vertigo 101

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V ertigo Case Report Presentation Cruz – Cusi – Dairo – Daz De Grano – De Jesus – Dela Rosa – Young

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Page 1: Vertigo 101

Vertigo

C a s e R e p o r t P r e s e n t a t i o n

Cruz – Cusi – Dairo – DazDe Grano – De Jesus – Dela Rosa – Young

Page 2: Vertigo 101

Anatomy & Physiology

• System of balance• Membranous and bony

labyrinth embedded in petrous bone

• 5 distinct end organs– 3 semicircular canals:

• Superior• Lateral• Posterior

– 2 otolith organs:• Utricle• saccule

Page 3: Vertigo 101

Anatomy & Physiology

• Semicircular canals sense angular acceleration

• Otolithic organs (utricle and saccule) sense linear acceleration

Page 4: Vertigo 101

• Semicircular canals are orthogonal to each other

• Lateral canal inclined to 30 degrees

• Superior/posterior canals 45 degrees off of sagittal plane

Anatomy & Physiology

Page 5: Vertigo 101

• Utricle is in horizontal plane

• Saccule is in vertical plane

Anatomy & Physiology

Page 6: Vertigo 101

• There are five openings into area of utricle– Saccule in spherical

recess– Utricle in elliptical

recess

Anatomy & Physiology

Page 7: Vertigo 101

• 45% from AICA• 24% superior cerebellar

artery• 16% basilar• Two divisions:– anterior vestibular – common cochlear artery

Anatomy & Physiology

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• Superior vestibular nerve: superior canal, lateral canal, utricle

• Inferior vestibular nerve: posterior canal and saccule

Anatomy & Physiology

Page 9: Vertigo 101

• Membranous labyrinth is surrounded by perilymph

• Endolymph fills the vestibular end organs along with the cochlea

• Perilymph– Similar to extracellular fluid– K+=10mEQ, Na+=140mEq/L– Unclear whether this is ultrafiltrate of CSF or blood– Drains via venules and middle ear mucosa

Anatomy & Physiology

Page 10: Vertigo 101

• Endolymph– Similar to intracellular fluid– K+=144mEq/L, Na+=5mEq/L– Produced by marginal cells in stria vascularis from

perilymph at the cochlea and from dark cells in the cristae and maculae

– Absorbed in endolymphatic sac which connected by endolymphatic, utricular and saccular ducts

Anatomy & Physiology

Page 11: Vertigo 101

Sensory structures

• Ampulla of the semicircular canals– Dilated end of canal– Contains sensory

neuroepithelium, cupula, supporting cells

• Crista ampullaris is made up of sensory hair cells and supporting cells

Anatomy & Physiology

Page 12: Vertigo 101

• Sensory cells are either Type I or Type II

• Type I cells are flask shaped and have chalice shaped calyx ending

• One chalice may synapse with 2-4 Type I cells

• Type II cells – cylinder shaped, multiple efferent and afferent boutons

Anatomy & Physiology

Page 13: Vertigo 101

Hair cells have 50-100 stereocilia and a single kinocilium.

Anatomy & Physiology

Stereocilia are not true cilia, they are graded in height with tallest nearest the kinocilium.

Page 14: Vertigo 101

• Kinocilium is located on one end of cell giving each cell a polarity

• Has 9+2 arrangement of microtubule doublets

• Lacks inner dynein arms, and central portion of microtubules not present near ends – may mean they are immobile or weakly mobile

Anatomy & Physiology

Page 15: Vertigo 101

Anatomy & Physiology• Each afferent neuron has

a baseline firing rate• Deflection of stereocilia

toward kinocilium results in an increase in the firing rate of the afferent neuron

• Deflection away causes a decrease in the firing rate

Page 16: Vertigo 101

Anatomy & Physiology

• AMPULLOPETAL FLOW (toward the ampulla) excitatory in lateral canals, inhibitory in superior/posterior canals

• AMPULLOFUGAL FLOW (away from the ampulla) has opposite effect

Page 17: Vertigo 101

• Saccule has hair cells oriented away from the striola

• Utricle has hair cells oriented towards the striola

• Striola is curved so otolithic organs are sensitive to linear motion in multiple trajectories

