Physiology of balance FINAL.pptxhtjydrjryjj

Navya525509 5 views 85 slides Sep 16, 2025
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About This Presentation

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Slide Content

PHYSIOLOGY OF BALANCE Moderator: Dr. Satish S. Raju Presenter: Dr. K. Navya Kiron

CONTENTS Introduction Components of vestibular system Peripheral vestibular system- Semicircular canal, Utricle and Saccule Central vestibular system-Vestibular nuclei and their projections Reflexes Nystagmus Important tests of Vestibular System

Introduction

Role of the vestibular system To ensure gaze stabilization To enable balanced locomotion and body position To provide general orientation of the body with respect to gravity To readjust autonomic functions after body orientation

ORIENTATION OF THE VESTIBULAR APPARATUS

Components of vestibular system PERIPHERAL CENTRAL

PERIPHERAL VESTIBULAR SYSTEM The non-auditory part of the inner ear - Vestibular Labyrinth Consists of two functional subdivisions: 1) The three Semicircular canals - two vertically oriented and one horizontally oriented 2) Otolithic organs - Saccule and Utricle Semicircular canals respond to Angular acceleration Otolithic organs are stimulated by Linear acceleration of the head, including the effects of gravity.

SEMICIRCULAR CANALS 3 in number- Lateral SCC, Anterior SCC, Posterior SCC They lie at right angles to each other and respond to Angular acceleration Due to this arrangement of the three canals in three different planes, any change in position of head can be detected

Every motion in space can be broken down into 6 degrees of freedom 3 rotational (roll, pitch and yaw) 3 translational (left-right, up-down, fore-aft).

SUPERIOR/ANTERIOR SEMICIRCULAR CANAL- Head nods up as in ‘YES’ motion (Pitch) POSTERIOR SEMICIRCULAR CANAL- When head tilt towards shoulder (Roll) LATERAL/HORIZONTAL SEMICIRCULAR CANAL- When head shakes side to side in ‘ NO’motion (Yaw )

CUMMINGS

Detection of head rotation by the Semicircular canals The moving endolymph in the SCCs is the key trigger for movement detection of the head Each semicircular canal has an enlargement at one of its ends called the AMPULLA Each ampulla contains a small crest called CRISTA AMPULLARIS

CRISTA AMPULLARIS It is a crest like mound of connective tissues on which lie the sensory epithelial cells. The cilia of the sensory hair cells project into the cupula, (gelatinous mass extending from the surface to the ceiling of the ampulla and forms a water tight partition) It get displaced to one or the other side like a swing door, with movements of endolymph. The gelatinous mass of cupula consists of polysaccharide and contains canals into which the cilia of sensory cells is projected

Ewald's three laws A stimulation of the semicircular canal causes a movement of the eyes in the plane of the stimulated canal In the horizontal semicircular canals, an ampullo -petal (towards ampulla) endolymph movement causes a greater stimulation than an ampullo -fugal one. In the vertical semicircular canals, the reverse is true.

Three forces act upon the endolymph and cupula in the Semi circular canal- while rotating about an axis The inertial force , proportional to the mass of the endolymph and cupula The elastic restoring force of the cupula that positions the cupula back to the centre position after stimulation The viscous forces that act upon the fluid when sliding past the internal wall of the tube - Dependent on the speed of relative movement of the endolymph with respect to the wall.

When a person’s head begins to rotate in any direction, the inertia of the fluid in one or more of the semicircular ducts causes the fluid to remain stationary while the semicircular duct rotates with the head. This process causes fluid to flow from the duct and through the ampulla, bending the cupula to one side Rotation of the head in the same direction causes the cupula to bend to the opposite side

HAIR CELLS Type I Hair cells- Flask-shaped and have “ chalice ”-type afferent-nerve endings that surround all except the kinocilium- or stereocilia-bearing end. Efferent-nerve terminals synapse with the afferent calyx near its base. Type II Hair cells - Cylindrical or test-tube shape and have several small bouton-type nerve endings that represent both afferent and efferent innervation only at the cell’s base. Type I hair cells are concentrated in the central apex of the cristae and the central part of the maculae Type II hair cells are more numerous toward the peripheral region of the end-organ

SHAMBAUGH BALLENGERS

Each hair cell has 50 to 70 small cilia called stereocilia, plus one large cilium, the kinocilium on its upper surface The kinocilium is thickest & largest among them and is located on the edge of the cell and the stereocilia become progressively shorter toward the other side of the cell The ion channels involved in mechanoelectrical transduction are located in the stereocilia Each hair cell of the equilibrium apparatus synapses with the vestibular nerve.  Directional Sensitivity of the Hair Cells—Kinocilium

Stereocilia deflection is the common mechanism by which all hair cells transduce mechanical forces. Stereocilia within a bundle are linked to one another by protein strands called Tip links that span from the side of a taller stereocilium to the tip of its shorter neighbor in the array. The tip links act as gating springs for mechanically sensitive ion channels When deflected in the open or “on” direction which is toward the tallest stereocilium, cations—which include potassium ions from the potassium-rich endolymph—rush in through the gates, and the membrane potential of the hair cell becomes more positive.

