Page 82 - IDF Journal 2023

IDF – Webinar Series IDF News – Spring 2023
Vertigo and Meniere’s Disease
Mr Solomon Abramovich
The history and timing of vertigo and hearing loss
are very important, and the following factors should be taken into consideration: the duration, onset, frequency and severity along with aggravating factors like head movements, special positions and walking.
Associated otological symptoms such
as hearing loss, fullness, tinnitus and ear discharge are common. Relevant medical history should be taken and the following examinations including examination of the ear, neurological examination, eye movements, Romberg test and gait, Hallpike’s manoeuvre and head thrust test should be done. Central vertigo, otherwise known as the disturbance of the vestibular ocular pathway in the brain, should be considered.
Audiometric and vestibular function tests are necessary to clarify peripheral failure or uncompensated vestibular dysfunction. Caloric balance testing identifies hypofunction of the lateral semi-circular canal. The Vestibular Head Impulse Test with recording of eye movement response in three directions, identifies whether there is a hypofunction separately in each semi-circular canal of balance.
Symptoms requiring patient referral
to a specialist without delay include patients who display vertigo and other neurological symptoms and signs, such as occipital headache, vertical nystagmus and sudden hearing loss. Isolated vertigo is unlikely to be due to central causes,
for example vascular, demyelination or tumours. Among patients with dizziness without other neurological symptoms and signs, only 0.7% were found to have had a stroke or TIA (Kerber KA et. al 2006). MRI is often of little use in establishing the cause of isolated symptoms of vertigo.
The most common causes of peripheral imbalance and vertigo (lesion in the labyrinth and nerve) are benign positional
paroxysmal vertigo (BPPV) (43%), vestibular neuritis (40%) and labyrinthitis, Meniere’s disease (<10%), vestibular schwannoma/acoustic neuroma, labyrinthine concussion, vascular causes, vestibular ototoxicity and chronic otitis media with destructive cholesteatoma leading to erosion fistula of the lateral semi-circular canal. Recurrent vertigo
in the presence of normal hearing and
a past history of migraine could be a manifestation of vestibular migraine and it is a diagnosis by exclusion.
Positive diagnosis of BPPV can be made with Dix-Hallpike Positional Test and Epley Manoeuvre by dislodging a floating otolith particle in the semi-circular canal of balance into the vestibule. The success of the first attempt is about 80%. The recurrence of BPPV is more common following head injury than in idiopathic cases. The diagnosis of vestibular neuritis can be made with the head thrust test. However, in patients with cervical spine problems these tests should be avoided.
Sudden hearing loss with imbalance may be present in up to 20% of patients with vestibular neuroma and unless one can confidently exclude infection or trauma, the patient with unilateral or asymmetric sensorineural hearing loss should have an MRI scan of the internal auditory meatus and cerebellar pontine angle.
Vestibular neuritis is usually a viral inflammation of the vestibular nerve
and the vestibular ganglion with sparing of the cochlear nerve, which is more common than labyrinthitis. It presents with episodes of true rotatory vertigo with delayed recovery, nausea and vomiting. Sudden sensorineural hearing loss with vertigo is labyrinthitis and not vestibular neuritis because the hearing loss is due to lesions of the receptors and neurones in the cochlea.
Sudden sensory neural hearing loss should be treated with a course of Prednisolone within 3-4 weeks of noticing the hearing loss. Intratympanic injections of steroids could be given to patients who have diabetes or severe gastric problems. They are absorbed from the middle ear cavity into the cochlea through the round window membrane. Whilst helpful for hearing loss, there is no good evidence that steroids speed up the clinical recovery of vertigo.
One should avoid vestibular sedatives once the acute stage has passed. Vestibular compensation and recovery could be speeded up and enhanced with balancing exercises which focus on central integration of visual input, proprioception, superficial sensation and labyrinthine activity. In poorly compensated patients, cognitive behavioural therapy may be necessary as some patients may exhibit avoidance behaviour, anxiety and depressive disorder, therefore calling for a more holistic approach.
A triad of symptoms of recurrent vertigo, sudden or fluctuation of hearing loss, tinnitus and sometimes a pressure in the ear is likely to be a diagnosis of Meniere’s disease. MRI scan for the diagnosis of endolymphatic hydrops may show the non-enhancing expanded endolymph compartment in the cochlea and vestibule which is thought to be pathological in Meniere’s disease.
Meniere’s disease in an acute phase should be treated with vestibular sedatives. A salt restricted diet may be of some help in underlying endolymphatic hydrops. Intratympanic injections of steroids is practiced by some surgeons. Intratympanic injections of vestibular toxic and ototoxic gentamicin could be considered in some patients who have unserviceable unilateral severe hearing loss in order to stop frequent recurrent disabling vertigo by destroying the remaining distorted vestibular labyrinth.
A period of imbalance will follow relying on one labyrinth only. However, in younger patients under 60 years old, central vestibular compensation will take place within months, aided by vestibular rehabilitation exercises.
Mr Solomon Abramovich MSc LRCP MRCS FRCS
Consultant ENT Surgeon
Platinum Medical Centre, Wellington Hospital, London, NW8 7JA
9 Harley Street London W1
T: 0207 9350604
E: solomon@abramovich.og.uk
82