Introduction

All too often the patient presents to the doctor complaining of ‘dizziness’, which is a ‘non-word’ as it is ambiguous and means different things to different people. ‘Dizziness’ can mean ‘true vertigo’ but it can also mean confusion, tiredness, light-headedness, loss of balance, headache, hunger or any other variety of words idiosyncratic to any particular patient. It follows that there can be no correct approach until the definition relevant to that patient has been established.

Patients will often get angry when asked to define ‘dizziness’ and, all too often, the doctor will accept ‘dizziness’ to mean something different to what the patient is trying to report. The doctor will translate ‘dizziness’ to mean ‘vertigo’ when in many cases it does not. As with all neurology, it is the history that is so important. The word ‘giddy’ is not a substitute for ‘dizzy’, and likewise is ambiguous and a ‘non-word’ meaning different things to different people.

Vertigo is a very specific word derived from two words, namely ‘vertere’, to turn and ‘igo’, a condition.¹ It implies an unreal sensation of motion, meaning that the patient perceives the sensation of movement when, in fact, the patient is stationary. Thus history taking when exploring what might prove to be true vertigo must explore the question of unreal motion, which can be objective, implying the external environment is perceived as moving, or subjective, in which the patient feels as if they are moving while the surroundings are stationary. Both equate to vertigo.

Perhaps the most common cause for vertigo to be referred to a neurologist is that of benign positional paroxysmal vertigo (BPPV), which can and should be successfully treated by the family doctor, although more often than not it does result in referral to either a neurologist or ear, nose and throat (ENT) surgeon.

What follows is a discussion of vertigo that will allow the general practitioner to take control in most instances. It aims to demystify vertigo and empower the general practitioner.

Taking the History

The most important part of history taking has already been discussed. It is absolutely imperative for both patient and doctor to read from the same text. Message sent must equate to message received. Causes for loss of balance can be quite different to those for vertigo. Differentiation will dictate appropriate management, namely diagnosis and its treatment.

Having confirmed that the basis for presentation is vertigo, the doctor needs to clarify its cause. The type and nature of the vertigo will help with diagnosis. Vertigo that occurs in bed, particularly after turning over in bed either right to left (or the converse), is more likely than not, going to be BPPV (see Table 8.1). Vertigo that follows an upper respiratory tract infection will probably be caused by labyrinthitis or vestibular neuronitis (see Table 8.1). Vestibular neuronitis (labyrinthitis) is usually of acute or subacute onset, causing rotatory vertigo together with nausea and postural loss of balance.

TABLE 8.1 Peripheral causes of vertigo

Vertigo associated with profound vomiting and deafness may be a case of Ménière’s disease (see Table 8.1). Ménière’s disease often has a greater problem with tinnitus, which may precede the complaint of loss of hearing. Other peripheral causes of vertigo are fairly rare (see Table 8.1).²

When considering vertigo, one should not overlook motion-induced vertigo that may relate to either peripheral vestibulitis or BPPV. Psychogenic causes of vertigo, as are reported in the patient who claims seasickness even when watching the ocean from dry land, may need desensitising and referral is warranted. Psychogenic vertigo may also occur in conjunction with panic disorders or hyperventilation.

There are also central causes of vertigo (Table 8.2),³ acknowledging that vertigo may be provoked by dysfunction anywhere along the vestibulo-cochlear pathway. This travels from the receptors in the ears, which record motion and position within the environment, and travel along the 8th cranial nerve to the pontine, brainstem connections. Hearing is also dependent upon competence of the 8th cranial nerve and, with mutual passage, both can be ‘interrupted’ by common aetiologies.

TABLE 8.2 Central causes of vertigo

Perhaps the most common central cause of vertigo, often associated with ataxia, incoordination and other definitive symptoms, is the ingestion of toxic amounts of substances such as alcohol or medications; for example, anti-epileptic medications. These causes will often have other associated histories that make their diagnosis quite straightforward (see Table 8.2).

