12.Wk9Assgn
Dizziness
D izziness is a symptom of a variety of conditions, including vertigo, lighthead
c:dneSS, and loss of balance. ln children, the symptom is frequently a new sensation and is usually poorly defined. Family members often state that the child has trouble walking • is irritable or that the child's behavior is cifferent. Older children, like adults, tend to c:Sgorize everything from lightheadedness ID(f unsteadiness to spinning and falling as dizziness. This chapter is limited to the dis cussion of vertigo. Patients with vertigo have die sensation of either their body moving (subjective vertigo) or their environment moving around them (objective), usually de scnbed as a spinning or rotary motion.
The sensation of balance depends on inter CD1DeCtions among the visual, vestibular, and semory systems. Vertigo can be thought of as a disruption of one of these three systems. Vertigo can be central, involving the brain *'° or cerebellum; be peripheral, involving 6e inner ear or vestibular apparatus; or result &om systemic causes.
Central vertigo is generally either neoplas tic or vascular in origin, although any central nervous system disorder, such as multiple 1elerosis, that disrupts the pathway between the vestibular apparatus and the brain can re sult in dizziness. Common vascular causes include recurrent intermittent vascular insuf ficiency, transient ischemic attack, or stroke. Migraine head.ache is a vascular-related central cause of vertigo.
Peripheral vertigo is typically produced by '-uption of the inner ear or vestibular appa lltbs. Common causes include idiopathic eti ologies, canalithiasis (tiny crystaJs of calcium carbonate migrate from their usual position 1o the semicircular canals), vestibular nerve ilOamm.ation, inner ear inflammation or in ~ or tumor. Systemic origins include
psychogenic, cardiovascular, and metabolic causes. Mixed or other causes include trauma and ototoxicity.
DIAGNOSTIC REASONING: FOCUSED HISTORY
What does the patient mean by dizziness?
Key Questions • Can you describe how you feel when you
are dizzy? • Do you feel yourself or the room spinning? • Do you feel your balance is off? • Do you feel like you are about to faint?
Sensation Vertigo produces the sensation of either the patient spipning or the environment spinning around the patient. Some patients describe a sensation of their body moving forward or accelerating.
Patients can also report loss of equilibrium accompanying the vertigo. Neoplasms and progressive vestibule loss typically produce a change in vestibular function that is slow in onset and manifested as imbalance.
Loss of balance and lack of coordination in the absence of vertigo can be the result of degenerative, neoplastic, vascul ar, or metabolic disorders. With these symptoms, look for other nervous system abnormalities. Imbalance can also occur in adults as a result of impaired sensory input, either visual or kinetic, such as occurs with peripheral neuropatby.
When interviewing children, using words such as swinging or being on a merry-go round helps give them ways to describe the feeling. Children who have a vague sense of unsteadiness can have peripheraJ neuropathy or a dysfunction of the vestibular or cerebellar
171
Chapter 13 • Dizziness
system, but children who report a feeling of motion are more likely to have an abnonnality of the vestibular system.
In contrast to dizziness and imbalance, lightheadedness is the feeling that one is about to faint (near syncope). Some patients describe it as a generalized weakness and the feeling that they are about to pass out if they do not lie down. True syncope, or a sudden transient loss of consciousness, with concur rent loss of postural tone, always has a spon taneous recovery (see Chapter 33).
Orthostatic hypotension is a frequent cause of lightheadedness and is most common in older patients, occurring as a result of abnor mal regulation of blood pressure. Neurologic causes of orthostatic hypotension are less common and are usually accompanied by neurologic findings.
In both children and adults, a report of lightheadedness can accompany anemia, hy poglycemia, or hyperventilation syndrome.
Is the vertigo from a systemic cause?
Key Questions • What other health problems do you have? • Would you describe yourself as anxious or
nervous? • Do the episodes occur with any specific
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 re duction in cardiac output that obstructs blood flow within the heart or pulmonary circula tion; 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 pos tural 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 thern. selves as anxious or nervous. Patients ca also have other psychiatric diagnoses. Stress~ ors and tensions affecting children, such as divorce, custody battles, and day care, can cause vertiginous-like symptoms in an 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 roll ing over in bed, is usually caused by vertigo. However, unsteadiness while walking is con sidered to be disequilibrium, which can be caused by many factors. Dizziness on stand ing can be the result of decreased cerebral perfusion.