This in turn activates voltage sensitive calcium channels at the basolateral aspect of the hair cell, and an influx of calcium leads to an increase in the release of excitatory neurotransmitters, principally glutamate, from hair cell synapses onto the vestibular primary afferents All of the hair cells on a semicircular canal crista are oriented or “polarized” in the same direction.

Cummings

SHAMBAUGH

VELOCITY STORAGE During constant speed rotations, elastic forces pull the cupula again back to its centre position. After sudden cessation of the rotation - the endolymph continues to move within the SCC and a nystagmus in the opposite direction becomes evident for another 20–30 seconds. The time constant during which the cupula repositions itself is determined as approximately 5–7 seconds, which implies that the cupula is almost entirely restored to its central position after 12 seconds. The fact that the nystagmus outlasts this mechanical phenomenon is due to the so-called ‘velocity storage mechanism’ (VSM) It is a process that maintains the sense of rotation even after the rotation has stopped This circuitry is therefore a mechanism that stores neural activity related to head and eye velocity and discharges it over its own time course.

OTOLITH ORGANS: UTRICLE & SACCULE UTRICLE : lies in the posterior part of bony vestibule It receives the five openings of the three semicircular ducts. SACCULE : lies anterior to the utricle and opposite the stapes footplate. Connected to utricle by utriculosaccular duct. Utricle lies relatively horizontal & Saccule lies in vertical plane

MACULA Maculae of the utricle and saccule are flat sheets of epithelium that are oriented at right angles to each other Utricle in the anterior–posterior plane & the Saccule in the superior–inferior plane Utricular macula -U-shaped and the Saccular macula- S-shaped Macula consists mainly of two parts: ( i ) Sensory neuroepithelium , made up of type I and type II hair cells. (ii) Otolithic membrane , which is made up of a gelatinous mass and on the top, the crystals of calcium carbonate called otoliths or otoconia The cilia of hair cells project into the gelatinous layer. The linear, gravitational and head tilt movements cause displacement of otolithic membrane and thus stimulate the hair cells

The Striola divides the macula into two halves, in which the hair cell ciliary polarization is in opposite directions In Utricular macula - hair cells are oriented toward the striola Saccular macula - hair cells are oriented away from the striola

Detection of orientation of head by Maculae The macula of the utricle lies mainly in the horizontal plane on the inferior surface of the utricle and plays an important role in determining orientation of the head when the head is upright. The macula of the saccule is located mainly in a vertical plane and signals head orientation when the person is lying down. Each macula is covered by a gelatinous layer in which many small calcium carbonate crystals called statoconia are embedded.

Macula contains thousands of hair cells -project cilia up into the gelatinous layer. The bases and sides of the hair cells synapse with sensory endings of the vestibular nerve. The calcified statoconia have a specific gravity two to three times the specific gravity of the surrounding fluid and tissues. The weight of the statoconia bends the cilia in the direction of gravitational pull. Hair cells are all oriented in different directions in the maculae of the utricles and saccules so that with different positions of the head, different hair cells become stimulated. The “patterns” of stimulation of the different hair cells apprise the brain of the position of the head with respect to the pull of gravity.

Detection of linear acceleration by Maculae When the body is suddenly thrust forward—that is, when the body accelerates—the statoconia fall backward on the hair cell cilia, and information of disequilibrium is sent into the nervous centers, causing the person to feel as though he or she were falling backward. This sensation automatically causes the person to lean forward until the resulting anterior shift of the statoconia exactly equals the tendency for the statoconia to fall backward because of the acceleration. At this point, the nervous system senses a state of proper equilibrium and leans the body forward no farther. Thus, the maculae operate to maintain equilibrium during linear acceleration in exactly the same manner as they operate during static equilibrium

VESTIBULOOCULAR REFLEX (VOR) It is a reflex ,where activation of vestibular system of the ear causes eye movement ,which is to stabilize image on the centre of the retina The left and right Semicircular canals are oriented in the head such that any movement always induces an antagonistic response in both canals

Push–pull principle of the VOR : (yaw-plane rotation –Horizontal semicircular canal) During head rest, hair cells in both SCCs have a resting discharge rate of 90 spikes per second. Head rotation is to the right Endolymph fluid lags behind, i.e. moves relative to the left within each SCC due to inertia The cupula bends to the left in each canal In the (leading) right SCC the stereocilia bend towards the kinocilium. In the (following) left SCC the stereocilia bend away from the kinocilium. The discharge rate increases in the leading right ear (e.g. from 90 to 300 spikes per second). The discharge rate decreases in the following left ear (e.g. from 90 to 20 spikes per second) The vestibular nuclei interpret the difference in discharge rates between left and right SCCs as movement to the right, and therefore trigger the oculomotor nuclei to drive the eyes to the left to maintain gaze stabilization.

