1. Anatomy 1000
   1. Intro:
      1. – Dizziness is one of the most common complaint adults report to their physicians & prevalence increases with age – Older than 75 years of age, dizziness is the most common reason to see a physician – Peripheral vestibular system = most common origin for patient signs & symptoms
   2. Peripheral Vestibular Syst
      1. 3 Primary Functions of the Peripheral Vestibular Syst:
         1. Stabilization of visual images on the fovea of the retina during head movement to allow clear vision
         2. Maintaining postural stability, especially during movement of the head
         3. Providing information used for spatial orientation
      2. Semicircular Canals
         1. – Within the Petrus portion of each temporal bone lies the membranous vestibular labyrinth – Each labyrinth contains 5 neural structures that detect head acceleration: A. 3 semicircular canals (SCC) (horizontal, post, ant) B. 2 otolith organs – 3 semicircular canals respond to angular acceleration & are orthogonal w/respect to each other – Angular head rotation stimulates each canal to varying degrees – SCC-filled w/endolymp that moves freely w/in each canal in responses to the direction of the angular head rotation –The SCCs enlarging one end to form the ampulla; within the ampulla lies the cupula-gelatinous barrier that contain sthe sensory hair cells –Kinocilia and stereocilia of the hair cells are seated in the crista ampullaris – Motion of the stereocilia TOWARD the kinocilia causes EXCITATION (depolarization) and motion of the stereocilia AWAY from the kinocilia leads to INHIBITION (hyperpolarization) – Each of the SCCs respond best to motion in its own plane with coplanar payers exhibiting a push-pull dynamic – The brain detects the direction of head movement by comparing input from the coplanar labyrinthine mates
      3. Otolith Organs
         1. – Composed of the saccule & utricle & respond to linear acceleration & static head tilt – Sensory hair cells project into a gelatinous material which provides the otolith organs w/an inertial mass – Motion toward the kinocilia causes excitation while motion away leads to inhibition – Utricular excitation occurs during horizontal linear acceleration &/or static head tilt – Saccular excitation occurs during vertical linear acceleration
   3. Central Vestibular Syst
      1. – Vestibular reflexes = controlled within brainstem – Parietal & insular regions/lobes=location for vestibular cortex/cortical location for processing vestibular info – Connections with the vestibular cortex, thalamus & reticular formation to enable the vestibular system to contribute to the integration of arousal & conscious awareness of the body, as well as to discriminate between movement of self & the environment – Cerebellar connections help maintain calibration of the vestibulo-ocular reflex (VOR), contribute to posture during static & dynamic activities, & influence the coordination of limb movements
2. Physiological & Motor Control
   1. Important Principles of the vestibular System include:
      1. 1. Tonic firing rate 2. VOR 3. Push-pull mechanism 4. Inhibitory cut off 5. Velocity storage system (VSS)
   2. Tonic Firing Rate
      1. – The presence of high tonic firing rate means each vestibular system can detect head motion through excitation or inhibition – During angular head rotations, ipsilateral vestibular efferents & ipsilateral central vestibular neurons are excited – Such head movements also result in inhibition of peripheral afferent & of many central vestibular neurons receiving innervation from the contralateral labyrinth
   3. Vestibulo-Ocular REflex & Vestibulo-Ocular Reflex Gain & Phase
      1. VOR is responsible for:
         1. Maintaining stability of an image on the fovea of the retina during rapid head movements – to do this the VOR must generate rapid compensatory eye movements in the direction opposite the head rotation
      2. The pathways controlling the VOR=described as 3-neuron arc
         1. In the case of the anterior SCC: 1. Primary vestibular efferents from the anterior SCC synapse in the ipsilateral vestibular nuclei 2. Secondary vestibular neurons receiving innervation from ipsilateral labyrinth decussates & synapse in the contralateral oculomotor nucleus 3. Motor neurons from the oculomotor nucleus then synapse at the NMJ of the ipsilateral superior rectus & contralateral inferior oblique muscles respectively
      3. Normally, as the head moves in one direction, the eyes move in the opposite direction with equal velocity
      4. VOR Phase
         1. Second useful measure of the vestibular system & represents the timing relationship for eye & head position
      5. Head Velocities:
