BPPV
The posterior semicircular canal is the most common site of canalithiasis. Less common are diseases of the anterior (superior) and horizontal semicircular canals; these also have slightly different clinical manifestations.
- Posterior canal BPPV is idiopathic in 35 percent of cases. Prior head trauma, which can be relatively minor, or whiplash injuries are present in approximately 15 percent. In the remainder, BPPV is a residual effect of a variety of vestibular pathologies, most commonly Meniere disease (30 percent), but also vestibular neuronitis, ear surgery, herpes zoster oticus, and inner ear ischemia/sudden sensorineural hearing loss.
- Most cases of horizontal canal BPPV (HC-BPPV) are idiopathic or due to minor head trauma. This problem is occasionally a complication of the maneuvers used to treat posterior canal BPPV.
CLINICAL MANIFESTATIONS
Approximately half of patients complain of imbalance between attacks, even after successful treatment. Episodes recur periodically for weeks to months without therapy. In one study, the median duration of BPPV recurrences was two weeks; a subset of these patients was treated
Response to provoking maneuvers — Observing nystagmus during a provoking maneuver solidifies the diagnosis of BPPV in patients with a typical history and identifies the side and the specific canal affected. These features help direct appropriate treatment.
Posterior canal BPPV
Diagnostic criteria employing the Dix-Hallpike maneuver have been proposed for PC-BPPV:
- Nystagmus and vertigo usually appear with a latency of a few seconds and last less than 30 seconds
- Nystagmus has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes beating toward the ground
- After nystagmus stops and the patient sits up, the nystagmus will recur but in the opposite direction
- The patient should then have the maneuver repeated to the same side; with each repetition, the intensity and duration of nystagmus will diminish
Sometimes patients have typical symptoms of posterior canal BPPV but no nystagmus visualized during the Dix-Hallpike maneuver. If symptoms are otherwise typical of posterior canal BPPV, the patient may have so-called "subjective" BPPV and still respond to treatment.
Horizontal canal BPPV
Horizontal canal BPPV (HC-BPPV) is provoked by turning the head while lying down, sometimes by head turns while upright, but not by getting in or out of bed or by extending the neck
The nystagmus is elicited by a lateral head turn in the supine position (sometimes called the head-roll or log-roll test). This may induce geotropic or apogeotropic nystagmus:
- In geotropic HC-BPPV, horizontal nystagmus beating toward the floor begins after one to eight seconds of turning the affected ear down; it lasts approximately one minute, and after a few seconds of inactivity may be followed by a reversal of the nystagmus, which also lasts up to one minute. A milder nystagmus is seen with the normal ear down, again beating toward the ground. This distinction between the normal versus the affected ear is important for treatment.
- In apogeotropic HC-BPPV, the induced nystagmus beats toward the uppermost ear
Another method of diagnosing HC-BPPV is the "bow and lean" test. The seated patient first bends head forward, aligning the horizontal canal with the gravity vector, and then leans his or her head backward, flipping the horizontal canal 180°. Right horizontal canalithiasis will cause a right beating nystagmus during the bow and a left beating nystagmus during the lean. This test may be better than the head-roll test at lateralizing the problem
Anterior canal BPPV
Anterior canal BPPV (superior canal BPPV) has similar provoking factors as classic posterior canal BPPV, but the nystagmus is downbeat and torsional, with the top of the eye torting away from the lower ear ( apogeotropic). The latency, duration, and fatigability are similar. It is rare, accounting for only approximately 1 to 2 percent of patients with BPPV, likely due to its anatomic position that makes it difficult for debris to enter.
Pure torsional BPPV — Approximately one-half of patients with a history of BPPV have a pure torsional nystagmus by the Dix-Hallpike maneuver. Time to remission with repeated repositioning maneuvers is prolonged for pure torsional BPPV compared with posterior BPPV
Subjective BPPV — Some patients report symptoms that suggest BPPV but do not have elicitable nystagmus, and have been suggested to have so-called "subjective" BPPV.
DIFFERENTIAL DIAGNOSIS
Chronic unilateral vestibular hypofunction — Chronic unilateral vestibular hypofunction from any cause is associated with transient dizziness after rapid head turns, but these are fleeting, lasting only one to two seconds. By contrast, vertigo from BPPV does not require rapidity of the head turn, and it typically lasts 30 to 60 seconds. Furthermore, vertigo in posterior canal BPPV is provoked by looking up or down, whereas these maneuvers are not necessarily problematic for patients with chronic unilateral vestibular hypofunction.
Vestibular paroxysmia — Vestibular paroxysmia refers to a syndrome of brief attacks of vertigo that last one to several seconds and recur several times a day. In some patients, attacks are unprovoked; in others, they are precipitated by head turn or other action. Magnetic resonance imaging (MRI) may reveal evidence of neurovascular compression.
