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226 CHAPTER 7: The Head and Neck
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it also occurs in isolation. Its severity varies from a complete cleft of the entire
soft and hard palate, including the alveolar ridge, to a partial cleft of the soft
palate alone.
Bid uvula. This results from incomplete fusion of the soft palate and may
be accompanied by disoriented palatal muscles.
Deviation of the uvula and soft palate asymmetry suggest a muscular
abnormality.
Teeth and Gum Signs
Wide interdental spaces. This occurs congenitally and is acquired in acromegaly as the jaw enlarges.
Caries. Tooth cavities can be subtle or obvious. Decreased saliva following
irradiation or with sicca syndrome increases risk for caries.
Enamel loss. Enamel is destroyed by regurgitated stomach acid and acidic
water in swimming pools with excessive chlorination. Enamel loss suggests
bulimia nervosa.
Fluoride pits. Opaque chalk-white spots, 1–2 mm in diameter, are scattered
on the surface of multiple teeth, indicating exposure to large amounts of uoride during childhood.
Notched teeth—Hutchinson teeth. In congenital syphilis the permanent
upper central incisors are misshapen, and the tips are notched (Fig. 7-61A).
They are smaller than normal, and peg topped, resembling the frustum of
a cone. Notching, interstitial keratitis, and labyrinthine deafness are the
Hutchinson triad.
Periapical abscess. An abscess forming within bone at the root tip increases
intraosseous pressure producing severe pain. Suspect an abscess when tap-
ping the tooth accentuates toothache pain. Tender swelling in the adjacent
gum and a draining sinus tract may form.
Test elevation of the uvula.
Bleeding gums. Gum bleeding signals local gum lesions or systemic blood
vessel or hemostatic disorders. The patient complains of bleeding with brush-
ing or notices blood in expectorated phlegm.
Gum recession. In older persons, the gingival margins may recede exposing
the rough, lusterless cementum, below the enamel border.
Periodontitis. Adherent dental plaque inames the gums leading to reces-
sion and erosion of the dental ligament. The receding gums are inamed with
deep pockets (>3 mm) between gum and tooth. The roots are exposed, and
the teeth may be loose (Fig. 7-61B). The breath is often foul, and the gums
bleed easily. A particularly virulent form is associated with methamphetamine abuse, meth mouth.
Necrotizing stomatitis (trench mouth, vincent stomatitis). Inammation
of the gums and adjoining mucosa is caused by a symbiotic infection with
A. Hutchinson notched teeth
C. Epulis D. Lead or bismuth line
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B. Periodontitis
(pyorrhea alveolaris)
FIG. 7-61 Dental Abnormalities. A. Hutchinson notched teeth. B. Periodontitis: In t he drawing, some of the
lower te eth are involve d: the gums are ret racted, and pus is exuding from behind the ging ival margins. C. Epulis: It is sessile,
lighter in color than the gums. D. Lead or bismuth line in the gums.
Borrelia vincentii and Fusobacterium plauti-vincenti. Punched-out ulcers on the
gums are covered with a gray–yellow membrane. The infection can remain
localized to the gums or extend to pharyngeal structures, including bone.
Swollen gums—scurvy. The gums are deep red or purple and become swollen,
tender, spongy and bleed easily. Other signs are subperiosteal hemorrhages
and perifollicular purpura.
Gingival hyperplasia. Increasing gum volume occasionally covers the teeth.
Phenytoin is the most common cause. In monocytic leukemia, gums inltrated with monocytes have a similar appearance.
Epulis.
This brous tumor of the gum arises from alveolar periosteum and
emerges between the teeth. It is a nontender sessile mass (Fig. 7-61C), lighter
in color than the gum, and rarely pedunculated. A similar tumor, but bright
red, is a broangiomatous epulis.
Blue gums—lead and bismuth lines, quinacrine. With chronic exposure to
lead (occupational) or bismuth (therapeutic), blue lines appear on the gums
~1 mm from the gingival margin where the heavy metals are deposited. The
line, appearing solid to the unaided eye (Fig. 7-61D), is composed of small,
discrete dots. Chronic quinacrine ingestion colors the gums diffusely blue or
purple.
Tongue Signs
Dry tongue without longitudinal furrows. The surface dries from mouth
breathing or lack of saliva. Tongue volume remains normal, so longitudinal
furrows don’t develop.
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FIG. 7-62 Paralysis of the Left Side of the Tongue. Deviation is toward the paralyzed side.
