Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2749_Библиотеки_им_академика_М_И_Перельмана
.pdf
Chapter 13 • Dizziness
https://t.me/med1917
149
a sudden transient loss of consciousness, with concurrent loss of postural tone, always has a spontaneous recovery (see Chapter 33).
Orthostatic hypotension is a frequent cause of lightheadedness and is most common in elderly patients,
occurring as a result of abnormal regulation of blood
pressure. Neurological causes of orthostatic hypotension are less common and are usually accompanied by
neurological ndings.
In both children and adults, a report of lightheadedness can accompany anemia, hypoglycemia, or
hyperventilation syndrome.
Is the vertigo from a systemic cause?
Key Questions
l
What other health problems do you have?
l
Would you describe yourself as anxious or nervous?
l
Do the episodes occur with any specic activity or
movement?
Other Health Problems
Cardiovascular problems are a common cause of vertigo
that is systemic in origin. The mechanism of vertigo can
include vasomotor instability that decreases systemic
vascular resistance, venous return, or both; severe reduction in cardiac output that obstructs blood ow within the
heart or pulmonary circulation; or cardiac dysrhythmia
that leads to transient decline in cardiac output. Patients
with hypertension can experience vertigo while taking
antihypertensives, potassium-depleting medications, or
as a result of postural hypotension.
Anxiety
Psychogenic dizziness is one of the most common causes
of vertigo. Symptoms tend to be vague and can include
other symptoms such as fatigue, fullness in the head,
light-headedness, and a sense of feeling apart from the
environment. Patients may describe themselves as anxious or nervous. Patients can also have other psychiatric
diagnoses. Stressors and tensions affecting children, such
as divorce, custody battles, and day care, can cause vertiginous-like symptoms in the older child. Anxiety with
hyperventilation can cause lightheadedness in a child,
who then reports the symptom as dizziness.
Relationship to Activity or Movement
Dizziness when turning, especially when rolling over in
bed, is usually caused by vertigo. However, unsteadiness while walking is considered to be disequilibrium,
which can be caused by many factors. Dizziness on standing can be the result of decreased cerebral perfusion.
In children, episodes of dizziness that occur with
sudden changes of posture can be the result of hypotension, vascular disease, or positional vertigo.
Is the vertigo central (brainstem or cerebellar)
or peripheral (vestibular) in origin?
Key Questions
l
Do you have migraine headaches?
l
Do you have other symptoms that bother you?
l
Do you have nausea and vomiting?
l
When do the episodes occur?
Headaches
Headache is a vascular-related cause of central vertigo.
Approximately one-third of patients with migraine
headaches experience vertigo. The vertigo can appear
as an aura occurring during the headache or separately.
Patients with vestibular-type migraine headaches often
experience photophobia, phonophobia, and visual aura
during the episodes of vertigo. Patients with basilartype migraines can have other symptoms consistent
with vertebrobasilar vascular abnormalities such as visual changes, tinnitus, decreased hearing, ataxia, or
paresthesia. Migraine, both with and without headache,
is recognized as a source of dizziness in children.
Other Symptoms
Patients with central vertigo nearly always have neurological symptoms such as double vision, facial numbness, and hemiparesis.
Cerebellar causes can produce other symptoms,
such as loss of balance, that closely resemble those of
a peripheral disorder; therefore neurological examination ndings are important in differentiating the two.
Pay particular attention to reports of motor dysfunction
or lack of coordination.
Vertigo that is peripheral in origin does not produce
additional neurological signs or symptoms. If the patient has nausea and vomiting, suspect a peripheral
vestibular apparatus problem rather than a central
cause. Nausea and vomiting are common with vestibular neuronitis and labyrinthitis and occur less often
with brainstem lesions.
Timing
Vertigo that occurs on rst arising in the morning is
usually the result of a vestibular disorder. Vertigo that
150
https://t.me/med1917
Chapter 13 • Dizziness
occurs while turning over in bed is characteristic of
benign paroxysmal positional vertigo (BPPV).
What do characteristics of the episodes tell me?
Key Questions
l
How long do the episodes of dizziness last?
l
Is the onset sudden or gradual?
l
Do you have any hearing loss?
l
Do you have ringing in your ears?
Duration of Episodes
Episodes that last a few seconds are typically caused
by BPPV and are usually elicited by rapid head movement. Episodes lasting minutes to hours can be caused
by Meniere disease or recurrent vestibulopathy.
Episodes that last days or weeks are commonly
produced by vestibular neuronitis. Patients usually feel
better when they lie completely still. Stroke can also
produce long-lasting episodes. The two can be differentiated based on medical history and physical examination ndings.
