Vestibular Rehabilitation

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Vestibular Rehabilitation by Mind Map: Vestibular Rehabilitation

1. Diagnoses

1.1. Meniere's Disease

1.1.1. Sx: Low-frequency hearing loss, episodic vertigo, sense of fullness in the ear, tinnitus; gradually increase in severity and can last several hours per episode

1.1.2. During episodes, exercise is not recommended. However, in chronic Meniere's, rehab is appropriate.

1.1.3. Other treatments include contolled diet, diuretics, surgery, etc.

1.2. Perilymphatic Fistula

1.2.1. Rupture of oval or round windows resulting in leakage of perilymph into middle ear. Sx: vertigo and hearing loss

1.2.2. Treatment includes initial bedrest and surgical patching of fistula. Early PT is contraindicated but may be beneficial for pts who have continual dysequilibrium or vestibular hypofunction post-op.

1.3. Vestibular Schwannoma

1.3.1. Benign tumors arising from CN 8. Sx: tinnitus and hearing loss, vestibular hypofunction

1.3.2. Treatment includes surgical excision of the tumor and PT for dysequilibrium and oscillopsia.

1.4. Motion Sickness

1.4.1. Occurs when proprioceptive, vestibular, and visual inputs do not match patterns the brain recognizes. Sx: pallor, nausea, emesis, diaphoresis, motion sensitivity

1.4.2. Treatment includes PT for reduction in motion sensitivity, cognitive-behavioral therapy, medications, biofeedback, and habituation training

1.5. Migraine-Related Dizziness

1.5.1. May be similar to BPPV or UVH. Sx: vertigo, dizziness, imbalance, motion sickness.

1.5.2. Treatment: neurologist referral, medication, diet

1.6. Multiple Sclerosis

1.6.1. If affecting CN 8, may cause sx similar to UVH. MRI is needed to be sure.

1.7. Multiple System Atrophy

1.7.1. Progressive degenerative disease of the NS involving cerebellar ataxia, autonomic dysfunction, PD-like sx, and corticospinal dysfunction. May be a cause of dizziness and imbalance.

1.8. Cervicogenic Dizziness

1.8.1. Cause of dizziness or imbalance is derived from the cervical spine or nearby soft tissue.

2. Contraindications to Vestibular Rehabilitation

2.1. 1. Unstablle Meniere's

2.2. 2. Uncontrolled migraine

2.3. 3. Perilymphatic fistula

2.4. 4. Unrepaired superior SCC dehisence

2.5. 5. Sudden loss of hearing, increasing feeling of pressure or fullness to the point of discomfort in one or both ears, severe ringing in one or bothe ars

2.6. 6. Observation of discharge from ears or nose which may be indicative of CSF leak

2.7. 7. Patients with acute neck injuries

3. New Knowledge

3.1. 1. From a study, 100% of persons with a migraine demonstrated abnormal nystagmus during a migraine episode if positionally tested in a CN3 exam.

3.2. 2. Use of head-shaking induced nystagmus test (HSN) - different from the HIT or DVAT which we discussed in class, the HSN occludes vision and assesses nystagmus after head has been shaked and eyes have been opened.

3.3. 3. There is a recommended 3-step bedside CN3 exam when trying to detect for stroke: 1.) HIT, 2,) Nystagmus, 3.) Test of skew

3.4. 4. Discussed in class as "red flags" for central etiology were horizontal or vertical diplopia, purely vertical nystagmus, or spontaneous up-beating nystagmus. Newly learned red flag includes that of a positive test for skew deviation which analyzes how VOR changes in upright vs supine.

