Neuro-Ophthalmology & Neuro-Otology
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Positional vertigo …
- Updated 01.11.2024
- Released 07.12.2001
- Expires For CME 01.11.2027
Positional vertigo
Introduction
Overview
Positional vertigo is triggered by and occurs after a change of head position in space relative to gravity. The most common cause is benign paroxysmal positional vertigo, which can be cured highly effectively with positioning maneuvers. The differentiation from central positional vertigo is discussed by the authors. This article includes a rare differential diagnosis to positional vertigo: light cupula. Patients with this condition present with persistent geotropic positional nystagmus in both lateral head positions. Alcohol consumption and vestibulocerebellar lesions need to be ruled out. This type of nystagmus can be best explained by changes of the density of the cupula that render this organ sensitive to head changes with respect to gravity.
Key points
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• Positional vertigo is triggered by and occurs after a change of head position in space relative to gravity. | |
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• The most common cause of positional vertigo is due to canalolithiasis of the labyrinth. | |
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• Central positional vertigo should be suspected when features of nystagmus differ from those of benign paroxysmal positional vertigo or when brainstem and cerebellar signs are present. |
Historical note and terminology
By definition, positional vertigo is triggered by and occurs after a change of head position in space relative to gravity (07). Some authors distinguish between positional and positioning vertigo. The former term has been used for vertigo that continues as long as the head is kept in the provocative position, whereas the latter term is used for vertigo that subsides when the head remains in the critical position (08); however, this nomenclature has not been widely accepted, as it does not reliably allow to separate peripheral from central vestibular disorders.
Clinical manifestations
Presentation and course
The most common cause of positional vertigo is benign paroxysmal positional vertigo, accounting for about 20% of referrals to specialized dizziness clinics. Patients typically experience attacks when turning over in bed, lying down from the sitting position, sitting up from supine, extending the neck to look up, or bending over. A single attack of benign paroxysmal positional vertigo of the posterior canal usually lasts no longer than 30 seconds. Typically, benign paroxysmal positional vertigo manifests itself with symptomatic episodes lasting from a few days to several months, interspersed by asymptomatic periods of several months to years. It may affect any one of the three semicircular canals, with the posterior canal being most common (around 80%).
Benign paroxysmal positional vertigo of the posterior canal is confirmed by the provocation of vertigo and observation of typical nystagmus with the Dix-Hallpike maneuver. The diagnosis can be made reliably when the positional nystagmus fulfills the following criteria (03):
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(1) Torsional-vertical nystagmus. The most prominent direction of nystagmus is a torsional component, rotating with the upper pole of the eyes toward the undermost and affected ear. In addition, a smaller vertical, upbeating component of nystagmus exists that is most prominent in the uppermost eye. | |
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(2) Latency. Typically, nystagmus and vertigo start a few seconds after the precipitating head position is reached. Nystagmus intensity increases rapidly and then decays (crescendo-decrescendo). | |
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(3) Duration. Nystagmus usually lasts 10 to 20 seconds and only exceeds 60 seconds in exceptionally rare cases. | |
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(4) Reversal. A few seconds after the patient has returned to the sitting position, a transient nystagmus of lesser intensity beating in the opposite direction can be observed. | |
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(5) Fatigability. Vertigo and nystagmus decrease in most cases with repeated positioning. |
In benign paroxysmal positional vertigo, symptoms occur typically in bouts lasting several weeks, with spontaneous remittance and reoccurrence after weeks to years; therefore, the diagnosis of benign paroxysmal positional vertigo is highly likely in a patient with repeated bouts of positional vertigo over several years with no neurologic abnormalities on examination.
