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Dizziness And/Or Vertigo Which Are Not Always Easy to Differentiate

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Dizziness And/Or Vertigo Which Are Not Always Easy to Differentiate PRESCRIBING IN PRACTICE n A practical approach to managing the dizzy patient Diego Kaski PhD, MRCP S P A variety of common causes L can lead to dizziness and/or vertigo which are not always easy to differentiate. Here we review these causes with a focus on making a positive diagnosis izziness accounts for over 20 per cent Dof GP visits in the UK and is associ - ated with significant morbidity. 1 Although in the acute setting the most frequent diagnostic errors concern differentiating central from peripheral causes of vertigo, 2 even when a peripheral cause of vertigo is identified, it is often incorrectly labelled as “viral labyrinthitis” to encompass most inner ear disorders of presumed benign Caloric reflex test of the vestibulo-ocular reflex origin. A good long-term clinical outcome settings. When making a diagnosis in in these patients depends on a correct ini - such patients, it may be helpful to have tial diagnosis. Here we will review the com - in mind these common diagnoses and mon causes of dizziness with a focus on determine into which the patient best fits, making a positive diagnosis and initiating rather than attempting to formulate a appropriate treatment. large differential based on the history and examination findings. What does the patient mean by “dizziness”? Benign paroxysmal positional vertigo Vertigo is simply the illusion of movement, Benign paroxysmal positional vertigo but patients often use the terms “vertigo” (BPPV) is the commonest cause of dizzi - and “dizziness” to describe a variety of ness among the general population, with subjective sensations. If the patient finds an incidence of 64 per 100,000 popula - it difficult to explain their sensation, offer tion per year. 3 Although it is commoner in words like “merry-go-round”, “rocking like the elderly, 4 it can affect people of any on a boat”, “unsteadiness” or “light-head - age but in children migraine or malig - edness”. The duration and time course of nancy should be excluded first. BPPV is vertigo may not be helpful because the characterised by brief episodes of vertigo subjective recall of time is inaccurate, and imbalance associated with nystag - particularly when episodes are brief (sec - mus. Nausea may occur but vomiting is onds or minutes). rare. While a history of recurrent episodes of vertigo triggered by movement (looking Common causes of acute up, bending down, or turning over in bed) vertigo suggests BPPV, the diagnosis can only be Table 1 summarises the commonest confirmed with the Dix–Hallpike manoeu - causes of vertigo in acute and chronic vre or its modified form. BPPV is caused prescriber.co.uk Prescriber 19 June 2015 z 27 n PRESCRIBING IN PRACTICE l Vertigo Diagnosis Clinical features Examination Investigation Treatment Peripheral Benign Sudden onset brief attacks of Positive Hallpike manoeuvre Nil Particle repositioning manoeuvre paroxysmal spinning vertigo, and with vertigo, and nystagmus (Epley or Semont) positional imbalance triggered by (torsional and upbeat for vertigo (BPPV) changes in head position posterior canal BPPV) (bending down, looking up, or turning over in bed) Vestibular Vertigo, nausea/vomiting and Unidirectional horizontal Nil Bedrest and anti-emetics for neuritis imbalance developing over (+ torsional) spontaneous Diagnosis can be maximum of 3 days. Encourage minutes to hours nystagmus. Abnormal head confirmed with mobility early. Symptoms are worse on impulse test, when turning bithermal caloric Vestibular rehabilitation if movement the head towards the side symptoms persist Constant oscillopsia initially of the lesion (hours) Imbalance Meniere’s Sudden onset severe vertigo, Spontaneous nystagmus with Audiogram +/- High-dose betahistine, disease nausea, vomiting, imbalance, horizontal/torsional caloric and intratympanic dexamethasone hearing loss, tinnitus, and component. Abnormal head vestibular evoked or gentamicin aural fullness impulse test, impaired hearing myogenic potentials Central Vestibular Episodic vertigo and imbalance Normal, or there may be May require magnetic Anti-migraine prophylaxis migraine often associated with nausea, nystagmus (spontaneous, resonance imaging (propranolol, amitriptyline, photophobia, phonophobia gaze-evoked or positional) (MRI) scan if first topiramate, pizotifen etc ) and aversion to movement. presentation Headache may or may not be present Posterior Sudden onset vertigo, Gaze-evoked nystagmus, Computed Treatment of stroke circulation headache, vomiting and broken smooth pursuit, tomography or MRI stroke imbalance limb ataxia, gait ataxia, brain positional downbeat nystagmus Non-vestibular Postural Recurrent