Dizziness and Vertigo

Nahihilo ako!
Dizziness
…difficult to define, impossible to measure, a challenge to diagnose, and
troublesome to treat.

Medical History
• Description of dizziness by the patient
• Secondary symptoms
• Previous history

Type 4: LIGHTHEADEDNESS
• A vague sensation
• Very difficult to describe
• Reserved for patients who do not experience one of the three more
discrete types of dizziness sensations—vertigo (spinning),
presyncope (fainting), or disequilibrium (falling)
• Psychogenic causes, such as depression, anxiety, or somatoform
disorders, typically have fatigue, insomnia, pain, or other physical
Drachman Dizziness and emotional symptoms in addition to dizziness
• Type 1: vertigo
o Rotational sensation Common Medications that Cause Dizziness
• Type 2: Presyncope • Anti-epileptic drugs (carbamazepine, phenytoin)
o Impending faint • Antidepressants
• Type 3: Dysequilibrium • Antihypertensive
o Loss of balance without head sensation • Antihistamines
• Type 4: Lightheadedness • Antiarrhythmic
o Ill-defined, not otherwise classifiable • Antibiotics (streptomycin, tobramycin, gentamicin)
• Precise classification is often difficult and multiple cause of the same • Analgesics
symptoms are common • Neuroleptics (phenothiazine)
• Tranquilizer (diazepam, chlordiazepoxide)
Type 2: PRESYNCOPE
• The sensation of near fainting Type 3: DYSEQUILIBRIUM
• Reflects diminished cerebral perfusion • Sense of being “dizzy in the body” rather than in the head
• Think of medical conditions that affect blood flow to the brain or • More common in the elderly—falling down sensation
decreased oxygen delivery to the brain • Often multifactorial—problems in hearing, vision, cerebellar
• Think of CIRCULATION dysfunction, peripheral neuropathy, parkinson’s disease and
• Think of the heart and BV polypharmacy
• Cardiac causes: • Diagnosis
o Electrical (tachy or bradyarrhythmias) o Assess gait, strength, coordination, reflexes and sensory
o Structural (especially aortic outflow obstruction) function
• Vascular causes of syncope: o Broad-based gait—cerebellar disorder
o Orthostatic hypotension o Bilateral vestibular loss—(+/-) hearing loss
o Temporary reactions due to vagal stimulation o Decreased or absent response to caloric and rotational
• Postural symptoms without orthostatic blood pressure changes are stimulation
particularly common in elderly persons
• Diagnostics Type 1: VERTIGO
o Head-Up-Tilt Test (HUTT)
o Electrocardiogram Duration of Common Causes of Vertigo
o Holter-test Monitoring Seconds Benign positional vertigo
• Management Minutes Vertebrobasilar insufficiency
o The first steps in treatment of orthostatic hypotension are Hours Migraine
diagnosis and management of the underlying cause Meniere’s Disease
Days Vestibular neuritis

Acute Prolonged Vertigo

• Vestibular neuritis
• Cerebellar/BS infarction or hemorrhage
 Objectives
• Perform a thorough screening examination for patients presenting
with dizziness
• Establish at the bedside the difference between central and
peripheral mechanisms
• Generate and appropriate differential diagnosis

Spontaneous Nystagmus

Recurrent Vertigo
• Benign positional vertigo
• Meniere’s disease
• Transient Ischemic Attacks (TIA)
• Migraine
• Anxiety

