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Clinical Bedside Examinations for the evaluation of VOR

Clinical Bedside Examinations for the evaluation of VOR

The assessment of the nystagmus, and therefore of the VOR, is fundamental in vestibology. Being often absent as spontaneous, it must be researched by means of specific tests.

An important concept is certainly that of Positioning Nystagmus, which corresponds to the pathological triggering of the Vestibulo-Ocular Reflex (VOR) as a consequence of different head positions, and that are due to alterations of the endolymphatic and labyrinthine functions in general. Whereas pathological events that can occur with Positioning Nystagmus triggered by central (cortical / cerebellar) dysfunctions, albeit important, are rarer.

Positioning Nystagmus can be divided into Paroxysmal and Non-Paroxysmal.  Paroxysmal nystagmus means one that is of a short duration, particularly intense, and episodic in its manifestation.

Typical Positioning Nystagmus is characterized by the following parameters:

  1. Latency, which indicates the period of time necessary for it to become manifest during the vestibular manoeuvre performed
  2. Increment with reaching the apex or plateau of the manifestation, with subsequent Decrement
  3. Inversion upon returning to the starting position before the manoeuvre
  4. Strength reduction of the nystagmus, whereby it is meant the reduction of intensity and amplitude that occur with the progressive repetition of the vestibular manoeuvres.

When at least one of these four parameters is missing when performing vestibular manoeuvres, we speak of Atypical Positioning Nystagmus, which may be indicative of a central (cortical / cerebellar) pathology.


Vestibular Bedside Examination Tests

  • Head Shaking Test (HST)

Introduced by Kamei in 1964, it is a useful test for the evaluation of vestibular asymmetry given by both peripheral and central lesions.

The patient is seated on the examination bed with the head flexed by about 30° so as to make the lateral semicircular canal horizontal. The patient’s head is shaken 25-30 times at a frequency as close as possible to 2Hz, with an abrupt stop of the induced movement, after which the possible onset of nystagmus is evaluated (defined as Head Shaking Nystagmus-HSNy) which, if positive, will appear within a latency of 20 seconds with at least 3 nystagmus shocks. The HSNy is horizontal, facing the labyrinth with greater reflectivity, progressively losing intensity and amplitude, with a duration generally contained within 30 seconds. Beating towards the less reactive side is not uncommon.

Decidedly rarer is nystagmus capable of subsequently reversing its direction (biphasic nystagmus). In this case, the first phase corresponds to the peripheral lesion, while the second phase of reversal would refer to a compensation or recovery mechanism. This second phase of inversion in biphasic nystagmus is of reduced in intensity, but often longer lasting (Harvey al. 1997).

The appearance of vertical, polyphasic or downbeat nystagmus, or with a torsional component with HST is rare. In such case, the diagnostic orientation focuses on the presence of a central vestibular lesion. This nystagmus is defined as Perverted HSNy and does not provide side indications. (Califano al. 2001) (Cherchi and Hain 2010) (Minagar al. 2001) (Huh and Kim 2011).

The HST is a rather specific test for a unilateral peripheral deficit, although its negativity does not exclude the presence of the same deficit (possible false negatives). It may be indicative of a central pathology if there is an overexpression of the nystagmus in intensity, amplitude, and duration.

In normal subjects, or even in the case of bilateral vestibular deficit, there will be no appearance of HSNy.

If the patient in videonystagmoscopy presents a spontaneous nystagmus within the first 5-6 seconds, the HSNy should be considered positive only if at the end of the HST there is a difference of at least 5°/ s within the first 5 seconds after performing the test (Wei al. 1989).

In summary, the HST is a vestibular test certainly indicatory for peripheral vestibular lesions, even if the width of the induced nystagmus (HSNy) is not correlated to the clinical or symptomatic severity. It can also be indicatory of any central lesions. It is recommended the test is always carried out it in videonystagmoscopy.


  • Head Impulse Test (HIT)

The HIT Test was devised by Halmagy and Curthois in 1988, it evaluates the canal function, allows to identify the deficient side in peripheral vestibular pathologies, and above all identifies the presence of an uncompensated peripheral vestibular deficit, which is an unfavourable index of compensatory recovery.


  1. patient is on examination bed
  2. the examiner holds the patient’s head and makes sharp, rapid rotations of about 10° – 20° on both sides
  3. Rotations should not be systematic or predictable by the patient
  4. During the execution of the test, the patient must gaze at a fixed point or target (in videonystagmoscopy the patient can gaze at some lights that are projected from inside the mask).

In an unaffected subject who has no peripheral vestibular pathology, during the execution of the HIT Test, the gaze remains fixed on the target.

On the other hand, if a peripheral vestibular pathology is present, the eyes will sway from the fixed target during the rotation of the head, owing to the speed of the head movement not being compensated, or coordinated to the speed of movement of the vestibular oculomotor reflex (VOR). The gaze sway is therefore followed by a horizontal corrective saccade in order to return visual fixation to the original target.

