Vestibular Neuritis

Vestibular neuritis which is caused by vestibular nerve dysfunction shows symptoms such as isolated and acute vertigo. Dix and Hallpike in 1952 explained vestibular neuronitis and differentiated it from Meniere’s disease[1]. The most likely etiology that is considered for vestibular neuritis is a viral cause[2]. Vestibular neuritis is seen in 3/2-9% of patients in dizziness centers. The usual onset age of the disease is 30 to 60 years old [3]. There is no significant difference between females and males in the incidence of the disease. Specific signs of vestibular neuritis include vertigo, nausea/vomiting, oscillopsia (motion of surroundings and blurred vision), gait abnormality, unsteadiness and postural imbalance[4]. These symptoms may appear suddenly or within several hours.


In order to detect Vestibular neuritis, initially, neurological disorders, especially those resulting from the brain stem or cerebellum, as well as other hearing impairments, should be ruled out[4]. This would be done by an accurate history taking and appropriate diagnostic tests.

In the early stages of Vestibular neuritis, in addition to the mentioned symptoms, horizontal nystagmus with beating far from the lesion side is seen. Moreover, patients are deviating toward the lesion side especially when walking. Assessments such as the Fukuda stepping test, which are usually performed as a screening of vestibular disorders, are designed based on this fact. In vestibular neuritis, vestibular symptoms are seen in isolation, that is, there are not any symptoms such as hearing loss and tinnitus. It is not a dangerous disease, but it is important because in some central vestibular diseases, which need urgent intervention, similar symptoms are seen. Basic assessments which are routinely performed for diagnosis of vestibular neuritis include hearing evaluation for ruling out other diseases related to vertigo such as Meniere’s disease, videonystagmography and video head impulse test (vHIT). If the patient has other symptoms, the otolaryngologists will also propose further examinations.


Vestibular neuritis treatments are focused on reducing symptoms of nausea, vomiting, nystagmus, and vertigo in the initial stage, the first one to three days after the onset of symptoms, which patient’s symptoms are more severe. In this stage, vestibular suppressants are used. Moreover, corticosteroids are also used to accelerate the improvement of peripheral vestibular function. In the next stages, based on the patient’s symptoms, vestibular rehabilitation would be recommended and performed by an audiologist. The aim of vestibular rehabilitation exercises is to accelerate central vestibular compensation[5]. The required time for vestibular rehabilitation in unilateral vestibular dysfunction is 1-3 months.

  1. Dix, M.R. and C.S. Hallpike, The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Ann Otol Rhinol Laryngol, 1952. 61(4): p. 987-1016.
  2. Baloh, R.W., Clinical practice. Vestibular neuritis. N Engl J Med, 2003. 348(11): p. 1027-32.
  3. Depondt, M., [Vestibular neuronitis. Vestibular paralysis with special characteristics]. Acta Otorhinolaryngol Belg, 1973. 27(3): p. 323-59.
  4. Strupp, M. and T. Brandt, Vestibular neuritis. Semin Neurol, 2009. 29(5): p. 509-19.
  5. Walker, M.F., Treatment of vestibular neuritis. Curr Treat Options Neurol, 2009. 11(1): p. 41-5.

Benign Paroxysmal Positional Vertigo

Benign Paroxysmal Positional Vertigo (BPPV) is the most common cause of vertigo[1]. This disease has the most effective treatment option among vestibular disorders[2]. BPPV is caused by a change in the position of the individual and it has been reported that up to 90% of positioning vertigo/nystagmus are related to BPPV and in 85% of BPPV cases, involvement of posterior canal is seen [3, 4]. The onset of BPPV is usually in the fifth and seventh decades of life [1]. In Tan study (2018) on 500 BPPV patients, the age of disease onset was 56 years-old and it was more prevalent in women [5]. This disease is probably the most common diagnosis in vertigo clinics and is the cause of vertigo in 20-40% of all cases with vertigo [6, 7]. Moreover, it is a comorbid condition in menieres disease, vestibular neuritis and vestibular migraine. The main symptom of BPPV is vertigo that is caused by changes in the head position of the patient in relation to the gravity [8]. Episodes of vertigo in BPPV last 10-20 seconds and occasionally last up to one minute [9]. Most of BPPV patients report that they feel a transient vertigo when they are lying, turning in bed, bending or picking something up from cabinet. These patients do not have any symptom of vertigo when they are not moving. Other problems that are reported with BPPV include disequilibrium which happens in few hours to few days after the vertigo attack and other vague feelings such as light-headedness and feeling of being suspended in the air [10].

