Vertigo is a type of dizziness whereby patients experience the sensation that objects around them are moving when they are not. This is often described as feeling like a spinning or swaying motion and is usually accompanied by nausea and loss of balance. Differentiating between the various causes of vertigo can be difficult, and for this reason it is a common exam topic.

 

Central and peripheral vertigo

The causes of vertigo can be classified as either being central or peripheral, and understanding the distinction between these is essential for management.

Central vertigo is caused by pathology in the cerebral cortex, cerebellum or brainstem. Examples of central causes include cerebrovascular disease, migraine, multiple sclerosis, acoustic neuroma, and alcohol intoxication.

Peripheral vertigo is caused by pathology in the vestibular labyrinth, semicircular canals or vestibular nerve. Examples of peripheral causes include viral labyrinthitis, vestibular neuronitis (vestibular neuritis), benign paroxysmal positional vertigo (BPPV), Meniere’s disease, and herpes zoster (Ramsey Hunt syndrome).

Although there is considerable overlap between the presentation of central and peripheral vertigo, the presenting features provide clues as to the origin of the pathology.

 

Peripheral vertigoCentral vertigo
Sudden onset
More severe vertigo symptoms
Intermittent vertigo symptoms
Severe nausea and vomiting
Positional vertigo that is affected by head movement
Absence of associated focal neurology
Nystagmus away from the side of the lesion
Hearing can be impaired (Meniere’s disease and labyrinthitis)
Gradual onset
Milder vertigo symptoms
Constant vertigo symptoms
Milder nausea and vomiting
Fixed vertigo that is not affected by head movement
New-onset headache may be present
Presence of associated focal neurology
Nystagmus towards the side of the lesion
Hearing usually intact (but can have unilateral acute hearing loss in some cases)

 

Red flags and indications for urgent referral

It is crucial when assessing patients with vertigo to exclude red flags that would warrant urgent referral for investigation of a possible central cause, e.g. cerebrovascular accident:

  • Unilateral acute hearing loss
  • Abnormal neurological clinical features e.g. CN palsies, diplopia, dysarthria, truncal ataxia, gait disturbance
  • New onset headache
  • Vertical nystagmus
  • Normal vestibulo-ocular reflex on head impulse testing

 

Severe nausea and vomiting and an inability to tolerate oral fluids or symptomatic drug treatment is also an indication for an urgent referral/admission.

 

Vestibular neuronitis and labyrinthitis

The terms vestibular neuronitis (or neuritis) and labyrinthitis are frequently used interchangeably; however they are two distinct conditions.

Vestibular neuronitis refers to cases where there is inflammation confined to the vestibular nerve and the sensory neurons of the vestibular ganglion alone. This results in vertigo and dizziness, but no alteration in hearing or tinnitus.

Labyrinthitis refers to cases in which both branches of the vestibulocochlear nerve and the labyrinth are affected. This results in a combination of vertigo and hearing loss/tinnitus. Labyrinthitis is less common than vestibular neuronitis.

The features of vestibular neuronitis and labyrinthitis are summarised in the table below:

 

Vestibular neuronitisLabyrinthitis
Infection of vestibular nerve alone
Can be viral or bacterial
Often preceded by sinus infection or URTI
Severe vertigo
Vertigo is non-positional
No hearing loss or tinnitus
Nausea and vomiting common
Nystagmus away from the side of the lesion
Loss of vestibulo-ocular reflex on affected side
Episodes may recur over an 18 month period
Infection of both branches of the vestibulocochlear nerve
Usually attributed to viral infection
Can affect entire inner ear and 8th cranial nerve
Severe vertigo
Vertigo can be positional
Can be sensorineural hearing loss and tinnitus
Nausea and vomiting common
Nystagmus away from the side of the lesion
Loss of vestibulo-ocular reflex on affected side

 

The management of these two conditions is identical:

  • Use prochlorperazine or antihistamines for three days only
  • Longer treatment than 3 days suppresses vestibular compensation and can delay recovery
  • Referral is indicated if symptoms persist without improvement for >1 week, or symptoms persist for >6 weeks.

 

 Benign paroxysmal positional vertigo (BPPV)

Benign paroxysmal positional vertigo (BPPV) is caused by dysfunction of the inner ear. The otoliths situated there become dislodged from their usual position within the utricle, and migrate over time into one of the semi-circular canals. These detached otoliths continue to move after head movement has stopped, resulting in vertigo from the conflicting sensation of ongoing movement with other sensory inputs.