episodes of Usually normal Postural blood Adequate hydration, reducing or hypotension dizziness, lightheadedness, pressure stopping offending medication, or imbalance. Worse in the recordings compression stockings, tilting morning. Triggered by head of bed. standing from sitting, or Fludrocortisone for resistant sitting from lying orthostatic hypotension Anaemia Recurrent episodes of light- Pallor Full blood count Treatment of underlying cause; headedness, often iron replacement; blood associated with palpitations. transfusion May present with blackouts Anxiety Episodic or chronic dizziness, Normal Thyroid function Reassurance, explanation of usually a sensation of self- tests, ECG symptoms. Cognitive behavioural motion, accompanied by therapy. Anxiolytics or autonomic symptoms, and antidepressants catastrophic fears. Avoidance behaviour Table 1. Common causes of vertigo in general practice 28 z Prescriber 19 June 2015 prescriber.co.uk Vertigo l PRESCRIBING IN PRACTICE n by calcium carbonate crystals (otoconia, or canaliths) settling within the endolym - phatic fluid of the semicircular canal, almost always the posterior semicircular canal. Horizontal canal BPPV accounts for only 10–20 per cent of cases, and ante - rior canal BPPV 5 per cent. 5 The direction of the nystagmus allows the identification of the affected semicircular canal. In a patient with posterior canal BPPV, the examiner sees upbeat and torsional nys - tagmus beating towards the lowermost ear during this manoeuvre (see Figure 1). PPV can be very disabling and is eas - ily treated, either with the traditional Epley manoeuvre or the Semont manoeuvre, which is easier to perform and equally effective. 6 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 Figure 1. Upbeat and torsional (rotatory) nystagmus beating towards the lowermost ear in role in BPPV management. left-sided posterior canal BPPV Vestibular neuritis or “labyrinthitis” ally rare for VN to recur in the same ber of oculomotor abnormalities (in up to Vestibular neuritis (VN) refers to inflam - patient, in which case a diagnosis of 60 per cent of cases), including nystag - mation of the vestibular nerve with spar - BPPV or vestibular migraine should be mus of a central type ( eg vertical or pure ing of the cochlear nerve, but is often considered. Physical activity should be torsional). Thus, acute brain imaging may mistakenly referred to as “labyrinthitis” encouraged as soon as the nausea set - be required on first presentation. (in which both hearing and balance are tles, with bedrest and anti-emetics rec - Between attacks the examination is nor - affected, and is exceptionally rare). VN ommended for a maximum of three mal. The diagnosis is aided by a previous has an incidence of approximately 3.5 per days. The norm is gradual recovery over history of similar symptoms, or a strong 100,000 population. 8 weeks following a process of central personal or family history of migraine. It presents with a sudden attack of compensation. Lifestyle adjustments to prevent iden - rotational vertigo, nausea, vomiting, and tified triggers may avoid the need for phar - imbalance. The vertigo and nausea typi - Vestibular migraine macotherapy. Where attacks continue to cally last hours to days, during which the A diagnosis of vestibular migraine is not be severe or unacceptably frequent, pro - vertigo is constant, even when the head widely recognised outside specialist prac - phylactic medications can be considered, is held completely still. This contrasts with tice but approximately half of patients with including beta blockers (propanolol), tri - BPPV where vertigo is only induced by classical migraine will report dizziness cyclic antidepressants (amitriptyline), head movements. The imbalance in VN and vertigo, with another 20 per cent ful - antiepileptics (valproate, topiramate, consists of “furniture-walking” type in con - filling the criteria for migrainous vertigo gabapentin), or antiserotonergic (pizo - trast to cerebellar stroke where patients (see Table 2). Patients with vestibular tifen) drugs. Visually-induced dizziness are typically unable to stand. migraine commonly report spontaneous (visual vertigo) is a mal-adaptive strategy Patients with acute VN will have spon - or positional vertigo lasting hours to days. that may complicate vestibular migraine. taneous nystagmus ie , looking straight The typical patient is a migraineur who It should be treated with anti-migraine ahead. The nystagmus of VN is horizontal has noticed a recent increase in prophylactic drugs first, with the addition with some rotatory (torsional) component headache frequency and, over the same of vestibular rehabilitation exercises if and is unidirectional, eg right-beating period, developed dizzy episodes, with required later. whether looking to the left, right, up or
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