Sudden onset of prolonged dizziness (lasting
60 minutes or longer) suggests central causes such
as infection, brainstem infarction, inammation, or
vestibular hemorrhage. Trauma can also produce
prolonged dizziness.
The child with chronic recurrent dizziness (episodes lasting less than 30 minutes) can have central
causes such as seizure problems or migraine headache. The cause can also be peripheral, such as BPPV.
Chronic persistent episodes can indicate brainstem
lesions, anemia, diabetes, thyrotoxicosis, or a psychosomatic disorder.
Onset
A gradual onset of dizziness is typical of an acoustic neuroma or other neoplastic process that is slow-growing.
BPPV can also have a gradual onset.
Acute or sudden onset of vertigo is characteristic of
labyrinthitis, Meniere disease, stroke, or vertebrobasilar causes.
Recurrent episodes are typical of BPPV, vertebrobasilar causes, and Meniere disease.
identical to those of Meniere disease. Tinnitus, hearing
loss, and ear pain point to lesions in the inner ear or
acoustic nerve (cranial nerve VIII).
Patients with labyrinthitis and perilymphatic stulas
may also experience hearing loss, but without tinnitus.
An acoustic neuroma will produce unilateral hearing
loss with tinnitus. Patients with recurrent vestibulopathy usually do not report hearing loss.
What else should I consider?
Key Questions
l
What medications are you taking?
l
Are you now or have you recently been ill?
l
Have you had any recent injury to your head? Did
you have dizziness before the head injury?
l
Have you had any previous ear surgery?
Medications
Mediations that are salt-retaining or ototoxic can
produce vertigo, lightheadedness, or unsteadiness.
Salt-retaining drugs include steroids and phenylbutazone. Ototoxic medications include ethacrynic acid,
streptomycin, gentamicin, aminoglycosides, aspirin,
and furosemide.
Psychotropic drugs can also produce vertigo. Antihypertensive drugs can cause hypotension leading to
lightheadedness. Sedatives, alcohol, and anticonvulsants can cause a sense of disequilibrium.
Current or Recent Illness
Vestibular neuronitis is associated with recent viral
infection, often an upper respiratory tract infection.
If a patient is currently ill, consider labyrinthitis because it is frequently associated with concomitant
bacterial and viral infection. Current ear or sinus
infection can produce dysfunction of the vestibular
apparatus, resulting in vertigo. Recent abnormalities
of middle ear ventilation and middle ear effusion are
the most common cause of balance disturbance in
childhood. In balance disturbance, transmission of
pressure gradients through the labyrinthine windows
to the inner ear uids and the vestibular sensory receptors is altered.
Hearing Loss and Tinnitus
A classic triad of symptoms—vertigo, hearing loss,
and tinnitus—denes Meniere disease. Patients can
also report a sensation of fullness in the ears. The hearing loss can be unilateral or bilateral. Patients with
secondary or early tertiary syphilis can have symptoms
History of Head Trauma
Trauma to the head or ear can cause disturbance of both
peripheral and central balance mechanisms. Certain
traumas can cause acute destruction of the inner ear and
produce vertigo. Direct trauma can occur to the labyrinth from a temporal bone fracture. A blow to the head
Chapter 13 • Dizziness
https://t.me/med1917
151
or a whiplash injury can also produce a concussive
effect on the labyrinth. Children who have a history of
head trauma can present with vertigo caused by labyrinthine damage.
Vertigo often occurs as a residual symptom and usually gradually improves over the course of a year. Trauma
can also produce a stula between the middle and inner
ear, causing tympanic membrane (TM) damage and
ossicle disruption.
Previous Otology History and Procedures
Patients with cholesteatoma usually have a history of
chronic middle ear infection, otorrhea, and conductive
hearing loss. Prior surgical procedures of the ear can
produce peripheral vertigo through disruption of the
vestibular apparatus or through formation of a perilymph
stula.
DIAGNOSTIC REASONING: FOCUSED
PHYSICAL EXAMINATION
Take Vital Signs and Note Blood Pressure
Assess orthostatic blood pressure to rule out postural hypotension as the cause of vertigo. Assessment is made by measuring the blood pressure in
both the supine and standing positions. A drop in
arterial blood pressure of at least 30 systolic and
20 diastolic mm Hg when the patient changes from
the supine to the standing position indicates orthostatic hypotension.
Note General Appearance
In a patient who is currently ill, suspect labyrinthitis. In
a patient who is acutely nauseated and vomiting, suspect vestibular neuronitis.
