Strategies to Distinguish Benign Paroxysmal Positional Vertigo from Rotational Vertebrobasilar Ischemia
Article Outline
Vertigo provoked by head rotation is a classic symptom of rotational vertebrobasilar ischemia (RVBI). Inner ear disease can cause positional vertigo and mimic RVBI. We review the case of a patient with vertigo consistently triggered by leftward head rotation when supine. Computed tomography angiogram and dynamic arteriogram failed to show compression of the vertebral arteries with head rotation. Further evaluation revealed benign paroxysmal positional vertigo (BPPV) as the underlying etiology. Treatment of her BPPV led to complete resolution of her symptoms. A succinct overview of this common otologic disorder is provided, and strategies to help distinguish it from RVBI are discussed.
Case Report
A 48-year-old woman was referred to a tertiary care vascular surgery practice for evaluation of vertigo consistently triggered by leftward head rotation. She had a history of a severe vestibular crisis 4 months earlier that manifested with intense rotary vertigo lasting 48 hours, followed by weeks of severe motion-provoked disequilibrium, which gradually resolved. However, she started having spells of positional vertigo in bed triggered with head rotation to either side or with rolling over. Symptoms were most intense with leftward head rotation or rolling onto her left side. She began sleeping on six pillows in bed to avoid the vertigo. She denied any hearing loss or tinnitus.
Examination in clinic revealed a healthy appearing woman with normal, symmetric blood pressure in both the right and left upper extremities. Upper extremity and neck pulses were equal and synchronous. Sensory and motor examination of the upper and lower extremities was normal. Cranial nerve testing was unremarkable. With the patient supine and the head rotated to either the left or right, she developed severe vertigo and nystagmus after a brief 2- to 3-second delay. Symptoms were worse with leftward head rotation.
A computed tomography (CT) angiogram was ordered to evaluate for rotational vertebrobasilar ischemia (RVBI). In the neutral position, the vertebral arteries were patent and of intermediate caliber bilaterally. Imaging with the patient's head turned 90 degrees to the left showed no significant encroachment on the distal cervical carotid or vertebral arteries. Dynamic arteriogram was performed next and confirmed the findings seen on CT.
The patient was subsequently referred to otolaryngology. Exam showed horizontal nystagmus in the supine position that would change direction as she was rolled from the right to left side. Caloric testing revealed a 41% right peripheral vestibular weakness. She was diagnosed with active right horizontal semicircular canal (HSC) benign paroxysmal positional vertigo (BPPV) following right vestibular neuritis. She was treated with a particle repositioning maneuver and home exercises and reported rapid resolution of her positional vertigo. At her last appointment, leftward head rotation when supine failed to elicit vertigo or significant nystagmus.
Discussion
Vertebrobasilar ischemia (VBI) may be due to fixed stenosis, microembolic events, dissection, or extrinsic compression. VBI secondary to extrinsic compression is called RVBI and occurs in patients whose dominant or only patent vertebral artery is transiently occluded with head rotation. The vertebral artery can be compressed at any point along its extracranial course, but the most common site is at the third segment and typically is secondary to impingement from cervical osteophytes.
Patients with untreated RVBI are at risk for impending posterior circulation infarction.1 The mechanism for stroke in patients with RVBI appears to be due to microembolization of thrombus formed in the setting of intimal injury caused by repeated compression and stretching of the artery.2, 3 Surgical decompression of the involved vertebral artery or carotid-to-distal vertebral artery bypass are effective treatments and reduce the risk of stroke.4, 5
Correct identification of patients with RVBI is challenging. It is important to recognize that this is a fairly rare disorder; one study at a tertiary center found that over a 10-year period, 100 patients presented with symptoms strongly suggestive of RVBI, but only 16 were ultimately found to have the condition.5 The workup for RVBI routinely includes noninvasive screening tests such as transcranial Doppler or CT angiogram, followed by dynamic arteriogram in patients with positive or equivocal findings to determine the precise site and extent of compression.
Patients who are initially suspected to have RVBI but who lack the confirmatory findings on imaging studies are usually found later to have inner ear disease as the underlying cause of their positional vertigo.6 The most common cause of vertigo originating from the inner ear is BPPV, and it can closely mimic RVBI. Patients with BPPV report discrete episodes of vertigo triggered by changes in head position. Unlike RVBI, it is very common; the overall prevalence in the population is 10-64 per 100,000, and it is estimated that the lifetime prevalence reaches 2.4%.7 BPPV is caused by loose calcium carbonate crystals in the inner ear—called otoconia—which detach from their normal location in the utricle and fall into any one of the three semicircular canals (Fig. 1). Changes in head position, often initiated by supine head rotation, force the displaced otoconia to migrate under the influence of gravity within the lumen of the semicircular canals. This in turn leads to movement of inner ear fluid, which triggers the sensation of vertigo. Different variants of BPPV exist, based on which of the three semicircular canals is affected. The most common form is posterior semicircular canal BPPV (PSC BPPV), and it accounts for 85-90% of cases. HSC BPPV is seen in 5-15% of patients. Superior canal BPPV is exceedingly rare.
Fig. 1
Inner ear anatomy. BPPV is a disorder of the inner ear where loose otoconia that normally reside in the utricle detach and fall into the semicircular canals. Most cases are unilateral and affect a single semicircular canal. The most common canal affected is the posterior semicircular canal, followed by the horizontal semicircular canal. Superior (anterior) canal BPPV is rare. (Reprinted with permission of the Barrow Neurological Institute.)