4. Anatomy

4.1. Peripheral Vestibular System

4.1.1. Semicircular Canals - respond to angular acceleration and are orthagonal to one another

4.1.1.1. Horizontal

4.1.1.1.1. Horizontal pairs form coplanar pair

4.1.1.2. Posterior

4.1.1.2.1. RALP/LARP forms coplanr pairs

4.1.1.3. Anterior

4.1.1.3.1. RALP/LARP forms coplanr pairs

4.1.1.4. Endolymph

4.1.1.4.1. Fluid filling each SCC that moves freely within each canal in response to the direction of angular head rotation

4.1.1.5. Ampulla

4.1.1.5.1. The enlargement at one end of the SCC

4.1.1.6. Cupula

4.1.1.6.1. Lies within the ampulla and is a gelatinous barrier containing sensory hair cells

4.1.1.7. Crista ampullaris

4.1.1.7.1. Sensory organ of angular rotation; contains kinocilia and sterocilia

4.1.2. Otholith Organs - respond to linear acceleration and static head tilt

4.1.2.1. Saccule

4.1.2.1.1. Vertical linear acceleration

4.1.2.2. Utricle

4.1.2.2.1. Horizontal linear acceleration and/or static head tilt

4.1.2.3. Otoconia

4.1.2.3.1. Calcium carbonate crystallines embedded in a gelatinous material in which sensory hair cells project into

4.2. Central Vestibular System

4.2.1. Brainstem

4.2.1.1. Provides primary control of many vestibular reflexes

4.2.2. Vestibular Nuceli, Reticular Formation, Thalamus, Cerebelleum

4.2.2.1. Tracing techniques from source to termination

4.2.2.2. Vestibular pathways terminate in a unique cortical area - the junction of the parietal and insular lobes is the location of the vestibular cortex

4.2.2.3. Connections between the vestibular cortex, thalamus, and reticular formation contribute to integration of arousal and conscious awareness of the body, as well as the ability to discriminate between movement of self and environment

4.2.2.4. Cerebellar connections also help to maintain VOR

5. Physiology and Motor Control

5.1. Tonic Firing Rate

5.1.1. Vestibular afferents function at a resting firing rate of 70-100 spikes/second

5.1.2. High tonic firing rate means the vestibular system can detect head motion through excitation or inhibition

5.1.3. During angular head rotations, ipsi vestibular afferents and ipsi central vestibular neurons are excited; this also inhibits peripheral afferents and central vestibular neurons receiving contra innervation from the labyrinth

5.2. Vestibulo-Ocular Reflex

5.2.1. Stabilizes images on the retina during head movements, contributes to posture during static and dynamic activities, and influences the coordination of limb movements

5.2.2. 3-Neuron Arc

5.2.2.1. Primary vestibular afferents from the anterior SCC synapse in the ipsi vestibular nuceli

5.2.2.2. Secondary ipsi vestibular neurons receiving innervation from the ipsi labyrinth decussate and synapse in the contra oculomotor nucleus

5.2.2.3. Motor neurons from the contra oculomotor nucleus synpase at the NMJ of the ipsi superior rectus and contra inferior oblique muscles

5.2.3. Gain and Phase

5.2.3.1. Gain

5.2.3.1.1. As the head moves in one direction, the eyes move in the opposite direction with equal velocity

5.2.3.2. Phase

5.2.3.2.1. As the head moves in one direction, the eyes move in the opposite direction with equal amplitude

5.3. Push-Pull Mechanism

5.3.1. Comparison between two vestibular systems to detect head movement and direction via coplanar fashion

5.3.2. Faulty interpretation of these comparisons will lead to difficulties in gaze stability, postural stability, and motion perception

5.4. Inhibitory Cutoff

5.4.1. The point that the inhibition of hair cells in opposite labyrinth during angular head rotation can only reduce the firing rate to 0

5.4.2. For ipsi rapid head rotations, the contra vestibular afferents cannot detect head rotation when the head velocity is greater than the inhibitory cutoff of those contra afferents

5.5. Velocity Storage System

5.5.1. The signal generated by movement of cupula is brief, but the response is sustained by a circuit of neurons in the medial vestibular nucelus, lasting longer than 10 seconds in normal vestibular functioning people.

