ClinicalSigns, Symptoms and Treatment of
Dysphagia in the Neurologically Disabled
Norman H. Bass, MD
The comprehensive evaluation and treatment of pa-
tients with neurogenic dysphagia requires detailed clinical
history, neurological examination and videoradiography
of swallow. Eliciting of a clinical history may immediate-
ly reveal information about swallowing difficulties. How-
ever, it must be emphasized that a neurologically disabled
patient with compensated dysphagia may only report that
feeding has become more arduous and time-consuming.
The clinician must then pursue a detailed feeding history
to elicit the less obvious symptomatic and behavioral
manifestations, which include changes in eating habits.
These habit patterns may have become so adapted to
activities of daily living that patients are often unaware of
their modified behavior. For example, a history of altered
patterns of phonation should alert the clinician to compro-
mise of the pharyngeal and laryngeal airway in dysphagic
patients. The subjective subtlety of oral, pharyngeal and
esophageal dysphagia and its’ compensations, when com-
pounded by cognitive deficits inherent in many neuro-
logical illnesses, emphasizes the need to focus on detailed
and often subtle behavioral changes in feeding habits
which at times can only be elicited from family members,
friends, or carepersons ( 1 -4).
Oral Dysphagia
Neurogenic dysphagia involving the oral stage of feed-
ing may present with complaints of oral spill at the lips
(drooling), difficulty chewing, and difficulty in initiating
swallow (Table 1). The patient may complain of excess
saliva volume, when actually its volume is normal or dim-
From the Department of Rehabilitation Medicine, Harmarville Re-
habilitation Center and Department of Neurology, University of Pitts-
burgh School of Medicine, Pittsburgh, PA
Address correspondence and reprint requests to Dr. Norman H. Bass,
Harmarville Rehabilitation Center, Guys Run Road, P.O. Box 1 460,
Pittsburgh, PA 15283
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inished. Bolus preparation may be impaired by deficient
salivation, and patients may also report &dquo;dry mouth,&dquo; with
the implication of deficiency of saliva or increase in its
viscosity (5,6). In fact, some neurologically impaired per-
sons have a diminution in neurosecretory function which
can be demonstrated by quantitative assessment of salivary
secretions with and without pharmacologic stimulation (7).
If muscles of lingual manipulation are weak or excessively
fatiguable, the patient may report arduous efforts with the
bolus in the oral cavity or often mistakenly complain of
poorly fitting dentures and pay numerous visits to their
dentist (8). Patients may restrict their diets to pureed food
or may be noted to exert excessive chewing efforts in
order to conform with the time constraints implicit in
social dining. Frequent small meals and avoidance of certain
foods which cannot readily be particulated may make
feeding easier, but may fail to maintain daily nutritional
requirements (9). Although weight loss is commonly
found, it is not always a concomitant of dysphagia, based
on the fact that some patients consume excessive quanti-
ties of high calorie swallow-ready foods, such as ice cream.
Family, friends, or carepersons may observe voluntary
compensation measures for oral dysphagia (Table 2).
These may include craniocervical flexion followed by
slow extension of the neck to control the transfer of the
food bolus at the junction of the mouth and pharynx.
Occasionally, patients may use fingers to push the food
bolus toward the oropharynx. They also use fingers to
place the bolus on the molar teeth when muscles of the
tongue are weakened and exhibit vertical as opposed to
rotary chewing. Some patients will prefer to drink liquids
through a straw, thereby using the suckle feeding behavior
of infancy to overcome impairments associated with the
oral dysphagia. However, this compensation may become
inadequate with increasing facial paralysis, and may re-
sult in difficulty with straw feeding, drooling and loss of
food out of the mouth, etc., as a result of impaired lip
227
 Table 1. Clinical symptoms of tteurogettic dysphagia.
closure. Such patients with abnormal sensorimotor func-
tion of the face and tongue may report retention of food
in the buccal area, referred to clinically as &dquo;squirreling&dquo;
behavior. Finally, we must mention those neurological
patients with cognitive dysfunction who simply do not
know what to do with the food placed in front of them, or
even with food placed in their mouth. In such cases, the
patient is unlikely to report the problem but carepersons
can provide more pertinent feeding history. Milder forms
of cognitive dysfunction may lead to improper bolus sizing
associated with inappropriate speaking and/or breathing
during feeding (Tables 1, 2).
