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Dizziness is a very common complaint and is often difficult to evaluate. By
using a systemic history, the dizziness can be classified into vertigo,
presyncope, dysequilibrium, or lightheadedness. This classification
significantly narrows the differential diagnosis, helps target the affected
organ system, and can help define the appropriate specialist referral for
persistent cases. In some patients, the etiology cannot be determined, but it is
important to rule out significant pathology.
Introduction. Dizziness is one of the most common complaints in ambulatory care,
accounting for nearly 8 million outpatient visits annually in the United States.1 It is also often a perplexing problem for physicians in primary care
office practice, resulting in frequent referrals to specialists. Because of its
complexity, patients with dizziness frequently see numerous physicians before an
accurate diagnosis can be made and a treatment plan instituted.
Spatial orientation depends on the proper function and central integration of
information from several organ systems.
These include the eyes, the vestibular system (vestibular labyrinth, eighth
nerve, and vestibular nuclei in the brain stem), central pathways from the
vestibular nuclei to the cerebral cortex, cerebellum, and proprioceptive system.
Because each system may be affected by many different disease states, the number
of diagnostic possibilities in a patient complaining of dizziness is great.
To accurately diagnose a patient with dizziness, the clinician must use a
systemic approach, eliminating some diagnoses by a thorough history, a careful
neurologic examination, and still others with the use of special diagnostic
tests. The first and most important diagnostic step in evaluating a patient with
the broad complaint of dizziness is a thorough history. Various sensations may
be described by patients as “dizziness.” These include vertigo, presyncope,
dysequilibrium, and lightheadedness. By accurately classifying the dizziness
into one of these categories, the differential diagnosis can be limited. This
classification will be used in this article to summarize the diagnostic features
and
medical management of common disorders that cause dizziness.
Vertigo. Vertigo is the true sensation of movement, and refers to a spinning or
rotating sensation. True vertigo generally reflects disease of the vestibular
system. In a study of patients presenting with dizziness to an ambulatory care
clinic, 54% complained of vertigo.2 In patients with true vertigo, it is helpful
to ask, “What is the nature and length of attacks? Does head motion incite or
aggravate the vertigo? Are there associated cochlear symptoms, such as hearing
loss, tinnitus, or a sensation of aural fullness? Are these exaggerated when the
dizziness is worse? Was there antecedent head injury, pressure change, or
symptoms of a viral syndrome?”
Benign Paroxysmal Positional Vertigo (BPPV). The vertigo caused by BPPV,
which was first described by Barany in 1921,3 occurs only in certain positions,
and the true vertigo lasts only seconds. The spinning typically occurs when the
affected ear is in
the dependent position, or when the head is turned sharply to the right, the
left, or by looking upward. Schuknecht attributed this condition to inorganic
deposits on the cupula of the posterior semicircular canal, the sensitivity of
their mass to gravitational force being the proposed mechanism of stimulation.
He designated the condition cupulolithiasis.4
The diagnosis is confirmed by the Hallpike maneuver during which the head is
turned to the involved side and extended over the edge of the table. The
observer looks for nystagmus and patient subjectively reports vertigo. The word
nystagmus stems from the Greek nystazein, which means to nod, especially in
sleep. Clinically, it refers to an involuntary rapid alternating movement of
the eyes. In BPPV, the nystagmus is horizontal, vertical or rotary, delayed in
onset, and fatigues when the head position is assumed repeatedly.
During acute events, treatment is primarily symptomatic. Medications are usually
ineffective, and the most obvious treatment is to avoid the offending position.
In the majority of cases, BPPV is a self-
limited disease with resolution of symptoms in 90% of patients receiving no
treatment within 3 months. The goal of treatment, however, is to habituate the
vestibular system rather than suppress it. Head positioning exercises, patient
specific habituation training, and the canolith repositioning maneuver have been
shown to be very effective in quickly controlling vertigo in the majority of
patients with BPPV.
