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Saleh Fares Aal-Ali FRCP-R3
“As the world Turns” Saleh Fares Aal-Ali FRCP-R3
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Objective to be addressed:
Difference between dizziness and vertigo. Diagnostic approach to True vertigo. Characteristics of peripheral vertigo. Characteristics of central vertigo. Treatment Considerations.
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Patients refer to Dizziness as:
Light headedness Sense of strangeness Faintness Giddy Imbalanced “out-of-it”
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Most dizzy patients can be placed in to one of four categories:
1- True Vertigo (50%)
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2-Pre-syncope: Transient sensation that a faint in about to occur.
May present as nausea ,weakness, SOB or change in vision. Transient.
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3-Dysequilibrium: No illusion. No sense of faintness.
A sensation of imbalance when standing or walking. No illusion. No sense of faintness.
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4-Vague lightheadedness:
Holds the reminder of symptoms of dizziness (which can’t fit to the other categories) Psychiatric disorders, Hyperventilation syndrome Encephalopathies
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What is Vertigo?
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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.
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How do we maintain equilibrium?
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Visual input Proprioceptiual input Vestibular input labyrinths.
equilibrium Proprioceptiual input Vestibular input labyrinths.
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Anatomy: Semicircular canals
Semicircular Canals (SCC) Horizontal Anterior Posterior Cupula End organ receptors Endolymph
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Anatomy: Utricle Utricle Connected to SCC Contains endolymph
Otoliths (otoconia) Calcium carbonate Attached to hair cells Macule (end organ)
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Vestibular system Tells brain which way the head moves without looking
SCC: angular acceleration Utricle: linear acceleration
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How can we clinically evaluate the patient with vertigo?
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labyrinth Vertigo Brainstem Cerebellum CN VIII (Vestibular portion)
nuclei
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Vertigo Central peripheral
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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?
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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?
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Key points in the physical examination:
Vital signs Bruits Ear exam Eye exam Positional testing Neurological exam (including gait)
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SPINNED PERIPHERAL CENTRAL Yes Slow, gradual No Severe Ill defined
Sudden (Onset) Yes Slow, gradual Positional No Intensity Severe Ill defined Nausea/Diaphoresis Frequent Infrequent Nystagmus Torsional/horizontal Vertical Ear (hearing loss) Can be present Absent Duration Paroxysmal Constant CNS signs Usually present Carvalho et al. CTU , Oct, 2004
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Case 1
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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.
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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.
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BPPV Benign Paroxysmal Positional Vertigo Age 60- 70 (F:M 2:1)
Head trauma
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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
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“BPPV” “B” = Benign Not a brain tumor Can be severe and disabling
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“BPPV” “P” = Paroxysmal Episodic, not persistent
Helpful feature in the differential diagnosis
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“BPPV” “P” = Positional Occurs with position of head
Turning over in bed Looking up Bending over
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“BPPV” “V” = Vertigo An illusion of motion “The room is spinning”
Other descriptions Rocking Tilting Somersaulting Descending in an elevator
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Pathophysiology of BPPV
Otoliths become detached from hair cells in utricle Inappropriately enter the posterior semicircular canal . Parnes LS, McClure JA. Laryngoscope 1992;102:
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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”
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Pathophysiology of 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
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Dix-Hallpike 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, Nylen, or Hallpike maneuver
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Dix-Hallpike 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.
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Lab studies In a straightforward case, no lab studies are needed!
Hemoglobin Fingerstick glucose Electrolytes if prolonged vomiting BHCG
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ED Therapy: 1-The 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. Epley J. Otolaryngol Head Neck Surg 1992;107: Lynn S, et al. Otolaryngol Head Neck Surg 1995;113:
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Epley Maneuver: Randomized controlled trials reported success rates ranging from 44% % Froehling et al. Mayo clin proc Jul 2000 Wolf et al. Clin otolaryngol feb 1999 Asawarichianginda et al ENT J Sep 2000
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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
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Epley maneuver 1. Repeat Hallpike
Previously performed diagnostic Hallpike test tells you the starting position (right or left)
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Epley maneuver 2. Turn head 90 degrees in the other direction
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Epley maneuver 3. Patient rolls onto shoulder, rotates head and looks down towards floor
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Epley maneuver
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Epley maneuver Repeating the Epley maneuver Post procedure
Remain upright for 8-24 hours
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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:
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Complications Vomiting Converting to horizontal canal BPPV
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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)
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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)
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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:
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The Vast majority of peripheral vertigo can be managed conservatively.
Surgery for intractable and incapacitating symptoms.
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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 middle-aged adults Often after respiratory infections self-limiting
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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) Self-limiting
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Meniere’s disease: Characterized by triad of: vertigo tinnitus
hearing loss (sensorineural) Chronic relapsing illness (? familial) Due to a build-up of endolymphatic pressure in the labyrinth. Treatment: vestibular suppressants.
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Meniere’s disease
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When to D/C? 1- Peripheral vertigo. 2- Healthy 3- Help at home.
4- Symptoms controlled. 5- Able to ambulate.
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F/U with PMD to arrange further evaluation if patient does not improve.
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Case 2
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Central vertigo May include disorders with significant potential morbidity. Warrants the initiation of further work-up.
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SPINNED PERIPHERAL CENTRAL Yes Slow, gradual No Severe Ill defined
Sudden (Onset) Yes Slow, gradual Positional No Intensity Severe Ill defined Nausea/Diaphoresis Frequent Infrequent Nystagmus Torsional/horizontal Vertical Ear (hearing loss) Can be present Absent Duration Paroxysmal Constant CNS signs Usually present Carvalho et al. CTU , Oct, 2004
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Differential Diagnosis:
Vertebral-basilar circulation events: Vestibular nuclei (TIA or stroke) Cerebellar infarction or hemorrhage Lateral medullary infarction (Wallenberg’s syndrome) 15
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4. Vertebral artery dissection
Migraine Post concussive syndrome. Tumors (acoustic reuromas) Multiple sclerosis Infection (encephalitis, meningitis)
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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.
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Twenty four patients with risk factors with stroke with history of vertigo (>48 hrs) and normal neurologic exam (except nystagemus) % had inferior cerebellar infarction. Norrving et al. Acta Neurol Scand. Jan 1995
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CT vs MRI: MRI/MRA for vertebrobasilar disease and cerebellar ischemia . CT is more sensitive for hemorrhage negative CT is not always reassuring.
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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."
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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”.
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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."
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