The diagnosis of the etiology of vertigo has always been a clinical problem for many doctors. In recent years, with the popularization of theory and the advancement of auxiliary examination techniques, most vertigo can be diagnosed; however, because the occurrence of vertigo involves many fields such as neurology, otorhinolaryngology and internal medicine, some basic issues such as pathophysiology are still not clear, and the etiology of some vertigo is still difficult to be clarified theoretically, thus posing difficulties to clinical practice. This expert consensus focuses on the standardized treatment of common vertigo, and at the same time outlines the clinical features of rare vertigo as comprehensively as possible, in addition, this article will also cover some of the dizziness.
I. Concept and etiological classification of vertigo
Vertigo refers to the sensation of rotation and oscillation of oneself or the environment, which is a kind of motion illusion; dizziness refers to the sensation of instability of oneself; and lightheadedness refers to the sensation of mental unclearness. The pathogenesis of vertigo and dizziness is not quite the same, but sometimes they are two manifestations of the same disease at different times.
Depending on the location of the disease, vertigo is often divided into peripheral and central, with the former occurring relatively more frequently; dizziness can be both a manifestation of the recovery period of the above-mentioned diseases and can also be caused by psychiatric disorders and certain systemic diseases. Peripheral vertigo accounts for 30% to 50%, with benign episodic positional vertigo having the highest incidence of single disease, followed by Meniere’s disease and vestibular neuritis; central vertigo accounts for 20% to 30%; dizziness associated with psychiatric and systemic diseases accounts for 15% to 50% and 5% to 30%, respectively; there are still 15% to 25% of vertigo with unknown causes [4-8]. There are some differences between children’s vertigo and adults, but the overall trend is that the proportion of central vertigo (mainly post-traumatic vertigo and migraine-related vertigo) is significantly higher than that of adults, accounting for about 19%-49%; the higher incidence of single diseases are: benign paroxysmal vertigo, post-traumatic vertigo and otitis media-related vertigo [9-12].
II. Problems of domestic neurologists in vertigo diagnosis and treatment
The main problem at present is the lack of theoretical knowledge. Firstly, it is manifested in the diagnosis, and the lack of relevance when asking the medical history, often
The etiology, form of onset, duration, concomitant symptoms and mode of remission are often missed [13-14], while 70%-80% of vertigo can be diagnosed or clearly directed by effective questioning. The limited equipment and evaluation level of auxiliary examinations for vertigo need to be improved, such as the examination process of nystagmography is not standardized enough; the MRI examination site is not targeted enough; some cases of post vertigo cerebrovascular stenosis are not sexually related examinations and missed diagnosis. In the daily treatment, vertigo is often confined to a few vague diseases, such as vertebrobasilar artery insufficiency, cervical spondylosis, Ménière’s disease and vestibular neuritis, or generally called “vertigo syndrome”. The second aspect is the treatment. Due to the lack of understanding of the importance of vestibular rehabilitation, the recovery of vestibular function is delayed by the long-term application of vestibular inhibitory drugs; the rate of benign episodic positional vertigo treated by manual repositioning is too low, etc.
Common causes of vertigo and treatment suggestions
The clinical manifestations, auxiliary examinations, treatment and prognosis of peripheral and central lesions of vertigo are completely different. In view of this, vertigo caused by brainstem, cerebellar nuclei and supranuclear lesions is called central vertigo in practice, and conversely, it is called peripheral vertigo [17-18].
(i) Central vertigo
Most of the symptoms are accompanied by other neurological damage, and physical examination reveals signs of focal neurological damage; most of the foci of central vertigo are located in the posterior cranial fossa. The clinical treatment should follow the principles of localization and qualitative diagnosis in neurology. It should be emphasized that vertical nystagmus and nonconjugate nystagmus are only seen in central lesions, and positional nystagmus without fatigue often suggests central nystagmus [13-14].
1, Vascular origin: The onset is acute and is mostly the result of vascular lesions in the vertebrobasilar system. The diagnosis and treatment should follow the guidelines of cerebrovascular diagnosis and treatment. TIA of the vertebrobasilar system: the symptoms are stereotypically recurrent and manifest as: vertigo lasting several minutes, total or partial presence of symptoms of brain nerve, brainstem, cerebellar or occipital lobe damage, no signs of neurological damage between episodes, and no fresh infarct lesions on magnetic resonance diffusion-weighted image (DWI) scan. Ultrasound, TCD, CT angiography (CTA), magnetic resonance angiography (MRA), and digital subtraction angiography (DSA) were performed to determine the presence or absence of stenosis in the vertebrobasilar artery.
