Dizziness is a common presentation of many disease processes and it is, therefore, essential to have a clear understanding of possible differential diagnoses.
Many terms can be used to describe dizziness and it is important to establish what each patient means when they use these terms, a useful question is always “Tell me more…” or “What exactly do you mean by that?”.
Loss of balance
Once you understand the nature of their complaint you can begin to sift through a list of differentials which may be central or peripheral in origin. The most important part of assessing a dizzy patient is to exclude central causes first, as these can be life-threatening.
It is also important to establish if the patient has come to any harm from their dizzy episodes such as frequent falls, car accidents or accidents at work. Dizzy patients must inform the DVLA and may not be insured to drive.
Here we will describe the key points in history taking from a patient complaining of dizziness and then go through some common ENT causes. This list of underlying disease processes is not exhaustive and sometimes a cause cannot be found.
Ask an open question to allow the patient to speak freely about their dizziness and how it affects them.
History of Presenting Complaint
Ask specifically about the first episode, followed by any changes they have noticed in their symptoms over time.
Are there any precipitating or exacerbating factors?
Food, lifestyle factors and hormonal changes
Does anything relieve the dizzy spells?
Are there any associated symptoms?
Aural fullness or pain
Facial asymmetry or numbness
Past Medical History
Specifically ask about risk factors for stroke (heart disease/arrhythmias, previous TIAs/strokes, diabetes mellitus).
Specifically ask about illicit drug use
Alcohol consumption is an important factor
Family history of ischaemic/haemorrhagic stroke, brain tumours, migraines
Benign Paroxysmal Positional Vertigo (BPPV)
This is a very common cause of vertigo. The classical presentation is of sudden onset vertigo with the sensation of “the room spinning” around the patient. When rolling over in bed, the patient may experience extreme nausea and vomiting, but fixating on a point in the room may help settle the symptoms. Episodes last only seconds to minutes but the patient may feel unwell and unsteady for a number of hours. This is usually self-limiting and resolves within 6 weeks if no treatment is given.
Debris from the otoconial membrane of the utricle, known as otoliths, may flow into a semicircular canal and strike the cupula on head movement. This causes a mismatch in the vestibular and ocular stimuli received by the brain resulting in vertigo. The posterior semicircular canal is most commonly affected (>80% of cases).
BPPV is most commonly idiopathic but may be caused by:
Chronic middle ear disease
Spontaneous degeneration of the labyrinth
Risk factors include:
Concurrent Meniere’s disease
The Dix-Hallpike manoeuvre is diagnostic of BPPV, but only the posterior semicircular canal is tested. If the history is typical and Dix-Hallpike is positive further investigations are not required. However, if there is asymmetric hearing loss or atypical nystagmus, imaging is required, either in the form of CT temporal bones or MRI.
Active monitoring – most cases resolve spontaneously within 6 weeks
If Dix-Hallpike is positive, the examiner should go on to perform Epley’s manoeuvre which aims to dislodge the otolith from the posterior semicircular canal. These manoeuvres are successful in abating the symptoms in approximately 90% of cases.
Vestibular rehabilitation with home exercises such as Cawthorne’s manoeuvres.
Vestibular suppression with prochlorperazine. This is only for short term use as it reduces central compensation and can prevent full recovery.
Reserved only for refractory and debilitating disease. There are a number of methods including intratympanic aminoglycosides, vestibular nerve section, posterior canal occlusion and as a last resort, labyrinthectomy.
Meniere’s disease can be unpredictable and severe. When attacks occur, common symptoms include a preceding feeling of aural fullness followed by severe rotatory vertigo and tinnitus. During the episodes patients also complain of hearing loss. This hearing loss is progressive and initially affects low pitch hearing but goes on to affect all frequencies. Episodes last several hours and patients often want to lie down with their eyes closed. Meniere’s is bilateral in 50% of cases. Occasionally loud sounds may exacerbate the symptoms, this is called Tulio’s phenomenon.
Meniere’s is the result of an expansion of the scala media part of the membranous labyrinth known as endolymphatic hydrops. This increased pressure distorts Reissner’s membrane which can rupture. When the membrane ruptures endolymph mixes with perilymph causing excitation of the vestibular system resulting in vertigo. Repeated rupture of Reissner’s membrane damages the Organ of Corti resulting in hearing loss.
Pure tone audiometry – classical picture of low frequency sensory neural hearing loss that is progressive, initially audiograms can be normal
Blood tests – To exclude systemic causes including FBC, TFT, ESR, U&E and syphilis screen (VDRL)
MRI brain – In cases of unilateral hearing loss to exclude other causes
Vestibular suppression with prochlorperazine, this is only for short term symptom relief as it prevents vestibular compensation and delays recovery.
Thiazide diuretics and betahistine reduce the frequency and severity of attacks.
Vestibular nerve section
Labyrinthectomy (bilateral labyrinthectomy results in vestibular hypofunction, patients can become wheelchair-bound and unable to move their heads)
Vestibular Neuronitis or Labyrinthitis
This usually occurs following an upper respiratory tract infection. Patients commonly describe waking up with severe, continuous rotatory vertigo. During the first episode, any movement can exacerbate the symptoms. Episodes can last for days and are often associated with nausea and vomiting. Movements may exacerbate the symptoms but episodes are not triggered by movement. Compensation occurs over weeks to months. Vestibular neuronitis solely affects the vestibular system whereas, in labyrinthitis, hearing loss also occurs.
