Vestibular Rehabilitation PDF - Past Paper

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21 Vestibular Rehabilitation Dara Meldrum, Rory McConn-Walsh OUTLINE Introduction, 445 Outcome Measures, 456 Epidemiology, 446 Prognosis, 457 Anatomy and Physiology of the Vestibular System, 446 Interventions, 460 Vestibular Ocular Reflex and Vestibulospinal Reflex, 449 Vestibular Paresis/Hypofunction, 460 Pathophysiology, 449 Balance and Gait Reeducation, 462 Peripheral Disorders, 449 Management of Benign Paroxysmal Central Disorders, 451 Positional Vertigo, 464 Vestibular Migraine, 451 Secondary Problems, 464 Persistent Postural Perceptual Dizziness, 451 Other Considerations, 464 Diagnosis, 452 Multidisciplinary Team, 464 Medical and Surgical Management, 452 Specialist Centres and Support Groups, 464 Ménière’s Disease, 454 Support Groups, 466 Persistent Benign Paroxysmal Positional Vertigo, 454 Useful Resources, 466 Acoustic Neuromas, 454 Conclusion, 466 Assessment, 455 Case Studies, 466 Physical Impairments, 455 Case 1: Peripheral Vestibular Neuritis, 466 Functional Ability, 455 Case 2: Benign Paroxysmal Positional Vertigo, 467 The overwhelming vertigo, the awful sickness and the vestibular system. Vestibular dysfunction is characterised by turbulent eye movements – all enhanced by the slight- a number of signs and symptoms including vertigo, oscillop- est movement of the head, combine to form a picture of sia (a false sensation that the visual surround is oscillating), helpless misery that has few parallels in the whole field gait and balance impairment, nausea and nystagmus (Table of injury and disease. 21.1). Patients with such dysfunction present the physio- therapist with specific problems and require specialised —Terence Cawthorne 1946 Copyright © 2018. Elsevier. All rights reserved. assessment and treatment techniques, collectively referred to as vestibular rehabilitation. Vestibular rehabilitation has its roots in the empirical work of Cawthorne and Cooksey, who INTRODUCTION in the 1940s first documented the important role of exer- Normal postural stability, or ‘balance’ as it is commonly cise in recovery after a vestibular injury (Cooksey 1946). The known, is fundamental to activities of daily living. Visual, evidence base is now well established for the effective role vestibular and somatosensory systems all have important and of physiotherapy in the management of patients with ves- integrated roles in the maintenance of balance, and the neu- tibular disorders (Hansson 2007, Hillier & McDonnell 2011, rological patient can present with problems in any or all of Porciuncula et al 2012, Ricci et al 2010), and vestibular reha- these components. This chapter will focus on the assessment bilitation is recognised as a specialist area within physiother- and treatment of patients who have a primary problem in the apy (http://www.csp.org.uk/professional-networks/acpivr), 445 Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  446 SECTION 3 Specific Aspects of Management TABLE 21.1 Signs and Symptoms of 2009). Prevalence of dizziness rises to one in three in the older than 65 years age group (Colledge et al 1994), and diz- Vestibular Disorders That Should Be ziness is the most common complaint of patients presenting Evaluated During History Taking to primary care in those aged older than 75 years (Sloane Primary Symptoms 1989). However, approximately 40% of patients with dizzi- and Signs Associated Problems ness do not consult their general practitioner, demonstrat- Vertigo Neck and back pain ing a probable underestimation of the problem (Yardley Dizziness/light- Physical deconditioning et al 1998b). There is a very low prevalence of dizziness in headedness individuals younger than 25 years, and women are more Nausea and vomiting Agoraphobia likely to experience dizziness. Dizziness rarely results in hos- Oscillopsia Hyperventilation pitalisation, and the majority of patients are managed at the Nystagmus Falls primary care level with medication (Sloane 1989). Disequilibrium/impaired Hearing loss/tinnitus balance ANATOMY AND PHYSIOLOGY OF THE Panic/anxiety Aural fullness VESTIBULAR SYSTEM Gait abnormality Headache Fatigue The anatomy and physiology of the vestibular system are complex, but an understanding is crucial for successful treatment of vestibular disorders. A brief organisational and an independent prescriber physiotherapy post has overview is shown in Fig. 21.1. The vestibular system has recently been reported (Burrows et al 2017). Historically, both sensory and motor functions, and is generally divided vestibular rehabilitation has been associated with the ear, into peripheral and central components. The peripheral nose and throat (ENT) medical specialty, but in fact is appli- system consists of the vestibular end organ (housed in cable across many other areas. These include neurology the petrous temporal bone of the skull) and the vestibular (e.g. Parkinson’s, multiple sclerosis, stroke, traumatic brain nerve up to and including the dorsal root entry zone. The injury and vestibular schwannoma), care of the elderly, central system includes the vestibular nuclei in the brain- sports medicine (sports-related concussion) and paediatrics. stem and their central connections. Patients within these groups frequently present with vestibu- The vestibular end organ includes the semicircular canals lar impairment; therefore acquiring clinical