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Dr. Aseem MishraVestibular Physiology and Approach to a patient of vertigo

2This chart represents the basic organization of the vestibular system.

We see that the semicircs are primarily responding to head rotation or angular acceleration.

The Saccule and Utricle are responsive to Linear acceleration and the pull of gravity.

Together they form one of the three primary inputs to the central nervous system components dedicated to balance:visual// proprioception & tactileTo foreshadow, the outputs of this system include: the occulomotor muscles, the spinal cord and cerebellum, and the forebrain.Ascending PathwaysVestibular nerveVestibular nucleiCerebellumOculomotor complexCN 3, 4, and 6Along with vestibulospinal reflexes coordinate head and eye movementsRelay CentersThalamusConnection with vestibular cortex and reticular formation arousal and conscious awareness of body; discrimination between self movement vs. that of the environmentVestibular CortexJunction of parietal and insular lobeTarget for afferents along with the cerebellumBoth process vestibular information with somatosensory and visual inputNetter 1997

Neural Pathways for Equilibrium and Balance

Otolith organsUtricle and sacculeOtolith sensory structuresMaculaeOtolithic membraneOtoconiaMovement of gel membrane & otoconia cause a shearing action to occur over the hair cells sensitivity of otolithsOtolith FunctionRespond to:Linear head motion on accelerationStatic tiltTwo organs respond to respective accelerations or tilts in their respective planesSaccule has vertical orientation of maculaeUtricle has horizontal orientation of maculaeBear 1996

Striola of the MaculaStriola serves as a structural landmarkContains otoconia arranged in narrow trenches, dividing each otolithOrientation of the hair cells change over the course of the maculaAllows otoliths to have multidirectional sensitivity

Vertigo Vertigo(from theLatinvert"a whirling or spinning movement"[) is a subtype ofdizzinessin which a patient inappropriately experiences theperceptionof motion (usually a spinning motion) due to dysfunction of thevestibular system.It is often associated withnauseaandvomiting as well as abalance disorder, causing difficulties standing or walking. Types of vertigo There are three types of vertigo- objective subjective Pseudovertigo

Depending on the location of the dysfunction of the vestibular pathwayCentral vertigoPeripheral vertigo Differentiation Between Peripheral & Central Causes of Vertigo Peripheral Central

Nauseasevere moderateImbalance mild severeHearing Losscommon rareOscillopsiamild severeNeurologic Symptomsrare commonCompensationrapid slow(Furman JM, Whitney SL. 2000)Visual illusion of oscillating movement of stationary objectsCan arise with lesions of peripheral or central vestibular systemsIndicative of diminished VOR gainmotion of images on foveadiminished visual acuity Oscillopsia 15 NystagmusRapid alternating movement of eyes in response to continued rotation of the bodyPrimary diagnostic indicator in identifying vestibular lesionsPhysiologic nystagmusvestibular, visual, extreme lateral gazePathologic nystagmusspontaneous, positional, gaze evokedLabeled by the direction of the fast componentCentral vs. peripheral cause differentiated by duration Gaze-Evoked (Gaze-Paretic) NystagmusGaze-evoked nystagmus is elicited by the attempt to maintain an eccentric eye position, and it is the most common form of nystagmus encountered in clinical practice. Patients recovering from a central gaze palsy show a phase in which lateral gaze movement is possible but cannot be maintained in the deviated position; that is, the eyes drift back slowly toward primary position. A corrective saccade repositions the eyes eccentrically, and repetition of this pattern produces nystagmus, aptly designated "gaze-paretic."Saccades: Quick, darting conjugate movements which direct the eyes to a new target.

Smooth pursuit: A slower conjugate movement which allows for tracking of a moving object, or of a stationary object while we are moving.

Convergence: A dysconjugate movement of both eyes toward the midline to allow for focusing on a near object by adjusting the angle between the eyes. Targeting eye movements 18Variety of pathways contribute to saccadic control and smooth pursuit

19 Smooth Pursuit Two types:

Voluntary (actually termed smooth pursuit) movements - originate in the temporo-parietal lobe

Reflexive - which are under vestibular nuclear control alone and constitute what is called the vestibulo-ocular reflex (VOR).