Dry tongue with longitudinal furrows. Longitudinal furrows develop when
tongue volume is reduced. This is a reliable sign of severe volume depletion.
Enlarged tongue. The tongue is enlarged in Down syndrome, cretinism, and
adult myxedema. It increases in size during development of acromegaly and
amyloidosis. Transient swelling occurs with glossitis, stomatitis, neck cellulitis, and angioedema. Lymphatic obstruction by carcinoma and superior vena
cava obstruction often lead to enlargement.
Tremor. Tongue tremor is seen with increased sympathetic activity as in
hyperthyroidism, alcohol and drug withdrawal, and anxiety.
Fasciculation.
Fasciculation is characteristic of bulbar poliomyelitis, West Nile virus encephalitis, and amyotrophic lateral sclerosis.
Shortened frenulum (tongue-tied). The frenulum is congenitally short limiting protrusion and preventing the tongue tip from reaching the roof of the
mouth, thus impairing articulation of lingual consonants.
Limited tongue protrusion—carcinoma. See page 240.
Geographic tongue. This is a harmless condition of unknown cause. The
tongues surface develops circular areas of smooth red epithelium, without
papillae, surrounded by light-yellow rings of piled-up cells (Fig. 7-63B). The
patches heal in a few days and are succeeded by new ones in other areas.
DDX: Median rhomboid glossitis is lifelong and does not change over time.
Hairy tongue. Hyperplasia of liform papillae entangled with an overgrowth
of mycelial threads of Aspergillus niger or Candida albicans gives the tongue
Denervation leads to spontaneous motor unit ring.
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FIG. 7-63 Tongue Surface Patterns. A. Congenitally furrowed tongue. B. Geographic tongue. C. Black
hairy tongue. D. Syphilitic glossitis. E. Tuberculous ulcers. F. Carcinoma: A typical location of carcinoma of
the tongue is on the lateral edge.
a hairy appearance. Patients are asymptomatic. The distal two-thirds of the
dorsum looks as if it were growing short hairs, usually black (Fig. 7-63C) but
occasionally green from the fungus or because of chewing gum containing
chlorophyll. It is seen in debilitated patients and after antibiotics.
Congenital furrows (scrotal tongue). This is a harmless condition, frequently
inherited. The median sulcus is deep and the dorsal surface is interrupted
by deep transverse furrows (Fig. 7-63A). It must be distinguished from the
longitudinal furrowing in syphilitic glossitis.
Hairy leukoplakia. Epithelial hyperplasia results from Epstein–Barr virus
(EBV) infection in patients with AIDS. The sides of the tongue have elongated
“hairy” liform papillae.
Atrophic glossitis.
Nutritional deciency results in impaired mucosal proliferation. The very high turnover rate of cells in the oral mucosa and tongue
makes it susceptible to nutritional deciencies. The tongue's extreme sensitivity explains the prominent symptoms.
intermittent burning, and paresthesias of taste. The tongue becomes smaller, its
surface slick and glistening, and the mucosa thins. In the advanced stages, there
is considerable pain and swelling. The color is pink, red, or blue-red with
atrophied hyperemic papillae appearing as small punctate red dots.
CLINICAL OCCURRENCE: Vitamin B
gastrectomy, blind intestinal loop, extreme vegetarian diets, sh tapeworm
(Diphyllobothrium latum) infestation;
mia of pregnancy, chronic liver disease; Other Causes: Iron deciency anemia,
idiopathic gastritis, mixed B-complex vitamin deciency, idiopathic.
Pellagra. Dietary deciency of niacin (nicotinic acid and nicotinamide) is the
cause. Initially, the patient complains of tongue burning with hot or spicy
foods; the tongue appears normal. Later, the burning is constant. The tongue
tip and borders become reddened; later the erythema spreads and the tongue
The patient complains of dry tongue,
Deciency: Pernicious anemia, post-
12
Folic Acid Deciency: Megaloblastic ane-
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swells. The denuded surface presents a ery-red mucosa with ulcerations and
indentations from teeth. After treatment, the tongue is pallid and atrophied.
Other signs are Diarrhea, Delirium, and Dermatitis (the three Ds).
Magenta cobblestone tongue—riboavin deciency. Dietary riboavin deciency causes mild tongue burning. Swollen hyperemic fungiform and liform papillae produce rows of reddened elevations suggesting cobblestones.