Anatomy & Physiology

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Anatomy & Physiology

Page 19: Vertigo 101

• Senses and controls motion

• Information is combined with that from visual system and proprioceptive system

• Maintains balance and compensates for effects of head motion

Anatomy & Physiology

Page 20: Vertigo 101

• Vestibulo-Ocular Reflex

– Membranous labyrinth moves with head motion

– Endolymph does not causing relative motion

– Cupula on right canal deflected towards utricle causing increase in firing rate, left deflects away causing a decrease in firing rate.

– Reflex causes movement of eyes to the left with saccades to right

– Stabilizes visual image

Anatomy & Physiology

Page 21: Vertigo 101

• If acceleration stops, and spin to right is at constant velocity, sensation of motion stops after 14-20 seconds as does nystagmus

• Cupula only takes 8-10 seconds to return to equilibrium position

• Vestibular integrator is the term for the prolongation and is mediated by the vestibular nuclei and cerebellum

Anatomy & Physiology

Page 22: Vertigo 101

Vestibulospinal Reflex

• Senses head movement and head relative to gravity

• Projects to antigravity muscles via 3 major pathways:

• Lateral vestibulospinal tract• Medial vestibulospinal tract• Reticulospinal tract

Anatomy & Physiology

Page 23: Vertigo 101

Physiology

• No single structure is solely responsible for balance

• Depends on the vestibular organs of the inner ear and information from 3 different sources

• Eyes• Muscles• joints

• Any dysfunction affecting one of these three, or the brain itself can cause dizziness/vertigo

Anatomy & Physiology

Page 24: Vertigo 101

Physiology

• At rest baseline afferent vestibular input is balanced in normal conditions– neural activity in the right and left sides are equal

• When head is rotated to the right excitation in the right side; inhibition in the left

– Detected as an asymmetry between neural activity by the brain perception of motion

Anatomy & Physiology

Page 25: Vertigo 101

Reflexes

• VESTIBULAR-OCULAR REFLEX– Will manifest as eye movement to the

contralateral side, and a fast movement to the ipsilateral side

• VESTIBULAR-SPINAL REFLEX– Will manifest as limb extension in the ipsilateral

side, limb flexion on the contralateral side

Anatomy & Physiology

Page 26: Vertigo 101

• Balance does not only depend on vestibular, visual and proprioceptive components

– Cerebellar lesions and other systemic diseases affecting the vascular supply of the brain may also cause dizziness and vertigo

Anatomy & Physiology

Page 27: Vertigo 101

Head Shake Test

Page 28: Vertigo 101

Head Shake Test

Action:• Patient is seated• Head is oscillated for 15-20 secs in a horizontal position. • The head is abruptly immobilized in midposition and the induced

nystagmus is observed directly or through Frenzel’s glasses.

Page 29: Vertigo 101

Head Shake Test• Head Shake Nystagmus

– Initial Nystagmus: the direction of the fast phase towards the pathologic or normal side inpatients with unilateral loss of vestibular function

– Time course of HSN: 1) Monophasic: direction fixed 2) Biphasic: fast phase reverse

direction a few seconds after the head is immobilized.

Head Shake Test

Page 30: Vertigo 101

• The nystagmus is associated with the activation of a latent vestibular imbalance.

• It states that, for high velocities of head rotation, excitation is a more effective stimulus than inhibition.

• Vestibular afferents are silenced/driven into inhibitory cut-off at a velocity of head rotation that is lower than that which leads to saturation during excitation.

Head Shake Test

Page 31: Vertigo 101

Head Shake Test

• The effect of Ewald’s law is most apparent when the head is positioned so that the plane of the particular semicircular canal being tested is parallel to the plane in which the head is rotating.

Head Shake Test

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Head Thrus t / Impu lse Tes t

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• Introduced by Halmagyi and Curthoys in 1988

• It aims to identify the presence and lateralize the side of a unilateral vestibular weakness.

