Benign paroxysmal positional vertigo: provocation and liberation maneuvers

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1 4 rd Congress of the European Academy of Neurology Lisbon, Portugal, June 16-19, 2018 Hands-on Course 7 Neuro-otology - Level 2 Benign paroxysmal positional vertigo: provocation and liberation maneuvers Michael Leo Strupp & Thomas Brandt Munich, Germany michael.strupp@med.uni-muenchen.de thomas.brandt@med.uni-muenchen.de

2 Conflict of interest: M. Strupp is Joint Chief Editor of the Journal of Neurology, Editor in Chief of Frontiers of Neuro-otology and Section Editor of F1000. He has received speaker s honoraria from Abbott, Actelion, Auris Medical, Biogen, Eisai, GSK, Henning Pharma, Interacoustics, MSD, Otometrics, Pierre-Fabre, TEVA, UCB. He acts as a consultant for Abbott, Actelion, AurisMedical, Heel, IntraBio and Sensorion. Thomas Brandt has no conflict of interest in relation to this manuscript Benign paroxysmal positional vertigo (BPPV) is the most frequent and a well treatable vestibular disorder. Every neurologist should become familiar with the positioning maneuvers for diagnosis and treatment of this common condition. Its diagnostic criteria were re-defined by members of the Classification Committee of Vestibular Disorders of the Bárány Society in 2015 [60]. Patient History The leading symptoms of benign paroxysmal positional vertigo (BPPV) are recurrent second-long attacks of rotatory vertigo with and without nausea. They are caused by changes in head position relative to gravity. Typical triggers include lying down or sitting up in bed, rolling or bending over in bed, extending the head backwards or forwards. First attacks often occur in the morning ( my every morning vertigo ). The complaints can be so typical that a diagnosis can often be made solely on the basis of the patient history; often even the affected ear can be identified in this way. The diagnosis of BPPV requires positioning manoeuvres that result in a canal-specific positional nystagmus of the posterior, horizontal, or anterior semicircular canals (PC, HC, AC), which are affected in this order of frequency [5, 30]. 1

3 Clinical Features and Course Benign paroxysmal positional vertigo is the most common cause of vertigo, not only in the elderly, with a lifetime-prevalence around 3% [59]. This condition is characterised by brief attacks of spinning vertigo and simultaneous positioning nystagmus with a rotatory component beating toward the under-most ear and a linear component beating toward the forehead. It can be accompanied by nausea. BPPV is elicited positioning the head or body toward the affected ear. Rotatory vertigo and nystagmus occur after such positioning with a short latency of seconds in the form of a crescendo/decrescendo course of maximally seconds. The beating direction of the nystagmus is vertical and rotatory; it also depends on the direction of gaze, is primarily rotatory when gaze is directed to the under-most ear and mostly vertical (to the forehead) during gaze to the uppermost ear. In pc-bppv the nystagmus corresponds to an (ampullofugal) excitation of the posterior canal of the under-most ear. BPPV can appear at any time from childhood to senility, but the idiopathic form is typically a disease of old age, peaking in the sixth to seventh decades. More than 95% of all patients are classified as degenerative or idiopathic (women:men = 2:1), whereas the symptomatic patients (women : men = 1:1) are most frequently caused by head injury (17%) or vestibular neuritis (15%) [27]. BPPV occurs often after extensive bed rest in connection with other illnesses or after operations. About 5% of the spontaneous patients and 10% of the trauma patients show a bilateral, generally asymmetrical BPPV. The right posterior canal is affected about twice as often as the left, which might be related to the fact that more people sleep on their right side [33]. We found that the history of the disorder until its diagnosis had lasted more than 4 weeks in 50% of our 2

4 patients and more than 6 months in 10%. It is called benign because it generally resolves spontaneously within weeks to months; if not treated, BPPV persists in up to 30% of patients [24]. Pathophysiology and Therapeutic Principles The canalolithiasis hypothesis [7, 40] can explain all signs and symptoms of BPPV. According to this hypothesis, the attacks are induced by otoconia that move freely in the semicircular canal. The movement of the conglomerate causes an ampullofugal or ampullopetal deflection of the endolymph depending on the direction of sedimentation and thus leads to a stimulation or inhibition of the vestibular hair cells. This model of the pathomechanism of BPPV can predict the direction, latency, duration and fatigability of the typical nystagmus, as well as changes in these parameters after head manoeuvres. Latency. Rotatory vertigo and nystagmus appear as soon as the particles in the canal precipitate as a result of gravity. This causes a deflection of the cupula, which exceeds the stimulus threshold of the sensory epithelium after 1 5 seconds. Duration. After the change in position the particles move toward the lowest point within the canal. Depending on their size and composition, this takes about 10 seconds. Course of Attacks. After the positioning, the particles fall away from the curved canal wall. They are accelerated from standstill by the forces of gravity, reach a maximal speed during their fall, and return to standstill at the lowest point in the canal. This explains the temporal crescendo decrescendo-like course of the attacks; the cupula time constant 3