         1. – Head of velocities below 60° per second gaze stability can be maintained fairly well using smooth pursuit – Had velocity greater than 60° per second, vestibular system is primarily responsible for generating eye movement to maintain gaze on the target – The VOR operates at head velocities as great as 350- 400° per second
   4. Push-Pull Mechanism
      1. – The brain detects head movement & direction through comparison of inputs between the 2 vestibular systems – As the head is turned to the right, the right horizontal SCC will have an increased firing rate while the left horizontal SCC has a decrease firing rate = called the push-pull mechanism – The brain is then responsible for recognizing the difference & interpreting movement – Faulty interpretation = difficulties with gays stabilization, postural stability, & motion perception
   5. Inhibitory Cutoff
      1. – During angular head rotations ipsilateral vestibular efferents can be excited up to 400 spikes per second – concomitant hyperpolarization of the opposite labrum and it also occurs – The hyperpolarization of the hair cells in the opposite labrum and it can only decrease the firing rate to zero, at which point the inhibition is cut off (inhibitory cutoff) – The response to head movements that hyperpolarize the hair cells and limited to a velocity range up to 70 – 100° per second – Because the resting discharge rate of these efferents & Central vestibular neurons averages 70 – 100 spikes per second, inhibitory cutoff is more likely to occur than is excitation saturation
   6. Velocity Storage Syst
      1. – The signal generated by movement of the cupula is brief – The response is sustained by a circuit neurons in the medial vestibular nucleus & lasts longer than 10 seconds in people with normal vestibular function – The purpose of sustaining the vestibular input is thought to assist the brain in detecting low frequency head rotation
3. Examination
   1. Hx
      1. Key Elements of taking the Hx:
         1. 1. Identification of symptoms 2. Duration & circumstances under which the symptoms occur
      2. Identification of Symbols
         1. Most complaints of dizzy can be categorized as:
            1. Vertigo
            2. def: an illusion of movement
            3. Tends to be episodic & indicate pathology at one or more places along the vestibular pathways:
            4. Acute stage of a unilateral vestibular hypofunction (UVH)
            5. Most common!
            6. Displaced otoconia (benign paroxysmal positional vertigo)
            7. Acute unilateral brainstem lesion affecting the root entry zone of the peripheral vestibular neurons or vestibular nuclei
            8. Light-headedness
            9. – Feeling bad fainting is about to occur & can be caused by non-vestibular factors such as hypotension, hypoglycemia, or anxiety – Is vague & less localizing than vertigo
            10. Dysequilibrium
            11. def: the sensation of being off balance
            12. Causes:
            13. – Acute & chronic vestibular lesions – Is often associated with non-vestibular problems such as decreased somato sensation or weakness in the LEs
            14. Oscillopsia
            15. def: is the subjective experience of motion of objects in the visual environment that are known to be stationary
            16. – Can occur with head movements in patients with vestibular hypofunction sense of a similar system is not generating an adequate compensatory eye velocity during the head motion – such a deficit in the VOR results in motion of images on the fovea & in a decline in visual acuity
      3. Duration and Circumstances of Symptoms
         1. PT must determine the following concerning the attack of vertigo, lightheadedness, dysequilibirum or oscillopsia:
            1. How Recently the Pt has had it
            2. If Episodic:
            3. PT must attempt to determine the average duration of the episodes and seconds, minutes, or hours
            4. Vertigo lasting seconds to minutes:
            5. suggest benign Paroxysmal Positional Vertigo
            6. Vertigo lasting minutes to hours:
            7. suggest Meniere's disease
            8. Vertigo lasting for days:
            9. Implies Vestibular Neuronitis or Migraine associated dizziness
            10. Whether the Sx is Constant or Episodic
            11. Under what circumstances the Pt. Experiences Sx
            12. ie: w/particular movements, positions, or at rest
   2. Test and Measures
      1. VAS
      2. Dizziness Handicap Inventory
         1. – Measures a patient's self perceived handicap as a result of vestibular disorders – excellent test retest reliability (r=0.97) – good internal consistency reliability (r=0.89) – Useful to establish subjective improvement
         2. Table 24.3 p. 1005
      3. Functional Disability Scale
         1. – To determine a patient's response to PT – Authors reported patients who believe their vestibular disorders were more disabling did not improve as such as those who perceive themselves to be less disabled
