Dizziness and Vertigo

 Dizziness is a common symptom and can be classified into

o Vertigo—abnormal perception of movement (self vs. environment)
 Basic requirement for a patient to have vertigo: asymmetric vestibular function
 Acuity and degree of asymmetry correlate with severity of vertigo
 Although peripheral vertigo is less anatomically serious than central, peripheral is more severe in
symptoms than central.
o Presyncope—lightheadedness or near fainting
 Transient cerebral hypoperfusion as a result of three basic problems
 Cardiac pump
 Intravascular volume
 Vascular resistance
 Workup for pre syncope is similar to that of syncope
o Disequilibrium—sense of imbalance when ambulating
 Etiologies may include visual, vestibular, pyramidal, extrapyramidal, cerebellar, proprioceptive,
motor neuron, NMJ, and musculoskeletal
 Other multifactorial, encompassing many of these
 The physical exam is so important in this category.
o Nonspecific
 Essentially a category of exclusion after ruling out the prior three categories
 Vaguely describes symptoms
 Anxiety disorder may be the most common cause
 Could also be an exacerbating factor in the other three scenarios
 Other etiologies include
 Medication side effects
 Hyperventilation
 Hypoglycemia
 Post-concussion
 Dysautonomia
o EX: postural tachycardia syndrome
 Problems with above scheme
o Difficulties in individual perception and reporting of symptoms
o Multiple etiologies may coexist in a given patient, especially elderly
 For most part, use the four for test.
 Despite the above issues, history and examination are still paramount in correctly naming the neurologic
syndrome. Once the illness script is constructed, further workup can be ordered.
o Most potentially useful features of the history may be
 Time course
 Including timing, pattern, and stability
 Provoking factors
 Spontaneous
 Specific maneuvers
o EX: turning the head
 Exacerbating factors
 EX: medication, viral illness, psych stressor, etc.
o A few caveats on history
 All vertigo is worsened by head movement
 During an episode, patients report being terrified to move the head/neck.
 If the aptient reports dizziness but denies worsening with head movement, it is very
unlikely to be vertigo.
  Orthostatic hypotension and benign paroxysmal positional vertigo can both lead to
dizziness when getting out of bed.
o A key aspect is whether symptoms are provoked by head/neck movements that
do not alter cerebral perfusion or blood pressure.
 Three useful tempo-related categories in evaluating vertigo
 Acute prolonged vertigo
 Recurrent spontaneous vertigo
 Recurrent positional vertigo
 (last two MAY have a normal exam if patient not currently symptomatic)
 When trying to discern central vs. peripheral vertigo by history
 Features suggesting peripheral
o Associated hearing loss/tinnitus
o Nausea and vomiting more severe
o Patients tend to fall toward abnormal side
o Vertigo itself more severe
 Features suggesting central etiology
o Headache (esp migraine like)
o Other bulbar symptoms/neurologic problems
o Gait/posture may be more unstable
 History is the most sensitive tool in classifying a patient’s dizziness
 Issues with elderly patients
o Overall risk of morbidity and mortality
o Multiple contributing factors
 Most outpatients with dizziness are diagnosed with peripheral vertigo
o Benign paroxysmal positional vertigo
 Most common
o Vestibular neuronitis/labyrinthitis
o Meniere disease
 Important of the illness script in naming the neurologic syndrome
o Discriminates among the four categories of dizziness
o Discriminates peripheral from central vertigo
o A few caveats on physical exam of the dizzy patient
 While this needs to be thorough, the most useful aspects in narrowing the differential tend to be
 Orthostatic vital signs
 Observation of gait
 Detection and description of nystagmus
 Effect of various positional maneuvers
 The presence of nystagmus strongly suggests that vertigo is the most likely cause of the patient’s
dizziness. Further aspects of nystagmus may help determine if vertigo is central vs. peripheral in
origin
 Peripheral nystagmus tends to be
o Horizontal/rotatory NOT purely vertical
o Unidirectional irrespective of direction of gaze
o Suppressible on visual fixation
 Central nystagmus tends to be
o Any direction, including purely vertical
o Dynamic in direction with changes in gaze
o Nonsuppressible on visual fixation
 Patients with peripheral vertigo tend to fall toward the affected side when ambulating
 The physical examination may be normal in patients with recurrent episodic peripheral vertigo
 Other potentially useful physical findings
 Dix Hallpike Maneuver
o Primary role in evaluating suspected benign paroxysmal positional vertigo
o Attempts to provoke vertigo and nystagmus
o Rapid position change from seated to supine
o Findings classic for BPPV
 Vertigo/nystagmus develop
 Following brief latency (few seconds)
 Last up to 30 seconds
 Repeat maneuvers = fatiguability
o Nonfatigable findings, lack of latency, prolonged symptoms/nystagmus, and/or
multidirectional nystagmus, think central vertigo
o Up to 80% sensitive for BPPV
 Head Impulse Test
o AKA Head Thrust Test
o Vestibuloocular reflex allows visual fixation while head position changes
 As you turn your head from L to R, if you have normal vestibuloocular
coordination, you should be able to maintain steady fixation on object
without becoming dizzy.
