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Understanding and managing the dizzy patient

Key learning points:

- Benign paroxysmal positional vertigo is the most common cause of vertigo, and can be easily treated with a bedside repositioning manoeuvre

- Common differential diagnoses in patients presenting with acute vertigo include vestibular migraine, vestibular neuritis, and posterior circulation stroke

- Red flags for patients with vertigo include new onset headache, unilateral hearing loss, cranial nerve or limb signs, and a normal vestibulo-ocular reflex

Dizziness accounts for more than 20% of general practice visits in the UK and is associated with significant long-term morbidity. (1) A good clinical outcome in these patients depends on making the right diagnosis initially, and this requires an understanding of the common causes of dizziness.

To make a diagnosis, the first step is to understand what the patient means by dizziness. Vertigo is the term commonly used by health practitioners. In medical terms, vertigo is simply the illusion of movement, but patients often use the terms vertigo and dizziness to describe a variety of subjective sensations. If the patient finds it difficult to explain their sensation being offered words like merry-go-round, rocking like on a boat, unsteadiness, or light-headedness can help them understand and explain the sensation. The duration of vertigo may not be helpful because the subjective recall of time is inaccurate, particularly when episodes are brief (seconds or minutes).

Causes of acute vertigo

There are a few common causes of vertigo that can be useful for nurses to understand, so they can recognise them when dealing with patients in primary care.

Benign paroxysmal positional vertigo (BPPV)

This is the most common cause of dizziness among the general population (2) and is more common in the elderly. (3) BPPV is characterised by brief episodes of vertigo and imbalance associated with nystagmus - an involuntary eye oscillation. Nausea may occur but vomiting is rare. A history of recurrent brief episodes of vertigo triggered by movement would suggest BPPV, but the diagnosis can only be confirmed with a bedside test that triggers the symptoms; this is the Dix-Hallpike manoeuvre (see Table 1). BPPV is caused by calcium carbonate crystals (otoconia, or canaliths) settling within the endolymphatic fluid of the semicircular canals in the inner ear. These are our angular motion detectors, and the abnormal presence of otoconia within the canal sends erroneous signals of motion to the brain following rapid head movements (looking up, bending down, or turning over in bed). In a patient with BPPV, the patient will report dizziness and the examiner sees nystagmus during this manoeuvre, which confirms the diagnosis.

BPPV can be very disabling but is easily treated, either with the traditional Epley manoeuvre or the Semont manoeuvre, which is easier to perform and equally effective (see Table 1). (4) As these may trigger vertigo in patients with BPPV, clinicians must spend a few moments explaining what is done and why. Note that medications have no role in BPPV management.

Vestibular migraine

A diagnosis of vestibular migraine is not widely recognised outside specialist practice but approximately half of patients with classical migraine will report dizziness and vertigo, with another 20% fulfilling the criteria for migrainous vertigo (see Table 2). Patients with vestibular migraine usually report dizziness that may be present spontaneously at rest, or only be triggered by changes in head position (e.g. when lying down flat). Symptoms may last hours and sometimes days, with gradual recovery. The typical patient is a migraineur who has noticed a recent increase in headache frequency and, over the same period, developed dizzy episodes, with headache and vertigo not necessarily occurring together. Other migrainous features such as photophobia, phonophobia, a dislike for self or external movement, and nausea are often present during the vertiginous episode.

During an attack there may be abnormal eye movements, particularly nystagmus (in up to 60% of cases). Thus, brain imaging with an MRI may be required on first presentation. Between attacks the examination is normal. There may be a history of similar symptoms, or a strong personal or family history of migraine that may aid the diagnosis.

Lifestyle adjustments to prevent identified triggers may avoid the need for pharmacotherapy. Where attacks continue to be severe or unacceptably frequent, prophylactic medications can be considered, including beta blockers (propanolol), tricyclic anti-depressants (amitriptyline), antiepileptics (valproate, topiramate, gabapentin), or antiserotonergic (pizotifen) drugs. Dizziness triggered by visual motion (visual vertigo) is a mal-adaptive strategy that may complicate vestibular migraines. It should be treated with anti-migraine prophylactic drugs first, with the addition of vestibular rehabilitation exercises if required later. Therefore it is helpful for primary care nurses to be able to give advice on this.