Head Thrust/ Impulse Test

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Ask the patient to fixate on a target in front of the patient

Head Thrust/ Impulse Test

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Head Thrust or Impulse Test

Head Thrust/ Impulse Test

• The patient's head is gently grasped, and a small-amplitude (50-100) but high-acceleration (3,000-4,0000/s) thrust is applied by the examiner.

• During the head turn, patient’s eyes are observed for corrective saccade

Page 36: Vertigo 101

Head Thrust or Impulse Test• Corrective saccade is a rapid eye

motion that returns the eyes toward the target.

• Normal: eyes stay fixed on the target no corrective saccade

• Head impulse turns towards the side of vestibular weakness result in the eye moving with the head initially and then a saccadic movement back to the target canal paresis on the ipsilateral side

Head Thrust/ Impulse Test

Page 37: Vertigo 101

• The presence of this movement is due to contralateral horizontal semicircular canal being stimulated in an ampullofugal manner.

• Rapid head turns the discharge rate of the vestibular afferents are driven from about 90 spikes/s at rest to zero, thus the compensatory response is dependent on the ipsilateral canal’s stimulation

• Impairment of the ipsilateral canal: VOR does not function optimally and compensatory movement is not adequate to keep target fixated.

Head Thrust/ Impulse Test

Page 38: Vertigo 101

Fukuda Step Testing

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FUKUDA STEP TESTING

• Method of obtaining objective evidence of imbalance of labyrinthine function which is expressed by functional imbalance of the musculature of the lower extremities during stepping.

Tadashi Fukuda. The Stepping Test Two Phases of the Labyrinthine Reflex. Department of ORL Gifu Medical School

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• Method:1. The subject stands upright in the centre of the Fukuda ring, blindfold, his arms stretched out horizontally in front of him; he is invited to step on the spot, 50 time, raising his knees high. The manoeuvre is repeated, head at rest, then rotated to the right, then to the left.

Fukuda Step Testing

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• Method:2. With his head straight ahead, a normal subject when he marks time does not go out of the hatched area.

3. But with his head turned to

the right he deviates leftwards.

4.With his head turned to the left, he deviates rightwards.

Fukuda Step Testing

Page 42: Vertigo 101

Results

• Head at rest, a normal subject does not go out of the 45 deg quadrant situated just in front of him, he deviates to the left when his head is rotated to his right and vice versa

• Deviation usually occurs to side of lesion

Fukuda Step Testing

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RESULTS: Normal or abnormal?1. Hardly no rotation of body2. Right-handed persons show slight left rotation of the body3. Left-handed persons show slight right deviation of the body4. Forward progression of the body up to 50-100 cm after 50-

100 steps5. Angle of rotation within 30 ˚6. Angle of rotation within 45 ˚7. Otitis media purulenta acuta8. Obstruction of the auditory canal

Tadashi Fukuda. The Stepping Test Two Phases of the Labyrinthine Reflex. Department of ORL Gifu Medical School

Page 44: Vertigo 101

FUKUDA STEPPING TEST

Honaker JA, Boismier TE, Shepard NP, Shepard NT. Fukuda stepping test: sensitivity and specificity. J Am Acad Audiol. 2009 May

• A vestibulospinal test known as the Fukuda stepping test (FST) has been suggested to be a measure of asymmetrical labyrinthine function. However, an extensive review of the performance of this test to identify a peripheral vestibular lesion has not been reported.

• These findings suggest that the FST with and without head shake component is not a reliable screening tool for peripheral vestibular asymmetry in chronic dizzy patients; however, future research may hold promise for the FST as a tool for patients with acute unilateral disorders.

Page 45: Vertigo 101

Romberg’s Test

Page 46: Vertigo 101

Primarily a test of somatosensation and proprioception

Not a test of cerebellar function, as it is commonly misconstrued.

Patients with cerebellar ataxia will, generally, be unable to balance even with the eyes open;

Test cannot proceed beyond the first step and no patient with cerebellar ataxia can correctly be described as Romberg's positive.