o Method
 Patient focuses on distant object
 Examiner abruptly turns the patient’ head 15-20 degrees
o Normal Response: head turn should create asymmetric vestibular input so the
eyes “drift” to maintain visual fixation on a target
o Abnormal Response: head turn leads to eyes “dragged” off target, followed by
rapid “correcting” saccadic movements to refocus on the target
o Abnormal response = peripheral vertigo
 Skew Deviation
o This test is based on the fact that central lesions (mostly brainstem) may cause
vertical misalignment.
o On alternate eye cover testing, the uncovered eye has vertical “correction” to
maintain fixation on an object
o Skew deviation = central vertigo (most of the time)
 HINTS Testing
o Combines Head Impulse test, evaluation of Nystagmus, and Test of Skew deviation
in a vertiginous patient
o Peripheral vertigo is most likely when ALL three are met
 Abnormal head impulse test
 Nystagmus with peripheral features
 No skew deviation
o Central vertigo is most likely when ANY of these occur
 Normal head impulse test
 Nystagmus with central features
 Presence of skew deviation
 Many other maneuvers exist
o Cold Calorics
 Can cause significant distress and is less commonly done in the office but
helpful in the laboratory
o Response to Hyperventilation
o Head shaking visual acuity
  Laboratory assessment includes audiometric evaluation, ENG, provocative vestibular
testing, etc.
 Vertigo
o Intro
 Classically defines as an illusion of movement (self and/or environment)
 Problems with patient perception/reporting of symptoms
o Patients become quite anxious during episode so we must take their reporting
with a grain of salt
 Must be distinguished from other causes of dizziness
 Basic Requirement: asymmetric vestibular input
o Neuroanatomy of Vertigo
 Cerebral cortex receives input from the vestibular nucleus in the brainstem.
 There is so much interplay between the vestibular nucleus and so many other
neuroanatomic structures, including the vestibular nerve and ganglion, cerebellum, MLF,
ocular motor nuclei, spinal cord itself
 Input from BOTH vestibular systems must be equal to maintain balance.
 Tempo and severity of ASYMMETRY are key factors in presence/severity of vertigo.
o Most cases of vertigo are peripheral. However, the more neuroanatomically severe ones are central.
 Central (20%)
 Most common
o Brainstem ischemia/hemorrhage
o Migranous vertigo
 Cerebellar disease
 Space occupying lesion
 Multiple sclerosis
 Chiari malformation
 Brainstem encephalitis
 Note: If you suspect central vertigo, you need to pursue an MRI of brain. CT alon cannot
visualize structures involved especially in posteriof fossa as well.
 Peripheral (80%)
 Most common
o BPPV
o Vestibular neuronitis
o Meniere disease
 Acoustic neuroma
 Otitis media
 Drugs: aminoglycosides
 Perilymphatic fistula
 Herpes zoster oticus (Ramsay Hunt)
 Trauma
 Central Vertigo
 Associated Symptoms
o Headache
o Dysarthria, visual problems, other cranial nerve abnormalities
o Gait and posture may be unstable
 Will fall unpredictably to either side
 Physical Findings
o Cranial nerve or long tract abnormalities
 Nystagmus
o Nonsuppressible with fixation
  IE does not resolve after few seconds of fixing gaze on one thing
o Vertical (can be horizontal/rotatory)
o Direction changes with changing eye position
 L beating when look L. Up beating when look up.
 Peripheral Vertigo
 Associated Symptoms
o “sparing of central problems” IE CN
o Hearing loss
o Aural fullness
o Tinnitus
o Vertigo tends to be more severe
o May fall toward affected side
 Physical Findings
o Asymmetric hearing
 Nystagmus
o Suppressible
o Horizontal/rotatory
 NEVER pure vertical
o Direction does not change with changing eye position
o Benign Paroxysmal Positional Vertigo
 Most common cause of episodic vertigo
 Pathogenesis
 Calcium debris (canalithiasis) within the semicircular canals, most commonly posterior
 As a result, movement of endolymph with linear acceleration causes the erroneous
sensation of spinning and rotating when the head shifts
o IE linear movement is perceived as angular movement
 It may be idiopathic or a consequence of prior vestibular pathology, including Meniere disease,
vestibular neuritis, or trauma.
