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eyes open or closed the surroundings seem to be whirling or spinning about.
Nausea and vomiting accompany severe vertigo. The rst task is distinguishing between positional vertigo, which is common and usually benign,
and spontaneous vertigo unrelated to position. Next, identify the cause as
peripheral (labyrinth, CN-VIII) or central (brainstem). Nausea and vomiting are more common with peripheral lesions. Despite severe discomfort,
the patient can stand and walk with peripheral lesions. With central lesions,
they may be unable to stand without falling. Also, peripheral vertigo tends to
improve with prolonged xation of the eyes. Signs Distinguishing Central from
Peripheral Vertigo: 1. Bidirectional nystagmus: The direction of the nystagmus
changes with alteration of gaze without changing head position. It always has
a central etiology. 2. Head impulse test: With the patient xing his gaze on your
nose, quickly turn the head about 45 degrees to the right and then left. If the
eyes move to restore xation, indicating an abnormal vestibuloocular reex,
the cause is peripheral. 3. Vertical squint: Perform the cover–uncover test
(page 175) with the gaze directed rst upward then downward. Movement of
either eye to restore xation on uncover indicates a central cause. 4. The Dix–
Hallpike Maneuver: See page 173. A positive test indicates a labyrinthine disorder. 5. The Fukuda Stepping Test: Standing upright with the eyes closed and the
arms outstretched, have the patient march in place, keeping the eyes closed.
Rotation of >30 degrees is a positive test indicating asymmetric inner ear
function [Froehling DA, Silverman MD, Mohr DN, Beatty CW. The rational
clinical examination. Does this dizzy patient have a serious form of vertigo?
JAMA. 1994;271:385–388].
CLINICAL OCCURRENCE: Peripheral Labyrinthine System: Serous labyrinthi-
tis, perilymph stula, labyrinth stula, viral labyrinthitis, otosclerosis, otitis
media with effusion, benign paroxysmal positional vertigo, Ménière disease,
motion sickness, cholesteatoma, temporal bone fracture, postural vertigo;
Central Labyrinthine System: Migraine, vertebrobasilar insufciency, brain-
stem or cerebellar hemorrhage or infarction, posteroinferior cerebellar artery
thrombosis, infarction of the lateral medulla (Wallenberg syndrome), cerebellopontine angle tumors, intra-axial tumors (pons, cerebellum, medulla), craniovertebral abnormalities causing cervicomedullary junctional compression,
multiple sclerosis, encephalitis, meningitis, intracranial abscess (temporal
lobe, cerebellum, epidural, subdural), trauma; CN-VIII infections (acute meningitis, tuberculous meningitis, basilar syphilitic meningitis), trauma, tumors.
Acute labyrinthitis (vestibular neuritis). This is the most frequent cause of
vertigo. The patient gradually develops a sense of whirling that reaches a
climax in 24–48 hours. Nausea and vomiting may occur. The patient seeks
comfort in the horizontal position; raising the head may induce vertigo.
The patient is incapacitated for several days. The symptoms gradually subside, and disappear in 3–6 weeks. There is no accompanying tinnitus or
hearing loss.
Benign paroxysmal positional vertigo (BPPV). Dislodged calcium depos-
its (otoliths), usually in the posterior labyrinth, move in response to gravity
eliciting a feeling of motion. This is most common in older individuals and
may occur after head trauma or acute labyrinthitis. The onset is sudden,
often when rolling over in bed or arising in the morning. There is no headache
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or fever. There is often intense nausea and inability to stand. Symptoms are
minimized by avoiding any head motion. After a 1–2-second latent period the
Dix–Hallpike maneuver (page 173) produces mixed vertical and rotational
nystagmus, the fast components toward the dependent ear and upward
toward the forehead. The nystagmus may be accompanied by profound vertigo and nausea. Canalith repositioning is curative, but recurrences are not
uncommon.
Labyrinthine hydrops (Ménière disease).
labyrinthine spaces and degeneration of the organ of Corti. There are sud-
den attacks of whirling vertigo, tinnitus, and neurosensory hearing loss with
intervals of complete freedom from vertigo. Attacks last hours but not days.
Hearing loss and tinnitus persist. Fluctuating slowly progressive hearing loss
predominates on one side. Tinnitus also uctuates, accentuating before an
attack. The disease is self-limited. The cause is unknown. Labyrinthine tests
are normal or hypoactive on the involved side.
