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236 CHAPTER 7: The Head and Neck
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Meningitis. The neck is held stify in slight or extreme dorsiexion from pain
and reex muscle spasm. Forceful neck anteexion results in involuntary
exion at the hips, knees, and ankles, Brudzinski sign, indicating meningeal
irritation. See Chapter 14, page 671.
Septic thrombophlebitis of the internal jugular vein (Lemierre syndrome).
Local infection in the face or oropharynx leads to septic thrombophlebitis of the internal jugular vein. This is a medical and surgical emergency,
mandating early recognition. The patient is systemically ill with fever,
chills, and signs of septicemia. Septic emboli to the lungs cause multiple
pulmonary abscesses [Bliss SJ, Flanders SA, Saint S. A pain in the neck. N
Engl J Med. 2004;350:1037–1042].
Midline Cervical Mass
Thyroglossal cysts and stulas. Cysts arise from midline thyroglossal duct
remnants (Fig. 7-12, page 171). Thyroglossal cysts appear at any time in life.
Some cysts are translucent. A stula results from drainage of an inamed cyst or
incomplete excision of a thyroglossal remnant. The sinus tract opens in or near
the midline. Cysts occur at various levels, presenting diagnostic challenges.
Suprahyoid level. A thyroglossal cyst immediately above the hyoid bone
(Fig. 7-65A) must be distinguished from a sublingual dermoid cyst, visible
under the tongue as a white, opaque body shining through the mucosa.
Subhyoid level. The midline cyst is between the hyoid bone and thyroid
cartilage. Sometimes swallowing hides the mass temporarily under the
hyoid. Dorsiexing the neck and opening mouth, causes the cyst to reappear
(Fig. 7-65B).
Thyroid cartilage level. At this level a thyroglossal cyst may deviate from
the midline, usually to the left, the forward pressure of the thyroid cartilage
pushing it aside. To distinguish the mass from an enlarged lymph node, have
the patient protrude the tongue maximally. A thyroglossal duct cyst is tugged
upward.
Cricoid cartilage level. In this region, a thyroglossal cyst must be distinguished
from a pyramidal lobe mass. Tongue protrusion tugs the cyst upward.
Pyramidal thyroid lobe. See the preceding discussion on thyroglossal cyst at
the cricoid level. The pyramidal lobe may extend from the thyroid isthmus to
the hyoid bone (Fig. 7-66A). The base on the isthmus is usually wider than the
projection’s height. It may be palpable in Hashimoto thyroiditis.
Suprasternal notch mass—dermoid cyst. A nonpulsatile uctuant mass in
the suprasternal notch (Burns space) frequently is a dermoid cyst. The mass
doesn’t adhere to the trachea, or move upward with tongue protrusion.
Suprasternal mass—tuberculous abscess. Other than being slightly less uctuant, this has the same characteristics as the dermoid cyst. It arises from an
apical lung abscess or by drainage from deep cervical lymph nodes.
A. Suprahyoid cyst B. Subhyoid cyst
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FIG. 7-65 Thyroglossal Cysts and Sinuses. A. Suprahyoid cyst: This is above the hyoid bone. B. Subhyoid cyst.
FIG. 7-66 Thyroid-Associated Masses. A. Pyramidal lobe of thyroid gland. B. Delphian nodes.
Pulsatile suprasternal notch mass—aorta or innominate artery. Occasionally,
the aortic arch or innominate artery elongates, bowing the vessel up into
the suprasternal notch. This is not necessarily evidence of aneurysmal
dilatation.
Lateral Cervical Masses: Intermittent or persistent cystic feeling masses in
lateral neck compartments usually arise from normal structures that have
become, or are intermittently, distended. The history, exact location, and characteristics of the mass usually identies the probable etiology. Solid masses in
these locations frequently arise in lymph nodes and suggest neoplasms, usually malignant. A uctuant lymph node mass suggests infection, suppurative
bacteria if acute and tuberculosis if chronic.
Branchial cyst. Embryonic branchial cleft remnants undergo cystic enlargement, usually in adults. Commonly, there is a single cystic mass just anterior but deep to the upper third of the sternocleidomastoid. The mass feels
slightly soft and resilient; intercurrent inammation makes it tender and rm.
Aspirated uid appears to be pus, but oil droplets may be seen oating on
the surface.
Branchial stula. Arising from a branchial cyst, the stula may be either congenital or have developed from an inamed cyst. Probing usually discloses a
blind end in the lateral pharyngeal wall. Fistulas become intermittently infected.