Pharyngeal Dysphagia
Neurogenic dysphagia involving the pharyngeal stage
of swallowing can be potentially lethal if the shallow
fails to empty the pharynx of the bolus with or without
subsequent bolus penetration into the larynx (Table 1).
Fortunately, in many patients with such disability, there
is effective physiological compensation or adaptation
for pharyngeal dysphagia. This compensation may mask
the clinical abnormality so that it can only be detected
by videoradiography. Repeat swallowing may be used
to clear retained material in the pharyngeal recesses. Tilt-
ing the head forward or to the side may facilitate swal-
lowing, and some patients discover that manual pressure
against one side of the neck helps them to swallow,
particularly in the case of asymmetric pharyngeal
weakness. However, even after careful history-taking
in such patients, the clinician may fail to identify
patients who have adapted their feeding style to neuro-
muscular compensations within the pharynx. In such
cases, only videoradiographic examination will reveal
the existence of potentially life-threatening pharyngeal
neurogenic dysphagia which requires further neurological
evaluation.
228
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Table 2. Oral dysphagia of neurologic cause.
lobserve asymmetry in posterior-anterior views
~’Vhy should the clinician be concerned about patients
with compensated neurogenic dysphagia? The inform-
ation is more than academic, for decompensation may
occur abruptly. For example, patients who have compen-
sated neurogenic dysphagia who then suffer a second
lesion on the contralateral side, as in stroke or metastatic
tumor, or progression of their neurological lesions as in
amyotrophic lateral sclerosis, may become acutely symp-
tomatic and at risk for bronchopulmonary complications
(10). Signs of decompensation from neurogenic pharyn-
geal dysphagia are alarming to both patient and clinician
(Table 3). The passage of solids through the pharynx may
be delayed, with retention of the food bolus in the pharyn-
geal recesses and subsequent leakage into the laryngeal
vestibule, which may lead to frequent throat clearing and
a wet-sounding voice. Nasal regurgitation of liquids may
be noted, especially in compromising positions such as
bending over to drink from a water fountain. The liquids
may be retained in the pharynx or aspirated, resulting in
cough/choke episodes, laryngospasm, or pneumonia. Like
ingested liquids, oral and pharyngeal secretions are re-
tained in the valleculae and piriform recesses. Patients
sense an accumulation of &dquo;phlegm&dquo; or &dquo;mucus,&dquo; as if
there is an overproduction of secretions, although the real
problem is a swallowing impairment. Laryngeal pene-
tration may cause coughing, choking, stridor, and pneu-
monia. Sensory impairment of the larynx and airways
may result in a life-threatening situation in which airway
penetration occurs without respiratory response, leading
to recurrent pneumonia. Symptoms of retained secretions
during sleep include drooling onto the pillow and awaken-
 Table 3. Pharyngeal dysphagia of neurologic cause.
tObserve asymmetry in posterior-anterior views
ing with choking. Persons known to have compensated
neurogenic dysphagia who show changes in feeding
habits or difficulty handling secretions during sleep
should be seriously considered for re-examination by
videofluoroscopy. Additionally, such persons should have
endoscopic evaluation to observe intrinsic motor dis-
orders of the larynx, transverse shift (curtain movement)
of the pharyngeal constrictor wall, and structural deficits
such as a web, a site of inflammation, or a neoplasm
(Table 4). Such structural abnormalities of lower pharynx
or esophagus can become quite extensive without clinical
symptoms and can secondarily complicate the course of
neurogenic dysphagia ( 11 ).
