis results in a significant
amount of food residue coating the pharyngeal walls
after the swallow response has been triggered.
 Common sites of pharyngeal residue include:
The Pharyngeal Phase
 Bilateral or unilateral vallecular stasis
 Bilateral or unilateral pyriform sinus stasis
 When
residue is found in both the pyriform sinuses, the
dysfunction is usually at the cricopharyngeus.
 If residue in the pyriforms is combined with residue in
other parts of the pharynx, it is a symptom of
generalized pharyngeal dysfunction, and not an isolated
cricopharyngeal problem.
 With any location of pharyngeal stasis, the patient is at
risk for aspiration of the material after swallow, when
the airway is again open for breathing.
The Pharyngeal Phase
 At
the level of the larynx, reduced anterior movement
and/or closure of the larynx can result in penetration.
 When anterior movement is reduced, residual material
may remain on top of the larynx after swallow.
 Lack of anterior movement of the larynx may also
prevent the cricopharyngeus from opening to permit
passage of the bolus.
 Lack of adequate laryngeal closure may permit material
to fall to the level of the vocal folds.
 If sensation is decreased, material may not be
expectorated until farther down in the trachea.
The Pharyngeal Phase
 Material
may continue to trickle in to the bronchi and
pulled into the lungs.
 If the pharyngeal stage is not triggered by the time the
bolus head reaches the point where the mandible crosses
the tongue base, the pharyngeal swallow is said to be
delayed.
 However, in the elderly person, the swallow is often not
initiated until the bolus reaches the valleculae or even the
pyriform sinuses.
The Pharyngeal Phase
 Abnormal
pharyngeal swallow delay is often accompanied
by struggle behavior to stimulate the swallow.
 The tongue base may be moved forward and backward in
an attempt to life the larynx.
 In infants, pharyngeal triggering and delay time is quite
different from that of adults.
 The bolus may be collected in the valleculae before the
pharyngeal swallow is triggered.
 In an infant, an abnormal delay is defined as more than 1
second between the last tongue pump and the onset of
the swallow, or aspiration occurring during bolus
collection.
The Pharyngeal Phase
 If
the central pattern generator in the brainstem does not
program the entire pharyngeal swallow to trigger, the bolus
may fall to the pyriform sinuses, or into the unprotected
open airway.
 This is sometimes referred to as an absent swallow
response.
The Esophageal Phase
The esophageal phase of swallowing may be affected by
structural and/or motility changes in the esophagus.
 Common structural disorders consist of stenosis, or
narrowing of the esophageal lumen, luminal deformity,
and diverticula.
 Motility disorders affect the contraction amplitude,
duration, and wave progression of esophageal
peristalsis.

Part 3: Adult Etiologies
Neurological Disorders

Neurologic disorders affecting swallowing can be
categorized in many different ways:
 by
the anatomic site of the lesion, such as the central or
peripheral nervous system;
 by the pathologic process, such as ischemia or
degeneration;
 by the underlying etiology; or
 by the clinical presentation such as those accompanying
dementia and movement disorders.
Disorders of the CNS
Disorders of the CNS can be nondegenerative or
degenerative.
 Nondegenerative disorders of the CNS are outlined in
Table 1 and include vascular, traumatic, neoplastic,
congenital, and iatrogenic etiologies.
 Based on clinical progression, degenerative disorders may
be subclassified into progressive and relapsing disorders.
 Progressive degenerative disorders may be further
subclassified based on their salient clinical characteristic
into dementias and movement disorders (see Table 2).

Table 1
Nondegenerative Disorders Affecting Swallow
Vascular
Stroke
Trauma
Traumatic
brain injury
Neoplastic
Brain tumor
Congenital
Cerebral
palsy
Iatrogenic
Medication
Induced
Surgery Induced
Tardive
dyskinesia
Carotid
endarterectomy
Cervical spine
surgery
Table 2
Degenerative Disorders Affecting Swallow
Progressive Course
Dementia
Movement Disorders
Alzheimer’s disease
Parkinson’s disease
Frontotemporal
dementia
Progressive supranuclear palsy
Lewy body dementia
Olivopontocerebellar atrophy
Vascular dementia
Huntington’s disease
Wilson’s disease
Relapsing—Remitting Course
Multiple sclerosis
Epidemiology of Dysphagia in CNS
Disorders