Romberg’s Test

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Method

1. Have the patient stand with feet close together and arms at the side with eyes open and then eyes closed.

2. Observe for the relative amount of sway with vision present versus absent.

Results: Romberg's test is positive if the patient sways or falls(+) equal sway with eyes open and closed = proprioception problems(+) with eyes closed = vestibular weakness

Page 48: Vertigo 101

(website for video demos) http://www.vestibularseminars.com/officeexamvideos.html

Fukuda step testing & Romberg’s test

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DIX-HALLPIKE MANEUVER

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DIX-HALLPIKE MANEUVER

• A.K.A. Nylen-Barany test

• Diagnostic test used to identify Benign Paroxysmal Positional Vertigo

– The presence or absence of debris in the posterior semicircular canal of the inner ear

– If debris is present the test will induce vertigo and nystagmus

Page 51: Vertigo 101

• Dix-Hallpike test is the gold standard for posterior canal BPPV

• The test has been shown to have a sensitivity of 79-82% and a specificity of 71-75%

DIX-HALLPIKE MANEUVER

Page 52: Vertigo 101

DIX-HALLPIKE MANEUVER

Patient sitting upright with the legs extendedPatient's head rotated by approximately 45 degrees

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DIX-HALLPIKE MANEUVER

Clinician helps the patient to lie down backwards quickly with the head held in approximately 20 degrees of extension

Page 54: Vertigo 101

HOW

• The patient's eyes are then observed for about 45 seconds as there is a characteristic 5-10 second period of latency prior to the onset of nystagmus

• To complete the test, the patient is brought back to the seated position, and the eyes are examined again to see if reversal occurs. The nystagmus may come in paroxysms and may be delayed by several seconds after the maneuver is performed

DIX-HALLPIKE MANEUVER

Page 55: Vertigo 101

POSTIVE TEST

• If rotational nystagmus occurs then the test is considered positive for benign positional vertigo

NEGATIVE TEST

• If the test is negative, it makes benign positional vertigo a less likely diagnosis and CNS involvement should be considered

Page 56: Vertigo 101

• During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the ear closest to the ground

• The direction of the fast phase is defined by the rotation of the top of the eye, either clockwise or counter-clockwise

DIX-HALLPIKE MANEUVER

Page 57: Vertigo 101

• There are several key characteristics of a positive test:– Latency of onset (usually 5-10 seconds)– Torsional (rotational) nystagmus

• If no torsional nystagmus occurs but there is upbeating or downbeating nystagmus, a CNS dysfunction is indicated

• Upbeating nystagmus indicates that the vertigo is present in the posterior semicircular canal of the tested side

• Downbeating nystagmus indicates that the vertigo is in the anterior semicircular canal of the tested side.

DIX-HALLPIKE MANEUVER

Page 58: Vertigo 101

• There are several key characteristics of a positive test:– Fatigable nystagmus• Multiple repetition of the test will result in less and less

nystagmus– Reversal• Upon sitting after a positive maneuver the direction of

nystagmus should reverse for a brief period of time

DIX-HALLPIKE MANEUVER

Page 59: Vertigo 101

FINGER-TO-NOSE TEST

Page 60: Vertigo 101

• Ask the patient to point to their nose, and then reach out to point to your index finger

• Ensure that they fully extend their elbow while doing this

• Look for intention tremor and over-reaching (indicative of cerebellar pathology)

Finger to Nose Test

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CEREBELLAR EXAMINATION• The main role of the cerebellum is to

coordinate voluntary muscular contractions.

• The cerebellum adjusts the rate, regularity, and force of willed movements and regulates muscle tone.

• Coordination of movement is not an isolated function and is obviously influenced by the whole functioning of the nervous system.

• The cerebellum receives many sensory afferents as well the “brain command” of what to move.

Page 62: Vertigo 101

CEREBELLAR EXAMINATION

• From this information the cerebellum coordinates the range, velocity and strength of contractions to produce steady volitional movements and steady volitional postures.

• Incoordination (ataxia) is the main feature of cerebellar dysfunction.