Vestibular Neuronitis. As the name implies, vestibular neuronitis is caused by
an inflammatory reaction of the vestibular division of the eighth cranial nerve.
The majority of cases referred to as acute labyrinthitis, inner ear infection,
epidemic vertigo and toxic labyrinthitis are examples of vestibular neuronitis.
Numerous causes for this inflammatory reaction have been proposed including
vascular insufficiency; viral, diabetic neuropathy, toxic and allergic
etiologies.
The diagnosis is based on a single, severe, prolonged episode of vertigo of
sudden onset, often with vomiting and complete debilitation. Unlike Meniere’s
disease, there is usually no involvement of the auditory system. After the acute
episode, which usually lasts
3 or 4 days, the patient may experience residual unsteadiness or postural
dizziness
for a prolonged period, but usually recovers completely within 6 months. Caloric
testing during electronystagmography (ENG) demonstrates a unilateral reduced
vestibular response. Because of the paretic vestibular nerve, it is important to
rule out a vestibular neuroma by brain stem-evoked response audiometry or a
magnetic resonance imaging study with gadolinium enhancement.
Since the course is usually one of gradual improvement, treatment is supportive
during the acute phase. Bed rest, sedation, and intravenous fluids are
supplemented with vestibular suppressing drugs, such as diazepam or
dimenhydrinate. Short term use of steroids has also been effective.5 If
positional dizziness persists after the acute attack, positional compensating
exercises may be helpful to hasten resolution.
Meniere’s Disease. Patients with
classic Meniere’s disease complain of intermittent spells of spinning vertigo
associated with fluctuating hearing impairment, tinnitus, and a sensation of
pressure or fullness in the involved ear. It is
a capricious disease with variations in this classic constellation of symptoms
being the rule rather than the exception.
The severe vertigo usually lasts for hours, following which the patient may have
the auditory symptoms for several days. After the initial attacks, the hearing
usually returns to normal, but on subsequent occasions, there is a progressive
permanent hearing loss. Occasionally, the patient will present with only the
vertigo (vestibular Meniere’s syndrome) or only the auditory symptoms
(cochlear Meniere’s syndrome).
Histologically, Meniere’s disease is characterized by distention of the
membranous labyrinth (endolymphatic hydrops). The cause for this is unknown
despite many decades of study. Theories include electrolyte imbalance,
autoimmune disease, allergies, vasomotor reactions, trauma, metabolic disorders,
infectious processes (eg, viral, syphilitic), and hereditary factors. While
there is no definitive test for this disorder, ENG, electrocochleography (ECOG),
dehydration testing, and screening blood profiles can be helpful.
There are a myriad of medications employed in the management of Meniere’s
disease, and in vestibular disorders in general. The mainstay of therapy is
diuretics, with concurrent restriction of dietary sodium, caffeine, and alcohol.
In certain cases, vasodilators, steroids, and other anti-inflammatory drugs may
be helpful. Recently, there is some evidence that perfusion of the labyrinth
with steroids given transtympanically may be of some benefit. Surgical
procedures for patients who fail medical management include endolymphatic sac
procedures, use of ototoxic antibiotics, such as gentamycin to ablate the
affected vestibular system, labyrinthectomy, and vestibular nerve section.
Other Causes Of Vertigo. Discussion of all causes of vertigo is beyond the scope
of this article. However, it should be emphasized that the clinician should not
direct attention too strongly to the inner ear, even if the dizziness is
vertiginous in nature because other central portions of the vestibular system
may produce identical symptoms. Examples of central causes of vertigo include
multiple sclerosis, vestibular migraines6, brain stem and cerebellar tumors,
impaired circulation to the vestibular nuclei as occurs in atherosclerosis and
vertebrobasilar insufficiency, vestibular epilepsy, cervical vertigo, and
vascular compression syndromes.