Have Patient Hyperventilate and Perform Valsalva
Maneuver
Perform this testing if you suspect psychogenic vertigo
because the maneuver can reproduce the vertigo in
these patients. Ask the patient to perform a Valsalva
maneuver and to breathe in and out or blow vigorously
for 1 to 3 minutes.
Perform Vision Examination
A recent change in visual acuity or new corrective
lenses can cause transient episodes of imbalance.
Perform Ear Examination
Look for the presence of effusion or infection that
signals serous otitis or otitis media. Look for the
pre sence of a cholesteatoma. It will appear as a shiny
white irregular mass; foul-smelling discharge can also
be present. Note the integrity of the TM; trauma can
sometimes cause its disruption. Perform pneumatic
otoscopy (see Chapter 15), which will enable you to
determine whether changes in pressure trigger an episode of vertigo. If the patient has a stula, changes in
pressure transmitted directly to the inner ear will
cause a sudden episode of vertigo.
Perform Screening Hearing Tests
Perform Rinne (air conduction [AC] greater than bone
conduction [BC]) and Weber (lateralization) tests. Expect sensorineural loss with Meniere disease, labyrinthitis, perilymph stula, and acoustic neuroma. In
sensorineural loss, the sound lateralizes to the unaffected ear. With sensorineural hearing loss, bone and
air conductions are both reduced in Rinne tests but the
ratio remains the same (AC greater than BC). Patients
with a cholesteatoma, serous otitis, or otitis media may
have conductive hearing loss (see Differential Diagnosis table).
Assess Nystagmus
A test for nystagmus assesses the function of the
vestibular branch of the acoustic nerve (cranial nerve
VIII). The presence and characteristics of nystagmus
are important in determining central versus peripheral causes of vertigo. Nystagmus is dened by the
axis on which it occurs (horizontal, vertical, rotary,
or mixed) and by the direction in which it occurs.
Nystagmus is composed of quick and slow components that can be observed. With the eye xated, a
slow drift away from the position of xation is corrected by a quick movement back to the original
position. The direction of the nystagmus is determined by the quick component because it is easier to
see. The quick component depends on the interaction
between the vestibular system and the cerebral cortex and represents the compensatory response to
vestibular stimulation. The slow component moves
in the direction of the movement of the endolymph,
a clear uid within the membranous labyrinth of the
inner ear.
Fixed nystagmus, which always beats in the same
direction, occurs with peripheral disorders of BPPV,
Meniere disease, vestibular neuronitis, or labyrinthitis.
Vestibular nystagmus typically consists of a horizontalrotary, jerk motion of both the slow and fast components.
The nystagmus associated with central causes can be
horizontal, vertical, rotary, or inconsistent. Pronounced
152
https://t.me/med1917
Chapter 13 • Dizziness
Table 13-1
Comparison of Nystagmus
in Central and Peripheral
Vertigo
CHARACTERISTICS CENTRAL PERIPHERAL
Severity Can be dispropor-
Axis Horizontal, vertical,
Consistency of
direction
Type Irregular or
tionate to vertigo
rotary; unidirectional upgaze or
downgaze
Can be inconsistent Consistent;
rapid in both
directions
rotary, unidirectional upgaze or downgaze nystagmus
always arises from central processes. Nystagmus that
is equally rapid in both directions is characteristic
of central causes. In vertigo of peripheral origin, nystagmus generally resolves on xation within 24 to
48 hours, whereas nystagmus associated with central
vertigo does not. See Table 13-1 for a comparison of
characteristics.
Perform Positional Nystagmus Testing/Provoking
Maneuvers
If the patient does not have nystagmus at rest, perform
position testing or provocation maneuvers.
Positional Maneuver (Dix-Hallpike Maneuver)
To determine the origin of vertigo and accompanying
nystagmus, seat the patient on the table with the patient’s head turned to the left or right at 45 degrees. Holding the head in that position, quickly lower the patient
to a lying position with the head 20 to 30 degrees
Proportionate
to vertigo
Horizontal,
rotary
always beats
in same
direction
Has both slow
and quick
components
lower than the table edge so that the ear faces the
oor. Repeat with the head turned to the other side
and then again with the head in the midline. The
maneuver produces intense vertigo in patients with
vestibular problems and can cause mild vertigo in patients with central causes. The patient’s eyes should be
kept open to observe the duration and direction
of nystagmus. The nystagmus associated with peripheral causes has a 3- to 10-second delay in onset,
lessens with repetition, and is in a xed direction (see
Evidence-Based Practice box). In contrast, the nystagmus associated with central causes begins immediately, does not fatigue with repetition, and can occur
in any and changing directions. With inner ear damage, the rapid phase of nystagmus is always in the
same direction regardless of the direction of gaze. For
a demonstration of the maneuver see www.youtube.
com/watch?v5kEM9p4EX1jk.