In children, episodes of dizziness that oc cur 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 • Do you have migraine headaches? • Do you have other symptoms that bother
you? • Do you have nausea and vomiting? • When do the episodes occur?
Headaches Headache is a vascu lar-related cause of central vertigo. Approximately one-third of patients with migraine headaches experi ence vertigo. The vertigo can appear as an aura occurring during the headache or separately. Patients with vestibular-type migraine headaches often experience photo phobia, phonophobia, and visual aura during the episodes of vertigo. Patients with basi lar-type migraines can have other symptoms consistent with vertebrobasi lar 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 centra l vertigo nearly a lways have neurologic symptoms such as double vision, facial numbness, and hemiparesis.
Cerebellar causes can produce other symp toms, such as loss of balance, that closely re semble those ofa peripheral disorder; therefore neurologic examination findings are important in differentiating the two. Pay particular atten tion to reports of motor dysfunction or lack of coordination.
Vertigo that is peripheral in origin does not produce additional neurologic signs or symp toms. 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 first ansmg in the morning is usually the result of a vestibular disorder. Vertigo that occurs while turning over in bed is characteristic of benign parox ysmal positional vertigo (BPPV).
What do characteristics ofthe episodes tell me?
Key Questions • How long do the episodes of dizziness
last? • Is the onset sudden or gradual? • Do you have any hearing loss? • 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 com monly produced by vestibular neuronitis. Pa tients us ually fee l better when they lie com pletely still. Stroke can also produce long-lasting episodes. The two can be differentiated based
Chapter 13 • Dizziness
on medical history and physical examination findings.
Sudden onset of prolonged dizziness (las ting :> 60 minutes) s uggests central causes such as infection, brainstem infarc tion , inflammation, or vestibular hemor rhage. Trauma can also produce prolonged dizziness.
The child with chronic recurrent dizziness (episodes lasting < 30 minutes) can have cen tral causes such as seizure problems or migraine headache. The cause can also be peripheral, such as BPPV. Chronic persistent episodes can indicate brainstem lesions, ane mia, diabetes, thyrotoxicosis, or a psychoso matic 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 charac teristic of labyrinthitis, Meniere disease, stroke, or vertebrobasilar causes.
Recurrent episodes are typical of BPPV, vertebrobasilar causes, and Melliere disease.
Hearing Loss and Tinnitus A classic triad of symptoms-vertigo, hear ing loss, and tinnitus-defines Meniere dis ease. Patients can also report a sensation of fullness in the ears. The hearing loss can be unilateral or bilateral. Patients with second ary or early tertiary syphi li s can have symp toms identical to those of Meniere disease. Tinnitus, hearing loss, and ear pain point to lesions in the inner ear or acoustic nerve (cranial nerve [CN] VIII).
Patients with labyrinthitis and perilym phatic fistulas may a lso experience hearing loss but without tinnitus. An acoustic neu roma will produce unilateral hearing loss with tinnitus . Patients with recurrent vestibulopa thy u s ually do not report hearing loss.
What else should I consider?
Key Questions • What medications are you taking? • Are you now or have you recently been ill?
Chapter 13 • Dizziness
• Have you had any recent injury to your head ? Did y ou have dizziness before the head injury?
• Have you had any previous ear surgery?
Medications Mediations that are salt-retaining or ototoxic can produce vertigo, li g htheadedness , or unsteadiness. Salt-retaining drugs include steroids and phenylbutazone. Ototoxic medi cations include ethacrynic acid, streptomycin, gentamicin, aminog lycosides, aspirin, and furosem ide.
Psychotropic drugs can a lso produce ver tigo. Antihypertensive drugs can cause hypo tension leading to ligbtheadedness. Sedatives, alcohol, and anticonvulsants can cause a sense of disequilibrium.
