Vertigo - “As the world Turns” Saleh Fares Aal­Ali...

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Unformatted text preview: “As the world Turns” Saleh Fares Aal­Ali FRCP­R3 Objective to be addressed: Objective to be addressed: Difference between dizziness and vertigo. • Diagnostic approach to True vertigo. • Characteristics of peripheral vertigo. • Characteristics of central vertigo. • Treatment Considerations. Patients refer to Dizziness as: Patients refer to Dizziness as: • Light headedness • Sense of strangeness • Faintness • Giddy • Imbalanced • “out-of-it” Most dizzy patients can be placed in to one of four categories: 1- True Vertigo (50%) 2­Pre­syncope: 2­Pre­syncope: Transient sensation that a faint in about to occur. • May present as nausea ,weakness, SOB or change in vision. • Transient. 3­Dysequilibrium: 3­Dysequilibrium: A sensation of imbalance when standing or walking. • No illusion. • No sense of faintness. 4­Vague lightheadedness: 4­Vague lightheadedness: Holds the reminder of symptoms of dizziness (which can’t fit to the other categories) 1.Psychiatric disorders, 2.Hyperventilation syndrome 3.Encephalopathies What is Vertigo? What is Vertigo? True vertigo: True vertigo: Defined as an “illusion” or “hallucination” of movement. • Both vertigo and dysequilibrium imply a loss of balance, but vertigo involves a sense of motion. How do we maintain How do we maintain equilibrium? Visual input Visual input equilibrium Proprioceptiual Vestibular input input labyrinths. Anatomy: Semicircular canals Anatomy: Semicircular canals Semicircular Canals (SCC) Cupula Horizontal Anterior Posterior End organ receptors Endolymph Anatomy: Utricle Anatomy: Utricle Utricle Connected to SCC Contains endolymph Otoliths (otoconia) Calcium carbonate Attached to hair cells Macule (end organ) Vestibular system Vestibular system Tells brain which way the head moves without looking SCC: angular acceleration Utricle: linear acceleration How can we clinically evaluate How can we clinically evaluate the patient with vertigo? CN VIII labyrinth Cerebellum (Vestibular portion) Vertigo Brainstem Vestibular nuclei Vertigo Vertigo Central peripheral Key points in History: Key points in History: •Is true vertigo present? •Are there associated neurologic symptoms? •What is the pattern of onset ? •What is the duration of the symptoms? •Have there been auditory symptoms? •Are there other associated symptoms? •What medications is the patient taking? •What is the patient’s past medical history? •Any recent or remote head or neck injury? Key points in the physical Key points in the physical examination: •Vital signs •Bruits •Ear exam •Eye exam •Positional testing •Neurological exam (including gait) SPINNED SPINNED PERIPHERAL CENTRAL Sudden (Onset) Positional Intensity Nausea/Diaphoresis Yes Yes Severe Frequent Nystagmus Torsional/horizontal Ear (hearing loss) Can be present Paroxysmal Absent Slow, gradual No Ill defined Duration CNS signs Carvalho et al. Infrequent Vertical Absent Constant Usually present CTU , Oct, 2004 Case 1 Case 1 Peripheral vertigo: Peripheral vertigo: •Approximation 85% of ED patients with vertigo. •Due to dysfunction of one of vestibular organs. •Asymmetry of input •Sensation of rotation •Associated with nausea, pallor and diaphoresis. Differential Diagnosis Differential Diagnosis Benign paroxysmal positional vertigo (BPPV) (50%) Vestibular neuritis Labyrinthitis (suppurative, serous, toxic, chronic) Meniere’s disease FB in ear canal A cute otitis media Perilymphatic fistula. BPPV BPPV Benign Paroxysmal Positional Vertigo Age 60­ 70 (F:M 2:1) Head trauma Characteristic story Characteristic story Turn head After a few seconds delay, vertigo occurs Resolves within 1 minute if you don’t move If you turn your