skills to evaluate (SCCs) and the otoliths (utricle and saccule). The SCCs the vestibular system is important for all physiotherapists. consist of three canals on each side (horizontal, anterior and posterior), which are orientated at 90-degree angles to KEY POINTS each other (Figs. 21.1 and 21.2). Each canal is coupled func- tionally with a canal in the opposite end organ with both Vertigo is the sensation of self-motion (of head/body) horizontal canals, the left anterior and right posterior and when no self-motion is occurring or the sensation of the right posterior and left anterior canals, coupled together distorted self-motion during an otherwise normal head (see Fig. 21.2). Specialised sensors known as hair cells are movement (Bisdorff et al 2015). Dizziness is the sensa- located in the SCCs in a region known as the cupula and tion of disturbed or impaired spatial orientation without respond to angular velocity of head movement in different a false or distorted sense of motion (Bisdorff et al 2015). planes. Each canal responds best to movement in its own Dizziness and vertigo are further classified into being plane. For example, when the head rotates to the right, the spontaneous or triggered (Bisdorff et al 2009). hair cells in the right horizontal SCC increase their firing Copyright © 2018. Elsevier. All rights reserved. rate and those in the left horizontal SCC decrease their fir- ing rate (Fig. 21.3). Thus the central nervous system (CNS) EPIDEMIOLOGY gains information relating to the velocity and direction of The prevalence of dizziness has been estimated to be one in head movement from both sides. This means that if one side five in the 18 to 64 years age group, with 50% reporting pos- is damaged and no longer providing input, the contralateral tural unsteadiness (Yardley et al 1998a). In a large cross-sec- side can provide information about head movement (but tional study including a random sample of more than 6500 only at lower velocity head movements). The otoliths have community-dwelling Americans aged older than 40 years, different hair cells in a region known as the macula. Hair 27% reported dizziness and 35.4% were unable to stand on cells in the maculae are covered by a layer of calcium car- foam with eyes closed for 30 seconds, indicating problems bonate crystals called otoconia. They respond to the force of with using vestibular information for balance (Agrawal et al gravity and thus can provide the CNS with information on Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  Peripheral Semicircular canals -Anterior -Posterior -Horizontal Sensors Otoliths -Utricle -Saccule Vestibular nerve Dorsal root entry zone Central Cerebellum Integration and Vestibular nuclei modulation Oculomotor Vestibulospinal Autonomic Reticular Vestibular Nuclei (Cranial tract nervous system formation cortex nerves III, IV, VI) Eye movements Postural control Medullary Arousal- Vestibulo-ocular Vestibulospinal vomiting centre Anxiety reflex reflex FIG. 21.1 Functional Organisation of the Vestibular System and Vestibular Labyrinth. Semicircular canals Anterior Anterior Posterior Posterior Copyright © 2018. Elsevier. All rights reserved. Lateral Lateral (Cochlea) (Cochlea) Right side Left side FIG. 21.2 Arrangement of the Semicircular Canals and Their Pairings. Adapted from aVOR App Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  448 SECTION 3 Specific Aspects of Management Eyes steady Right horizontal canal Left horizontal canal (firing rate of hair cells) (firing rate of hair cells) I I I I I I I I I I Head stationary Eyes move to left (left lateral and right medial rectus muscles) IIIIIIIIIIIIII I I I Head turned to right Eyes move to right (right lateral and left medial rectus muscles) I I I IIIIIIIIIIIIII Head turned to left Left beating nystagmus IIIII Head stationary: right peripheral pathology of vestibular system FIG. 21.3 Function of the Horizontal Canals in Generating a Vestibulo-Ocular Reflex (VOR) During Turning of the Head and Effect of Loss of Hair Cell Function. With loss of tonic firing on the right, there is a relative increase in firing on the left; the brain interprets this as movement to the left (patient feels dizzy) and generates a VOR so that the eyes move to the right. The central nervous system corrects the eye movement with a saccadic movement to left and a left- beating nystagmus is seen. (Firing rate is for illustrative purposes only.) head tilt and linear acceleration (i.e. going up and down in a the resultant disturbance in cortical spatial orientation are Copyright © 2018. Elsevier. All rights reserved. lift or going forwards or backwards in a car). thought to form the basis of vertigo and produce the nystag- The peripheral system is a tonically active system; that mus seen in unilateral peripheral vestibular (Brandt 2000). is, it always has a certain firing level (approximately 40–90 The vestibular nerve sends fibres to two main areas: spikes per second which can increase or decrease with head the vestibular nuclei and the cerebellum (see Fig. 21.1). movement) (Goldberg & Fernandez 1971, Lacour et al The vestibular nuclei are responsible for integrat- 2009). The CNS interprets any asymmetry in the firing rate ing information received from the end organ with that as movement. This fact is of utmost importance when con- received from other sensory systems and the cerebellum. sidering a patient who has loss