Current or Recent Illness Vestibular neuronitis is associated with recent v iral infection, often an upper respiratory tract infection. If a patient is currently ill, consider labyrinthitis because it is frequently associ ated with concomitant b acterial and viral in fection. Current ear or sinus infection can produce dysfunction of the vestibular appara tus, resulting in vertigo. Recent abnormalities of middle ear ventilation and middle ear effu sion are the most common cause of balance disturbance in childhood. In balance distur bance, transmission of pressure gradients through the labyrinthine w indows to the inner ear fluids and the vestibu lar sen sory receptors is a ltered.
History of Head Trauma Trauma to the head or ear can cause distur bance of both peripheral and central balance mechanisms. Certain traumas can cause acute destruction of the inner ear and pro duce vertigo. Direct trauma can occur to the labyrinth from a tempora l bone fracture. A blow to the head or a whiplash injury can a lso produce a concussive effect on the laby rinth. Children who have a history of head trauma can present with vertigo caused b y labyrinthine damage.
Vertigo often occurs as a residual symptom and usually gradually improves over the course of a year. Trauma can also produce a
fistula between the middle and inn· er causi n g tympanic membrane (TM) da eai, and ossicle disruption. fl'lage
Previous Otology History and Procedu res Patients vvith cholesteatoma usually h
· f hr · ·ddl · ave ahistory o c on1c mi e ear mfection rhea, and conductive hearing loss. Prior'~~ cal procedures of the ear can produce perj~ eral vertigo through disruption of ~ vestibular apparatus o r throu gh formati on of perilymph fistula. a
DIAGNOSTIC REASON I N G: FOCUSED PHYSICAL EXAMINATI ON Take Vital Signs and Note Blood Pressure Assess orthostatic blood pressure to rule ow postural hypotension as the cause of vertigo. Assessment is made by measuring the blOOd pressure in both the supine and standing posj. tions. A drop in arterial blood pressure of at least 30 mm Hg systol ic 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 vvh o is currently ill , suspect laby rinthitis. In a patient who is acutely nauseated and vomiting, suspect vestibular neuronitis.
Have the Patient Hyperventilate and Perform Valsalva Maneuver Perform this testing if you s uspect psycho genic vertigo because the maneuver can re produce the vertigo in these p a ti e nts. Ask the patient to perform a Valsalva maneuver and to breathe in and out or blow vig orously for I to 3 minutes.
Perform Vision Examination A recent change in visual acuity or new cor· r ective lenses can cau se transient episodes of imbalance.
Perform Ear Examination Look for the presence of e ffi.Js ion or infection that signal s serous otitis or otitis media. Look for the presence of a cho lesteatoma. It will
Chapter 13 • Dizziness
appear as a shiny, white, irregular mass; foul smelling discharge can also be present. Note the integrity of the TM; trauma can some times 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 fistula, 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 (later alization) tests. Expect sensorineural loss with Meniere disease, labyrinthitis, perilymph fis tula, and acoustic neuroma. In sensorineural loss, the sound lateraliz es 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 cholestea toma, serous otitis, or otitis media may have conductive hearing loss (see Differential Diagnosis table).
Assess Nystagmus A test for nystagrnus assesses the function of the vestibular branch of the acoustic nerve (CN VIII). The presence and characteristics of nystagmus are important in determining central versus peripheral causes of vertigo. Nystagmus is defined by the axis on which it occurs (horizontal, vertical, rotary, or mixed) and by the direction in which it occurs. Nys tagmus is composed of quick and slow com ponents that can be observed. With the eye
fixated , a slow drift away from the position of fixation 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 cere bral cortex and represents the compensatory res ponse to vestibular stimulation. The slow component moves in the direction of the movement of the endolymph, a clear fluid 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, vestibu lar neuronitis, or labyrinthitis. Vestibular nys tagmus typically consists of a horizontal rotary, jerk motion of both the slow and fast components. The nystagmus associated with central causes can be horizontal, vertical, ro tary, or inconsistent. Pronounced rotary, uni directional upgaze or downgaze nystagrnus always arises from central processes. Nystag mus that is equally rapid in both directions is characteristic of central causes. In vertigo of peripheral origin, nystagmus generally re solves on fixation within 24 to 48 hours, whereas nystagmus associated with central vertigo does not. See Table 13.1 for a com parison of characteristics.
