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Central Vertigo and Nystagmus

Central vertigo and nystagmus

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Central Vertigo and Nystagmus

Distinctions Between Central and Peripheral Dizziness

Effect of Fixation on Nystagmus

Vestibular versus Central Nystagmus

Alexanders Law in Peripheral Vestibular Disease

Spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy earNystagmus 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

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.

Direction Changing Nystagmus

Nystagmus has a gaze-evoked component Note the asymmetry of movement between each eyeFailure of gaze-holding circuits in the cerebellum or brainstemDiagnosis here is acute cerebellar infarction

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.

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 peduncleBenign paroxysmal positional vertigo

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.

Pendular Nystagmus

Multivectorial nystagmus (ie, horizontal, vertical, circular, elliptical) with an equal velocity in each directionOften there is marked asymmetry and dissociation between the eyesAmplitude of the nystagmus may vary in different positions of gazeDemyelinating disease, monocular or binocular visual deprivation, oculopalatal myoclonus, internuclear ophthalmoplegia, brainstem or cerebellar dysfunction

Internuclear Ophthalmoplegia

Named for the ADducting eye and ipsilateral to the affected MLFHorizontal nystagmus in the ABducting eyeFrequently associated with upbeating vertical nystagmusBilateral is almost pathognomonic for MS

Convergence-retraction nystagmus (induced convergence-retraction)

Part of the dorsal midbrain syndrome (Piranauds Syndrome) associated with:paralysis of upward gazedefective convergence eyelid retraction pupillary lightnear dissociationBest elicited on attempted upgaze saccades (eg, by asking the patient to track a downwardly rotating OKN drum)

Light Near Dissociation

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 cycleThe interstitial nucleus of Cajal (INC), adjacent to the medial longitudinal fasciculus in the midbrain tegmentum, has been frequently implicated in the pathogenesis of SSN

Rebound Nystagmus

Rebound is nearly always pathological, and is related to brain stem or cerebellar diseasePontine ischemia, brainstem MS, lesions of the cerebellar floccus, degenerative cerebellar diseaseEvoked 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.