of vestibular function on one Vestibular nuclei send fibres to the oculomotor nuclei, side (i.e. decrease or absence of firing) because there will vestibulospinal tracts, contralateral vestibular nuclei, be a relative increase of firing on the intact side even when reticular formation, cerebellum, autonomic nervous sys- the head is not moving (see Fig. 21.3). This asymmetry and tem and the cortex. The symptoms of nausea, vomiting Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  CHAPTER 21 Vestibular Rehabilitation 449 and anxiety associated with vestibular disorders are as a TABLE 21.2 Peripheral and Central result of abnormal activation of the autonomic and retic- Vestibular Disorders ular pathways, respectively (see Fig. 21.1). For a more detailed description of vestibular anatomy and physiol- Peripheral Central ogy, the reader is referred to Hain and Helminski (2007) Viral: vestibular neuritis/ Ischaemia, e.g. lateral and Kingma and van de Berg (2016). labyrinthitis medullary syndrome (Wallenberg’s syndrome) VESTIBULAR OCULAR REFLEX AND Benign paroxysmal Vertebrobasilar VESTIBULOSPINAL REFLEX positional vertigo insufficiency Perilymph fistula Infection The motor functions of the vestibular system include the vestibular ocular reflex (VOR) and the vestibulospinal Ménière’s disease Head injury reflex (VSR). The function of the VOR is to maintain sta- Vascular occlusion Degenerative disease, ble vision when the head is moving. A good example of e.g. multiple sclerosis, this is being able to focus on an object when walking. If Friedreich’s ataxia the eyes moved with the head as it goes up and down when Iatrogenic (ototoxic Base of skull abnormalities, walking it would be impossible to see clearly. The VOR drugs, surgery) e.g. Arnold–Chiari enables the eyes (through activation of the appropriate malformation ocular muscles) to move in the opposite direction and Head injury (labyrinthine Tumours of the at an equal velocity to the head. The image of the object concussion) cerebellopontine angle thus remains stable on the retina. For the VOR to func- Acoustic neuromas Drugs tion normally, velocity of eye movement must be equal (may have a central Epilepsy to and in the opposite direction to the head movement. component) Migraine This is known as the ‘gain’ of the VOR. Patients who have problems with the vestibular system have impairment of the gain of the VOR and therefore demonstrate prob- PERIPHERAL DISORDERS lems with gaze stability. They often describe that during Vestibular neuritis (also called neuronitis) is a common self-motion objects seem as if they are moving. The func- peripheral vestibular problem thought to be caused by tion of the VSR is primarily to maintain and regain pos- a virus (Strupp & Brandt 2010). It results in varying tural control, and it does this through monosynaptic and degrees of hair cell loss and unilateral vestibular paresis polysynaptic vestibulospinal pathways. (or hypofunction). Patients present with an acute onset of vertigo, nausea and vomiting that are severely inca- PATHOPHYSIOLOGY pacitating and worsened by head and eye movements. A classification system for vestibular disorders has recently been proposed (Bisdorff et al 2009, 2015), but disorders KEY POINTS can broadly be classified anatomically into peripheral or Nystagmus is a rhythmical oscillation of the eyes. There central, depending on which area pathology affects. They is a slow movement or ‘phase’ in one direction and a are further classified by duration: acute, episodic or chronic fast corrective movement in the opposite direction. By (Bisdorff et al 2015). Common peripheral and central ves- convention, nystagmus is named by the direction of the tibular disorders are listed in Table 21.2. Notably, vertigo fast phase. For example, left beating horizontal nystag- Copyright © 2018. Elsevier. All rights reserved. and dizziness are not always caused by pathology affect- mus is one in which the slow phase of the nystagmus ing the vestibular system; there may be many other causes is horizontal movement of the eyes towards the right including orthostatic hypotension, cardiac disorders, psy- and the fast phase of the nystagmus is horizontal eye chiatric disorders and hyperventilation, and these should movement towards the left. There are many causes of be evaluated before referral to physiotherapy. The exact nystagmus. In the patient with an acute peripheral ves- cause of dizziness frequently remains uncertain, and a trial tibular disorder, a spontaneous nystagmus can be seen of vestibular rehabilitation may be suggested in the absence with its fast phase beating away from the side of the of a specific diagnosis. The pathology of disorders that can lesion. After a few days, the nystagmus is not visible affect the central vestibular system (e.g. cerebrovascular in room light but may be evident indefinitely with infra- accidents, traumatic brain injury and multiple sclerosis) is red goggles (visual fixation is removed; see Fig. 21.6). considered in other chapters. Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  450 SECTION 3 Specific Aspects of Management On examination, a spontaneous horizontal nystagmus can be seen, the fast phase of which beats away from the involved side. This is caused by the asymmetri- cal tonic firing of the vestibular nerves (see Fig. 21.3). Balance and gait abnormalities are also evident (Allum & Adkin 2003, Fetter et al 1990). Hearing is not gener- ally affected, but if it is, the condition is called labyrin- thitis. Symptoms generally resolve over a period of 2 to 6 weeks. Benign paroxysmal positional vertigo (BPPV) is the commonest cause of vertigo in peripheral vestibular dis- orders (Bhattacharyya et al 2017). It has a lifetime prev- alence rate of 2.4% and a 1-year incidence rate of 0.6% (von Brevern et al 2007). Prevalence increases with age and is almost seven times higher in those older than the age of 60 years compared with those aged 18 to 39 years (von Brevern et al 2007). In the elderly, BPPV is often undiagnosed (Oghalai et al 2000). The name encompasses the associated features: FIG. 21.4 The Hallpike–Dix test for diagnosis of be- benign: the prognosis for recovery is favourable nign paroxysmal positional vertigo. paroxysmal: the associated vertigo is short-lived, gener- ally less than 1 minute positional: the vertigo is provoked by certain head made using the Hallpike–Dix (HPD) manoeuvre (Fig. positions 21.4) in which the head is moved into a provocative vertigo: a spinning sensation is experienced position. BPPV most commonly affects the posterior In addition, nausea and anxiety can be reported, and SCC (approximately 85%–95% of cases) but can also occasionally vomiting occurs. Imbalance is reported in affect the horizontal (5%–15% of cases) (Parnes et al 50% of patients, and most patients report vertigo when 2003, White et al 2005) and, very rarely, the anterior turning over in bed (von Brevern et al 2007). canal (De La Meilleure 1996). Multiple canal involve- BPPV is thought to be caused by detached utricu- ment can also occur. lar otoconia entering one of the SCCs and either float- Patients with BPPV report vertigo associated with cer- ing free in the canal (canalithiasis) or adhering to the tain head movements, that is, rolling over in bed, looking cupula (cupulolithiasis) (Epley 1980). This has the effect up or bending down, and will usually avoid these move- of making the SCCs responsive to gravity when they ments. Treatment consists of physical manoeuvres, some- normally are not. The SCCs usually respond to head times repeated a few times during one session (Gordon & movement in their respective planes and increase their Gadoth 2004), that aim to reposition the displaced otoco- firing rate during head movement, returning to normal nia back into the utricle (Gold et al 2014, Hilton & Pinder tonic firing level when the head has stopped moving. 2004). These manoeuvres are highly effective in most cases However, if the head moves into a dependent position and lead to full resolution of symptoms (Bhattacharyya and then stops, the displaced otoconia are heavier and et al 2017, Hilton & Pinder 2004). BPPV has a high recur- will continue to move in the canal, stimulating the hair rence rate of 25% (von Brevern et al 2007), necessitating Copyright © 2018. Elsevier. All rights reserved. cells in the canal to continue firing. The central vestibu- further treatment. lar system interprets this as further movement and gen- Ménière’s disease is thought to be caused by an increase erates a VOR for that canal, and the patient experiences in the volume of and/or a problem with absorption of nystagmus and vertigo. This nystagmus has a latency of the endolymph (the fluid in the inner ear). This results 1 to 50 seconds, is generally transient (it stops when the in dilation of the endolymphatic spaces (endolymphatic otoconia come to a resting position) and, in the case of hydrops). This happens episodically and unpredictably, posterior semicircular canal (PSCC) BPPV is torsional and an attack is characterised by a complaint of a fullness towards the affected ear. If the patient repeatedly moves in the ear, reduction of hearing and tinnitus (a ringing into the provoking position, the vertigo and nystagmus sound in the ear). This is followed by vertigo, vomiting and will decrease because of habituation of the response postural imbalance, and nystagmus is observed. The epi- (Baloh et al 1987). The diagnosis of BPPV is generally sodes may last from 30 minutes to 72 hours and then the Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  CHAPTER 21 Vestibular Rehabilitation 451 patient gradually improves (Committee on Hearing and post-event (von Brevern et al 2005). Abnormalities include Equilibrium 1995). Episodes are generally managed with gaze-induced nystagmus, central positional nystagmus, medication, diet and rest, but in severe cases surgery may abnormal saccades and abnormal smooth pursuit (von be indicated (see later). Vestibular rehabilitation can be Brevern et al 2005). Management is mainly pharmacolog- helpful in patients with Ménière’s disease whose symptoms ical to either prevent or abort the migrainous events, and of disequilibrium and dizziness continue between attacks this is recommended as first-line treatment (Bisdorff 2011). (Clendaniel & Tucci 1997, Garcia et al 2013, Gottshall et al Physiotherapy can be offered as a second line of treatment 2005). if vestibular symptoms persist. There is weak evidence (in Bilateral vestibular hypofunction can be caused by infec- the form of retrospective and observational studies) to tions (e.g. meningitis), tumours (e.g. bilateral acoustic support vestibular rehabilitation in improving the physical neuromas in neurofibromatosis), Ménière’s disease, auto- symptoms associated with vestibular migraine (Sugaya