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Vertigo and Nystagmus - 2
Yasser A. Alzainy
Al-Azhar University
Agenda
• Nystagmus
“and other ocular oscillations”
• Classification of nystagmus
• Physical examination in dizzy
patient
• Central causes of dizziness
• Peripheral causes of dizziness
Nystagmus
“and other ocular oscillations”
• Classification
• Non-neuropathologic Nystagmus
• Neuropathologic Nystagmus
• Nystagmus mimics
Nystagmus
• Rhythmic
• Biphasic
Classification
 Pendular vs Jerk
 Spontaneous vs Induced
 Physiologic vs Pathologic
 Other Specifiers
o Rapid / Slow
o Coarse / Fine
o Manifest / Latent
o Horizontal /Vertical /Torsional
Grading
1st degree
• Only in eccentric gaze
2nd degreee
• In primary gaze
3rd degree
• Even upon gazing towards
the slow phase
Alexander Law
Jerk nystagmus increases in the direction of the fast phase
Nystagmus
Non-Neuropathologic
Physiologic
End-point
nystagmus
OKN
Induced
Vestibular
Voluntary Congenital Ocular disease
Visual loss
induced
nystagmus
Spasmus
nutans
Neuropathologic
Spontaneous Positional Gaze-evoked
Drug-induced Gaze paretic
Non-Neuropathologic
Physiologic
End-point
nystagmus
OKN
Induced
Vestibular
Voluntary Congenital Ocular disease
Visual loss
induced
nystagmus
Spasmus
nutans
End-point nystagmus
 At extremes of lateral gaze
o Down to as little as 30º in some normal individuals
 Low amplitude
 Irregular
 Variably sustained
 Symmetrical
 Dysconjugate (Abducting > Adducting
eye)
 Can be abolished
Optokinetic nystagmus (OKN)
 Striped drum / tape; Mobile App
 Ask the patient to “count” the stripes
 PTOJ mediates pursuit
 When ready to break off, signals ipsilateral
FEF to generate a saccade
 Fast phase opposite tape movement
 LocalizingValue
 Occipital vs Parietal lobe (optic radiation)
Normal OKN vs Blunted / Absent
Induced vestibular nystagmus
Voluntary nystagmus
 High frequency
 Irregular
 Low amplitude
 Pendular
 Cannot be sustained for long (>30 s)
 Eyelid twitches
Congenital nystagmus
 Since infancy
 Horizontal
o Even in vertical gaze
 Null point
o Head tilt
 Damps with convergence
o Holds what he reads extremely close
 Inversion of OKN
Ocular Disease
Blindness-induced nystagmus Spasmus nutans
Neuropathologic
Spontaneous Positional Gaze-evoked
Drug-induced Gaze paretic
Spontaneous nystagmus
 Diminish by visual fixation
 Possible triggers (vestibular):
 Mastoid tapping
 Hyperventilation
 Head Shaking
Positional nystagmus
 Dix-Hallpike Maneuver
 ~= BBPV in the
posterior SCC of the
dependent ear
 Wait until symptoms
subside
 Assess for recurrence
 Nystagmus is torsional
and geotropic
Central positional nystagmus
 No latency
 Vertical (upbeat / downbeat)
 If torsional component (rare) = ageotropic
 Persists > 40 s or even as long as position is maintained
 Vertigo, Nystagmus, Nausea mismatch
Dix-Hallpike Maneuver
History items
Central Peripheral
Nausea Variable Variable “more prominent”
Positional Rare Common
Diplopia, dysarthria,
dysphagia
Common Rare
Long tract dysfunction Common Rare
Hearing loss, tinnitus Rare Common
Imbalance Variable, often severe Variable, often mild/moderate
Oscillopsia Severe Mild
Recovery Months Days-weeks
Recurrence Rare Variable
Examination items
Central Peripheral
Neurological Signs:
“Cr.N. dysfunction {strabismus,
dysphagia}, weakness, sensory loss”
Common Rare
Nystagmus • Vertical or horizontal
• Multidirectional:Gaze-evoked
• Dysconjugate
• No suppression with fixation
• Torsional or horizontal
• Unidirectional
• Conjugate
• Suppresses with fixation
Head Impulse test Maintains fixation (NL) Catch-up saccade (Impaired)
Alternate cover testing Skew Deviation No skew deviation
Ocular
movements with
high localizing
value
Downbeat nystagmus
Upbeat nystagmus
Rebound nystagmus
Convergence retraction
nystagmus
Bruns’ nystagmus
Seesaw nystagmus
Ocular Bobbing
Opsoclonus
Ocular Flutter
Central Causes of
Dizziness
Central Causes of Dizziness
• Cerebrovascular disorders
• Multiple Sclerosis
• Migraine
• Seizure
• CPA tumors
• Cranio-cervical junction disorders
• Other: Cerebellar degeneration / Cerebellitis, Hereditary ataxias, Psychiatric.
Cerebrovascular disorders
Multiple Sclerosis
• Can mimic peripheral (root entry zone)
• INO
• Pendular nystagmus
Cranio-cervical Junction disorders
• Symptom worsen w/neck extension & cough
• Spontaneous & positional vertigo, tinnitus, hearing loss,
dysarthria/dysphonia, ataxia
• Shortness of neck, low neck hair line, limited neck ROM
• Lower CN signs
• May develop hydrocephalus
Peripheral Causes
of Dizziness
Vestibular Neuritis
Meniere's Disease
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo
• Most common cause of vertigo
• Canalithiasis
• 85-95% in posterior canal (5-15% in horizontal)
• Brief (<1 min) spells provoked by Δs in position
• +ve Dix-Hallpike maneuver (80% sensitive and specific).
• Spontaneous recovery after weeks, but may recur
• Treatment with reposition maneuvers: Eply maneuver and
habituation exercises (Brandt-Daroff)
Vestibular Neuritis
• Vertigo and nystagmus last for hours / days
• Mimic posterior circulation CVA
• No hearing loss or other neurological symptoms
• Post- or Para-infectious (e.g., HSV)
• Unilateral hearing loss may implicate labyrinthitis
• MRI + DWI is a must if CVA risk factors
• Subsides in weeks, but may recur
• Steroids can be used within days from onset
Meniere’s disease
• Caused by endolymphatic hydrops.
• Recurrent attacks of vertigo lasting >20 min
• Horizontal rotatory nystagmus, hearing loss (may remain
between attacks)
• Sense of fullness and/or tinnitus
• Vertigo often severe w/ days of disequilibrium/N/V
• often progresses to bilateral
Thank you
YasserA. Alzainy

