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Vertigo and Dizziness

Presented by A. Hillier, D.O.
        EM Resident
St. John West Shore Hospital
Vertigo and Dizziness
 Prevalence
  1  in 5 adults report dizziness in last month
   Increases in elderly
   Worsened by decreased visual acuity,
    proprioception and vestibular input
 Dizziness
   Non-specific term
   Different meanings to different people
     Could    mean
        -   Vertigo    - Syncope         - Presyncope
        -   Weak       - Giddiness       - Anxiety
        -   Anemia     - Depression      - Unsteady
Vertigo and Dizziness
 Vertigo
   Perception of movement
   Peripheral or Central



 Syncope
   Transient  loss of consciousness with loss of
    postural tone
Vertigo and Dizziness
 Presyncope
   Lightheadedness-an     impending loss of
    consciousness
 Psychiatric   dizziness
   Dizziness   not related to vestibular dysfunction
 Disequilibrium
   Feeling of unsteadiness, imbalance or
    sensation of “floating” while walking
Vestibular Labyrinth
 Pathophysiology
   Complex   interaction of visual, vestibular and
     proprioceptive inputs that the CNS integrates as
     motion and spatial orientation
3   semicircular canals
   rotational   movement
   cupula
2   otolithic organs
   utricle& saccule
   linear acceleration
   Macula
Vertigo and Dizziness
 Normally there is balanced input from both
 vestibular systems

 Vertigo   develops from asymmetrical vestibular
 activity

 Abnormal  bilateral vestibular activation results
 in truncal ataxia
Vertigo and Dizziness
 Nystagmus
   Rhythmic   slow and fast eye movement
      Direction
               named by fast component
      Slow component due to vestibular or brainstem activity
      Slow component usually ipsilateral to diseased structure
      Fast component due to cortical correction

 Physiologic      Vertigo
   “motion sickness”
   A mismatch between visual, proprioceptive and
    vestibular inputs
   Not a diseased cochleovestibular system or CNS
Vertigo-Differential Diagnoses
 Etiologies         of Vertigo      CNS infection (TB, Syphillis)
     BPPV                           Tumor (Benign or Neoplastic)
     Labyrintitis                   Cerebellar infarct
        Acute suppurative           Cerebellar hemorrhage
        Serous                      Vertebrobasilar insufficiency
        Toxic                       AICA syndrome
        Chronic
                                     PICA syndrome
     Vestibular neuronitis          Multiple Sclerosis
     Vestibular ganglionitis        Basilar artery migraine
     Ménière’s                      Hypothyroidism
     Acoustic neuroma               Hypoglycemia
     Perilymphatic fistula          Traumatic
     Cerumen impaction              Hematologic (Waldenstroms)
Vertigo-History
 Is it true vertigo?     Unusual  eye
 Autonomic                movements?
                          Any past head or
  symptoms?
                           neck trauma?
 Pattern of onset and
                          Past medical history?
  duration
                          Previous symptoms?
 Auditory
                          Prescribed and OTC
  disturbances?            medications?
 Neurologic              Drug and alcohol
  disturbances?            intake?
 Was there syncope?
Vertigo-Physical Exam
   Cerumen/FB in EAC
   Otitis media              Auscultate for carotid bruits
   Pneumatic otoscopy        Orthostatic vital signs
   Tympanosclerosis or TM  BP and pulse in both arms
    perforation               Dix-Hallpike maneuver
   Nystagmus                 Gross hearing
   Fundoscopic exam          Weber-Rinne test
   Pupillary abnormalities   External auditory canal vesicles
   Extraocular muscles       Muscle strength
   Cranial nerves            Gait and Cerebellar function
   Internuclear ophthalmoplegia
Dix-Hallpike Maneuver