Central positional vertigo should generally be suspected either when features of nystagmus differ from those of benign paroxysmal positional vertigo or when brainstem and cerebellar signs are present. Single characteristics of benign paroxysmal positional vertigo, such as latency, duration, the time course of nystagmus, and fatigability with repeated positioning, can also occur in central positional vertigo syndromes (13); however, it is unlikely that a central lesion mimics the entire nystagmus pattern of benign paroxysmal positional vertigo of the posterior canal. Of note, central lesions can simulate the nystagmus pattern of other variants of benign paroxysmal positional vertigo, in particular, cupulolithiasis of the horizontal canal (18). The most common types of central positional nystagmus are downbeating nystagmus in the head-hanging position and apogeotropic horizontal nystagmus in the lateral supine position (06; 16; 15; 51). Usually, the direction of central positional nystagmus is aligned with the plane of the head motion during the positioning, ie, vertical nystagmus in the head-hanging position and horizontal nystagmus in the lateral supine position (51). Central positional nystagmus may present with direction-changing apogeotropic nystagmus in the supine roll test, mimicking cupulolithiasis of the horizontal canal. However, in this type of central positional nystagmus, the intensity of nystagmus is at its peak initially and decreases exponentially over time (16), whereas it gradually builds up over 10 to 20 seconds and then decreases slowly in cupulolithiasis of the horizontal canal. In addition, patients with apogeotropic positional nystagmus usually exhibit horizontal nystagmus in the upright and in the supine position that may help to differentiate central positional vertigo from benign paroxysmal vertigo: in the latter, the intensity of this nystagmus increases from the upright to the supine position whereas in the former this is usually not the case (15a). Central positional nystagmus often persists as long as the precipitating head position is maintained; it usually does not fatigue with repetitive positioning. It is often of low frequency compared to benign paroxysmal positional nystagmus. Typically, patients with central positional nystagmus present with additional neurologic findings that cannot be explained by benign paroxysmal positional vertigo, such as truncal ataxia, perverted head-shaking nystagmus, gaze-evoked nystagmus, and impaired smooth pursuit (06; 16; 15a). A central lesion must always be assumed when positional nystagmus occurs without concomitant vertigo (05) or when vomiting is induced by head positioning without nystagmus (23). Purely vertical or torsional nystagmus, verified by examination under Frenzel glasses, should always be considered of central origin; however, positional vertigo and transient positional predominantly downbeating nystagmus during the Dix-Hallpike maneuver or in the straight head hanging position have also been attributed to canalolithiasis of the anterior semicircular canal in some patients (05). These patients had normal imaging studies, and further neurologic examination was unremarkable, except for signs of posterior canal canalolithiasis in some of them. In contrast, patients with central positional downbeating nystagmus rarely complain about positional vertigo.
Neurovascular compression of the eighth cranial nerve is probably a rare cause of positional vertigo. The syndrome was initially described by Jannetta, who coined the term "disabling positional vertigo" and reported good response to surgical decompression of the nerve (40). However, many case series have been criticized for their lack of reliable diagnostic criteria (83; 75), the insufficient exclusion of other disorders causing vertigo, and the frequency of asymptomatic neurovascular contacts (12; 09). Furthermore, the identification of neurovascular contacts by MRI may be misleading because there appears to be no consistent relationship between neurovascular cross-compression and the laterality of cochlear or vestibular abnormalities (22; 36); therefore, even the surgical finding of a neurovascular contact does not confirm the diagnosis; some authors doubt that symptomatic neurovascular compression of the eighth cranial nerve even exists (31). On the other hand, the existence of the syndrome is supported by the concurrence of vestibulocochlear symptoms in patients with established neurovascular compression syndromes (ie, hemifacial spasm) (85). Neurovascular compression of the neighboring seventh and eighth cranial nerve has been found intraoperatively in several of these patients. Brandt and Dieterich termed the condition “vestibular paroxysmia” and reported a series of patients with short attacks of vertigo precipitated by changes of head position. All patients responded to treatment with carbamazepine (09). In a follow-up study of 32 patients, symptoms were most frequently precipitated by a head turn. Unilateral canal paresis was present in 62% of patients and hyperventilation-induced nystagmus, as measured by electronystagmography, in 70% of patients.