Videoradiography of Swallow
Radiographic imaging has become an essential tool for
the comprehensive evaluation and care of dysphagia in
patients with neurologic disabilities. Video- and cine-
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Table 4. Dysphagia caused by esophageal disease with
secondary liettroloric comvlications.
radiography have been used for several years in the evalu-
ation of the esophageal stage of feeding, in association
with endoscopy, manometry, and pH probe recording
(Table 4). However, since 1975, videoradiography has
been increasingly utilized for the evaluation of oral and
pharyngeal stages of swallowing (12-16). Radiographic
recording has made possible the detailed study of these
feeding behaviors, which occur in such schedule and
complexity that description based on the actual speed of
the swallowing performance is inadequate. Additionally,
radiographic imaging is now employed as a method for
devising strategies of dysphagia rehabilitation. Such
methods are based on sensorimotor facilitation of oral and
pharyngeal swallow by measures such as variations in the
physical character of foods, position of the head and
neck, and the effect of voluntary routines of respiration
designed to facilitate swallow. Single radiographs of the
oral and pharyngeal area also contribute useful inform-
ation about the mobility and spatial configuration of the
pharynx during conditions of voluntary inspiration and
speech { 1 fi,17).
Videoradiography continues to be the definitive
method for demonstration of abnormalities of feeding
performance in the neurologically impaired and is often
not performed in dysphagic patients with neurologic dis-
abilities (Tables 2, 3). Such studies are indicated in all
patients who have signs and symptoms of dysphagia as
observed not only by the patient but also by family and
carepersons. In addition, all tube-fed patients that are
229
being considered for graduation to oral feeding should be
similarly evaluated. The functional anatomy of pharyn-
geal swallowing acquired by this examination may prove
to be life saving based on availability of a wide array of
treatment strategies offered by the dysphagia rehabilita-
tion team.
The protocol for videoradiographic evaluation of
swallowing should be tailored to the individual patient
based on clinical history and examination. During the
radiographic procedure, frequent video-playback is used
to perform current assessment and modification of such
variables as bolus size, physical character of the bolus,
and adaptations of craniocervical posture. To diminish
radiation exposure, the feeding should be carefully
planned with respect to viscosity and amount, as assessed
by clinical evaluation prior to the radiographic procedure.
The procedure should only be repeated if change occurs in
the clinical status of dysphagia which requires repeated
documentation.
Compensated Neurogenic Dysphagia
The basic radiographic evaluation of feeding is de-
signed to evaluate the gathering and sizing of the bolus in
the swallow preparatory area (oral cavity) and the initi-
ation of swallow by voluntary delivery of the bolus from
the mouth into the pharynx. By successive displacements
of the radiographic apparatus, the bolus is followed
through pharyngeal and esophageal swallow. Abundant
videoradiographic observations have documented numer-
ous compensatory or adaptive behaviors of oral and phar-
yngeal stages of feeding in patients who have experienced
transient symptomatic episodes of neurogenic dysphagia
(15,18,19). Although the feeding process is arbitrarily
divided into oral, pharyngeal and esophageal stages, it
must be viewed as a totally integrated and interdependent
series of behaviors in which an abnormality at any stage
will result in abnormal compensatory behavior of the
entire feeding process. For example, during the oral stage
immediately prior to initiation of swallow, the bolus may
leak into the pharynx from the mouth in patients with
sensorimotor disorders of the tongue and muscular palate.
Symptoms associated with this neurological deficit may
spontaneously recover by virtue of behavioral compen-
sation, which may include greater convergence of the
pharyngeal constrictor muscles and upward displacement
of the tongue to compensate for palatal weakness or
downward displacement of the palate to compensate for
selective weakness and/or incoordination of the tongue.
Additionally, compensatory behavioral changes in cervi-
cal posture, such as flexion of the neck, may be observed
as compensation for leakage during the oral stage of swal-
lowing.
230
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Videoradiography may also be utilized in devising and
revising strategies for therapy by delineating the optimal
circumstances for the feeding performance. For example,
the best posture of the head and neck for the oral stage
may be in craniocervical flexion if the person lacks ade-
quate control of the junction of mouth and pharynx (20).
The oral performance of mastication of a barium-coated
cracker or barium impregnated hamburger meat can be
clearly shown by radiography in the antero-posterior or
lateral projections (21 ). During normal mastication, there
is a characteristic rotation of the tongue in the transverse
plane which places the food mass on the molar table.