Vertebrobasilar artery insufficiency (VBI): There is a consensus that the diagnosis of VBI is too generalized. However, it is debated whether this completes the denial of the name VBI. Some scholars deny the ischemic state of brain tissue in the posterior cranial fossa and advocate the abolition of VBI, while some scholars hold the opposite opinion. There is a lack of evidence on both sides of the denial and affirmation.
Subclavian artery steal syndrome: The clinical presentation often presents in two ways. One is vertigo, visual impairment or cerebellar ataxia, and the other is weakness of the affected upper extremity with diminished radial artery pulsation and a decrease in systolic blood pressure of 20 mm Hg (1 mm Hg = 0.133 kPa) or more compared to the healthy side. Ultrasound, TCD, CTA, MRA and DSA are used to make a definitive diagnosis. Treatment is mainly interventional or surgical to reconstruct normal blood flow in the subclavian artery.
Blood flow or brainstem infarction [8, 13-14]: the disease may start with episodic vertigo, often combined with signs of cerebral nerve damage such as medullary palsy, diplopia, facial palsy, facial sensory disturbances, and sometimes combined with Horner’s sign. Imaging examinations, especially DWI scans early in the course of the disease, confirm cerebral tissue infarction. It can be seen in severe stenosis or occlusion of large vessels of the vertebrobasilar system, including the posterior inferior cerebellar artery, vertebral artery, basilar artery, and anterior inferior cerebellar artery; sometimes it is also seen in deep penetrating branch lesions of the basilar artery. Imaging is required to determine this. Cerebellar or brainstem hemorrhage: mild symptoms are sudden dizziness or vertigo, and cerebellar ataxia is seen on physical examination; dizziness may occur during the recovery period of massive hemorrhage; imaging such as cranial CT is required to confirm the diagnosis. Internal symptomatic treatment is based, and surgery is required if necessary.
2. Tumor: It is often subacute or chronic in origin, and the diagnosis can be made clearly by imaging when typical symptoms and signs appear. Cerebellar or brainstem tumors: Dizziness attacks are common, which can be seen as cerebellar ataxia, cerebral nerve or crossed cone damage, sometimes combined with vertigo or dizziness attacks. Pontocerebellar horn tumor: dizziness attacks are common, cerebellar ataxia, lateral sensory deficits and adductor nerve palsy, facial palsy and other signs are seen. Pathologically, they are commonly known as auditory neuroma, meningioma and cholesteatoma.
3. Brainstem or cerebellar infections: acute onset, with fever and other systemic inflammatory reactions, often with a history of antecedent infections such as upper respiratory tract infections or diarrhea. In addition to the clinical manifestations of cerebellar and brainstem damage, vertigo is sometimes present. Cerebrospinal fluid examination is the main basis for confirming the diagnosis. According to the pathogenic findings, antiviral agents, antibiotics or hormones are applied respectively.
4.Multiple sclerosis: vertigo may appear when the lesion involves brainstem or cerebellum; the vertigo manifestation is not specific, it may be positional and may last for several days or even weeks. The diagnosis and treatment refer to NICE criteria [28].
5. Craniocervical junctional area malformation: Chari malformation, skull base depression, and dentate subluxation are common, which can present with cone bundle damage, cerebellar symptoms, and manifestations of posterior group cerebral nerve and high cervical medullary damage, sometimes combined with vertigo; vertigo can sometimes be induced by the Waldorf expiratory maneuver. Imaging examination is the basis for diagnosis; surgical treatment is needed.
6.Drug origin: some drugs can damage the vestibular end sensory apparatus or vestibular pathway and cause vertigo.
Carbamazepine can cause reversible cerebellar damage, long-term application of phenytoin sodium can cause cerebellar degeneration, long-term exposure to heavy metals such as mercury, lead and arsenic can damage the cochlea, vestibular apparatus and cerebellum, and organic solvents such as formaldehyde, xylene, styrene and trichloromethane can damage the cerebellum. The postural instability and ataxia seen in acute alcoholism are the result of reversible damage to the semicircular canals and cerebellum.