Provocation Maneuvers
In patients who experience vertigo associated with
position changes or rapid movement of the head, provoke nystagmus and vertigo by having the patient assume the positions that cause the vertigo. Provocation
assists in the diagnosis of BPPV. If you suspect a perilymph stula, perform pneumatic otoscopy. The pressure applied to the middle ear can provoke nystagmus
and vertigo.
Assess the Vestibular Ocular Reflex
Assessment of the vestibular ocular reex (VOR) is
useful in conrming a vestibular origin of vertigo and
in determining which labyrinth is abnormal. This is
demonstrated when the head is moved in the direction
of the damaged labyrinth (or vestibular nerve). Assess
the VOR using the head impulse (head thrust test)
(Figure 13-1). The test assesses horizontal semicircular
canal function. Hold the patient’s head and ask him/her
to xate on your nose. Then very quickly thrust the
EVIDENCE-BASED PRACTICE
In this systematic review the authors conclude that the reference standard for BPPV is a positive Dix-Hallpike maneuver
(intense vertigo and fixed nystagmus with a 3- to 10-second
delay in onset). The conclusion is based on randomized trials
that demonstrate the success of canalith repositioning procedures in patients with no focal neurologic findings or central
Data from David L, Simel DL, Froehling DA, Bedlack R: Update: Vertigo. In DL Simel, R Drummond (eds.): The rational clinical examination: Evidence-
based clinical diagnosis,
New York, 2009, McGraw Hill.
Dix-Hallpike Maneuver to Diagnose BPPV
nervous system disease, whose diagnosis of BPPV is confirmed with the Dix-Hallpike maneuver. The randomized trials
demonstrated that within 1 month of treatment, patients with
a positive Dix-Hallpike maneuver benefit from the repositioning procedures with symptom resolution, and that the
Dix-Hallpike maneuver result returns to normal.
A
https://t.me/med1917
B C
FIGURE 13-1 VOR or head thrust test. (From Cameron MH,
Monroe LG: Physical rehabilitation: Evidence-based examination, evaluation, and intervention, St. Louis, 2007, Saunders.)
patients head to one side. In healthy patients the VOR
is intact, and when the head is rotated, the eyes will
remain xed on your nose regardless of the head position. If the VOR is unilaterally impaired, when the
head is rotated the patient’s eyes will momentarily
move with the head and lose their xation on your
nose. Look for one or more catch up corrective eye
movement directed back towards your nose. This quick
corrective eye movement is the abnormality. Carry out
several trials in each direction, in no recognizable pattern. In a patient with a labyrinthine abnormality, the
eyes will move with the head when turned to the side
of the abnormality.
Chapter 13 • Dizziness
153
Perform Neurological Examination
Look for brainstem or cerebellar dysfunction, which
could cause abnormal neurological ndings. Specically test cranial nerves, looking for sensory and/or
motor decits. With the exception of hearing loss, cranial nerve function should be normal in patients with
peripheral vertigo. Patients with brainstem dysfunction
typically have diplopia and changes in sensory and
motor function.
Test cerebellar function. Testing gait differences while
blindfolded can be helpful. Ataxia from bilateral vestibular loss is worsened by loss of visual input, whereas
ataxia from cerebellar disease remains about the same.
The sensitivity of gait testing is increased by watching
tandem gait (heel to toe). When trying to walk a straight
line, the patient with a cerebellar lesion will tend to fall
toward the side of the lesion. However, gait disturbances
can also be present with peripheral vertigo.
Test the patient’s ability to perform rapid alternating
movements (RAMs) either through pronation-supination
or through touching thumb to ngers sequentially. Movements should be smooth and rhythmic, and the patient
should be able to gradually increase speed. Stiff, slowed,
or jerky movements indicate cerebellar dysfunction.
Perform the past-pointing test. Have the patient sit
with one arm extended forward and the index nger
pointed while you sit in the same position facing the
patient. The tips of your ngers should touch. Then ask
the patient to close the eyes, raise the arm above the
head, and bring the arm and nger back to the same
position. In patients with central lesions or unilateral
vestibular abnormalities, the arm will deviate toward
the side of the lesion.
Test sensory and motor function. Look for focal
decits that can occur with central vertigo. Many patients with vertigo also report generalized weakness;
therefore it is important to distinguish between generalized weakness and focal motor impairment caused by
brainstem disorder.