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FIG. 7-67 Single Tumors of the Lateral Neck II. A. Carotid body tumor. B. Laryngocele.
Hygroma. The mass is formed by many cysts of occluded lymphatic channels. The soft, irregular, and partially compressible mass is usually present
from childhood. It occupies the upper third of the anterior cervical triangle
but may extend downward or under the jaw. Its brilliant translucence distinguishes it from all other cysts. Its size may vary from time to time and it may
become inamed.
Carotid body (glomus) tumor. This arises from the carotid body chromafn
tissue, can be familial or sporadic. It appears in middle life and grows very
slowly. The mass is palpated near the carotid bifurcation (Fig. 7-67A). Usually
shaped like a potato (potato tumor), it is freely movable laterally, but cannot be
moved in the long axis of the artery. Although growing in the carotid sheath,
it does not always transmit arterial pulsations. Early it may feel cystic, later
becoming hard. Pressure on the tumor sometimes slows the heart rate producing lightheadedness. Some tumors produce vasoactive amines, and palpation
can produce pupillary dilatation and hypertension, a useful diagnostic sign.
Regional extension upward along the carotid sheath eventually occurs in 20%.
Zenker diverticulum (pharyngeal pouch). A pharyngeal diverticulum occurs
cephalad to the cricopharyngeus muscle. The patient complains of gurgling
in the neck, especially during swallowing. Regurgitation of food is common
while eating or lying on the side. An intermittent swelling may be seen in the
side of the neck, usually the left. If not apparent, the swelling may be induced
by swallowing water. Pressure on the distended pouch causes regurgitation
of old food.
Laryngocele. Herniation of a laryngeal diverticulum through the lateral thy-
rohyoid membrane causes intermittent neck swelling (Fig. 7-67B). Blowing
the nose will often induce an air-lled swelling that is resonant to percussion.
It is usually caused by chronic severe coughing or sustained blowing on a
musical instrument.
Cavernous hemangioma. As in other parts of the body, the swelling is soft,
compression partially empties the cavity of blood and relling is slow. A faint
blue color under the skin may be discerned.
Thyroid Signs
Tracheal displacement and compression by goiter. A large or strategically located goiter can cause tracheal compression and/or displacement
(Fig. 7-68). Patients complain of tightness or pressure in the throat. Stridor is
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FIG. 7-68 Tracheal Displacement: The retrosternal goiter on the patient’s left compresses the trachea transversely
pushing it to the right. The tracheal deviation can be demonstrated by palpation.
rarely the presenting complaint. The trachea is most vulnerable to compression at the thoracic inlet, especially in small patients with short necks. Usually
the trachea is narrowed transversely. Small degrees of compression are not
apparent from history or physical exam. With severe narrowing, slight pressure on the lateral thyroid lobes produces stridor (Kocher test). Lateral trachea
deviation in the neck is present when the midpoints of the tracheal rings are
not centered in the suprasternal notch (Fig. 7-68).
Tender thyroid—thyroiditis. See page 258.
Thyroid bruit. As the thyroid undergoes hyperplasia the increased blood
ow produces a thyroid bruit, suggesting Graves disease.
bruit may be confused with a carotid bruit; the latter radiates to the angle of
the jaw. An aortic murmur originates at the base of the heart and can be followed into the neck. A venous hum has a different pitch and is abolished by
light compression of the jugular vein.
DDX: A thyroid
Thyroid enlargement—goiter. See page 256.
Thyroid nodules. See page 258.
Enlarged Delphian lymph nodes. A few lymph nodes are normally present
in the thyrohyoid membrane. When enlarged, they are termed the Delphian
because they may foretell thyroid cancer. Enlarged Delphian nodes indicate
either subacute thyroiditis or thyroid cancer (Fig. 7-66B).
HEAD AND NECK SYNDROMES
Squamous Cell Cancers of the Head and Neck: Tobacco and alcohol are
cocarcinogens for aerodigestive system squamous cell carcinoma. Muscle
inltration by neoplasm limits functions, e.g.,
cancers. Regional lymph node spread may be the rst sign of disease. The
enlarging nodes are stony hard. Lymph node biopsy is contraindicated since
it violates tissue planes adversely affecting prognosis. Aspiration cytology is
indicated for suspicious nodes. Complete panendoscopic evaluation of the
upper aerodigestive tract is necessary in all cases to establish the primary site
and disease extent, and for treatment planning.
tongue protrusion with deep
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Tongue carcinoma. Carcinomas in the oor of the mouth are often symptomatic, ulceration producing pain, and tongue motion causing discomfort.