Schucknecht, for the first time, described the pathophysiology of BPPV and in 1969 introduced the cupulolithiasis theory based on pathologic studies[11]. In 1979, Hall introduced canalolithiasis theory which was a basis for canalith repositioning maneuvers for treatment of BPPV [12, 13]. In this disease, each of lateral, superior and posterior canals could be involved and type of BPPV is diagnosed based on nystagmus patterns in Dix-Hallpike and other diagnostic maneuvers. Posterior semicircular canal (right side) is usually more affected than lateral and superior canals [1, 14].

The first mention of the disease was by Shakespeare in Romeo and Juliet in Act I, Scene II[15]. In medical articles, the first description of BPPV was by Adler[16] and Then Barany[17] which believed that this disease is the consequence of otolith organs dysfunction. In 1952, Margaret Dix and Charles Hallpike developed a positional test for BPPV[1].

BPPV can be caused by different disorders which damage inner ear and lead to detachment of otolith from utricular macula. However, in most cases, the cause of BPPV is unknown [8]. The primary or idiopathic BPPV is a kind of BPPV which is seen alone is and includes almost 50-70% of BPPV cases. Secondary BPPV is the result of other causes, and the most common cause is head trauma (7-17% of BPPV cases). Other causes of secondary BPPV are viral neurolabiryntitis or vestibular neuronit (up to 15% of BPPV cases), Menieres disease (5%), migraine, otologic or non-otologic surgeries and long-term bed rest [6]. In sum, each inner ear disease which detach otoconia but does not totally damage semicircular canal function can lead to secondary BPPV. Recurrences of endolymphatic hydrops cause macular fibrosis and detachment of otoconia. It has been shown that repositioning maneuvers are a better treatment option for idiopathic BPPV patients [18].

Dix-Hallpike Test

Dix-Hallpike positioning test is designed to stimulate subjective vertigo and nystagmus created by BPPV. Symptoms of posterior canal BPPV are sudden onset and short term vertigo and nystagmus which are caused by changing head position of patient. Dix-Hallpike maneuver only assesses posterior and anterior canal BPPV. For diagnosis of anterior canal BPPV, other maneuvers such as roll maneuver should be used [19].


Medication does not have a significant role in treatment of BPPV, and is prescribed only in the early stages in which dizziness may not be tolerated. In fact, the main effective treatment options of BPPV are rehabilitation maneuvers which in more than 70% of cases lead to complete recovery. It is believed that repositioning maneuvers treat BPPV by moving the otoconia particles from the semicircular canal to the vestibular system, where they are re-absorbed [7]. The number of maneuvers required to treat BPPV range from one to three (with an average of 1.5) maneuvers. However, there are some cases which need 10 or more than 10 maneuvers [20].

Initially, BPPV was treated with vestibular suppressor drugs and restriction of position change in order to prevent vertigo attacks. This type of treatment prolonged the course of the disease. In 1980, Brandt-Daroff exercises were introduced for treatment of this disease in which, patients should perform active exercises. These exercises are known as habituation exercises because patient will be taught to move in to exciting position until there is no symptom. The purpose of these exercises is diffusing the particles of the otoconia into the affected canal, and not necessarily the outflow of these particles from the canal. As the result of these exercises, vertigo and nystagmus subsides. It has been shown that using these exercises, the duration of BPPV treatment decreased to 3-14 days and after this time period, 98% of patients did not have any symptoms. However, most patients do not perform Brandt-Daroff exercises because they cannot tolerate symptoms. BPPV patients were not treated effectively until the late 1980s and early 1990s in which repositioning maneuvers were introduced. In 1998, Semont Liberatory maneuver was introduced. In this maneuver, patient should not move for 2-3 minutes. After 1-2 maneuvers, 73-93% of patients would not have any symptoms. John Epley’s therapeutic maneuver was introduced in 1992. In this maneuver, patient should remain stable for 2-4 minutes. It has been reported that 60-90% of patients were effectively treated with this maneuver. Although a similar success rate has been reported for different types of CRM, one study showed that the effect of the epley maneuver is greater than that of Samont maneuver [21]. In a study, it was shown that home repositioning maneuvers reduce the likelihood of BPPV recurrence[22].

Factors such as depression and anxiety reduce the success of repositioning maneuvers and also increase the likelihood of recurrence of BPPV. In women, the same effect has been observed [23].


