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Dizziness & Vertigo. Moritz Haager Oct 16, 2003. WADO. 111 yo female presents to the ED with the complaint of feeling “weak and dizzy all over” How do you approach this? What are some of the key questions you should ask?. Objectives. Clearly define terminology Dizziness Vertigo
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Dizziness & Vertigo Moritz Haager Oct 16, 2003
WADO • 111 yo female presents to the ED with the complaint of feeling “weak and dizzy all over” • How do you approach this? • What are some of the key questions you should ask?
Objectives • Clearly define terminology • Dizziness • Vertigo • Syncope & pre-syncope • Examine the differential diagnosis for each • Look at what tests are useful • Look at what drugs are useful & when • Develop an approach to the weak & dizzy pt
Dizziness • Causes of dizziness in a outpatient neurology clinic specializing in dizziness
Dizziness is not a medical term • Breaks down into 4 general categories • Vertigo • e.g. BPPV • Syncope or pre-syncope • E.g. orthostatic hypotension • Dysequilibrium syndrome • Undifferentiated dizziness • Psychogenic • E.g. anxiety • Systemic illnesses w/ malaise • E.g. pyleonephritis, hypoglycemia • Who-kows-whats-the-&#@# -is-going-on-here
The Dizzy History • What do you mean by dizzy? • Vertigo vs. pre-syncope/syncope vs. weakness/malaise • What precipitates it? • How fast does it come on? How long does it last? • Are there any associated hearing changes? • Is there any evidence of other neurologic abnormalities? • What meds are you on, or have you been on recently? • Any head trauma?
Dysequilibrium Syndrome • Age-related degeneration of visual, proprioceptive, and vestibular systems • Pts have great difficulty with getting about especially at night with diminished light • Present to ED with hip fractures
Vertigo • Definition • The illusion or sensation of movement of the pt or the pts surroundings (aka “the spins” in EtOH intoxication) • Usually 2o to pathological basis, but need to differentiate benign from sinister • Start by differentiating peripheral vertigo from central
Anatomy for Dummies • Semi-circular canals • 3 semi-circular canals at right angles to each other to detect angular acceleration • Crista ampullaris = sensory organ • Sits in ampulla, and sends cilia from hair cells into gelatinous matrix (cupula) which moves opposite to direction of head movement due to surrounding viscous endolymph
Anatomy for Dummies • Utricle & Saccule • detect linear acceleration & changes in head position relative to gravity • Maculae are the sensory organs w/in these • Ca-carbonate crystals (= otoliths) in gelatinous matrix w/ embedded hair cells sense motion
Otoconia • Otoconia = debris in SCC either displaced otoliths (2o to trauma, infection etc) or clotted blood; can cause abnormal endolymph flow and hence inappropriate stimulation of vestibular systems
Peripheral Vertigo • SPINNED • S – Sudden onset / offset • P – Positional & fatigable • I – Intense (more than central) • N – Nausea & vomiting (more than central) • N – Normal neuro exam • E – Episodic (never lasts > 2weeks) • D – no neuro deficits
Central Gradual onset Milder intensity Continuous for wks – mos Min influenced by position Associated neuro findings Absence of auditory deficits Nystagmus Any direction Uni- or bilateral Not supressed by visual fixation (may enhance) Non-fatigable Mild intensity Sustained duration Short latency Peripheral Sudden onset Severe intensity Never lasts > 2 weeks Positional Normal neuro exam May have auditory complaints e.g. tinnitus Nystagmus Horizontal or rotatory Never vertical Bilateral Supressed by visual fixation Transient (lasts sec’s – mins) Episodic Mild – severe intensity Fatigable Long latency Central vs. Peripheral
Peripheral FB in ear canal Cerumen impaction AOM BPV Labyrinthitis (suppurative, serous, toxic, chronic) Meniere’s Dz: Vestibular neuronitis Acoustic neuroma Central Infection (meningitis, encephalitis, abscess) Vertebrobasilar insufficiency Cerebellar stroke Wallenberg’s syndrome PICA occlusion Subcalvian steal Head or neck trauma Vertebrobasilar migraine Multiple sclerosis Temporal lobe epilepsy Tumor Hypoglycemia Vertigo DDx