If the patient complains of discomfort, dysphagia, or inability to protrude the
tongue, yet no lesions are visible, palpate the root of the tongue. Inspection
usually reveals an ulcerated, whitish lesion. On palpation it is harder than
surrounding muscle. Carcinoma is usually seen on the sides, base, and
undersurface of the tongue (Fig. 7-63F) as an ulcerating mass with rolled and
everted margins. It is not tender unless ulcerated. A unilateral neoplasm hindering muscle action, causes deviation toward the side of the lesion. Fixation
to the mandible and metastases to submental or anterior jugular lymph nodes
occur early.
Tonsil carcinoma.
than half of tonsillar cancers. The patient complains of earache from referred
pain. The breath is foul with a bleeding ulceration. Palpation discloses characteristic tonsil induration.
Larynx neoplasms. Larynx tumors are benign or malignant, pedunculated or
sessile, localized or inltrative. Inltrative lesions are malignant. Localized
masses must be biopsied for diagnosis (Figs. 7-64E and F)
Scalp, Face, Skull, and Jaw Syndromes
Headache. See Chapter 14, page 651, for a full discussion of headache. Discussed below are regional causes of headache related to extracranial disease.
Fever. Many febrile illnesses are associated with headache. The location varies, the pain may be slight or severe, throbbing or steady. Pain is thought to
arise from distention of the cranial arteries.
Giant cell arteritis, temporal arteritis. See Chapter 8, page 361. Temporal
headache resulting from ischemia in the temporal artery distribution are constant and relatively severe. Scalp tenderness is often present and exquisite
scalp sensitivity is nearly diagnostic. Search for nodularity and decreased
temporal artery pulsation.
Occipital neuritis. Pain over the ear and posterior scalp suggests occipital
neuritis from occipital nerve entrapment.
Paranasal sinusitis. See page 248.
Ice cream headache. Applying cold to the palate triggers intense medial
orbital pain. It is precipitated by eating very cold foods, classically ice cream,
and lasts 2–120 seconds. It may be more common in migraineurs.
Human papilloma virus, especially type 16, causes more
TMJ pain. Pain in front of the ear, episodic or constant, worsened with eating, and accompanied by clicking or grating sensations is typical of TMJ disease (Fig. 7-69). Common causes are trauma and being edentulous. Loss of
correct maxilla-mandible spacing for chewing places abnormal forces on the
TMJ. Other diseases affecting the TMJ are RA, rheumatic fever, SLE, gout,
Sjögren syndrome, and familial Mediterranean fever. DDX: Pain in the side
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FIG. 7-69 Palpation of the TMJ. P lace the tips o f your index finger s in each extern al acoustic meatus and have the pat ient
open and close his mouth. Clicking or crepitation is felt with TMJ arthritis; the joint will be tender if rheumatoid arthritis is the cause.
of the head with chewing suggests giant cell arteritis with claudication of the
masticators. The mechanical symptoms identify TMJ pain. TMJ tenderness
distinguishes RA from rheumatic fever.
Periorbital abscess.
through the lateral sinus wall forming an abscess between the ethmoid plate
and periosteum lining the orbit.
movement, and edema between the inner canthus and the bridge of the nose.
The edematous region is tender, and edema may extend to both lids. The pus
may push the globe slightly downward and laterally. No chemosis is present.
Surgical drainage is essential.
Orbital cellulitis. A periorbital abscess may extend producing diffuse orbital
cellulitis. Invasion is heralded by a chill, high fever, and dull pain in the eye.
The eyelids become edematous, particularly near the inner canthus, and chemosis develops. Ultimately, the eye becomes xed. The patient appears very
ill and requires immediate surgical care.
Eye Syndromes
Sjögren syndrome—keratoconjunctivitis sicca. Lymphocytes inltrate the
salivary and lacrimal glands with loss of exocrine function. This autoimmune
disorder was rst described as keratoconjunctivitis sicca and xerostomia in
rheumatoid arthritis patients.
mon with symptoms of fatigue, dry mouth, eyes, and other mucosal surfaces,
arthralgias and arthritis, and nephritis. Both central and peripheral neurologic symptoms may be present. In addition to rheumatoid arthritis other
autoimmune diseases may accompany the syndrome. There is an increased
risk of non-Hodgkin lymphomas.