Perform Positional Nystagmus Testing or Provoking Maneuvers If the patient does not have nystagmus at rest, perform pos ition testing or provocation maneuvers.
Table 13.1 Comparison of Nystagmus in Central and Peripheral Vertigo
CHARACTERISTICS CENTRAL PERIPHERAL
Severity Axis
Consistency of direction
Can be disproportionate to vertigo Horizontal, vertical, rotary; unidi
rectional upgaze or downgaze Can be inconsistent
Proportionate to vertigo Horizonta I, rotary
Consistent; a lways beats in same direction
Type Irregular or rapid in both directions
Has both slow and quick components
Chapter 13 • Dizziness
Posldonal maneuver (Dix-HaUpike maneuver)
To determine the origin of vertigo and accom panying nystagmus, seat the patient on the table with the patient's head turned to the left or right at 45 d egrees. Holding the h ead in this position , quickly lower the patient to a lyin g pos ition with the head 20 to 30 d egrees lower than the table edge so that the ear faces the floor. Repeat with the head turned to the other s ide and then again with the head in the midline. The maneu ver produces intense vertigo in patients with vestibular problems and can cause mild vertigo in patients with central causes. The patient's eyes sh ou ld be kept open to observe the dura tion and direction of nystagmus. The nystag mus associated with peripheral cau ses has a 3- to 10-second delay in onset, lessens with repetition, and is in a fixed direction (see Evidence-Based Practice box). In contrast, the nystagmus associated with central causes be gins immediately, does not fatigue with repeti tion, and can occur in any and changing direc tions. With inner ear damage, the rapid phase of nystagmus is always in the same direction
regardless of the direction of gaze. For a dein. onstration of the maneuve r, see httpJ/ youtube.com. Wl\' :
Provocation nraneuvers
In p a tients who experie n ce v~rtigo associa~ with pos ition changes or rapid movement of the head, provoke nystagmu s and vertigo by having the pa~ient assume ~he pos!tions that cause the vertigo. Provocation assists in the diagnosis of BPPV. If you s uspect a J>eri. lymph fi s tula, p erform pneumatic otoscopy, The pressure applied to the middle ear caq provoke n ystagmus and vertigo.
Assess the Vestibular Ocular Reflex A s sessment of the vestibu lar ocular reflex (VOR ) is u seful in confirming a vestibular origin of vertigo and in dete rmining which labyrinth is abnormal. T hi s is demonstrated when the head is moved in the direction of the damaged labyrinth (or vestibular nerve). Assess the VOR u sing the head impulse ( head thrust test) (Fig. 13 . l ). The test
B
FIGUR~ . 1~. 1 Ve~tibular ocu lar reflex or head thrust test. (From Cameron MH , Monroe LG : Physical rehab111tatt0n: Evidence-based examination, evaluation, and intervention , St. Louis, 2007, Saunders.)
Chapter 13 • Dizziness
2 EVIDENCE-BASED PRACTICE Dix-Hal/pike l \4a11e11ver to Diagnose Ben(t.:11 Paroxys11u1/ Positional Vertigo
In this systematic review, the authors con clude that the reference standard for benign paroxysmal positional vertigo (BPPV) is a pos itive 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 suc cess of canalith repositioning procedures in patients with no focal neurologic findings
or central nervous system disease, whose diagnosis of BPPV is confi rm ed with the Dix Hallpike maneuver. The randomized trials demonstrated that within 1 month of treat ment , patients with a positive Dix-Hallpike maneuver benefit from the repositioning pro cedures with symptom resolution and that the Dix-Hallpike maneuver result returns to normal .
Reference: David et al, 2009.
assesses horizontal semicircular canal func tion. Hold the patient's head and ask him or her to fixate on your nose. Then very quickly thrust the patients head to one side. In healthy patients, the VOR is intact, and when the head is rotated, the eyes will remain fixed on your nose regardless of the head position. If the VOR is unilaterally impaired, when the head is rotated, the patient' s eyes will mo mentarily move with the head and lose their fixation on your nose. Look for one or more catch-up corrective eye movements directed back toward 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.