Vascular disease. Transient vertigo may be caused by arterial spasm or
obstruction producing low ow. Severe prolonged symptoms suggest
thrombosis or dissection of a brainstem artery. There is sudden vertigo with
nystagmus, loud tinnitus, and sudden deafness. Partial recovery is usual in
3–4 weeks.
Trauma. Skull fracture through the inner ear, concussion, or a loud noise in-
duces symptoms like a stroke. Tinnitus and hearing loss are present. Labyrin-
thine tests show delay and hypoactivity on the affected side.
Trauma.
vertigo and nystagmus. Disorders of CN-VIII (e.g., acoustic neuroma) are
accompanied by hearing loss, which is absent with brainstem lesions, except
when other CNs are also damaged.
Nose and Sinus Syndromes
Rhinosinusitis. Infection, allergic inammation, or irritation of the respira-
tory epithelium lining the nose and paranasal sinuses lead to hyperemia,
edema, increased mucous production, and exudation of inammatory cells.
Patients experience congestion, nasal and postnasal discharge, sneezing,
facial pressure, and sometimes fever. Diagnosis depends upon an accurate
history noting time of year, exposures, and current infectious disease activity
in the home and community. DDX: Rhinovirus infections do not cause sore
throat or fever. Fever, purulent or bloody discharge, or pain in the upper teeth
beginning several days after onset of a cold suggests suppurative sinusitis.
Sneezing and itchy eyes suggest allergic rhinosinusitis with allergic conjunctivitis.
Damage to CN-VIII or brainstem nuclei. Lesions, at either level, produce
There is swelling of endolymphatic
Acute rhinitis—the common cold.
nasal and sinus mucous membranes causing inammation and increasing nasal secretions. The sinuses are involved in 75% of patients.
4–6 episodes annually. The onset is abrupt with a watery discharge (rhinor-
rhea) and sneezing, often with malaise and mild myalgia, but without fever or
Rhinoviruses, and many others, infect the
Most people have
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sore throat. Nasal secretions may become purulent, possibly accompanied by
fever and malaise. Mucosal edema obstructs nasal passages. Symptoms last
3–10 days. Severe local pain suggests bacterial sinusitis.
Chronic rhinitis. Chronic bilateral rhinorrhea suggests chronic environmental
irritants (dust, smoke, perfume, dry or cold air), allergic rhinitis (seasonal or
perennial), rhinitis medicamentosa, or vasomotor rhinitis.
Atrophic rhinitis. The patient complains of nasal discomfort or stufness. The
membranes are dry, smooth, and shiny, and studded with crusts. A foul odor
(ozena) may be present. The cause is unknown.
Allergic rhinosinusitis.
sure to specic allergens to which the patient has been sensitized by previous
exposure. Nasal and ocular itching, rhinorrhea, and lacrimation are accompa-
nied by sneezing. Headache is common. The mucosa is usually pale, swollen,
and edematous, but may be dull red or purplish. Allergic rhinitis is seasonal
or perennial. Common allergens are pollens, molds, animal danders, house
dust mite, and cockroach antigens. Seasonal symptoms are associated with
exposure to pollens (trees in the spring; grasses in the summer; ragweed
in the fall) or to antigens associated with a specic environment. Perennial
allergic rhinitis suggests environmental antigens in the home, e.g., house dust
mite and/or animal danders (usually cats).
Vasomotor rhinitis. Environmental, hormonal, and drug exposures cause na-
sal vasodilatation increasing mucous production by nonallergic mechanisms.
Environmental irritants, e.g., smoke, perfumes, strong odors, and cold air, are
a common cause. Pregnancy and therapeutic estrogens and progestins have
been implicated. Chronic vasomotor rhinitis reects persistent mucosal overreaction to environmental exposures.
Rhinitis medicamentosa. Using topical vasoconstrictors for more than a few
days leads to rebound hyperemia on withdrawal, triggering more medication
Looking like allergic rhinitis, the history of nasal vasoconstrictor use, and
use.
absence of eosinophils in nasal secretions suggest the diagnosis.
Suppurative paranasal sinusitis. Most viral upper respiratory infections
are accompanied by sinus inammation. Obstruction of the narrow sinus
orices leads to mucous accumulation which becomes infected by bacteria
(S. pneumoniae, H. inuenzae, Moraxella
The maxillary sinus with its dependent antrum and superiorly positioned
orice is at greatest risk. Severe face pain 7–14 days after onset of an acute
upper respiratory infection suggests complicating acute suppurative bacterial sinusitis. Pain and pressure without fever earlier in the illness suggests
sinus obstruction requiring decongestants [Williams JW, Simel DL. The
rational clinical examination. Does this patient have sinusitis? Diagnosing
acute sinusitis by history and physical exam. JAMA. 1993;270:1242–124].