What is the most difficult central cause to detect? • Cerebellar infarction • Why? Scandinavian studies have shown that of older pts presenting with what appears to be peripheral vertigo 25% will actually have a cerebellar lesion • Makes sorting out the older pt with acute vertigo & imbalance more difficult • CT will NOT help you -- if you want to r/o post fossa stroke you need a MRI
Cerebellar Stroke • Account for ~1.5% of all strokes • Sudden onset severe vertigo, H/A, N & V, ataxia • May see ipsilateral CN VI deficit • 2 common presentations are Anterior inferior cerebellar artery infarct & posterior inferior cerebellar artery infarct • The things that will kill you: • brainstem compression secondary to edema • brainstem infarction • hydrocephalus • Tx • Hydrocephalus may be amenable to surgical Tx • Phenothiazines or odansetron for Sx control; • Antiplatelet Tx +/- warfarin, CVS Dz RF modification • Vestibular rehab once past acute phase • Reasonable to start ASA in these pts & arrange close f/u if otherwise well
AICA • Ant inf Cerebellar a. infarct: • AICA supplies lateral cerebellum, dorsolateral pons, and labyrinth • Sx depend on which of these are occluded • Vertigo, N & V, ataxia = ant vestibular branch of labyrinth a. • Hearing loss & tinnitus = common cochlear branch of labyrinth a. • Dysarthria, ipsilateral facial palsy & trigeminal sensory loss, Horner’s syndrome, dysmetria, contralateral pain & temp loss = pontine a.
Wallenberg’s Syndrome • PICA occlusion • Infarcts post inf cerebellum & dorsolateral medulla • Sx: • Vertigo (vestibular nucleus in lateral medulla) • N & V • Nystagmus that (if horizontal) may reverse direction on gaze toward affected side • loss of pain & temp sensation on ipsilateral face and contralateral body, • Ataxia & lateropulsion towards affected side • hoarseness due to paralysis of palate, pharynx, and larynx • Horners syndrome
Pharmacological Management • Diazepam • 2-10 mg tid • Anticholinergics • Indicated for vestibular neuronitis (incl. RH Syndrome), & labyrinthitis • Meclizine (anti-vert) 25 mg q8h • Diphenhydramine (benadryl) 25-50 mg q6-8h • Promethazine (Phenergan) • 25-50 mg PO/PR/IM q6-8h • 12.5-25 mg IV • Droperidol 2.5 mg IV • Ondansetron • Indicated for severe refractory N & V from central causes • 4 mg q8h x 3 d
Pharmacological Management • Prednisone • Indicated for Acute vestibular neuronits, RH Syndrome, & severe N & V from central causes • 60 mg PO qd, then taper over 10d • Acyclovir • Indicated for Ramsay Hunt syndrome • Important to start ASAP (ideally within 3 d of onset) to reduce facial nerve degeneration & hearing loss) • 400 mg 5x/d x10 d • Antibiotics • As indicated for Tx of OM in labyrinthitis
Non-Pharmacological Mgmt • Vestibular Rehabilitation • Not effective for central processes where nystagmus & vertigo don’t fatigue or habituate • Will discuss more later
BPPVBenign Paroxysmal Positional Vertigo • Short-lived (usually seconds) • Positional • often one triggering position or certain head positions w/ horizotorotary nystagmus that can be reproduced at bedside • Fatigable • Associated N & V • Most common cause of “dizzy spells” in elderly; incidence increases with age • Debris (otoconia) from utricle floats into post semicircular canal in supine position – vertical head movements cause debris movement and stimulation of cupula causing Sx • Often follows vestibular neuritis or minor head trauma
Roll Test • For horizontal SCC BPPV • Often won’t see nystagmus w Hallpike • Roll in plane of horizontal SCC • A. start supine • B. rapidly roll head to one side and look for nystagmus & vertigo • C. repeat other side – affected side down will cause more nystagmus & vertigo • Can tell free-floating otoconia (canalithiasis) from otoconia fixed to cupula (cupulolithiasis) based on direction & duration of nystagmus • Canalithiasis – geotropic & fatigable • Cupulolithiasis – ageotropic & sustained
BPPV • Tx • Vestibular suppressants short-term and prior to canalith repositioning maneuvers • Canalith repositioning maneuvers (Epley or Semont) • Said to be effective in 85-95% of pts w/ one treatment • Pts can be taught to do this at home • Continue until no further vertigo even w/ maneuver