Vestibular migraine — Migraine is a frequent cause of episodic vertigo, and vestibular migraine, also known as migrainous vertigo, can present as an isolated positional vertigo mimicking BPPV. A migraine headache with or following the vertiginous spell makes for an easy diagnosis, but this sequence does not always occur.
Central positional vertigo — Central positional vertigo and nystagmus may occur with lesions of the cerebellum, particularly the cerebellar vermis. The classic sign of central positional vertigo is downbeat nystagmus. In contrast with BPPV, the nystagmus is static and persists as long as the provocative position is maintained. In some patients, the downbeat nystagmus is present or increased only when lying down, more so when prone than supine
TREATMENT
- The Epley maneuver and modified Epley maneuver
- The Semont maneuver and modified Semont maneuver
The treatment maneuvers encourage the debris to migrate toward the common crus of the anterior and posterior canals and exit into the utricular cavity. These maneuvers may be effective when the history is highly suggestive of BPPV, even if nystagmus is not seen on examination.
After successful repositioning treatment, up to 37 percent of subjects can still have some mild nonpositional vague imbalance and dizziness for two to three weeks; this is more common in older patients and in those whose BPPV had been present for over a week before treatment. In some patients, debris may re-enter another canal, most commonly the horizontal, causing "transitional BPPV". This may resolve on its own or require treatment with the horizontal canal maneuvers below.¸
Maneuvers for other BPPV variants
Horizontal canal BPPV – One better-studied maneuver for the horizontal canal variant involves stepwise rotations of the non-tilted head in the supine position moving 360° from the affected to the unaffected ear . This is performed two to four times or until nystagmus disappears. This method has been dubbed the "barbecue rotation" maneuver, and is also known as the Lempert roll maneuver. The efficacy of this maneuver may depend upon correct determination of the side of the problem, which may be improved by the "bow and lean" test
Dizziness and Imbalance in the Elderly
The underlying cause of dizziness in the elderly is complex and multi-factorial. Postural stability is maintained by the integration of somatosensory, visual and vestibular inputs to the central nervous system, followed by outputs to the musculo-skeletal system. Dizziness and imbalance can be caused by changes in any of the factors associated the balance system, be they of sensory, visual, vestibular, neurologic, and muscular origin. Function of all these components deteriorates with age.
Tinetti et al. (2000) proposed that dizziness in the elderly should be considered as a multifactorial geriatric syndrome involving many different symptoms and originating from many different causes, including cardiovascular, neurologic, sensory, psychological and medication-related problems.
Peripheral vestibular disorders in the elderly
In most studies regarding dizziness in the elderly, peripheral vestibular dysfunction is the first or the second most frequent cause of dizziness. Benign paroxysmal positional vertigo (BPPV) is the most frequent form of peripheral vestibular dysfunction, followed by Meniere’s disease and vestibular neuritis.
BPPV is the most common cause of vertigo and dizziness from childhood through to old age, peaking at about 60 years.
Johkura et al. (2008) reported that about 50% of elderly patients with chronic dizziness who visited an emergency unit showed extremely weak, horizontal, direction changing apogeotropic nystagmus, which is characteristic of horizontal canal BPPV, and that some of symptoms in these patients was improved by daily positional exercises for BPPV.
The cause of BPPV is thought to be small particles trapped in the semicircular canals . These particles most likely consist of otoconia dislodged from the utricula maculae. Several studies have demonstrated that a high proportion of otoconia of the utricular macula degenerates in the elderly, and many have fractures.
Functional deterioration of vestibular systems in the elderly
The stability of posture and gaze during standing and walking is maintained by the rapid processing of vestibular, visual and somatosensory inputs in the central nervous systems, followed by outputs to the musculoskeletal and visual systems. Every factor in this system deteriorates during aging.
Age-related deterioration of peripheral vestibular function has been documented by measuring the vestibulo-ocular reflex. Function of the semicircular canals as well as the otolith organs decline with age
Management of dizziness in the elderly
Vestibular rehabilitation was first introduced by Cawthorne and Cooksey (1946) to rehabilitate patients with vestibular disorders. The rehabilitation includes 1) VOR adaptation exercises to assist the central nervous system to adapt to a change or loss in inputs to the vestibular system, 2) habituation exercises to reduce pathologic responses to a provoking stimulus, and 3) substitution exercises to promote the use of the remaining sensory system.
Currently, these exercises are found to be effective in treating people with dizziness caused by vestibular dysfunction, anxiety, head injury, cerebellar dysfunction, or Parkinson’s disease
Common characteristics of BPPV include rotational vertigo (86%), imbalance (49%), fear of falling (36%), nausea (33%), oscillopsia (objects appearing to oscillate in the visual field with head movement; 31%), vomiting (14%), and falls (1%). The risk of falls is also greater in older adults. BPPV has adverse psychosocial consequences, including poorer health-related quality of life, interruption of daily activities, and avoidance of leaving the house, and individuals with BPPV are more likely to have depression.