Edema at the bases of the papillae produces the magenta color, contrasting
with the ery red pellagrous tongue, in which the epithelium is denuded.
Cheilosis and angular stomatitis are common. A painless gray papule at one
or both corners of the mouth enlarges and ulcerates producing indolent ssures with piled-up yellow crusts that leave permanent scars. Similar lesions
can occur at the ocular canthi and nasolabial folds. Supercial keratitis and
conjunctival injection are common.
Nonspecic glossitis. Pharyngeal infections may also involve the tongue,
producing redness and swelling. The tongue may burn and feel tender.
Strawberry tongue (raspberry tongue).
infection release exotoxins (e.g., scarlet fever, toxic shock syndrome). The lingual papillae become swollen and reddened.
strawberry tongue was given to the stage when the inamed and hyperplastic
papillae show through a white coat. Later, the epithelium desquamates, carrying away the coat and leaving a ery-red, denuded surface surmounted by
hyperplastic papillae; this has also been termed a strawberry tongue, others
preferring the more accurately descriptive term raspberry tongue. During the
desquamated period, taste is diminished.
Menopausal glossitis. Ascribed to estrogen deciency, intense burning and
slight mucosal atrophy occurs at menopause or in other estrogen deciency
states. The symptoms and signs improve with estrogen administration.
Syphilitic glossitis. The furrows of syphilitic glossitis are mainly longitudinal and deeper than the congenital type. The intervening epithelium is desquamated (Fig. 7-63D).
Herpetic glossitis. A painful inamed tongue with longitudinal ssures has
been described with herpes infection in HIV-infected patients.
Leukoplakia. Thin and white, often wrinkled or pearly areas obliterate the
papillae. Later, the lesions coalesce, thicken, and become chalk white. In
advanced stages, they look like dried, cracked white paint. Leukoplakia is a
premalignant condition.
Dental ulcer. A projecting tooth or an ill-tting denture causes ulceration on
the sides or undersurface of the tongue. The ulcer margin may be elevated
and surrounded by induration, suggesting carcinoma. Removal of the irritating surface should result in a trend toward healing in a few weeks. Lacking
improvement, biopsy is indicated.
Streptococcal or staphylococcal
According to Osler, the name
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Sublingual mass—ranula. Cystic distention of sublingual or submandibular
salivary ducts is caused by obstruction at the orice. Because it looks like a
frog’s belly, Hippocrates used the Greek word for “little frog” to describe this
A translucent mass is seen beside the frenulum and may extend to
lesion.
the other side. Bimanual palpation often tracks the mass to the submandibular gland. Transillumination reveals the submandibular duct traversing the
upper part of the cyst.
Sublingual varices—caviar lesions. With aging, supercial sublingual veins
develop varicosities resembling a mass of purple caviar (Chapter 6, Fig. 6-18A,
page 131). They are of no clinical signicance.
Posterior lingual mass—lingual thyroid.
roglossal duct remnant.
at the base of the tongue, near the foramen cecum. It may be the only functioning thyroid tissue.
Pharynx Signs
Oropharyngeal soft tissue hypertrophy. Enlargement of the tongue's base
and narrowing of the pharynx by soft tissue hypertrophy combine to compromise the airway, especially when the tongue relaxes during sleep in the
supine position.
sitting and the tongue relaxed in the oor of the mouth predict both the ease
of tracheal intubation and the risk of upper airway obstruction during sleep.
The modied Mallampati score is based upon visualization of the complete tonsillar bed, base of the uvula, and soft palate. Loss of visualization proceeds
sequentially. A score of 1 means all structures are visualized; 2 means the
full tonsillar bed is not seen; 3 means the base of the uvula is not seen; and 4
means the soft palate is not seen. Scores of 3 and 4 indicate high-risk.
Tonsil enlargement—hyperplasia. Children’s tonsils are large, shrinking at
puberty. Normal adult tonsils seldom protrude beyond the faucial pillars.
Hyperplasia, usually bilateral, is usually attributed to chronic infection, but it
may be associated with obesity, hyperthyroidism, or lymphoma.
Tonsillar exudates.
exudate which may spread to the lateral and posterior pharyngeal walls. The
most common causes are viral infections, including acute mononucleosis (EB
virus) and Group A streptococcal pharyngitis (see page 250 for a complete
discussion).