Figure 1. Dix-Hallpike maneuver (used to diagnose benign paroxysmal
   positional vertigo). This test consists of a series of two maneuvers: With the
   patient sitting on the examination table, facing forward, eyes open, the
   physician turns the patient's head 45 degrees to the right (A). The physician
   supports the patient's head as the patient lies back quickly from a sitting to
   supine position, ending with the head hanging 20 degrees off the end of the
   examination table. The patient remains in this position for 30 seconds (B).
   Then the patient returns to the upright position and is observed for 30
   seconds. Next, the maneuver is repeated with the patient's head turned to
   the left. A positive test is indicated if any of these maneuvers provide vertigo
   with or without nystagmus.
Vertigo-Characteristics
                    Peripheral        Central
Onset               Sudden            Usually slow
Severity of Vertigo Intense           Usually mild
Pattern             Paroxysmal        Constant
Exac. by movement Yes                 Variable
Autonomic           Frequent          Variable
Laterality          Unilateral        Uni or bilat
Nystagmus           Horizontorotary   Any
Fatigable/Fixation  Yes               No
Auditory symptoms Yes                 No
TM                  May be abnormal   Normal
CNS symptoms        Absent            Present
Vertigo-Ancillary Tests
 CT-if cerebellar mass, hemorrhage or
  infarction suspected
 Glucose and ECG in the “dizzy” patient
 Cold caloric testing
 Angiography for suspected VBI
 MRI
 Electronystagmography and audiology
Peripheral Vertigo-Differential
 Labyrinthine   Disorders
   Most  common cause of true vertigo
   Five entities
    Benign paroxysmal positional vertigo (BPPV)
    Labyrinthitis
    Ménière disease
    Vestibular neuronitis
    Acoustic Neuroma
Benign Paroxysmal Positional
              Vertigo
 Extremely  common
 Otoconia displacement
 No hearing loss or tinnitus
 Short-lived episodes brought on by rapid
  changes in head position
 Usually a single position that elicits vertigo
 Horizontorotary nystagmus with crescendo-
  decrescendo pattern after slight latency period
 Less pronounced with repeated stimuli
 Typically can be reproduced at bedside with
  positioning maneuvers
Otoconia in BPPV
Labyrinthitis
 Associated  hearing loss and tinnitus
 Involves the cochlear and vestibular
  systems
 Abrupt onset
 Usually continuous
 Four types of Labyrinthitis
   Serous
   Acute   suppurative
   Toxic
   Chronic
Labyrinthitis
 Serous
   Adjacent   inflammation due to ENT or meningeal
    infection
   Mild to severe vertigo with nausea and vomiting
   May have some degree of permanent impairment



 Acute   suppurative labyrinthitis
   Acute bacterial exudative infection in middle ear
   Secondary to otitis media or meningitis
   Severe hearing loss and vertigo
   Treated with admission and IV antibiotics
Labyrinthitis
 Toxic
   Due    to toxic effects of medications
   Still relatively common
   Mild tinnitus and high frequency hearing loss
   Vertigo in acute phase
   Ataxia in the chronic phase
   Common etiologies

    -Aminoglycosides            -Vancomycin
    -Erythromycin               -Barbiturates
    -Phenytoin                  -Furosemide
    -Quinidine                  -Salicylates
    -Alcohol
Labyrinthitis
 Chronic


   Localizedinflammatory process of the inner
   ear due to fistula formation from middle to
   inner ear

   Most   occur in horizontal semicircular canal

   Etiology
           is due to destruction by a
   cholesteatoma
Vestibular Neuronitis
 Suspected    viral etiology

 Sudden  onset vertigo that increases in
 intensity over several hours and gradually
 subsides over several days

 Mild   vertigo may last for several weeks

 May    have auditory symptoms

 Highest   incidence in 3rd and 5th decades
Vestibular Ganglionitis
 Usually   virally mediated-most often VZV

 Affects vestibular ganglion, but also may affect
  multiple ganglions

 May   be mistaken as BPPV or Ménière disease

 Ramsay    Hunt Syndrome
  -Deafness             -Vertigo
  -Facial Nerve Palsy   -EAC Vesicles
Ménière Disease
 Firstdescribed in 1861
 Triad of vertigo, tinnitus and hearing loss
 Due to cochlea-hydrops
   Unknown   etiology
   Possibly autoimmune

 Abrupt, episodic, recurrent episodes with
  severe rotational vertigo
 Usually last for several hours
Ménière Disease
 Often  patients have eaten a salty meal
  prior to attacks
 May occur in clusters and have long
  episode-free remissions
 Usually low pitched tinnitus
 Symptoms subside quickly after attack
 No CNS symptoms or positional vertigo
  are present
Acoustic Neuroma
 Peripheral  vertigo that ultimately develops
  central manifestations
 Tumor of the Schwann cells around the 8 th CN
 Vertigo with hearing loss and tinnitus
 With tumor enlargement, it encroaches on the
  cerebellopontine angle causing neurologic signs
 Earliest sign is decreased corneal reflex
 Later truncal ataxia
 Most occur in women during 3rd and 6th decades
Central Vertigo-Differential
 Central   Vertigo

