Vestibular assessment

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Vestibujlar assessment

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  • http://www1.imperial.ac.uk/medicine/research/researchthemes/neuroscience/movement_balance/mabdandv/
  • The sensation that viewed objects are moving or wavering back and forth. Also called oscillating vision
  • http://stroke.ahajournals.org/content/40/11/3504/suppl/DC1
    1a – acute right vestibular neuritis
  • Evans JG. Transient neurological dysfunction and risk of stroke in an elderly English population: the different significance of vertigo
    and non-rotatory dizziness. Age Ageing 1990; 19: 43-49.
  • 2/3 > 1 cause in >65s (Maarsingh, 2010)
    Value in communicating a disorder – needs clarification
    Tinetti ME, Williams CS, Gill TM. Dizziness among older adults: a possible geriatric syndrome. Ann Intern Med 2000; 132:337.
  • Kroenke K, Mangelsdorff AD. Common symptoms in ambulatory care: incidence, evaluation, therapy, and outcome. Am J Med 1989;86:262-6.
    Sloane P, Blazer D, George LK.Dizziness in a community elderly population.J Am Geriatr Soc1989;37:1018.
    Neuhauser HK, Radtke A, von Brevern M, et al. Burden of dizziness and vertigo in the community. Arch Intern Med 2008; 168:2118. in one Germany cohort of 18-79 year olds
  • Referral processes
  • A group of 5 sensory receptors responsible for detecting linear and rotational accelerations of the head.
    Formed of the Utricle, Saccule, and three semi circular canals.
    Arranged identically bilaterally
  • Here we see that the hair cells project into a gelatinous layer, which itself is weighed down by calcium carbonate crystals or otoconia. Therefore when the head accelerates or decelerates, there is inertial drag on the weighted gelatinous layer, so the hair cells are displaced.
    Such signals are important for mediating the vestibulospinal reflex in particular.
  • Afferent information from the peripheral vestibular system is relayed to vestibular nuclei located within the floor of the 4th ventricle of the hindbrain.
    Numerous projections from nuclei to:
    Thalamus / cortex
    Oculomotor nuclei
    Spinal cord
    Cerebellum
    Autonomic medullary centres
  • This diagram shows how the semicircular canals give rise to the vestibulo-ocular reflex and thereby help ensure steady vision during movement of the head.
    Instead of a weighted gelatinous layer, the hair cells within the SCCs project into a gelatinous blob called the cupula. This gets deflected when the head rotates.
    Note that the SCCs work in pairs. Here we see that when the head rotates right, there is increased firing along the vestibular nerve on that side, but decreased firing on the contralateral left side. As a result, signals are sent to activate the appropriate muscles to turn the eyes left, equal but opposite in direction to the original head movement.
  • Bilateral vestibular disorder – genetic, trauma, ototoxicity – gentamicin, infections, auto immune, idiopathic
  • some interpret this as self-motion, others as motion of the environment
  • Chronic dizziness: a practical approach PN 2010;10:129-139 . A M Bronstein, T Lempert, B M Seemungal.
    Pract Neurol 2008;8:211-221. A practical approach to acute vertigo. B M Seemungal, A M Bronstein
  • http://www1.imperial.ac.uk/medicine/research/researchthemes/neuroscience/movement_balance/mabdandv/
    Cover test – reveal heterotopias – misalignment of the visual axis when both eyes are viewing a single target
    Peripheral
    Spontaneous in the absence of optic fixation;
    Dominantly horizontal jerk nystagmus that beats only in one direction and increases in intensity when the patient looks in the direction of the nystagmus fast phase.
    Central
    Gaze evoked nystagmus;up or down beat;
  • http://stroke.ahajournals.org/content/40/11/3504/suppl/DC1
    1a – acute right vestibular neuritis
    1b – pseudolabyrinthine presentation of stoke - right cerebellar stroke
    3 – Skew deviation in lateral medullar syndrome
    http://content.lib.utah.edu/cdm4/item_viewer.php?CISOROOT=/ehsl-dent&CISOPTR=2
    Gaze evoked nystagmus changing direction on eccentric gaze
    utah
  • Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor
    examination more sensitive than early MRI diffusionweighted imaging. Stroke 2009;40:3504-10.
