Video 1. Systematic Examination of the Vestibular System. Professor M Strupp, University of Munich

 

(vv)VestibularSystemExamination.mp4(tt)

The topics covered in the video are the following:

  1. Check for spontaneous nystagmus using Frenzel lenses
  2. Head Shaking nystagmus 
  3. Head Impulse Test
  4. Determinging vertical (Subjective Visual Vertical)
  5. Visual fixation suppression of the VOR

     

    The important features on examination which help to identify the type of nystagmus, and aid in distinguishing peripheral from central lesions include1:

  Clinical Characteristics

 
  Dysfunction

  Vertigo    Severe
  Tinnitus or hearing loss   Common
  Horizontal nystagmus with torsion   Typical
  Horizontal nystagmus without torsion   Rare
  Pure vertical or horizontal nystagmus   Almost never
  Duration of symptoms   Days to weeks
  Visual fixation   Dampens nystagmus

1. Waveform: The nystagmus trajectory should align with the approximate plane of the affected semicircular canal(s). When a horizontal canal or its afferents are involved (as is typically the case), in straight-ahead gaze the nystagmus usually appears predominantly horizontal with additional small torsional and/or vertical components (depending on what additional structures are affected, if any).

The typical waveforms seen in peripheral vestibular nystagmus can be explained by the combined effects of one or more canals on either side: combined involvement of all three canals on one side results in a mixed horizontal–torsional nystagmus, indicating involvement of the entire vestibular nerve or all the semicircular canals within one labyrinth.  This is most commonly due to a peripheral vestibular lesion, although the same horizontal-torsional vestibular nystagmus may result from a lesion affecting the intrapontine vestibular nerve fascicles, vestibular nucleus, or cerebellar structures modulating resting vestibular tone1.

Spontaneous horizontal-vertical-torsional nystagmus is seen most often in superior division vestibular neuritis, where dysfunction in the horizontal canal afferents contributes to the horizontal component and dysfunction in the anterior canal afferents contributes to the torsional and small upbeat components. Note, however, that a similar nystagmus trajectory can occur in central disorders such as the lateral medullary (Wallenberg) syndrome

 - By contrast, pure vertical or pure torsional nystagmus invariably has a central origin because of the improbability of involving both anterior or both posterior semicircular canals selectively (for a pure vertical nystagmus) or just the anterior and posterior semicircular canals in one labyrinth (for a pure torsional nystagmus). 

2. Direction: The direction of the linear slow phases in vestibular nystagmus is determined by the imbalance in tonic neural activity at the level of the vestibular nuclei. If a process reduces unilateral vestibular tone, activity from the vestibular nuclei on the unaffected side will drive the eyes in a slow phase drift toward the affected side, and the nystagmus will beat away from the affected side of reduced function. 
Spontaneous peripheral vestibular nystagmus should be direction-fixed or unidirectional: it follows Alexander’s law, which states that nystagmus intensity increases during gaze in the direction of the quick phases.  A subtle peripheral vestibular nystagmus may be present only when the eyes are fixing in the direction of its fast phase2. The nystagmus intensity is dictated by the degree of asymmetry in vestibular tone.
Depending on the severity of the lesion, the nystagmus may be evident in primary position.

 - By contrast, if of central origin, nystagmus may reverse depending on the direction of gaze, or may be unidirectional.

3. Suppression: by vision and smooth pursuit. It is important to ensure that spontaneous nystagmus (which is typically seen in vestibular neuritis) is not present in patients with an acute vestibular syndrome. To assist with distinguishing central from peripheral spontaneous nystatmus, all vertiginous patients need to be examined with a technique which removes visual fixation (such as Frenzel lenses).

 - By contrast, if of central origin, not supressed by vision or smooth pursuit, especially if affecting the vestibulocerebellum (flocculus, paraflocculus). Some central lesions may have nystagmus which is suppressed by visual fixation1.

4. Additional symptoms: vertigo, hearing loss, tinnitus.

 - By contrast, if of central origin, brainstem or cerebellar signs are present.  Severe truncal ataxia is only seen in central lesions (inability to sit without the use of arms or assistance). It is commoner for central lesions to involve both semicircular canal and utricular function, whereas peripheral lesions, such as acute vestibulopathy, most commonly involve the horizontal and anterior semicircular canals.

5. Latency and fatigueability: nystagmus of peripheral origin may have a latency and is fatigueable.

 - By contrast, if of central origin, nystagmus is nonfatigueable, lasting for more than 30 seconds.


 

Video 2.  Acute vestibulopathy. Spontaneous nystagmus to the left (even with visual fixation)


(vv)AV1.mp4(tt)

From: Kim JS. When the Room Is Spinning: Experience of Vestibular Neuritis by a Neurotologist. Front Neurol. 2020 Mar 3;11:157. doi: 10.3389/fneur.2020.00157. PMID: 32194499; PMCID: PMC7062794.


 

Video 3.  Nystagmus increased when fixation was removed using Frenzel lenses.

The nystagmus decreased during rightward gaze and increased during leftward gaze, obeying the Alexander's law.

(vv)AV2.mp4(tt)

From: Kim JS. When the Room Is Spinning: Experience of Vestibular Neuritis by a Neurotologist. Front Neurol. 2020 Mar 3;11:157. doi: 10.3389/fneur.2020.00157. PMID: 32194499; PMCID: PMC7062794.


 

 

 

 

References

  1. Eggers SDZ, Bisdorff A, von Brevern M, et al. Classification of vestibular signs and examination techniques: Nystagmus and nystagmus-like movements. J Vestib Res. 2019;29(2-3):57-87.
  2. Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998;339(10):680-685. doi:10.1056/NEJM199809033391007