Vestibular System Vestibular Ocular Reflex Vertigo Vestibular

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Vestibular System Vestibular Ocular Reflex Vertigo Vestibular Powered By Docstoc
					    Vestibular System, Vestibular-Ocular Reflex, Vertigo, Vestibular Disorders
    Robert Peterka, Ph.D. Alar Mirka, M.D., Ph.D.; 01.15.09 @ 9:30 a.m. pg 193

  - A "dime" sized region located in the temporal bone
     - Bony labyrinth consists of the complex cavities which contain
       the vestibular organs
     - Membranous Labyrinth in a delicate epithelial membrane
       contained within the bony labyrinth and separates the vestibular
       labyrinth into two fluid filled spaces
     - Endolymph: fills the interior of the membranous labyrinth;
       composition of intracellular fluid - high K, low Na
     - Perilymph: surrounds the membranous labyrinth; composition
       of extracellular fluid - high Na, low K
     - Continuous production and reabsorption of endolymph and

 DISEASE)                                                                  VESTIBULAR HAIR CELLS AND TRANSDUCTION
 ►Case 1
                                                                           - Vestibular hair cells: mechanoreceptors common to all 5 vestibular motion sensors
 - Pathology: Distention of the membranous labyrinth due to
                                                                              - Morphological polarization
 abnormal fluid regulation of endolymphatic fluid leading to
                                                                                   - Each hair cell has a hair bundle with one kinocilium located at on one side of a
 ruptures in the membrane separating endolymph from
                                                                                   bundle of 40-70 stereocilia.
 perilymph.                                                                -Transduction
 - History: Episodic, recurrent attacks of vertigo that are
                                                                                - Deflection of hair cell bundle towards the kinocilium → hair cell depolarization → ↑
 spontaneous, but worsened by head movement. Symptoms
                                                                                transmitter release → ↑ 8th nn activity
 improve over hours, but last up to several days before                         - Deflection of hair cell bundle away from the kinocilium → hair cell hyperpolarization
 resolving completely. Associated symptoms include fluctuating
                                                                                → ↓ transmitter release → ↓ 8th nn activity
 aural fullness or pressure, tinnitus, and low frequency hearing
                                                                                - Deflection of hair cell bundle at 90° to either of the above directions → no change in
 loss that may lead to a progressive permanent hearing loss.

  - Each of the three semicircular canals, horizontal (also called lateral), posterior, & anterior (also called superior), have a bulge in the circular duct called an
  - Hair cells are arrayed on a saddle shaped structure called the ampullar crista
  - The hair bundles stick above the crista which is covered by a gelatinous structure called the cupula.
  - Rotational motion of the head → movement of endolymph in the canal → movement of the cupula → deflection of the hair bundles
  - All of the hair cells in a particular canal crista are oriented in the same direction, so cupula movement in a given canal causes 8th nn afferents innervating
    that canal to ↑ or ↓ their activity together.
  - Spatial Orientation
       - Each canal responds only to the component of rotation in its plane
       - Canals in the two ears are oriented in pairs; pair operate in push-pull manner
          - Right anterior & left posterior are in the same plane
          - Left anterior & right posterior
          - Right horizontal & left horizontal
  - High spontaneous activity in afferent nn fibers
  - Brain compares activity coming from canal pairs in order to determine if movement
    is occurring & the direction of movement
  - Abnormal disruption of canal activity leads to vertigo (false sense of rotation)