Central Oculomotor Functions

Gaze Nystagmus
• Eccentric gaze
o Control of the brainstem and midline cerebellum,
particularly the vestibulocerebellum (especially the
flocculonodular lobes)
• Fail to hold the eye in the eccentric position
o Eye drifts toward the midline (exponentially decreasing
velocity), followed by refixation saccades toward the
target
o Central in origin and always beats in the direction of
Insidious Slowly Progressive Course intended gaze
• Disequilibrium associated with hearing loss and later facial paralysis • Peripheral spontaneous nystagmus
and numbness o Linear slow component velocity
o Vestibular Schwanomma o Without direction change when gazing in the direction of
• Ataxia associated with headache and signs of increased ICP the fast phase
o Cerebellar Mass (Neoplasms, Abscess) • Cause of gaze-evoked nystagmus
o Drug effect (sedatives, antiepileptic), alcohol, CNS
tumors, and cerebellar degenerative syndromes
Smooth Pursuit
• Action. Ask the patient to follow your finger as you slowly move it
left and right, up and down. Make sure the patient can see the target
clearly and you do not exceed 60 degrees in total arc or 40 degrees
per second
• Interpretation
o Cerebellar or BS disease
§ Saccadic eye tracking in which the patient
repeatedly loses the target and the catches up
with a small saccade
§ In most cases, abnormal pursuit is
Neurologic Evaluation nonlocalizing with in the CNS
Where is the lesion?
• Peripheral vestibular
o End organ (labyrinth)
o Vestibular nerve
• Central vestibular pathway
o Brainstem
o Cerebellum

How can I differentiate central from peripheral dizziness?

The 10-minute examination of dizzy patient
1. Spontaneous nystagmus
2. Central occulomotor function
3. The vestibule-ocular reflex (VOR) battery—headshake, head thrust,
dynamic visual acuity, and Hallpike positioning
4. Coordination
5. Posture
6. Gait
7. Special examinations
 § Small reversal phase
Saccades o Central etiology
• Action. Ask the patient to look back and forth between two § Prolonged nystagmus
outstretched fingers held about 12 inches apart in the horizontal and § Vertical nystagmus following horizontal
vertical plane. Observe for latency of onset, speed, accuracy, and headshake ("cross coupling")
conjugate movement § Disconjugate nystagmus
• Interpretation
o Saccadic eye movements: refixation movements Dynamic Visual Acuity
§ Frontal lobes (voluntary saccades) • Action. Ask the ptient to read the lowest (smallest) line possible on
§ BS reticular formation (voluntary and a Snellen eye chart with best corrected vision (glasses, contact
involuntary saccades) lenses). Repeat the maneuver while passively shaking the patient's
§ Oculmotor nuclei III, IV, and VI head at 2 Hz, and record the number of lines of acuity "lost" during
o Delayed saccades the headshake
§ Cortical and BS lesions • Interpretation
o Slow saccades o Excessive retinal slippage during head movement
§ BS disease § Vestibular dysfunction
o Inaccurate saccades (especially overshoots) § Most frequent etiology: bilateral vestibular loss
§ Lesions of the cerebellar vermis and fastigial related to ototoxicity or aging
nuclei o Poorly compensated unilateral dysfunction
o Disconjugate eye movements with slowing of the § Loss of dynamic visual acuity but is harder to
adducting eye and overshoots of the abducting eye identify with this clinical test
§ MLF pathology frequently associated with o Examiner shakes the patient's head to avoid pauses
multiple sclerosis during which the patient can see the target