According to the International Classification of Vestibular Disorders, vestibular paroxysmia can be diagnosed when the following criteria are fulfilled (79):
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A. At least 10 attacks of spontaneous spinning or nonspinning vertigo |
Diagnostic criteria for probable vestibular paroxysmia (79):
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A. At least five attacks of spontaneous spinning or non-spinning vertigo |
The sensitivity and specificity of these criteria remain unclear, however, being that no gold standard exists for the diagnosis of neurovascular compression of the eighth cranial nerve.
Vestibular migraine can manifest itself with positional vertigo (42) and can mimic benign paroxysmal positional vertigo (86). Various patterns of positional nystagmus can be observed during the attack, most of which have been attributed to a central origin (69; 86; 89; 49; 91). One study found positional nystagmus of a central type in eight out of 20 patients during acute vestibular migraine (89). In another study, all 26 patients with acute vestibular migraine showed central positional nystagmus, and about half of them complained of positional vertigo (69). A third study used a custom-made home-video oculography system and reported isolated positional nystagmus in 16 of 67 patients with acute vestibular migraine; in most of them, horizontal direction-changing nystagmus in both lateral supine positions was observed (91). Another large case series by the same group with 101 patients reported isolated positional nystagmus in 26% and a combination of spontaneous and positional nystagmus in 70% of patients. Positional nystagmus was persistent in all patients. About half of the patients showed positional nystagmus also in the symptom-free interval but with much lower intensity than ictal nystagmus (93). The following factors help to distinguish migrainous positional vertigo from benign paroxysmal positional vertigo: short-duration symptomatic episodes and frequent recurrences, manifestation early in life, migrainous symptoms during episodes with positional vertigo, and atypical positional nystagmus (86). Positional nystagmus is usually persistent and horizontal, beating either towards the lower ear (geotropic nystagmus) or towards the upper ear (apogeotropic nystagmus) in both lateral supine positions (69; 49; 91). The diagnosis of vestibular migraine can be challenging because many patients do not show a fixed association of headache and vertigo (21; 61). When headache is not a prominent feature of the attacks, the diagnosis of vestibular migraine rests on other symptoms that relate the vertiginous attacks to migraine (ie, sensitivity to light or scintillating scotoma). Furthermore, the time course of vertigo in patients with migraine is variable and often exceeds the duration of a typical aura. The diagnosis can be made when the following criteria are met (52):
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(1) At least five episodes with vestibular symptoms of moderate or severe intensity, lasting 5 minutes to 72 hours | ||
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(2) Current or previous history of migraine with or without aura according to the criteria of the International Classification of Headache Disorders (ICHD) | ||
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(3) One or more migraine features with at least 50% of the vestibular episodes: | ||
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• headache with at least two of the following characteristics: 1-sided location, pulsating quality, moderate or severe pain intensity, aggravation by routine physical activity | ||
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• photophobia and phonophobia | ||
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• visual aura | ||
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(4) Not better accounted for by another vestibular or ICHD diagnosis | ||
In addition, migraine is a predisposing factor for benign paroxysmal positional vertigo (39).
Rarely, vestibular schwannoma (acoustic neurinoma) and Menière disease can present with positional vertigo (81; 49; 19). Persistent apogeotropic positional nystagmus mimicking cupulolithiasis of the horizontal canal has been described in both conditions (49). In a large case series, 39% of patients with Meniere disease examined with video Frenzel goggles showed horizontal positional nystagmus of low intensity in the asymptomatic interval (82).
In perilymph fistulas, vertigo can occasionally be evoked during changes of head position. Conflicting data are available on the frequency of this manifestation. Although positional vertigo has been a frequent finding in some case series (29; 78), it has been an exception in others (28). Detailed studies on the clinical features of positional vertigo and nystagmus are lacking in these patients. Vertigo provoked by Valsalva maneuvers during coughing, sneezing, and lifting heavy objects is more typical. Superior canal dehiscence is another third mobile window syndrome that may rarely present with positional vertigo and vertical-torsional nystagmus arising from stimulation of the superior semicircular canal (92). Typical symptoms of superior canal dehiscence are pressure- and sound-induced vertigo, pulsatile tinnitus, and autophony.