Extension beyond the sinus into surrounding soft tissue and bone is a serious
complication, the symptoms and signs being specic to the sinus involved.
Transillumination may reveal an opaque maxillary or frontal sinus and plain
IgE-mediated mast cell degranulation follows expo-
spp.) leading to suppurative sinusitis.
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lms may show clouding of the sinus or a uid level. CT imaging is denitive. Pain is not present with chronic inammation or infection of the paranasal sinuses. DDX: Many patients with migraine are misdiagnosed with
“sinus headaches.” Nasal and sinus symptoms are common with migraine
and cluster headache. Persistent or progressive symptoms raise concern for
serious diseases, e.g., Wegener granulomatosis, nasopharyngeal carcinoma,
and lethal midline granuloma.
Maxillary sinusitis. There is dull throbbing pain in the cheek and the ipsilateral upper teeth. Thumb pressure reveals localized maxillary tenderness.
Examination discloses a reddened, edematous mucosa and swollen turbinates. A purulent blood-tinged discharge may be seen. Pus in the posterior
middle meatus may be seen in the nasopharyngeal mirror.
DDX: Painful teeth
from maxillary sinusitis must be distinguished from dental apical abscess
where only one tooth is painful and is tender when tapped.
Frontal sinusitis. There is pain above the supraorbital ridge and pressure
there elicits tenderness. Ipsilateral eyelid edema is infrequent.
Ethmoid sinusitis. Pain is medial to the eye, seemingly deep in the head or
orbit. Although lid edema is common, there is no localizing tenderness.
Sphenoid sinusitis. There is pain either behind the eyes, in the occiput, or in
the vertex of the skull; no tenderness is elicited.
Chronic suppurative sinusitis. When a purulent nasal discharge persists
>3 weeks, subacute or chronic sinusitis is suspected. Sinus pain is not prominent and tenderness is frequently absent. Exam after instilling a vasoconstrictor may reveal the source of the pus. DDX: Chronic suppurative sinusitis, especially with unusual organisms (e.g., fungi like Aspergillus spp. or Mucor spp.)
or resistant to medical therapy, suggests common variable immunodeciency.
Sinusitis and ocular palsies—cavernous sinus thrombosis. Usually
infection spreads from the nose through the angular vein to the cavernous sinus, where septic thrombosis occurs. This is the most feared
complication of nasal infections because it can cause blindness and
death. There are sudden chills, high fever, and pain deep in the eyes.
The patient becomes prostrate and may rapidly become comatose. Early,
there is ocular palsy involving the oculomotor (CN-III), trochlear nerve
(CN-IV), or abducens nerve (CN-VI) within the cavernous sinus. Both
eyes are involved early, with immobilization of the globes, periorbital
edema, and chemosis. Death may occur within 2–3 days. DDX: Selective
ocular palsy occurs early in cavernous sinus thrombosis, whereas orbital
abscess produces complete immobilization of the globe gradually, without preliminary disorder of a single nerve. Bilaterality strongly suggests
cavernous sinus thrombosis.
Midline granuloma. The cause is unknown, but some classify it as an angio-
centric immunoproliferative lesion. Inammation is attended by granuloma formation. It is most common in fth and sixth decades, with a slight
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preference for women. Symptoms include sneezing, nasal stufness, obstruction, and pain. Signs are rhinorrhea, nasal congestion, and paranasal sinusitis
progressing to inammation and ulcerations of the nasal septum, palate, and
nasal ali. Advanced disease is indicated by destruction of midfacial structures
including pharynx, mouth, sinuses, and eyes with death from cachexia, pneumonia, meningitis, or hemorrhage. Indolent ulceration and mutilation suggest the diagnosis.
there is no systemic involvement or primary vasculitis.
Oral Syndromes (Lips, Mouth, Tongue, Teeth, and Pharynx)
Acute pharyngitis. The chief problem is distinguishing treatable bacterial
pharyngitis from viral infection. Use antigen detection and throat culture to
make a specic diagnosis when this is felt necessary.