 More common in women
 More prevalent with advancing age
 Clinical Presentation
 Recurrent, brief (less than a minute) vertigo
o Provoked by specific head movements
o EX: rolling over, standing up, looking up while sitting
 Nausea and vomiting may occur
 Hearing is preserved and tinnitus is absent
o Unless there is preexisting or coexisting vestibulocochlear disease
 Some patients may have a sense of “imbalance” between attacks, even if treatment was
effective
 Dix Hallpike maneuver should be performed
o Latency period
o Vertigo with torsional/upward nystagmus
o Brief in duration (< 30 seconds)
o Less severe with repetition IE fatiguability
 Most patients respond to office-based particle repositioning maneuvers and education on home-
based techniques.
 Some require surgical intervention
o Meniere Disease
 Average age onset 20-40 years old
 Pathogenesis focuses on endolymphatic hydrops
  Excessive accumulation of endolymph leading to physical distortion of the labyrinthine
system
 Multiple mechanisms have been proposed IE infectious, immunologic, genetic, traumatic,
mechanical, etc. that culminate in several symptoms
 Classic Triad
 Sensorineural hearing loss (may be low frequency early on)
 Episodic vertigo
 Tinnitus (may be low pitched or “roaring” early)
 Other common symptoms include sensation of ear (aural) fullness, nausea, and nonspecific
sensation imbalance
 Signs and symptoms tend to be episodic: 20 minutes to 24 hours
 Clinical presentation and natural history can be quite variable in terms of
 Severity of each of the three characteristic symptoms
 Whether attacks occur in clusters or isolated
 Unilateral or bilateral
 Response to therapy
 Hearing loss is sensorineural, often fluctuating, and (unlike most other processes leading to
hearing loss) may be initially worse at lower frequencies.
 Since tinnitus pitch often matches the frequency of hearing deficit, it may be low-
pitched/roaring in Meniere disease.
 However, variants of this exist as many patients have high and low frequency hearing loss
at disease onset
 Some patients with recurrent attacks may end up with permanent hearing impairment
 Vertigo is usually spinning or rocking in nature and also tends ot be fluctuating and episodic
 Diagnosis requires a consistent hitoryof episodic symptoms, audiometric confirmation of SNHL,
and with proper imaging and other otologic studies, considering exclusion of mimickers
 Therapy
 Lifestyle
o Salt restriction
o Limitation alcohol, nicotine, caffeine
 Medical
o Acute: possible low dose benzos as vestibular suppressants
o Long Term: diuretic therapy commonly used
 May be a role for betahistine
 Nonmedical
o There may be a role for vestibular rehabilitation
o Surgical therapy may be destructive or nondestructive
 Most of these options are reserved for patients with debilitating
symptoms, especially those who idd not respond to above options
o Vestibular Neuritis/Labyrinthitis
 This is a benign acute self-limited peripheral vestibulopathy
 Without hearing loss = neuritis
 With heading loss = labyrinthitis
 Pathogenesis is most likely related to ongoing inflammatory injury of the vestibular system that is
most likely related to a current or recent viral illness.
 Most patients, however, do not recall recent symptoms attributable to viral illness
 Clinical presentation is that of an acute spontaneous bout of severe vertigo, nausea, vomiting,
and gait instability. It can be dramatic enough to raise concern over acute cerebrovascular event
involving the cerebellum or the brainstem.
 Peaks early (within hours to a day), remains severe for 1-2 days, the gradually resolves.
  Recurrences are very uncommon, but there is a risk of later development of BPPV, as
stated earlier.
 Examination must aim to ensure no features suggest central pathology.
 The HINTS assessment is very useful at distinguishing vestibular neuritis from
cerebrovascular disease in patients with vestibular syndromes.
 HINTS alone may not fully exclude an acute central event as, rarely:
o Infarcts of the internal auditory artery can lead to acute vertigo an hearing
changes that suggest a peripheral cause
o Some cerebellar infarcts can also mimic symptoms of peripheral vestibulopathy
 Treatment
 Medical
o Given the suggested pathophysiology, a 10-14 day trial of glucocorticoid therapy is
reasonable
o No role for antiviral therapy.
o Early use of antiemetics and vestibular suppressants may be needed, at least until
clinical improvement takes place (a few days)
 Nonmedical
o There is a role for early vestibular rehabilitation
o