  1. Hornibrook, J., Benign Paroxysmal Positional Vertigo (BPPV): History, Pathophysiology, Office Treatment and Future Directions. Int J Otolaryngol, 2011. 2011: p. 835671.
  2. von Brevern, M., Benign paroxysmal positional vertigo. Semin Neurol, 2013. 33(3): p. 204-11.
  3. Hotson, J.R. and R.W. Baloh, Acute vestibular syndrome. N Engl J Med, 1998. 339(10): p. 680-5.
  4. Furman, J.M. and S.P. Cass, Benign paroxysmal positional vertigo. N Engl J Med, 1999. 341(21): p. 1590-6.
  5. Tan, F., C. Bartels, and R.M. Walsh, Our experience with 500 patients with benign paroxysmal positional vertigo: Reexploring aetiology and reevaluating MRI investigation. Auris Nasus Larynx, 2018. 45(2): p. 248-253.
  6. Fife, T.D., et al., Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 2008. 70(22): p. 2067-74.
  7. von Brevern, M., et al., Benign paroxysmal positional vertigo predominantly affects the right labyrinth. J Neurol Neurosurg Psychiatry, 2004. 75(10): p. 1487-8.
  8. Lee SH, K.J., Benign Paroxysmal Positional Vertigo. J Clin Neurol, 2010: p. 6.
  9. Fife, T.D. and M. von Brevern, Benign Paroxysmal Positional Vertigo in the Acute Care Setting. Neurol Clin, 2015. 33(3): p. 601-17, viii-ix.
  10. Kollen, L., et al., Benign paroxysmal positional vertigo is a common cause of dizziness and unsteadiness in a large population of 75-year-olds. Aging Clin Exp Res, 2012. 24(4): p. 317-23.
  11. Schuknecht, H.F., Cupulolithiasis. Arch Otolaryngol, 1969. 90(6): p. 765-78.
  12. Semont, A., G. Freyss, and E. Vitte, Curing the BPPV with a liberatory maneuver. Adv Otorhinolaryngol, 1988. 42: p. 290-3.
  13. Epley, J.M., The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg, 1992. 107(3): p. 399-404.
  14. Silva, C., A.M. Amorim, and A. Paiva, Benign paroxysmal positional vertigo–a review of 101 cases. Acta Otorrinolaringol Esp, 2015. 66(4): p. 205-9.
  15. Kaga, K., “Personal communication: historical discovery of vestibular peripheral system and new insights on bilateral vestibular neuropathy in patients,” Proceedings of the Barany Society XXIII Congress, Paris, France,. July 2004.
  16. Adler, D., Ubeden ‘einseitigen Drehschwindel. Dtsch Z Nervenheilkd, 1897: p. 18.
  17. Barany, R., Diagnose von krankheitserch-eingungen im mereiche de otolithenapparates. Acta Otolaryngol, 1921. 2: p. 5.
  18. Riga, M., et al., Inner ear disease and benign paroxysmal positional vertigo: a critical review of incidence, clinical characteristics, and management. Int J Otolaryngol, 2011. 2011: p. 709469.
  19. Kim, J.S. and D.S. Zee, Clinical practice. Benign paroxysmal positional vertigo. N Engl J Med, 2014. 370(12): p. 1138-47.
  20. Perez, P., et al., Recurrence of benign paroxysmal positional vertigo. Otol Neurotol, 2012. 33(3): p. 437-43.
  21. Lee, J.D., et al., A multicenter randomized double-blind study: comparison of the Epley, Semont, and sham maneuvers for the treatment of posterior canal benign paroxysmal positional vertigo. Audiol Neurootol, 2014. 19(5): p. 336-41.
  22. Ismail, E.I., A.E. Morgan, and M.M. Abdeltawwab, Home particle repositioning maneuver to prevent the recurrence of posterior canal BPPV. Auris Nasus Larynx, 2018.
  23. Wei, W., et al., Presence of Anxiety and Depression Symptoms Affects the First Time Treatment Efficacy and Recurrence of Benign Paroxysmal Positional Vertigo. Front Neurol, 2018. 9: p. 178.
menieres disease

Meniere’s disease

Meniere’s disease is a chronic disease of the inner ear which causes episodes of vertigo and hearing loss. This disease affects many people and is very important because it causes to very severe vertigo. The severity of vertigo is so high that some patients in the first attack of Meniere’s disease feel that they are dying. The positive point is that this severe vertigo will not be repeated so strongly and will subside overtime in a period of 7-10 years.