Viral pharyngitis. Pharyngeal inammation accompanies many viral infec-
tions, the most common are EBV, respiratory syncytial virus (RSV), parainuenza, inuenza, adenovirus, and coxsackievirus. The patient complains
of sore throat, often with mild rhinorrhea and hoarseness. In inuenza, the
patient is febrile and usually complains of malaise, myalgia, and often a moderately sore throat and rhinorrhea. Oral inspection discloses swelling of mucosal lymphoid tissue on the posterior oropharyngeal wall, seen as elevated
oval islands (Fig. 7-70). The mucosa may be dull red and the faucial pillars
slightly edematous. Herpes simplex produces painful ulcers of the posterior
pharynx, soft palate, buccal mucosa, and/or tongue, with punched-out edges
surrounded by a rim of erythema.
Streptococcal and staphylococcal pharyngitis. Onset is often sudden, throat
pain is severe, and the temperature rises to 39.5°C (103°F) or higher. The pharyngeal mucosa is bright red, swollen, and edematous, especially the fauces
and uvula, and studded with white or yellow follicles. When the tonsils are
present, they are swollen and stippled with prominent follicles. Tender, swollen cervical lymph nodes are common. Group A Streptococcus is much more
common than Staphylococcus. Scarlet fever presents as an extremely painful
throat with few follicles but brilliant red oropharyngeal mucosa extending
forward to end abruptly near the back of the soft palate and fauces, as if red
paint had been applied. Streptococcus is the presumptive cause unless proven
DDX: Unlike granulomatosis with polyangiitis (Wegener),
FIG. 7-70 Granular Pharyngitis in Viral Infections. Elevated islands of lymphoid tissue are seen in the oropharyn-
geal mucosa. The mucosa is only slightly reddened; seldom is there any edema or exudate.
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otherwise. DDX: Hoarseness and cough are decidedly uncommon with bacterial pharyngitis, either arguing strongly against empiric antibiotic therapy.
Acute epiglottitis. Bacterial infection of the epiglottis produces severe
edema which can compromise the airway leading to asphyxiation.
The
condition is both more common and more dangerous in children. Patients
present with sore throat and painful swallowing, decreased voice, and
signs of pharyngitis. Stridor and the need to sit erect to breathe indicate
impending airway compromise.
Pharyngeal diphtheria. The fauces rst become dull red and a patch of
white membrane appears on the tonsil or oropharyngeal mucosa which
is reddened, swollen, and edematous. The membrane becomes thick,
gray or yellow, and tenaciously adherent to the mucosa, which bleeds
when it is removed. The membrane spreads rapidly to other structures
including the larynx. The cervical lymph nodes are enlarged and tender,
and the patient is quite ill, with severe constitutional symptoms. A pharyngeal membrane requires culture on media appropriate for the diphtheria bacillus.
DDX: The throat is not nearly as sore as in streptococcal
pharyngitis. A membrane limited to a tonsil must be distinguished from
Vincent angina (acute necrotizing ulcerative stomatitis) in which the
membrane is limited to the tonsil and not tenacious and unaccompanied
by severe constitutional symptoms.
Oropharyngeal candidiasis (thrush). Shiny, raised white patches, surrounded
by an erythematous rim, appear on the posterior pharynx, buccal mucosa,
and tongue. They may be painful. An atrophic erythematous mucosal lesion
without white exudate also occurs. If there is pain on swallowing, Candida
esophagitis is likely, especially in the immunosuppressed or diabetic patient.
Infectious mononucleosis. An acute acquired infection of lymphocytes with
EBV leads to lymphadenopathy and atypical circulating lymphocytes. The
identical clinical picture can be caused by acute HIV, CMV, HHV6 and toxoplasma infections.
Sore throat is the most common symptom, accompanied
by slight fever, malaise, cough, and headache. The pharynx is red and edematous, often with enlarged tonsils coated with exudate, making distinction
from streptococcal infection difcult. The tonsils may reach the midline and
impair speech and, rarely, respirations. There may be petechiae on the palate and uvula. The cervical lymph nodes are usually enlarged and tender.
Disproportionate cervical lymph node enlargement suggests a generalized
disease, so the physician should search for axillary and inguinal lymphadenopathy and splenomegaly. A morbilliform rash, conjunctivitis, splenomegaly, and occasionally jaundice with a tender, enlarged liver are seen.