Graves ophthalmopathy. Mucopolysaccharide deposition and brotic
degeneration of the extraocular muscles and orbital fat displace the globe
forward, impairing eye movement. Acquired bilateral exophthalmos is most
commonly associated with Graves disease.
dently of thyroid function, so the patient may be hyperthyroid, euthyroid,
or hypothyroid. The proptosis is often permanent, although treating acute
inltration and edema may lead to resolution. Accompanying signs are lid
edema, periorbital swelling, lid lag, lid retraction, and scleral show (page 175).
Proptosis may initially be unilateral, raising concern for other intraorbital
In suppurative ethmoid sinusitis, pus may extend
This is accompanied by fever, pain on eye
Primary Sjögren syndrome is relatively com-
The proptosis occurs indepen-
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pathology. Patients may present with diplopia because of asymmetric muscle
involvement.
Down syndrome (trisomy 21). The four ocular signs of Down syndrome are
an epicanthic fold persisting after age 10 years; unilateral or bilateral slanting
eyes in which the lateral canthus is elevated >2 mm above a line through
both medial canthi; Brusheld spots, accumulations of light-colored tissues in a
concentric band of the outer third of the iris; and hypoplastic iris seen as dark
discoloration of the iris.
Uveal tract inammation—uveitis (iritis, iridocyclitis, and choroiditis).
uveal tract, the vascular layer of the eye, is inamed. It may involve only
the iris (iritis), extend to the ciliary body (iridocyclitis), or involve the choroid (choroiditis) or retina (retinitis).
miosis, accompanied by deep pain, photophobia, blurring, and lacrimation.
The inamed iris may adhere to the anterior lens forming posterior synechiae,
manifest by pupil irregularity. Cells cast off into the anterior chamber form
a sterile hypopyon (Fig. 7-34B). Yellow deposits or white dots of aggregated
inammatory and pigmented cells, keratic precipitates, appear on the cornea’s posterior surface. Uveitis, most commonly idiopathic, also results from
trauma, infection, allergy, sarcoidosis, collagen vascular diseases, and autoimmune conditions such as ankylosing spondylitis.
Red eye. A red eye may be caused by a benign self-limited condition or indicate serious sight-threatening eye disease. DDX: Generalized redness of the
bulbar and tarsal conjunctivae, with minimal discharge and no visual loss, is
usually viral conjunctivitis or blepharitis. Localized lid redness and swelling
suggests hordeolum or chalazion. Severe photophobia, ciliary ush, visual
loss, elevated intraocular pressure, corneal haze, acute proptosis, and acute
scleritis require urgent evaluation by an ophthalmologist.
CLINICAL OCCURRENCE: Benign Disorders: Environmental irritant, aller-
gic and viral conjunctivitis, external hordeolum (sty), internal hordeolum
(chalazion), and blepharitis; Serious Disorders Requiring Urgent Ophthalmology
Referral: Acute keratitis (herpes simplex, bacterial, trauma, foreign body),
gonococcal and chlamydial conjunctivitis, acute glaucoma, acute iridocyclitis,
uveitis, and acute scleritis.
Glaucoma. Increased intraocular pressure produces ischemic damage to the
nerve bers at the optic disk. A progressive increase in cup-to-disk ratio dis-
covered by sequential observations suggests increasing intraocular pressure
(Fig. 7-37). Early damage leads to nasal steps and arcuate defects. Later, there
is general visual eld constriction from optic nerve injury from increased
intraocular pressure or vasculopathy of the nerve head (Fig. 7-39C). Detection
of early visual eld loss requires automated perimetry. Pupillary dilation is
often present.
Iritis is characterized by ciliary ush and
The
Narrow angle glaucoma. Drainage of aqueous from the anterior chamber is
obstructed by narrowing the chamber angle and/or increasing aqueous production. Acute symptoms are extreme ocular pain with nausea and vomit-
ing, and loss of vision. Chronic symptoms include halos around lights, tunnel
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vision, ocular pain, and headache. Chemosis, corneal edema, ciliary ush,
and a xed dilated pupil are seen on exam.
Open angle glaucoma. There is increased aqueous secretion and obstruction
to outow with normal chamber angles. The most common type of glaucoma,
it occurs in older persons who may see colored halos around lights and experience insidious, painless blindness.
Sudden vision loss. This always requires urgent attention by an ophthalmologist.