20Voluntary Smooth Pursuitoriginates near the angular gyrus - Area 39 at the temporal parietal occipital junction

cells in this region are able to compute the speed and direction of a moving object

results in ipsilateral smooth pursuit

IPSI21 SaccadesUnder the control of three different areas in the brain:

voluntary saccades - frontal eye fields (Brodmanns area 8)

reflexive saccades to complex stimuli - parietal lobes (Brodmanns area 7)

reflexive saccades to elementary stimuli - superior colliculi22

SaccadesPause cells inhibitBurst Neurons which stimulate:III & VI (horizontal)

orIII & IV (vertical)23CEREBRAL HEMISPHEREMIDBRAINPONSPPRFPPRFVIVIFEFFEFIIIIIIVoluntary Horizontal Saccades

24 Reflexive Saccades

- to complex stimuli originates in area 7 of the parietal lobe

- to elementary stimuli originates in superior colliculi

dorsolateral prefrontal cortex involved in planning of eye movements25 Optokinetic ReflexCombination of saccades and smooth pursuit that allow tracking of targets in turn (e.g. counting sheep as they jump over a fence).

smoothly pursue one target, then saccade in the opposite direction to pick up the next target

parieto-temporal junction (smooth pursuit area) projects down to ipsilateral vestibular nucleus, inhibits it allowing ipsilateral smooth pursuit

then, the FEF of the same hemisphere generates a saccade back (contralateral) to the next target

26 Vestibular-Ocular Reflex (VOR)Causes eyes to move in the opposite direction to head movementSpeed of the eye movement equals that of the head movementAllows objects to remain in focus during head movements27 Reflexive Smooth Pursuit - VORmaintains gaze on a target despite head movement

reflex arc semicircular canal opposite the head turn detects motion and activates the ipsi vestibular n. which deactivates its inhibitory input on the ipsilateral VI

results in eyes turning opposite to the head turn

VIIIp339 Medical Neuroscience, Nadeau et al28

Head impulse test

Peripheral Vestibular DisordersVestibular NeuronitisLabyrinthitisMenieres Migranous VertigoMotion Sickness/ mal de Debarquement SyndromeFistulaBenign Paroxysmal Positional Vertigo (BPPV)35Central Vestibular DisordersVascularWallenbergs SyndromeHead InjuryCerebellar InfarctPostconcussive SyndromeDemyelinating DiseaseCongenital36 Risk Factors

4 risk factors, 78% chance of falling in an older adultSedativesCognitive impairmentLE disabilityFoot problemsBalance abnormalitiesDizziness dependence on visual cuesFear of fallingOrthostatic hypotension

(Tideiksaar R 1998)Objective of Clinical ExamEstablish location & severity of lesion (central or peripheral)Typical examination- history (hearing status)- cranial nerves- vestibularspontaneous nystagmus (imbalance in tone)postural instability (abnormal tone & gain; proprioceptive loss)VOR gain (maintained fixation, dynamic visual acuity)head shaking (compensated UVL; not necessarily PVL)caloricspressure sensitivity (fistula)positional nystagmus (Hallpike-Dix test)hyperventilation (anxiety; acoustic neuroma) History Site of lesionSymptomCommentPeripheral ( Labyrinth or VIII nerve )Tinnitus Special cases : LabyrinthineEar fullnessMenire's disease CP angleV , VI, VII VII + VIII neuritisEAC vesicles + VIIRamsay HuntBrainstem Diplopia(III, IV, VI or skew deviation) Facial numbness ( V ) Difficulty in swallowing, choking (IX, X ) Slurred speech ( XII and cerebellum ) Uni bilateral numbness, weakness, ataxia ( long tracts, cerebellum )Hemisphere Unilateral numbness, weakness Hemianopia (parieto-occipital lobe) Blindness ( both occipital lobes ) Loss of consciousness : Syncope, cardiac arrhythmia epilepsyMCA\PCABoth PCAs