Fixation Suppression Test Dix-Hallpike Maneuver

• Action. Ask the patient to fixate on his or her own index finger held
out in front at arm’s length. Unlock the examination chair and rotate
the patient up to 2 Hz while the patient stars at the finger moving
with them. The examiner observes for a decrease in the visual-
vestibular nystagmus that is evoked during rotation without ocular
fixation
• Interpretation
o Modulation of nystagmus invoked by rotation
§ Dependent on the cerebellar flocculus
o Failure of fixation suppression in the presence of
adequate visual acuity
§ Floccular dysfunction
§ Similar in nature to the fixation suppression
performed after caloric stimulation during
electro-oculography
Head Thrust Test (Head Impulse Test)
• Action. Ask the patient to fixate on a target on the wall in front of the
patient while the examiner moves the patient’s head rapidly (>2000
deg/sec2) to each side
• Any movement of the pupil during the head thrust and a refixation
saccade back to the target
• Direct observation or use of an ophthalmoscope to document eye
movement
• Interpretation
o Reliable sign of reduced vestibular function in the plane
of rotation of the ear ipsilateral to the head thrust
o Eye movement during the maneuver
§ Decreased neural input from the ipsilateral ear
the the VOR
§ Contralateral ear is in inhibitory “saturation”
and cannot supply enough neural activity to
stabilize gaze
Post head Shake Nystagmus
• Action. Tilt the head of the patient forward 30 degrees and shake
the head in the horizontal plane at 2 Hz for 20 seconds. Observe
for postheadshake nystagmus and note direction and any reversal.
Fresnel lenses are preferred to avoid fixation The maneuver may
be repeated in the vertical direction
• Interpretation
o Pathologic sign of imbalance in the vestibular inputs in
the plane of rotation
o Peripheral cause
§ Nystagmus directed toward the stronger ear
• Action. With the examination chair unfolded like a bed, turn the
patient's head 45 degrees to one side while seated and rapidly but
carefully have the patient recline
• Observe the eyes for nystagmus and, if present, note the following
five characteristics: latency, direction, fatigue (decrease on repeated
maneuvers), habituation (duration), and reversal upon sitting up.
• Intepretation
o Diagnostic for benign position vertigo
§ Otoconial debris: floating (canalithiasis) or
fixed (cupulolithiasis) within the posterior
semicircular canal of the undermost ear
Limb Coordination Tests
• Action. Ask the patient to perform a series of coordination tasks
such as finger-nose- finger, heel-shin, rapid alterna.ng motion, and
fine finger motion (coun.ng on all digits). Observe for dysmetria or
dysrhythmia
• Intepretation
o Limb dysmetria or dysdiadochokinesia
§ Cerebellar cortical disease
§ May or may not accompany midline or
vestibulocerebellar oculomotor dysfunction
Romberg Test
• Action. Have the patient stand with feet close together and arms at
the side with eyes open and then eyes closed. Observe for the
rela.ve amount of sway with vision present versus absent.
Gait Observation
• Action. Ask the patient to walk 50 feet in the hall, turn rapidly, and
walk back without touching the walls. Observe for initiation of
movement, stride length, arm swing, missteps and veering, and
signs of muscle weakness or skeletal abnormality (kyphoscoliosis,
limb asymmetry, limp).
• Interpretation
o Loss of otolithic function
§ Veer toward the side of the lesion
o Central brain stem and musculoskeletal lesions
§ Lateral deviation during ambulation
o Extrapyramidal disease
§ Difficulties with gait initiation and turns and
decreased arm swing can be seen in.
Tragal Compression, Pneumatic Otoscopy, Tullio Phenomenon, Valsalva • Positional vertigo or head motion discomfort
With Pinched Nostrils And Closed Glottis • Accompanied by migrainous symptoms
• Action. With Fresnel lenses in place, observe for nystagmus or • Normal between attacks
tonic eye deviations with symptoms of dizziness under four test • Central or peripheral spontaneous nystagmus
conditions: • Pathophysiology unknown
• 1st attack may require imaging to rule out posterior fossa lesion
(1) steady tragal compression to increase pressure in the external • Treatment
auditory canal o Vestibular suppressants
(2) positive and negative pressure applied with the pneuma.c o Triptans
otoscope o Migraine Prophylaxis for frequent and severe attacks
(3) presentation of loud tones via tuning fork or impedance bridge
(4) increased pressure during breath holding against pinched Causes of Peripheral Vertogo
nostrils or closed glottis. • BPPV – Benign Paroxysmal Positional Vertigo
• Interpretation • Vestibular Neuritis
o Superior canal dehiscence syndrome
• Meniere’s Disease
§ Eye elevation and intorsion with loud sounds
• Labyrinthithis
or Valsalva maneuver against pinched nostrils
o Cranial-cervical junction abnormalities (Arnold-Chiari • Vestibular Paroxysmia
malformation in particular)
§ Vertical downbeat nystagmus with any BPPV
maneuver that increases intracranial pressure • The most common cause of vertigo
• It results from free floating calcium carbonate crystals that
inadvertently enter the long arm of the posterior semicircular canal