During chewing, the food mass is repeatedly arranged
upon the molar table by the combined action of the tongue
and buccinator. The normal motions of the jaws are both
vertical and transverse in a rotary pattern (21,22). De-
pending particularly upon the relative strength of muscles
which converge upon the tongue, hyoid, and larynx, the
optimum position for pharyngeal swallow may be either
in flexion or in extension. It is also possible to evaluate,
by videoradiography, the effect of voluntary increase in
intrathoracic pressure during swallow followed by effort-
ful valved expiration after swallocv, i.e., the &dquo;supraglottic
swallow&dquo; (23).
When the pharyngeal swallow has been initiated, dys-
functional sensorimotor performances of the pharyngeal
musculature may fail to propel the food bolus, resulting in
retention of food particles in the valleculae and piriform
recesses. Symptoms from such dysfunction may undergo
spontaneous recovery by compensatory motor activity
resulting in exaggerated upward and posterior displace-
ment of the tongue and larynx. A clinical problem which
is occasionally seen with this type of neurogenic dyspha-
gia presents as cough secondary to an increased post-
swallow liability to laryngeal penetration of liquids during
the inspiratory phase of respiration The problem of aspir-
ation can be more severe if there is an associated weak-
ness of intrinsic laryngeal muscles resulting in a failure of
closure of the laryngeal chambers. In such cases, rapid
compensation may occur with increased upward and for-
ward displacement of the larynx. Lastly, a failure of relax-
ation of the cricopharyngeus muscle, with resultant failure
in adequate opening of the pharyngoesopha~eal segment,
may be compensated in part by forward tilting of the head
and forward thrusting of the jaw. This emphasizes the
importance of postural reflexes of the neck in neural
mechanisms of spontaneous compensation for neurogenic
dysphagia.
In summary, videoradiographic study of feeding per-
formances is indicated in all patients who have signs and
symptoms of dysphagia, as observed not only by the
patient but also by the family and carepersons. Moreover,
such study of swallowing should be considered for pa-
tients that are being fed by non-oral methods (nasogastric
tube or gastrostomy), particularly those being considered
for removal of such non-oral feeding devices (24-27).
Therapy
The initial design of therapy for oral and pharyngeal
dysphagia is based on a detailed evaluation by direct
clinical examination and by videoradiography. A better
understanding of each person’s mode of adaptation is
progressively clarified with respect to improvement or
increasing disability during continued care. In particular,
repair of nutritional deficiency may result in restitution of
normal patterns of appetite and restore the feeding in-
centive ; craniocervical positioning and feeding schedules
optimized to avoid inadvertent exacerbation of dysphagia;
etc. Although evaluation and therapy are initiated by the
physician experienced in rehabilitation, it is the speech-
language pathologist, occupational therapist, rehabilita-
tion nurse and nutritionist (the dysphagia rehabilitation
team) who assume daily management of feeding problems
and make critical clinical observations in order to achieve
clinical goals, which include restoration of feeding with
optimum nutrition.
It is commonly observed that neurologically impaired
adults with disorders of the oral and pharyngeal stages of
feeding prefer foods with a consistency of gels or purees
(9). This subjective impression is readily confirmed by
videoradiographic abnormalities seen during swallowing
of watery fluids, which include: decreased efficiency of
formation of a swallow-ready bolus, leakage through the
junction of mouth and pharynx, incomplete emptying of
the pharynx, and penetration into the larynx. On the other
hand, dense solids may be incompletely particulated prior
to swallow, or may be partially retained in the pharynx. To
achieve the optimum swallow-ready bolus for the neuro-
logically impaired with dysphagia requires either the
homogenization of particulated solids to the consistency
of purees or the gelling of watery liquids. In such patients,
attention should be given to the fact that oral medications
must be prepared by a pharmacist in a manner which
matches the consistency of the food substrate without
loss of pharmacologic potency and administered at the
onset of feeding. In this way, it may be possible to prevent
drug-induced diffuse esophagitis (28) or localized nec-
rosis at the site of a slowly dissolving pill or capsule (29).