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Vertigo and Nystagmus - Clinical approach part-2.pptx

Editor's Notes

  1. Pendular nystagmus rarely signifies neurological disease; usually horizontal
  2. Pendular nystagmus rarely signifies neurological disease; usually horizontal
  3. Pendular nystagmus rarely signifies neurological disease; usually horizontal
  4. The significance of OKN asymmetry lies in the vascular anatomy and the differing pathologies that affect the parietal and occipital lobes. Tumors are rare in the occipital lobe and much more common in the parietal lobe. Furthermore, the OKN pathways in the deep parietal lobe are outside the distribution of the posterior cerebral artery. Therefore, a patient with a hemianopsia and normal OKN responses is more likely to have an occipital lesion, and more likely to have had a stroke. With asymmetric OKNs, the lesion is more likely to reside in the parietal lobe, and more likely to be nonvascular, that is, a tumor (Cogan’s rule).
  5. The significance of OKN asymmetry lies in the vascular anatomy and the differing pathologies that affect the parietal and occipital lobes. Tumors are rare in the occipital lobe and much more common in the parietal lobe. Furthermore, the OKN pathways in the deep parietal lobe are outside the distribution of the posterior cerebral artery. Therefore, a patient with a hemianopsia and normal OKN responses is more likely to have an occipital lesion, and more likely to have had a stroke. With asymmetric OKNs, the lesion is more likely to reside in the parietal lobe, and more likely to be nonvascular, that is, a tumor (Cogan’s rule).
  6. Spasmus nutans: 6-12 months of age, triad of nystagmus, head nodding and torticollis; benign course: disappear before age of 4 yr; low amplitude, high frequency and dysconjugate Blindness-induced nystagmus: continuous, pendular
  7. Rolls test for horizontal canal
  8. Rolls test for horizontal canal
  9. Rolls test for horizontal canal