The 3 arc neuron representation of VOR HEAD MOVED TO RIGHT

Cummings

CENTRAL VESTIBULAR SYSTEM

VESTIBULAR NERVE Vestibular or Scarpa's ganglion is situated in the lateral part of the internal acoustic meatus. It contains bipolar cells. The distal processes of bipolar cells innervate the sensory epithelium of the labyrinth while its central processes aggregate to form the vestibular nerve Vestibular Portion of C.N. VIII Superior division : Utricle, Horizontal & Anterior Canals and anterior part of Saccule Inferior division: Posterior canal & posterior part of Saccule

CENTRAL VESTIBULAR CONNECTIONS The fibres of vestibular nerve end in vestibular nuclei and some go to the cerebellum directly. In the brain stem there are 4 Vestibular nuclei: Superior ( Bechterew’s or angular) Lateral (Deiters’) Medial (Schwalbe’s or principal or triangular) Descending (Spinal or Inferior)

The cell bodies of the 19,000 neurons supplying the cris­tae and maculae on each side are located in the vestibular ganglion. Each vestibular nerve terminates in the ipsilateral four-part vestibular nucleus and in the floc­culonodular lobe of the cerebellum. The vestibular nuclei also project to the thalamus and from there to two parts of the primary somatosensory cortex. The ascending connec­tions to cranial nerve nuclei are largely concerned with eye movements (via MLF)

Efferents from vestibular nuclei go to: Nuclei of CN III, IV, VI via Medial longitudinal fasciculus ( Vestibulo -Oculomotor ) Motor part of spinal cord (Vestibulospinal fibres) - coordinates the movements of head, neck and body in the maintenance of balance Cerebellum ( Vestibulocerebellar fibres) - coordinate input information to maintain the body balance. Autonomic nervous system: This explains nausea, vomiting, palpitation, sweating and pallor seen in vestibular disorders (e.g. Ménière's disease). Vestibular nuclei of the opposite side - commissural pathway Cerebral cortex (Temporal lobe). This is responsible for subjective awareness of motion

REFLEXES

VESTIBULOSPINAL REFLEX Through the lateral vestibulospinal tract. Projects to cervical, thoracic, and lumbar segments via the ventral funiculus Entirely ipsilateral Originates in the lateral vestibular nucleus, predominantly an otolith signal Allows the limbs to adjust for head movements. Provides excitatory tone to extensor muscles Decerebrate rigidity is the loss of inhibition from cerebral cortex and cerebellum on the LVST, and exaggerates the effect of the tonic signal in the LVST

VESTIBULO-COLLIC REFLEX Through the Medial Vestibulospinal Tract Originates in the medial vestibular nucleus, predominantly a SCC canal signal Projects to cervical segments via the medial longitudinal fasciculus Predominantly ipsilateral. Keeps the head still in space mediating the vestibulo-collic reflex

CERVICO-OCULAR REFLEX When the head is fixed but the body is rotated, nystagmus may be observed. This reflex is based on the stimulation of neck receptors. In humans, this reflex is very unreliable and unpredictable Only in subjects with congenital peripheral vestibular loss, does this alternative strategy for gaze stabilization become helpful.

T ests of Vestibular System CLINICAL TESTS LABORATORY TESTS

Clinical tests of Vestibular function SPONTANEOUS NYSTAGMUS HEAD THRUST POSITIONAL TEST FISTULA TEST ROMBERG TEST UNTERBERGER'S TEST

SPONTANEOUS NYSTAGMUS Defined as - Involuntary, rhythmical, oscillatory movement of eyes It may be horizontal , vertical or rotatory Vestibular nystagmus has a slow and a fast component, and by convention, the direction of nystagmus is indicated by the direction of the fast component. Intensity of nystagmus is indicated by its degree Slow component - mediated by Abnormal vestibular system  uninhibited labyrinth Fast component – mediated by central (brainstem) corrective mechanism

