Despite being the most common cause of peripheral vertigo, (Froehling, et al., 2000) BPPV is still often underdiagnosed or misdiagnosed (von Brevern, et al., 2004). Causes of vertigo that may be confused with BPPV can be divided into otological, neurological, and other entities. In subspecialty settings, BPPV caused 10.1% of vertigo, while neurological causes were rare (Bruintjes, et al., 2007).

The most common diagnoses that require distinction from BPPV are listed in Table 3.1. These conditions require distinction from BPPV because their natural history, treatment, and potential for serious medical sequelae differ significantly.

Otologic disorders

Other otological disorders causing vertigo may be differentiated from BPPV by their clinical characteristics including their temporal pattern and the presence or absence of hearing loss. Whereas BPPV is characterized by acute, discrete episodes of brief positional vertigo without associated hearing loss, other otological causes of vertigo manifest different temporal patterns and may additionally demonstrate associated hearing loss (Kentala, et al., 2003). In distinction to BPPV, Ménière’s disease is characterized by discrete episodic attacks, with each attack exhibiting a characteristic triad of sustained vertigo, fluctuating hearing loss, and tinnitus (Baloh, et al., 1987), (Wladislavosky-Waserman, et al., 1984). Recurrent vestibulopathy is characterized by similar episodic attacks of vertigo, but lacks any auditory symptoms (van Leeuwen et al., 2010).As opposed to BPPV, the duration of vertigo in an episode of Ménière’s disease or recurrent vestibulopathy typically lasts longer (usually on the order of hours) and is typically more disabling owing to both severity and duration. In addition, an associated contemporaneous decline in sensorineural hearing is required for the diagnosis of a Ménière’s attack, whereas acute hearing loss should not occur with an episode of BPPV (Thorp, et al., 2003). Protracted nausea and vomiting are also more common during an attack of Ménière’s disease or recurrent vestibulopathy.

Acute peripheral vestibular dysfunction syndromes, such as vestibular neuritis or labyrinthitis, present with sudden, unanticipated, severe vertigo with a subjective sensation of rotational (room spinning) motion. If the auditory portion of the inner ear is affected, hearing loss and tinnitus may also result (Baloh, et al., 2003). These syndromes are commonly preceded by a viral prodrome. The time course of the vertigo is often the best differentiator between BPPV and vestibular neuritis or labyrinthitis. In vestibular neuritis or labyrinthitis, the vertigo is of gradual onset, developing over several hours, followed by a sustained level of vertigo lasting days to weeks (Kentala, et al., 2003) (Kentala, et al., 1996) (Kentala, et al., 1999). The vertigo is present at rest (not requiring positional change for its onset), but it may be subjectively exacerbated by positional changes. These acute peripheral vestibular syndromes may also be accompanied by severe levels of nausea, vomiting, sweating, and pallor, which are also typically sustained along with the vertigo.

Tabel 3.1

Differentiaaldiagnose BPPD

Superior canal dehiscence syndrome (SCD) is clinically characterized by attacks of vertigo and oscillopsia (the sensation that viewed objects are moving or wavering back and forth) often brought on by loud sounds, Valsalva maneuvers, or pressure changes of the external auditory canals (Minor, et al., 2001). Similar to perilymphatic fistula, it differs from BPPV in that vertigo is induced by pressure changes and not position changes. SCD may also present with an associated conductive hearing loss and is diagnosed through CT of the temporal bones (Rosowski, et al., 2004).

Posttraumatic vertigo can present with a variety of clinical manifestations including vertigo, disequilibrium, tinnitus, and headache (Marzo, et al., 2004). Although BPPV is most often idiopathic, in specific cases, traumatic brain injury is associated with BPPV (Davies, et al., 1995). BPPV has been described as occurring in conjunction with or as a sequelae to other vestibular disorders as well, such as Ménière’s disease and vestibular neuritis (Karlberg, et al., 2000). Therefore, clinicians must consider the possibility of more than one vestibular disorder being present in any patient who does not clearly have the specific symptoms of a single vestibular entity.