Foods which are irritative to the mucosa should be
avoided so as to diminish the risk of esophageal reflux and
regurgitation with increased liability to laryngeal pene-
tration (30-33).
The importance of feeding as a basic psychosocial
behavior must not be underestimated in patients with
dysphagia (25,34). Deprivation of oral food intake by
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nasogastric bypass or gastrostomy may produce psycho-
logical disturbances that far exceed those that can be
accounted for by satisfactions associated with the caloric
demands of hunger or the pleasurable qualities of taste.
Those patients who have mild or moderate dysphagia
should be encouraged to dine in familiar circumstances,
preferably in the company of family or friends (34-37).
The goals of therapy should be to encourage the patient
with dysphagia to continue living in a manner that approx-
imates as closely as possible his/her life style and routines,
and to acknowledge the role of feeding in maintaining
the patient’s self image. In this regard, it is important to
note that abnormal feeding behavior in tube feeding de-
pendent dysphagic patients, such as that made possible by
&dquo;hedonic feeding&dquo; (repeated oral expectoration of chewed
and savored foods) is preferable to self-induced or pre-
scribed deprivation of oral feeding.
In circumstances in which neurologic impairment has
resulted in motor dysfunction of the upper extremities,
manual feeding may require the assistance of a caretaker
(25). In such cases, the volume of food as well as the
extent and duration of the feeding effort should be adapted
patient’s capacity for oral and pharyngeal feeding.
to the
Although fluid intake can be conveniently assessed by
measurements of urine volume and specific gravity in
those patients without renal disease, dietary purees, gels,
and solids should, in most instances, be measured/
weighed before and after feeding. In many instances,
pleasurable feeding with adequate dietary consumption
can only be achieved when feeding is distributed into 5-7
mealtimes. In all instances, the environment should be
adapted to the patient’s physiologic and psychological
capabilities, and although encouragement and persuasion
to conform to a convenient routine may be effective, in
some cases it may be detrimental. It is essential that the
patient’s nutritional state be frequently evaluated by daily
weighing, and supplemented by determination of skin fold
thicknesses and other measures familiar to dieticians (26).
Evaluation and Treatment of Mild
Decompensation
Patients with mild neurogenic dysphagia may have a
wide variety of neurologic lesions and may have already
made major compensations in feeding behavior which can
be identified by descriptions of the physical character of
the food consumed and the manner of its oral delivery, as
well by the patient’s general state of health (weight
as
loss, obesity, or malnutrition) and his psychosocial inter-
actions (mental and emotional status). In addition, the
patient and clinician should be alert to the occurrence of
symptoms and signs of decompensation caused by incom-
plete oral particulation, leakage of oral content into the
231
pharynx prior to the initiation of swallow, emptying of the
pharynx during swallow, and penetration of foodfliquid
into the larynx during or after swallow. When it is con-
cluded that the patient has neurogenic dysphagia with
mild decompensation upon the basis of history, examina-
tion, radiography, or other specialized study, the clinical
leader of the dysphagia rehabilitation team sets rehabilita-
tion goals and informs the patient of specific mechanisms
and circumstances of feeding effective in preventing or
diminishing the dysphagia. An optimal diet associated
with an individualized routine and schedule of feeding is
prescribed. The patient must be warned about alcohol
ingestion or inordinate use of medications that may affect
alertness and concentration. The patient is encouraged to
focus on the many available techniques for preparation of
highly palatable food with the goal of insuring successful
oral intake of a swallow-ready -bolus. In addition, the
patient is urged to focus his attention on swallow and
modulation of reflexive cough, if indicated. If esophageal
regurgitation into the pharynx is detected and incom-
pletely controlled with medication, the patient is cau-
tioned to remain in an upright position for one hour after
feeding, and omit feeding one to two hours before sleep.