Visual loss is usually monocular resulting from detached retina, vitreous
hemorrhage, retinal artery occlusion (embolus, thrombus, or vasculitis), optic
nerve compression, or anterior ischemic optic neuritis (AION), arteritic and
nonarteritic. Transient 5–15-minute unilateral visual loss (amaurosis fugax) is
usually caused by embolic retinal artery occlusion. On fundoscopy, refractile
cholesterol emboli may be seen at retinal artery bifurcations. Loss of vision
in one visual eld (right or left hemianopsia) indicates a lesion between the
optic chiasm and visual cortex. Patients are often unaware of this visual eld
loss. Sudden bilateral visual loss with nystagmus and/or confusion suggests
thiamine deciency, from dietary deciency or increased metabolic demand.
Monocular visual loss—amblyopia.
normal eye occurs during visual development in the rst few years of life
from one of the three causes: misalignment of the optic axes (strabismus), large
differences in refractive error between the two eyes (anisometropia), or depri-
vation of vision in one eye resulting from bilateral severe refractive errors.
Amblyopia causes preventable visual loss in ~3% of the population. Early
childhood screening, recognition, and treatment helps to prevent and, in
some cases restore visual acuity.
Ear Syndromes
Acute external otitis. A variety of organisms can cause inammation, but the
usual offenders are Pseudomonas aeruginosa, or, less commonly, streptococci,
staphylococci, or Proteus vulgaris. This may be the result of increased pH in
the canal (“swimmer's ear”). Pain may be mild or severe and is accentuated
by movement of the tragus or pinna. The epithelium appears either pale or
red; it may swell closing the canal and impairing hearing. The tragus may
also swell. A discharge is often present. Fever is not uncommon. Tender, palpable lymph nodes may appear in front of the tragus, behind the pinna, or in
the anterior cervical triangle.
Chronic external otitis. Bacteria and fungi are the chief causes, although it
can accompany a chronic dermatitis, e.g., seborrhea or psoriasis. Pruritus, not
pain, is the chief symptom. Ear discharge may be present. The epithelium of
the pinna and meatus is thickened and red; it is abnormally insensitive to the
pain during instrumentation.
Malignant (necrotizing) external otitis. Pseudomonas aeruginosa invades the
soft tissues, cartilage, and bone of patients with diabetes mellitus. Although
some patients have minimal clinical ndings, others experience pain, discharge, and fever with swelling and tenderness of the tissues around the
Monocular visual loss in an otherwise
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ear. Auditory canal exam may reveal edema, redness, granulation tissue,
and pus obscuring the TM. Complications are osteomyelitis of the mastoid,
temporal bone, and skull base with involvement of CNs, especially CN-VII.
Otolaryngology consult is mandatory.
Middle ear glomus tumor.
the jugular bulb or middle ear mucosa.
the involved ear. Sometimes the glomus jugular type is associated with paralysis of CN-IX and CN-XI which pass through the jugular foramen. Glomus
tumors appear as red masses behind the TM. Identical tumors arise from the
carotid artery bifurcation. Rarely, tumors are multiple, malignant, and/or
secreting vasoactive amines. If biopsied, they bleed profusely. Familial forms
occur.
Acute otitis media with effusion (serous otitis media).
obstruction prevents middle ear aeration. Resorption of trapped air produces
negative middle ear pressure leading to an effusion, while atmospheric pressure displaces the TM inward. This usually follows an upper respiratory
infection. Initially, the TM retracts around the malleus, becoming more distinct and curving the light reex (Fig. 7-28B). Later, serous amber uid is seen
behind the TM (Fig. 7-28C). A uid meniscus forms a ne black line, and
sometimes air bubbles are visible (Fig. 7-28E).
Acute suppurative otitis media. Bacteria from the nasopharynx (Streptococcus
pneumonia, Haemophilus inuenza, Moraxella catarrhalis) enter the middle
ear via the Eustachian tube; uid in the chamber favors purulent infection.
Throbbing earache, frequently with fever and hearing loss, is the chief complaint. The bright red and lusterless TM bulges obliterating normal landmarks
(Fig. 7-28D). Perforation rapidly relieves pain and pus appears in the canal. If
the infection extends into the mastoid air cells, pressure on the mastoid process may elicit pain. Fever and constitutional symptoms are more prominent
in children than adults.
cause pain, unlike acute external otitis.
Acute mastoiditis.