CommonRare Non vestibular causes of dizzinessCauses Endocrine HypoglycemiaAdrenal failurePheochromocytoma Cardiovascular Vasovagal syncopeOrthostatic hypertensionEmbolic diseaseCardiac dysrhythmias Hematological Hyperviscosity syndromes Anemia Psychological Anxiety Phobias Panic attacks DrugsAlcoholAminoglycosidesAnticonvulsantsAntidepressantsDiureticsMarijuanaMethadoneQuinine/choloroquineSalicylatesSedativesVESTIBULAR SUPPRESANTSRombergs TestSharpened Rombergs TestDysdiadochokinesiaFukuda Marching/Unterbergers TestFukuda Writing TestTandem Gait testGaze Paretic nystagmusDynamic Visual AcuityScreening for Hyperventilation SyndromeTesting for Orthostatic HypotensionRombergs Test

Benign Paroxysmal Positional Vertigo (BPPV)Signs & symptoms attacks of vertigo precipitated by certain head positions & movementse.g., rolling over, neck extension, bending forwardlightheadedness; nauseaanxietyavoids movementdirection & duration of nystagmus differentiates between BPPV & a central vestibular lesion (CVL)Benign Paroxysmal Positional Vertigo (BPPV)5 criteria crucial in diagnosis (Hallpike-Dix Test):torsional/linear-rotary nystagmus; reproduced by provocative positioning with affected ear downnystagmus of 1-5 sec. latency nystagmus of brief duration (5-30 sec.)reversal of nystagmus direction on returning to upright positionresponse diminishes with repetition of maneuver (fatigability)(Massoud 96)

BPPVCupulolithiasisDebris, probably fragments of otoconia from the utricle, adhere to the cupulaTreatmentSemont, liberatory maneuver46BPPVMost commonly posterior SCC 65-70%Horizontal SCC in 15-20%

DiagnosisDix Hallpike TestPostererior and Anterior canalRoll TestHorizontal canal

The test to be repeated 3 times on 2 separate visitsHyperventilationHallpike-Dix ManeuverGold standard used to check for the presence of benign paroxysmal positional vertigo (BPPV)Nystagmus induced by this test is an objective measurement from which we can determine SSC dysfunction and assess a response to treatment49Canalolith Repositioning Epleys ManeuvreSemonts repositioning maneuvreSemonts Liberatory maneuvre270 barbecue Roll360 Yaw RollGuffonis ManeuvreForced Prolonged positioningBrandt Daroff ExerciseEpleys Repositioning maneuvre

360 Yaw Roll

When not to prescribe a Vestibular SuppresantsBPPV (Canalolithiaisis/Cupulolithiasis)Chronic MenieresChronic vestibular disorder

There is inhibition of the central compensation mechanism.Interferes with clinical interpretation of diagnostic tests.MedicationsAnti cholinergicsAnti HistaminesCalcium channel antagonist

Other Medications DiureticsAnxiolyticsVestibular neuritisSudden Spontaneous vertigoAggravated by head movementHorizontal torsional NystagmusPositive head Impulse TestSubjective Visual Horizontal TestShort course of SteroidsBilateral VestibulopathyBilateral vestibular or labyrinthine damageOtotoxictityPostural imbalance most marked while walkinngNo Spontaneous NystagmusHead Impulse TestVestibular RehabilitationVestibular MigraineEpisodic headache with vertigoRecurrent attacks with positional vertigoAuraPhonophobia/photophobiaAnti migranous treatment Vestibular Exercise ProgramObjectivesComplement CNS natural compensationdiminish dizziness & vertigoenhance gaze stabilizationenhance postural stability in static & dynamic situationsIncrease overall functional activitiesPatient educationnature of pathologyepisodic nature, prognosiscontrol of exacerbationsFactors affecting CompensationVisual ImpairmentImpaired PropricoceptionHyperventilationSomatizationAutonomic SymptomsVestibular Supressant DrugsHead InjuryCerebellar degeneration

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