5 increases the duration of the nystagmus and vertigo). This was more recently confirmed by a mechanical model of BPPV [40, 41]. Direction of Nystagmus. The ampullofugal stimulation of the posterior canal causes compensatory eye movements around the axis of ocular rotation, which is perpendicular to the canal plane, by means of the vestibulo-ocular reflex (VOR). To the physician this will appear to be a combination of linear (toward the forehead) and rotatory eye movements. Reversal of Nystagmus. If the positioning movement is reversed by sitting up, the particles move in the opposite direction. Now the cupula is deflected in the opposite (ampullopetal) direction. This results in a reversal of both the rotatory vertigo and the direction of nystagmus due to inhibition of the vestibular hair cells. Fatigability. The particles that form a plug or clump are loosely held together. During changes in the head position they tend to fall apart. Small particles cannot cause suction or pressure on the cupula independently of each other, as does a single clumpwith a diameter almost filling the canal. If the patient holds his head still for several hours (e.g., during sleep), the particles, which had fallen apart before, coalesce into a clump in the lowest place within the canal and again induce vertigo when the head position is changed (for Ref see [5]). Liberatory Manoeuvres The efficacy of repositioning (liberatory) manoeuvres of the head can only be explained by the canalolithiasis hypothesis, i.e., a clot that moves freely within the canal. By quickly turning the patient s head to the opposite side, the plug is washed out of the canal and then can no longer cause any positioning vertigo [7, 8]. Brandt and Daroff in 1980 [4] first 4

6 devised an exercise programme, which, by means of simple head positioning, loosens the heavy degenerative otolithic material and distributes it into other areas of the labyrinth, where it no longer impairs canal function. We nowadays recommend that the patient s position according to the modified liberatory manoeuvre of Semont et al. from 1988 [48] is changed from a side-lying position by a tilt of 180 to the opposite side. Based on the findings of a mechanical model we recommend a tilt of at least 210 (the so-called SemontPlus manoeuvre) which should theoretically further improve the efficacy of the Semont manoeuvres [41]. This is currently studied in a multi-center RCT. The angular velocity of the movements should be between 90 and 180 /s [41]. In 1992, Epley proposed another liberatory manoeuvre [17] that involved turning the patient from a supine position into a head-hanging position. Evidence-based reviews conclude that all manoeuvres are effective [2, 18, 23] and can be explained by the mechanism of canalolithiasis [8, 53]. The success rate of the Semont as well as the Epley manoeuvre is around 90% after several applications (meta-analyses). Pragmatic Therapy Liberatory manoeuvres. When correctly performed, the physical liberatory manoeuvres according to Semont [48] or Epley s repositioning manoeuvre [16] are successful in almost all patients [2, 18, 23, 53]. There is evidence that these manoeuvre lead to a repositioning of the otoconia to the utricle [9]. 5

7 Semont manoeuvre According to the liberatory manoeuvre developed by Semont even before the mechanism of canalolithiasis was known the patient s head is first rotated by 45 to the side of the healthy labyrinth, in order to bring the posterior canal into the plane of the positional manoeuvre [48] (Figure 1). Then the patient is turned 90 to the side of the affected labyrinth; he/she holds this position for about 1 min. Afterwards the patient is turned by 180 to the side of the unaffected labyrinth, where he/she again has to remain lying for at least 1 min. Positional nystagmus to the uppermost ear, so-called orthotopic nystagmus, indicates that the plug has left the canal, i.e., the therapy is successful. Conversely, positional nystagmus to the lowermost healthy ear indicates that the liberatory manoeuvre failed and the procedure must be repeated. Finally the patient sits up. This manoeuvre should be repeated three times each: in the morning, afternoon, and evening until the patient is symptom-free. The efficacy of the Semont manoeuvre appears to be somewhat less than that of the Epley manoeuvre (see below). There has been a randomised study with an untreated control group: after one or multiple treatments 94% of the patients as opposed to only 36% of the controls were symptom-free [47]. In another double-blind sham-controlled study one hour after one Semont manoeuvre 79% and 24 hours later 87% were symptom-free compared to none within the sham group [35]. The success rate of the Semont manoeuvre is around over 90-98% after several treatments [32]. Epley manoeuvre Epley s repositioning manoeuvre requires that the supine patient s head and trunk be rotated after being tilted backward into a lateral headhanging position on the affected side [16] (Figure 2). Its efficacy has been 6