      4. Motion Sensitivity Quotient
         1. – Provide a subjective score of an individual's dizziness – Test involves placing patients into positions incorporating head or entire body motion to determine whether the movement reproduces dizziness
         2. Figure 24.8 p. 1006
      5. Eye Movements
         1. Owing to the direct relationship between vestibular receptors in the inner ear & I movements produced by the VOR, the examination of eye movements can be of primary importance and defining & localizing vestibular pathology
         2. Key Tests include observation for:
            1. 1. Nystagmus 2. VOR at high acceleration (head thrust test) 3. Head shaking induce nystagmus (HSN) 4. Positional testing 5. Dynamic visual acuity (DVA)
         3. Nystagmus
            1. Is the primary diagnostic indicator used in identify most peripheral & central vestibular lesions
            2. – In involuntary eye movement, nystagmus due to a peripheral vestibular lesion is composed of both slow & fast component eye movements
            3. For Individuals w/unilateral vestibular lesion:
            4. – The flow component is due to relative excitation of one-sided vestibular system – the past component is generated from the parapontine reticular formation in the brainstem & repositions the eye to the center of the orbit – The direction opposite the quick component of the nystagmus localizes the side of the vestibular lesion
            5. Spontaneous Nystagmus:
            6. – Nystagmus due to a vestibular lesion – Occurs in the absence of motion because of asymmetry between the functioning & nonfunctioning vestibular systems – Brain perceives the asymmetry as active stimulation from the healthy side – May always be present in the dark after a unilateral loss of vestibular function – Resolution of spontaneous the statements in the light or dark occurs when symmetry between the resting fire rates of both vestibular systems is reestablished
         4. Observation for Nystagmus
            1. – Can be suppressed in light & a person visually fixate on a target – observation should be performed under conditions in which the person can't see surrounding environment: Frenzel lenses or Infrared Camera Syst
         5. Head Thrust Test
            1. – Used to examine the semicircular canal function – Cervical are 0M should be determined prior to – Provides a sensitive indication of vestibular hypofunction in patients with complete loss of function in the affected labyrinth that occurs following ablative surgical procedures (labyrinthectomy) – Is less sensitive and detecting hypofunction in patients with incomplete loss of function
            2. Procedure:
            3. 1. Performed by having the patient first fixate on a near target (PT's nose) 2. When testing the horizontal SCC , the head is flexed 30° 3. Patients are asked to keep their eyes focused on a target while their head is manually rotated in unpredictable direction using small amplitude, high acceleration angular thrust
            4. Pt w/normally functioning VOR:
            5. The eyes move in the direction opposite to the head movement & gaze will remain on the target
            6. Pt. w/loss of vestibular fnx
            7. Will not move the eyes as quickly as the head rotation & the eyes move off target – patient will make corrective saccade to reposition the eyes (fovea) on the target
            8. Corrective Saccade:
            9. – Corrective saccade - rapid eye movement used to reposition the eyes of the target of interest – Appearance of corrective saccade's indicates vestibular hypofunction as determined by the headdress test & occurs because inhibition of vestibular afferent & central vestibular neurons on the Intech side (persons with unilateral vestibular hypofunction) are less effective in encoding the amplitude of a head movement than excitation (inhibitory cut off)
            10. Pt. w/unilateral peripheral lesion or patho of central vestibular neurons:
            11. Will not be able to maintain gaze when the head is rotated quickly toward the side of the lesion
            12. Pt. w/bilateral loss of vestibular fnx:
            13. Will make corrective saccades after a head thrust to either side
         6. Head-Shaking Induced Nystagmus
            1. – Useful aid in the diagnosis of a unilateral peripheral vestibular defect – The presence of vertical nystagmus after either horizontal or vertical headshaking suggest a central lesion
            2. Procedure:
            3. 1. Vision is occluded and the patient is instructed to close eyes 2. PT flexes had 30° & oscillates the head horizontally for 20 cycles at a frequency of 2 repetitions per second (2 Hz) 3. Upon stopping the oscillation, patient opens eyes & PT checks for nystagmus
            4. Pts w/normal vestibular fnx:
            5. Nystagmus will not be present – an asymmetry between the peripheral vestibular inputs to central vestibular nuclei, however may result in headshaking induce nystagmus (HSN)
            6. Pt. w/UVH (unilateral vestibular hypofnx)
            7. Will manifest a horizontal HSN, w/the quick phases of the nystagmus directed toward the healthy ear & the slow phases directed toward the lesioned ear – not all patients with UVH will have HSN
            8. Pts. w/a complete loss of vestibular fnx bilaterally:
            9. Won't have HSN because neither systems functioning – As a result, there is no asymmetry between the tonic firing rates
         7. Positional Testing
            1. – Commonly used to identify whether otoconia have been displaced into the SCC, causing a condition referred to as Benign Paroxysmal Positional Vertigo (BPPV) thus making the SCCs sensitive to changes in head position – The direction & duration of the resultant nystagmus can help determine whether the patient has BPPV or a central lesion
            2. Hallpike-Dix Test Fig 24.10 p. 1009
            3. – Most common positional test used to examine for Begign Paroxysmal Positional Vertigo (BPPV) 1. Patient is moved from sitting with head rotated 45° to one side, to a supine position with the head extended 30° beyond horizontal, head still rotated 45° 2. Maneuver places each of the SCC and a gravity dependent position & PT should observe the eyes for nystagmus (direction of nystagmus is unique to be involved SCC)
            4. Alt Hallpike-Dix Test
            5. Pt. is asked to move into a sidelying position Fig 24.11 p. 1009
            6. In Both TESTS:
            7. – The ear toward the ground is the labyrinth being tested – Is horizontal SCC BPPV is suspected, the role test can be used instead
            8. Roll Test Fig 24.12 p.1010
            9. 1. Patient is positioned supine with head flexed 20° 2. Rapid rotations to the sides are done separately & PT observes for nystagmus
         8. Dynamic Visual Acuity Test
            1. – Is the measurement of visual acuity during horizontal motion of the head – a bedside & computerized form of the test can be used to identify the functional significance of the vestibular hypofunction – Head velocities need to be greater than 100° per second at the time DVA is measured to ensure that the vestibular afferents from the contralateral side are driven into inhibition & the letters are not identified with a smooth pursuit eye movement
            2. Procedure:
            3. 1. Static visual acuity is determined first 2. Patient asked to read the lowest line they can see on a wall-mounted acuity chart 3. Patient then attempts to read the chart while the PT horizontally oscillates the patient's head at a frequency of 2 Hz (or a metronome can be used)
            4. Pts. w/normal vestibular fnx:
            5. Head movement results and little or no change of visual acuity compared with the head still (<1 line difference)
            6. Pts. w/loss of vestibular fnx:
            7. – Eyes will not be stable in space during head movements – this causes a decrement in DVA compared with visual acuity when the head is still – a 3 or more line decrement in visual acuity during head movement is suggestive of vestibular hypofunction
      6. Gait & Balance Testing
         1. Common Balance Tests & Expected Results Table 24.5 p.1010
      7. Vestibular Function Tests
         1. Semicircular Canal Tests
            1. More common vestibular fnx tests incld:
            2. 1. Caloric testing 2. Rotary chair test
            3. Caloric Testing
            4. – Useful for determining the side of the deficit, because each labyrinth is stimulated separately – Provides limited information because only the horizontal SCCs are stimulated & that stimulation corresponds to a frequency (0.025 Hz) that is much lower than the natural frequency of head movement (1-2 Hz)
            5. Procedure:
            6. 1. Involves infusing the external auditory canal with air/water 2.The stimulus introduces a temperature gradient 3. In the presence of gravity, this temperature gradient results in the convective flow of endolymph that deflects the cupula & generates nystagmus within the horizontal SCC
            7. Rotary Chair Test
            8. – Stimulates each vestibular system by rotating subjects in the dark – Is limited because only the horizontal SCCs are routinely tested to determine extent of pathology
            9. Pts. w/normal vestibular fnx:
            10. Nystagmus should be generated by the rotations
            11. Pts. w/a vestibular disorder:
            12. The extent of pathology can be determined by comparing VOR gain & phase from rotations toward one ear with rotations toward the opposite ear
         2. Otolith Tests
            1. Vestibular -Evoked Myogenic Potentials (VEMP)