Perform Neurologic Examination Look for brainstem or cerebellar dysfunction, which cou ld cause abnormal neurologic find ings. Specifically test CNs, looking for sen sory and motor deficits. With the exception of hearing loss, CN function should be nor mal in patients with periphera l vertigo. Pa tients with brainstern dysfunction typically have diplopia and changes in sensory and motor function.
Test cerebellar function. Testing gait dif ferences while the patient is blindfolded can be helpful. Whereas ataxia from bilateral ves tibular loss is worsened by loss of visual
input, 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, a 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 fingers sequentially. Movements should be smooth and rhythmic, and the pa tient should be able to gradually increase speed. Stiff, slowed, or jerky movements indi cate cerebellar dysfunction.
Perform the past-pointing test. Have the patient s it with one arm extended for ward and the index finger pointed while you sit in the same position facing the patient. The tips of your fingers should touch. Then ask the patient to close the eyes, raise the arm above the head, and bring the arm and finger back to the same position. In patients with central lesions or unilateral vestibular abnormali ties, the arm will deviate toward the side of the lesion.
Test sensory and motor function. Look for focal deficits that can occur with central vertigo. Many patients with vertigo also report generalized weakness; therefore, it is important to distinguish between genera l ized weakness and focal motor impairment caused by brainstem disorder.
Chapter 13 • Dizziness
2 EVIDENCE-BASED PRACTICE Ro111be1:~ Test to Assess Balance? This study of 103 patients assessed the sensitiv ity, specificity, and positive and negative predic tive value of the Romberg Test of Standing Bal ance on Firm and Comp liant Support Surfaces (RTSBFCSS) for the identification of patients with vestibular system impairments. The crite rion standards were the caloric test and the cervical vestibular evoked myogenic potential
(cVEM P) test. Sensitivity ranged from Sscy, to 61 % , and spec ificity ranged from 58% to 64%. Positive and negative predictive value~ r anged from 39% to 55% and 64% to 78cy, respectively. The authors concluded that tho, RTSBFCSS is a test of balance, not vestibulae function, and should not be used as a screeni/ measure for vestibular impairment. g
Reference: Jacobson et al, 2011.
Perform Cardiovascular Evaluation Note the heart rate and rhythm and attempt to detect d ysrhythmias. Auscultate carotid and temporal arteries for bruits that can alert you to a cardiovascu lar cause for the vertigo.
Con genita l heart disease can produce episodes of syn cope that mig ht b e falsely interpreted as vertiginou s e pisodes (see Chapter 33).
LABORATORY AND DIAGNOSTIC STUDIES Audiometry Audiometry is used to quantify hearing loss. The patient is tested at specific frequenc ies (pure tones) and specific intensities. Hearing loss is measured in d ecibels. Audiometry is used anytime the patient presents w ith both vertigo and hearing loss (i.e., Meniere dis ease, acoustic neuroma, labyrinthitis, peri lymph fistula , or use of ototoxic medications) (see Chapter 15).
Electronystagmography Electronystagmography e lectronica lly d e tects nystagmus that cannot be detected v is u a lly . Vestibular function is evaluated using gaze testing, pos itional changes, and ca loric stim ulation . Eye movements a r e recorded e lec tronically. Caloric stimulation is produced by ear irrigation with warm and then cool water.
E lectronystagmograph y is most u sefu l in diagnosi ng chronic peripheral disorders ( i.e. , Meniere disease a nd persistent BPPV) to determine the degree and progression of the vestibular deficit. It can also be u seful in
patients with psychogenic vertigo to provid reassurance that no organic di sease is presen~
Magnetic Resonance Imaging Magnetic res onance imag ing (MRI) of the brain is indicated when the hi story and physj. ca l examination point to acoustic neuroma or a central cause of the vertig o. Consider urgent MRI if vertigo is of sudden o n set; is accom. panied by severe h eadache, direction-changing nystagmus, or n eurologic s igns or if the pa. tient h as risk factors for stroke.