Vestibular neuritis or 'labyrinthitis'

Vestibular neuritis (VN) refers to inflammation of the vestibular nerve with sparing of the cochlear nerve (and therefore hearing), but is often mistakenly referred to as labyrinthitis (in which both balance and hearing would be affected). VN has an incidence of approximately 3.5 per 100,000 population. (5)

It presents with a sudden attack of rotational vertigo, nausea, vomiting, and imbalance. The vertigo and nausea typically last hours to days, during which the vertigo is constant, even when the head is held completely still. This contrasts with BPPV where vertigo is only induced by head movements. The imbalance in VN consists of “furniture-walking” type in contrast to cerebellar stroke where patients are typically unable to stand.

Patients with acute VN will have spontaneous nystagmus i.e. present when the eyes are in the straight-ahead position. The vestibulo-ocular reflex (VOR) will also be impaired on the side of the lesion (the area of the abnormal tissue change) and can be evaluated with the 'head impulse test' (6) in a clinic.

Steroids are not used routinely in the UK as it is unclear whether they result in long-term clinical improvement. (7) Physical activity should be encouraged as soon as the nausea settles, with bed-rest and anti-nausea medication recommended for a maximum of three days. The norm is gradual recovery over weeks following a process of central compensation.

Posterior circulation stroke

The abrupt onset of vertigo (within seconds), often accompanied by occipital headache (in up to 50% of cases) should raise the suspicion of a posterior circulation stroke. Other associated signs may include gait or limb ataxia, facial numbness, Horner's syndrome, hearing loss, contralateral hemiparesis and hemisensory loss, suggesting involvement of cerebellar or brainstem structures. Importantly, the head impulse test (that evaluates the integrity of the vestibular nerve) tends to be normal in posterior circulation stroke. Urgent brain imaging is indicated where a posterior circulation stroke is suspected as these patients may require thrombolysis or even surgical intervention.

Meniere's disease

Meniere's disease (MD) is over-diagnosed in general practice. Patients will present with spontaneous, episodic, and disabling vertigo (lasting minutes to hours) in association with unilateral tinnitus, a sensation of fullness in the ear and unilateral fluctuating deafness. This is usually accompanied by nausea and vomiting, with imbalance that may last several days. Examination will reveal nystagmus in the acute phase, the head impulse test may be impaired, and hearing is typically affected. Specialist investigations are required to make a diagnosis of MD, including hearing tests and tests of vestibular function.

High-dose betahistine may have a prophylactic effect on the frequency of attacks of MD, at least in the first year, (8) although its effect on vestibular and audiological function is unknown. There is also weak evidence that intratympanic dexamethasone may reduce attacks of meniere's, without significant systemic side-effects. (9)

Other causes to consider

Patients with postural hypotension and syncope may also express their symptoms of light-headedness using the term dizziness. It is therefore important to ask the patient whether symptoms can occur in bed, or while sitting/lying (e.g. BPPV), or whether they occur exclusively when upright (suggesting postural hypotension). Accompanying symptoms such as chest pain, palpitations, or signs of pallor, and brief loss of consciousness would suggest a non-vestibular cause. Finally, anxiety and panic attacks often manifest as dizziness in patients, where there may also be tingling in the fingertips or around the mouth, and a sensation of chest tightness, difficulty breathing, or hyperventilation. It must remembered that any attack of dizziness, is often accompanied by anxiety, partly due to the connections between the vestibular and limbic systems, partly due to the intensity of such episodes.

Red flags in a patient with acute vertigo

Red flags in cases of acute dizziness include; unilateral hearing loss, abnormal neurological symptoms or signs, new headache, and a normal (head impulse test). If present, more serious causes such as posterior circulation stroke should be considered.

Conducting a successful consultation

For nurses in primary care who come across patients who are suffering from 'dizziness' it is important for them to know how to conduct a relevant and successful consultation, there are a few ways to do this. First it important establish what the patient means by the term 'dizziness', and to enquire about possible triggers, symptom duration, and the pattern - whether episodic (e.g. BPPV or migraine), isolated (e.g. vestibular neuritis or

stroke), or continuous (migraine, decompensated vestibular neuritis, anxiety etc.). Given the interplay between vestibular disturbance sand psychological symptoms, in part related to
the rich connections between the vestibular system and both limbic system and autonomic nervous system, patients with dizziness of any aetiology often report anxiety-related symptoms. It is worthwhile both acknowledging this, but also treating underlying psychological disturbances as these feed into chronic dizziness.


Department of Neuro-otology, Imperial College London

Department of Neuro-otology, The National Hospital for Neurology

and Neurosurgery, London

The Meniere's Society


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