EVIDENCE-BASED PRACTICE
This study of 103 patients assessed the sensitivity, specificity, and positive and negative predictive value of the Romberg
Test of Standing Balance on Firm and Compliant Support
Surfaces (RTSBFCSS) for the identification of patients with
vestibular system impairments. The criterion standards were
the caloric test and the cervical vestibular evoked myogenic
Data from Jacobson GP, McCaslin DL, Piker EG, et al: Insensitivity of the “Romberg test of standing balance on firm and compliant support surfaces” to the results of caloric and VEMP tests, Ear Hear 32: 5, 2011.
Romberg Test to Assess Balance?
potential (cVEMP) test. Sensitivity ranged from 55% to 61%,
and specificity ranged from 58% to 64%. Positive and negative predictive values ranged from 39% to 55% and 64% to
78% respectively. The authors concluded that the RTSBFCSS
is a test of balance, not vestibular function, and should not
be used as a screening measure for vestibular impairment.
154
https://t.me/med1917
Chapter 13 • Dizziness
Perform Cardiovascular Evaluation
Note the heart rate and rhythm and attempt to detect
dysrhythmias. Auscultate carotid and temporal arteries
for bruits that can alert you to a cardiovascular cause
for the vertigo.
Congenital heart disease can produce episodes of
syncope that might be falsely interpreted as vertiginous
episodes (see Chapter 33).
LABORATORY AND DIAGNOSTIC STUDIES
Audiometry
Audiometry is used to quantify hearing loss. The
patient is tested at specic frequencies (pure tones)
and specic intensities. Hearing loss is measured in
decibels. Audiometry is used anytime the patient
presents with both vertigo and hearing loss (i.e.,
Meniere disease, acoustic neuroma, labyrinthitis,
perilymph stula, or use of ototoxic medications)
(see Chapter 15).
Electronystagmography
Electronystagmography (ENG) electronically detects
nystagmus that cannot be detected visually. Vestibular
function is evaluated using gaze testing, positional
changes, and caloric stimulation. Eye movements are
recorded electronically. Caloric stimulation is produced
by ear irrigation with warm and then cool water.
ENG is most useful in diagnosing chronic peripheral disorders (i.e., Meniere disease and persistent
BPPV) to determine the degree and progression of the
vestibular decit. It can also be useful in patients with
psychogenic vertigo to provide reassurance that no
organic disease is present.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) of the brain is indicated when the history and physical examination
point to acoustic neuroma or a central cause of the
vertigo. Consider urgent MRI if vertigo is of sudden
onset; is accompanied by severe headache, directionchanging nystagmus, or neurological signs; or if the
patient has risk factors for stroke.
Computed Tomography
Computed tomography (CT) scanning of the brain is
indicated whenever there is persistent vertigo and in all
cases with additional signs of neurological disturbance.
In patients with medical conditions such as renal failure, hypertension, or a hematological malignancy and
who have sudden onset of vertigo, CT scanning is used
to look for hemorrhage into the cerebellum, brainstem,
or labyrinth.
Electroencephalography
An electroencephalogram (EEG) should be obtained
for patients who have vertigo associated with alterations of consciousness.
Cardiac Monitoring
An electrocardiogram (ECG) or Holter monitoring can
provide conrmatory information on cardiovascular
causes of vertigo.
Hematology and Urinalysis
Complete blood count (CBC) can reveal anemia, which
can cause presyncopal light-headedness. Urine or
serum glucose levels will detect diabetes mellitus,
which can produce vertigo. Urine testing and blood
urea nitrogen (BUN) level can reveal renal failure,
which can also be associated with vertigo.
Serological Testing for Syphilis
Because secondary syphilis or early tertiary syphilis
can produce the same symptoms that occur in Meniere
disease, screening high risk individuals is advocated to
rule out syphilis as a cause.
DIFFERENTIAL DIAGNOSIS
Central Causes
Brainstem Dysfunction and Cerebellar Dysfunction
Central vertigo produced by disorders of the brainstem and cerebellum is usually caused by neoplastic
or vascular processes including recurrent intermittent vascular insufciency, transient ischemic
attack, and stroke. Neoplasms are usually slow growing; therefore vestibular dysfunction is of gradual
onset and usually manifests as a problem with
equilibrium.
Vascular causes are more common and can produce
acute-onset, long-lasting, or recurrent transient episodes
of vertigo. Patients usually manifest other neurological
decits. With brainstem disorders, patients can have reports of diplopia, dysarthria, dysphagia, and paresthesia.