Damage to the pontine or cerebellar connections, as may occur with trauma, ischaemia (be it transient ischaemic attack or stroke), tumours of the cerebello-pontine angle (such as acoustic neuromas or pontine tumours like gliomas) or vascular anomalies, can all provoke true vertigo.⁴ Lesions in the brainstem may also have other cranial nerve abnormalities.

Tumours located in the cerebellopontine angle, such as acoustic neuromas or schwannomas, may evoke vertigo. The onset of symptoms may be slower than is the case with other causes. Less common causes of central vertigo may include migraines or multiple sclerosis, but the history should be self-explanatory. Vascular malformations may cause centrally-induced vertigo.

From the above it is established that vertigo can result from lesions anywhere along the vestibulo-cochlear pathway. Knowing the symptoms that attach to each location may enhance diagnostic acumen (see Table 8.3).

TABLE 8.3 Vertigo-associated symptoms that may assist with localisation

Examination

Examination starts at the time of calling the patient into the consultation. Coordination and gait ataxia should have been noted even before talking to the patient. How the patient stands up from the chair or whether they heard their name being called are all valuable signs.

The history will direct attention in the appropriate direction. Cranial nerve examination is the usual formal starting point. The ophthalmoscope is particularly useful. It may allow the definition of nystagmus even in the primary position, as patients often have difficulty focusing on a distant object with the bright light of the ophthalmoscope. Evidence of raised intracranial pressure may suggest a brainstem or cerebellar pontine angle space-occupying lesion if vertigo is the initial complaint. Ophthalmoplegia may suggest multiple sclerosis; while 6th or 7th cranial nerve deficit may imply pontine lesion; and deafness suggests vestibulo–cochlear damage, either centrally or peripherally.

Having used the ophthalmoscope it is wise to also examine the ears with an otoscope. The tympanic membrane should be viewed for inflammation. Signs of previous damage with perforation of the drum may be seen. There may be associated pus. Pressing on the tragus of the ear may provoke vertigo, suggestive of perilymphatic fistula (Hennebert’s sign).

Central subtle nystagmus, provoked during ophthalmoscopic examination and possibly not seen otherwise, has already been alluded to. Horizontal nystagmus may be either central or peripheral but if it always presents as the fast component moving to the same unilateral direction irrespective of eye position, it suggests peripheral cause for nystagmus. Vertical nystagmus, especially down-beat nystagmus, suggests a central cause.

One of the best-known tests, used specifically for BPPV, is Hallpike’s manoeuvre. In this the patient sits upright on the examination couch, is drawn back quickly and advised to keep the eyes open. The head is turned such that the ear is lowermost and the head is held at an angle of 45° to the horizontal. The patient is asked to keep the eyes open and to look down to the floor. This evokes a torsional affect on the calcium carbonate laden hairs in the inner ear, causing a sensation of rotation towards the lowermost ear, which occurs after a brief latent period. This is repeated so that both sides are tested (see Fig 8.1).⁵ Absence of the latent period is more indicative of a central cause for the vertigo.

FIGURE 8.1 Hallpike’s manoeuvre.

Other useful tests include the ‘head impulse test’ and the Fukuda-Unterberger test.⁶ The ‘head impulse test’ assesses acute vestibulopathy with head turn to the affected ear evoking a delayed response with the need for a corrective saccade, eye movement, to maintain focus on an object. The Fukuda-Unterberger test causes the patient to deviate to the affected side when ‘marking time’, namely stepping or marching on the spot.

Romberg’s test has the patient standing to attention in military fashion, closing their eyes. This will evoke enhanced dysequilibrium rather than vertigo. The navy has refined this test to have the patient stand with one foot in front of the other (heel touching toe) with arms crossed over the chest, known as Heightened Romberg’s test. If the patient is already unsteady this test will add nothing: its original use was for testing proprioception in patients with tabes dorsalis rather than vertigo. Personal preference dismisses use of Romberg’s test when assessing vertigo, but its discussion was thought necessary as most general practitioners insist on its inclusion in the assessment of patients with vertigo.