Common ototoxic drugs include: antibiotics such as aminoglycosides, vancomycin, viomycin and sulfonamides, antineoplastics such as cisplatin, chlorhexidine and vincristine, quinine, high-dose salicylates, diuretics such as tachykinuria and diuretic acid, and some local anesthetics applied in the middle ear, such as lidocaine. Dimethylaminetetracycline damages only the vestibule, and the vestibular toxins of gentamicin and streptomycin are much more toxic than their cochlear toxicity. Nystagmographic tracings (ENG) and rotational tests sometimes reveal a bilateral decrease in vestibular function; hearing tests reveal sensorineural deafness.
Diagnostic recommendations.
(1) From history, signs and relevant ancillary tests and exclude other etiologies.
(2) Vestibular function tests and/or audiograms may be abnormal or normal.
Treatment recommendations: discontinue medication, remove from the environment; bilateral vestibular function impairment, vestibular rehabilitation training is feasible.
7.Other rare central vertigo: including the following.
Migrainous vertigo (MV): the pathogenesis is the same as migraine, and related names in the literature include vestibular migraine, migraine-associated vertigo, benign recurrent vertigo, and migraine-associated vestibulopathy [29-32].
The identified criteria for MV include.
(i) moderate or severe episodic vestibular symptoms, including rotational vertigo, positional vertigo, other self-motion illusions, and head movement intolerance (due to head movement-induced imbalance sensation or illusion of movement of self or surrounding objects, etc.). The severity of vestibular symptoms is classified as III poles: mild as not interfering with daily activities, moderate as interfering but not limiting daily activities, and severe as limiting daily activities.
②Migraine in accordance with the International Headache Classification (HIS).
③At least 2 episodes of vertigo with 1 of the following migraine symptoms: pulsating headache, photophobia, phonophobia, visual or other aura.
(iv) Other etiologies are excluded.
Possible MV criteria are.
① Moderate or severe episodic vestibular symptoms.
②At least 1 of the following symptoms: migraine meeting HIS criteria, migrainous concomitant symptoms during vertigo attacks, migraine-specific triggers (e.g., specific foods, irregular sleep, endocrine disorders), and effective treatment with anti-migraine medication.
③ Exclude other etiologies.
Recommendations.
(1) Diagnosis needs to be based on the above criteria.
(2) Medication should be administered with reference to the treatment or preventive measures for migraine.
Epileptic vertigo (epileptic vertigo): It is rare clinically, internationally classified as focal epilepsy, usually lasting for seconds or tens of seconds, and the seizure is not associated with postural changes. The sites that can produce vertigo epilepsy include: the intraparietal sulcus, the posterior superior temporal gyrus, the middle posterior parietal gyrus, the left middle frontal gyrus, and the temporoparietal junctional area. It is rare to find epilepsy in which vertigo is the main or only manifestation of vertigo; vertigo can be a precursor symptom of partial epilepsy, especially temporal lobe epilepsy. Confirmation of the diagnosis requires an EEG showing epileptiform wave discharges in the corresponding leads.
Diagnostic recommendations.
(1) Abnormal discharges on the EEG in the corresponding leads during vertigo seizures.
(2) Other etiologies need to be excluded.
Treatment recommendation: administer medication as for partial seizures.
Cervical vertigo (cervical vertigo): There are no uniform criteria, and the exclusion method is preferred. At least the following features should be present.
(1) Dizziness or vertigo accompanied by pain in the neck.
(2) Dizziness or vertigo mostly occurs after neck activity.
③Some patients have positive neck distortion test.
④Abnormal neck imaging, such as cervical retroflexion, conus instability, disc herniation, etc.
⑤ Most of them have a history of neck trauma.
⑥Other causes were excluded.
Diagnosis basis: The diagnosis needs to be in accordance with the above characteristics.
Treatment suggestion: The main treatment measures are correction of poor head and neck posture, physical therapy and local closure.
Post-traumatic vertigo (PTV): A transient sense of self rotation, sometimes a persistent sense of self instability, that occurs after head trauma.
It includes.
(1) Temporal bone fracture and inner ear penetration injury: Some stab wounds and gunshot wounds involving the temporal bone also damage the inner ear, and if the patient is fortunate enough to recover from the trauma, hearing impairment and vertigo are often left behind. Some patients may wake up with only a sense of instability and hearing loss without vertigo attacks; symptomatic treatment is the mainstay, and those who are left with permanent vestibular impairment need to try vestibular rehabilitation training.