Central Vertigo
• Cerebellar infarction
• Cerebellar hemorrhage Eppley Maneuver for BPPV
• Lateral medullary infarction (Wallenberg’s syndrome) • Canalith repositioning maneuver
• Other • 5 step head hanging maneuver
• Moves otoliths out of the posterior semicircular canal and back into
Vertibrobasilar Insufficiency utricle where they belong
• Vertigo with associated neurological signs
o Diplopia
o Ataxia
o Drop attacks
o Dysarthria
o Paralysis/weakness/numbness
o Headache
o Risk factors (HTN, DM, Coronary disease)

Dorsolateral Medullary Infarction: Wallenberg’s Syndrome

• Vertigo with nystagmus
• N&V
• Ataxia and ipsilateral asynergia
• Hoarseness
• Ipsilateral Horner’s Syndrome
• Ipsilateral facial analgesia, contralateral body analgesia
• No weakness
Meniere’s Disease
Vestibular Migraine • Sudden and recurrent (paroxysmal) attack of severe vertigo
• Most common cause of recurrent spontaneous vertigo • Low-tone hearing loss
• 2nd most common vestibular disorder after BPPV • Low-tone tinnitus
• 10% of migraineurs • Sense of fullness in the ear
• Any age • Vertigo lasts for hours to a day then burn out
• F:M 3:1 • Hearing loss may progress
• Familial
• Attacks of spontaneous vertigo
 • Combination of abruptly occurring attacks with vestibular and/or • Vestibular and/or cochlear deficits increase during the attack and
trochlear symptoms with fluctuating, slowly progressive hearing loss; are less pronounced during the attack-free interval (audiogram,
tinnitus; and in the course of time vestibular deficits acoustic-evoked potentials, caloric testing)
• CAUSES • Attacks are improved or lessened by administering carbamazepine
o The cause of endolymphatic hydrops are many (even low dosage effective).
o Autoimmunological and infectious diseases • No central vestibular/ocular motor disorders or brainstem signs are
o Hypotheses that ion-channel-related diseases or present.
aquaporins can play an important role • Clincal Features
• Betahistine o Short attacks of rotatory or postural vertigo last for
o Higher doses (3x 48mg/day) superior to usual doses seconds to minutes with instability of posture and gait.
(3x16mg, 3x24mg/day) o Attacks may be triggered by particular head positions and
o After 12 months number of attacks declined from 7.6 hyperventilation, or be influenced by changing the head
months to 4.4 in the low dosage group; 8.8 to 1.0 in the position.
high dosage group o Unilateral hypoacusis or tinnitus occurs during the
o (p=0.0002) Strupp et al 2008 attacks, occasionally or permanently.
• Higher Betahistine Dosage for Prophylaxis • MRI
o Goal of treatment
§ Freedom from attacks for at least 6 months
§ Dosage can be tapered slowly to maintenance
dosage
• Ineffective treatment
o Salt free diet
o Diuretics
o Saccotomy
• MRI

Vestibular Neuronitis
• Can be paroxysmal, single attack of vertigo w/c diminishes over 2
weeks
• Spontaneous nystagmus and unsteadiness
• Associated with nausea, vomiting and previous URTI
• NO auditory symptoms unlike labyrinthitis
• Inflammation of vestibular nerve
• Treatment
o Corticosteroids—methylprednisolone initially 100mg/day,
reduce 20mg every 4th day
o Symptomatic therapy—1st 3 days
§ Dimenhydrinate or other antivertigo meds
o Improvement of central vestibular compensation
• Ineffective therapy
o Treatment with measures to improve circulation—
vasodilators, LMW dextrans
• Differential diagnosis
o Meniere’s Disease
o Vestibular migraine
o Vestibular paroxysmia
o Vestibular pseudoneuritis secondary to brainstem or
cerebellar lesion
• How to differentiate from central vertigo
o Skew deviation of the eyes—ocular tilt reaction
o Normal head impulse test
o Central fixation nystagmus
o Saccadic smooth pursuit
• Acute vestibular vertigo with spontaneous nystagmus and normal
head impulse test indicates a CENTRAL ORIGIN

Vestibular Paroxysmia
• Attacks of rotatory or postural vertigo lasting seconds to a few
minutes
• w/ or w/o ear symptoms
• Hearing loss and tinnitus can also be present during attack-free
intervals