   Vertebrobasilar   Insufficiency
      Atheromatous  plaque            Head Trauma
      Subclavian Steal Syndrome
                                       Neck Injury
      Drop Attack
                                       Temporal lobe seizure
      Wallenberg Syndrome
                                       Vertebral basilar
   Cerebellar Hemorrhage
                                        migraine
   Multiple Sclerosis
                                       Metabolic
                                        abnormalities
                                          Hypoglycemia
                                          Hypothyroidism
Vertebrobasilar Insufficiency
 Important   causes of central vertigo

 Related to decreased perfusion of
 vestibular nuclei in brain stem

 Vertigo
        may be a prominent symptom with
 ischemia in basilar artery territories

 Unusualfor vertigo to be only symptom of
 ischemia
Vertebrobasilar Insufficiency
 Most   commonly will also have:
       -Dysarthria       -Ataxia     -Facial numbness
       -Hemiparesis      -Diplopia   -Headache


 Tinnitus   and hearing loss unlikely

 Verticalnystagmus is characteristic of a
  (superior colliculus) brain stem lesion

 Up to 30% of TIA’s are VBI with pontine
  symptoms and a focal neurologic lesion
Drop attack
 Abruptlyfalls without warning, but does
 not loose consciousness

 Believed
         to be caused by transient
 quadraparesis due to ischemia at the
 pyramidal decussation
Subclavian Steal Syndrome
 Rare,   but treatable

 Armexercise on side of stenotic
 subclavian artery usually causes
 symptoms of intermittent claudication

 Blood  is shunted away from brainstem into
 ipsilateral vertebral artery

 Classic   history occurs only rarely
Wallenberg Syndrome

 Occlusion    of PICA

 Relatively   common cause of central vertigo

 Associated  Symptoms:
     -nausea      -vomiting       -nystagmus
     -ataxia      -Horner syndrome
     -palate, pharynx and laryngeal paresis
     -loss of pain and temperature on ipsilateral
      face and contralateral body
Cerebellar Hemorrhage
 Neurosurgical   emergency

 Suspected in any patient with sudden onset
  headache, vertigo, vomiting and ataxia

 May    have gaze preference

 Motor-sensory   exam usually normal

 Gait disturbance often not recognized because
  patient appears too ill to move
Multiple Sclerosis
 Vertigo is presenting symptom in 7-10%
 Thirty percent develop vertigo in the course of
  the disease
 May have any type of nystagmus
 Internuclear ophthalmoplegia is virtually
  pathognomonic
 Onset during 2nd to 4th decade
 Rare after 5th decade
 Usually will have had previous neurological
  symptoms
Head and Neck Trauma
 Due   to damage to the inner ear and central
  vestibular nuclei, most often labyrinthine concussion
 Temporal skull fracture may damage the labyrinth or
  eighth cranial nerve
 Vertigo may occur 7-10 days after whiplash
 Persistent episodic flares suggest perilymphatic
  fistula
 Fistula may provide direct route to CNS infection
Vertebral Basilar Migraine
 Syndrome   of vertigo, dysarthria, ataxia, visual
  changes, paresthesias followed by headache
 Distinguishing features of basilar artery migraine
  -Symptoms precede headache
  -History of previous attacks
  -Family history of migraine
  -No residual neurologic signs
 Symptoms    coincide with angiographic evidence
  of intracranial vasoconstriction
Metabolic Abnormalities

 Hypoglycemia
   Suspected in any patient with diabetes with associated
    headache, tachycardia or anxiety