Difculty swallowing—dysphagia. Swallowing is a complex voluntary and
reex event requiring normal sensory and neuromuscular function of the
tongue, mouth, and pharynx. Impairment of any of these structures can produce difculty swallowing. Patients generally attach symptoms to the oral,
pharyngeal, or esophageal phase of swallowing. Careful patient observation
during attempts to swallow thin and thickened liquids, soft foods, and solid
boluses helps identify the site and nature of the problem. Speech therapists
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should assist with the evaluation and videouoroscopy. See also page 190,
and Chapter 9, page 411.
CLINICAL OCCURRENCE: Congenital: Cerebral palsy, intellectual impair-
Endocrine: Hypothyroidism; Degenerative/Idiopathic: Parkinson
ment;
disease, hypoglossal nerve palsy;
nucleosis, epiglottitis, mumps, retropharyngeal abscess, chancre,
gumma, actinomycosis, rabies, oral and esophageal herpes simplex,
Candida;
Inflammatory/Immune: Myasthenia gravis, amyloidosis, Sjögren
syndrome, scleroderma; Mechanical/Traumatic: Fractures, jaw dislocation,
TMJ ankylosis, irradiation; Metabolic/Toxic: Botulism; Neoplastic: Sarcoma
of the jaw, carcinoma; Neurologic: Stroke, bulbar paralysis, pseudobulbar
paralysis, bilateral facial nerve palsy, myasthenia gravis, diphtheritic
palsy, hypoglossal nerve palsy, Parkinson disease; Psychosocial: Hysteria;
Vascular: Stroke.
Infectious: Tonsillitis, quinsy, mono-
Peritonsillar abscess (quinsy).
Pyogenic infection of the tonsil spreads into
the peritonsillar and pharyngeal spaces. The affected side is very painful and
edematous. Mouth opening is always limited and may be difcult because
of muscle spasm (trismus). An anterior abscess between the tonsil and anterior faucial pillar is easily seen, displacing the uvula to the opposite side
(Fig. 7-71A). The adjacent soft palate is edematous and bulging. When the
abscess is posterior to the tonsil, earache accompanies the sore throat and the
tonsil is pushed forward, much of the swelling is hidden from direct vision.
Surgical drainage is necessary.
Retropharyngeal abscess. Pus accumulates between the pharynx and the
prevertebral fascia. This is most common in children <5 years old. With the
tongue depressed, oropharyngeal swelling is seen on the posterior pharyngeal wall, and gentle palpation (Fig. 7-71B) discloses a unilateral soft swelling. In the nasopharynx, or opposite the larynx, the swelling is never directly
visible. Suspect nasopharyngeal swelling when nose breathing is impaired
(often attributed to adenoids), and laryngeal swelling with respiratory distress or difculty swallowing. Urgent surgical drainage is necessary to avoid
airway obstruction.
Aberrant right subclavian artery (dysphagia lusoria).
The right subclavian
artery, arising anomalously from the descending aorta distal to the left subclavian artery (Fig. 7-72), to reach the right axilla crosses left to right and
upward, either behind the esophagus, between the esophagus and trachea,
or rarely anterior to the trachea. In the rst two positions, it puts pressure
on the esophagus. Symptom starts in adolescence or early adulthood with
difculty swallowing solid food. An esophagram shows a pressure notch in
the esophagus.
Larynx Syndromes
Acute laryngeal obstruction—aphonia, choking (“the cafe coronary”).
An acutely obstructed larynx requires instant treatment. Even physicians
may fail to recognize and treat laryngeal obstruction in time to save a life.
Usually during a meal, the victim rises suddenly with a look of panic or
anguish, often with a hand to the throat, unable to speak or breathe. Ask
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FIG. 7-71 Lesions of the Oral Cavity. A. Peritonsillar abscess (quinsy). B. Palpation of a retropharyn-
geal abscess: The sagittal section shows the relation of the abscess to the palpating finger. The gloved finger feels a boggy
indentable mass as it presses gently against the anterior surfaces of the vertebral bodies.
FIG. 7-72 Aberrant Right Subclavian Artery. The right subclavian artery arises in the descending aorta, distal to
the origin of the left subclavian artery. It crosses the midline either behind the esophagus, between the esophagus and the
trachea, or anterior to the trachea. In either of the first two patterns, the artery may compress the esophagus producing
difficulty in swallowing, “dysphagia lusoria.” A transverse compression band in the esophagram suggests the diagnosis.
the patient if he/she can speak. He/she may rush from the room, with
face rapidly changing from pale to blue. This behavior is presumptive
evidence of choking (in contrast, myocardial infarction permits speech
and breathing), and there are fewer than 5 minutes in which to intervene
before death.