Presyncope. Presyncope can be defined as a sensation of impending loss of
consciousness or faintness. This symptom accounted for 16% of patients
presenting to an ambulatory care clinic with the complaint of dizziness.2
Orthostatic Hypotension. One common cause of presyncope is orthostatic
hypotension. These patients present with symptoms occurring only at the
assumption of a more upright posture, that is, lying to sitting, or sitting to
standing. Upon standing, documentation of a 10mm Hg drop in systolic blood
pressure or any drop in diastolic blood pressure is diagnostic. In a large study
of patients presenting to a neurotology practice, 18.67% had abnormal blood
pressures (hypotension, hypertension, and orthostatic hypertension).7
Arrhythmias. Cardiac arrhythmias commonly present with symptoms of presyncope.
Diagnosis is by electrocardiogram or rhythm monitoring documenting tachycardia
(other than sinus), bradycardia (rate <50), or sinus pauses (>3 seconds).
Dysequilibrium. The sensation of dysequilibrium is defined as a sensation of
imbalance, often with a feeling of falling, when standing or walking, usually
without cephalic sensation. This sensation is usually continuous without an
episodic nature. In the ambulatory care setting, dysequilibrium accounted for 2%
of patient’s primary complaint of dizziness, but it was a contributing factor
in 17% of patients presenting with the complaint of dizziness.2
Vestibular Nerve Injury. The most common cause of dysequilibrium is vestibular
nerve injury with a reduced vestibular response to caloric stimulation seen on
ENG testing. This may be the end result from vestibular neuronitis, Meniere’s
disease, vascular occlusion, peripheral neuropathy, multiple sclerosis, or
acoustic tumor.
Other Causes. Other causes for dysequilibrium include noncorrectable visual
impairment, metabolic disorders, peripheral neuropathy, cervical spondylosis,
orthopedic disorders interfering with ambulation, or gait disturbances related
to neurological or musculoskeletal disease (eg, hemiparesis or arthritis).
Often, the cause of the dysequilibrium is multifactorial. In these cases, a
customized program of vestibular rehabilitation is often extremely effective to
force compensation of other organ systems and increase the patient’s
independence and safety.
Lightheadedness. One of the most challenging groups of patients is that
presenting with non-specific symptoms of lightheadedness. These patients often
present a vague history of dizziness, which makes diagnosis difficult. In a
large percentage of these patients, psychiatric problems are either the primary
cause of the complaint, or a significant contributing factor. In the ambulatory
care study, psychiatric factors contributed to the dizziness in at least 40% of
patients, and was felt to be the primary cause in 16%.2 Whether primary or
contributory, psychiatric disorders should be recognized as potentially
treatable comorbid conditions.
Conclusion. In summary, dizziness is often self-limited, but when it does
persist,
a directed history and physical examination can establish a presumptive cause in
most patients.Vestibular function testing, radiographic imaging, and psychiatric
evaluation are the most useful supplemental measures. The etiology of dizziness
is often multifactorial, and in some patients, no etiology can be identified. It
is important in these patients to exclude serious conditions, but fortunately,
serious treatable causes of dizziness are rare.
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References
1. Sloane PD. Dizziness in primary care: Results from the National Ambulatory
Medical Care Survey. J Fam Pract. 1989;29:33-38.
2. Kroenke K, Lucas CA, Rosenberg ML. Causes of persistent dizziness. Ann Intern
Med. 1992;117:898-904.
3. Barany R. Diagnose von krankheitsercheinungen im bereiche des
otolithenapparates. Acta Otolaryngol. 1921;2:434.
4. Schuknecht HF. Cupulolithiasis. Arch Otolaryngol. 1969; 90:765.
5. Ariyasu L. The beneficial effect of methylprenisolone in acute vestibular
vertigo. Arch Otolaryngol. 1990;116:700.
6. Parker W. Migraine and the vestibular system in adults. Am J Otology.
1991;12:25.
7. Ohashi N, Imamura J, Nakagawa H, Mizukoshi K. Blood pressure abnormalities as
background roles for vertigo, dizziness, and dysequilibrium. ORL.
1990;52:355-359.
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