5.5.2. The purpose of this sustained input is to assist the brain in detecting low-frequency head rotation.

6. PT Examination

6.1. History and Systems Review

6.1.1. ID of Symptoms

6.1.1.1. Dizziness - common term used; but may be vertigo, lightheadedness, dysequilibrium, or oscillopsia. Generally, dizziness is vaguely defined as sensation of whirling or feeling a tendency to fall

6.1.1.2. Vertigo - an illusion of movement; "spinning"; episodic; indicative of UVH or BPPV most often

6.1.1.3. Lightheadedness - a feeling that fainting is about to occur can may be attributed to hypotension, hypoglycemia, or anxiety; less localizing than vertigo

6.1.1.4. Dysequilibrium - the sensation of being off balance, typically due to acute and chronic vestibular lesions but may be associated with nonvestibular problems like decreased sensation or LE weakness

6.1.1.5. Oscillopsia - experience of objects "bouncing"

6.1.2. Duration and Circumstances of Symptoms

6.1.2.1. Duration

6.1.2.1.1. Short episodes (seconds-minutes) of vertigo = BPPV

6.1.2.1.2. Long episodes (minutes-hours) of vertigo = Meniere's

6.1.2.1.3. Longer episodes (days) of vertigo = Vestibular neuritis or migraine-associated dizziness

6.1.2.2. Circumstances

6.1.2.2.1. Positional? Associated with movements? Better with rest? Motion sensitive?

6.2. Tests and Measures

6.2.1. Visual Analogue Scale

6.2.1.1. Subjective intensity of vertigo, lightheadedness, dysequilibrium, and oscillopsia

6.2.2. Dizziness Handicap Inventory

6.2.2.1. Self-perception of degree of handicap in physical, emotional, and functional domains

6.2.3. Functional Disability Scale

6.2.3.1. Specifies the benefit from vestibular PT including questions that address avoidance behavior

6.2.4. Motion Sensitivity Quoient

6.2.4.1. Subjective score of individual's sensitivity to motion

6.2.5. Examination of Eye Movements

6.2.5.1. VOR assessment via nystagmus observation, head impulse test, head-shaking induced nystagmus test, positional testing, & the DVAT

6.2.6. Examination of Gait and Balance

6.2.6.1. Vestibular function tests - SCC and otolith tests

7. Vestibular System Dysfunction

7.1. Peripheral Pathology

7.1.1. Mechanical

7.1.1.1. Cupulolithiasis

7.1.1.2. Canalithiasis

7.1.2. Decreased Receptor Input

7.1.2.1. UVH

7.1.2.2. BVH

7.2. Central Nervous System Pathology

7.2.1. Cerebrovascular Insults

7.2.2. Vertebrobasilar Insufficiency

7.2.3. Traumatic Brain Injury

7.2.4. Multiple Sclerosis

7.3. Discerning Peripheral vs Central Vestibular Pathology

7.3.1. Peripheral

7.3.1.1. Ataxia mild, smooth pursuit and saccades usually normal; positional testing may produce nystagmus, possible hearing loss, fullness in ears, and tinnitus, acute vertigo suppressed by visual fixation and more intense, nystagmus with slow and fast phases

7.3.2. Central

7.3.2.1. Ataxia severe, abnormal smooth pursuit and saccades, no hearing loss, may have diplopia, altered consciousness, lateropusion, acute vertigo not suppressed by visual fixation, pendular nystagmus, persistent vertical nystagmus

8. Interventions

8.1. BPPV

8.1.1. Canalith repositioning maneuver

8.2. UVH

8.2.1. Gaze stability exercises

8.2.2. Postural stability exercises

8.2.3. Habituation exercises (motion sensitivity)

8.3. BVH

8.3.1. Gaze stability exercises

8.3.2. Balance exercises

8.4. Abnormal Central Vestibular Function

8.4.1. Treatment similar to UVH beginning with habituation along with gait and balance exercises

8.5. Patient Education

8.5.1. The vestibular system requires movement to recover - educate on returning to daily activity and exercising at home through a tolerable and effective amount