The incidence of neurogenic dysphagia worldwide is
400,000 to 800,000 new cases per year.
The reported incidence of dysphagia in specific
neurologic diseases is variable, owing in part to patient
selection methods (e.g., consecutive patients, case
series) and evaluation methods (e.g., questionnaire,
clinical evaluation, diagnostic evaluation).
Determination of dysphagia based on patient complaint
or clinical swallowing evaluation generally
underestimates the incidence.
Table 3 summarizes dysphagia prevalence for specific
neurological diseases.
Table 3. Prevalence of dysphagia for specific
neurologic diseases
Disease
Prevalence of dysphagia
Stroke
65% dysphagia in acute stroke (Daniels et al.)
Traumatic brain injury
25% (Winstein)–61% (Mackay et al.)
Cervical spine surgery
Carotid endarterectomy
50% (Smith-Hammond et al.)
2.5% (AbuRahma & Lim)–42% (Ekberg et al.)
Alzheimer's dementia
32% (Volicer et al.)–84% (Horner et al.)
Frontotemporal dementia
30% (Ikeda et al.)
Parkinson's disease
50% (Lieberman et al.)–63% (Fuh et al.)
Progressive supranuclear palsy
Initially: 16%, later stages: 83% (Litvan et al.)
Olivopontocerebellar atrophy
44% (Landis et al.)–75% (Schut)
Huntington's disease
85% (Edmonds)
Multiple sclerosis
34% (Calcagno et al.)
Amyotrophic lateral sclerosis
100% (Kawai et al.)
Non-Degenerative Disorders: Stroke



Stroke is the most common cause of neurogenic
dysphagia.
When identified by VFSS, dysphagia is documented in
approximately 65% of acute stroke patients, with the
incidence of aspiration ranging from 43% to 58%.
Prevalence of dysphagia following stroke depends on
when in the course of recovery the detection of a
swallowing impairment was made:
In patients with acute stroke--less than 5 days after onset--the
prevalence of dysphagia is as high as 50%;
 Two weeks after stroke the prevalence may be only 10% 28%.

Stroke

Swallowing abnormalities in stroke are variable and
may include:
oral lateral sulci retention
 delayed oral transfer
 delayed elicitation of a pharyngeal swallow
 decreased hyolaryngeal elevation, and
 aspiration.

Non-Degenerative Disorders: TBI



Dysphagia following TBI is common and depends on the
brain region involved.
Brain injury resulting from trauma is generally more
diffuse than that following stroke, and cognitive
impairments are often prominent depending on the site
and severity of injury.
The secondary effects of head injury on cortical and
respiratory function may necessitate tracheostomy with
or without ventilation, which interfere with swallow
ability.
Traumatic Brain Injury (TBI)
Patients who are semicomatose cannot concentrate or
cooperate during attempts at feeding.
 Prevalence data for patients who survive TBI and enter a
rehabilitation setting vary.
 Lazarus and Logemann (1987) found that approximately
45% of patients admitted to rehab during a nine-month
period had signs of dysphagia.
 Winstein (1983) found that 33% were dysphagic upon
admission and that only 6% were dysphagic after five
months of rehab.