Alexander’s law Alexander's law describes eye movements seen in patients with an acute unilateral vestibular loss After unilateral vestibular loss, a central process called the " Leaky integrator " contributes to eye motion and nystagmus allowing the eye to drift to center, regardless of its position. This is due to imbalance in vestibular activity between the two labyrinths cause nystagmus to be more pronounced when looking away from the lesion

In straight-ahead gaze (A), the vestibular slow phase is only manifest. When the eyes look to the direction of the fast phase (right, B ), the leaky integrator causes eye to drift to Left. This drift adds to the vestibular slow phase, and net Slow Phase Velocity(SPV) increases – Nystagmus is more pronounced When eyes look to the direction of slow phase(left, C)the leaky integrator causes eye to drift to right. It subtracts from the vestibular slow phase, and the net SPV decreases

HEAD THRUST TEST A brief, high acceleration rotation of head in the horizontal plane are applied while instructing the patient to look carefully at the examiner's nose. In normal individual there is no delay (A) In case of hypofunctional horizontal canal- fails to drive eyes to opposite side (B) A catch-up saccade brings them into position after a delay. A B

POSITIONAL TEST - DIX HALLPIKE TEST Benign paroxysmal positional vertigo (BPPV) is the most common cause of dizziness in patients It is usually caused by pathology in the posterior semicircular canal, but can affect the horizontal, superior, or multiple canals Diagnosis of BPPV is made by Dix- hallpike test /Positional test method.

Patient sits on a couch. For testing Right posterior SCC BPPV, head is turned 45 degree, so chin towards right shoulder and then place the patient in a supine position so that head hangs 30 degree below the horizontal and neck is extended. This positioned is maintained for at least 30sec. Nystagmus typically begins after a latency of 2 to 10 sec, increases in amplitude over about 10 sec, and declines over the next 30 sec. Patient also complains of vertigo when the head is in critical position. On subsequent repetition nystagmus disappears altogether, i.e. nystagmus is fatigable METHOD:

PERIPHERAL NYSTAGMUS CENTRAL NYSTAGMUS Latency 2-20 sec No latency Duration Less than 1 min More than 1 min Direction of Nystagmus Direction – fixed i.e towards the undermost ear Direction changing Fatiguability Fatiguable Non fatiguable Accompanying Symptoms Severe vertigo None or Slight Positional Nystagmus – Central vs Peripheral lesions

FISTULA TEST Basis of this test is to induce nystagmus by producing pressure changes in the external canal which is then transmitted to the labyrinth. Stimulation of labyrinth results in nystagmus and patient complains of vertigo. INTERPRETATIONS: Normally test is Negative. Positive in - erosion of horizontal canal by cholesteatoma, fenestration operation (surgically created), abnormal opening in oval window (post stapedectomy) or the round window (rupture of round window membrane)– Implies that labyrinth is functional False negative test seen in cholesteatoma covering the fistula site. False positive test seen in congenital syphilis, and in about 25% cases of Meniere's disease - ( Hennebert's sign).

ROMBERG TEST Patient is asked to stand with feet together and arm by the side with eyes first open and then close. In peripheral vestibular lesion with eyes open patient can compensate but with eyes closed patient can't, and sways to the site of lesion. In central lesion, patient shows instability

UNTERBERGER'S TEST Patient is asked to close his eyes with out-stretched hands in front and asked to step up and step down his feet alternately go times in 1 sec. Rotation to one side indicates vestibular hypofunction of that side or hyperfunction of the opposite. Fukuda stepping test - turning while marching in place for 30 sec with eyes closed --are signs of vestibulospinal asymmetry due to vestibular lesions

Laboratory tests of vestibular function CALORIC TEST ELECTRONYSTAGMOGRAPHY OPTOKINETIC TEST ROTATION TEST GALVANIC TEST VESTIBULAR EVOKED MYOGENIC POTENTIALS (VEMP)

CALORIC TEST The basis of this test is to induce nystagmus by thermal stimulation. The advantage of this test is that each labyrinth can be tested separately. 3 TYPES- Modified Kobrak Test Fitzgerald-Hallpike Test Cold Air Caloric Test

1) MODIFIED KOBRAK TEST : Ear is irrigated with ice water for 60 sec, first with 5ml and if there is no response, 10, 20, 40ml. Normally, nystagmus towards opposite ear will be seen in 5ml of ice water. If response is seen in between 5ml to 40ml, labyrinth is considered hypoactive. No response to 40ml, indicates dead labyrinth.