Vestibular neuronitis is often caused by reactivation of Herpes simplex which resides in the vestibular ganglion following primary infection. The superior division of CNVIII travels through a long bony canal where it is susceptible to ischaemic injury due to swelling (another possible cause).
Other viruses and bacteria can also cause inflammation of the labyrinth.
Routine blood tests and blood cultures are indicated if a bacterial cause is suspected.
In cases of hearing loss, pure tone audiometry can be useful to characterise the severity of this.
MRI of the internal auditory meatus (IAM) is required if suppurative labyrinthitis develops. If a middle ear effusion is present, the fluid should be sent for culture and sensitivities.
CT or MRI is helpful to rule out a central cause in patients with risk factors for an ischaemic or haemorrhagic stroke.
Vestibular rehabilitation exercises
Vestibular suppression with prochlorperazine – short term use only (corticosteroids, antivirals and benzodiazepines are not recommended)
Not usually required as the condition is often benign and self-limiting
Vertiginous or vestibular migraine may or may not be associated with headache, although attacks are often preceded or followed by a headache. Disequilibrium and vertigo can last from seconds to hours and sometimes days but episodes are not associated with tinnitus or hearing loss. Loud sounds and bright lights may worsen symptoms and triggers can often be identified by keeping a symptom diary. Common triggers include stress, poor sleep, hunger, hormonal changes (associated with periods) and diet (bread, processed meats and smoked fish).
Unknown, but the condition is known to run in families and there is an association with Meniere’s disease.
There is usually no abnormality on clinical examination.
All patients should undergo an MRI to rule out a central cause for their symptoms.
Active monitoring with a lifestyle diary to identify and exclude triggers
Calcium channel blockers
No role for surgical management
Superior semi-circular canal dehiscence
Patients usually present with sound or pressure-induced dizziness, imbalance or vertigo. Tulio’s phenomenon (dizziness worsened by loud noises) is characteristic of this condition and patients often avoid noisy environments. Patients sometimes complain of being able to hear their own eye movements (gaze-evoked tinnitus) or pulse. Hyperacusis (increased sensitivity to sound) can occur but is not specific for this condition.
This condition is often due to a congenitally absent or thin layer of bone over the superior semicircular canal. When associated with trauma, dehiscence of the bone over the canal can occur creating a “third window” to the bony labyrinth. This allows intracranial pressure to be transmitted to the membranous labyrinth resulting in symptoms of vertigo.
CT temporal bones can demonstrate an area of dehiscent bone over the superior semicircular canal.
Pure tone audiometry is normal in this condition and helps rule out a retrocochlear cause for vertigo.
Short term vestibular suppression with prochlorperazine
Both open and minimally invasive techniques have been described to repair the dehiscent area of bone or reinforce the round window. However, surgery is reserved for patients with severe and debilitating symptoms.
Vestibular schwannomas (VS) can present with a variety of symptoms due to a pressure effect on the vestibular nerve and surrounding structures. A classical presentation is that of progressive unilateral hearing loss associated with vertigo and tinnitus. Patients may present with symptoms of raised intracranial pressure such as nausea, vomiting and headache. Other cranial nerves close to the cerebellopontine angle (the origin of the vestibular nerve) may be affected including the facial nerve (resulting in facial palsy) or the trigeminal nerve (causing facial numbness). Occasionally patients may present with sudden unilateral hearing loss.
VS is a nerve sheath tumour predominantly affecting the vestibular nerve although they can also affect the cochlear nerve. They are usually slow-growing lesions resulting in progressive symptoms. Symptoms occur earlier if the lesion is within the internal acoustic meatus but can be delayed if the tumour is at the cerebellopontine angle.
Bilateral VS is pathognomonic of Neurofibromatosis type 2.
Pure tone audiometry reveals a unilateral sensorineural hearing loss.
MRI internal auditory meatus is essential in all patients presenting with unilateral sensorineural hearing loss.
Active monitoring with serial imaging if patients have small tumours and good preservation of hearing.
No role for medical management.
The surgical approach depends on the size and location of the tumour and the importance of preserving hearing. Most tumours can be completely excised.
MUST EXCLUDE CENTRAL CAUSES
Central causes of vertigo and dizziness must be excluded in the history, during the examination and with further investigation if appropriate.
Common central causes of vertigo, dizziness and light-headedness include…
Multiple sclerosis (dizziness is the presenting symptom in 5% of cases)
Abnormal blood pressure
Screening questions include:
Are you on any blood thinners?
Have you ever had a stroke or heart attack?
How’s your blood pressure?
Do you suffer from diabetes?
Do you have any weakness or numbness? (constant/intermittent)
How’s your vision?
Characteristics of nystagmus can be a useful way to differentiate between central and peripheral causes of vertigo.
Characteristic of Nystagmus
Bidirectional or PURELY vertical/horizontal
Hall and Colman’s. Diseases of the ear, nose and throat. Fifteenth edition. 2000. Chapter 6 pages 63-70.
Moorhouse et al. An Essential Exam Revision Guide to Diploma in Otolaryngology and Head and Neck Surgery. First edition. 2012. Pages 47-55.
Kuller et al. MasterPass ENT OSCEs a guide to passing the DO-HNs and MRCS(ENT) OSCE. First edition. 2012. Chapter 1 pages 57-60.
Tysome and Kanegaonkar. ENT an Introduction and Practical Guide. Second edition. 2018. Chapter 32 pages 152-160.