Non-Degenerative Disorders: Brain Tumor
 As
with stroke and TBI, brain tumors may result in
dysphagia depending on which brain region is involved.
 Pathologically, brain tumors may be benign or malignant.
 However, their space-occupying nature can result in
significant neurologic dysfunction.
 Swallowing may be affected by infiltration of the tumor
into brain regions important in deglutition.
Brain Tumor
 In
addition, the treatment modalities for the tumor
including surgery and radiation therapy may affect
swallowing.
 Unlike the dysphagia resulting from stroke or TBI,
swallowing disorders secondary to a brain tumor may be
progressive as the tumor invasion increases.
Iatrogenic—Medication Induced
 Any
drug capable of causing extrapyramidal side effects
(EPS) and tardive dyskinesia (TD) is by definition a
neuroleptic (Latin for “seize the neuron”).
 EPS, especially TD, can occur in up to 20% of patients
receiving neuroleptics.
 Neurologic symptoms include repetitive movement of the
lower face, lips, and tongue (orobuccolingual dyskinesia),
and movement of the trunk and pelvis.
 Neuroleptics are a class of drugs which includes antipsychotics used for schizophrenia; anti-emetics; antispasmodics; and the prokinetic medications commonly
used in gastroenterology (reglan, propulsid, zantac).
Iatrogenic—Medication Induced
Symptoms suggestive of EPS or isolated reports of
movement disorders are associated with medications used
to treat irritable bowel syndrome, ulcerative colitis,
inflammatory bowel disease, and GERD.
 These medications are capable of causing potentially
permanent side effects which may range from dramatic
and debilitating to very subtle.
 Symptoms may be reversible if identified early and the
medication changed to newer medications which do not
produce these symptoms.

Iatrogenic--Surgery Induced

Surgery involving the neck, such as cervical spine surgery
and carotid endarterectomy, may produce dysphagia
generally owing to manipulation of cranial nerves.
 The anterior approach to cervical spine surgery results in
dysphagia and co-occurring postoperative dysphonia
more frequently than a posterior approach due to
retraction and stretch injury to the cranial nerves of the
pharyngeal plexus.
 Injury of the VII, X, and XII cranial nerves may occur with
carotid endarterectomy, as these nerves are close to the
carotid bifurcation.
 Postoperative edema may also contribute to the
dysphagia.
Progressive Degenerative: Dementia
Patients with dementia not only have problems with
swallowing but also with feeding; limb apraxia may affect
their ability to use eating utensils; visual agnosia may affect
their ability to recognize and accept food.
 Deficits in transfer of the bolus in the oral cavity are also
prominent.
 Because of the progressive nature of these disease
processes, dysphagic symptoms can occur anywhere in the
disease progression.
 Some patients complain of dysphagia as the initial
symptom of the disease; others may never complain of
dysphagia.
 In general, as disease severity increases, so does dysphagia.

Progressive Movement Disorders
Movement disorders constitute a group of degenerative
metabolic disorders of the CNS involving the
extrapyramidal and cerebellar pathways.
 The characteristics of the disordered movement allow for
their easy clinical recognition.
 Such disorders include:

Parkinson’s disease (PD) and its variants;
 progressive supranuclear palsy (PSP);
 amyotrophic lateral sclerosis (ALS);
 Huntington’s disease (HD);
 multiple sclerosis (MS);
 myasthenia gravis (MG).

Progressive Movement Disorders
Dysphagia occurs in about 50% of those individuals with
PD.
 The prevalence of dysphagia is probably higher in those
patients with PD who also have significant dementia
 Common dysphagic manifestations include:

Abnormal
lingual peristalsis;
Reduced pharyngeal peristalsis;
Delayed swallow response; and
CP dysfunction.
Progressive Movement Disorders
Progressive supranuclear palsy (PSP) is a rare, generally
sporadic, rapidly progressive disease involving the basal
ganglia, frontal lobes, midbrain, and brainstem.
 Onset typically occurs between the ages of 50 and 60
years.
 Symptoms include vertical ophthalmoplegia, axial rigidity,
pseudobulbar (upper motor neuron) palsy, and dementia.

Progressive Movement Disorders
The bulbar presentation of ALS includes dysarthria,
dysphonia, dysphagia, sialorrhea, muscle atrophy, and
fasciculations.
 Approximately 25% of ALS patients will have bulbarrelated symptoms at onset.
 When ALS affects the bulbar (pontine) musculature,
dysphagia may be one of the first symptoms of the
disease.

Progressive Movement Disorders
In the early stages of ALS, oral phase problems are due to
either a dysfunction in the transport of the bolus at the
anterior part of the tongue, or in the holding of the bolus
at the posterior part of the tongue (Kawai, Tsukuda,
Mochimatsu, Enomoto, Kagesato, Hirose, Kuroiwa, &
Suzuki, 2003).
 Aspiration is more often associated with impaired
holding function (oral containment) at the posterior part
of the tongue, than to transport dysfunction.
 There is almost no delay in swallowing at the pharyngeal
level, nor problems with esophageal peristalsis.

