Practical Neurology Part 4: Dizziness on head movement

Miriam S Welgampola, Andrew Bradshaw and G Michael Halmagyi
Med J Aust 2011; 195 (9): 518-522. || doi: 10.5694/mja11.11001
Published online: 7 November 2011

Rose’s story

Rose, who is 63 years old, presented to a balance clinic after experiencing multiple episodes of dizziness and unsteadiness over 10 days. These had begun abruptly on waking one morning, with a sensation of disequilibrium on getting out of bed. She had also felt herself being pushed to the right after rising from a stoop. The initial symptoms resolved, but over the ensuing days she had been troubled by spells of vertigo that lasted seconds. These spells were brought on by arching backwards while putting in eye drops and by returning to the upright position after bending down. In bed, Rose had noticed a spinning sensation brought on by turning to her left side. She recalled a similar episode 1 year earlier, which resolved within days. She had no history of head injury or any prolonged episode of acute spontaneous vertigo that might suggest previous vestibular neuritis. She had a history of occasional migraine with aura but there was no temporal relationship between these headaches and her vertigo. The vertigo was not accompanied by aural symptoms such as tinnitus, aural fullness or hearing loss.

On examination, Rose had no signs of a unilateral vestibulopathy. Specifically, there was no nystagmus at rest or evoked by gaze or head-shaking. The result of a horizontal head impulse test (in which the examiner manually delivers high acceleration, 20°–30° head rotations in the horizontal plane to assess the horizontal vestibulo-ocular reflex while the patient fixes their gaze on a target) was normal, with no evidence of a “catch-up saccade” after head movement. A left Dix–Hallpike test (in which the patient is arched backwards by the examiner while their head is turned 45° to the left) revealed vigorous upbeating counterclockwise (leftward) torsional nystagmus that appeared after a latency of 5–10 seconds, reached a crescendo over 30 seconds and then rapidly slowed down (Video 1).

Differential diagnoses

The differential diagnoses for episodic positional vertigo are summarised in Box 1. In Rose’s case, positional vertigo lasted only seconds and was not associated with aural symptoms or headache. Her sensation of being pushed to one side (“lateropulsion”) was probably caused by movement of otoconia within the duct of the left posterior semicircular canal.

The typical nystagmus of BPV that results from canalithiasis (Box 2) is preceded by a latency of 2–15 seconds after head movement. It is paroxysmal, rises to a crescendo and abates within 60 seconds. It is elicited by positioning the head in a way that the affected canal is vertical and aligned with gravity. Stimulation of a given canal by the movement of otoconia provokes nystagmus in the plane of that canal, and is thus unique to that canal. The nystagmus reverses direction by moving the head in the opposite direction (eg, returning to the upright position). The nystagmus fatigues on repetition of the Dix–Hallpike test.

Observations from electrical stimulation of nerves innervating individual semicircular canals and three-dimensional analysis of eye movements recorded from single-canal BPV confirms that activation of a given canal evokes nystagmus with a rotational axis perpendicular to that canal.2 The left Dix–Hallpike test in this patient evoked paroxysmal upbeating and counterclockwise torsional nystagmus (from the patient’s perspective) indicative of left posterior canal activation (Box 3, Video 1).


Posterior canalithiasis — BPV affecting one of the posterior canals — is the most common canalithiasis. It can be treated at the bedside with an Epley manoeuvre (Box 4, Video 4), which has been shown to be effective in randomised controlled trials (Grade A evidence).4 The manoeuvre is easy to learn and can be performed by medical practitioners, allied health professionals and, in some instances, patients themselves.

Achieving the correct head position is the key to successful treatment. When the repositioning is successful, upbeating torsional nystagmus (ie, in a direction identical to the nystagmus elicited in the head-hanging position) can be observed even in Steps 3 and 4, indicating flow of the otoconia away from the ampulla and towards the common crus of the anterior and posterior canals, to reach the final destination — the utricle. Conversely, “wrong direction nystagmus” (ie, downbeating clockwise [rightward] torsional nystagmus in this instance) implies a failed manoeuvre due to otoconia falling back towards the ampulla. When downbeating nystagmus is observed in this context, the repositioning manoeuvre should be repeated.

During an Epley manoeuvre, otoconia can sometimes inadvertently be dislodged from the posterior canal and drop into the horizontal canal, resulting in severe vertigo accompanied by horizontal nystagmus. The side-lying test (or roll test) can be used to test for horizontal canal BPV. The patient is quickly turned to the left and right lateral positions as the examiner observes the eyes. In left horizontal canal BPV, left-beating horizontal nystagmus will be observed in the left lateral position. Less intense right-beating horizontal nystagmus will be observed in the right lateral position. Iatrogenic horizontal canalithiasis should be treated with the same manoeuvre used for treatment of BPV affecting the horizontal canal;4 this is sometimes called the barbecue manoeuvre, as the patient imitates a spit roast being rotated (Box 5, Video 5).

Anterior canal BPV is exceedingly rare. Left anterior canal BPV can be treated by placing the patient in the right Hallpike position and performing an Epley manoeuvre. Alternatively, a deep Dix–Hallpike test (with the right ear down) followed by a rapid return to the upright position can also be used (Video 6).