Investigations

Most investigations, such as vestibular function studies, brainstem-evoked responses or even MRI, are beyond general practitioner involvement but are not usually routinely indicated in the assessment of vertigo.

The majority of patients with vertigo do not need sophisticated testing and the symptoms will be self-limiting. If this is not the case then specialist referral is appropriate.

Treatment

As already stated, the majority of cases of vertigo, especially those of peripheral aetiology—such as labyrinthitis—are self-limiting and will only require symptomatic assistance. Such treatment may adopt Maxolon® (metoclopramide hydrochloride) given as 5–10 mg t.d.s. for adults or Stemetil® (prochlorperazine maleate) 5 mg t.d.s., as may be needed. In severe cases parenteral administration may be necessary.

If these fail, Serc® (betahistine dihydrochloride) given as 8–16 mg t.d.s. may give symptomatic relief. Avomine® (promethazine theoclate) is used especially in motion sickness but may also be helpful with vertigo in a dosage of 25 mg up to q.i.d.

Treatment of BPPV does not usually require pharmacologic intervention unless the vertigo is so intrusive as to preclude quality of life. The most effective intervention is to use fatiguing exercises (see Fig 8.2) and the BPPV is also usually self-limiting, although it may recur. The best-known manoeuvre is the Epley manoeuvre, but it is not the one personally favoured. The one favoured is self-administered by the patient and is a variant of the Semont manoeuvre. The patient sits on the edge of the bed and drops to one side, waits for the vertigo and associated symptoms to improve, and then sits up again before performing the identical drop to the opposite side (see Fig 8.2). The patient does this, dropping to each side five to ten times in the morning upon waking and before getting up from bed, and at night before going to sleep.

FIGURE 8.2 Fatiguing exercises in benign paroxysmal positional vertigo.

This allows the deposits of calcium carbonate that attach to the hairs in the inner ear to be dislodged and thence reabsorbed. The described procedure is usually very effective and will empower the general practitioner to treat BPPV without need to refer the patient to a specialist, once a positive Hallpike’s manoeuvre has confirmed the diagnosis. It should be remembered that the procedure may evoke nausea and vomiting, so it is wise to advise the patient to have a receptacle, such as a bucket, available by the bed when performing the manoeuvre.

Ménière’s disease requires specific intervention and usually requires specialist involvement both for diagnosis and treatment. It is caused by dilatation of the endolymphatic organ, which causes the vertigo, tinnitus, feeling of fullness in the ears and impaired hearing. This is the most debilitating form of vertigo, often necessitating bed rest and antiemetics such as Maxolon®, Stemetil® or Serc®. Patients are prescribed a low salt diet limited to less than 3 g per day and may require use of a diuretic, such as hydrochlorthiazide at a dosage of 25 mg per day.

Serc® (betahistamine) acts as a vasodilator thought to increase vascular supply to the inner ear, although it may also have other benefits for Ménière’s disease, at a dosage of 8–16 mg b.i.d.

Other treatments, such as surgical intervention (with endolymphatic sac decompression or nerve section) are beyond general practitioner involvement, as is intra-tympanic gentamicin in those with deafness.

The remaining treatments of vertigo are dependent upon the underlying diagnoses, which demand primary attention. Symptomatic intervention, as discussed above, remains relevant but is secondary to treating the condition that provoked the vertigo. The most important message is to remain within one’s comfort zone and, if in doubt, it is time to involve a specialist when that comfort zone is breached.

Conclusion

This chapter has aimed to demystify vertigo and to show that the bulk of vertigo remains within the domain of the general practitioner to manage. Exact history is imperative to ensure that the patient truly is complaining of vertigo rather than many other conditions also covered by the word ‘dizziness’. Once that is confirmed then the majority of causes are self-limiting and peripheral, such as vestibular neuronitis or BPPV. Both of these are properly managed by the general practitioner, but when in doubt the involvement of a specialist is warranted.