Positional alcohol nystagmus and vertigo appear within 30 minutes after ingestion of alcohol whenever the patient turns his head to either side in the supine position. Positional nystagmus is horizontal with respect to the head and beats persistently toward the lower ear. It changes direction when the patient turns the head to the other side, beating again to the lower ear. This initial response decreases a few hours after alcohol consumption and is followed by a silent period lasting about 2 hours. Then, positional nystagmus reappears with reversed direction; thus, beating to the upper ear in each head lateral position (58). Oral ingestion of glycerol (70), as used for diagnostic purposes in Ménière disease, and deuterium oxide (59) evoke positional nystagmus towards the uppermost ear in the lateral supine position.
Persistent geotropic direction-changing positional nystagmus in the supine lateral head positions may also occur in patients without alcohol consumption or central neurologic signs and with normal results in cerebral imaging. This condition has been termed “light cupula” (35; 38).
Finally, vertigo and auditory symptoms can be manifestations of Waldenstrom macroglobulinemia, with positional vertigo occurring as a rare variant (43).
Rotational vertebral artery syndrome is a rare cause for vertigo induced by fierce head rotations but only exceptionally presents with positional vertigo in the proper sense (74). Typically, vertigo develops with a latency of several seconds during a head rotation to one side and ceases shortly after the patient has resumed the neutral head position. Transient vertigo can be accompanied by tinnitus (80; 17), blurred vision (72), other brainstem symptoms, and syncope (20) or may occur in isolation (55). During attacks of vertigo, transient nystagmus can be typically observed with a mixed downbeat, horizontal, and torsional direction (17; 55). Reversal of nystagmus may be observed, either when the provoking head position is maintained or after rotating the head back to the neutral position.
Prognosis and complications
Positional vertigo is a symptom and can reflect pathophysiological disorders as diverse as benign paroxysmal positional vertigo and cerebellar hemorrhage; therefore, prognosis depends on the underlying pathology. A prospective study has observed spontaneous remission of benign paroxysmal positional vertigo of the posterior canal on average 39 days after onset (37). Benign paroxysmal positional vertigo has a recurrence rate of about 50%, with 80% of recurrences occurring within the first year after treatment (10).
Biological basis
Anatomic localization
Benign paroxysmal positional vertigo, perilymph fistulas, and positional alcohol nystagmus arise from the labyrinth. The peripheral origin of benign paroxysmal positional vertigo has been proven by surgical procedures like selective dissection of the posterior ampullary nerve (27) and occlusion of the posterior canal (67), which completely abolish the attacks. Likewise, positional alcohol nystagmus does not occur when labyrinthine function is lost (64). A symptomatic neurovascular compression of the eighth cranial nerve can presumably occur along the entire course of the nerve within the subarachnoid space (36). Central positional vertigo is caused by lesions of vestibular pathways in the brainstem or the cerebellum involving the dorsal vermis (73), nodulus (41; 60; 45), the dorsal pontomedullary brainstem (54), and a region dorsolateral to the fourth ventricle involving the brachium conjunctivum (08; 01). Vestibular migraine may involve both central and peripheral vestibular structures, but a central vestibular syndrome is more common (89; 69).
In rotational vertebral artery syndrome, the analysis of nystagmus is compatible with either unilateral or bilateral dysfunction of the inner ear, involving predominantly the superior labyrinth (17; 55). Ischemia of the vestibular nuclei has also been suspected but is less likely when vertigo and tinnitus occur in isolation (17).
