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I ANATOMY                

 

II PHYSIOLOGY OF        EYE MOVEMENTS 

III EXAMINATION: EYE MOVEMENTS & NYSTAGMUS 

IV FIXATION INSTABILITY   

V SUPRANUCLEAR to NUCLEAR  

 VII CEREBELLAR EYE   MOVEMENTS 

VIII CN PALSIES, VISUAL FIELDS, PUPIL & THE EYE

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Video 1. An introduction to Neuro-Otology. Prof A Moodley Neurology Registrar Weekend, 2019

 

(vv)Neurotology.mp4(tt)

 

 

Peripheral and brainstem vestibular dysfunction causes pathological sense of self-motion and visuo-vestibular conflict.  GOldberg
 

 

Rotation of the head is sensed by reciprocal changes in activity between pairs of semicircular canals, one in each labyrinth. This difference, relayed centrally to the vestibular nuclei, generates the eye movement command that compensates for head movements when we attempt to stabilize retinal images of objects that are stationary in the environment.

This simple reflex, the vestibulo-ocular reflex (VOR), is called:

Imbalance in these systems is shown by distinct phenomena:

If there is loss of activity from the affected labyrinth, the patient initially develops a strong spontaneous nystagmus as a result of the central imbalance in tone that is created by the asymmetry in the levels of afferent activity from the semicircular canals transmitted to the vestibular nuclei from the two labyrinths. The nystagmus subsides, but usually taking days to weeks to completely resolve, as central balance is restored and a new stable set-point is achieved.Zee 17

There are several possible reasons why most vestibular syndromes involve both the semicircular canal and otolith functions. The different receptors for perception of angular and linear accelerations are housed in a common labyrinth. Their peripheral (VIIIth nerve) and central (e.g. medial longitudinal fasciculus) pathways take the same course. Finally, there is a convergence of otolith and semicircular canal input at all central vestibular levels, from the vestibular nuclei to the vestibular cortex.BrSTr

A disorder of otolithic function at peripheral or central level should be suspected if a patient describes symptoms of falls, sensations of linear motion or tilt, or else shows signs of specific derangements of ocular motor and postural orienting and balancing responsesBrSTr

Many vestibular syndromes are mixed with involvement of both semicircular canal and utricular dysfunction:BrSTr

Examination of the vestibular system and for nystagmus  Static vs Dynamic Imbalance (pg 52  WOng)

  1. Spontaneous nystagmus: Vestibular, ideally with Frenzel). this is due to an imbalance of vestibular tone and is initially assessed when the patient is looking straight ahead.  Signal to suppress nystagmus is retinal slip, as occurs in an isolated peripheral lesion.
  2. Head shaking test: 2 Hz for 20 seconds, head down by 30o.
  3. Head impulse test: vestibulo-ocular reflex (VOR)
  4. Bucket test: subjective visual vertical
  5. Visual fixation suppression of the vestibulo- ocular reflex (VOR)
  6. Dynamic VA: normal < 3 line decrease at 2 Hz; abnormal > 3 line decrease

 

  1. Head position
  2. Eye position: alternating cover; first one eye and then the other (1-2 seconds per eye). This is to try and assess whether there is a skew deviation present: as you move the cover away look at that eye to see whether it is moving.
  3.  
  4. Saccades: horizontal and vertical
  5. Smooth pursuit: this is generated by original slip; retinal slip is used as a signal in order to suppress nystagmus of peripheral origin: 30 degrees to the side in horizontal plane.
  6. Examine for positioning nystagmus.
  7. Examination of gaze-holding function: Gaze Evoked Nystagmus: other central or peripheral;
  8. VOR: HIT and the VOR suppression test where one combines head and target.
  9.  
  10. Romberg: legs apart and together/tandem Romberg/ stand on one leg x 5 seconds

Symptoms and signs of vestibular disease:

Mnemonic: RAPT:
Patients report that the rooms spins away (Rotate Away) from the lesion, and they point in the direction of the slow drift, that is, towards the lesion (Point Towards). 
The patient themselves rotate and fall towards the lesion, again, following the slow phase.

Oscillopsia in association with peripheral vestibular lesions often resolves quickly as compensatory mechanisms come into play whereas such compensation generally does not occur rapidly with brainstem disorders.

 

By contrast:

Peripheral Vestibular Nystagmus

1. Waveform
? Purely vertical, torsional, horizontal, or mixed (e.g., RAC + LAC = ↑ or RAC + RPC = )
? Linear, increasing, or deacreasing velocity waveforms
? Jerk nystagmus 
2. Reverse direction with gaze or unidirectional
3. Not suppressed by vision or smooth pursuit
4. No adaptation: nystagmus often persists
5. No other vestibular symptoms
6. Other brainstem or cerebellar signs present

Peripheral vestibular diseases often cause a positioning nystagmus, which is caused by the actual head movement (this is in contrast to positional nystagmus, which is caused by a specific head position secondary to a central lesion).
Positioning nystagmus is paroxysmal, and can be found in disorders such as benign paroxysmal positioning vertigo (BPPV), Ménière’s disease, perilymph fistula, vestibular atelectasis, physiological “head extension vertigo” or “bending over vertigo.”

 

EggersFor example, benign paroxysmal positional vertigo from the left posterior semicircular canal elicits eye movements about an axis parallel to the affected canal’s axis (which is approximately 45◦ from the anterior and left ends of the naso-occipital and interaural axes, respectively), regardless of the direction of gaze [38, 43]. When the subject’s gaze is directed 45◦ to the left of center, the nystagmus with respect to the eye appears purely torsional about the line of sight, butwhen the subject’s gaze is directed 45◦ to the right of center, the nystagmus with respect to the eye appears purely vertical. Using an eye frame of reference would therefore result in a confusing description complicated by dependence on instantaneous eye orientation. Choosing a head frame of reference is only modestly better, because the nystagmus will include two nearly equal components (roll and pitch), neither of which is intuitively linked to the source of dysfunction. In contrast, choosing a canal frame of reference (i.e., three mutually perpendicular axes comprising the mean axes of the left-anterior/right-posterior [LARP], right-anterior/left-posterior [RALP] and left-horizontal/right-horizontal [LHRH] canal pairs) greatly simplifies the description, because the nystagmus is almost entirely about the RALP axis.