The majority of cases of BPPV are idiopathic, but a cause can recognised in approximately 40% of cases, and these include:

  • Head injury
  • Spontaneous labyrinthine degeneration
  • Post-viral illness
  • Middle ear surgery
  • Chronic middle ear disease

 

The main clinical features of BPPV are

  • Provoked by head movement, rolling over and upward gaze
  • Brief episodes – last less than 5 minutes
  • Symptoms typically worse in the mornings
  • No hearing loss or tinnitus
  • Nausea common, vomiting rare
  • Positive Dix-Hallpike test

 

The Dix- Hallpike test can be used to confirm the diagnosis of BPPV. The following short video by Dr Christopher Chang demonstrates how this test is performed:

 

There is no proven benefit for the use of vestibular suppressant medications in the management of BPPV. These medications do not improve symptoms or reduce the duration of the disease.

The treatment of choice for BPPV is the Epley manoeuvre. It aims to reposition otoliths back into the utricles from the semicircular canals. A 2014 Cochrane review concluded that the manoeuvre is a safe, effective treatment for BPPV, with a number needed to treat of 2-4. The following short video by Dr Christopher Chang nicely demonstrates how the Epley manoeuvre is performed:

 

Referral for patients with BPPV is indicated if:

  • The treating clinician is unable to perform or access the Epley manoeuvre
  • The Epley manoeuvre has not been beneficial after repeated attempted (minimum two)
  • The patient has been symptomatic for >4 weeks
  • The patient has suffered >3 periods of BPPV

 

Meniere’s disease

Meniere’s disease is a disorder of the inner ear caused by a change of fluid volume within the vestibular labyrinth. Progressive distension of the labyrinth (endolymphatic hydrops) causes damage to the vestibular system, causing vertigo, and/or the cochlea, causing hearing loss. The classical triad of symptoms associated with Meniere’s disease is vertigo, hearing loss and tinnitus.

The main clinical features of Meniere’s disease are

  • Attacks of vertigo usually 2-3 hours in duration
  • Attacks of vertigo last less than 24 hours
  • Hearing loss (usually gradually progressive and unilateral)
  • Associated tinnitus common
  • Sensation of fullness or pressure in ear(s)
  • Nausea and vomiting common
  • Nystagmus away from the side of the lesion
  • Increased prevalence in migraine sufferers

 

The management of Meniere’s disease should aim to alleviate acute attacks, reduce the severity and frequency of attacks, and to improve hearing and reduce the impact of tinnitus. Patients should be referred routinely to ENT if the diagnosis is suspected.

Management of acute attacks:

  • Prochlorperazine, cinnarizine, cyclizine can help to reduce nausea and vertigo symptoms (If vomiting is present buccal or intramuscular administration may be needed)
  • If the symptoms are severe, hospital admission may be needed to avoid dehydration.

 

For prophylaxis:

  • Lifestyle measures can be helpful.
    • Avoid caffeine, chocolate, alcohol and tobacco.
    • Excessive fatigue should be avoided.
    • Low-salt diet possibly beneficial
  • Drug prophylaxis is with betahistine (initially 16 mg TDS) to reduce the frequency and severity of attacks.
  • Diuretics can be beneficial, but are not usually recommended for use in the primary care setting.

 

Acoustic neuroma

An acoustic neuroma (also commonly referred to as vestibular schwannoma) is a benign primary intracranial tumour of the myelin-forming cells of the vestibulocochlear nerve. The tumour is classically situated close to the cerebellopontine angle, and large tumours can compress other cranial nerves in the area, most commonly the trigeminal nerve (CN V).

The clinical features of an acoustic neuroma include:

  • Gradually worsening unilateral sensorineural hearing loss
  • Facial numbness and tingling (CN V
  • Tinnitus
  • Vertigo
  • Nystagmus towards the side of the lesion

 

In addition, the patient may also have a history of headaches, and rarely the 7th, 9th and 10th cranial nerves may be involved.

Patients with a suspected acoustic neuroma should be referred to ENT or neurosurgery for an MRI and further assessment. The main treatments are surgery, radiotherapy and stereotactic radiosurgery.

 

Vestibular Migraine

Migraine is one of the most common neurological complaints with a lifetime prevalence of 16%. Vestibular migraine is the association of migrainous symptoms with recurrent vertigo and/or unsteadiness.

It is one of the commonest causes of vertigo and the most common cause of spontaneous episodic vertigo. Vestibular disturbance can predominate as part of the aura presentation or can occur outside of the classic aura timing. The duration of attacks can vary from seconds to days, usually lasting minutes to hours, and they often occur independently of headaches. Vestibular migraine is largely a diagnosis of exclusion. Long-lasting individual attacks are treated with antivertiginous and antiemetic drugs. Specific antimigraine drugs are unlikely to be very effective for rescue. The mainstay of the management of vestibular migraine is prophylactic medication.

Referral to neurology may be needed to confirm the diagnosis, particularly if the patient is presenting acutely for the first time.

 


Thank you to the joint editorial team of MRCGP Exam Prep for this exam tips post.

Header image used on licence from Shutterstock

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