BPPV is one of the most common causes of dizziness. This type of vertigo is caused by the release of otoconia in the otoconial membrane, which with changes in the position of the head, move to the ampullae of the semicircular canals and activate vestibular sensory hair cells.
Treatment depends on the stage at which the patient is seen. If the patient sees the doctor during an attack or during a relapse, treatment is based on liberatory manoeuvres.
The liberatory manoeuvre consists of mobilising the patient’s head to displace the cupulo- or canalithiasis. This manoeuvre often cures positional vertigo. It can be repeated during another session if the positional vertigo is still present. If the positional vertigo is refractory to two or three correct manoeuvres, the practitioner should revise the diagnosis. These manoeuvres should never be repeated frequently.
Vestibular neuritis is one of the most common causes of peripheral vertigo. It is a good example of sudden unilateral vestibular deafferentation.
This results in the sudden onset of rotary vertigo with nausea and vomiting. It is essential to note that no auditory problems are detected (deafness, tinnitus) when the patient is questioned. The bed examination identifies a spontaneous peripheral nystagmus: the latter is horizontal and rotary, unidirectional and less substantial and less frequent during ocular fixation. The rapid phase of this nystagmus is directed towards the healthy ear as it is a destructive nystagmus. Other aspects of the examination, in particular the neurological examination, are normal.
The caloric and rotary tests confirm areflexia of the horizontal canal nerve. The patient does not respond to hot or cold stimulation, nor to rotating the head horizontally to the damaged side. Otolithic evoked potentials induced by sound stimuli show normal reflexes in the saccules and the sacculospinal pathways in 2/3 of cases. This demonstrates that normal sensitivity is preserved in the saccular nerve. These examinations confirm that the vestibular neuritis most often results from damage to the superior vestibular nerve.
This condition is thought to be caused by viral infection. In some cases the cause may be vascular, particularly in hypertensive patients or those prone to vascular problems.
Treatment serves first and foremost to relieve the patient: the patient is isolated and prescribed major vertigo medication, antiemetics, and even sedatives. Strong doses of systemic corticosteroids and antiviral medication are also often recommended. The patient should be regularly monitored using the different tests referred to above. The VNG and balance tests (EquiTest, static and dynamic posturography) enable the doctor to assess:
1/ vestibular nerve function recovery and
2/ the quality of central vestibular compensation over the weeks following the initial attack.
These tumours are often discovered through imaging conducted after atypical vertigo or other warning signs such as balance disorders, deafness or tinnitus. An otoneurological examination is used to detect which branches of the eighth nerve are damaged. In such cases it is important to conduct an MRI when there is any kind of unexplained unilateral problem in the eighth cranial pair.
Treatment consists of monitoring with MRI, gamma knife treatment or surgery depending on tumour growth, size and location.
Meniere’s disease is a common condition that can be crippling due to the consequences of the vertigo on the patient’s work, family and social life.
The diagnosis is based on four types of argument:
- The onset of major rotary vertigo
- Concomitant unilateral auditory signs:
1) tinnitus causing a non-pulsating buzzing, whistling or humming sensation.
2) perceptive deafness, which, at first, is predominant in low frequencies and fluctuates enormously. This is also accompanied by the feeling of having a blocked ear, fullness or pressure that wanes after an acute attack.
- Predisposing factors: patients often have a specific psychological background that includes stress, anxiety, fatigue and emotional trauma. In general, patients are perfectionists, intelligent and obsessive.
When Meniere’s disease is suspected, a full cochleovestibular examination must be conducted.
Treatment of the vertigo attack is based on patient isolation and administering vertigo medication, a sedative and/or an antiemetic.
Constitutional treatment is aimed at preventing recurring vertigo and is subdivided into conservative, destructive, medical or surgical treatment, according to whether the latter preserves or destroys the patient’s vestibular function.
Destructive treatments serve to destroy the vestibular receptors (chemical labyrinthectomy) or to section the vestibular nerve (vestibular neurotomy).
Gentamicin-type aminoglycosides are used more and more locally. They destroy the vestibular receptors while preserving cochlear function. In practice, gentamicin is injected (2 to 6 injections: chemical labyrinthectomy) under local anaesthetic through the eardrum into the middle ear to achieve definitive relief from vertigo.
There are many causes. The most common causes are multiple sclerosis, vestibular epilepsy, Wallenberg’s syndrome, vertebral basilar insufficiency, hereditary ataxia and anomalies of the cervico-occipital hinge.
Inner ear disorders are common causes of rotary vertigo and unsteadiness. Accompanying signs, the context in which they occur and, most importantly, the VNG examination, will usually enable the doctor to determine the cause. Further examinations, caloric tests, the audiogram, and VEMP often confirm diagnosis and prevent the patient from having to undergo more invasive examinations. Any atypical vertigo combined with non-peripheral nystagmus requires an MRI, the only means of confirming or invalidating the diagnosis suspected following clinical examination. Treatment is aimed at relieving the patient of the vertigo and eradicating their balance problems.