et al immune diseases and ototoxic drugs (e.g. aminoglycoside 2017, Whitney et al 2000, Wrisley et al 2002). Clinical expe- antibiotics) (Lucieer et al 2016, Rinne et al 1998). In some rience suggests that these patients are usually motion sen- cases, the cause is unknown. Patients with bilateral vestib- sitive and their symptoms can be exacerbated easily; thus ular hypofunction do not usually report vertigo when ves- caution is needed in the early stages to allow them to build tibular loss is symmetrical. Their main problems include up a tolerance to head movements and optokinetic stimu- balance and gait impairments. They also have decreased lation. In our migraine clinic, we found evidence of balance gaze stability caused by loss of VOR function, report disturbance in patients with migraine, particularly when that they cannot see clearly during head movements, and they stood on a moving surface with their eyes closed indi- describe their surroundings as bouncing or jumping. This cating a reduced ability to utilise vestibular function ade- is termed oscillopsia. Vestibular rehabilitation is indicated quately. Balance retraining can be offered to these patients. in patients with bilateral vestibular loss, but outcomes are not as favourable (Brown et al 2001, Herdman et al 2015, PERSISTENT POSTURAL PERCEPTUAL Krebs et al 2003). DIZZINESS CENTRAL DISORDERS Persistent postural perceptual dizziness (PPPD) is a recently agreed term for a disorder that in the past has also Vestibular Migraine be named as space and motion discomfort, phobic pos- Considered to be one of the most common causes of epi- tural vertigo, visual vertigo or chronic subjective dizziness sodic vertigo, vestibular migraine is underdiagnosed, par- (Dieterich & Staab 2017). The core features that suggest ticularly at primary care level (Sohn 2016). It is hypothesised a diagnosis include symptoms of dizziness, unsteadiness to be a CNS disorder with spreading cortical depression as or non-spinning vertigo that are present on most days the hypothesised mechanism (Bisdorff 2011). Diagnostic for more than 3 months. Symptoms may be precipitated criteria have been developed by the International Headache by, or comorbid with, a neuro-otological event (such as Society and International Barany Society (Lempert et al vestibular neuritis) or a psychiatric disorder but also may 2012). These are a history of migraine with or without aura exist in isolation. PPPD is therefore considered a chronic and vestibular symptoms of moderate to severe intensity functional vestibular disorder whose pathophysiological lasting 5 minutes to 72 hours. At least five episodes should processes are not fully understood (Dieterich & Staab have occurred, and 50% of episodes should have at least 2017). Patients commonly report that their symptoms one of three migrainous symptoms (headache, phonopho- increase with postural changes such as sitting to stand- bia/photophobia or visual aura). ing. Symptoms are provoked by a variety of visual stimuli Copyright © 2018. Elsevier. All rights reserved. Using these criteria, Cho et al (2016) found a 10.3% (still or moving), including crowds, supermarket aisles, prevalence rate of vestibular migraine in migraineurs, and busy backgrounds (such as patterned carpets or walls) Neuhauser et al (2006) estimated a lifetime prevalence rate and computer screens. Head movements can also exacer- of 1% and a 1-year prevalence rate of 0.9%. Symptoms are bate their symptoms. episodic and include vertigo (spontaneous and motion Examination of the patient may reveal normal neuro- provoked), head motion intolerance and unsteadiness. otological testing. Posturography (Fig. 21.5) is useful and Significantly, more anxiety has been found in those vestib- may reveal difficulties with easier balance tasks (and larger ular migraines when compared with either healthy controls variability) when compared with controls (Dieterich & or non-vestibular migraine (Kutay et al 2017). Oculomotor Staab 2017, Sohsten et al 2016). Vestibular rehabilitation testing can reveal abnormalities in up to 70% of patients (habituation exercises and balance retraining) along with during a vestibular migraine but return to normal counselling and medications (selective serotonin reuptake Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  452 SECTION 3 Specific Aspects of Management inhibitors or serotonin and norepinephrine reuptake canal. As well as assessing peripheral vestibular func- inhibitors have shown some promise) are the mainstays of tion, oculomotor testing can also detect oculomotor treatment for this patient group (Bittar & Lins 2015, Schaaf disturbance (abnormal saccades, smooth pursuit) sug- & Hesse 2015, Thompson et al 2015). gestive of a central disorder. 3. Magnetic resonance imaging (MRI): Any patient who presents with dizziness that is persistent or progressive DIAGNOSIS should have an MRI scan (preferably with gadolinium Patients presenting with vertigo and dizziness may be enhancement) of the brain and cerebellopontine angle referred for specialised audio-vestibular testing to evaluate to exclude lesions such as a brain tumour, acoustic whether a central or peripheral vestibular disorder is the neuroma, multiple sclerosis or embolic/haemorrhagic cause of their symptoms. events. 