(2) Labyrinthine concussion: It belongs to peripheral vertigo. It occurs after the inner ear is shocked by violence or vibration wave, and manifests as vertigo that lasts for several days, sometimes for weeks or longer, often accompanied by hearing loss and tinnitus, and positional nystagmus on ENG examination, and in a few patients, semicircular canal paralysis, temporal bone and ear imaging are not abnormal; treatment is mainly symptomatic and rest.
(ii) Peripheral vertigo
Most of the lesions below the nucleus of the brainstem nerve are caused by ear diseases. Except for nystagmus and sometimes may be accompanied by hearing impairment, patients do not have corresponding signs and symptoms of neurological damage.
1. Peripheral vertigo without hearing impairment: The common diseases are described below, and the rare diseases are shown in Table 1.
Benign paroxysmal positional vertigo (BPPV): It is caused by the dislodgement of calcium carbonate particles from the otolith membrane of the ellipsoidal sac into the semicircular canal. 85% to 90% of ectopic otoliths occur in the posterior semicircular canal, and 5% to 15% in the horizontal semicircular canal. The majority of BPPV is of the “canal stone type” and is characterized by.
(1) Episodes of vertigo occurring during head position changes;
(2) Dix-Hallpike or Roll test can induce vertigo and nystagmus at the same time, and there is a latency period of 5~20S between head position change and vertigo attack and nystagmus. “When the patient sits up from the prone position, “reverse nystagmus” often occurs.
Very few BPPVs are of the “crestal cap stone type”, which differs from the “tubular stone type” in that the former has no latency and a long duration of nystagmus on examination by Dix-Hallpike et al. The so-called central positional vertigo caused by a few lesions in the posterior cranial fossa and high cervical segment is similar to the “potbelly crest otolith” and requires careful history, physical examination, and neuroimaging if necessary [43].
The diagnostic guidelines of the American Academy of Otolaryngology-Head and Neck Surgery do not advocate the diagnostic name of “subjective BPPV”, but in clinical practice, there are a number of patients with a typical BPPV history, but Dix-Hallpike examination did not induce vertigo and nystagmus, which may be related to the timing of the examination and the number of ectopic otoliths. number, and as long as a central cause is ruled out, treatment with Epley or Semont manipulation repositioning can be tried.
Diagnosis is based on.
(1) Vertigo attacks are associated with changes in head position. The vertigo usually lasts less than 1 min without signs of cochlear damage.
(2) There are no positive neurological signs. vertigo and groundward nystagmus are induced during Dix-Hallpike and other examinations.
Treatment recommendation: otolith manipulation and repositioning treatment.
Vestibular neuritis (vestibular vertigo): also known as vestibular neuronitis (VN), is the result of a viral infection of the vestibular nerve or vestibular neurons. Most patients have a history of upper respiratory tract infection or diarrhea in the days or weeks prior to the disease. The severe peripheral spinning sensation often lasts for more than 24 h, sometimes for several days, and is accompanied by severe vomiting, palpitations, sweating, and other autonomic responses. Most of them heal spontaneously within a few weeks, and recurrence is rare. More than half of the patients may develop transient instability within 1 year after the disease, and some patients later develop BPPV manifestations, and abnormalities of cold and heat tests may last longer.
Diagnosis is based on.
(1) Vertigo attacks often last more than 24h, and some patients have a history of viral infection before the disease.
(2) No cochlear symptoms; stroke and traumatic brain injury are excluded.
(3) ENG examination shows one side of vestibular hypofunction.
Treatment suggestions: apply glucocorticoids; stop vestibular inhibitors after vomiting stops, and perform vestibular rehabilitation training as early as possible.
2. Peripheral vertigo with hearing impairment: common diseases are as follows.
Meniere’s disease: The etiology is not completely clear, and the pathological mechanism is mostly related to endolymphatic effusion. There is no gender difference, and the first onset is rare in people younger than 20 years old or older than 70 years old.
The Chinese Medical Association’s Otolaryngology-Head and Neck Surgery Branch proposed the diagnostic criteria for this disease in 2006.
① 2 or more episodes of vertigo lasting 20 min to several hours. It is often associated with autonomic dysfunction and balance disorders. There is no loss of consciousness.