Neurological disorders

One of the key issues facing clinicians attempting to diagnose the etiology for vertigo is the differentiation between peripheral causes of vertigo (those causes arising from the ear or vestibular apparatus) and CNS causes of vertigo. Although at times this distinction may be difficult, several clinical features may suggest a central cause of vertigo rather than BPPV (Labuguen, et al., 2006) (Baloh, et al., 1998). Nystagmus findings that more strongly suggest a neurological cause for vertigo, rather than a peripheral cause such as BPPV, include down-beating nystagmus on the Dix-Hallpike maneuver, direction-changing nystagmus occurring without changes in head position (ie, periodic alternating nystagmus), or baseline nystagmus manifesting without provocative maneuvers. Among the central causes of vertigo that should be distinguished from BPPV are migraine-associated vertigo, vertebrobasilar TIA, and intracranial tumors.

Vestibular migraine has been described as a common cause of vertigo in the adult population (Reploeg, et al., 2002) and may account for as many as 14 percent of cases of vertigo (Kentala, et al., 2003). Diagnostic criteria include 1) episodic vestibular symptoms; 2) migraine according to International Headache Society criteria; 3) at least two of the following migraine symptoms during at least two vertiginous episodes: migrainous headache, photophobia, phonophobia, or visual or other aura; and 4) other causes ruled out by appropriate investigations (Headache Classification Subcommittee of the International Headache Society, 2004). Migraine-associated vertigo is heterogeneous in that both central disorders and peripheral disorders have been described, although more often it is believed to be central in nature (Neuhauser, et al., 2001), (von Brevern, et al., 2005). It is distinguishable from BPPV by virtue of the necessary migraine/headache components, which are not associated with classic BPPV.

Several reports have suggested that isolated attacks of vertigo can be the initial and only symptom of vertebrobasilar insufficiency (Fife, et al., 1994), (Grad, et al., 1989) (Gomez, et al., 1996). Isolated transient vertigo may precede a stroke in the vertebrobasilar artery by weeks or months. The attacks of vertigo in vertebrobasilar insufficiency usually last less then 30 minutes and have no associated hearing loss. The type of nystagmus (typically gaze-evoked in central lesions), the severity of postural instability, and the presence of additional neurological signs are the main distinguishing features between vertebrobasilar insufficiency and BPPV (Gomez, et al., 1996) (Hotson, et al., 1998). In addition, the nystagmus arising in vertebrobasilar insufficiency does not fatigue and is not easily suppressed by gaze fixation, helping to separate this diagnosis from BPPV.

Intracranial tumors and other brain stem lesions may rarely present with a history and symptomatology similar to those of BPPV (Dunniway, et al., 1998). In these cases, associated symptoms such as tinnitus, aural fullness, new-onset hearing loss, and/or other neurological symptoms should help differentiate these diagnoses from BPPV. Atypical nystagmus during Dix- Hallpike testing (eg, sustained down-beating nystagmus) argues against BPPV and suggests a more serious cause. Finally, failure to respond to conservative management such as the PRM or vestibular rehabilitation should raise concern that the underlying diagnosis may not be BPPV (Dunniway, et al., 1998).

Other disorders

Several other non-otological and non-neurological disorders may present similarly to BPPV. Patients with panic disorder, anxiety disorder, or agoraphobia may complain of symptoms of lightheadedness and dizziness. Although these symptoms are usually attributed to hyperventilation, other studies have shown high prevalences of vestibular dysfunction in these patients (Jacob, et al., 1996) (Furman, et al., 2006). These conditions may also mimic BPPV. Several medications, such as Mysoline, carbamazepine, phenytoin, antihypertensive medications, and cardiovascular medications, may produce side effects of dizziness and/or vertigo and should be considered in the differential diagnosis.

Postural hypotension also may produce episodic dizziness or vertigo. The dizziness or vertigo in postural hypotension, however, is provoked by moving from the supine to the upright position in distinction to the provocative positional changes of BPPV.

Although the differential diagnosis of BPPV is vast, most of these other disorders can be further distinguished from BPPV on the basis of responses to the Dix-Hallpike maneuver and the supine roll test. Clinicians should still remain alert for concurrent diagnoses accompanying BPPV, especially in patients with a mixed clinical presentation.