The disease is largely known and there are many articles about it. However, in some cases the person’s disease is misdiagnosed as the Meniere’s disease. The reason is that although the prevalence of this disease is high, its diagnosis is difficult and a specialized team and appropriate diagnostic tools are required. One of the issues that make it difficult to diagnose this disease is the comorbidity of it with other diseases like vestibular neuritis (VN), benign paroxysmal positional vertigo (BPPV) and migraine. On the other hand, this disease has a progressive course in which in the early stages, all symptoms of the disease are not evident. Moreover, in some patients, all signs are not seen together. Therefore, high knowledge and clinical experience with this disease and other illnesses associated with hearing impairment and dizziness play an important role in diagnosing it.


This disease was first explained by a French physician, Prosper Meniere (1799-1862), in 1861. Before this scientist, it was thought that Meniere’s symptoms were caused by a brain lesion. Prosper Meniere linked these symptoms to a disorder in the inner ear. He and other scientists called it “inner ear glaucoma”[1, 2].

In most cases, these patients with symptoms of sudden onset of dizziness present to the emergency rooms. At this stage, due to accompaniment of hearing impairment with these symptoms, they may be mistakenly diagnosed as “labyrinthitis” or “sudden sensorineural hearing loss”. In these cases, if Vertigo is repeated, Meniere’s disease will be considered in the diagnosis.

Meniere’s disease is divided into two categories. The first one is typical Meniere’s disease in which all cochlear (hearing loss, tinnitus and ear fullness) and vestibular (vertigo and ear fullness without hearing loss or tinnitus) signs are seen. In atypical Meniere’s disease, cochlear signs or vestibular signs are seen[3].

Due to the difficulties in the diagnosis of Meniere’s disease, it is difficult to determine its prevalence and the results of studies are also different. Prevalence of Meniere’s disease has been reported from 3.5 in 100000 to 513 in 100000[4]. Its prevalence in women is 1-3 times higher than in men. This disease is more common in adults and in fourth and fifth decades of their life. Of course, this disease has also been reported in children. In most patients, a family history of the disease is reported. It seems that the disease affects white people of North European descent more than the African and Black races[5, 6].


The main histopathologic correlate of this disease is endolymphatic hydrops which results as the excessive production of endolymphatic fluid or its lower than needed re-absorption. Endolymphatic Hydropse can happen secondary to high blood pressure, metabolic disorders or taking especial medications. Meniere’s disease is a type of episodic and recurrent endolymphatic hydropse that is idiopathic.


The main sign of this disease is its fluctuations and changes in its severity. Common symptoms of typical Meniere’s disease include episodic vertigo which lasts from minutes to hours (with positional vertigo in and between attacks). Moreover, almost all patients, report the sense of pressure in the ear or ear fullness and tinnitus.

Most of patients experience unilateral symptoms and they will experience bilateral symptoms several years after the disease onset.

Although numerous tests and evaluations are used in the diagnosis of this disease, its diagnosis is still clinical. That is, a precise history taking and complete physical evaluation is required. The main necessary evaluations for Meniere’s disease include a thorough audiometric assessment, CHAMP, videonystagmography and electrocochleography. In all of the unilateral cases, Brain MRI with and without contrast is required to rule out other retrocochlear lesions which can lead to hearing loss, tinnitus and vertigo. Temporal bone CT-scanning is of less value in the diagnosis of the Meniere’s disease.

Most of these patients show up-sloping low frequency sensorineural hearing loss which is fluctuating and becomes flat over time. Serial audiograms are very helpful in diagnosis of this disease because in addition to determining the type and form of hearing loss, its fluctuations are confirmed over time.

Patients who manifest the signs of Meniere’s disease must complete hematological tests, including fat and blood glucose tests in order to rule out more common causes of their symptoms.


  1. Knapp, H., A clinical analysis of the infl ammatory aff ectation of the inner ear. Arch Ophthalmol Otolaryngol, 1871. 4: p. 79.
  2. Portmann, G., Vertigo: surgical treatment by opening of the saccus endolymphaticus. Arch Otolaryngol, 1927. 6.
  3. Committee on Hearing and Equilibrium guidelines for the diagnosis and evaluation of therapy in Meniere’s disease. American Academy of Otolaryngology-Head and Neck Foundation, Inc. Otolaryngol Head Neck Surg, 1995. 113(3): p. 181-5.
  4. Alexander, T.H. and J.P. Harris, Current epidemiology of Meniere’s syndrome. Otolaryngol Clin North Am, 2010. 43(5): p. 965-70.
  5. Caparosa, R., Medical treatment of Meniere’s disease. Laryngoscope Investig Otolaryngol, 1963. 73: p. 6.
  6. Nsamba, C., A comparative study of the etiology of vertigo in the African. J Laryngol Otol, 1972. 86: p. 8.