1. Vertigo ("Dizzy, lightheaded")
Presentation
This may be a nonspecific complaint which must be refined further into either
an altered somatic sensation (giddiness, wooziness); orthostatic blood
pressure changes (lightheadedness, sensation of fainting); or the sensation of
the environment (or patient) spinning (true vertigo). In inner ear disease,
vertigo is virtually always accompanied by nystagmus, which is the ocular
compensation for the unreal sensation of spinning; but the nystagmus may be
extinguished when the eyes are open and fixed on some point (by the same
token, vertigo is usually worse with the eyes closed). Nausea and vomiting
are common accompanying symptoms, but less common (depending on the
underlying cause) are hearing changes, tinnitus, cerebellar or adjacent cranial
nerve impairment.
What to do:
• Have the patient tell you in his own words what it feels like (without
using the word "dizzy"). Ask about any sensation of spinning, factors
which make it better or worse, and associated symptoms. Ask about
drugs or toxins which could be responsible.
• Determine whether the patient is describing vertigo (a feeling of
movement of one's body or surroundings) or a sensation of an
impending faint or a vague unsteady feeling.
• If the problem is near syncope or orthostatic lightneadedness, then
consider potentially serious etiologies such as heart disease, cardiac
dys- rhythmias or blood loss.
• With a sensation of dysequilibrium or an elderly patient's feeling that
he is going to fall, look for peripheral neuropathy, cervical spondylosis,
stiff legs and vasodilator medication. These patients should be referred
to their primary care physicians for management of their underlying
medical problems and adjustment of their medications.
• If there is light-headedness that is unrelated to changes in position and
posture and there is no evidence of disease found on physical
examination and laboratory evaluation, then instruct the patient to
hyperventilate by breathing deeply in and out fifteen times. If this
reproduces the symptoms, assess the patient's emotional state as a
possible cause of his symptoms.
• If the patient is having true vertigo, examine for nystagmus, which can
be horizontal, vertical or rotatory (pupils describe arcs). Have the
patient follow your finger with his eyes as it moves a few degrees to
the left and right (not to extremes of gaze) and watch whether there
are more than the normal 2 to 3 beats of nystagmus before the eyes
are still. You may detect nystagmus when the eyes are closed by
watching the bulge of the cornea moving under the lid.

2. • If nystagmus is not clearly evident and the patient can tolerate it,
attempt a provocative maneuver for positional nystagmus by having
the patient sit up and then lie back, quickly hang his head over the
stretcher side and turn his head and eyes to one side. Repeat to the
other side. When this maneuver produces positional nystagmus, it
indicates a benign inner ear dysfunction. A negative test is not helpful.
• Examine ears for cerumen, foreign bodies, otitis media, and hearing
loss.
• Examine the cranial nerves. Test cerebellar function (rapid alternating
movement, finger-nose, gait). Check the corneal blink reflexes: if
absent on one side in a patient who does not wear contact lenses,
consider acoustic neuroma.
• Decide, on the basis of the above, whether the etiology is central
(brainstem, cerebellopontine angle tumor, multiple sclerosis) or
peripheral (vestibular organs, eighth nerve). Central lesions may
require further workup, otolaryngologic or neurologic consultation, or
hospital admission, while peripheral lesions, although more
symptomatic, are more likely self-limiting.
• In the emergency department, treat moderate to severe symptoms of
vertigo with intravenous diazepam (Valium) 10 mg or diphenhydramine
(Benadryl) 50mg. Add promethazine (Phenergan) 25mg iv for nausea.
If there are no contra- indications (e.g. glaucoma) then a patch of
transdermal scopolamine can be worn for three days. Some authors
recommend hydroxyzine (Vistaril, Atarax) while others suggest
corticosteroids (Solu-Medrol, Prednisone). Nifedipine (Procardia) had
been used to alleviate notion sickness but is no better than
scopolamine patches, and should not be used for patients with postural
hypotension or who take beta blockers. If the patient does not
respond, he may require hospitalization for further parenteral
treatment.
• Treat vertigo symptoms in outpatients with diazepam (Valium) 5-10mg
qid, meclizine (Antivert) 12.5-25mg qid, diphenhydramine (Dramamine,
Benadryl) 25-50mg qid, promethazine (Phenergan) 25mg qid,or
hydroxyzine (Vistaril) 25mg qid, and bedrest as needed until symptoms
improve.
• Arrange for followup if there is no clear improvement in 2 days or if
there is any suggestion of a central etiology.
What not to do:
• Do not attempt provocative maneuvers if the patient is symptomatic
with nystagmus.
• Do not give anti-vertigo drugs to elderly patients with dysequilibrium.
These medications have sedative properties which can make them
worse.
• Do not make the diagnosis of Meniere's disease (endolymphatic
hydrops) without the triad of paroxysmal vertigo, sensorineural

3. deafness, and tinnitus, along with a feeling of pressure or fullness in
the affected ear.
Discussion
In general, the more violent and spinning the sensation of vertigo, the more
likely the lesion if peripheral. Central lesions tend to cause less intense vertigo
and more vague symptoms. Peripheral etiologies of vertigo or nystagmus
include irritation of the ear (utricle, saccule, semi- circular canals) or the
vestibular division of the eighth cranial (acoustic) nerve by toxins otitis, viral
infection, or cerumen or a foreign body against the tympanic membrane. The
term "labyrinthitis" should be reserved for vertigo with hearing changes, and
"vestibular neuronitis" for the common short-lived vertigo without hearing
changes usually associated with viral upper respiratory infections. Paroxysmal
positional vertigo may be related to dislocated otoconia in the utricle and
saccule. If it occurs following trauma, suspect a basal skull fracture with
leakage of endolymph or perilymph, and consider otolaryngologic referral for
further evaluation and positional Central etiologies include multiple sclerosis,
temporal lobe epilepsy, basilar migraine and hemorrhage in the posterior
fossa. A slow-growing acoustic neuroma in the cerebellopontine angle usually
does not present with acute vertigo but rather a progressive unilateral
hearing loss with or without tinnitus. The earliest sign is usually a gradual loss
of auditory discrimination.
Vertebrobasilar arterial insufficiency can cause vertigo, usually with associated
nausea, vomiting and cranial nerve or cerebellar signs. It is commonly
diagnosed in dizzy pateints who are older than 50, but more often than not
the diagnosis is incorrect. The brainstem is a tightly-packed structure in which
the vestibular nuclei are crowded in with the oculomotor nuclei, the medial
longitudinal fasiculus, cerebellar, sensory and motor pathways. It would be
unusual for ischmia to produce only vertigo without accompanying diplopia,
ataxia, sensory or motor disturbance. Although vertigo may be the major
symptom of an ischemic attack, careful questioning of the patient commonly
uncovers symptoms implicating involvement of other brainstem structures.
Objective neurologic signs should be present in frank infarction of the
brainstem.
Either central or peripheral nystagmus can be due to toxins, most commonly
alcohol, tobacco, aminoglycosides, minocycline, disopyramide, phencyclidine,
phenytoin, benzodiazepines, quinine, quinidine, aspirin, salicylates, non-
steroidal anti-inflammatories and carbon monoxide. Nystagmus occuring in
central nervous system disease may be vertical and disconjugate, whereas
inner ear nystagmus never is. Central nystagmus is gaze-directed (beats in
the direction of gaze) whereas inner ear nystagmus is direction-fixed (beats in
one direction regardless of the direction of gaze). Central nystagmus is
brought out by visual fixation, which supressed inner ear nystagmus.