Computed Tomography Computed tomography (CT) scanning of the brain is indicated w h enever there is persistent vertigo and in all cases with additional signs of neurologic disturbance . In patients with medical conditions s uch as renal failure, by. pertension, or a hematologic malignancy and who have s udden onset of vertigo, CT scan ning is u sed t o look for h emorrhage into the cerebellum, brainstem, or labyrinth.
Electroencephalography An e lectroenceph a logram s hould be obtained for patients who hav e vertigo associated with alterations of consciousness.
Cardiac Monitoring An e lectrocardiogram or Holter monitoring can provide confirmatory in formation on car· diovas cular cau ses of vertigo.
Hematology and Urinalysis Complete blood count (CBC) can reveal ane mia, w hi c h can cause presyn copa l lighthead· edness. Urine or serum g lu cose levels will
detect diabetes m e lJitus, w h ich can produce ,-ertjgo. Urine testing and blood urea nitrogen (BUN) level can revea l renal fai lure, w hich can also be associated with vertigo.
serologic Testing for Syphilis Because secondary syphi lis o r early tertiary syphilis can produce the same symptoms that occur in Meniere disease, screening high-risk individuals is advocated to rule o ut syphi lis as a cause.
DIFFERENTIAL DIAGNOSIS
Central Causes
Brai11stem dysfunction and cer e b e llar dysf1111ction
Central vertigo produced by disorders of the brainstem and cerebellum is usually caused by neoplastic or vascular processes, including re current intermittent vascular insufficiency, tran sient ischemic attack, and stroke. Neoplasms are usually s low 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 recur rent transient episodes of vertigo. Patients usually manifest other neurologic deficits. With brainstem disorders, patients can h ave reports of diplopia, dysarthria, d ysphagia, and paresthesia. They can demonstrate sensory and motor deficits. Cerebellar d ysfunction usually res ults in gait disturbance and diffi culties in fine motor coordination, including RAMs a nd finger-to-finger testing.
M11ltiple scl erosis
Multipl e sclerosis can produce a range of neurologic symptoms. Vertigo occurs in up to 50% of patients with multiple sclerosis. Dis ease o nset is u sually in the th ird or fourth decade of life. MRI s h ows c haracteristic demyelinating plaques.
Migraine h eadach e
Approx imately 30% of p eop le with mi gra ine headaches have vertigo. It can be present
Chapter 13 • Dizziness
before the headache begins, during the h ead ache, or independent of th e headache. Patients with vestibular- type migraine headaches often experience photophobia, phonophobia, and v is u al aura during the episodes of vertigo. Patients with bas ilar-type migraine may have other symptoms consistent with vertebrobasi la r vascular abnormalitjes such as visu a l changes, tinnitus, decreased h earing, ataxia, or paresthesia. Diagnosis is usually made on the basis of the history.
Peripheral Causes
B e nign paroxysmal positional vertigo
Episodes of BPPV are characterized by acu te onset of vertigo associated with rapid h ead movement or position changes. Many women report dizziness with pos1t1on change around the time of the ir menses . The ep isodes are brief, lasting a few seconds. Nystagmus can be e lic ited by the Dix Hallpike maneuver. Testing positional changes can provoke the vertigo. There is no h ear ing loss . Diagnosis is made on the basis of the history and clinica l finding s . This is one of the most common cau ses of vertigo, especia lly in o lder adults . In patients with BPPV, tiny crystals of calcium carbonate (otoliths) in the inner ear that monitor head position relative to gravity become di s lodged and migrate into one of the semicir cu lar canals. When the head moves, the gravity-d ependent movement of the o to liths in the affected semic ircular canal causes endolymph displacement and a sensation of vertigo.
B enign paroxysmal vertigo ofchildhood
Benign paroxysmal vertigo of chi ldhood occurs most often in ch ildren 2 to 3 year s old. The disorder tends to be recurrent with one to four e pisodes p er month. The epi sodes occur s udden ly and are often associ ated with vomiting, pallor, sweating, and n ystagmus. The n e urologic a nd audio logic examinations produce normal findings. Some chi ldre n ca n have a hypoactive or absent response to caloric tes ting (ear irrigation with warm and then cool water) .