 Hypothyroidism
   Clinicalpicture of vertigo, unsteadiness, falling, truncal
    ataxia and generalized clumsiness
Management
 Based   on differentiating central from peripheral
  causes
 VBI should be considered in any elderly patient with
  new-onset vertigo without an obvious etiology
 Neurological or ENT consult for central vertigo
 Suppurative labrynthitis-admit and IV antibiotics
 Toxic labrynthitis-stop offending agent if possible
Management
 Severe  Ménière disease may require chemical
  ablation with gentamicin
 Attempt Epley maneuver for BPPV
 Mainstay of peripheral vertigo management are
  antihistamines that possess anticholinergic
  properties
    -Meclizine       -Diphenhydramine
    -Promethazine    -Droperidol
    -Scopolamine
Epley Maneuver
Epley Maneuver
 University   of Baltimore
   107 patients
   Diagnosed with BPPV
   Right ear affected 54%
   Posterior semicircular canal in 105 patients
   Treated with 1.23 treatments
   Successful in 93.4%


                      Laryngoscope. 1999 Jun;109(6):900-3
Summary
 Ensure  you understand what the patient means
  by “dizzy”
 Try to differentiate central from peripheral
   Often   there is significant overlap
 Not every patient needs a head CT
 Central causes are usually insidious and more
  severe while peripheral causes are mostly
  abrupt and benign
 Most can be discharged with antihistamines
Questions
1. Nystagmus due to peripheral causes has
    all
    of the following features except:
     a. Diminishes with fixation
     b. Unidirectional fast component
     c. Can be horizontorotary or vertical
     d. Nystagmus increases with gaze in
        direction of fast component
     e. Can be accentuated by head
             movement
Nystagmus due to peripheral causes has all
         of the following features except:


c. Can be horizontorotary or vertical

 Peripheral nystagmus is typically
 horozonto-rotary, not pure horizontal or
 rotary and is definitely not vertical.
2. Nystagmus due to central causes has all
of the following features except:
a. Does not change with gaze fixation
b. Can be unidirectional or bidirectional
c. Can be horizontal, rotary or vertical
d. Nystagmus increases with gaze in
     direction of fast component
e. Can be dramatically accentuated by
  head movement
Nystagmus due to central causes has all of
      the following features except:
e. Can be dramatically accentuated
    by head movement

 Vertigo and nystagmus produced by
 central causes does not significantly
 worsen with head movement
3. All of the following will have hearing loss
and tinnitus associated with the vertigo
except:
a.   Vestibular neuronitis
b.   Acute labrynthitis
c.   BPPV
d.   Acoustic neuroma
e.   Ménière Disease
All of the following will have hearing loss
     and tinnitus associated with the vertigo
                        except:
c.    BPPV will not have associated hearing
      loss or tinnitus

      All of the other responses will have
      hearing loss and tinnitus to varying
      degrees
4. T or F The Dix-Halpike maneuver is
   useful in the treatment of BPPV?

   False

   The Dix-Halpike is used to precipitate the
   nystagmus if the nystagmus and vertigo
   have resolved so a correct diagnosis can
   be made.
   The Epley maneuver is used to relocate
   the otoliths and therefore treat the BPPV.
5. All of the following have been implicated in
    causing vertigo except:
    a. Loop diuretics         e. Fluoroquinolones

    b. Anticonvulsants     f.   All of the above
    c. Aminoglycosides
    d. NSAIDS

F All of the above
Many everyday medications can cause vertigo
   which is easily reversible if recognized.