After a single successful Epley manoeuvre, it is reassuring to repeat the Dix–Hallpike test and demonstrate absence of nystagmus and vertigo. Repeated testing can cause habituation of the canal receptors, resulting in a false negative result from the Dix–Hallpike test. Patients can be advised to sleep on two or three pillows, on the unaffected side, for 1 week. Although disequilibrium may persist for several days, they should remain physically active and maintain a normal range of head movements. Neck immobilisation with soft collars promotes fear of head movement and may contribute to neck pain and tension headaches. If positional vertigo persists, patients should have a follow-up assessment within 1 week. Patients have previously been advised to sleep upright for 48 hours after treatment of BPV, but recent studies show no advantage of this (Grade B evidence).5

Bedside treatment of BPV is within the capability of any medical practitioner, and some physiotherapists and nurses are adept at treating BPV. Websites that show patients how they can self-treat their BPV have also led to home Epley manoeuvres. When the patient is able to clearly identify the affected side and when the Epley manoeuvre is not technically difficult (ie, when the patient is mobile enough to perform the manoeuvre unassisted), he or she can be taught (by a health care professional) how to self-treat. It is important to caution the patient that there are many BPV subtypes, of which the home Epley manoeuvre treats only one (albeit the most common one). If no improvement is noticed after a home repositioning manoeuvre, further medical advice should be sought. For patients with a limited range of neck movements, the Semont manoeuvre is an alternative method of treating posterior canalithiasis (Box 6, Video 7).

Treatment challenges

Subjective BPV: Benign positional nystagmus is more likely to be detected when the patient does not fix their gaze. In contrast, when bedside examination with visual fixation elicits clearly lateralised positional vertigo without nystagmus (subjective BPV, in which the patient feels as though they are spinning), the symptomatic side should be treated with a particle-repositioning manoeuvre.6 If the patient’s history is characteristic of BPV but neither nystagmus nor vertigo can be provoked, and there are no physical signs of vestibular impairment, it is more fruitful to repeat the bedside assessment on one or more symptomatic days, rather than seek an alternative diagnosis.7

BPV with motion sensitivity that impedes treatment: Motion-sensitive patients with BPV — including those with migraine, severe post-traumatic BPV or horizontal canal BPV — can develop intense nausea and vomiting during testing and treatment. Such patients should fast for 4 hours before treatment and be premedicated with an antiemetic (eg, intramuscular prochlorperazine or sublingual ondansetron) and a vestibular suppressant (eg, oral diazepam or oral lorazepam). However, these drugs do not reduce time to symptom resolution.4

Recurrent BPV: Long-term follow-up studies show a 50% recurrence rate for BPV over 10 years; in most cases, BPV recurs in the first year after repositioning.8 In a few patients, BPV is refractory to multiple bedside repositioning treatments. If the patient can perform the Epley manoeuvre (perhaps with the help of a family member), daily home Epley manoeuvres, with weekly supervised manoeuvres by a trained physician, therapist or nurse, are recommended. Mechanical particle-repositioning devices (see below) have high success rates for treating recurrent BPV that is refractory to multiple bedside repositioning treatments2,9 but it is not known whether these devices are more efficacious than frequent regular bedside repositioning manoeuvres.

Atypical positional nystagmus: Rarely, central vestibular disorders can give rise to positional nystagmus, which can be mistaken for BPV. For example, posterior fossa lesions, especially small cerebellar strokes, can produce paroxysmal positional nystagmus, which can be difficult to differentiate from BPV.10 In addition, spontaneous horizontal nystagmus from acute peripheral vestibulopathies may be enhanced by Dix–Hallpike testing. However, unlike the horizontal (paroxysmal) nystagmus observed in horizontal canal BPV (which changes direction with either ear down), enhanced spontaneous nystagmus is consistently unidirectional. For example, spontaneous nystagmus from a right-sided vestibular neuritis will be left beating in the left lateral and right lateral positions. In contrast, nystagmus from left horizontal canal BPV will be vigorously left beating in the left lateral position and will beat less vigorously to the right in the right lateral position. Low-velocity sustained horizontal, vertical or torsional nystagmus can be found in patients with clinically definite vestibular migraine.11

Advanced therapies

Mechanical repositioning: The Epley Omniax System (Vesticon, Portland, Ore, USA) is a multi-axial motorised chair that can position and move a seated patient in the plane of any one of the six semicircular canals. It uses real-time infrared video-oculography to enable observation of nystagmus during provocative testing. Studies indicate success rates of 99.3%, 89.2% and 63.2%, respectively, for treatment of posterior, horizontal and anterior canal BPV in a single manoeuvre, which are higher than success rates reported for bedside particle-repositioning manoeuvres.9 However, no randomised trials have directly compared the efficacy of bedside repositioning with that of mechanical repositioning.

Canal plugging: Posterior semicircular canal occlusion is an effective treatment option for debilitating posterior canal BPV that is unresponsive to bedside repositioning. In the largest case series reported to date, all but one of 44 patients who underwent this procedure were relieved of BPV on follow-up between 6 months and 12 years.12 One patient with normal preoperative hearing developed delayed sudden hearing loss in the treated ear at 3 months. Postoperative imbalance and motion sensitivity (up to 4 weeks) was reported in all patients, with more prolonged symptoms in six.

Video 1: Nystagmus of left posterior canal BPV

A left Dix-Hallpike test evokes upbeating counterclockwise (leftward [ie, fast phase torting to the left]) torsional nystagmus (from the patient's perspective).

  • Miriam S Welgampola1,2
  • Andrew Bradshaw1
  • G Michael Halmagyi1,2

  • 1 Department of Neurology, Royal Prince Alfred Hospital, Sydney, NSW.
  • 2 Central Clinical School, University of Sydney, Sydney, NSW.



Miriam Welgampola and Michael Halmagyi are supported by a National Health and Medical Research Council grant for research on diagnosis and management of intractable BPV (NHMRC Project Grant APP1010017). Miriam Welgampola is the recipient of a Garnett Passe and Rodney Williams Memorial Foundation Senior/Principal Research Fellowship.

Competing interests:

No relevant disclosures.

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