The Heimlich maneuver (Fig. 7-73). Stand behind the victim wrapping your
arms around their waist. Grasp your st with the other hand, placing the
thumb side of the st against the victim’s abdomen between the navel and
xiphoid. With a quick upward thrust press your st deep into the abdomen;
repeat several times, if necessary. Heimlich calculated that his maneuver
could forcefully expel approximately 940 mL of residual and tidal air at an
average pressure of 31 mm Hg, enough to force the bolus out.
Acute laryngitis. The most common cause of hoarseness, acute viral laryngitis, is often accompanied by an unproductive cough, producing pain or
a burning dryness in the throat. The true cords are reddened, their edges
rounded by swelling. Erythema of other laryngeal membranes is present;
edema of the larynx is common.
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Violent jerk upward
Heimlich maneuver
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The bolus
is forcefully
ejected
with fist into
the epigastrium
FIG. 7-73 Heimlich Maneuver. This is used to dislodge foreign bodies from the larynx. Standing at the subject’s back,
encircl e the subjec t’s waist with you r arms. Grasp yo ur fist with th e other hand an d give it a sudden f orceful jerk t hat thrus ts the
fist upward into the subject’s epigastrium. Repeat until the obstructing bolus is forcefully expelled from the throat.
Croup. Acute upper airway narrowing occurs with infection, allergy, for-
eign body, or neoplasm and is accompanied by a hoarse, brassy cough
and dyspnea. Parainuenza infection causing acute laryngotracheobronchitis is the most frequent cause in children redundant. Inammatory croup
is an acute laryngitis. The cords may appear normal and edema may be
greatest in the sub-epiglottic region. Attacks increase danger of asphyxia.
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In spasmodic croup, the child awakens with a barking cough, dyspnea, and
stridor; cyanosis is frequent. The larynx looks normal. Recovery is sudden
and complete. The cause is unknown.
Chronic laryngitis. Hoarseness and unproductive cough are usually present.
Pain is negligible. The true cords are dull and thickened or edematous and
polypoid. Frequently, the false cords are similarly affected. Chronic laryngitis
is associated with chronic overuse of the cords, tobacco smoking, syphilis,
and tuberculosis of the cords complicating cavitary pulmonary tuberculosis.
Hysterical aphonia. When viewed the cords are normal. The organic causes
of aphonia are readily diagnosed by inspecting the larynx. Even before laryngeal examination, hysterical aphonia is demonstrated by the patient’s ability
to make a sharp normal cough.
Laryngeal dyspnea. Shortness of breath has many causes (Chapter 8, page
294). In laryngeal disease, dyspnea indicates advanced obstruction, milder
obstruction producing hoarseness and stridor. In laryngeal dyspnea, the
harder the attempt to inhale, the greater the obstruction. Exhalation is unopposed, so quiet breathing is more efcient.
Paradoxical vocal cord motion.
doxically close narrowing the airway and producing wheezing. Patients
often present with episodic wheezing and shortness of breath unresponsive
to treatment appropriate for asthma. On auscultation, the wheeze is loudest
over the larynx, not the lungs. Diagnosis requires direct visualization of the
cords during an episode.
Dysphonia plicae ventricularis. Intermittent or chronic hoarseness occurs
when the false vocal cords close over the true cords instead of remaining passive during phonation. A single cord examination may disclose no abnormal-
ity; with repeated examinations, one eventually coincides with the false cords
closing partially or completely over the true cords. When this occurs, the
voice breaks, as in a boy whose “voice is changing.” The false cords may also
be active when the true cords are separated by tumor, cricoarytenoid arthritis,
voice abuse, or emotional instability.
Speech disorders. See Chapter 14, page 705.
Salivary Gland Syndromes
Dry mouth—xerostomia. Generalized abnormalities of salivary gland func-
tion result in inadequate wetting of the mucosa. The patient complains of a
dry mouth and difculty swallowing dry foods such as crackers. The patient
is often consuming liquids attempting to wet the mouth. Extensive caries are
frequent, often leading to loss of teeth. Common causes are anticholinergic
drugs, head and neck irradiation, and immune salivary gland destruction in
Sjögren syndrome (page 202). Ask about dry eyes and xerophthalmia.
Parotid tumors. Parotid neoplasia is benign or malignant. Pleomorphic
Adenoma (Mixed Parotid Tumor) presents as a rm, painless, nontender
During inspiration, the vocal cords para-
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