            2. Procedure
            3. 1. VEMP test exposes patients to a series of loud clicks 2. During the sound application, the ipsilateral SCM muscle is tested for myogenic potentials –The Saccule has been implicated as the site of afferent stimulation during VEMP testing because saccular efferents provide ipsilateral inhibitory disynaptic input to the SCM muscle, are responsive to click noises, & are positioned close to the footplate of the stapes & therefore are subject to mechanical stimulation
            4. Pt. w/healthy vestibular fnx:
            5. An initial inhibitory potential (occurring at a latency of 13 msec after the click) is followed by an excitatory potential (occurring at a latency of 21 msec after the click)
            6. Pt. w/vestibular hypofnx:
            7. the VEMPs are absent the side of the lesion
4. Vestibular Syst Dysfnx
   1. Peripheral Patho
      1. Mechanical
         1. Most common cause of Vertigo, BPPV(Benign Paroxysmal Positional Vertigo):
            1. Biomechanical Disorder
         2. Sx of BPPV:
            1. 1. Vertigo with change in head position 2. Nausea with or without vomiting 3. Disequilibrium
         3. What occurs:
            1. – In the most common form, a latency of onset of the vertigo & nystagmus occurs within 15 seconds once the head is in the provoking position – The duration is usually less than 60 seconds – The vertigo & the segments are direct impairments caused by the misplaced otoconia
         4. Mechanisms/Theories to explain the occurrence of BPPV, both of which involve the Otoliths becoming dislodged from the utricle & falling into the SCCs
            1. Cupulolithiasis
            2. – Fragments of otoconia breakaway & adhere to the cupula of one of the SCCs – When the head is moved into certain positions, the weighted cupula is deflected by the pool of gravity – This abnormal signal result in vertigo & a status, which persists as long as the patient is in the provoking position – However, this does not explain the brief duration of vertigo common in BPPV
            3. Canalithiasis
            4. – Otoconia are floating freely in one of the SCCs – When a patient changes had position, the pull of gravity causes the freely floating otoconia to move inside the SCC resulting in endolymph movement & deflection of the cupula
      2. Decreased Receptor Input
         1. Unilateral Vestibular Hypofunction (UVH)
            1. Most common cause of UVH (Unilateral Vestibular Hypofunction) leading to decreased or eliminated receptor input incld:
            2. 1. Viral insults 2. Trauma 3. Vascular events
            3. Pts. w/sustained UVH:
            4. – Will experience direct impairments of vertigo, spontaneous nystagmus, oscillopsia w/head movements, postural instability & disequilibrium – patient will initially experience vertigo & nystagmus impairments due to asymmetry created when 1 vestibular system is no longer functioning which resolves within 3-7 days – Spontaneous nystagmus beyond this time ==>possible central lesion or an unstable peripheral vestibular lesion – Direct impairments of visual blurring, postural instability & disequilibrium respond to PT intervention
         2. Bilateral Vestibular Hypofunction (BVH)
            1. Most common cause of BVH:
            2. OTOTOXICITY
            3. Certain classes of antibiotics such as aminoglycosides (gentamicin, streptomycin) are readily taken up by hair cells of the vestibular apparatus & con't to build in the system even after the person has stopped using the antibiotic
            4. Less common cause of BVH:
            5. Meningitis, autoimmune disorders, head trauma, tumors on each 8th CN, transient ischemic episodes of vessels supplying the vestibular system & sequential unilateral vestibular neuronitis
            6. Primary Complaint:
            7. Dysequilibrium
            8. although, oscillopsia & gait ataxia=common clinical signs (all direct impairments)
            9. Unless BVH is asymmetric, the patient will not experience nausea or vertigo, because there is no asymmetry in the tonic firing rate of the vestibular neurons
   2. CNS Patho
      1. Cerebrovascular insults involving the following may cause vertigo, though other associated signs are present:
         1. Anterior-Inferior Cerebellar Artery (AICA)
            1. AICA vs PICA hard to determine but hearing loss=moreso AICA
         2. Posterior-Inferior Cerebellar Artery (PICA)
         3. Vertebral Artery
            1. May affect the cerebellum only & can mimic a peripheral vestibular hypofunction
      2. Pts w/TBI due to labyrinthine or skull fx may c/o Vertigo
      3. Vertebroasiliar Insufficiency (VBI)
         1. S&S:
            1. Drop attacks, transient blindness, or dysarthria (don't usually invovle vestibular patho sx)
   3. Discerning Peripheral Vestibular Patho from Central Vestibular Patho