8 proven in the meantime by several controlled, randomised studies and meta-analyses (for Ref see [23]). For the Epley manoeuvre to be successful the following details must be kept in mind: (1) The transition from one position to the next is performed quickly but not abruptly. (2) Patients with restricted movement of the neck are treated either on an examination couch with lowered headrest or alternatively with the Semont method. (3) In cases of pronounced fear or nausea we recommend administering premedication with dimenhydrinate or other antivertigious drugs about 30 min before beginning the exercises. (4) The success rate is improved by repeating the manoeuvre 2 3 times in one session [19]. (5) The success rate is not improved by Epley s original suggestion to vibrate the mastoid bone during the manoeuvre [21, 34, 46]. (6) Remaining upright for 48 h after a successful treatment to avoid early recurrences improves the outcome only marginally (NNT=10) and can be decided individually with the patient [36, 45]. Staying upright after a Semont manoeuvre was ineffective in a single study [37]. The occurrence of nystagmus (so-called liberatory nystagmus) in the second step of the Epley manoeuvre indicates that the treatment will be successful [7, 42]. Direct comparisons of the Epley and the Semont manoeuvre found no differences [14, 22, 23, 37, 49, 51]. The choice of the manoeuvre to be used should depend on which manoeuvre the therapist has experience with or if there are any individual contraindications. Very obese patients are easier to treat with the Epley method, while the Semont manoeuvre is suitable for patients with shoulder-neck problems. 7

9 Transient nausea can occur as an adverse effect, above all during repeated positionings within one sitting (prophylaxis with, e.g., 100 mg dimenhydrinate or another antivertiginous substance is indicated). About 20 40% of the successfully treated patients experience 1 3 days of lightheadedness or postural vertigo with gait instability (most likely otolith vertigo) due to the partial repositioning of the otoconia toward the utricle [10, 61]). Occasionally a positional vertigo of the posterior canal converts into the horizontal or anterior canal variants during treatment [22]. Figure 1. Semont manoeuvre for treatment of posterior canal BPPV on the left. The procedure can be easily performed by the patient after getting instructions. All movements are to be performed with moderate angular velocity. 8

10 Figure 2. Epley s manoeuvre for treatment of LEFT posterior canal BPPV. Self-treatment The Epley and Semont manoeuvres can be successfully applied by the patient himself [44]). The treatment is performed three times per day applying between one and three manoeuvres per session until symptoms have disappeared. A thorough guidance by personal demonstration and an illustrated instruction is necessary. The success rates (50 90% after 1 week = 21 treatment sessions) are not as high as when a physician performs the manoeuvre. Thus the self-therapy can be used in a complementary way, for example in patients with remaining complaints or frequent recurrences. 9

11 Recurrences after successful liberatory manoeuvres According to follow-up observations over an average of 10 years, the recurrence rate in treated patients totals about 50%. Of these patients 80% have recurrences in the first year independently of the type of liberatory manoeuvre applied [6]. Women have a rate of 58% and thus are more often affected than men who have a rate of 39%. Additional medication Patients who develop severe nausea after a single manoeuvre can take an antiemetic, e.g. dimenhydrinate (100 mg) half an hour before undergoing the liberatory manoeuvre. Patients with excessive anxiety may require premedication with sublingual lorazepam or another benzodiazepine. An association between osteoporosis, vitamin D deficiency and BPPV was described in many studies [11, 15, 26, 43, 55, 57, 58, 63, 64]; this can probably also explain the predominance of women (2:1) in the idiopathic type of BPPV. Therefore, we determine in every patient vitamin D and if necessary substitute it. BPPV of the Horizontal Canal (hc-bppv) BPPV of the horizontal canal [38] is less frequent than posterior canal BPPV but is still diagnosed too seldom. Its key features differ from those of posterior BPPV: It can be induced by turning the head along the longitudinal axis of the supine body (either to the right or to the left) (Figure 2.5). This results in vertigo with horizontal geotropic nystagmus, i.e. nystagmus beating toward the ground in either head lateral position. Nystagmus is more intense when the head is turned to the side of the affected ear. 10