1. Hearing tests (pure tone audiogram/speech discrimina- 4. Posturography (see Fig. 21.5): This provides a quantita- tion): Certain conditions that cause dizziness may also tive measure of certain functional aspects of dynamic result in hearing loss. These include Ménière’s disease, equilibrium (Di Fabio 1995, Fetter et al 1990, Visser ototoxic medications, head trauma, acoustic neuromas et al 2008). It therefore has a role to play in the assess- and previous middle ear surgery. A hearing test will ment of the disabled patient with dizziness and can also provide valuable information on the inner ear (cochlea) be used in monitoring their rehabilitation. To date, and middle ear function of these patients. however, it has been used mainly as a research tool. 2. Caloric/oculomotor testing: This is the most commonly used test of peripheral vestibular function and provides MEDICAL AND SURGICAL MANAGEMENT a quantitative measure of lateral SCC function in each inner ear (Luxon & Davies 1997). This is performed by The acute rotatory vertigo suffered during an acute measuring the response of the VOR (nystagmus) to the peripheral vestibular upset is caused by sudden asymme- instillation of cold and warm water down the external try in vestibular input to the CNS. Vestibular sedatives Copyright © 2018. Elsevier. All rights reserved. A FIG. 21.5 Computerised Posturography. (A) The EquiTest system which consists of force plat- form and visual surround, both of which can be sway referenced (move in tandem with postural sway). (B) Postural sway under six conditions is generally tested in the sensory organisation test (right-hand side). Reprinted with permission from EquiTest®, NeuroCom® International, Inc. Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  CHAPTER 21 Vestibular Rehabilitation 453 Sensory organisation test (SOT) – Six conditions Condition Sensory systems Normal vision 1 Fixed support Absent vision 2 Fixed support Sway-referenced vision 3 Fixed support Normal vision 4 Sway-referenced support Absent vision 5 Sway-referenced support Sway-referenced vision 6 Sway-referenced support Copyright © 2018. Elsevier. All rights reserved. Visual input Blue denotes ‘sway-referenced’ input. Visual surround follows subject's body sway, providing orientationally inaccurate information Vestibular input Somatosensory input Blue denotes ‘sway-referenced’ input. Support surface follows subject's body sway, providing orientationally inaccurate information B FIG. 21.5, cont’d. Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  454 SECTION 3 Specific Aspects of Management are a group of drugs that have a well-established record where it selectively destroys vestibular and not cochlear of controlling such attacks. These drugs have variable hair cells. Success rates of more than 80% have been anticholinergic, antiemetic and sedative properties. They reported. The main disadvantage is that there is a risk for include phenothiazines (e.g. prochlorperazine, per- sensorineural hearing loss. Endolymphatic sac decom- phenazine), antihistamines (e.g. cinnarizine, dimenhydri- pression entails a mastoidectomy with removal of all bone nate, promethazine, meclizine) and benzodiazepines (e.g. over the endolymphatic sac/duct and possibly inserting a diazepam, lorazepam) (Moffat & Ballagh 1997). These drain into it (Moffat 1994). The sac is the proposed site of drugs are of particular value in the management of acute obstruction of endolymphatic reabsorption in Ménière’s vertigo, and they can be administered by intramuscular or disease, and this procedure enables the sac to expand intravenous injection, suppository, buccal absorption or during the active disease process. Vestibular neurectomy orally, depending on the individual drug. However, they entails transecting the vestibular nerves in the posterior should be avoided in the management of chronic periph- cranial fossa. The main disadvantages are damage to the eral labyrinthine disorders because they may suppress facial and cochlear nerves together with intracranial com- central vestibular activity and thereby delay compensa- plications. Vestibular rehabilitation is important after tion and symptomatic recovery. these procedures. Ménière’s Disease Persistent Benign Paroxysmal Positional Vertigo There are many treatment options for the manage- Cases of intractable (>1 year) and incapacitating BPPV can ment of Ménière’s disease, but no firm consensus on be treated by occlusion of the PSCC (Parnes & McClure the best option (Clyde et al 2017). Betahistine and thi- 1990). This involves a mastoidectomy with isolation and azide diuretics have been advocated (Clyde et al 2017). then occlusion of the PSCC. This is a safe and effective oper- Betahistine is a vasodilator that works directly on the ation with success rates of more than 90% to 95% (Walsh inner ear and is thought to improve its microcircula- et al 1999). Before this operation, singular neurectomy was tion. Thiazide diuretics are thought to work in Ménière’s advocated, but this is a technically more demanding opera- disease by reducing the endolymphatic pressure by tion with a risk for sensorineural hearing loss. means of a systemic diuretic effect. However, much of the data reported regarding the efficacy of these drugs Acoustic Neuromas in Ménière’s disease are conflicting (Burgess & Kundu There are currently three methods of managing acoustic 2006). Intratympanic injection of steroids is also a treat- neuromas. These include conservative management, sur- ment option (Clyde et al 2017). gery (combined ENT and neurosurgery) and stereotactic In those patients with unilateral Ménière’s disease that radiosurgery. Conservative management is reserved for are symptomatic for 6 months to 1 year despite conser- small tumours that are not growing or for patients who vative management (betahistine, thiazide diuretic, salt/ are unfit or express a desire not to have surgery (Walsh caffeine restriction), then surgery should be considered et al 2000). In those tumours that are growing, causing (Dorion 1998). The type of surgery is dependent on the symptoms, and those tumours greater than 1 to 2 cm in level of hearing in the affected ear. If the hearing is not diameter, then surgery should be considered. The aim of serviceable or useful (50% speech reception threshold), then a labyrinthec- facial nerve, and when indicated to preserve hearing. Three tomy is the preferred choice. This entails a mastoidectomy surgical approaches are possible, and the type depends and drilling out the three SCCs under general anaesthesia. on the level of remaining hearing. If the hearing is not This is very effective at treating the vertiginous episodes by serviceable or useful, then a translabyrinthine approach Copyright © 2018. Elsevier. All rights reserved. destroying all peripheral vestibular function, although all is performed (House & Hitselberger 1985, Schwartz et al residual hearing is destroyed. 2017). The main advantage of this technique is that there If the hearing is useful, then the surgery should is minimal brain retraction and the access is excellent, attempt to preserve the remaining hearing. This can be although all remaining hearing is sacrificed. If the hear- done by means of topical gentamicin ablation therapy, ing is useful, then the tumour is approached either via endolymphatic sac decompression or vestibular neurec- a retrosigmoid or a middle cranial fossa approach in an tomy. Topical gentamicin therapy involves the transtym- attempt to preserve the hearing (Sekhar et al 1996). The panic instillation of gentamicin solution into the middle main disadvantage of the former is that there is cerebellar ear (Nedzelski et al 1992). The gentamicin then diffuses retraction, whereas the latter is technically demanding. into the inner ear across the round window membrane, Stereotactic radiosurgery entails the accurate application Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  CHAPTER 21 Vestibular Rehabilitation 455 of radiotherapy from an external source to the site of the TABLE 21.3 Special Questions During acoustic neuroma with minimal surrounding tissue dam- History Taking age. Treatment success with stereotactic radiosurgery has been reported as 97.7% with an acceptable toxicity profile Have you noticed any loss of hearing? (Patel et al 2017). Have you any ringing in your ears or a feeling of fullness? ASSESSMENT Have you ever fallen? Have you ever lost consciousness? A thorough assessment of the vestibular patient is a cru- Have you any double vision, trouble swallowing or cial prerequisite to any treatment. Although many aspects speaking during an attack? of the examination are similar to that of any physiother- Any other neurological symptoms such as weakness, apy assessment, there are specific tests that should be per- numbness or pins and needles? formed. The patient should be made aware that aspects of the examination often provoke symptoms and leave the Do you have a history of migraine or other headaches? patient feeling unwell. It is advisable to request the patient Have you any neck pain or stiffness? have someone with him or her on the first assessment who can accompany him or her home if required. A history is It is not always visible in room light when the patient can taken of the present complaint, the onset, nature, severity, fixate on something and suppress it. Specialised infra-red duration and irritability of symptoms, and the aggravat- goggles (Fig. 21.6) can be used to view the eyes with fixa- ing and alleviating factors. True vertigo (asking ‘Do you tion removed. Nystagmus of peripheral origin is generally spin?’ or ‘Does the room spin?’) should be differentiated direction fixed and increases when the patient gazes in from dizziness, light-headedness, giddiness and disequilib- the direction of the fast phase. Spontaneous upbeating, rium. A history should also be taken of any other associated downbeating or a pure torsional nystagmus indicates a symptoms (see Table 21.1). It should be ascertained how CNS lesion (Kerber & Baloh 2011). Ocular range of move- long the patient has had the symptoms, and what was his or ment (gaze up, down, left and right), smooth pursuit and her initial presentation. The history relating the very first saccadic eye movements, and the ability to cancel the episode, if there has been more than one, and although it VOR are then assessed (see Table 21.4). These eye move- may have been a long time previously, is critically import- ments are centrally programmed, and deficits observed ant. These previous episodes and their outcomes should are indicative of CNS disorders (Tusa 2010). Specific tests be explored. Pertinent medical history includes problems of peripheral vestibular loss include the head impulse test with vision, other peripheral nervous system or CNS dis- or head thrust test (Kerber & Baloh 2011). orders (e.g. migraine, epilepsy, previous head injury), The assessment of