head back, vertigo recurs in the opposite direction “BPPV” “B” = Benign Not a brain tumor Can be severe and disabling “BPPV” “P” = Paroxysmal Episodic, not persistent Helpful feature in the differential diagnosis “BPPV” “P” = Positional Occurs with position of head Turning over in bed Looking up Bending over “BPPV” “V” = Vertigo An illusion of motion “The room is spinning” Other descriptions Rocking Tilting Somersaulting Descending in an elevator Pathophysiology of BPPV Pathophysiology of BPPV Otoliths become detached from hair cells in utricle Inappropriately enter the posterior semicircular canal . Parnes LS, McClure JA. Laryngoscope 1992;102:988-92. Physiology Physiology Normal situation As one turns head to the right Endolymph moves SCC receptors fire “head turning right” Stop turning head endolymph stops moving SCC receptors stop firing “head has stopped moving” Pathophysiology of BPPV Pathophysiology of BPPV BPPV Stop turning head otoliths keep moving drag endolymph receptors continue to fire inappropriately “head is still moving” Eyes “head is NOT moving” Brain room must be spinning in the opposite direction Dix­Hallpike Maneuver Dix­Hallpike Maneuver •The diagnosis of BPPV is generally from the history. •Can confirm the diagnosis of BPPV •First described by Dix and Hallpike in 1952. •Also called the Nylen-Bárány, Bárány, Bárány Nylen, or Hallpike maneuver Dix­Hallpike Maneuver Dix­Hallpike Maneuver They include: 1- Nystagmus 2- Provocative head position 3- Brief latency to symptoms after change in position 4- Short duration of attack 5- Fatigability of nystagmus on repeat testing 6-Reverse of nystagmus on returning to upright position. Lab studies Lab studies In a straightforward case, no lab studies are needed! Hemoglobin Fingerstick glucose Electrolytes if prolonged vomiting BHCG ED Therapy: 1­The Epley Maneuver 1­The Epley Maneuver First described in 19922 Bedside Immediate relief Epley reported an 80% success rate after a single time and 100% success rate after more than one session 30% recurrence rate over a 30-month period. 2. 3. Epley J. Otolaryngol Head Neck Surg 1992;107:399-404 Lynn S, et al. Otolaryngol Head Neck Surg 1995;113:712-20. Epley Maneuver: Epley Maneuver: Randomized controlled trials reported success rates ranging from 44% ­ 88% •Froehling et al. •Wolf et al. Mayo clin proc Clin otolaryngol •Asawarichianginda et al. Jul 2000 feb 1999 ENT J Sep 2000 Epley maneuver Epley maneuver Canalith repositioning maneuver 5 step head hanging maneuver Moves otoliths out of the posterior semicircular canal and back into utricle where they belong Epley maneuver Epley maneuver 1. Repeat Hallpike Previously performed diagnostic Hallpike test tells you the starting position (right or left) Epley maneuver Epley maneuver 2. Turn head 90 degrees in the other direction Epley maneuver Epley maneuver 3. Patient rolls onto shoulder, rotates head and looks down towards floor Epley maneuver Epley maneuver Epley maneuver Epley maneuver Repeating the Epley maneuver Post procedure Remain upright for 8­24 hours The Epley Maneuver The Epley Maneuver Contraindications Unstable heart disease High grade carotid stenosis Severe neck disease Ongoing CNS disease (TIA/stroke) Pregnancy beyond 24th week gestation (relative) Furman JM, Cass SP. N Engl J Med 1999;341:1590-96 Complications Complications Vomiting Converting to horizontal canal BPPV ED therapy ED therapy 2- Vestibular Suppressants: •Meclizine is the most commonly used (H1 – antagonist) •Can significanthy reduce symptoms. Cohen et at. Arch Nenrol. Aug 1972(RCT) •Dimenhydrinate (Gravol) and diphenhydramine (Benedryl) have also been used. •Their efficacy is likely mediated by their anticholinergic activity. •They inhibit muscarinic acetylcholine receptors involved