Vertigo

Vertigo: What Is It?

Vertigo is defined as the disabling sensation in which the affected individual feels that he himself or his surroundings are in a state of constant movement. It has a reported 1-year incidence of 1.4%. Like syncope Opens in new window, it is a symptom not a diagnosis, and has as many causes. The difficulty is that whereas many of the causes of vertigo are benign, it may be a symptom of serious neurological conditions such as vertebrobasilar stroke.

Aetiology

The causes of vertigo may be divided into peripheral and central. We'll discuss these two as the study progresses.

Clinical Features

It is vital to establish whether the patient is suffering true vertigo, as opposed to pre-syncope, loss of consciousness or mild unsteadiness. It is also necessary to clarify whether they have a sense of continuous motion (vertigo) or whether they fell ‘light-headed’ or ‘dizzy.’ If the patient feels they are moving in relation to their surroundings this is termed subjective vertigo; however, if the patient feels that the surroundings are spinning around them, this is termed objective vertigo.

As previously described, vertigo may be central or peripheral in origin. Peripheral vertigo tends to be more intense and associated with nausea, vomiting, diaphoresis and auditory symptoms such as tinnitus or hearing loss (although hearing loss can rarely occur with vascular insufficiency in the posterior cerebral circulation, as the auditory apparatus is supplied via the anterior inferior cerebellar artery or the posterior inferior cerebellar artery). There may also be a history of ear trauma, barotrauma, ear infection or generalized illness. The onset of the vertigo tends to be sub-acute, coming on over minutes to hours.

Central vertigo tends to be less severe and associated with neurological symptoms and signs such as headache, weakness of the limbs, ataxia, incoordination and dysarthria. These symptoms may be the harbinger of more serious causes, such as cerebellar lesions or demyelinating diseases.

Physical examination concentrates on any positional factors plus a detailed search for neurological signs, in particular nystagmus. This is the main objective sign of vertigo. Any spontaneous movement of the eyes needs to be noted, plus direction and persistence. Peripheral vertigo tends to produce unidirectional nystagmus with the slow phase towards the affected side. In addition, patients with vestibular nystagmus are often able to suppress it by fixating on a stationary object. Cardiovascular examination should focus on the risk factors for central nervous system thromboembolic events, such as arrhythmias, murmus and bruits.

Clinical Investigations

Most patients who present with vertigo do not need laboratory tests, apart from a blood glucose level. If there is a history of trauma or a space-occupying lesion is suspected, then a CT or MRI scan of the brain is indicated. An ECG should also be performed to help rule out arrhythmias if syncope Opens in new window is the possible problem.

Dynamic maneuvers can be both diagnostic and therapeutic. The Dix-Hallpike test can diagnose benign paroxysmal positional vertigo (BPPV). It should not be performed on patients with carotid bruits, and patients must be warned that the test may provoke severe symptoms.

Initially, the patient should be seated upright, close enough to the head of the bed so that when they are supine the head will be able to extend back a further 30–45^o. To test the right posterior semicircular canal, the head is initially rotated 30–45^o to the right. Keeping the head in this position, the patient is quickly brought to the horizontal position with the head placed 30–45^o below the level of the bed. A positive test is indicated by rotary nystagmus towards the affected ear. The test is then repeated on the left side.

Treatment

Treatment depends on the cause. Benign paroxysmal positional vertigo (BPPV) has the classic history of positon-induced vertigo lasting only seconds. If BPPV is suspecte, the Dix-Hallpike test is performed to identify the affected ear.

The Epley maneuver or ‘canalith repositioning maneuver’ aims to move any unwanted particles out of the semicircular canals and thus ease the symptoms for which they are responsible. The steps of this maneuver are:

1. The patient is seated as for the Dix-Hallpike test with the head turned 45^o toward the affected ear.
2. The patient is brought to the horizontal position with the head hyperextended 30–45^o below the bed.
3. The head is gently rotated 45^o towards the midline.
4. The head is then rotated a further 45^o towards the unaffected ear.
5. The patient rolls onto the shoulder of the unaffected side, at the same time rotating the head a further 45^o.
6. The patient is returned to the sitting position and the head returned to the midline.

These movements may induce nystagmus in the same direction as that seen during the Dix-Hallpike test. Be aware that nystagmus in the opposite direction indicates an unsuccessful test. The maneuver may need to be repeated a few times.

Vestibular neuritis is unilateral and thought to be caused by a viral infection or inflammation. Episodes are acute in onset and may be severe, lasting for days, usually associated with nausea and vomiting.

The sense of perpetual movement is present even with the eyes closed, and is made worse by movement of the head. Symptomatic treatment, with medications such as antihistamines, antiemetics and benzodiazepines, is often all that is indicated. If nausea and vomiting are severe, intravenous fluid therapy may be needed. There are some reports of trials using steroids for vestibular neuritis, but this treatment remains unproven.

Acute labyrinthitis may be viral or bacterial in origin. If it is viral, the course and treatment are similar to those of vestibular neuritis. Bacterial labyrinthitis may develop from an otitis media. The key feature here is severe vertigo with hearing loss. Patients are febrile and toxic and require admission for intravenous antibiotics.

Ménière’s disease has the classic triad of vertigo, sensorineural hearing loss and tinnitus. Attacks last from minutes to hours, and may recur with increasing frequency as the disease progresses. It is caused by dilation of the endolymphatic system due to excessive production or problems with reabsorption of the endolymph (endolymphatic hydrops). Medical arrangement traditionally involves salt restriction and diuretics, although a Cochrane Review has questioned the efficacy of this.

Vertebrobasilar insufficiency can produce vertigo, often accompanied by unsteadiness and visual changes. Symptoms may be provoked by head position and often include headache. Importantly, however, patients with cerebeller infarction occasionally present with vertigo without other symptoms or signs of neurological impairment. Treatment involves addressing cardiovascular risk factors as well as anticiplatelet therapy.

Migrainous vertigo is an increasingly recognized condition that is incompletely understood. In the acute setting it poses a diagnostic challenge that will often necessitate exclusion of other central causes for vertigo, such as cerebrovascular disease.