② fluctuating hearing loss, mostly low-frequency hearing loss in the early stage, with progressive hearing loss gradually increasing. At least 1 pure tone audiometry for sensorineural hearing loss, which may appear as reverberation.
③It may be accompanied by tinnitus and/or and a feeling of fullness.
④Vestibular function examination: there may be spontaneous nystagmus and/or abnormal vestibular function.
⑤ Exclude vertigo caused by other diseases. Early clinical stage is normal intermittent hearing or mild low frequency hearing loss; middle stage out of 2KHZ, hearing loss in both low and high frequencies; late stage is full frequency hearing loss up to moderate to severe or more, no hearing fluctuation.
Patients with Ménière’s disease need to restrict food intake, diuretics, calcium antagonists vasodilators, etc. have not been proven effective; European RCT trial results support the effectiveness of betahistine in the treatment of Ménière’s disease. After failure of medical treatment, gentamicin intra-dural injection or surgery such as endolymphatic sac decompression, vestibular nerve or vagotomy may be considered.
Diagnostic basis: Refer to the ENT diagnostic criteria mentioned above.
Treatment recommendations.
(1) Symptomatic treatment in the acute phase; the intake of nasal salt can be restricted in the interictal phase.
(2) Surgery may be considered if medical treatment is ineffective.
Labyrinthitis: vertigo can be caused by infection of bone vagus or membrane vagus, and generally divided into 3 types of labyrinthitis.
(1) Limited labyrinthitis: Mostly caused by chronic purulent otitis media or mastoiditis eroding the bone vagus, and the lesion is limited to the bone vagus. The vertigo mostly occurs during postural changes, head shocks, pressure on the ear screen or digging for cerumen in the ear canal, and lasts for several minutes to hours; the fistula test is mostly positive, with normal or hyperactive vestibular function; the hearing impairment is mostly conductive, and in a few severe cases it is mixed.
(2) Plasmacytic vaginitis: predominantly plasma or plasmacytic fibrinoid exudation, which can be the result of untreated limited vaginitis. The degree of vertigo is severe and long-lasting, and the patient prefers to lie on the affected side; the fistula test may be positive; the cochlear damage is more severe than the vestibular damage, and the hearing damage is often sensorineural.
(3) Acute septic vaginitis: septic bacteria destroy the bony vagus and membrane vagus. In the acute septic phase, the patient is bedridden due to severe vertigo; the patient’s hearing decreases sharply; the body temperature is usually not high; however, if there is fever and headache, the patient needs to be alert to the spread of infection into the skull. After the symptoms of the acute phase disappear 2~6 weeks into the compensatory phase, vertigo disappears and the patient is totally deaf and unresponsive to hot and cold stimulation test. All the above 3 cases require early surgery after the infection is controlled.
(iii) Dizziness associated with mental disorders and other systemic disorders
The main manifestation is a sense of self instability, sometimes even a fear of balance disorder, and patients are usually accompanied by a sense of mental unclearness; anxiety symptoms such as difficulty in falling asleep and irritability, easy early awakening, depressive manifestations such as easy fatigue and decreased interest, somatization symptoms such as palpitations, poor sodium, and pain [57], which may be accompanied by excessive sweating and chilliness. The diagnosis can usually be confirmed if the questioning is comprehensive; appropriate targeted ancillary tests are necessary when organic pathology needs to be excluded.
There is some debate as to whether the two are co-morbid or not, as there is a higher percentage of dizziness in patients with anxiety and depression and a higher percentage of dizziness and vertigo with psychiatric disorders. Treatment is mainly anti-anxiety, depression and psychological interventions.
Dizziness associated with other systemic diseases also manifests itself mainly as a sense of instability, and can be triggered by vertigo when the lesion damages the vestibular system. It is seen in: hematological disorders (leukemia, anemia, etc.), endocrine disorders (including hypoglycemia, hypo- or hyperthyroidism, etc.), decreased ejection in cardiac disorders, hypotensive, ionic and acid-base disorders of body fluids from various causes, ocular disorders (ocular muscle paralysis, ocular clonus, significant inconsistency in binocular vision, etc.).
(iv) Unexplained nature
There are still 15%-25% of patients with vertigo in whom the cause is not clear despite detailed history taking, physical examination and auxiliary examinations. It is recommended to follow up such patients along with symptomatic treatment.