Uvula edema. Allergic or nonallergic angioedema causes edema of the uvula
and has occurred with thrombosis of an internal jugular vein containing a
central venous line. Edema of the uvula together with bronchitis, asthma, and
rhinopharyngitis suggests inhalational injury, often from recreational drug
use (e.g., recent heavy smoking of marijuana, crack cocaine, hashish).
It presents as a round, smooth, red, nontender mass
Normal oropharyngeal structures visualized with the patient
Bacterial and viral infections produce a purulent tonsillar
A lingual thyroid arises from a thy-
Larynx and Trachea Signs
Stridor. Extrathoracic airway narrowing worsens as transtracheal pressure
increases during inspiration. A high-pitched sound is heard during inspiration,
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FIG. 7-64 Laryngeal Lesions in the Mirror. A. Laryngeal edema: The mucosa on the vocal cords, arytenoid
prominences, and epiglottis is swollen and glistening. B. Singer’s nodules: Apposing swellings on the free margins of the
vocal cords at a distance one-third posteriorly in their extent. C. Contact ulcers apposed on the free margins of the cords
at their junctions with the arytenoid cartilages. D. Laryngeal polyp on the free margin of the left cord. E. Laryngeal
carcinoma in the left piriform sinus. F. Squamous cell carcinoma along the anterior half of the right cord.
having the same pitch and intensity throughout inspiration indicating a high
degree of airway obstruction. Stridor is almost always accompanied by significant dyspnea. It is caused by mass lesions, such as carcinoma, which restrict
vocal cord mobility or reduce the size of the glottic aperture, by bilateral vocal
cord paralysis, which limits the effective glottic opening, or a swollen epiglottis in acute epiglottitis or inhalation injury.
Laryngeal edema. The signs of laryngeal obstruction range through hoarseness, dyspnea, and stridor. Inspection through the mirror is diagnostic.
Glistening, swollen mucosa is seen on the vocal cords, arytenoid prominences,
and epiglottis (Fig. 7-64A). Laryngeal edema may occur with acute laryngitis,
lymphatic obstruction by neoplasm or abscess, radiation, anaphylaxis, angioedema, myxedema, and trauma to the larynx from instrumentation.
Hoarseness.
Paralysis, edema or inltration of a vocal cord, and vocal cord
masses change the vibratory response to airow. Hoarseness focuses atten-
tion on the larynx. A multitude of disorders cause hoarseness.
CLINICAL OCCURRENCE: Recent Onset—Overuse: Shouting, cheer-
ing; Infection: Upper respiratory infections, chlamydia, diphtheria, mea-
Drugs: Anticholinergic drugs, strychnine (laryngeal spasm), aspirin
sles;
aspiration (chemical burn), potassium iodide, and uremia (cord edema);
Angioedema: Insect bites, drug allergy, angiotensin-converting enzyme
inhibitors, hereditary angioedema; Foreign Body: Food aspiration, after
endotracheal intubation; Laryngeal Spasm: Croup, tetany, tetanus; Burns:
Inhalation of irritant gases, swallowing of hot or caustic liquids. Chronic
Course—Occupational Overuse: In the clergy, orators, singers, teachers;
Foreign Body: Food aspiration, prolonged endotracheal intubation; Lack of
Mucus: Sjögren syndrome; Chronic Vocal Cord Inammation: Nonspecic
chronic laryngitis, gastroesophageal reux, alcoholism, gout, tobacco smoking; Cord Edema: Myxedema, chronic nephritis; Surface Lesions: Keratosis,
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pachyderma, herpes, leukoplakia, pemphigus; Ulcers: Tuberculosis, syphilis, leprosy, SLE, typhoid fever, trauma, contact ulcer;
ules, sessile or pedunculated polyp, vocal process granuloma, vallecula
cyst, leukoplakia, carcinoma in situ, epidermoid carcinoma, papilloma,
angioma;
aortic aneurysm, large left atrium of the heart, mediastinal neoplasm, mediastinal lymphadenopathy, retrosternal goiter, injury during thyroidectomy;
Weak Cord Muscles: Debilitating diseases, severe anemia, myasthenia gravis,
myxedema, hyperthyroidism, normal aging process; Laryngeal Bones and
Cartilages: Perichondritis of cricoid or arytenoids, ankylosis of cricoarytenoid
joints (rheumatoid arthritis); Larynx Compression: Retropharyngeal abscess,
tuberculosis of cervical vertebrae, neoplasm of pharynx, large goiters, actinomycosis;
Vocal cord paralysis.
in the neck and chest inferior to the larynx. In unilateral cord paralysis, the
affected cord may be immobilized near the midline or slightly more laterally in the paramedian position. In the latter case, vocal cord approximation
is poor, and the voice is husky. During phonation, laryngoscopy shows the
normal cord crossing the midline to meet the abducted immobile cord. In
bilateral cord paralysis, the cords are usually xed near the midline, so the
voice is normal, but dyspnea is extreme and inspiratory stridor with strenuous exertion is pronounced. Cord paralysis is associated with thyroidectomy,
aneurysm of the left aortic arch (left cord), mitral stenosis with enlarged left
atrium (left cord), and mediastinal tumors.