12 Repeated positioning manoeuvres cause hardly any fatigue of the positional nystagmus. The duration of the attacks and the nystagmus is longer than in pc- BPPV (20-60 s) because of the horizontal canal s so-called central storage mechanism of velocity. Positional nystagmus frequently shows a reversal of direction during the attacks; this corresponds to postrotatory nystagmus (so-called P I and P II). Typical hc-bppv can also be explained by canalolithiasis [52], although occasionally the mechanism switches from canalolithiasis to cupulolithiasis [50]. In the rare form of hc-bppv due to cupulolithiasis nystagmus beats horizontally to the uppermost ear with weaker nystagmus when the head is turned to the affected side. ( the zero point of positional nystagmus (beyond which direction changes) can be determined by turning the patient s head around the longitudinal axis while in the supine position; this is possible because the cupula of the ipsilateral horizontal canal is then parallel to the gravity vector [3]. In this way one can also determine which side is affected by horizontal BPPV. Therapy for hc-bppv Canalolithiasis. Therapy involves rotations around the patient s longitudinal axis while recumbent. In essence this is an altered version of the Epley manoeuvre. For canalolithiasis the supine patient is rotated in three 90 -steps around the longitudinal axis toward the healthy ear. The patient holds each position for 30 sec [31]. An effective alternative is to assume a lateral recumbent position on the side of the healthy ear for 12 hours [56]. A comparative study showed success rates of 70% for both 11

13 manoeuvres after one application as opposed to 30% in the untreated controls [39]. The combination of both manoeuvres (the modified Epley manoeuvre followed by a lateral recumbent position) is successful in about 90% of the patients [13]. Alternatively one can perform the so-called Gufoni manoeuvre [20] with which patients with either a canalolithiasis or a cupulolithiasis can be successfully treated [28, 29]. The advantage of this manoeuvre is that it is quick and that one needs not to determine which form of hc-bppv is present. From a sitting position, the patient is simply laid down on the side exhibiting less nystagmus. Afterwards the head is turned 45 downwards [1, 13, 20]. However, the authors are not convinced about the efficacy of this manoeuvre. Cupulolithiasis. For hc-bppv due to cupulolithiasis the treatment of choice is head-shaking with the nose down to transform the cupulo- into a canalothiasis [29]. This is indicated by the changing of direction of the nystagmus. Subsequently, the same manoeuvre as for canalolithiasis can be performed. BPPV of the anterior canal (ac-bppv) The main symptoms of ac-bppv correspond to those of pc-bppv. The clinical examination during the diagnostic positioning manoeuvres shows, however, a primarily vertical nystagmus that beats downward and has torsional components [25]. The relative frequency of ac-bppv is low: a study reported that it occurred in 2.2% of 577 patients with BPPV [62]. The same group devised a new and simple manoeuvre to treat ac-bppv. From a midline head-hanging position, the patient must bow his head 30 12

14 degrees toward the chest and sit up after 1 minute. This study reported a success rate of 85% after one single manoeuvre [62]. This high success rate does not correspond to our experience. Further studies should verify their findings. Finally, the authors have doubts about the clinical relevance of the ac-bppv. Differential Diagnosis and Clinical Problems The diagnosis of BPPV can be made on the basis of a typical patient history (brief rotatory vertigo when turning over or sitting up/lying down in bed) and the clinical findings. Especially in patients with therapyrefractory positional vertigo (despite correct positioning exercises), the following syndromes should be considered in the differential diagnosis: central positional nystagmus (infrequent, see below), vestibular migraine, bilateral BPPV, particularly post-traumatic (ca. 10%), BPPV of the horizontal canal (too rarely diagnosed, see above), and vestibular paroxysmia [54]. Central Positional Vertigo/Nystagmus Central positional vertigo and central positional nystagmus are caused by infratentorial lesions that affect connections between the vestibular nuclei in the medulla oblongata and cerebellar structures close to the midline (vermis). It is important to distinguish between peripheral and central vestibular disorders, as the Four characteristic forms of central positional vertigo/ nystagmus can be distinguished, although the symptoms overlap and combinations occur: central downbeat nystagmus, in head-hanging position (with or without accompanying vertigo), typically in lesions of the nodulus; central positional nystagmus (without vertigo); 13

15 central paroxysmal positional vertigo with nystagmus, typically in nodulus lesions, and central position vomiting. These central vestibular disorders occur much more seldom than typical BPPV. However, it can be difficult to distinguish peripheral and central disorders in an individual patient (Table 2.2). The following clinical rules are important for diagnosing a central positional vertigo/nystagmus [12]: persisting positional nystagmus (slow-phase velocity >5 /s) without associated vertigo; positioning-induced vomiting after single head movements without any substantial vertigo or nystagmus; positional vertigo with nystagmus of purely torsional or vertical character (downbeat or upbeat directions); a purely horizontal direction of nystagmus is typical for hc-bppv; and positional nystagmus that does not correspond to the plane of the semicircular canal stimulated by the head positioning (e.g., torsional nystagmus after stimulation of the horizontal canal). In clinical practice the latter seems to be the most important feature by which a central positional nystagmus can be identified. According to traditional, positional nystagmus beating toward the uppermost ear or lasting longer than 1 minute indicated a central pathology; this is no longer considered a reliable differentiating feature, as both features occur with the cupulolithiasis variant of BPPV. 14

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