2) FITZGERALD-HALLPIKE TEST/ BITHERMAL CALORIC TEST: Patient lies supine with head tilted 30° forward so that horizontal canal is vertical. Ear is irrigated for 40 sec alternately with water at 30 degree C and 44 degree C . Eyes are observed for nystagmus. Time taken from the starting point of irrigation to the end point of nystagmus is recorded and charted on a calorigram . If no nystagmus in any ear, test is repeated with water at 20 degree C for 4min before labelling the labyrinth dead. A gap of 5 min should be allowed between two ears. Depending upon the response Canal paresis and Directional preponderance can be understood.

W arm caloric test transmits heat to the lateral semicircular canal, causing the endolymph to be warmed and less dense and to rise and flow toward the cupula ( ampullopetal flow). This is stimulatory to the lateral canal, and nystagmus is generated with the fast phase beating toward the irrigated ear. C ool caloric stimulus cools the endolymph, making it more dense and causing it to fall away from the cupula ( ampullofugal flow )  inhibitory  nystagmus away from the irrigated ear. Cold-Opposite Warm-Same (COWS ) is a simple way to remember the association

3) DUNDAS GRANT COLD-AIR CALORIC TEST It is done when there is perforation of TM. Dundas Grant tube is a coiled copper tube wrapped in cloth. The Air in the tube is cooled by pouring Ethyl chloride and then blown into the ear. It is only a rough qualitative test

ELECTRONYSTAGMOGRAPHY Method of detecting and recording of nystagmus, which is spontaneous or induced by caloric, positional, rotational or optokinetic stimulus The test depends on the presence of corneo -retinal potentials which are recorded by placing electrodes at suitable places round the eyes. The test is also useful to detect nystagmus, which is not seen with the naked eye.

Patient is asked to follow a series of vertical stripes on a drum moving first from right to left and then from left to right. Normally it produces nystagmus with slow component in the direction of moving stripes and fast component in the opposite direction. Optokinetic abnormalities are seen in brainstem and cerebral hemisphere lesions Thus, this test is useful to diagnose a central lesion OPTOKINETIC TEST

GALVANIC TEST H elps in differentiating an end organ lesion from that of vestibular nerve. Patient stands with his feet together, eyes closed and arms outstretched and then a current of 1 mA is passed to one ear. Normally, person sways towards the side of anodal current. Body sway can be studied by a special platform. POSTUROGRAPHY To evaluate vestibular function by measuring postural stability and is based on the fact that maintenance of posture depends on three sensory inputs—visual, Vestibular and somatosensory. It uses either a fixed or a moving platform

ROTATION TEST Patient is seated in Barany’s revolving chair with his head tilted 30° forward and then rotated 10 turns in 20 s. The chair is stopped abruptly and nystagmus observed. Normally there is nystagmus for 25–40 s. Disadvantage of the test is that both the labyrinths are simultaneously stimulated during the rotation process and cannot be tested individually.

Test to study function of otolith organs—the saccule and utricle. Normally their function is linear acceleration. They can also be stimulated by loud sound of air or bone conduction. Even tapping the head can stimulate them. Myogenic potentials can be picked up from either the sternocleidomastoid (cervical) muscle or ocular muscle (inferior oblique or superior rectus) and have respectively been called cVEMP and oVEMP . Reflex arc is: From Saccule —inferior vestibular  vestibular nucleus  ipsilateral vestibular spinal tract  spinal accessory nerve (CN XI)— sternocleidomastoid From Utricle —superior vestibular nerve  vestibular nuclei  medial longitudinal fasciculus—oculomotor (CN III) nerve  inferior oblique muscle VESTIBULAR EVOKED MYOGENIC POTENTIALS (VEMP)

References Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's review of medical physiology. 25th ed. New York: McGraw-Hill Education; 2016. Gleeson M, Browning GG, Burton MJ, Clarke R, Hibbert J, Jones NS, et al. Scott-Brown’s otorhinolaryngology: head and neck surgery. 8th ed. Boca Raton: CRC Press; 2018.Cummings CW, Flint PW, Haughey BH, Lund VJ, Niparko JK, Richardson MA, et al. Cummings otolaryngology: head and neck surgery. 6th ed. Philadelphia: Elsevier Mosby; 2015. Hall JE, Guyton AC. Guyton and Hall textbook of medical physiology. 13th ed. Philadelphia: Elsevier Saunders; 2016. Schuknecht HF, Pathak S. Schuknecht’s pathology of the ear. 6th ed. Shelton: People’s Medical Publishing House; 2010.(Shambaugh’s) Snow JB, Ballenger JJ. Ballenger’s otorhinolaryngology: head and neck surgery. 18th ed. Shelton: PMPH-USA; 2016.Netter FH. Atlas of human anatomy. 6th ed. Philadelphia: Elsevier Saunders; 2014.

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