Canalith Repositioning Maneuvers • Side effects • Neck pain ~6% • Tx failure or displacing otoconia into another SCC ~6% • Emesis ~1% • Canalith jam • Conversion of transient nystagmus to persistent nystagmus irrespective to head position (Tx w/ vibrator or repeat maneuver) • Contraindications • Severe cervical spine disease • Unstable cardiac disease • High grade carotid stenosis
Canalith Repositioning Maneuver: How effective are they? • Reports vary from 66-100% success in alleviating or decreasing Sx • 30-50% will have recurrence requiring repeat Tx • Problems • no ED-based studies • Small sample sizes • Numerous outcome variables studied • Highly selected populations • Bottom-line: • Appear to be efficacious & safe – perhaps we are underutilizing them in the ED
Epley Maneuver • Best for post SCC canalithiasis • A. sitting upright turn head 45 deg towards affected side • B. lie down into Dix-Hallpike position for min until Sx abate (20 sec – 4) • C. slowly turn head toward unaffected side keeping neck extended & maintain for 20 secs • D. Roll onto side with head turned 45 deg down towards floor. Maintain for 20 sec. • E. Sit pt up slowly keeping head pitched down and deviated toward unaffected side • Final instructions should be minimal had movements, no bending over, lying down, or head tilting for rest of day. F/U in 2 days -- 50% will have recurrence
Semont Maneuver • Best for post SCC cupulolithiasis • 2nd choice for canaltithiasis • Difficult in elderly b/c requires fast movements • A. rotate head 45o to unaffected side; maintain this head position throughout • B. rapidly lie pt down sideways onto affected side – wait 20 sec • C. rapidly move pt through sitting position into affected side down – wait 20 sec • D. Move slowly into sitting position • Repeat entire procedure again • Same post-procedure care as Epley’s
Brandt-Daroff TxVestibular Rehabilitation Therapy • 3d line Tx for mild BPPV • Can take up to 2 weeks to work • A. turn head 45o to unaffected side • B. lie down rapidly on affected side – hold for 20 sec or until vertigo stops • C. sit up slowly, wait 20 sec • D. turn head 45o to other side & repeat procedure on other side • Repeat 5 times in each direction 1-3x/d for until no vertigo for 2 consecutive days (up to 2 weeks) • Works by moving otoconia back & forth allowing it to move out of SCC & break up & dissolve
Bar-B-Q Tx • For Tx of horizontal SCC BPPV • A. lie supine w/ affected ear down • B. Slowly roll head into supine position – hold for 15 sec or until vertigo stops • C. Roll head onto other side -- hold for 15 sec or until vertigo stops • D. Roll head and body in same direction into prone position -- hold for 15 sec or until vertigo stops • E. Roll head and body in same direction back into original starting position • Slowly bring into sitting position • For cupulolithiasis same procedure but more rapid head turning to try & dislodge otoconia
Serous Labyrinthitis • Mild – severe positional Sx • Usually follows ENT infection • Acute severe vertigo, N & V,a associated hearing loss of variable severity & onset • Minimal fever, not toxic • Bacterial or viral etiology
Acute Suppurative Labyrinthitis • Sx • Coexisting acute exudative bacterial inner ear infection • Severe N & V & hearing loss • Febrile toxic pt • Tx • Admit for IV Abx +/- surgical I & D
Toxic Labyrinthitis • Sx • Gradually progressive Sx • Secondary to ototoxic meds • Can get hearing loss & severe N & V • Gent more toxic to vestibular hair cells than cochlear function • No positional nystagmus • Tx • Stop toxic drug • ?steroids
Vestibular Neuronitis • Presentation • Peak incidence in 30’s -50-s • Acute severe vertigo; Inc’s rapidly in intensity (hrs) & subsides gradually (days) • Can have mild persistent positional vertigo for wks – mos • Get N & V, but NO auditory Sx : Primary difference b/w neuronitis & labyrinthitis is lack of tinnitus or hearing loss in neuronits • Antecedent common cold in ~50%, or ototoxic exposure • Likely reactivation of dormant HSV infection in Scarpas ganglia within vestibular nerve • Ramsay Hunt Syndrome = rare variant of vestibular neuronitis due to varicella zoster w/ CN VII & VIII deficits. • Tx with acyclovir & prednisone • Tx • Prednisone for 10d may shorten course • Vestibular rehab