- Change in afferent discharge rate is proportional to cupula deflection
- Cupula deflection is proportional to rotational head velocity over the range of most
  naturally occurring motions, but during sustained rotational motions the canal response                 UNILATERAL LOSS OF VESTIBULAR FXN
  declines and therefore does not accurately signal rotational head motion (e.g. during long              ►Case 2A - Acoustic Neuroma
  duration, constant velocity rotations)                                                                  - Pathology: A vestibular schwannoma that begins on
- Cupula deflection is controlled by three factors                                                          the vestibular nerve in the internal auditory canal and
     1. Inertia of the endolymph in the canal - The endolymph's inertia causes it to lag                    slowly compressed the 8th nerve.
      behind the movement of the head, therefore causing relative movement of                             - History: Insidious onset of imbalance and
      endolymph within the canal which deflects the cupula                                                  dysequilibrium with rare vertigo.
     2. Viscosity of endolymph in the canal - This frictional force wants to cause the                    Associated symptoms include tinnitus and high
      endolymph to move with the head                                                                       frequency hearing loss.
     3. Spring-like properties of the cupula - When deflected, the cupula exerts a restoring              ►Case 2B - Labyrinthitis and Neuronitis
      spring force to return to its neutral position                                                      - Pathology: Viral infection leading to inflammation
- The cupula is normally neutrally buoyant in its surrounding endolymph - static head                       and subsequent atrophy of the vestibular end organ
  position changes with respect to gravity do not cause cupula movements and the canals                     (labyrinthitis) or vestibular nerve trunks (neuronitis).
  are therefore only responsive to rotational head motions                                                - History: Sudden onset of spontaneous vertigo that
                                                                                                            lasts days up to weeks, associated with nausea and
                                                                                                            vomiting frequently and hearing loss occasionally.
 OTOLITH ORGANS (UTRICLE AND SACCULE)                                                                      BENIGN PAROXYSMAL POSITIONAL VERTIGO
 - Anatomy                                                                                                 (BPPV)
    - Hair cells arrayed on a receptor surface w/ a wide variety of orientations of the hair bundles       ►Case 3
    - The hairs of the hair cells project into otolithic membrane which covers receptor surface            - Pathology: Distorted function of a semicircular canal due
    - Otolithic membrane is gelatinous w/ imbedded otoconia (dense calcium carbonate crystals)             to degenerative debris in the canal endolymph
 - Physiology                                                                                              (canalithiasis) or on the cupula of the canal crista
    - Head tilt with respect to gravity and other linear accelerations cause a shift of the otolithic      ampullaris (cupulolithasis). Clinically the posterior
      membrane with respect to the hair cells, deflecting the hair cells, and causing a change of          semicircular canal is most commonly involved due to
      afferent neural discharge in proportion to the applied linear acceleration                           debris settling in the anatomically lowest canal.
    - Static sensitivity refers to the fact that head position in space is encoded by the pattern of       - History: Brief episodes of vertigo lasting up to 30
      otolith organ discharge rates                                                                        seconds and triggered by position change. Typically
    - Dynamic sensitivity refers to the fact that the otolith organs also respond to linear                worse in the mornings when turning over in bed, bending
      accelerations, in fact they respond to vectoral sum of gravity with the linear acceleration of       over and straightening up, or extending the neck to look
      the head in space.                                                                                   up. Occasional milder vertigo during the day.

                                                                                           VESTIBULO-OCULAR REFLEX (VOR)
                                                                                           - Purpose of the VOR - to maintain gaze stability during head movements in
                                                                                             order to maintain clear vision
                                                                                           - Properties of the VOR
                                                                                               - Conjugate eye movements
                                                                                               - Works best for transient motions, poor for sustained motion (e.g.
                                                                                                 constant rotational velocity)
                                                                                               - Sustained motions produce vestibular nystagmus
                                                                                               - Eye movements evoked with short latency (~15 ms)
                                                                                               - VOR eye movements occur during rotations in the dark - this allows for
                                                                                                 clinical tests of vestibular function without the influence of visually
                                                                                                 induced eye movements
                                                                                           - VOR Neurophysiology
                                                                                               - CNS projection of 8th nn afferents - main projection to vestibular
                                                                                                 nuclei, also to cerebellum
                                                                                               - Vestibular nuclei projections - oculomotor nuclei (III, IV, VI), pontine
                                                                                                 reticular formation, cerebellum, spinal cord tracts, other pontine and
                                                                                                 midbrain nuclei involved in eye movement control
                                                                                               - VOR "3 neuron arc"
                                                                                           - Nystagmus
                                                                                               - Slow phase component in direction opposite to head movement
                                                                                               - Fast (or quick) phase component resets the eye towards the center
  CENTRAL VERTIGO OR DIZZINESS = BRAINSTEM LESIONS                                               position so the compensatory slow phases can continue
  ►Case 4                                                                                      - Nystagmus direction is referred to in terms of the fast phase direction
  - Pathology                                                                                    (e.g. right beating) since the fast phase direction is easiest to visualize
    - Multiple Sclerosis - demyelinating disease of the CNS that causes vertigo or         - Visual/vestibular interactions – Visual information used by the smooth
      dysequilibrium if vestibular nuclei are involved.                                      pursuit and optokinetic systems can be used to enhance or suppress the
    - Cerebellopontine angle (CPA) tumors - meningiomas and epidermoid cysts                 VOR depending on the goal of the subject (e.g. reading a book in a moving
      as primary tumors, and rarely metastatic breast, kidney, lung, laryngeal, and          car requires suppression of the VOR)
      thyroid cancer may invade the CPA                                                    - Adaptive changes of VOR – cerebellum exerts an inhibitory influence on
    - Vertebrobasilar Insufficiency (VBI) - ischemia of brainstem, labyrinth, and            the VOR, the magnitude of inhibition can be altered (with visual "error"
      vestibular nuclei seen in the elderly                                                  signals feeding back to the cerebellum through the inferior olive) to adjust
    - Cerebellar or brainstem infarction - occlusion of vertebral, cerebellar, or            the amplitude, direction, and symmetry of compensatory eye movements
      smaller branches leas to various syndromes depending on infarcted area                 generated in response to a given head movement
  - History: Imbalance and dysequilibrium may develop along with other                         - Compensation for lesions, aging
  neurologic deficits due to cranial nerve involvement. Vertigo is common in                   - Slow time course
  VBI (abrupt onset lasting minutes along with other posterior fossa symptoms                  - Clinical problem - compensation can mask slowly developing disease
  such as diplopia, dysphagia, drop attacks), and in cerebellar and brainstem                    processes (acoustic neuroma)
  infarctions (prolonged, spontaneous, direction-fixed nystagmus and vertigo).