Symptomatic characteristics of common vertigo attacks
1. Duration of the attack.
(1) Several seconds or tens of seconds: BPPV, vestibular paroxysm, varicose vertigo, cervical vertigo, epileptic vertigo and pre-syncope, etc.
(2) Several minutes: TIA, MV, vestibular paroxysm, epileptic vertigo, superior semicircular fissure, and varicose vertigo, etc.
(3) More than 20min: Meniere’s disease and MV.
(4) Several days: stroke, vestibular neuritis and MV, etc.
(5) Persistent dizziness: bilateral vestibular hypofunction and psychiatric disorders.
2. Accompanying symptoms.
(1) Cerebral nerve or limb paralysis: posterior cranial fossa or skull base lesions.
(2) Deafness, tinnitus or ear swelling: Meniere’s disease, auditory neuroma, sudden deafness, labyrinthitis, exolymphatic fistula, large vestibular aqueduct syndrome, vestibular paroxysm, otosclerosis and autoimmune inner ear disease.
(3) Photophobia, headache or visual aura: MV.
3. Triggering factors.
(1) Head position change: BPPV, posterior cranial fossa tumor and MV, etc.
(2) Menstruation-related or sleep deprivation: MV, etc.
(3) Large body or tile movement: superior hemimelia and ectolymphatic fistula.
(4) Standing position: postural hypotension, etc.
(5) Object movement in the visual field: bilateral vestibular disease.
4. Frequency of seizures.
(1) Single or first time: vestibular neuritis, brainstem or cerebellar stroke or demyelination, first episode of MV, first episode of Ménière’s disease, labyrinthitis, ectolymphatic fistula and pharmacologic.
(2) Recurrent: BPPV, Meniere’s disease, TIA, MV, vestibular paroxysm, exolymphatic fistula, epileptic vertigo, autoimmune inner ear disease, auditory neuroma, otolithic dysfunction, and unilateral hypoplastic vestibular insufficiency.
V. Diagnostic process.
The diagnostic process of vertigo is shown in Figure 1.
VI. Treatment of vertigo
Etiological treatment: Those with clear etiology should take timely and targeted treatment measures, such as patients with otoliths should be reset by different postural methods according to the different involved semicircular canals; for acute vertebrobasilar artery ischemic stroke, thrombolytic treatment can be carried out for suitable patients with 3-6h onset, etc.
Symptomatic treatment: For vertigo attacks lasting several hours or frequent attacks, patients with severe autonomic reactions and
For those who need clinical bed rest, vestibular depressants are usually needed to control the symptoms. Currently, vestibular depressants are mainly divided into antihistamines (iproniazid, diphenhydramine, etc.), anticholinergics (scopolamine) and benzodiazepines; antiemetics include gastroflucan and chlorpromazine, etc. Vestibular inhibitors work mainly by inhibiting neurotransmitters, but if applied for too long, they can inhibit the establishment of central compensatory mechanisms, so it is advisable to discontinue them when the patient’s acute phase symptoms are controlled; inhibitors are not suitable for use with patients with permanent impairment of vestibular function, and dizziness is generally not treated with vestibular inhibitors [14]. Psychotherapy can eliminate the fear psychology and anxiety and depressive symptoms caused by vertigo, and antidepressant and anxiolytic drugs such as paroxetine should be used when needed.
Surgical treatment: for patients with persistent severe peripheral vertigo that is difficult to be controlled by medication, inner ear surgery should be considered.
Vestibular rehabilitation training: It is mainly for patients with balance disorders due to low vestibular function or loss of vestibular function, which often last for a long time and conventional medications are ineffective. Commonly used trainings include adaptation, substitution, habituation, and Cawthorne-Cooksey training, which aim to rebuild the integration function of visual, proprioceptive and vestibular afferent information, improve the patient’s balance function, and reduce vibration hallucinations.
Other: betahistine is a strong antagonist of histamine H3 receptors, and some European RCT studies have confirmed its effectiveness in the treatment of Ménière’s disease [61-63]. The application of calcium antagonists, Chinese herbal medicines, nicergoline, acetylleucine, ginkgo preparations, and even carbamazepine and gabapentin have been reported for the treatment of vertigo; baclofen, epinephrine, and amphetamine have also been reported to accelerate vestibular compensation.