Usually, mastoid infection results from inadequate treatment of acute suppurative otitis media. The symptoms of otitis gradually increase and there is
low-grade fever. The eardrum is lusterless and edematous. Deep pain is elicited by percussing the mastoid process. Clouding of the mastoid air cells on
imaging conrms the diagnosis. Bone destruction becomes evident after 2–3
weeks. Extension can cause a subperiosteal abscess of the mastoid process.
Less commonly, erosion of bone damages the facial nerve (CN-VII) with facial
paralysis. Extension through the inner table can cause meningitis, epidural
abscess, or abscess of the temporal lobe or cerebellum. Infection of the internal ear can produce labyrinthitis.
Fibrovascular tumors arise from glomus bodies in
They present with pulsatile tinnitus in
Eustachian tube
DDX: Movement of the pinna and tragus does not
The mastoid air cells communicate with the middle ear.
Chronic suppurative otitis media. This is associated with a permanent TM
perforation. A marginal annulus perforation is more common than a central
defect. The chief symptom is painless aural discharge. Hearing is always
impaired. Discharge volume may wax and wane, but recurrence is invariable.
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Painless discharge accompanying a URI suggests an old perforation. Pain
and vertigo indicate a complication, e.g., subdural irritation, brain abscess, or
labyrinth involvement.
Cholesteatoma. In chronic suppurative otitis media with a deep retraction
pocket in the attic or posterior superior quadrant of the TM, the squamous
epithelium of the meatus may grow into the attic of the tympanic cavity.
Desquamation produces a caseous mass of cells, keratin, and debris, which,
becoming infected and slowly enlarging, extends into the mastoid antrum
ultimately eroding bone.
Patients have ear fullness, pain, headache, and
hearing loss. Signs include chronic foul-smelling suppurative middle ear discharge, hearing loss, and a pearly gray mass visible with the otoscope.
Hearing loss. Sensorineural loss (nerve deafness) results from disorders of
the cochlea or acoustic nerve (CN-VIII). Conductive loss means failure to
conduct TM vibrations to the neurosensory apparatus. Causes of sensorineu-
ral loss include hereditary deafness, congenital deafness, trauma, infections,
drug toxicity, and aging (presbycusis). Unilateral hearing loss and tinnitus may
be the rst symptoms of an acoustic neuroma. Conductive loss occurs with
external acoustic meatus obstruction, TM and middle ear disorders, and xation of the stapes by bone overgrowth (otosclerosis). Hearing loss screening
involves questioning patient and family members about hearing difculty.
Follow afrmative or equivocal responses with the whispered voice test.
Dizziness. Symptoms described as dizziness may arise from problems in the
inner ear, CN-VIII, or vestibular nucleus; from loss of proprioception due to
peripheral neuropathy or visual impairment; from autonomic dysfunction
or intravascular volume depletion; and from anxiety and other psychiatric
disorders.
This common complaint requires a careful history. Never suggest
descriptive terms (spinning, lightheaded, unsteady, etc.). The patient must describe
the symptoms without using the word dizzy. From the description, put the symp-
toms into one of four general categories: 1. true vertigo (an illusion or hallucination of motion); 2. near syncope (e.g., orthostatic lightheadedness, and
hypotension); 3. postural unsteadiness caused by sensory abnormalities or
weakness; and 4. the last group, for whom no clear physiologic explanation
is suggested.
CLINICAL OCCURRENCE: Endocrine: Hypothyroidism, pregnancy, hypo-
parathyroidism, aldosteronoma; Degenerative/Idiopathic: Multisystem atrophy,
migraine, absence seizures, peripheral neuropathy;
Infectious: Meningitis,
encephalitis, brain abscess, syphilis; Inammatory/Immune: Vestibular
neuritis; Mechanical/Traumatic—Ears: Utricular trauma from skull fracture,
otosclerosis, leakage from tears in the oval or round windows, perilymph
stula; Mechanical/Traumatic—Eyes: Muscle imbalance, refractive errors,
glaucoma; Metabolic/Toxic: Nutritional: Pellagra, alcoholism, vitamin B
deciency; cerebral hypoxia, uid and electrolyte disturbances; Neoplastic:
Brain tumors (primary, metastatic);
Psychosocial: Panic attack, generalized
12
anxiety disorder; Vascular: Hypotension, orthostatic hypotension.
Vertigo. When the head is at rest, persistent stimulation of the semicircular
canals or vestibular nucleus produces a hallucination of motion. With the
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