    Chen L, Lee W, Chambers BR, et al. Diagnostic accuracy of acute vestibular syndrome at the bedside in a stroke unit. J Neurol
    2010;258:855-61.
  • Nystagmus evident with visual fixation always beats in the same direction and increases when the patient gazes in the direction of the fast phase. Nystagmus decreases or disappears when the patient gazes in the direction opposite to the fast phase. This pattern is often seen in peripheral vestibular disorders and occasionally in central disorders.
  • MRI  Head  :  Technique:  Axial  DWI,  T2,  PD  weighted,  sagittal  T1  weighted, and  coronal  FLAIR  images  of  the  brain  obtained  without  and axial  and  coronal  T1W  images  after  iv  GD.FINDINGS:  There  is  abnormal  high  T2/Flair  gyral  signal,  some  internal low  T2  signal  with  restricted  diffusion,  without  enhancement in  the  basal  antero  frontal  and  basal  antero  temporal  lobe on  the  left  hand  side.  There  is  also  diffuse  sulcal  high  T2 signal  changes  in  both  parieto  occipital  lobes  and  bilateral fronto  parietal  meningeal  enhancement;  findings  are consistent  with  meningo-encephalitis.  In  addition  there  is  a small  rounded  in  the  anterior  and  a  small  wedge  shape  area of  abnormal  high  T2/Flair,  some  internal  low  T2  signal (haemorrhagic  change  ?)  with  restricted  diffusion  in  theposterior  inferior  cerebellar  hemisphere  on  the  left  hand side,  most  in  keeping  with  focal  encephalitis  orencephalitis  related  ischemia. No  abscess.  There  are  a  few  non-specific  small  bilateral high  T2  signal  changes  in  the  periventricular  cerebralfrontal  white  matter  on  both  sides  of  uncertain  significance with  no  abnormal  diffusion/acute  ischaemia.  No  intracranial collection  or  other  haemorrhage.  No  intracranial  space occupying  mass  lesion  or  other  structural  pathology.  Normalventricles.  No  signs  of  increased  intracranial  pressure. Marked  right  middle  ear  and  mastoid  fluid/disease  and bilateral  mucosal  swelling  of  the  sphenoid  and  ethmoid  cells is  noted.CONCLUSION:Findings  are  most  consistent  with  meningo-encephalitis  (HSV?  ,  LP  correlation  ?);  clinical  correlation  is  advised.
  • http://www1.imperial.ac.uk/medicine/research/researchthemes/neuroscience/movement_balance/mabdandv/
  • Y Agrawal, JP Carey, CC Della Santina, MC Schubert, LB Minor. Disorders of Balance and Vestibular Function in US Adults Data From the National Health and Nutrition Examination Survey, 2001-2004.. ARCH INTERN MED/VOL 169 (NO. 10), MAY 25, 2009
  • Three important facts: proximal branches supply brain stem, brain stem signs are common with cerebellar stroke! Internal auditort artery is from AICA, inner ear symptoms such as hearing loss and vertigo can accompany cerebellar stroke, thirdly variations of normal anatomy are common!