Page 63: Vertigo 101

WRIST SLAPPING

Page 64: Vertigo 101

• Rapid alternating movements test for dysdiadochokinesia

• Rapid alternating movements, such as wiping one palm alternately with the palm and dorsum of the other hand.

Wrist Slapping

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OVERSHOOTING

• Clinical examination for postural or position “overshooting”

• Test for overshoot by having the patient raise both arms suddenly from their lap to the level of your hand.

• In addition, you can apply pressure to the patient's outstretched arms and then suddenly release it.

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• Normal performance of these motor tasks depends on the integrated functioning of multiple sensory and motor subsystems.

• These include position sense pathways, lower motor neurons, upper motor neurons, the basal ganglia, and the cerebellum.

• Thus, in order to convincingly demonstrate that abnormalities are due to a cerebellar lesion, one must first test for normal joint position sense, strength, and reflexes and confirm the absence of involuntary movements caused by basal ganglia lesions.

Wrist Slapping

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Common Disorders

COMMON DISORDERS

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Meniere’s Disease• Idiopathic endolymphatic hydrops• distortion of the membranous

labyrinth due to overaccumulation of endolymph

• clinical triad of vertigo, tinnitus and hearing loss

Management• Diuretics (Hydrochlorothiazide)• Salt restriction• Antiemetics for vomiting • Surgery if with intractable vertigo

Page 69: Vertigo 101

BENIGN PAROXYSMAL POSITIONAL VERTIGO

• Dislodgement of calcium crystals (otoconia) from the utricle with migration to the semicircular canals (most commonly the posterior canal)

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BENIGN PAROXYSMAL POSITIONAL VERTIGO

• When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris within the affected semicircular canal causes abnormal fluid endolymph displacement and a resultant sensation of vertigo

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Dix Hallpike Test: NystagmusThe nystagmus associated with BPPV has several important

characteristics which differentiate it from other types of nystagmus.• Positional: the nystagmus occurs only in certain positions• Latency of onsent: there is a 5-10 second delay prior to onset of

nystagmus• Nystagmus lasts for 5–120 seconds• Visual fixation does not suppress nystagmus due to BPPV• Rotatory/Torsional component is present or (in the case of lateral

canal involvement)the nystagmus beats in either a geotropic (towards the ground)or ageotropic (away from the ground) fashion

• Repeated stimulation, including via Dix-Hallpike maneuvers, cause the nystagmus to fatigue or disappear temporarily

Page 72: Vertigo 101

Management• Watchful waiting• Canalith repositioning procedure– Employs gravity to move the calcium buildup

• Vestibulosuppressant medication• Surgical management

– Semicircular canal occlusion

Page 73: Vertigo 101

VESTIBULAR NEURITIS

• acute, sustained dysfunction of the peripheral vestibular system with secondary nausea, vomiting, and vertigo

• sudden disruption of afferent neuronal input from 1 of the 2 vestibular apparatuses

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VESTIBULAR NEURITIS

• abrupt onset of severe, debilitating vertigo with associated unsteadiness, nausea, and vomiting.

– They often describe their vertigo as a sense that either they or their surroundings are spinning.

– Vertigo increases with head movement.

Page 75: Vertigo 101

LABYRINTHITIS

• inflammatory disorder of the inner ear or labyrinth caused most commonly by bacterial or viral infection or by an autoimmune

cause

Page 76: Vertigo 101

LABYRINTHITIS• Viral– characterized by a sudden, unilateral loss of vestibular

function and hearing– The acute onset of severe, often incapacitating, vertigo,

frequently associated with nausea and vomiting– Vertigo eventually resolves after several days to weeks;

however, unsteadiness and positional vertigo may persist for several months

Page 77: Vertigo 101

Bacterial Labyrinthitis• potential consequence of meningitis and otitis media and

may occur by either direct bacterial invasion (suppurative labyrinthitis) or through the passage of bacterial toxins and other inflammatory mediators into the inner ear (serous labyrinthitis).

• Profound hearing loss, severe vertigo, ataxia, and nausea and vomiting

Management• Treat underlying infection• Antiemetic medications• Steroids for recovery of peripheral vestibular function

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Thank You!