Meniere’s Dz • Presentation • Recurrent sudden onset episodic severe rotational vertigo • Last hrs - days • Get long Sx-free remissions • Associated N & V, tinnitus, & fluctuating hearing loss (low frequency senorineural) • Felt to be due to decreased endolymph resorption in endolymphatic sac • Tx • Low Na diet (<2 g/d), avoid caffeine & EtOH, quit smoking • Vasodilators, diuretics (acetazolamide 250 bid) • Chemical ablation of vestibular function (streptomycin, gentamicin) • Surgery
Acoustic Neuroma(= vestibular schwannoma) • Gradual onset & increasing severity of: • Progressive or sudden unilateral sensorineural hearing loss • Tinnitus • Vertigo = presenting Sx in up to 38% of pts • Ataxia (truncal) • Neuro findings (diminution or absence of corneal reflex; CN VIII deficit • Predisposed to females b/w 30-60 yo • Dx • look for speech discrimination deficits (light, right, might) • MRI w/ gadolinium 100% sensitive; CT & unenhanced MRI will miss it! • Tx • Observation w/ serial imaging • Surgical resection or XRT
Vertebrobasilar Insufficiency • Get isolated vertigo lasting secs – mins • Often associated: • Headache • Neuro Sx (dysarthria, ataxia, weakness, numbness, diplopia) • TIA’s • Dx • MRI, doppler U/S of carotids & vertebrals • Tx • CVD risk factor modification, ASA, +/- warfarin
Subclavian Steal Syndrome • May present w/ syncopal episodes but usually w/ more subtle Sx: • Arm fatigue & cramps • Lightheadedness • Vertigo • Dec’s or absent radial pulse on affected side • Investigate w/ doppler U/S of carotid & vertebral vessels +/- angiogram
Head & Neck Trauma • Usually onset within 10 days of trauma • May last wks – mos • Positional & episodic lasting secs – mins • Usually self-limited • Related to inner ear fistula or otoconia usually
Vertebrobasilar Migraine • Typically begins in adolescence: • Multiple neuro Sx followed by headache: • Vertigo • Dysarthria • Ataxia • Visual disturbances • Paresthesias • Complete resolution of neuro abnormalities after attack subsides
Multiple Sclerosis • Onset usually in 20’s-40’s • Bilateral internuclear opthalmoplegia virtually pathognomonic • Vertigo develops in ~30% at some point • Associated ataxic eye movements • N & V
Temporal Lobe Epilepsy • Spectrum of Sx: • Vertigo • Memory impairments • Hallucinations • Trance-like state • Blatant seizure activity • aphasia
Vestibular Hypofunction • Present w/ chronic unsteadiness and oscillopsia (illusion of motion in visual environment) • ~50% have associated hearing loss • Usually bilateral loss of vestibular function most commonly idiopathic (degenerative), ~30% due to ototoxicity (gent) • Don’t usually have vertigo b/c of bilateral nature of vestibular loss • Tx • Vestibular rehab
Meds that cause the Spins • Vestibular Suppressants • Meclizine • Diazepam • Short term use only as interfere with central compensation & can lead to withdrawal effects • Anti-convulsants • Phenytoin, carbamezapine, barbiturates • Anti-hypertensives • HCTZ, lasix (ototoxic also), beta-blockers, alpha-blockers (prazosin, terosine), CCB’s • NSAIDs • ASA is ototoxic
Meds that cause the Spins • Antiarrythmics • Amiodarone, quinine • Anti-depressants • amitryptiline, imipramine • BDZ’s • Muscle relaxants • Cyclobenzaprine, orphenidriine, methocarbomol • Antibiotics • Streptomycin, gentamicin, tobramycin (ototoxicit) • Chemotherapy agents • Cisplatin (ototoxic)
Definition • Sudden & temporary transient loss of consciousness and concurrent loss of postural tone with spontaneous recovery
The Trouble w/ Syncope • Syncope is a Sx, not a disease • > 40 causes listed in Rosen’s • By the time pt arrives they’re usually asymptomatic • DDx ranges from benign causes to potentially fatal • Lack of clear guidelines for investigations • Difficult area to research given transient nature of Sx, and lack of gold standard diagnostic tool or work-up • Precludes a one-size-fits-all approach