  • Vestibular assessment

    1. 1. Assessing the vertiginous patient in ED Jim Fleet
    2. 2. Vestibular assessment - Objectives 1. The differential diagnosis of “dizziness” 2. Clinical anatomy and clinical physiology of the vestibular apparatus 3. Diagnostic strategy 4. Clinical assessment techniques
    3. 3. History • 62 year old male shop worker • Brought into A&E via ambulance 06:00 – Complaining of “room spinning around him” • Walked downstairs after waking normally and felt suddenly unwell – Sweaty, clammy, nauseated • Collapsed to ground, unsure if LOC
    4. 4. History • • • • • Vomited 3 to 4 times Difficulty hearing Mild frontal headache Oscillopsia Some rhinorrhea in preceding days previously, otherwise well • Nothing like this previously
    5. 5. History • No ongoing medical conditions and no regular medication • Smokes 20-30/day since youth • No alcohol
    6. 6. Examination • • • • • G.C.S 15/15 BP - 141/94; P - 88, reg; T – 35 0 C Sats 99% air, BM 5.4 No meningism Cardio-respiratory and abdominal systems normal
    7. 7. Examination • • • • • Truncal instability with ongoing vertigo Gait not assessed Pupils equal and responsive No ophthalmoplegia Loss of hearing right ear
    8. 8. Examination • Other cranial nerves normal • Tone, power, sensation all normal • Reflexes – 2+ and symmetrical – Plantars down-going
    9. 9. Nystagmus • http://stroke.ahajournals.org/content/4 0/11/3504/suppl/DC1 • 1a
    10. 10. Investigations • ECG – sinus rhythm, normal axis • Blood – normal haematology and biochemistry
    11. 11. Summary • 62 year old smoker • Collapse and acute vertigo – Symptoms setting • Vomiting • Nystagmus and hearing loss • Investigations normal
    12. 12. How to Proceed? • Differential diagnosis? • Additional information – Further history? – Further investigation? – Further investigation? • Inpatient or outpatient?
    13. 13. Dizziness • Non-specific term used by patients • Summation of symptoms and pathology – Vertigo – Disequilibrium • Any pathology of balance homeostasis – Pre-syncope – Nonspecific “dizziness” • Vestibular pathology important in the dizzy patient – 40% peripheral – 10% central (higher in older age)
    14. 14. How common is it? • Common! – 3 rd most common medical symptom reported in general medical clinics – Most common complaint in over 75s – 22-30% annual prevalence (Neuhauser, 2009) (Kroenke, 1989) (Sloane, 1989)
    15. 15. Aetiology • Broad spectrum of causes • Surprisingly similar in varying settings – – – – A&E Primary care Medical clinics Dizziness clinics
    16. 16. Anatomy
    17. 17. Inner ear anatomy
    18. 18. Inner ear anatomy
    19. 19. The Hair Cell
    20. 20. Central integration
    21. 21. Vestibulo- ocular reflex Lateral rectus Medial rectus Oculomotor nucleus Abducens nucleus Vestibular nucleus Neural firing rate Head turning
    22. 22. Diagnostic strategy • Stepwise approach • First identify possible vestibular pathology – Does my dizzy/falling/unsteady/vertiginous patient have vestibular deficit? • Acute/intermittent vs chronic – Based on history • Peripheral vs central – History and examination
    23. 23. Acute causes • Peripheral – Often common and self limiting – Often outpatient management and follow up • Central – Rare but more serious – Often inpatient investigations
    24. 24. Differential diagnosis Acute/intermittent Chronic Peripheral Vestibular neuritis BPPV Meniere’s disease Central Stroke Vertiginous migraine Tumour/nerve compression Bilateral vestibular disorder Cholesteatoma Age related changes? Stroke Tumour Demyelination
    25. 25. Peripheral vs Central Disorder: Symptoms PVD Symptoms CVD Severe Vertigo Not always Severe at onset Nausea/Vomiting Rare Mild Imbalance Severe Common Hearing loss Rare Mild (except bilateral PVD) Oscillopsia Severe Rare Neurological symptoms Common Fast Compensation Slow
    26. 26. Identifying the vestibular patient - History • What do you mean by dizzy? – “…do you just feel lightheaded or do you see the world spin around you as if you had just got off a play-ground roundabout ?” (Evans, 1990) • Notoriously unreliable E.g. movement descriptions in syncope (Newman-Toker, 2007) – Timing • ?Acute onset • ?Recurrent – Trigger • ?Spontaneous – Triage • ?Red flags
    27. 27. Red flags in acute vertigo (adapted from Barraclough, 2009) • Any central neurological symptoms or signs – General neurological – HINTS testing • New type of headache (esp. occipital) – Suggests possible vascular event • Acute deafness – Suggests acute ischaemia/damage of the labyrinth or brainstem • Altered conscious – Needs syncope risk stratification if T-LOC – Encephalopathic process
    28. 28. Neurological examination – eyes • Eye movements – Assessment for nystagmus • Is it up/down beating? • Is it uni-directional? • Skew – Cover test • VOR assessment - Head thrust test • Dix-Hallpike to Epley manoeuvre if considering BPPV
    29. 29. Head Thrust Test
    30. 30. Videos • • • • Head thrust test – Gaze evolved nystagmus Cover test/skew deviation Dix-Hallpike 1a +/- 1b - bmj - utah - 3
    31. 31. HINTS testing • Abnormal head trust test less helpful • Can we improve bedside analysis • HINTS study (Kattah, 2009) – Head Impulse test – Nystagmus – direction changing, vertical – Test of Skew • 100% sensitive and 96% specific • Better than DW MRI up to 48 hours • Junior neurology residents similar ability 2010) (Chen,
    32. 32. Examination – ears and face • Tympanic membranes • New onset deafness • Pupils – ? Horners’ • Ataxia/cerebellar signs • Sensory loss • General neurological examination
    33. 33. Vertigo – what then?
