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Central vertigo and nystagmus

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Dizziness and the physical manifestation that exemplify central etiologies

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Central vertigo and nystagmus

  1. 1. Central Vertigo and Nystagmus
  2. 2. Distinctions Between Central and Peripheral Dizziness
  3. 3. Effect of Fixation on Nystagmus
  4. 4. Vestibular versus Central Nystagmus
  5. 5. Alexander’s Law in Peripheral Vestibular Disease • Spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear • Nystagmus is greatest when gaze is directed toward the healthy ear is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. • The third element says that spontaneous nystagmus with central gaze is augmented when vision fixation is denied
  6. 6. Central Positional Vertigo (CPV) • CPV is a rare cause of positional vertigo. It is especially common due to structural lesions in the cerebellum, especially the cerebellar nodulus and uvula (Lee et al, 2014). • There are a number of potential causes -- CPV is nearly universal in persons with medulloblastoma, (tumor that arises in the cerebellar nodulus.) • CPV is also somewhat common in the Arnold-Chiari malformation and the related disorder of basilar invagination, and after strokes, tumors or multiple-sclerosis lesions involving the brainstem or cerebellum area. There are numerous rare cerebellar degenerations that can also result in central positional vertigo. • Ordinarily this diagnosis is made by noting a positional vertigo, finding that it does not respond to exercises for BPPV, and then further investigation.
  7. 7. Direction Changing Nystagmus • Nystagmus has a gaze-evoked component • Note the asymmetry of movement between each eye • Failure of gaze-holding circuits in the cerebellum or brainstem • Diagnosis here is acute cerebellar infarction
  8. 8. Upbeating Vertical Nystagmus • Two varieties: • Large amplitude nystagmus that increases in intensity with upward gaze. • Suggestive of a lesion of the anterior vermis of the cerebellum. • Small amplitude nystagmus that decreases in intensity with upward gaze and increases in intensity with downward gaze • Suggestive of lesions of the medulla.
  9. 9. Vertical Upbeating Nystagmus • Causes: • Medullary lesions, including perihypoglossal nuclei, the adjacent medial vestibular nucleus, and the nucleus intercalatus (structures important in gaze holding) • Lesions of the anterior vermis of the cerebellum and superior cerebellar peduncle • Benign paroxysmal positional vertigo
  10. 10. Vertical Downbeating Nystagmus • The presence of downbeat nystagmus suggests a lesion in the cervicomedullary junction. • Causes include Arnold-Chiari's syndrome, spinocerebellar degeneration, stroke and multiple sclerosis.
  11. 11. Pendular Nystagmus • Multivectorial nystagmus (ie, horizontal, vertical, circular, elliptical) with an equal velocity in each direction • Often there is marked asymmetry and dissociation between the eyes • Amplitude of the nystagmus may vary in different positions of gaze • Demyelinating disease, monocular or binocular visual deprivation, oculopalatal myoclonus, internuclear ophthalmoplegia, brainstem or cerebellar dysfunction
  12. 12. Internuclear Ophthalmoplegia • Named for the ADducting eye and ipsilateral to the affected MLF • Horizontal nystagmus in the ABducting eye • Frequently associated with upbeating vertical nystagmus • Bilateral is almost pathognomonic for MS
  13. 13. Convergence-retraction nystagmus (induced convergence-retraction) • Part of the dorsal midbrain syndrome (Piranaud’s Syndrome) associated with: • paralysis of upward gaze • defective convergence • eyelid retraction • pupillary light–near dissociation • Best elicited on attempted upgaze saccades (eg, by asking the patient to track a downwardly rotating OKN drum)
  14. 14. Light Near Dissociation
  15. 15. See Saw Nystagmus • Localizes to lesions supra/parasellar region (Large sellar and hypothalamic lesions) • In one half cycle, the eye will rise and intort and the other eye will fall and extort; then, in the next half cycle • The interstitial nucleus of Cajal (INC), adjacent to the medial longitudinal fasciculus in the midbrain tegmentum, has been frequently implicated in the pathogenesis of SSN
  16. 16. Rebound Nystagmus • Rebound is nearly always pathological, and is related to brain stem or cerebellar disease • Pontine ischemia, brainstem MS, lesions of the cerebellar floccus, degenerative cerebellar disease • Evoked patient follow ones finger to one side, hold gaze there for 10 seconds (with constant encouragement by the examiner to keep looking), and then rapid return to central gaze. At that point, the examiner looks for a nystagmus that beats away from the previous direction of gaze holding, lasting for at least 5 beats.

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