The Hit is therefore based on the evaluation of the neuronal pathways of the VOR ranging from the labyrinthine semicircular canals to the extrinsic eye muscles. It is an important expression of a lack of vestibular compensation.


  • Head Heave Test (HHT)

This test us useful for evaluating any dysfunctions of the utricle and therefore of the superior vestibular nerve. It is based on rapid translation movements on the horizontal plane (Nuti et al 2005).


1. The patient is placed on the examination bed, preferably with a videonystagmoscopic mask, and fixes the gaze on a target.

2. Rapid movements of the head are performed on the horizontal plane with a maximum displacement of 5-6 cm

3. If the utricle is functional, the gaze remains stable on the fixed target

4. If there is functional asymmetry of the utricle, a correction saccade appears at the end of the movement, which is an indication of functional deficit of the side towards which the movement of the head was made.

The small saccadic movements that are detected, however, can be non-specific. For this reason, HTT should be placed in a much broader context of vestibular evaluation, especially an instrumental one of the vestibular patients.


  • Hyperventilation Test

Hyperventilation induces an increase in forced pulmonary ventilation which leads to hyperoxygenation and a net reduction in PaCO2 with a consequent increase in arterial pH. This leads to an intracellular alkalosis resulting from the passage of hydrogen ions from the cells to the extracellular liquids, activating the ionic exchanges K+ and Na+. This leads to an increase in intracellular Ca++ and a net reduction in plasma bicarbonates.

Such a situation of hypocapnia induces in sequence:

1. vasoconstriction of arterioles

2. cellular hypoxia

3. increase in the pH of the cerebrospinal fluid

4. impaired haemoglobin dissociation

5. further tissue / cellular hypoxia

6. middle ear and intracranial hypotension.

These events induce a neurogenic excitatory state (Manto / Bosset 2003).

Hyperventilation Syndrome, which can be Voluntary, Compensatory for Breathing Disorders or Psychogenic, is characterized by the possibility of inducing symptoms that can be characterized by:

  • sweating
  • anxiety / light-headedness / concentration difficutly
  • dyspnoea
  • asthenia
  • dizziness / vertigo
  • paraesthesia
  • headache / migraine
  • tetany / convulsions
  • may give cerebellar functional interference by triggering nystagmus.

This activity can happen owing to two conditions:

1. Primary pathology of the cerebellum

2. inhibition of normal cerebellar function which is compensating for a dysfunction of the peripheral vestibular system.

Hyperventilation seems to alter the central compensation mechanism created in vestibular pathology.

For instance, in Acute Vestibular Neuritis or in Acoustic Neuroma, the Hyperventilation Test can induce the onset of nystagmus, more often “Deficitary” Nystagmus (i.e., rapid phase of nystagmus that beats towards the unaffected side) than “Excitatory” (rapid phase that beats towards the pathological side).

The Hyperventilation Test, which is always recommended to be performed in videonystagmoscopy, according to our clinical experience at Vestibology Medical, can also take advantage of a stabilometric assessment through an appropriate programme, both during the test and immediately after the test is suspended.

This test can highlight dysfunctions of the vestibular system that we can define as latent, or in the phase of symptomatic compensation given by the cortical / central structures.

The Hyperventilation Test should be performed for about 60-90 seconds and as previously mentioned, in videonystagmoscopy. Stabilometry with a specific programme may be useful. It is definitely useful for central pathologies such as Acoustic Neuroma or Multiple Sclerosis.

The test should be considered positive for the appearance of at least 5 nystagmus shocks lasting at least 5 seconds.

If, on the other hand, a spontaneous nystagmus is present and the Hyperventilation Test is performed, it should be considered positive for at least one of the following conditions: strengthening by intensity, inhibition or inversion of the nystagmus for at least 5 seconds.

The Hyperventilation Test has the merit of having a low number of false positives.


 But what are the pathologies in which the Test finds greater application?


Superior Semicircular Canal Dehiscence Syndrome (SCDS or Third Window).

Appearance of downbeat nystagmus with a torsional component.

Acute Vestibular Neuritis

Often there is a reinforcement of the spontaneous horizontal nystagmus present in the acute phase of the clinical manifestation. Over time, an inversion of the nystagmus may occur which can be detected even after months or even years.

Neuroma of the eighth pair of cranial nerves (or acoustic neuroma)

Appearance of horizontal nystagmus in a pathology generally devoid of spontaneous nystagmus.

Multiple sclerosis

With the Hyperventilation Test in the case of MS, two different manifestations can generally occur:

1. complete or partial inhibition of a spontaneous nystagmus

2. onset of horizontal, vertical, or rotary nystagmus (especially in the case of inhibition of vertical nystagmus, there is almost certainty of pathology).

Cerebellum pathologies

The Hyperventilation Test can induce the onset of a Downbeat Nystagmus.