This change in feeding habits reduces the risk of aspira-
tion and regurgitation from the residual bolus in the pyri-
form recesses and valleculae of the pharynx. The ultimate
outcome for successful rehabilitation of neurogenic dys-
phagia with mild decompensation will depend on the
patient’s ability to modify his feeding behavior and the
skills of the clinician in the educational process. A prob-
lem inherent in those patients with progressive neurologic
illness relates to the fact that even neurogenic dysphagia
with mild decompensation may become life-threatening
when associated with progressive cognitive impairment
and nonspecific factors such as intercurrent illness, injury,
stress, or fatigue. In many instances, successful therapy
will require supplementary explanations and advice given
to significant persons in the patient’s psychosocial environ-
ment, telephone availability of the clinician, and follow-
up outpatient visits.
Evaluation and Treatment of Moderate
Deoompensation
Symptoms of moderate decompensation from neuro-
genic dysphagia are alarming, and in cases of previously
identified mild dysphagia, usually come immediately to
the clinician’s attention (4,18,23,27). In those circum-
stances where feeding compensations have not previously
been identified, complete diagnostic evaluation should be
considered. Despite all attempts to conform with rehabil-
itative strategies, the patient with mild dysphagia may
experience swallowing problems of moderate severity
232
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such as choking episodes, retention of food in the phar-
ynx, spill of oral content into the pharynx, obstructive
apnea, or pneumonia. The clinical examination confirms
the symptoms, but videoradiography demonstrates ab-
normalities responsible for these symptoms. In addition,
dynamic radiographic study may also assist the clinician
in determining the optimal treatment strategy. For ex-
ample, videoradiographic study may suggest the optimal
posture of head and neck necessary for preparation of a
swallow-ready bolus in the mouth, or adaptive respiratory
maneuvers by which intrathoracic pressure is increased
during swallow followed by forcible expiration or cough
after swallow.
Fortunately, most patients with neurogenic dysphagia
who have this degree of decompensation are under the
watchful supervision of a family member or other care-
person. Accordingly, detailed instructions or &dquo;coaching&dquo;
and demonstration designed to maintain oral feeding
without risk must be presented to both the patient and
the caretaker (5,23,27,38). If therapy is successful, the
dysphagic person who has a non-progressive neurologic
impairment may, with modification of diet, become inde-
pendent in feeding performances. In those patients who
have progressive neurologic disease, continued attention
is required not only to prevent aspiration and progressive
bronchopulmonary disease, but to avoid malnutrition and
debilitation leading to further feeding impairment.
A specific feeding impairment commonly found in
patients with moderate neurogenic dysphagia is a failure
to initiate a sensory-cued pharyngeal swallow by volun-
tary conveyance of a bolus through the faucial isthmus.
For those persons with such a sensorimotor impairment,
thin liquids may fail to elicit swallow as compared with
liquids of thick consistency. For others, the impairment
may become apparent only when swallow of a solid bolus,
such as meat, candy bits, or pills is attempted. The second-
ary psychological problems that result may be consider-
able, and videoradiography of a pharyngeal swallow that
the person has struggled to initiate may fail to show
any abnormality. Logemann (23) and Lassara et al (38)
found that application of a cold stimulus to the side of the
faucial isthmus facilitated pharyngeal swallow in such
patients.
Suckle feeding has also been shown to be a strategic
alternative resource in patients with neurogenic dysphagia
exhibiting failure of elicitation of pharyngeal swallow (39).
During early human development, the neuroanatomic and
neurophysiologic basis for swallowing changes and dram-
atic evidence has been presented to show that some
severely dysphagic adults can feed safely by reverting to
infant-patterned suckle feeding (40,41). This pattern of
suckle feeding continues to be available to the adult with
neurogenic dysphagia and the utility of this infantile
mechanism can be demonstrated by videoradiography. In
some instances of neurologenic dysphagia, infantile suckle
feeding appears to be more effective in recruiting motor
function of the oral and pharyngeal musculature than
rehabilitative strategies seeking to directly restore the
mature pattern of feeding. Pharyngeal swallow follows
promptly upon suckle, particularly if the patient has
achieved the periodicity of &dquo;established&dquo; suckle feeding.