    34. 34. Benign paroxysmal positional vertigo • Free floating otoconia in canals – Usually posterior • Most common cause of vertigo • Short lived intense rotatory vertigo related to reproducible head position • Vomiting unusual, hearing normal • Rotatory upbeating, non-sustained nystagmus (beware down beating) – Dix-Hallpike 79% sensitivity and 75% specificity (Halker, 2008) • Epley manoeuvre rapidly fix problem – 92% at 6 months and falls reduction (Gananca, 2010) (Richard, 2005)
    35. 35. Video – Epley manoeuvre
    36. 36. Summary • 62 year old smoker • Collapse and acute vertigo – Symptoms setting • Vomiting and ataxia • Nystagmus and hearing loss
    37. 37. Other points - examination • External ear normal • Nystagmus – Spontaneous bi-ocular leftwards horizontal jerk nystagmus accentuated by left gaze, suppressed by fixation • Hearing – Weber’s test to left • Thrust test positive to right
    38. 38. MRI
    39. 39. Progress • Remained ataxic • Stayed for further inpatient investigation • Neurology and ENT review – CVA? – Acute labyrinth failure ? cause • Sent to tertiary centre
    40. 40. Progress • Images r/v – ? Maturing frontal and cerebellar contusions and evolving subdural haematoma • CT head – R transverse petrous fracture involving labyrinth and petrous potion of semicircular canals • Gradual compensation • For local follow up with ENT and falls service
    41. 41. Summary 1. Vestibular anatomy/physiology explains vertigo 2. Careful history can exclude mimics 3. Care examination can differential peripheral and central causes
    42. 42. Mechanisms of Vertigo/dizziness • Baloh & Honrubia, 2001 Type Mechanism Physiological Sensory conflict due to unusual combination of sensory inputs e.g. motion Imbalance in tonic vestibular signals Vertigo Visual Multi-sensory Psychological Disequilibrium/ataxia Mismatch of visual and vestibular signals e.g. Ocular and vestibular pathology Impairment of 2 or more sensory inputs of balance Impairment of central integration of sensory inputs Loss of neurological function: proprioception, motor, cerebellar
    43. 43. Vestibular pathology - is it important? • Increasingly recognised – Associated with reduced quality of life – Symptoms often impairing • 80% in vestibular dizziness – Greatly increased risk of falls • x12 (Agrawal, 2009)
    44. 44. Vestibular pathology - is it important? • Asymptomatic prevalence exceptionally common • Also increased risk of falls • 35.4% of US adults aged 40 years • 84.8% in over 80s (Agrawal, 2009) – Accumulation of damage with poor compensation – Depletion of vestibular hair cells and otoliths – Dysfunction of the remaining hair cells – Loss of vestibular ganglion cells
    45. 45. Relevance to elderly care? • Age groups concerned • Non-specific presentation – Often referred to elderly care • Multi-factorial – Non speciality specific condition – Patient preference • Important sequelae – Falls/fractures/function • Treatable
    46. 46. Blood Supply
    47. 47. • http://www.asha.org/aud/articles/Centr alVestib/

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