They can demonstrate sensory and motor decits. Cerebellar dysfunction usually results in gait disturbance
and difculties in ne motor coordination, including
rapid alternating movements (RAM) and nger-tonger testing.
Chapter 13 • Dizziness
https://t.me/med1917
155
Multiple Sclerosis
Multiple sclerosis can produce a range of neurological
symptoms. Vertigo occurs in up to 50% of patients
with multiple sclerosis. Disease onset is usually in the
third or fourth decade of life. MRI shows characteristic
demyelinating plaques.
Migraine Headache
Approximately 30% of people with migraine headaches
have vertigo. It can be present before the headache begins, during the headache, or independent of the headache. Patients with vestibular-type migraine headaches
often experience photophobia, phonophobia, and visual
aura during the episodes of vertigo. Patients with
basilar-type migraine may have other symptoms consistent with vertebrobasilar vascular abnormalities such as
visual changes, tinnitus, decreased hearing, ataxia, or
paresthesia. Diagnosis is usually made on the basis of
the history.
Peripheral Causes
Benign Paroxysmal Positional Vertigo
Episodes of BPPV are characterized by acute onset of
vertigo associated with rapid head movement or position
changes. Many women report dizziness with position
change around the time of their menses. The episodes
are brief, lasting a few seconds. Nystagmus can be elicited by the Dix-Hallpike maneuver. Testing positional
changes can provoke the vertigo. There is no hearing
loss. Diagnosis is made on the basis of the history and
clinical ndings. This is one of the most common causes
of vertigo, especially in older adults. In patients with
BPPV, tiny crystals of calcium carbonate (otoliths) in
the inner ear that monitor head position relative to gravity become dislodged and migrate into one of the semicircular canals. When the head moves, the gravity-dependent movement of the otoliths in the affected
semicircular canal causes endolymph displacement and
a sensation of vertigo.
Benign Paroxysmal Vertigo of Childhood
Benign paroxysmal vertigo (BPV) of childhood occurs
most often in children 2 to 3 years old. The disorder
tends to be recurrent with one to four episodes per
month. The episodes occur suddenly and are often
associated with vomiting, pallor, sweating, and nystagmus. The neurological and audiological examinations
produce normal ndings. Some children can have a
hypoactive or absent response to caloric testing (ear
irrigation with warm and then cool water).
Meniere Disease
Meniere disease is characterized by a classic triad of
symptoms: vertigo, hearing loss, and tinnitus. A sensation
of ear fullness can also be present. The attacks are abrupt
and recurrent and last for minutes to several hours. The
interval between attacks can be weeks or months. Be-
tween episodes, the patient is asymptomatic. On physical
examination, sensorineural hearing loss is present in the
affected ear, or it can be bilateral. Nystagmus is lateral
or rotary. The visual ocular reex will lateralize to the
symptomatic ear.
Vestibular Neuronitis
Vestibular neuronitis is frequently preceded by an acute
viral infection. These patients usually present with severe
vertigo, nausea, and vomiting. The vertigo lasts for days
to weeks. Remaining completely motionless can help al-
leviate the symptoms. Auditory function is not affected.
Physical examination reveals nystagmus that intensies
in amplitude when the gaze is directed away from the af-
fected ear. Visual xation minimizes the nystagmus. The
visual ocular reex will lateralize to the affected side.
Labyrinthitis
Frequently associated with a concurrent viral or bacterial
illness, labyrinthitis produces severe vertigo that lasts for
several days. Labyrinthitis can be a complication of otitis
media or meningitis. This condition is distinguished from
vestibular neuronitis by the accompanying hearing loss
that occurs as a result of destruction of the inner ear. The
visual ocular reex will lateralize to the affected side.
Acoustic Neuroma
Also called a vestibular schwannoma, acoustic neu-
roma is a benign tumor that originates most often in the
vestibular portion of the acoustic nerve (cranial nerve
VIII). It usually causes unilateral sensorineural hearing
loss, tinnitus, and loss of equilibrium. The neuroma
grows slowly; therefore loss of equilibrium is more
often a symptom than is vertigo. Acoustic neuroma can
also occur in the trigeminal nerve (cranial nerve V)
with symptoms of paresthesia consistent with the nerve
distribution. Large tumors of the abducens nerve (cranial
nerve VI) can compress the brainstem.