Chapter 13 • Dizziness
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 recur rent and la st for minutes to several hours. The interval between attacks can be weeks or months . Between episodes, the patient is as ymptomatic. On physical examination, senso rineural hearing loss is present in the affected ear, or it can be bilateral. Nystagmus is lateral or rotary. The visual ocular reflex will lateral ize 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 las ts for days to weeks. Remaining completely motionless can help alleviate the symptoms. Auditory func tion is not affected. Physica l examination re veals nystagmus that intensifies in amplitude when the gaze is directed away from the affected ear. Visual fixation minimizes the nystagmus. The visual ocular reflex will later alize to the affected side.
Labyrinthitis
Frequently associated with a concurrent viral or bacterial illness, labyrinthiti s produces se vere vertigo that lasts for several days. Laby rinthitis can be a complication of otitis media or meningitis. This condition is distinguished from vestibular neuronitis by the accompany ing hearing loss that occurs as a result of de struction of the inner ear. The visual ocular reflex will lateralize to the affected side.
Acoustic neuroma
Also called a vestibular schwannoma, acous tic neuroma is a b e nign tumor that originates most often in the vestibular portion of the acoustic nerve (CN 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. A neuro1na can also occur in the trig~0U.stic nerve (CN V) with symptoms of pare ~1~1 consistent with the nerve distribution s~es1a tumors of the abducens nerve (CN Vt)arge compress the brainstem. can
Perilymph .fistula
Fistula formation can occur as a result of . trauma, from a direct blow, secondary to
0 :
logic surgery, or indirectly from strainin coughing, or pressure changes. In thfa cond~'.
1 ti on, there is leakage ofperi lymph from eith the round or the oval window into the midd~ ear. Sensorineural hearing loss and venig~ are frequently present. The fis tula will often heal s pontaneously but sometimes can require surgery.
Sinusitis and otitis
Serous otitis, otitis media, a nd s inusitis can cause disruption of the vestibular apparatus, producing vertigo. History and physical examination findings will be consistent with the specific disorder (see Chapters 15 and 25).
Cholesteatoma
Collection of s quamous debris, often associ· ated with chronic middle ear infection, can form a cholesteatoma, which enlarges and destroys structures in its way. On physical examination, the cholesteatoma will appearas 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 themse lves as anxious or n e rvou s and may have p sychiatric diagno ses (see Chapter 4 ). Their symptoms ~ vague and imprecise. Neurologic examinauon findings are normal. No nystagmus is present or elicited. The vertigo can be reproduced
Chapter 13 • Dizziness
\\'ith hyperventilation. MRI can be useful to pro,·ide reas s urance.
Cardiovascular
Orthostati c hypotension and card iac dys rhythmias can pro~uce vertigo. Po_stural hy potension can be diagnosed by takmg ortho stat ic 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 pres ent with symptoms similar to those ofMeniere disease. The patient demonstrates various clin ical symptoms, including papilledema, apha sia, monoplegia or hemiplegia, CN palsies, pupillary abnormalities, or focal neurologic deficits. 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 wi ll be positive for syphilis.
Other Causes
Ototoxic drugs and drugs cau sing salt r etention
Medications that are ototoxic, salt-retentive, or psychotropic can produce vertigo, light headedness, or unsteadiness. Drugs causing salt retention include steroids and phenylbuta zone. Ototoxic medications include as pirin, ethacrynic acid, streptomycin, gentamicin, aminoglycosides, and furosemide. Psychotro pic drugs can a lso produce vertigo. Ototoxic drugs can produce a sensorineural hearing loss. Audiometry should be p erformed with any noted hearing loss.
Trauma
Injury to the h ead or ear from labyrinthine concussion, temporal bone fracture , or peri lymph fistula can produce disturbance of the vestibular apparatus and result in vertigo. Head trauma can also produce cerebral con cussion involving the anterior tip of the tem poral lobe. Trauma from otologic procedures can a lso cause vertigo.
