Dizziness and Vertigo _________________________________________________________________________
Episodic positional symptoms are common to all causes of t-EVS, differentiated by targeted history and exams. BPPV is identified by maneuvers that reproduce dizziness combined with an observed pattern of nystagmus. Orthostatic hypo- tension is diagnosed by observing a significant fall in blood pressure upon sitting and standing. Dangerous t-EVS mimics are identified by careful attention to the corresponding signs and symptoms that differentiate these benign conditions from potentially more serious disorders [36]. Positional triggers, such as rolling over in bed or reclining, are common in BPPV but should not occur in orthostatic hypotension [8]. Unlike head position changes in BPPV, the vertigo and oscillopsia attacks in superior canal dehiscence syndrome are triggered by pressure-related changes of the external auditory canals (e.g., loud sounds, Valsalva maneuver) [21]. The nystagmus characteristics of BPPV and central paroxysmal positional vertigo are distinct. Atypical nystagmus (downbeat or horizontal) is suggestive of central paroxysmal positional vertigo, and pure vertical (up- or downbeating) nystagmus should be considered of central origin until proven otherwise [8; 22]. Central mimics of BPPV less often involve strokes and more often involve posterior fossa neoplasm, hemorrhage, or demyelination recognized by association with other abnormali- ties [105; 114]. Central paroxysmal positional vertigo also includes common, benign causes, such as alcohol or sedative intoxication. Such patients are more apt to complain of continuous, persistent dizziness exacerbated (not triggered) by position change, often readily diagnosed based on context and other signs of intoxication [8; 36]. In general, BPPV is not associated with vertiginous episodes provoked simply by head and body movements in general, but by sudden positional changes relative to gravity. Moreover, unprovoked (spontaneous) episodes while immobile or the constant sensation of unsteadiness also suggest a diagnosis other than BPPV [21]. BPPV Within any (semicircular) canal, BPPV is caused by abnormal stimulation of the cupula by otoconia that are free-floating (canalithiasis) or have attached to the cupula (cupulolithiasis) [115]. With head motion in the plane of the affected canal, cupula stimulation produces error signaling that triggers eye movement patterns (nystagmus) specific to the afflicted canal [21]. BPPV should be differentiated from other causes of imbal- ance, dizziness, and vertigo. Patients should also be assessed for factors that modify management, including impaired mobility or balance, CNS disorders, lack of home support, and increased risk for falling. In patients meeting BPPV diagnostic criteria, it is not necessary to obtain radiography or order vestibular testing in the absence of signs/symptoms inconsistent with BPPV [21].
Provoked nystagmus is used clinically to diagnose BPPV by positioning the head to spatially align the plane of the affected canal with gravity. Gravity challenge moves otolithic debris in the canal, inducing excitation and resultant nystagmus. This identifies the afflicted canal, determines the canal-specific therapy, and distinguishes BPPV from central causes of vertigo [15; 23; 39; 115]. Head movement tests are canal-specific. Because posterior canal BPPV is the most common type, the Dix-Hallpike maneu- ver is used first. For this maneuver, the patient is moved quickly from sitting upright with head turned 45° in the direction of the involved ear, to supine position with head still turned 45° and neck extended 20° off the end of the exam table with the affected ear down [20; 21]. Before initiating physical maneuvers that involve head rotation, the neck should be evaluated to determine if the procedure should be modified or avoided. The Dix-Hallpike maneuver should be performed with caution or avoided in patients with a current or past neck or back injury, surgery, or painful condition [23; 115]. A diagnosis of BPPV affecting the posterior canal (pc-BPPV) is confirmed by vertigo with torsional (rotatory), upbeating (toward the forehead) nystagmus, with onset 5 to 20 seconds after completion of the Dix-Hallpike maneuver (latency) and duration less than 60 seconds. Provoked nystagmus that lasts longer than 60 seconds with no or brief latency identifies cupulolithiasis [20; 21]. If the initial maneuver is negative, it should be repeated with the opposite ear down. Before performing the Dix-Hallpike maneuver, the patient should be advised that sudden, intense vertigo or nausea is possible but should subside within 60 seconds. The sequen- tial steps and expected results of the maneuver should be explained, orienting the patient to the supine position and location of the head and providing reassurance that the head and body will be supported and guided safely and securely through the maneuver [20; 21]. There are two types of BPPV affecting the lateral canal (lc- BPPV)—geotropic or apogeotropic—with two types of direction- changing positional nystagmus [21; 39]. When BPPV is sus- pected and the Dix-Hallpike maneuver is negative, the supine roll test should be used to assess for lc-BPPV. The supine roll test provokes a linear, horizontal nystagmus in patients with lc-BPPV. In cases of lc-BPPV caused by canalithiasis, the nystag- mus beats to the ear under the head (i.e., higher intensity on the affected side). If the condition results from cupulolithiasis, the nystagmus beats to the upward ear (i.e., higher intensity on the non-affected side).
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