posture, tone, strength, sensation, cardiorespiratory disease (low or high blood pressure), proprioception, coordination and reflexes provides use- endocrinological diseases (e.g. diabetes), musculoskeletal ful information (particularly where a central lesion is problems (particularly cervical spine problems) and any suspected or known). A musculoskeletal examination is previous vestibular surgery. The effects of the problem on carried out on the trunk and extremities if indicated. the patient’s occupational and leisure activities should also be noted. Medications – type, dosage, effect and plans for Functional Ability cessation – should also be discussed. Results of any inves- Dynamic visual acuity is a functional measure of the VOR tigations should be noted. Special questions are listed in and objectively quantifies how visual acuity degrades Table 21.3. during head movement (Badke et al 2004, Herdman et al Copyright © 2018. Elsevier. All rights reserved. 1998). The patient sits in front of a visual acuity chart (e.g. Physical Impairments an early treatment for diabetic retinopathy study (ETDRS) The examination of the vestibular patient commences chart; Fig. 21.7). The patient is asked to verbalise the letters with a screening of the cervical spine (range of movement on the chart, starting at the top of the chart and working and any symptoms with movement). Subsequent to this, his or her way down. The lowest line at which he or she can the oculomotor examination is performed (Table 21.4). accurately identify three out of (usually) five letters is noted The patient is firstly examined for the presence of spon- as the static visual acuity. The examiner stands behind the taneous nystagmus and the direction (of the fast phase) patient and holds the patient’s head while rotating it left- noted. Nystagmus can be upbeating, downbeating, hori- wards and rightwards in the horizontal plane at a rate of 2 zontal, torsional or a mixture (e.g. upbeating torsional). Hz and at an amplitude of about 30 degrees. The patient Physical Management for Neurological Conditions E-Book : Physical Management for Neurological Conditions E-Book, edited by Sheila Lennon, et al., Elsevier, 2018. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/utas/detail.action?docID=5485007. Created from utas on 2024-03-04 07:17:11.  456 SECTION 3 Specific Aspects of Management TABLE 21.4 Key Assessment Findings Oculomotor Examination Test Procedure and Findings Spontaneous nystagmus Patient looks straight ahead. The eyes are observed for a nystagmus, and the direction is Room light (visual noted. Frenzel lenses both remove visual fixation and magnify the eyes (see Fig. 21.6). fixation) Nystagmus arising from a peripheral vestibular disorder can be suppressed by visual Frenzel lenses (no visual fixation. fixation) Gaze-evoked nystagmusa Ability to hold eyes steady on a stationary object. If abnormal, the eyes will make jerky movements in an effort to remain on the object. Smooth pursuita Ability to track a moving object with the eyes when the head is stationary. In the normal, the eyes make smooth movements, abnormalities include jerky movements of the eyes. Saccadesa Ability to move the eyes from one stationary target to another when the head is station- ary. In the abnormal, the eyes may over- or under-shoot the target. VOR cancellationa Ability to suppress the VOR and move the eyes in phase with the head. Patient is asked to follow a moving target as the examiner moves the head in the same direction. VOR A normal VOR is when the eyes can make a compensatory movement to stay on a sta- Gaze stabilisation with tionary target when the head moves. Patient is asked to keep eyes steady on a target head movement whilst the examiner moves the patient’s head in a small range of movement from side Slow head movement to side and then up and down slowly. This is repeated with faster movements of the Fast head movement head. Abnormalities would involve a saccadic movement of the eyes to stay on the target. Positional tests The patient is long sitting on plinth with eyes open. The head is turned 45 degrees to Hallpike–Dix test (see the side that is being tested. The patient is brought quickly into a lying position with Fig. 21.4) the head in 30-degree extension by the examiner. This position is maintained for 50 seconds, and the presence, duration and direction of nystagmus are noted. Symptoms are also noted. This test is diagnostic for BPPV. The nystagmus observed will usually be upbeating and torsional towards the affected side, i.e. towards the left in the left Hallpike Dix position. This indicates a posterior semicircular canal BPPV. In extremely rare cases, the anterior canal can be affected and the nystagmus will be downbeating and torsional towards the affected side. Horizontal roll test The patient lies supine, the examiner rolls the head to the left, and the patient’s eyes are examined for nystagmus, direction and intensity. The head is then rolled to the right and the patient’s eyes are examined for nystagmus, direction and intensity. If the nystag- mus is horizontal and the fast phase is towards the ground (geotropic nystagmus) when the head is turned to either side, this is likely to be canalithiasis of the horizontal canal. Usually the nystagmus is more intense on one side and this is the affected side. If the nystagmus is horizontal and the fast phase is away from the ground (apogeotropic)