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Vertigo and dizziness

  • 1. Vertigo and Dizziness Presented by A. Hillier, D.O. EM Resident St. John West Shore Hospital
  • 2. Vertigo and Dizziness  Prevalence 1 in 5 adults report dizziness in last month  Increases in elderly  Worsened by decreased visual acuity, proprioception and vestibular input  Dizziness  Non-specific term  Different meanings to different people Could mean - Vertigo - Syncope - Presyncope - Weak - Giddiness - Anxiety - Anemia - Depression - Unsteady
  • 3. Vertigo and Dizziness  Vertigo  Perception of movement  Peripheral or Central  Syncope  Transient loss of consciousness with loss of postural tone
  • 4. Vertigo and Dizziness  Presyncope  Lightheadedness-an impending loss of consciousness  Psychiatric dizziness  Dizziness not related to vestibular dysfunction  Disequilibrium  Feeling of unsteadiness, imbalance or sensation of “floating” while walking
  • 5. Vestibular Labyrinth  Pathophysiology  Complex interaction of visual, vestibular and proprioceptive inputs that the CNS integrates as motion and spatial orientation 3 semicircular canals  rotational movement  cupula 2 otolithic organs  utricle& saccule  linear acceleration  Macula
  • 6. Vertigo and Dizziness  Normally there is balanced input from both vestibular systems  Vertigo develops from asymmetrical vestibular activity  Abnormal bilateral vestibular activation results in truncal ataxia
  • 7. Vertigo and Dizziness  Nystagmus  Rhythmic slow and fast eye movement  Direction named by fast component  Slow component due to vestibular or brainstem activity  Slow component usually ipsilateral to diseased structure  Fast component due to cortical correction  Physiologic Vertigo  “motion sickness”  A mismatch between visual, proprioceptive and vestibular inputs  Not a diseased cochleovestibular system or CNS
  • 8. Vertigo-Differential Diagnoses  Etiologies of Vertigo  CNS infection (TB, Syphillis)  BPPV  Tumor (Benign or Neoplastic)  Labyrintitis  Cerebellar infarct  Acute suppurative  Cerebellar hemorrhage  Serous  Vertebrobasilar insufficiency  Toxic  AICA syndrome  Chronic  PICA syndrome  Vestibular neuronitis  Multiple Sclerosis  Vestibular ganglionitis  Basilar artery migraine  Ménière’s  Hypothyroidism  Acoustic neuroma  Hypoglycemia  Perilymphatic fistula  Traumatic  Cerumen impaction  Hematologic (Waldenstroms)
  • 9. Vertigo-History  Is it true vertigo?  Unusual eye  Autonomic movements?  Any past head or symptoms? neck trauma?  Pattern of onset and  Past medical history? duration  Previous symptoms?  Auditory  Prescribed and OTC disturbances? medications?  Neurologic  Drug and alcohol disturbances? intake?  Was there syncope?
  • 10. Vertigo-Physical Exam  Cerumen/FB in EAC  Otitis media  Auscultate for carotid bruits  Pneumatic otoscopy  Orthostatic vital signs  Tympanosclerosis or TM  BP and pulse in both arms perforation  Dix-Hallpike maneuver  Nystagmus  Gross hearing  Fundoscopic exam  Weber-Rinne test  Pupillary abnormalities  External auditory canal vesicles  Extraocular muscles  Muscle strength  Cranial nerves  Gait and Cerebellar function  Internuclear ophthalmoplegia
  • 11. Dix-Hallpike Maneuver Figure 1. Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient's head 45 degrees to the right (A). The physician supports the patient's head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient's head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.
  • 12. Vertigo-Characteristics Peripheral Central Onset Sudden Usually slow Severity of Vertigo Intense Usually mild Pattern Paroxysmal Constant Exac. by movement Yes Variable Autonomic Frequent Variable Laterality Unilateral Uni or bilat Nystagmus Horizontorotary Any Fatigable/Fixation Yes No Auditory symptoms Yes No TM May be abnormal Normal CNS symptoms Absent Present
  • 13. Vertigo-Ancillary Tests  CT-if cerebellar mass, hemorrhage or infarction suspected  Glucose and ECG in the “dizzy” patient  Cold caloric testing  Angiography for suspected VBI  MRI  Electronystagmography and audiology
  • 14. Peripheral Vertigo-Differential  Labyrinthine Disorders  Most common cause of true vertigo  Five entities Benign paroxysmal positional vertigo (BPPV) Labyrinthitis Ménière disease Vestibular neuronitis Acoustic Neuroma
  • 15. Benign Paroxysmal Positional Vertigo  Extremely common  Otoconia displacement  No hearing loss or tinnitus  Short-lived episodes brought on by rapid changes in head position  Usually a single position that elicits vertigo  Horizontorotary nystagmus with crescendo- decrescendo pattern after slight latency period  Less pronounced with repeated stimuli  Typically can be reproduced at bedside with positioning maneuvers