- Define what the patient means by "dizziness", since each person's experiences, culture, and education lead to unique use of this word.
- The potential differential diagnosis for dizziness is enormous, including psychiatric, drug-induced, neurologic, cardiovascular, endocrinologic, and
  rheumotologic – as well as vestibular - etiologies.
- History
      - Type of dizziness = vertigo, dysequilibrium
      - Onset = key to diagnosis
      - Triggering factors (positional, spontaneous, dietary, situational)
      - Associated symptoms (hearing loss, tinnitus, nausea, other neurological deficits)
      -Vestibular review of symptoms (ROS): trauma, ototoxic drug use, infections, family history
- Physical Exam
    - HEENT exam = look for nystagmus, extraocular movements, ear exam
    - Neurologic exam = cranial nerve exam, tuning fork test (Weber and Rinne), cerebellar and gait exam, Hallpike (Nylen-Barany) maneuver, Romberg test,
      visual suppression of VOR maneuver
- ENG (Electronystagmography ) Test - eye movements recorded using electrooculography
   - Ocular motor screening - tests of saccades, smooth pursuit, gaze stability
   - Positional tests - determines if nystagmus present in the dark and if it is modified by different head positions in space and different head on neck
   - Caloric tests - used to detect an asymmetry of vestibular function between the two ears
       - artificial stimulation of the horizontal semicircular canal using warm or cold water irrigations of the external ear canal
       - each ear stimulated separately and the amplitude of evoked nystagmus compared for the four irrigations
   - Hallpike test - test for BPPV
- Rotation Test - eye movements recorded using electrooculography while patient rotates in a chair controlled by computer
   - Provides natural stimulus to horizontal semicircular canals - detailed quantification or evoked nystagmus provides evidence for
   - Unilateral vestibular asymmetry and extent of compensation - bilateral vestibular loss
   - Addition of concurrent visual stimuli allow testing of visual/vestibular interactions, and therefore provides information on central vestibular function
      and eye movement control
- Moving Platform Posturography (Computerized Dynamic Posturography) – Provides functional characterization of postural control

- Endolymphatic Hydrops
   - ENG may show positional nystagmus if asymmetry of vestibular function exists.
       Caloric test may reveal unilateral hypofunction.
   - Audiogram may show low frequency hearing loss early in disease, and combined low and high frequency or flat hearing loss late.
   - ENG with Hallpike maneuver may show positionally triggered rotatory (torsional) nystagmus (but may miss it)
- Unilateral vestibular disorders
   - Caloric test shows unilateral hypofunction (asymmetry) in most cases of advanced acoustic neuroma and vestibular neuronitis, less often in
                                                                                             Nystagmus image that I forgot to add on page 2.