Pathophysiology
Benign paroxysmal positional vertigo is caused by heavy particles that have entered a semicircular canal where they move freely within the endolymph. The so-called canalolithiasis concept has become widely accepted, as it is compatible with all clinical features of benign paroxysmal positional vertigo (30; 11). Mobile particles that are heavier than endolymph may enter the posterior semicircular canal, where they tend to gravitate to the most dependent point. When the patient is upright, they are located at the base of the cupula and do not have any effect. During the Dix-Hallpike test, the head is rotated backward in the plane of the posterior canal, inducing movement of the particles within the long arm of the canal away from the cupula. A gravitating clot of otoconia debris acts like a plunger, causing ampullofugal endolymph and cupular displacement. The ensuing excitation of the posterior canal receptors results in the mixed torsional-vertical nystagmus. The latency of nystagmus may be attributed to the time taken for the particles to move because of inertia and their initial adherence to the membranous wall of the labyrinth. The nystagmus will subside after the particles have reached the most dependent point of the canal and the cupula has returned to its resting position. When the patient sits up again, the particles will be shifted in the opposite direction to induce deflection of the cupula in the other direction, resulting in a reversed nystagmus of lower intensity. The clot may disperse with repeated provocations that would lead to a fatiguing response.
Central positional vertigo and nystagmus are caused by lesions of vestibular structures in the brainstem or vestibulocerebellum (08). Most patients have lesions of the nodulus, the uvula, or the tonsil (18), but also the cerebellar peduncles, the lateral medulla, and the pons may be affected (51). Consequently, a change of the head with respect to gravitation may lead to an unphysiologic tone imbalance of the vestibulo-ocular system. Persistent apogeotropic positional nystagmus has been simulated by a mathematical model including lesions in cerebellar and brainstem circuits involved in generating centrally created estimates of gravity (15). Causes of central positional vertigo include lesions due to infarction (18), hemorrhage, tumor (14), multiple sclerosis, other inflammatory diseases, and cerebellar degeneration. Positional vertigo is a common complaint in spinocerebellar ataxia type 6 and can precede the development of ataxia (94). Rarely, paraneoplastic encephalitis can manifest with positional vertigo and nystagmus (24).
Positional vertigo and downbeat nystagmus in the straight head-hanging position has been described in patients with anti-GQ1b antibodies, usually presenting after an antecedent episode of upper respiratory infection (50). These patients usually show no classical anti-GQ1b syndrome, such as Miller Fisher syndrome.
In neurovascular compression of the eighth cranial nerve, vertigo is presumably caused by interaxonal ephaptic transmission with abnormal neuronal discharges; however, the pathophysiologic role of nerve compression is debated, even in established neurovascular compression syndromes, such as trigeminal neuralgia and hemifacial spasm, in regards to the frequency of asymptomatic contacts between nerves and vessels (12; 56).
The pathophysiology of vestibular migraine is unknown. It is unclear which central and peripheral vestibular structures are involved and how the vertigo relates with the pathophysiology of migraine. The following hypotheses have been discussed: (1) cortical spreading depression; (2) labyrinthine ischemia due to migrainous vasoconstriction (03); (3) release of neurotransmitters or neuropeptides during the migraine attack that might influence vestibular signal processing (21); and (4) ion channel dysfunction causing both migraine and vertigo (03; 89).
Positional vertigo and nystagmus in vestibular schwannoma can occur with large tumors compressing the brainstem (19). When it occurs in intrameatal tumors, compression or traction of the vestibular nerve exerted by head movements has been postulated (81).
Perilymph fistulas are abnormal communications between the perilymphatic space and the middle ear or the intracranial cavity. They may occur spontaneously, as a congenital malformation, and after trauma, ear surgery, or inflammation. Fistulas allow the transmission of external pressure changes into the labyrinth, resulting in mechanical irritation of vestibular structures. Typical provoking factors include Valsalva maneuver when sneezing or coughing, change of head position, or loud tones.