During suckle feeding, the sensorimotor responses of the
tongue, mandible and larynx may be effectively recruited
and may be better or more easily elicited than voluntary
single performances. For example, established suckle
feeding may relieve neurogenic dysphagia associated
with Parkinsons’ disease (42,43), cerebrovascular acci-
dent (44,45), head injury (46), and Amytrophic Lateral
Sclerosis (47,48). Use of a Ramsey feeding device for
some patients with decompensated neurogenic dysphagia,
may allow suckle feeding can become the principal mode
of food intake; in others, it may play a valuable supple-
mentary role (39).
The intermittent use of the nasogastric tube to maintain
nutrition in patients with decompensated neurogenic
dysphagia should be encouraged in order to maintain
optimal nutrition. However, enteric intubation should
not impede efforts to sustain the quality of life associated
with safe oral feeding, even when it becomes apparent
that only a small fraction of daily nutritional requirements
can be met by the oral route. For the patient with decomp-
ensated neurogenic dysphagia, intermittent use of the
nasogastric tube should be anticipated, and not necessar-
ily be considered an indication of therapy failure. However,
when increasing needs for repeated intubation become
apparent, a feeding gastrostomy avoids the many comp-
lications of the nasogastric tube and is the preferable
mode for maintaining nutrition. Emplacement of a gastro-
stoma can be readily performed as an outpatient procedure
by endoscopic intubation, and this procedure, termed
&dquo;percutaneous gastrostomy&dquo; (49), does not require gen-
eral anesthesia, requires only a small abdominal wall in-
cision, has a minimal complication rate, and only briefly
interrupts enteral feeding. Continued enteral intubation
should not preclude dysphagia therapy designed to
maintain oral feeding.
Recovery of oral feeding competence may occasion
unique problems. The dysphagic who has been pro-
longedly fed by enteric intubation becomes adapted to
this form of feeding. The person may also have con-
siderable apprehension about feeding, a fear which was
well-learned from choking episodes during evolving dys-
phagic symptoms. Such persons may resist attempts to
restore oral feeding performance and in such cases,
hedonic feeding may aid in diminution of such phobic
behavior.
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Evaluation and Treatment of Severe
Decompensation
In variety of clinical circumstances, patients may be
a
totally deprived of independence in performance of activ-
ities of daily living secondary to severe neurologic dys-
function (10,24,25,27,36). It is not uncommon for such
patients to be incapable of oral and pharyngeal feeding
performances. This may occur under such circumstances
as progression of neuromuscular disease (muscular dys-
trophy, myasthenia gravis, or polyneuropathy), brainstem
disease (amyotrophic lateral sclerosis, multiple sclerosis,
stroke), cerebral hemisphere and cerebellar disease
(recurrent cerebrovascular disease). These patients with
severe dysphagia may be unable to swallow their oral and
respiratory secretions between feedings and also have
impairments of reflexive cough. A familiar complication
of such severe oral and pharyngeal dysphagia is recurrent
gastroesophageal reflux and/or esophageal-pharyngeal
regurgitation, and recurrent pneumonitis (31,32,33). In
such patients, nutrition must be maintained by enteral or
parenteral intubation, and it may be necessary to protect
the airway by tracheotomy. After placement of a cuffed
tracheostomy tube, such patients may be orally fed. At
the initiation of oral feeding, the tracheostomy tube
cuff is inflated and the patient is taught to swallow at
the onset of artificial expiration, attempting expiratory
valving at the moment of swallow. To check for the
possibility of tracheobronchial food penetration during
such training, a tracheal aspirate is assessed for the pres-
ence of test foods marked with methylene blue.
Challenging clinical problems of feeding are frequently
encountered in neurologic patients who temporarily or
permanently require mechanically-assisted respiration
(27,50). Such patients often have severe disabilities of
oral and pharyngeal feeding and communication despite
maintenance of competent mentation and judgement. The
dysphagia team, enlarged to include respiratory thera-
pists, can be effective in dealing with the unique problems
of feeding in ventilator-dependent patients with chronic
neurologic disabilities.
References
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pharynx. Frontiers of oral physiology. 1976;2:78-107.
2. DeJong RN. Case taking and the neurologic examination.
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