Cricoarytenoid joint ankyloses. Inammatory or traumatic arthritis limits
motion at the cricoarytenoid joint.
true cords, resembling paralysis. Hoarseness and voice weakness are common. Passive mobility, tested by an otolaryngologist, is absent in ankylosing, but present with paralysis. If the joints are not completely immobilized,
crepitus over the larynx may be heard with a stethoscope. It may be so insidious that dyspnea is not recognized. Causes are rheumatoid arthritis and
prolonged contact with an esophageal feeding tube.
Innervation of cords: Compression of recurrent laryngeal nerve by
Neck Irradiation.
The recurrent laryngeal nerves are susceptible to injury
There is limited or absent motion of the
Neoplasm: Vocal nod-
Polypoid corditis. The entire free margins of the true cords are loose and sagging, hoarseness resulting from imperfect approximation of the edematous
cords. Causal factors include voice strain, irritation from alcohol and tobacco,
and upper respiratory allergy or infection.
Vocal nodules (singer’s nodules). With voice overuse, apposing 1–3 mm
nodules form on the free margins of the true cords at the junction of the anterior one-third and the posterior two-thirds (Fig. 7-64B). Early lesions appear
red, brosis later turns them white.
Laryngeal contact ulcer. Apposing ulcers occur on the free edges of both vocal
cords at their junctions with the arytenoid cartilages. The irregular ulcer borders cause hoarseness (Fig. 7-64C). They usually are caused by overuse, trauma
or instrumentation. Granulation tissue develops on one or both ulcers; enlargement can cause airway embarrassment.
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Larynx neoplasm. See Syndromes page 240 below.
Salivary Gland Signs
Xerostomia. Dry mouth is caused by mouth breathing, obstructed salivary
ducts, irradiation, and Sjögren syndrome.
enlargement accompany Sjögren syndrome (page 202).
Sialorrhea (ptyalism). Sialorrhea is excessive saliva production, but it often
refers to any condition of overabundant saliva, from rapid secretion, inability
to swallow, production of viscid difcult to swallow saliva, or failure of the
lips to contain the saliva.
CLINICAL OCCURRENCE: The common causes are poor neuromuscular
control of the lips, tongue, and perioral soft tissues. Other causes are drugs,
intoxicants, and local inammation stimulating salivary secretion. Drugs:
Mercury, copper, arsenic, antimony, iodide, bromide, potassium chlorate, pilocarpine, aconite, cantharides, carbidopa-levodopa; Stomatitis: Aphthous ulcers,
septic ulcers, suppurative lesions, periodontal disease, chemical burns; Specic
Oral Infections: Diphtheria, syphilis, tuberculosis; Single Oral Lesions: alveolar
abscess, epulis, salivary calculus; Reex Salivation: Gastric dilatation, gastric
ulcer or carcinoma, acute gastritis, pancreatitis, hepatic disease.
Enlarged salivary glands. Salivary gland enlargement can indicate local or
systemic disease. Painless enlargement of a single gland suggests tumor or an
obstructed duct. A painful enlarged gland suggests acute viral or suppurative
bacterial infection. Painless enlargement characterizes indolent mycobacterial and fungal infections. Generalized salivary gland enlargement suggests
a systemic disease involving the salivary glands either primarily or secondarily, or excessive salivary stimulation (e.g., bulimia).
CLINICAL OCCURRENCE: Degenerative/Idiopathic: Sarcoidosis; Infections:
Bacterial (staph, gonorrhea, syphilis, trachoma, actinomycosis); viral (mumps,
EBV, hepatitis C, HIV); mycobacterial (tuberculosis); fungal (histoplasmosis); Inammatory/Immune: Sjögren syndrome, amyloidosis; Metabolic/Toxic:
Diabetes mellitus, metal sensitivity (lead, iodide, copper); Neoplastic: Primary
salivary gland tumors, lymphoma, Warthin tumor; Psychosocial: Bulimia,
chronic alcohol consumption.