  • 17. Labyrinthitis  Associated hearing loss and tinnitus  Involves the cochlear and vestibular systems  Abrupt onset  Usually continuous  Four types of Labyrinthitis  Serous  Acute suppurative  Toxic  Chronic
  • 18. Labyrinthitis  Serous  Adjacent inflammation due to ENT or meningeal infection  Mild to severe vertigo with nausea and vomiting  May have some degree of permanent impairment  Acute suppurative labyrinthitis  Acute bacterial exudative infection in middle ear  Secondary to otitis media or meningitis  Severe hearing loss and vertigo  Treated with admission and IV antibiotics
  • 19. Labyrinthitis  Toxic  Due to toxic effects of medications  Still relatively common  Mild tinnitus and high frequency hearing loss  Vertigo in acute phase  Ataxia in the chronic phase  Common etiologies -Aminoglycosides -Vancomycin -Erythromycin -Barbiturates -Phenytoin -Furosemide -Quinidine -Salicylates -Alcohol
  • 20. Labyrinthitis  Chronic  Localizedinflammatory process of the inner ear due to fistula formation from middle to inner ear  Most occur in horizontal semicircular canal  Etiology is due to destruction by a cholesteatoma
  • 21. Vestibular Neuronitis  Suspected viral etiology  Sudden onset vertigo that increases in intensity over several hours and gradually subsides over several days  Mild vertigo may last for several weeks  May have auditory symptoms  Highest incidence in 3rd and 5th decades
  • 22. Vestibular Ganglionitis  Usually virally mediated-most often VZV  Affects vestibular ganglion, but also may affect multiple ganglions  May be mistaken as BPPV or Ménière disease  Ramsay Hunt Syndrome -Deafness -Vertigo -Facial Nerve Palsy -EAC Vesicles
  • 23. Ménière Disease  Firstdescribed in 1861  Triad of vertigo, tinnitus and hearing loss  Due to cochlea-hydrops  Unknown etiology  Possibly autoimmune  Abrupt, episodic, recurrent episodes with severe rotational vertigo  Usually last for several hours
  • 24. Ménière Disease  Often patients have eaten a salty meal prior to attacks  May occur in clusters and have long episode-free remissions  Usually low pitched tinnitus  Symptoms subside quickly after attack  No CNS symptoms or positional vertigo are present
  • 25. Acoustic Neuroma  Peripheral vertigo that ultimately develops central manifestations  Tumor of the Schwann cells around the 8 th CN  Vertigo with hearing loss and tinnitus  With tumor enlargement, it encroaches on the cerebellopontine angle causing neurologic signs  Earliest sign is decreased corneal reflex  Later truncal ataxia  Most occur in women during 3rd and 6th decades
  • 26. Central Vertigo-Differential  Central Vertigo  Vertebrobasilar Insufficiency  Atheromatous plaque  Head Trauma  Subclavian Steal Syndrome  Neck Injury  Drop Attack  Temporal lobe seizure  Wallenberg Syndrome  Vertebral basilar  Cerebellar Hemorrhage migraine  Multiple Sclerosis  Metabolic abnormalities  Hypoglycemia  Hypothyroidism
  • 27. Vertebrobasilar Insufficiency  Important causes of central vertigo  Related to decreased perfusion of vestibular nuclei in brain stem  Vertigo may be a prominent symptom with ischemia in basilar artery territories  Unusualfor vertigo to be only symptom of ischemia
  • 28. Vertebrobasilar Insufficiency  Most commonly will also have: -Dysarthria -Ataxia -Facial numbness -Hemiparesis -Diplopia -Headache  Tinnitus and hearing loss unlikely  Verticalnystagmus is characteristic of a (superior colliculus) brain stem lesion  Up to 30% of TIA’s are VBI with pontine symptoms and a focal neurologic lesion
  • 29. Drop attack  Abruptlyfalls without warning, but does not loose consciousness  Believed to be caused by transient quadraparesis due to ischemia at the pyramidal decussation
  • 30. Subclavian Steal Syndrome  Rare, but treatable  Armexercise on side of stenotic subclavian artery usually causes symptoms of intermittent claudication  Blood is shunted away from brainstem into ipsilateral vertebral artery  Classic history occurs only rarely
  • 31. Wallenberg Syndrome  Occlusion of PICA  Relatively common cause of central vertigo  Associated Symptoms: -nausea -vomiting -nystagmus -ataxia -Horner syndrome -palate, pharynx and laryngeal paresis -loss of pain and temperature on ipsilateral face and contralateral body
  • 32. Cerebellar Hemorrhage  Neurosurgical emergency  Suspected in any patient with sudden onset headache, vertigo, vomiting and ataxia  May have gaze preference  Motor-sensory exam usually normal  Gait disturbance often not recognized because patient appears too ill to move