Positional alcohol nystagmus can be explained by a transient transformation of the cupula into a gravity-sensitive receptor. Physiologically, the semicircular canals selectively transduce angular acceleration and are not sensitive to gravitation, as the cupula and the endolymph have the same specific gravity. According to the so-called buoyancy hypothesis, any specific gravity differential between the cupula and the surrounding endolymph renders this organ sensitive to head changes with respect to gravity (59). Alcohol has a lower specific gravity than both endolymph and the cupula. Shortly after ingestion, alcohol diffuses selectively into the cupula, which thereby becomes lighter than endolymph. This causes upward cupula displacement in the lateral head position during phase I of positional alcohol nystagmus, which beats to the lower ear. Then, alcohol diffuses in the endolymph, equalizing the gradient of gravity. Later, alcohol is washed out of the cupula before it diffuses out of the endolymph. Therefore, during phase II of positional alcohol nystagmus, the cupula becomes denser than endolymph, which leads to downward displacement of the cupula with nystagmus beating to the upper ear. Positional nystagmus after ingestion of glycerol or deuterium oxide can be explained by the same mechanism. As these substances are denser than endolymph, the direction of nystagmus changes sequentially, like positional alcohol nystagmus, but oppositely directed; thus, it initially beats to the upper ear and reverses after a silent period. The rare positional vertigo in macroglobulinemia is possibly due to a gravity gradient between cupula and endolymph as well (43).
The buoyancy hypothesis has also been suggested to explain persistent geotropic positional nystagmus in patients without alcohol consumption or central neurologic signs (light cupula). This type of nystagmus is neither compatible with mobile otoconia in a semicircular canal nor with dense otoconia attached to a cupula. However, there seems to be an association between this disorder and canalolithiasis and cupulolithiasis, as some of these patients have developed classical variants of benign paroxysmal positional vertigo at follow-up (35; 38; 68). Furthermore, an association with sudden sensorineural hearing loss has been described (44). It has been suggested that this type of positional vertigo and nystagmus may be due to changes of the density of the cupula or the endolymph (46), but this remains speculative.
Rotational vertebral artery syndrome is due to compression of the dominant vertebral artery during contralateral head rotation, usually at the atlantoaxial joint (17). The resulting ischemia of one or both labyrinths probably leads to transient excitation of the vestibular hair cells of the superior labyrinth, involving the anterior and horizontal canals (80).
Epidemiology
In a neurotologic survey, 43% of 243 unselected patients with vestibular vertigo had positional vertigo (63). The lifetime prevalence of benign paroxysmal positional vertigo has been estimated to be 3.2% in females and 1.6% in males (87). In a group of 100 patients with positional nystagmus, a peripheral cause--almost exclusively benign paroxysmal positional vertigo--was identified in 83% and a central cause in 12% (06). In a prospective case series with 58 patients presenting with persistent geotropic positional nystagmus 12% of patients showed a cerebellar lesion (18).
Differential diagnosis
The various etiologies of positional vertigo can usually be distinguished on the basis of history and clinical examination.