in feedback from the brainstem to the vestibular labyrinth. •If N/V promethazine (phenergan) or prochlorperazine (stemetil) (extrapyramidal effect) Benzodiazepines Benzodiazepines generalized inhibition of neural activity In a review article: Authors did not encourage the use of vestibular suppressants: • suppress the intensity of symptoms. • but do not reduce the frequency of attacks. Furman JM, Cass SP. N Engl J Med 1999;341:1590-96 The Vast majority of peripheral vertigo can be managed conservatively. Surgery for intractable and incapacitating symptoms. Labyrinthitis and Vestibular Labyrinthitis and Vestibular neuronitis A cute unilateral loss of peripheral vestibular function Associated with vertigo, N/V, and nystagmus Worsened by head movement Occurs in healthy young to middle­aged adults Often after respiratory infections self­limiting Perilymphatic fistula: Perilymphatic fistula: Due to a traumatic “fistula” at the round or oval window. After forceful cough, sneeze, scuba diving or direct blow to the ear. Recurrence of vertigo with pneumo­ otoscopy (Hennebert’s sign) Self­limiting Meniere’s disease: Meniere’s disease: Characterized by triad of: • vertigo • tinnitus • hearing loss (sensorineural) Chronic relapsing illness (? familial) Due to a build­up of endolymphatic pressure in the labyrinth. Treatment: vestibular suppressants. Meniere’s disease Meniere’s When to D/C? When to D/C? 1­ Peripheral vertigo. 2- Healthy 3- Help at home. 4- Symptoms controlled. 5- Able to ambulate. F/U with PMD to arrange further evaluation if patient does not improve. Case 2 Case 2 Central vertigo Central vertigo May include disorders with significant potential morbidity. Warrants the initiation of further work­up. SPINNED SPINNED PERIPHERAL CENTRAL Sudden (Onset) Positional Intensity Nausea/Diaphoresis Yes Yes Severe Frequent Nystagmus Torsional/horizontal Ear (hearing loss) Can be present Paroxysmal Absent Slow, gradual No Ill defined Duration CNS signs Carvalho et al. Infrequent Vertical Absent Constant Usually present CTU , Oct, 2004 Differential Diagnosis: Differential Diagnosis Vertebral­basilar circulation events: 1. Vestibular nuclei (TIA or stroke) 2. Cerebellar infarction or hemorrhage 3. Lateral medullary infarction (Wallenberg’s syndrome) 4. Vertebral artery dissection 4. Vertebral artery dissection Migraine Post concussive syndrome. Tumors (acoustic reuromas) Multiple sclerosis Infection (encephalitis, meningitis) Neuroimaging in vertigo: Neuroimaging in vertigo: Headache(sudden onset or severe) Hard neurological findings No imaging for patients with no risk factors and exam suggestive of peripheral vertigo. Twenty four patients with risk factors with stroke with history of vertigo (>48 hrs) and normal neurologic exam (except nystagemus) 25% had inferior cerebellar infarction. Norrving et al. Acta Neurol Scand. Jan 1995 CT vs MRI: CT MRI/MRA for vertebrobasilar disease and cerebellar ischemia . CT is more sensitive for hemorrhage negative CT is not always reassuring. Bad Excuses In Court: Bad Excuses In Court: 1. "I thought the medications would help…not cause her to fall and break her hip.“ 2. "I know it was vertical nystagmus, but there were no other neurological findings so I assumed it was peripheral vertigo." 3. "I thought it was obvious that the patient shouldn’t drive." 4. "The vertigo had subsided, so I thought it was okay for him to walk to the bathroom.“ 5. "The patient was too young to worry about a stroke”. 6. "I didn’t know that the patient had decreased hearing.“ 7. "The CT was normal, so I thought it was safe to send the patient home." 8. "The patient came from the psychiatric hospital, so I assumed that he was crazy." The end The end ...
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