DDX: Dry eyes and salivary gland
Painless bilateral parotid enlargement. Parotids enlarge in a number of con-
ditions: its mechanism is unknown.
CLINICAL OCCURRENCE: Endocrine: Diabetes mellitus, pregnancy, lacta-
tion, hyperthyroidism; Degenerative/Idiopathic: Fatty salivary gland atrophy;
Inammatory/Immune: Sjögren syndrome, sarcoidosis, amyloidosis; Metabolic/
Toxic: Malnutrition (cirrhosis, kwashiorkor, pellagra, vitamin A deciency),
poisoning (iodine, mercury, lead), drugs (e.g., thiouracil, isoproterenol, sulsoxazole), obesity, starch ingestion; Neoplastic: Lymphocytic leukemia, lymphoma, salivary gland tumors; Psychosocial: Bulimia nervosa, stress.
Acute nonsuppurative parotitis. There is brawny induration of the parotid
region, with swelling in front of the tragus, and behind the mandible and
earlobe, pushing it outward. The skin is warm and there is pain, accentuated
by mouth opening or chewing, and exquisite tenderness. Fever is common.
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The duct orice can be red, occasionally discharging pus. One or both sides
may be involved. Mumps is the classic cause; occasionally bacterial infection
is responsible. Iodine allergy can cause the same symptoms.
Acute suppurative parotitis. Acute bacterial parotid infection is seen in
debilitated, immunosuppressed, and previously irradiated patients. The
gland is swollen, tender, and painful; induration and pitting edema are often
present, accompanied by high fever. The duct orice discharges pus. Multiple
abscesses may form, but uctuance is difcult to detect.
Chronic suppurative parotitis. Repeated episodes of duct obstruction produces chronic inammation without fever or pain.
Submandibular duct obstruction. When there is a history of a mass appearing after meals, but no mass on exam, give sips of lemon juice and watch for
swelling. A new mass, or enlargement of a preexisting swelling, is diagnostic of duct obstruction. Compare duct orices on each side. Using bimanual
palpation, feel for a calculus or mass. Press the gland in the submandibular
triangle and look for drainage.
Neck Signs
Stiff neck. Pain and limited neck motion direct attention to the neck’s muscles, bones, and joints. Be sure the mental status is normal and there are no
signs of meningeal inammation (Chapter 14, page 670) before evaluating for
other causes.
CLINICAL OCCURRENCE: Congenital: Torticollis, syringomyelia, Chiari syn-
dromes; Degenerative/Idiopathic: Fibromyalgia, myofascial pain syndrome,
stiff-man syndrome, Parkinson disease; Infectious: Pharyngitis, laryngitis,
prevertebral or retropharyngeal abscess, cervical lymphadenitis, meningitis;
Inammatory/Immune: Osteomyelitis, epidural abscess, tuberculosis, RA,
ankylosing spondylitis, polymyalgia rheumatica; Mechanical/Traumatic:
Acquired torticollis, trauma to cervical vertebrae (fracture, dislocation, subluxation, disk herniation), muscles and soft tissues (e.g., whiplash), cervical spondylitis, spinal stenosis; Metabolic/Toxic: Strychnine, hypercalcemia,
tetanus;
metastatic carcinoma; Psychosocial: Malingering, pending injury litigation.
Neoplastic: Thyroid cancer, lymphoma, oropharyngeal carcinoma,
Torticollis (wryneck). Hematoma or partial rupture of the sternocleidomas-
toid during parturition results in unilateral muscle shortening and congenital torticollis. Dystonic drug reactions, e.g., to phenothiazines, frequently
precipitates torticollis. The head may tip to one side, the dystonic sterno-
cleidomastoid being prominent. If tipping is present but the muscles are
not prominent, straighten the head causing the sternal head of one muscle
to tense more than the other. In long-standing torticollis, the face, and even
the skull, may be asymmetrical. DDX: Distinguish the head tilt of torticollis from head posture correcting for vertical squint or ocular muscle palsy,
ocular torticollis (Chapter 14, page 662): slowly but rmly straighten the neck
while watching the eyes for squint. Asymmetrical erosion of the occipital
condyle from rheumatoid arthritis or neoplastic disease results in cranial
settling in a tilted position.
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