      1. Observation of nystagmus is a useful tool for assisting in determining a dx of CNS pathology
         1. Nystagmus from Cerebellar Lesion:
            1. – May be in a pure vertical direction – nystagmus may oscillated equal speed = pendulum nystagmus which is often indicative of congenital disorders such as absence of central vision (cortical visual processing) – nystagmus may never revolve (unlike nystagmus from peripheral vestibular lesion
      2. Pts. w/lesions of the Vestibular Nuceli
         1. – Can present with vertigo, nystagmus & disequilibrium similar to the patient with the peripheral vestibular lesion – However, central lesions above the level of the vestibular nuclei will manifest lateralpulsion (person's tendency to fall to 1 side), head tilt, & visual perceptual difficulties as well as oculomotor signs
      3. Brandt et al. reported that the m ost sensitive signs of Unilateral Brainstem Infarct are:
         1. Tilt of the Pt's SVV
         2. Ocular torsion
            1. def: refers to both eyes rotating downward toward the direction of tilt
            2. Ocular torsion combo w/head tilting & skew deviation =Ocular Tilt Reaction (OTR) -Skew Deviation: appears as 1 eye being superiorly displaced in comparison w/the other eye
            3. OTR
      4. Red Flags to Central Vestibular Etiology:
         1. Horizontal or vertical diplopia left in longer than 2 weeks after the onset of signs or symptoms thought to be due to: 1. UVH 2. Persistent pure vertical (positional nystagmus) (anterior canal cupulolithiasis should be ruled out) 3. Spontaneous up beating nystagmus (rare) **refer to neurologist if above S&S present
      5. Diff Btwn Central & Peripheral Vestibular Dysfnx
5. Intervention
   1. Benign Paroxysmal Positional Vertigo (BPPV)
      1. Most common peripheral vestibular pathology
      2. Nystagmus,Generated as a result of placing the SCC in gravity dependent positions, dictates which SCC is involved
      3. 3 Tx Approaches/Techniques:
         1. 1. Canalith Repositioning Maneuver 2. Liberatory (Semont) Maneuver 3. Brandt-Daroff Exercises
      4. Canalith Repositioning Maneuver Fig 24.15 p. 1015
         1. Based on the Canalithiasis theory of free-floating debris in the SCC
         2. 1. Patient's head is moved into different positions in a sequence that will move the debris out of the involved SCC & into the vestibule (location of the utricle & saccule) 2. Once the debris is in the vestibule, the signs & symptoms should resolve 3. After the treatment, the patient may be fit with a soft collar as a reminder to avoid vertical head movements that may again dislodge the otoconia
         3. PT GOAL:
            1. To replace the otoconia into the vestibule, where the calcium crystals can be reabsorbed
      5. Liberatory (Semont) Maneuver Fig 24.17 p. 1016
         1. – First offered as treatment for posterior SCC BPPV based on the cupulolithiasis theory – Recent evidence shows it's effective as an alternative treatment for canalithiasis, though it is more difficult for the patient to tolerate
         2. Involves rapidly moving the patient through positions designed to dislodge the debris from the cupula
         3. PT GOAL:
            1. To replace the otoconia into the vestibule, where the calcium crystals can be reabsorbed
      6. Brandt-Daroff Exercises Fig 24.18 p. 1017
         1. – Designed to habituate the CNS to the provoking position – They may also act to dislodge debrief from the cupula or by causing debris to move out of the canal – 5-10 reps 3x/day until Pt. has no vertigo for 2 consecutive days (may reduce to 3 reps 3x/day if Pt has severe vertigo & nausea)
         2. Important to inform the Pt that:
            1. 1. Movements must be performed rapidly & this will probably provoke vertigo 2. It is normal to have some residual symptoms of disequilibrium & nausea on completing the exercise which are usually temporary in the patient needs to continue the exercises
         3. Although originally designed to habituate the peripheral vestibular response, it is also led to a complete remission of symptoms, sometimes after the first exercise session
      7. Suggested Guidelines for use of CRT, Liberatory (Semont0 Manuever or Brandt-Daroff Exercises
   2. Unilat Vestibular Hypofnx
      1. Important to inform the Pt. that:
         1. Recovery time upon initiating vestibular rehabilitation averages 6-8 wks
      2. Gaze Stability Fig 24.19 p. 1017
         1. – Purpose of these exercises is to improve the VOR & other systems that are used to assist gaze stability with head motion – Computerized DVA test is a useful measure of improved gaze stability for individuals with UVH & TBI
         2. Vestibular adaptation exercises are designed to expose the Pts. to RETINAL SLIP