Depending on the location of the displaced fragments, BPPV can arise from canalolithiasis (particles in one or more semicircular canals) or cupulolithiasis (particles adherent to the cupula of one or more semicircular canals). The mere presence of fragments within the semicircular canal is not always sufficient to induce a change in the vestibular nerve activity; rather it is believed that a critical mass is needed to evoke clinical symptoms.
ETIOLOGICAL FACTORS
BPPV can arise in the setting of trauma (6.7% of all patients), ipsilateral Meniere’s disease (6.5%), ipsilateral vestibular neuritis (5.6%), severe systemic disease (4.6%), and recent otological surgery (1%). Carcinomas treated using radiotherapy or chemotherapy, recent myocardial infarction, leukemia treated with chemotherapy, sarcoidosis, and active ulcerative colitis have also been associated with BPPV, but for 61.9% of BPPV cases, an etiology cannot be identified (idiopathic). Aging appears to be a primary risk factor for idiopathic BPPV.
Prolonged bed rest (e.g., >24–48 hours) in older adults recuperating from illnesses or surgery can precipitate BPPV. It has been suggested that prolonged lying may facilitate the deposition of otoconia on the cupula or contribute to their loosening from the utricle. The above mechanism might also explain why the laterality of BPPV often corresponds to the preferred side of lying during sleep.
Associations have been reported between BPPV and diabetes mellitus. Another systemic link was described recently wherein lipid profiles and serum uric acid levels were found to be higher in individuals with BPPV than in controls.
The diagnosis of BPPV is based on the history and use of provocative maneuvers. Subjectively, the primary complaint at presentation is dizziness triggered by movement, such as looking up, turning the head, or rolling over in bed.
- The intense sensation of vertigo triggered typically is short, although people feel off balance even when avoiding sudden head movements.
- Repeated head movements in close temporal proximity trigger successively weaker symptoms, suggesting fatigability.
- Reflecting the natural course of the disease, BPPV episodes are typically self-limited.
- Episodes of BPPV are mostly short, with a median duration of 2 weeks.
- BPPV is a recurrent disease, with a recurrence risk of approximately 15% per year.
Special considerations are warranted in older adults, because older adults with BPPV usually report dizziness or imbalance but do not always describe a rotatory crisis. It is recommended that the Dix–Hallpike and supine roll tests be performed in older adults with dizziness, even if they do not complain of a spinning sensation with positional changes. There are also instances in older adult in which positional testing is not feasible or, despite compelling history, yields negative results. An example of the former instance involves frail older adults who have difficulty undergoing positional testing.
Although, BPPV is one of the most common causes of vertigo, other disorders can trigger BPPV or present with BPPV-like symptoms. There appears to be a variant condition in which recurrent vertigo associated with fast head movements and history consistent with BPPV is associated with absence of nystagmus on the Dix-Hallpike maneuver. This variant is known as “subjective BPPV” or “sitting-up or Type 2 BPPV.” It is characterized by vertigo or nausea in the absence of nystagmus during the Dix-Hallpike or roll test. It has been suggested that individuals with this type of vertigo could have small amounts of particles stuck to the cupula or floating in the affected semicircular canal (including the short arm of a canal) that may not be enough to cause nystagmus. An alternate explanation was put forward when it was noted that nystagmus may be present but may be too subtle to detect without additional instrumentation. Another explanation has been offered based on a change in calcium metabolism and the consequent nonabsorption of free otoliths, which would increase their quantity in the semicircular canals and enable the triggering of vertigo with head movement. It has been suggested that the affected labyrinth can be identified based on which side induced nausea or vertigo on positioning testing.
When history is suggestive of positional vertigo but positional testing is negative for BPPV, other etiologies should also be considered. For example, medications are a common cause of movement-associated dizziness, including anticonvulsants, antidepressants, anxiolytics, sedatives and hypnotics, strong analgesics, muscle relaxants, and antiarrhythmias. Cervicogenic vertigo is illusory motion deriving from a disturbance of the neck that may have a presentation similar to that of BPPV. This type of vertigo can arise from impingement of the vertebral arteries, whiplash, and degenerative cervical disorders. Although there are no specific, sensitive tests for cervicogenic vertigo, an important element of presenting history and physical examination is the sustained nature of vertigo or nystagmus with neck rotation or body rotation below the neck.
THERAPEUTIC INTERVENTIONS
Mechanical Repositioning
In older adults with BPPV, clinical and functional aspects of body balance, including postural instability, improved after treatment with the modified Epley maneuver, although the effectiveness of therapeutic repositioning maneuvers (see below) is less in older adults than in those younger than 70.
Residual symptoms such as lightheadedness or a floating sensation after a successful repositioning maneuver can occur in up to 57% of individuals.