Progressive Movement Disorders
Similar to ALS, not all patients with MS will be dysphagic
unless bulbar musculature is involved.
 Because of the disease’s tendency to produce ataxic
symptoms, the coordination of deglutition and breathing
may predispose these patients to dysphagia, as well as to
oral and pharyngeal muscle weakness and incoordination.
 Hartelius and Svensson (1994) found that more than 33%
of patients with MS had either chewing or swallowing
problems.
 Other common dysphagic manifestations include
aspiration:


before the swallow due to reduced lingual control;
Progressive Movement Disorders




before the swallow due to a delayed swallow response;
during the swallow due to reduced laryngeal closure;
after the swallow due to reduced pharyngeal peristalsis; and
after the swallow due to CP dysfunction.
In selected populations of patients with MG, approximately
one third are dysphagic.
 The prevalence of dysphagia largely depends on the extent
of muscle fatigue.

Progressive Movement Disorders
A recent study by Dolton-Hudson, Koopman, Moosa,
Smith, Bach and Nicolle (2002) found that 45% of their
participants with MS had oral preparatory phase
dysphagia, 65% had oral phase dysphagia, and 100% had
pharyngeal phase dysphagia.
 Specific oral preparatory phase problems included poor
bolus formation and extended chewing with reduced
buccal tension leading to spillage of material into the
lateral sulci.

Progressive Movement Disorders
Oral phase problems included slow bolus transports,
piecemeal deglutition, and poor retro-oral seal of the
tongue and palate, leading to residue on the tongue base
and soft palate.
 Pharyngeal phase dysphagia included delayed swallow
response and reduced tongue base retraction toward the
pharyngeal wall, resulting in residue in the valleculae and
pyriform sinuses.
 Aspiration occurred in about 1/3 of the patients, with the
majority aspirating during the swallow.

Systemic Rheumatic Diseases
 Systemic rheumatic diseases, such as
dermatomyositis,
polymyositis, rheumatoid arthritis, scleroderma, and
Sjogren’s syndrome are rarer than PD or MS, but
deserve consideration in a discussion of dysphagia and
neurologic disease.
 Dermatomyositis and polymyositis are characterized by
inflammation of the proximal skeletal muscles.
 Thus muscles of the pharynx are often affected but the
smooth muscles of the esophagus are spared.
Systemic Rheumatic Diseases
On VFSS,
there is usually prominence of the CP muscle,
decreased epiglottic tilt, and moderate to severe
pharyngeal residue (Murray & Carrau, 2001).
About 67% of patients with myositis have demonstrable
delayed transit through the cervical esophagus.
Rheumatoid arthritis (RA) is a chronic relapsing
inflammatory arthritis, usually affecting multiple
diarthrodial joints.
Women are more commonly affected than men, with a
ratio of 3:1.
Systemic Rheumatic Diseases
 RA
is associated with xerostomia, TMJ syndrome, cervical
spine arthritic disease, and decreased peristaltic
amplitude in the proximal esophagus, all contributing to
swallowing problems.
Rheumatic laryngeal involvement may result in
cricoarytenoid joint fixation, affecting laryngeal closure.
A study by Ekberg, Redlund-Johnell, and Sjoblom (1987)
found that 65% of patients with RA had pharyngeal
dysfunction.
Systemic Rheumatic Diseases




Scleroderma is a disorder characterized by progressive
fibrosis and vascular changes.
As many as 90% of patients with scleroderma have
complaints related to swallowing.
Dysphagia is first noticed while swallowing solids due to
poor motility through the inferior 2/3 of the esophagus.
Secondary effects on the oral and pharyngeal stages have
been reported.
Systemic Rheumatic Diseases
 Sjogren’s
syndrome (SS) is an autoimmune disorder that
produces dryness of the eyes, nose, and mouth.
 Xerostomia, oral pain, glossodynia, and dysgeusia are
prominent features of SS.
 As many as 75% of patients diagnosed with SS have
dysphagia, which has the potential to involve all stages of
swallowing function.