            1. – Retinal slip occurs when the image of an object moves off the fovea of the retina, resulting in visual blurring – Retinal slip is necessary as this is the signal used to improve the response of the residual vestibular system – Because the brain can tolerate small amounts of retinal slip yet see a target clearly, patient must try to keep the target and focus. Otherwise head motion that is to rapid will result in excessive retinal slip
         3. 2 Primary Paradigms of VEstibular Adaptation Fig 24.10 p. 1017
            1. X1 Exercise
            2. 1. Patient is asked to move the head horizontally (& vertically if appropriate) as quickly as possible while maintaining a focus on a stable target 2. Patient must learn to slow the head movement is target becomes blurred 3. The starting target (business card where pt focuses on a word/letter w/in a word) distance should be an arms length away
            3. X2 Exercise
            4. 1. Patient moves the head & target in opposite positions
      3. Postural Stability
         1. Purpose:
            1. To improve balance by encouraging the development of balance strategies within the limitations of the patient, be they somatosensory, visual, or vestibular
         2. Important to incorporate head movement into the exercises because many patients with vestibular loss tend to decrease their head movement
         3. Balance Exercises & Progressions
      4. Motion Sensitivity
         1. Habituation
            1. def: The reduction in response to a repeatedly performed movement
         2. Habituation Training
            1. – Warranted when a patient with a UVH has continual complaints of dizziness 1. PT should not treat all vestibular patients with this exercise and must determine the provoking positions first 2. When a position elicit a mild to moderate dizziness, the patient remains in the provoking position for 30 seconds or until the symptoms abate, whichever comes first 3. Patient is then provided with an HEP based on the results of the positional test 4. The provoking exercises are performed 3-5x each, 2-3x/day
         3. Purpose:
            1. Designed to reduce the dizziness – the patient should be encouraged that the symptoms normally decrease with the 2 weeks
   3. Bilat Vestibular Hypofnx (BVH)
      1. Treatment of Pts w/ BVH is designed to address the primary complaints of gays instability during head motion, disequilibrium, & gait ataxia
      2. Exercises/Interventions:
         1. Gaze Stability Exercises:
            1. – Can be similar to X1 paradigm – X2 not recommended b/c it may cause excessive retinal slip
            2. Exercises that incorporate sequenced eye and hand movements & the use of imaginary targets may improve gaze stability by enhancing central preprogramming of eye movements
         2. The patient on a walking program, daily if tolerated
         3. Pool Therapy & Tai Chi
         4. Vestibular Adaptation Exercises
            1. Excellent starting point for rehab of patients with UVH & BVH
         5. **NO Habituation exercises, they don't work w/bilateral vestibular loss
      3. BVH Pts depend on:
         1. Somatosensation &/or vision to maintain postural stability
         2. more likely to fall
   4. Central Vestibular Hypofnx
      1. – Generally, the time to recover will be 6 months or more & may be incomplete – Many of the adaptive mechanisms thought responsible for recovery of the vestibular system are central processes that may have been damaged in the initial central lesion – Though vestibular rehab offers promise for treating persons with TBI, it may not always be the treatment of choice owing to its irritating nature
      2. Exercises/Interventions:
         1. PT intervention for a central vestibular lesion at the level of the brainstem (vestibular nuclei) likely will be similar to a UVH, w/same expectations for recovery)
         2. Habituation Exercises
            1. These are good exercises to start w/since many pts with central vestibular lesions c/o dizziness
         3. Gait & Balance Exercises
            1. Designed to incorporate somatosensory, visual & vestibular contributions
   5. Pt. Education
      1. – The vestibular system requires movement to recover from most lesions – The vestibular system will not improve maximally without head motion
6. Diagnoses Involving Vestibular Syst
   1. Meniere's Disease
      1. – Dx by a documented low frequency hearing loss & episodic vertigo – Pt. may c/o sense of fullness in the ear & tinnitus – Sx gradually increase in severity & then last 1-2 hrs per episode – Chronic Meniere's disease=can result in a UVH (4 which rehab is appropriate)
      2. Pathophysiology
         1. Probably involves an increase in endolymphatic fluid causing distention of the membranous tissues
      3. Medical Mgmt/Tx
         1. Directed toward reducing or preventing fluid buildup
         2. Controlled Diet