  • 33. Multiple Sclerosis  Vertigo is presenting symptom in 7-10%  Thirty percent develop vertigo in the course of the disease  May have any type of nystagmus  Internuclear ophthalmoplegia is virtually pathognomonic  Onset during 2nd to 4th decade  Rare after 5th decade  Usually will have had previous neurological symptoms
  • 34. Head and Neck Trauma  Due to damage to the inner ear and central vestibular nuclei, most often labyrinthine concussion  Temporal skull fracture may damage the labyrinth or eighth cranial nerve  Vertigo may occur 7-10 days after whiplash  Persistent episodic flares suggest perilymphatic fistula  Fistula may provide direct route to CNS infection
  • 35. Vertebral Basilar Migraine  Syndrome of vertigo, dysarthria, ataxia, visual changes, paresthesias followed by headache  Distinguishing features of basilar artery migraine -Symptoms precede headache -History of previous attacks -Family history of migraine -No residual neurologic signs  Symptoms coincide with angiographic evidence of intracranial vasoconstriction
  • 36. Metabolic Abnormalities  Hypoglycemia  Suspected in any patient with diabetes with associated headache, tachycardia or anxiety  Hypothyroidism  Clinicalpicture of vertigo, unsteadiness, falling, truncal ataxia and generalized clumsiness
  • 37. Management  Based on differentiating central from peripheral causes  VBI should be considered in any elderly patient with new-onset vertigo without an obvious etiology  Neurological or ENT consult for central vertigo  Suppurative labrynthitis-admit and IV antibiotics  Toxic labrynthitis-stop offending agent if possible
  • 38. Management  Severe Ménière disease may require chemical ablation with gentamicin  Attempt Epley maneuver for BPPV  Mainstay of peripheral vertigo management are antihistamines that possess anticholinergic properties -Meclizine -Diphenhydramine -Promethazine -Droperidol -Scopolamine
  • 40. Epley Maneuver  University of Baltimore  107 patients  Diagnosed with BPPV  Right ear affected 54%  Posterior semicircular canal in 105 patients  Treated with 1.23 treatments  Successful in 93.4% Laryngoscope. 1999 Jun;109(6):900-3
  • 41. Summary  Ensure you understand what the patient means by “dizzy”  Try to differentiate central from peripheral  Often there is significant overlap  Not every patient needs a head CT  Central causes are usually insidious and more severe while peripheral causes are mostly abrupt and benign  Most can be discharged with antihistamines
  • 43. 1. Nystagmus due to peripheral causes has all of the following features except: a. Diminishes with fixation b. Unidirectional fast component c. Can be horizontorotary or vertical d. Nystagmus increases with gaze in direction of fast component e. Can be accentuated by head movement
  • 44. Nystagmus due to peripheral causes has all of the following features except: c. Can be horizontorotary or vertical Peripheral nystagmus is typically horozonto-rotary, not pure horizontal or rotary and is definitely not vertical.
  • 45. 2. Nystagmus due to central causes has all of the following features except: a. Does not change with gaze fixation b. Can be unidirectional or bidirectional c. Can be horizontal, rotary or vertical d. Nystagmus increases with gaze in direction of fast component e. Can be dramatically accentuated by head movement
  • 46. Nystagmus due to central causes has all of the following features except: e. Can be dramatically accentuated by head movement Vertigo and nystagmus produced by central causes does not significantly worsen with head movement
  • 47. 3. All of the following will have hearing loss and tinnitus associated with the vertigo except: a. Vestibular neuronitis b. Acute labrynthitis c. BPPV d. Acoustic neuroma e. Ménière Disease
  • 48. All of the following will have hearing loss and tinnitus associated with the vertigo except: c. BPPV will not have associated hearing loss or tinnitus All of the other responses will have hearing loss and tinnitus to varying degrees
  • 49. 4. T or F The Dix-Halpike maneuver is useful in the treatment of BPPV? False The Dix-Halpike is used to precipitate the nystagmus if the nystagmus and vertigo have resolved so a correct diagnosis can be made. The Epley maneuver is used to relocate the otoliths and therefore treat the BPPV.
  • 50. 5. All of the following have been implicated in causing vertigo except: a. Loop diuretics e. Fluoroquinolones b. Anticonvulsants f. All of the above c. Aminoglycosides d. NSAIDS F All of the above Many everyday medications can cause vertigo which is easily reversible if recognized.