Introduction
Peripheral vestibular end‐organ disease typified by a sudden, transient gyratory sensation accompanied by characteristic nystagmus.
- M/C peripheral vestibular end‐organ disease
- M/C cause of vertigo (up to 20%)
History:
Physiology
Vestibular system:
to perceive head motion and position
- Otolith organs (comprised of utricle & saccule): Detect linear acceleration and gravitational forces
- Semicircular canals: Detect rotational acceleration
- Endolymph hydrodynamics (within semicircular canals + influence on ampullary cupula): Sensation of angular movement in each of the 3 planes in which the canals are oriented
The symptomatology of BPPV is a direct result of aberrant semicircular canal signalling which creates an illusory sense of motion.
Aetiology
- Idiopathic (M/C)
- Head trauma
- Ear infections
Pathophysiology
BPPV occurs due to the displacement of calcium-carbonate crystals or otoconia within the fluid-filled semicircular canals of the inner ear. These otoconia are essential to proper functioning of the utricle of the otolithic membrane by helping deflect the hair cells within endolymph, which relays positional changes of the head including tilting, turning, and linear acceleration.
With BPPV, otoconia (also known as “otoliths” or “canaliths”) dislodge and settle within the endolymph of the semicircular canals. When the head remains static, there is no stimulus causing the hair cells to fire. With motion, however, the displaced otoconia shift within the fluid, and the subsequent stimulus is unbalanced with respect to the opposite ear, inappropriately causing symptoms of dizziness, spinning, and/or swaying. Hence, symptoms of BPPV are profound with movement but classically lessen with rest.
Variants:
These two variants of BPPV means different characteristics of the nystagmus elicited by the provoking manoeuvres.
- Canalithiasis (free-floating otoconia within canal duct)
- Nystagmus; Brief (< 1 minute), paroxysmal and latency (few seconds)
- Cupulolithiasis (otoconia adherent to the cupula)
- Nystagmus: No latency and lasts long (> 1 minute)
Classification
- Posterior canal BPPV (pc-BPPV) (M/C variant, 80–90% cases)
- Lateral canal BPPV (lc-BPPV)
- Anterior/superior canal BPPV (ac-BPPV) (rare, 1–2% cases)
Clinical features
Classically, the symptoms of BPPV are sudden in onset, provoked by movement, and decreased with rest.
Rotational vertigo (M/C feature)
Brief, discrete episodes of vertigo lasting seconds to minutes upon lying down, turning over or getting out of bed
- Severe cases associated with nausea & vomiting
Benign positional nystagmus:
Nystagmus direction, onset, intensity pattern and duration should be consistent with that expected of BPV
Diagnosis
Diagnosis of BPPV can be made based on the history and examination.
Dix–Hallpike maneuver:
Performed by rapidly moving head from upright to hanging position with one ear 45° to the side resulting in torsional upbeating nystagmus corresponding in duration to the patient’s subjective vertigo, and occurring only after Dix–Hallpike positioning on the affected side.
Supine head turn maneuver:
Diagnose horizontal BPPV by turning patient’s head to one side, then turning back to the supine face-up position. Then the head is turned to the other side. The nystagmus of horizontal canal BPPV, unlike that of posterior canal BPPV, is distinctly horizontal and changes direction with changes in the head position. The paroxysmal direction changing nystagmus may be either geotropic or apogeotropic.
Differential diagnosis:
Management
The treatment of BPV involves positional manoeuvres to direct the displaced otoconia back into the utricle. For patients with the cupulolithiasis variant this will involve first converting to canalithiasis. The nystagmus observed during the manoeuvre can be a useful indicator of the ampullofugal flow of otoconia towards the utricle.
Accepted recurrence rate of BPPV after successful treatment is 40%–50% at 5 years of average follow-up. There does appear to be a subset of individuals prone to multiple recurrences.
Repositioning maneuvers:
Mainstay of treatment
Epley maneuver:
Posterior canal BPPV treatment
Half-Somersault maneuver:
Posterior canal BPPV treatment
Gufoni maneuver:
Lateral BPPV treatment
Lempert (BBQ) maneuver:
Horizontal/lateral canal BPPV treatment
Deep head-hanging maneuver (DHM):
Superior/anterior canal BPPV
Other home exercises: CONTRAINDICATED
These are indicated in all causes of vertigo/diziness except those due to Meniere’s disease & BPPV
Vstibular suppressant therapy:
Cases with severe symptoms after a therapeutic maneuver, and patients who decline treatment although their symptoms are severe
- Antihistamines
- Benzodiazepines
- Anticholinergics
Surgical management:
Central adaption and postoperative vestibular physiotherapy required in conjunction with procedures
- Singular neurectomy (for p-BPPV): Transection of posterior ampullary nerve within singular canal (removes the resting input from the affected posterior canal ampulla, creating both a dynamic and static vestibular asymmetry)
- Posterior semicircular canal occlusion (treat intractable BPPV): Occluding the canal renders cupulaunresponsive to stimulation from natural head movements or gravitational pull on the canaliths (the resultant dynamic vestibular asymmetry leads to an initial period of postoperative imbalance)