A careful history and physical exam can differentiate BPPV from RVBI (Table I). While the majority of cases of BPPV are idiopathic, known risk factors include recent head trauma or a prior history of vestibular neuritis. Patients with BPPV suffer monosymptomatic attacks of vertigo. Complaints of associated tinnitus, acute hearing loss, syncope, dysarthria, or other symptoms suggestive of brainstem ischemia are not seen with this disorder. Unlike patients with RVBI, lateral head turns in the sitting or standing position usually do not pose a problem for patients with BPPV. Attacks are precipitated by changes in head position relative to gravity and thus are most commonly seen with reclining backward, rolling over when supine, neck extension, or bending over. Attacks of vertigo from BPPV do not always require head rotation; en bloc rotation of the body with the head such as when rolling over in bed is usually sufficient. When an attack occurs, there typically is a short delay from the moment the patient assumes the provocative position to the start of symptoms. This period of latency lasts seconds and is followed by vertigo that has a crescendo-decrescendo pattern of intensity and seldom lasts more than 1 minute. Rarely, patients can exhibit a form of BPPV called cupulolithiasis that manifests with immediate onset of vertigo and nystagmus which persist as long as the patient remains in the provocative position.
Table I. Comparison of symptoms and signs for BPPV and RVBI
| RVBI | BPPV | |
|---|---|---|
| Symptoms | Vertigo, syncope or near-syncope, tinnitus, blurred vision | Vertigo |
| Symptom triggers | Head rotation | Head or en bloc head and body rotation |
| Nystagmus patterns | Initially downbeating, followed by a mixed torsional horizontal trajectory that can reverse direction | Consistent patterns seen based on affected semicircular canal. PSC BPPV exhibits torsional nystagmus on Dix-Hallpike testing. HSC BPPV exhibits bidirectional horizontal nystagmus on supine roll test. |
There are two clinical tests that can be easily performed in the office setting to make the diagnosis of BPPV. These tests require the clinician to identify characteristic patterns of nystagmus when the patient is placed into specific positions. By convention, nystagmus is named by the direction of its fast component. The Dix-Hallpike test is the gold standard for diagnosing PSC BPPV and is shown in Figure 2.8 A positive Dix-Hallpike test manifests with nystagmus that is predominantly torsional where the eyes appear to rotate toward the undermost ear.
Fig. 2
The Dix-Hallpike test for diagnosis of posterior semicircular canal BPPV. To perform a right Dix-Hallpike test, begin with the patient seated on the examination table. Grasp the patient's head and rotate it 45 degrees to the right side (A). Then briskly bring the patient to a head-hanging position (B). The patient's eyes should be observed closely for the development of torsional nystagmus. A left Dix-Hallpike begins with the patient's head rotated 45 degrees to the left.
The supine roll test is shown in Figure 3 and is used to diagnose HSC BPPV, which was seen in this patient. With HSC BPPV, patients develop nystagmus that is horizontal but changes direction depending on which side they lie on. Two subtypes of HSC BPPV exist. In geotropic HSC BPPV, the nystagmus is directed toward the ground (geo = “earth”), so that in the right lateral position the patient has right-beating nystagmus, and in the left lateral position the patient develops left-beating nystagmus. In ageotropic HSC BPPV, the nystagmus beats away from the ground.
Fig. 3
Supine roll test for horizontal semicircular canal BPPV. In the supine roll test, the patient is brought from a sitting position to a supine position with the head center and the neck flexed forward 20-30 degrees (A). The patient's head and body are then rolled en bloc into the right lateral position, and then into the left lateral position (B, C). Each lateral position is maintained for at least 10 seconds, and the eyes are observed for development of horizontal nystagmus.
There may be a characteristic pattern of nystagmus associated with RVBI. Three papers looked at a total of six patients with RVBI and found that during head rotation contralateral to the dominant vertebral artery, these patients exhibited an unusual pattern of nystagmus that was initially downbeating, followed by a mixed torsional horizontal trajectory that would sometimes reverse direction.9, 10, 11 It is too early to determine if this is a reliable finding in patients with RVBI, but it may prove to be an important clinical sign for this rare disorder.
Treatment of BPPV is directed at returning the displaced otoconia back into their proper location in the inner ear. Various effective particle repositioning maneuvers have been developed and can be performed in the office setting by a physician, audiologist, or physical therapist familiar with BPPV. Motivated patients can even be taught to perform these maneuvers at home by themselves.12 A recent article by Fife et al.13 describes in detail the different repositioning maneuvers used to treat each variant of BPPV. Surgery for BPPV is reserved as a last resort and has only been extensively reported for PSC BPPV.
BPPV is a common cause of positional vertigo and can closely mimic RVBI. A careful history and exam focused on identifying characteristic patterns of nystagmus can help differentiate these two disorders and eliminate the need for costly testing in most cases. Depending on the variant of BPPV, office-based repositioning maneuvers are curative in 50–98% of cases, making this disorder one of the most treatable causes of vertigo.7, 13, 14, 15
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PII: S0890-5096(09)00341-0
doi:10.1016/j.avsg.2009.09.018
© 2010 Annals of Vascular Surgery Inc. Published by Elsevier Inc All rights reserved.
