Adverse effect of the Epley maneuver: Anterior canal crisis.

OBJECTIVE: In the Epley maneuver performed on patients with posterior semicircular canal-benign paroxysmal positional vertigo-canalolithiasis (P-BPPV-Can), an intense downbeat nystagmus and retropulsion rarely appear as soon as they reach the last upright sitting position. It is considered an anterior canal crisis that appears when the otoliths move to the ampullofugal direction in the anterior semicircular canal by changing head and body positions from the healthy-ear-down 135° head position (the third head position) to the upright sitting position (the fourth head position). This study aimed to determine the prevention of this anterior canal crisis. METHODS: The anterior canal crisis frequency was compared among the 178 cases that underwent general Epley maneuver (uncorrected Epley maneuver) and the 228 cases that underwent Epley maneuver (corrected Epley maneuver) by preventing head rotation beyond 135° to the healthy ear and the top of the head going down at the third head position. RESULTS: In 6% of patients with P-BPPV-Can who underwent the Epley maneuver, a transient mixed downbeat and torsional nystagmus to the affected ear and retropulsion were observed at the fourth head position (anterior canal crisis). The corrected Epley maneuver significantly reduced the incidence of unpredictable anterior canal crisis (p = 0.017). Additionally, there was no difference in the effect of the Epley maneuver the next day regardless of the anterior canal crisis appearance. CONCLUSION: Anterior canal crisis is an adverse effect of the Epley maneuver, and its prevention is important for safety. Avoiding head rotation beyond 135° to the healthy ear and/or the top of the head going down at the healthy-ear-down 135° head position is expected to reduce anterior canal crisis.

Subjective visual vertical deviation in patients with early-onset direction-changing horizontal positional nystagmus.

OBJECTIVE: Otolithic dysfunction is investigated in cases of direction-changing horizontal positional nystagmus (DCHPN) due to peripheral vestibular disorders. METHODS: The static-subjective visual vertical (S-SVV) was conducted in DCHPN cases within 48 h after onset. RESULTS: The absolute values of S-SVV deviations of patients with Light cupula and lateral canal-benign paroxysmal positional vertigo-cupulolithiasis (L-BPPV-Cup) were significantly different from those of healthy subjects (p < 0.001, p < 0.05, respectively), whereas there were no significant differences in those of patients with L-BPPV-Canalolithiasis-geotropic (L-BPPV-Can-g) or L-BPPV-Can-ageotropic (L-BPPV-Can-a) versus healthy subjects. Significant differences were found in S-SVV (+: deviation to the affected side, -: deviation to the unaffected side) between patients with Light cupula and those with L-BPPV-Can-g, L-BPPV-Can-a and L-BPPV-Cup (p < 0.01, p < 0.05, and p < 0.001, respectively), as well as between those with L-BPPV-Can-g and L-BPPV-Cup (p < 0.01). The S-SVV in patients with Light cupula, L-BPPV-Can-g, and L-BPPV-Can-a deviated more to the affected side, whereas that in patients with L-BPPV-Cup deviated more to the unaffected side. CONCLUSION: Mild otolithic dysfunctions were found in patients with DCHPN due to the presence of peripheral vestibular disorders within 48 h after onset. The extent of otolithic (utricular) disorders in patients with DCHPN is estimated in decreasing order as follows: Light cupula > L-BPPV-Cup > L-BPPV-Can-g and L-BPPV-Can-a. Many patients with L-BPPV-Cup likely suffer from disorders of the pars externa of the utricular macula, whereas many patients with L-BPPV-Can-g likely suffer from disorders of the pars interna of the utricular macula. L-BPPV-Can-a and L-BPPV-Can-g must be induced by a common mild utricular disorder.

Variants of benign paroxysmal positional vertigo in relation to head position during sleep.

BACKGROUND: Patients with posterior- and lateral-(canal)-benign paroxysmal positional vertigo (BPPV)-canalolithiasis sleep in the affected-ear-down head position. Posterior-BPPV-canalolithiasis typically affects the right than left ear; sleeping in the right-ear-down head position may be causal. OBJECTIVE: To investigate the relationship between habitual head position during sleep and the onset of BPPV variants. METHODS: Among 1,170 cases of BPPV variants with unknown etiology, the affected ears, habitual head positions during sleep based on interviews, and relationships among them were investigated. RESULTS: Posterior-BPPV-canalolithiasis and lateral-BPPV-canalolithiasis-geotropic affected the right ear significantly more often. Significantly more patients with posterior-BPPV-canalolithiasis and lateral-BPPV-canalolithiasis-apogeotropic habitually slept in the right-ear-down head position. Patients with posterior- and lateral-BPPV-canalolithiasis and light cupula were more likely to sleep habitually in the affected-ear-down position than in the healthy-ear-down head position; no relationship was observed in patients with posterior- and lateral-BPPV-cupulolithiasis. In patients with posterior-BPPV-canalolithiasis and lateral-BPPV-canalolithiasis-geotropic, the proportion of right-affected ears in those sleeping habitually in the right-ear-down head position was significantly greater than that for the left-affected ear. CONCLUSIONS: A habitual affected-ear-down head position during sleep may contribute to BPPV-canalolithiasis and light cupula onset, but not BPPV-cupulolithiasis onset. However, habitual sleeping in the right-ear-down head position cannot explain the predominance of right-affected ears.