Perilymph Fistula
Fistula formation can occur as a result of ear trauma,
from a direct blow, secondary to otologic surgery, or
indirectly from straining, coughing, or pressure
changes. In this condition there is leakage of perilymph
156
https://t.me/med1917
Chapter 13 • Dizziness
from either the round or the oval window into the
middle ear. Sensorineural hearing loss and vertigo are
frequently present. The stula will often heal spontaneously but sometimes can require surgery.
Sinusitis and Otitis
Serous otitis, otitis media, and sinusitis can cause disruption of the vestibular apparatus, producing vertigo. History and physical examination ndings will be consistent
with the specic disorder (see Chapters 15 and 25).
Cholesteatoma
Collection of squamous debris, often associated with
chronic middle ear infection, can form a cholesteatoma,
which enlarges and destroys structures in its way. On
physical examination, the cholesteatoma will appear as
a shiny white irregular mass. Foul-smelling discharge
may be evident, and there may be visible bone destruction. Conductive hearing loss can be present.
Systemic Causes
Psychogenic
Psychogenic causes of vertigo are common. Patients often describe themselves as anxious or nervous and may
have psychiatric diagnoses (see Chapter 4). Their symptoms are vague and imprecise. Neurological examination
is normal. No nystagmus is present or elicited. The vertigo can be reproduced with hyperventilation. MRI can
be useful to provide reassurance.
Cardiovascular
Orthostatic hypotension and cardiac dysrhythmias can
produce vertigo. Postural hypotension can be diagnosed by taking orthostatic blood pressure readings.
The diagnosis of cardiac conditions can involve CBC,
blood chemistry, ECG, cardiac stress testing, and
echocardiography.
Neurosyphilis
Secondary or early tertiary syphilis can present with
symptoms similar to those of Meniere disease. The patient demonstrates various clinical symptoms, including
papilledema, aphasia, monoplegia or hemiplegia, cranial nerve (CN) palsies, pupillary abnormalities, or
focal neurological decits. The Argyll Robertson pupil,
which occurs almost exclusively in neurosyphilis, is
a small irregular pupil that reacts normally to accommodation but not to light. Serological testing will be
positive for syphilis.
Other Causes
Ototoxic Drugs and Drugs Causing Salt Retention
Medications that are ototoxic, salt-retentive, or psychotropic can produce vertigo, light-headedness, or
unsteadiness. Drugs causing salt retention include
steroids and phenylbutazone. Ototoxic medications
include aspirin, ethacrynic acid, streptomycin, gentamicin, aminoglycosides, and furosemide. Psychotropic drugs can also produce vertigo. Ototoxic
drugs can produce a sensorineural hearing loss.
Audiometry should be performed with any noted
hearing loss.
Trauma
Injury to the head or ear from labyrinthine concussion,
temporal bone fracture, or perilymph stula can produce
disturbance of the vestibular apparatus and result in vertigo. Head trauma can also produce cerebral concussion
involving the anterior tip of the temporal lobe. Trauma
from otologic procedures can also cause vertigo.
DIFFERENTIAL DIAGNOSIS OF
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
CENTRAL CAUSES
Brainstem
dysfunction/
cerebellar
dysfunction
Multiple sclerosis Onset is often in third or
Migraine
headache
Common Causes of Dizziness
Elderly; acute-onset;
recurrent vertigo; tinnitus;
hearing OK
fourth decade of life
Headache history; other
migraine symptoms
Symptoms of brainstem/vertebrobasilar
vascular abnormality: ataxia, double
vision; lack of coordination; sensory/
motor deficits; vertical, lateral, rotary
nystagmus; hearing normal; cerebellar:
impaired RAM, finger-to-finger testing
Can have no other findings or can have
other neurological symptoms
Can have symptoms of vertebrobasilar
vascular abnormalities, as above
MRI
MRI
None
Chapter 13 • Dizziness
https://t.me/med1917
157
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Dizziness — cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
PERIPHERAL CAUSES
Benign paroxys-
mal positional
vertigo (BPPV)
Benign paroxys-
mal vertigo of
childhood
Meniere disease Sudden onset; lasts hours,
Vestibular
neuronitis
Labyrinthitis Sudden onset, lasts hours to
Acoustic neuroma Adults; gradual onset; mild
Perilymph fistula History of trauma; hearing
Otitis/sinusitis Pain in ear or face; history of
