Vestibular assessment
•Télécharger en tant que PPT, PDF•
13 j'aime•10,876 vues
Vestibujlar assessment
Recommandé
Recommandé
Contenu connexe
Tendances
Tendances (20)
En vedette
En vedette (20)
Similaire à Vestibular assessment
Similaire à Vestibular assessment (20)
Plus de SCGH ED CME
Plus de SCGH ED CME (20)
Dernier
Dernier (20)
Vestibular assessment
- 1. Assessing the vertiginous patient in ED Jim Fleet
- 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. 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. 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. History • No ongoing medical conditions and no regular medication • Smokes 20-30/day since youth • No alcohol
- 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. Examination • • • • • Truncal instability with ongoing vertigo Gait not assessed Pupils equal and responsive No ophthalmoplegia Loss of hearing right ear
- 8. Examination • Other cranial nerves normal • Tone, power, sensation all normal • Reflexes – 2+ and symmetrical – Plantars down-going
- 10. Investigations • ECG – sinus rhythm, normal axis • Blood – normal haematology and biochemistry
- 11. Summary • 62 year old smoker • Collapse and acute vertigo – Symptoms setting • Vomiting • Nystagmus and hearing loss • Investigations normal
- 12. How to Proceed? • Differential diagnosis? • Additional information – Further history? – Further investigation? – Further investigation? • Inpatient or outpatient?
- 15. 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)
- 16. 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)
- 17. Aetiology • Broad spectrum of causes • Surprisingly similar in varying settings – – – – A&E Primary care Medical clinics Dizziness clinics
- 18. Anatomy
- 21. The Hair Cell
- 23. Vestibulo- ocular reflex Lateral rectus Medial rectus Oculomotor nucleus Abducens nucleus Vestibular nucleus Neural firing rate Head turning
- 24. 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
- 25. Acute causes • Peripheral – Often common and self limiting – Often outpatient management and follow up • Central – Rare but more serious – Often inpatient investigations
- 26. 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
- 27. 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
- 28. 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
- 29. 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
- 30. 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
- 31. Head Thrust Test
- 32. Videos • • • • Head thrust test – Gaze evolved nystagmus Cover test/skew deviation Dix-Hallpike 1a +/- 1b - bmj - utah - 3
- 33. 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,
- 34. Examination – ears and face • Tympanic membranes • New onset deafness • Pupils – ? Horners’ • Ataxia/cerebellar signs • Sensory loss • General neurological examination
- 35. Vertigo – what then?
- 36. 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)
- 37. Video – Epley manoeuvre
- 38. Summary • 62 year old smoker • Collapse and acute vertigo – Symptoms setting • Vomiting and ataxia • Nystagmus and hearing loss
- 39. 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
- 40. MRI
- 41. Progress • Remained ataxic • Stayed for further inpatient investigation • Neurology and ENT review – CVA? – Acute labyrinth failure ? cause • Sent to tertiary centre
- 42. 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
- 43. Summary 1. Vestibular anatomy/physiology explains vertigo 2. Careful history can exclude mimics 3. Care examination can differential peripheral and central causes
- 46. 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
- 47. 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)
- 48. 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
- 49. 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
- 50. Blood Supply
Notes de l'éditeur
- 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!