Chapter 38 Posterior Semicircular Canal Occlusion for Benign Paroxysmal Positional Vertigo
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Benign paroxysmal positional vertigo (BPPV) is the most common vestibular end organ disorder; in one busy vestibular clinic, BPPV accounted for 17% of all diagnoses.1 Patients complain of brief vertigo spells, often accompanied by nausea, but rarely vomiting. The actual duration of the spells (5 to 15 seconds) is usually much shorter than what the patients describe. Spells are induced by characteristic head movements, such as rolling to the affected side while in bed or extending the neck while upright. Less common precipitating movements include bending forward, arising from a supine position, and rotating the head. When the disease is very active, in addition to the brief positional vertigo episodes, patients may complain of protracted, nonspecific imbalance and dizziness accompanied by mild lassitude.
BPPV is most often an idiopathic disorder. The most common identifiable cause is head or temporal bone trauma.2 Other, less common causes include viral labyrinthitis, vestibular neuronitis, stapedectomy, perilymph fistula, Meniere’s disease, and chronic otitis media.3–8 Various combinations of rotatory, vertical, and oblique nystagmus may be seen in response to the Dix-Hallpike maneuver, depending on the position of the globe within the orbit during nystagmus. The nystagmus profile correlates, however, with the known neuromuscular pathways arising from the crista of the undermost posterior canal.9–12
The classic diagnostic maneuver as described by Dix and Hallpike13 has the patient laying back from a sitting to a head-hanging position. Before lying the patient back, the head is turned 45 degrees toward the side being tested such that when lying back, that side is directed down toward the floor. In some patients, it may be impossible to extend the neck back into a “head-hanging” position because of arthritis, kyphoscoliosis, or vascular disease. For pure diagnostic testing purposes, the lack of hyperextension should not preclude a positive diagnostic test, but it becomes a factor later on when attempting the therapeutic repositioning maneuver (see later). The Dix-Hallpike maneuver serves to rotate the undermost posterior semicircular canal (SCC) in the earth’s vertical plane. This rotation results in an endolymph current and secondary cupular displacement, which produces the characteristic oculomotor response, primarily a rotatory nystagmus.
BPPV must be differentiated from other causes of vertigo and nystagmus. The history is usually typical, and a positive response to the Dix-Hallpike maneuver is virtually diagnostic, assuming that all features are present. Typical posterior canal BPPV, which produces a positive response to the Dix-Hallpike maneuver, must be differentiated from the much less common lateral canal BPPV14 and the extremely rare anterior canal BPPV. Lateral canal BPPV gives rise to more severe and prolonged vertigo spells. It is brought on by head movements that produce gravitational forces on the affected lateral canal and is diagnosed by rolling the patient from one lateral supine position to the other and observing the eyes for horizontal nystagmus. Vertigo usually resolves within days to weeks of onset, but similar to the classic posterior canal variant, it can also be treated with various repositioning maneuvers.15 The remainder of this discussion deals solely with the management of the classic posterior canal BPPV.
Untreated posterior canal BPPV has three clinical courses. Most commonly, patients experience a self-limited single episode that subsides spontaneously over weeks to months. A second group of patients experiences remissions and recurrences ranging from weeks to years. A third, smaller group has the more chronic form of this disorder. In one busy vestibular clinic, about 30% of untreated patients had symptoms lasting longer than 1 year.8
PATHOPHYSIOLOGY
Under normal physiologic conditions, the cupula has the same density as the surrounding endolymph. The SCCs are normally not sensitive to linear acceleration (e.g., gravity). A fixed cupular deposit would render the posterior canal crista sensitive to gravity, however.16 Rotation of the canal in the earth’s vertical plane during the Dix-Hallpike maneuver would produce cupular displacement through the gravitational pull on the deposit, resulting in nystagmus and vertigo. This condition, so-called cupulolithiasis, may represent the extremely rare, more chronic form of this disorder. Cupulolithiasis also seems to be more prevalent in lateral canal BPPV.15
The more common, self-limited variant and the variant with remissions and recurrences likely have a different pathophysiologic mechanism. Free-floating endolymph particles within the posterior canal produce a Dix-Hallpike response identical to that of a fixed cupular deposit.17 Because the posterior canal is the most gravity-dependent part of the vestibular labyrinth, free-floating endolymph particles have a predilection for settling in the posterior canal endolymph.