            1. – Placed on a 2g/d or less sodium diet – Avoid caffeine & alcohol
         3. Use of diuretic to control amt of water in body
         4. Surgery
            1. – To either prevent the fluid buildup in the inner ear (endolymphatic shunt placement) or to stop the abnormal vestibular signal (vestibular nerve section, or transtympanic gentamicin injection) may be indicated the episodes are frequent enough to disturb daily function
      4. Exercises/Interventions
         1. – PT is most beneficial although it will not stop the episode of vertigo – PT = useful in the treatment of disequilibrium occurring after vestibular neurectomy
         2. Gaze & Postural Stability Exercises
   2. Perilymphatic Fistula (PLF)
      1. – Most commonly caused by a rupture of the oval or around windows, membranes that separate the middle & inner ear resulting in leakage of the perilymph into the middle ear which leads to vertigo & hearing loss – Perilymph: normally bathes the SCCs & serves as protective barrier btwn bony & membranous labyrinth – Caused from a traumatic event such as excessive pressure changes as in deep water diving, blonde head trauma without skull fracture, or extremely loud noise
      2. Treatment:
         1. 1. Bed rest
            1. In hopes of allowing the membrane to heal
         2. Surgical Patches of the Fistula
         3. PT
            1. Contraindicated for most patients however can be beneficial in those patients who have continual disequilibrium or develop a vestibular hypofunction post-op
         4. Medical Mgmt:
            1. strict limitation son activities
   3. Acoustic Neuroma
      1. aka Vestibular Schwannomma
      2. Benign tumor located on CN VIII
      3. c/o:
         1. 1. Progressive hearing loss 2. Tinnitus 3. Disequilibrium
      4. Pre-op=no vertigo; Post-op=possible vertigo
      5. Treatment:
         1. Surgical excision of the tumor
         2. PT
            1. – Initiated during the early postoperative period to help the patient resolve symptoms of disequilibrium & oscillopsia – Outpatient treatment =sim to Tx for unilateral vestibular loss
   4. Motion Sickness
      1. Explanation/Theroy behind it:
         1. Sensory Conflict Theory
            1. – 3 sensory inputs of proprioception, vestibular, & visual information do not match stored neural patterns the brain expects to recognize – As a result, persons experience paler, nausea, emesis, diaphoresis, & motion sensitivity
      2. Tx:
         1. PT
         2. Cognitive-Behavioral Mgmt
         3. Meds
         4. Biofeedback
         5. Habituation Training using ground & flight situation
   5. Migraine-Related Dizziness
      1. Deceptively similar to a peripheral vestibular lesion because the vascular event occurs in a vestibular structures such as the vestibular nuclei
      2. Migraine related Sx
         1. 1. Vertigo 2. Dizziness 3. Motion sickness
      3. If migraine suspected=refer to neurologist
      4. Tx:
         1. Medication & diet
   6. MS
      1. – Can affect CN VIII where it enters the brainstem & causes identical Sxs to a unilateral vestibular pathology – MRI scan will ensure an accurate dx of MS
   7. Multiple System Atrophy
      1. – A progressive degenerative disease of the interest involving 4 clinical domains: 1. Cerebellar ataxia 2. Autonomic dysfunction 3. Parkinson's disease like symptoms 4. Corticospinal dysfunction – Has been found to be a cause of dizziness & M balance – PT effects= not investigated
   8. Cervical Vertigo
      1. Mechanisms of involvement are beleived to be from at least 2 sources:
         1. The upper cervical spine sends proprioceptive input to the contralateral vestibular nucleus
            1. – Soft tissue injury & joint dysfunction might alter the afferent input contributing to spatial orientation – Vestibular rehab may be warranted
         2. A patient might have vertebral basilar insufficiency (VBI)
            1. – If suspected, vascular compromise must first be rolled out as a cause – VBI test can be performed while Pt is seated: 1. Patient leans forward & extends neck 2. Neck is then rotated 45° to the suspicious side – Symptoms include: 1. Diplopia, dysarthria, syncope, headache & visual field deficits as well as vertigo & nystagmus – If suspected of VBI=immediate referral to neurologist
      2. Repeated episodes of vertigo without associated VBI Sx usually suggests a peripheral vestibular dx
   9. Contraindications to Vestibular Rehab
      1. 1. Unstable vestibular disorders such as Meniere's disease & PLF (no PT) 2. Sudden hearing loss 3. Increased feeling of pressure or fullness to the point of discomfort and one or both ears 4. Severe ringing in one or both ears 5. When treating surgical patients be observing for discharge of fluid from the ears or knows which may indicate CSF leak 6. Be careful with acute neck injury patients