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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 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 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

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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 (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 +/- 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

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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 headache and vertigo not necessarily down. The vestibulo-ocular reflex (VOR) occurring together. Other migrainous fea - Posterior circulation stroke will also be impaired on the side of the tures such as photophobia, phonophobia Posterior circulation stroke is charac - lesion and can be evaluated with the and nausea are often present during the terised by the abrupt onset of vertigo “head impulse test” 9 in the clinic. vertiginous episode, in addition to (within seconds), often accompanied by The utility of steroids in VN remains increased motion sensitivity, ie a dislike occipital headache (in up to 50 per cent unclear 10 and they are not used rou - for self- or external movement. of cases). Other associated signs may tinely in the UK. Of note, it is exception - During an attack there may be a num - include gait or limb ataxia, facial numb - prescriber.co.uk Prescriber 19 June 2015 z 29 n PRESCRIBING IN PRACTICE l Vertigo

should think of possible more serious Definite vestibular migraine causes such as posterior circulation stroke. Hearing and otoscopy are normal in VN and A. Episodic vestibular symptoms of at least moderate severity most other harmless causes of dizziness.

B. Current or previous history of migraine according to the 2004 criteria of the IHS References 1. Yardley L, et al . Prevalence and presenta - C. One of the following migrainous symptoms during two or more attacks of vertigo: tion of dizziness in a general practice commu - migrainous headache, photophobia, phonophobia, visual aura, or other aura nity sample of working age people. Br J Gen Pract 1998;48:1131–5. D. Other causes ruled out by appropriate investigations 2. Royl G, et al . Dizziness in the emergency room: diagnoses and misdiagnoses. Eur Note: Vestibular symptoms are rotational vertigo or another illusory self- or object- Neurol 2011;66:256–63. motion. They may be spontaneous or positional. Vestibular symptoms are “moder - 3. Froehling DA, et al . Benign positional ver - ate” if they interfere with but do not prohibit daily activities. “Severe” vestibular tigo: incidence and prognosis in a population- symptoms do not allow patients to continue daily activities. based study in Olmsted County, Minnesota. Mayo Clin Proc 1991;66:596–601. 4. von Brevern M, et al . Epidemiology of Probable vestibular migraine benign paroxysmal positional vertigo: a popu - lation based study. J Neurol Neurosurg A. Episodic vestibular symptoms of at least moderate severity Psychiatry 2007;78:710–5. 5. Parnes LS, et al . Diagnosis and manage - B. One of the following: (1) current or previous history of migraine according to the ment of benign paroxysmal positional vertigo 2004 criteria of the IHS; (2) migrainous symptoms during vestibular symptoms; (3) (BPPV). CMAJ 2003;169:681–93. migraine precipitants of vertigo in more than 50% of attacks; food triggers, sleep 6. Lopez-Escamez J, et al . [Meta-analysis of irregularities or hormonal changes; or (4) response to migraine medication in more the treatment of benign paroxysmal positional than 50% of attacks vertigo by Epley and Semont maneuvers]. Acta Otorrinolaringol Esp 1999;50:366–70. C. Other causes ruled out by appropriate investigations 7. Kaski D, Bronstein AM. Epley and beyond: an update on treating positional vertigo. Pract Table 2. Diagnostic criteria for vestibular migraine Neurol 2014;14:210–21. 8. Sekitani T, et al . Vestibular neuronitis: epi - demiological survey by questionnaire in Japan. ness, Horner’s syndrome, hearing loss, including audiography and tests of Acta Otolaryngol Suppl 1993;503:9–12. contralateral hemiparesis and hemisen - vestibular function. 9. Halmagyi GM, Curthoys IS. A clinical sign of sory loss, suggesting involvement of Given that the pathophysiological hall - canal paresis. Arch Neurol 1988;45:737–9. cerebellar or brainstem structures. mark of MD is endolymphatic hydrops, 10. Fishman JM, et al . Corticosteroids for the Importantly, the head impulse test tends salt restriction has been used prophylac - treatment of idiopathic acute vestibular dys - to be normal in posterior circulation tically, but this is not supported by evi - function (vestibular neuritis). Cochrane stroke. Urgent brain imaging is indicated dence. 11 Similarly, a Cochrane review of Database Syst Rev 2011;(5):CD008607. where a posterior circulation stroke is sus - diuretics for MD did not support their use 11. Harcourt J, et al . Meniere's disease. BMJ pected as these patients may require in MD. 12 High-dose betahistine may have 2014;349:g6544. thrombolysis or even surgical intervention. a prophylactic effect on the frequency of 12. Thirlwall AS, Kundu S. Diuretics for Meniere's disease or syndrome. Cochrane attacks of MD, at least in the first year, 13 Database Syst Rev 2006;(3):CD003599. Ménière’s disease although its effect on vestibular and audi - 13. Strupp M, et al . Long-term prophylactic Ménière’s disease (MD) is overdiagnosed ological function is unknown. There is treatment of attacks of vertigo in Meniere's in general practice. Patients will present also weak evidence that intratympanic disease – comparison of a high with a low with spontaneous, episodic and disabling dexamethasone may reduce attacks of dosage of betahistine in an open trial. Acta vertigo (lasting minutes to hours) in asso - Ménière’s, without significant systemic Otolaryngol 2008;128:520–4. ciation with unilateral tinnitus, aural full - side-effects. 14 14. Boleas-Aguirre MS, et al . Longitudinal ness and unilateral fluctuating deafness. results with intratympanic dexamethasone in This is usually accompanied by nausea Red flags in a patient the treatment of Ménière's disease. Otol and vomiting, with imbalance that may with acute vertigo Neurotol 2008;29:33–8. last several days. Examination will reveal Red flags in cases of acute dizziness horizontal-torsional nystagmus in the include: unilateral new onset hearing loss, Declaration of interests acute phase, the head impulse test may focal neurological signs ( eg , facial weak - None to declare. be impaired, and hearing is typically ness, diplopia or limb weakness), new affected. Specialist investigations are onset headache, and a normal VOR (head Dr Kaski is a specialist registrar in required to make a diagnosis of MD, impulse test). If present, the clinician neurology at the Royal London Hospital

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