~ DIFFERENTIAL DIAGNOSIS OF Co111111011 Causes of· Di-:.-:.iness CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
CENTRAL CAUSES
Brainstem O lder adult; acute Symptoms of brai n stem MRI dysfunction or onset; recurrent or vertebrobasilar cerebellar vertigo; tinnitus; vascular abnormal ity: dysfunction hearing OK ataxia, double vision;
lack of coordination; sensory or m otor deficits; vertical, lat era l , rotary nystagmus; hearing normal; cere bellar: impaired RAM, finger-to-finger testi ng
Multiple sclerosis Onset is often in Can h ave no other find- MRI third or fourth i ngs or can have other decade of Iife neurologic sympt oms
Migraine H eadache history; Can have symptoms N one headac he other migraine of vertebrobas ilar
symptoms vascular abnormalities , as above
Continued
Chapter 13 • Dizziness
•·''iiidjlliM+.!QQMi~l·'UMM&lldiM'•2*d~ CONDITION
Benign paroxys m a I positional vertigo (BPPV)
Benign paroxys m a I vertigo of childhood
M~niere disease
Vestibular neuronitis
Labyrinthitis
Acoustic neuroma
Perilymph fistula
Otitis/sinusitis
Cholesteatoma
HISTORY PHYSICAL FINDINGS
PERIPHERAL CAUSES
Adults: associated with positional changes; recurrent episodes; lasts seconds to min utes; some relief if motionless
Children: usually 2 - 3 yr old; sudden onset with crying by child
Sudden onset; lasts hours, recurrent; tinnitus and fullness in ears
Sudden onset; antecedent viral infection
Sudden onset, lasts hours to days
Adults; gradual onset; mild vertigo; per sistent tinnitus; facial numbness, weakness
History of trauma; hearing loss
Pain in ear or face; history of ear or sinus infections; gradual onset of verti go
History of chronic middle ear infections
Lateral or rotary nystag mus; no tinnitus or hearing loss
Vomiting, pallor, sweat ing, and nystagmus common; no loss of consciousness; neuro logic and audiologic examination can be normal
Lateral or rotary nystag mus; fluctuating hear ing loss: low tones; sensorineural
Nausea and vomiting; nystagmus; no hearing loss, loss of equ ilib rium 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 otos copy; sensorineural hearing loss
Serous otitis, otitis me dia; tenderness over sinuses; purulent nasal discharge; no nystagmus
Shiny, white, irregular mass on otoscopic examination; foul smelling discharge can be present; bone de struction can be visi ble; cond uctive h earing loss can be present
DIAGNOSTIC STUDIES '
~ Provoke nyst~
and_~ertigo by pos1t1on that
c~uses response; D1x-Hallpike maneuver; ENG
Can have hypoactive or absent resp0n to caloric testingse
Posi tional maneuvers positive VOR test ' audiometry, ENG,
Positional maneuvers· positive VOR test '
Positional maneuvers positive VOR test '
I
audiometry
MR I; audiometry
Audi ometry
See Chapters 15 and 25
Audiometry
Chapter 13 • Dizziness
Co111111011 Causes <~/' Diz-;.i11ess-co11t •t1DIFFERENTIAL DIAGNOSIS OF
HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
SYSTEMIC CAUSES
Vague symptoms; Normal neurologic and Hyperventilation to recurrent; can auditory examinations reproduce the describe self as vertigo anxious; can have other psychiatric diagnoses
Cardiovascular his Orthostatic blood pres Depends on client tory; antihyperten sure; dysrhythmias; condition and sive medications carotid or temporal symptoms
bruits Vertigo, tinnitus, Various clinical symp Serology for syph i I is
fullness in ears toms; papilledema, aphasia, monoplegia or hemiplegia, central nervous palsies, pupil lary abnormalities, Argyll Robertson pupil; focal neurologic deficits
OTHER CAUSES
Ototoxic and salt Medication history: Sensorineural hearing Audiometry retaining drugs steroids, phenylbu loss
tazone, ethacryn ic acid, aspirin, streptomycin, gen tamicin, aminogly cosides, furose mide, psychotropic drugs
Trauma History of trauma to Depends on nature and MRI or CT head or ear location of injury; can
exhibit peripheral or central symptoms
BPPV, benign paroxysmal positional vertigo; CT, computed tomography; ENG, electronystagmography; MRI, magnetic resonance imaging; RAM, rapid alternating movements.