A new variant of posterior canal-benign paroxysmal positional vertigo-canalolithiasis.

OBJECTIVE: The characteristics of typical posterior canal-benign paroxysmal positional vertigo-canalolithiasis (P-BPPV-Can) are well known. We found 10 patients with a new variant of P-BPPV-Can: Reverse (Rev)-P-BPPV-Can. The characteristics and pathophysiology of Rev-P-BPPV-Can are discussed. METHODS: For 4 years and 9 months, 10 patients with Rev-P-BPPV-Can (9 women and 1 man; mean age: 73 years) visited our clinic. Within the same period, 268 patients with unilateral typical P-BPPV-Can were treated. During the Dix-Hallpike and Epley maneuvers, nystagmus was recorded using an infrared charge-coupled device camera mounted on a pair of spectacles. RESULTS: The patients exhibited entirely opposite direction of nystagmus from typical P-BPPV-Can in both the Dix-Hallpike head position and upright sitting position. The patients had typical characteristics of nystagmus due to canalolithiasis, such as latency, duration of <1 min, linear-torsional nystagmus, and fatigability. Rev-P-BPPV-Can appeared after the Epley maneuver for typical P-BPPV-Can; in other patients, Rev-P-BPPV-Can changed to typical P-BPPV-Can. The affected sides of Rev-P-BPPV-Can were decided by those of typical P-BPPV-Can. CONCLUSION: Canalolithiasis in the non-ampullary distal portion of the posterior semicircular canal may be a potential pathophysiology of Rev-P-BPPV-Can. The Epley maneuver has little effect for treating Rev-P-BPPV-Can, but spontaneous transition to typical P-BPPV-Can or spontaneous recovery is expected.

Classification, diagnostic criteria and management of benign paroxysmal positional vertigo.

Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vertigo and the posterior and/or lateral semicircular canals are usually affected. BPPV is characterized by brief attacks of rotatory vertigo associated with positional and/or positioning nystagmus, which are elicited by specific head positions or changes in head position relative to gravity. In patients with the posterior-canal-type of BPPV, torsional nystagmus is induced by the Dix-Hallpike maneuver. In patients with the lateral-canal-type of BPPV, horizontal geotropic or apogeotropic nystagmus is induced by the supine roll test. The pathophysiology of BPPV is canalolithiasis comprising free-floating otoconial debris within the endolymph of a semicircular canal, or cupulolithiasis comprising otoconial debris adherent to the cupula. The observation of positional and/or positioning nystagmus is essential for the diagnosis of BPPV. BPPV is treated with the canalith repositioning procedure (CRP). Through a series of head position changes, the CRP moves otoconial debris from the affected semicircular canal to the utricle. In this review, we provide the classification, diagnostic criteria, and examinations for the diagnosis, and specific and non-specific treatments of BPPV in accordance with the Japanese practical guidelines on BPPV published by the Japan Society for Equilibrium Research.

Benign paroxysmal positional vertigo and head position during sleep.

To determine whether any particular head positions during sleep are associated with BPPV, head position during sleep was monitored for 3 days in 50 BPPV patients after the disappearance of positional nystagmus and in 25 normal control subjects. A gravity sensor was attached to the center of the subject's forehead at home. The positional angle of the head was measured at 5-second intervals during sleep. In BPPV, the posterior semicircular canal was involved in 40 patients and the lateral semicircular canal in 10 patients. Recurrence was found in 22 of 50 BPPV patients. BPPV patients with recurrence were significantly more likely to sleep in the affected-ear-down 45-degree head position than were patients with no history of recurrence (P< 0.02). When the head is in the affected-ear-down 45-degree head position, the non-ampullated half of the posterior semicircular canal and the non-ampullated half of the lateral semicircular canal are nearly in the earth-vertical position, making it easier for detached otoconia to fall into the posterior or lateral semicircular canal and to agglomerate and attain a certain size in the lowest portion of each semicircular canal. Our findings showed that the affected-ear-down 45-degree head position during sleep could be an etiological factor of BPPV, more particularly in patients with recurrent BPPV.

Otolith dysfunction during vertiginous attacks in Ménière's disease.

OBJECTIVE: Vertiginous attacks of Ménière's disease (MD) are characterized by various types of vertigo, namely rotatory vertigo, dizziness and drop attack. When a patient complains of dizziness without spontaneous nystagmus, otolith dysfunction cannot be ruled out. The purpose of this study was to evaluate otolith dysfunction during vertiginous attacks of MD or delayed endolymphatic hydrops. MATERIAL AND METHODS: Vestibular function tests were carried out daily for several days in 11 patients (MD, n = 9; delayed endolymphatic hydrops, n = 2) during vertiginous attacks. Otolith function was evaluated by means of the static torsional position of both eyes [static ocular torsion (OT)] whilst in an upright position. We defined otolith dysfunction as an abnormal change (range) in OT without spontaneous nystagmus or as an abnormal change in OT without a change in spontaneous nystagmus. RESULTS: Four patients had an abnormal change (range) in OT without spontaneous nystagmus or an abnormal change in OT without a change in spontaneous nystagmus during vertiginous attacks of MD. CONCLUSIONS: Otolith dysfunction occurs in patients during vertiginous attacks of MD. In cases of ataxia without spontaneous nystagmus, otolith dysfunction most likely causes atypical attacks of MD.