Cholesteatoma History of chronic middle ear
Adults: associated with posi-
tional changes; recurrent
episodes; lasts seconds to
minutes; some relief if
motionless
Children: usually 2-3 yr old,
sudden onset with crying
by child
recurrent; tinnitus and
fullness in ears
Sudden onset; antecedent
viral infection
days
vertigo; persistent tinnitus;
facial numbness, weakness
loss
ear or sinus infections;
gradual onset of vertigo
infections
Lateral or rotary nystagmus; no tinnitus or
hearing loss
Vomiting, pallor, sweating, and nystagmus
common; no loss of consciousness;
neurological and audiological examination can be normal
Lateral or rotary nystagmus; fluctuating
hearing loss: low tones; sensorineural
Nausea and vomiting; nystagmus; no hear-
ing loss, loss of equilibrium always to
the same side
Can currently be ill; lateral nystagmus;
hearing loss; rarely tinnitus; nausea and
vomiting can be present
Unilateral hearing loss, poor speech
discrimination
Nystagmus and vertigo with pneumatic
otoscopy; sensorineural hearing loss
Serous otitis, otitis media; tenderness
over sinuses; purulent nasal discharge;
no nystagmus
Shiny white irregular mass on otoscopic
examination; foul-smelling discharge
can be present; bone destruction can be
visible; conductive hearing loss can be
present
Provoke nystagmus
and vertigo by
position that
causes response;
Dix-Hallpike
maneuver; ENG
Can have hypoactive
or absent response
to caloric testing
Positional maneuvers,
positive VOR
test, audiometry,
ENG
Positional maneu-
vers; positive
VOR test
Positional maneuvers,
positive VOR test,
audiometry
MRI; audiometry
Audiometry
See Chapters 15
and 25
Audiometry
SYSTEMIC CAUSES
Psychogenic
Cardiovascular Cardiovascular history;
Neurosyphilis
Vague symptoms; recurrent;
can describe self as
anxious; can have other
psychiatric diagnoses
antihypertensive
medications
Vertigo, tinnitus, fullness
in ears
Normal neurological and auditory
examinations
Orthostatic blood pressure; dysrhythmias;
carotid or temporal bruits
Various clinical symptoms; papilledema,
aphasia, monoplegia or hemiplegia,
central nervous palsies, pupillary abnormalities, Argyll Robertson pupil; focal
neurological deficits
Hyperventilation to
reproduce the
vertigo
Depends on client
condition and
symptoms
Serology for syphilis
Continued
158
https://t.me/med1917
Chapter 13 • Dizziness
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Dizziness — cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
OTHER CAUSES
Ototoxic and salt-
retaining drugs
Trauma
BPPV, Benign paroxysmal positional vertigo; CT, computed tomography; ENG, electronystagmography; MRI, magnetic resonance imaging; RAM, rapid
alternating movements.
References and Readings
Benun J: Balance and vertigo in children, Pediatr Rev 32:84, 2011.
Casselbrant ML, Mandel EM: Balance disorders in children, Neurol
Clin 23:807, 2005.
Clark MM: How to sort out a complaint of dizziness, Patient Care
37:44, 2003.
Fetter M: Assessing vestibular function: Which tests, when? J Neurol
247:335, 2000.
Froehling DA, Silverstein MD, Mohr DN, Beatty CW: Does this
dizzy patient have a serious form of vertigo? JAMA 271:385,
1994.
Hanley K, O’Dowd T, Considine N: A systematic review of vertigo
in primary care, Br J Gen Pract 51:666, 2001.
Kerber KA: Vertigo and dizziness in the emergency department,
Emerg Med Clin North Am 27:39, 2009.
Medication history: steroids,
phenylbutazone, ethacrynic
acid, aspirin, streptomycin,
gentamicin, aminoglycosides, furosemide,
psychotropic drugs
History of trauma to head
or ear
Sensorineural hearing loss Audiometry
Depends on nature and location of injury;
can exhibit peripheral or central
symptoms
Labuguen R: Initial evaluation of vertigo, Am Fam Phys 73:244,
2006.
Maarsingh OR, Dros J, Schellevis FG, et al: Causes of persistent
dizziness in elderly patients in primary care, Ann Fam Med 8:196,
2010.
Murdin L, Seemungal BM, Bronstein AM: Dizziness, Medicine
40:431, 2012.
Seemungal BM, Bronstein AM: A practical approach to acute vertigo,
Pract Neurol 8:211, 2008.
Valente M, McCaslin DL: Vestibular disorders and evaluation of the
pediatric patient, ASHA Leader 16:3, 2011.
Wiener-Vacher SR: Vestibular disorders in children, Int J Audiol
47:578, 2008.
Woodworth, BA, Gillespie MB, Lambert PR: The canalith reposi-
tioning procedure for benign positional vertigo: A meta-analysis,
Laryngoscope 114:1531, 2009.
MRI/CT
Соседние файлы в папке Библиотека им академика М.И. Перельмана