With the head upright, the most dependent part of the canal is the area just posterior and inferior to the ampulla on the side of the cupula opposite the utricle. As the posterior canal rotates during the Dix-Hallpike maneuver, the particles initially rotate upward because of their inertia. After a short latent period, gravity pulls them down and away from the cupula (utriculofugal) to a more dependent position. Their hydrodynamic drag creates an endolymph current in the same direction, displacing the cupula away from the utricle. Utriculofugal displacement of the posterior canal cupula increases the resting discharge rate of the hair cells and first-order vestibular neurons. As known from previous animal studies, this action produces excitation of the ipsilateral superior oblique and contralateral inferior rectus muscles,9 which causes counterclockwise eye rotation with stimulation of the left posterior crista and clockwise rotation with right-sided stimulation. The compensatory fast component of the induced nystagmus is in the opposite direction, however, corresponding with the clinical findings of typical BPPV.
These free-floating posterior canal particles have been identified in vivo in patients undergoing surgery for BPPV.18,19 This theory of free-floating particles, also referred to as canalithiasis, is an important concept because it relates to the treatment of this condition.
PREOPERATIVE PATIENT COUNSELING AND CONSERVATIVE MANAGEMENT
First, the patient must be reassured that BPPV is an inner ear disorder that is relatively benign and most often self-limited. Medical management for BPPV is mostly ineffective.20 The most efficacious means of vertigo control is avoidance of the specific provocative head movements that induce the attacks. Most patients already use this approach by not lying on the affected side and by not extending the neck to look upward. Patients who stringently avoid these movements may have more prolonged courses because the absence of provocative movements prevents movement within and subsequent dispersement of the particles from the canal.
Most cases of BPPV resolve spontaneously over weeks to months without any treatment. Brandt and Daroff21 recommended a rigorous course of physiotherapy under heavy sedation during several days of hospitalization. They believed that the exercises shook free the otolithic debris from the cupula. Other clinicians could not reproduce their good results. Semont and associates22 reported excellent results using a technique termed the liberatory maneuver. They theorized that this technique liberated deposits from the cupula and reported a 92% success rate following two maneuvers.
The liberatory maneuver is difficult to perform in elderly, frail patients. The particle repositioning maneuver23–25 provides the same benefits as the liberatory maneuver, but is simpler to accomplish. It is based on the free-floating particle (canalithiasis) pathophysiologic theory of BPPV and is adapted from Epley’s canalith repositioning procedure.26 For the purpose of this discussion, it is important to remember that the cupula forms a complete barrier across the ampullated end of the canal that is impermeable to endolymph and free-floating particles. Free-floating posterior canal endolymph particles can enter and exit the canal only through the common crus.
The current particle repositioning technique (Fig. 38-1) begins with the patient seated lengthwise on the examining table. The first part of the Dix-Hallpike maneuver is performed by rotation of the posterior SCC of the undermost (affected) ear in the earth’s vertical axis (see Fig. 38-1B). The examiner should observe the classic nystagmus response, which confirms the diagnosis, and then reassure the patient as the vertigo subsides. The patient maintains this position for 30 to 60 seconds after resolution of the nystagmus, allowing the particles to settle in their new dependent position closer to the common crus. In the second stage, the patient rolls laterally through position C into position D onto the opposite side with the head turned 45 degrees downward. This stage is performed in a smooth, continuous motion, and the neck is kept extended throughout. This method rotates the affected posterior canal 180 degrees in the plane of gravity, allowing the free-floating particles to follow the natural curve of the canal and continue their relative course through the common crus into the utricle, presumably from whence they came.
Conversely, a secondary nystagmus that reverses direction from that of the initial head-hanging position (position B) may occur through two possible mechanisms. In one, the particles reverse their direction of movement because of an improperly performed maneuver, resulting in a utriculopetal endolymph current. This reversal usually occurs when the neck is not hyperextended enough during the roll. Cupulolithiasis is the other possible mechanism underlying reversal nystagmus. The gravitational effect on a fixed cupular deposit results in utriculofugal cupular deflection during the Dix-Hallpike maneuver (see Fig. 38-1B), as would be seen with free-floating particles. The position assumed during the second stage of the particle-repositioning maneuver effectively rotates the posterior canal 180 degrees in the earth’s vertical plane (see Fig. 38-1D). This action serves to flip the whole posterior canal and its cupula upside down, reversing the gravitational pull on the cupula and resulting in utriculopetal cupular displacement and a reversal of the nystagmus response.