In benign paroxysmal positional vertigo, symptoms occur typically in bouts lasting several weeks, with spontaneous remittance and reoccurrence after weeks to years; therefore, the diagnosis of benign paroxysmal positional vertigo is highly likely in a patient with repeated bouts of positional vertigo over several years with no neurologic abnormalities on examination. Single characteristics of benign paroxysmal positional vertigo, such as latency, duration, time course of nystagmus, and fatigability with repeated positioning can also occur in central positional vertigo syndromes (13); however, it is unlikely that a central lesion mimics the entire nystagmus pattern of benign paroxysmal positional vertigo of the posterior canal. However, central lesions can simulate the nystagmus pattern of other variants of benign paroxysmal positional vertigo, particularly cupulolithiasis of the horizontal canal (18). Central positional nystagmus is often not attributable to the plane of the stimulated semicircular canal (eg, may exhibit purely vertical nystagmus after the head of the supine patient is turned to the side, which stimulates the horizontal canal). Conversely, nystagmus in benign paroxysmal positional vertigo corresponds to the stimulated semicircular canal plane; for instance, in benign paroxysmal positional vertigo of the posterior canal, a mixed torsional-vertical nystagmus appears maximally after positioning in the plane of the affected canal, which reflects the known excitatory connections of the posterior canal with the ipsilateral superior oblique and the contralateral inferior rectus muscle. Purely vertical or torsional nystagmus, verified by examination under Frenzel glasses, should always be considered of central origin, as it cannot be explained by stimulation of a single semicircular canal. Most patients with central positional nystagmus exhibit gaze-evoked nystagmus or saccadic pursuit (06; 15). Central nervous symptoms may occur with brainstem or cerebellar lesions and during acute attacks of vestibular migraine. Concomitant auditory symptoms suggest neurovascular compression of the eighth cranial nerve, perilymph fistula, or vestibular migraine.
Diagnostic workup
Usually, a careful history and clinical examination are sufficient to identify the cause of positional vertigo. The history should comprise onset, duration, course, and provocative maneuvers of positional vertigo as well as associated autonomic, auditory, and central nervous system symptoms. Age of onset is not a criterion to identify a specific etiology of positional vertigo. The neurologic examination should emphasize oculomotor function, vestibulospinal tests, and provocative testing for positional vertigo with Frenzel glasses. Further testing with bithermal caloric irrigation, audiometry, auditory evoked potentials, and imaging can be helpful.
The diagnosis of benign paroxysmal positional vertigo is confirmed by the observation of typical nystagmus during positional testing. Further laboratory investigations are usually not required. In cases with suspected coexisting peripheral vestibular disease, the appropriate vestibular and audiologic tests should be performed. Variants of benign paroxysmal positional vertigo that can be mimicked by central lesions (eg, cupulolithiasis of the horizontal canal presenting with apogeotropic positional nystagmus in the lateral head positions) require meticulous neurologic examination, focusing particularly on ocular motor function.
When central positional vertigo is suspected, MRI of the posterior fossa is required to identify brainstem or cerebellar lesions.
The presumptive diagnosis of neurovascular compression of the eighth cranial nerve is based on the history of short attacks of vertigo, occurring spontaneously or precipitated by head movements, and the response to treatment with carbamazepine or oxcarbazepine (79). Other causes for positional vertigo, particularly benign paroxysmal positional vertigo, must be excluded. MRI is employed primarily to rule out pathologic structures compressing the eighth cranial nerve (02), whereas the radiologic or intraoperative finding of a close contact between blood vessels and the eighth cranial nerve is insufficient to prove a symptomatic neurovascular compression.
A history of ear or head trauma, barotrauma, ear surgery, or inflammatory ear disease can point to a perilymph fistula. The pressure fistula test, also known as Hennebert sign, is positive in about 25% of cases (78). The test is positive when a change of pressure within the external auditory canal, exerted with a Politzer balloon, induces vertigo, nystagmus, or ocular deviation. The role of imaging in suspected perilymph fistula is controversial. High-resolution computed tomography may show air bubbles at the prosthesis after stapedectomy (47) or abnormalities of the stapes (90), but the validity of these findings has not been evaluated. Fistulas between the labyrinth and the middle ear may be confirmed with exploratory tympanotomy, which can be performed under local anesthesia; however, the diagnostic reliability of this procedure is debated (78).
The diagnosis of vestibular migraine relies purely on the patient's history. The repeated occurrence of either migrainous headache or other symptoms during vertigo supports the diagnosis (52). Supportive evidence includes menstrual vertigo; precipitation by factors that may provoke migraine, such as lack of sleep, bright lights, or specific foods; and response to antimigrainous drugs.
Rotational vertebral artery syndrome can be documented with dynamic angiography, demonstrating compression of the vertebral artery during contralateral head rotation (17). Alternatively, transcranial Doppler and duplex sonography can demonstrate an increase of resistance in the vertebral artery during the challenging head position (55).
Management
Both Epley and Semont positional maneuver are highly effective for the treatment of benign paroxysmal positional vertigo of the posterior canal, although the body of evidence is stronger for the Epley maneuver (26; 34). They induce the displacement of the otolithic debris through the open end of the posterior semicircular canal into the utricular cavity, where they no longer produce positional vertigo (76; 25). Complete recovery is achieved in 50% to 80% of cases after a single maneuver when performed properly (76; 33; 77). In a randomized, double-blind trial, 80% of patients were free of positional vertigo and nystagmus 1 day after a single treatment session with up to three Epley maneuvers, compared to 10% in the control group (88). Additionally, therapeutic positioning maneuvers may be effective in patients who, in spite of a typical history, do not show nystagmus on Hallpike testing (32). Surgical elimination of posterior canal function is restricted to those rare patients with longstanding benign paroxysmal positioning vertigo who have not responded to appropriate and repeated therapeutic positioning (67; 27).
Treatment of central positional vertigo depends on the underlying cause, which may be infarction, hemorrhage, inflammation, tumor, antibody-mediated, or intoxication. Successful treatment of positional vertigo and positional downbeating nystagmus with 4-aminopyridine has been reported in a patient with a cerebellar vermis lesion (48). Patients with vestibular dysfunction associated with anti-GQ1b antibody typically recover spontaneously within a few months (50). Suppression of paroxysmal positional downbeating nystagmus and vertigo with clonazepam has been described in a patient with posterior fossa hemorrhage involving the fourth ventricle (66).
Vertigo due to neurovascular compression of the eighth cranial nerve should be treated with carbamazepine or oxcarbazepine (09). Treatment with oxcarbazepine was moderately effective in a randomized double-blind placebo-controlled trial, but discontinuation due to adverse effects was frequent (04). The role of surgery in suspected neurovascular compression of the eighth cranial nerve is controversial. In analogy with recognized vascular compression syndromes (ie, trigeminal neuralgia and hemifacial spasm), retromastoid craniectomy with microvascular decompression of the eighth cranial nerve has been performed (40). Intraoperatively, it was often found that the vestibular nerve was being compressed by blood vessels, most commonly a cerebellar artery (57). Good response to surgical treatment has also been described by other groups (75; 71); however, controlled studies are needed to exclude placebo effects that appear to be powerful after sham operations in patients with vertigo (84).
Vestibular migraine attacks may be severe, protracted, and frequent enough to warrant acute or prophylactic treatment. Unfortunately, current treatment recommendations are based on anecdotal experience and expert opinion rather than on randomized clinical trials (65). One small, controlled study on the use of zolmitriptan for acute vestibular migraine was inconclusive (62). There is limited evidence for prophylactic treatment from a single randomized trial using 10 mg flunarizine (not marketed in the United States), which showed a significant decrease in frequency and severity of attacks compared to placebo (53).
There is no treatment for positional vertigo associated with persistent geotropic positional nystagmus in patients without alcohol consumption or central neurologic signs (light cupula). However, spontaneous remission within 1 week has been described in 43% to 70% of patients (68).
Rotational vertebral artery syndrome can be treated causally with surgical decompression of the vertebral artery at the C1/C2 level (80; 20). The long-term outcome of conservative treatment with avoidance of head rotations and antiplatelet drugs has not been assessed systematically.
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Michael von Brevern MD
Dr. von Brevern of Charité University Hospital has no relevant financial relationships to disclose.
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Thomas Lempert MD
Dr. Lempert of Charite University Hospital has no relevant financial relationships to disclose.
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Douglas J Lanska MD MS MSPH
Dr. Lanska of the University of Wisconsin School of Medicine and Public Health and the Medical College of Wisconsin has no relevant financial relationships to disclose.
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