The Individual Components Can Differ1

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The individual components can differ, since there are probably other

pathogenesis besides the vestibular one with imbalance in the graviceptive VOR
(impairment in the projection of ctolithic information). E.g. imbalance disfunction
of the neuronal ocular motor integrator and of the saccade-burst generator.
Downbeat nystagmus is often the result of a bilateral lesion of the flocculus or
the paraflocculus (ex intoxication due to anticonvulsant drugs) or caused by a
lesion at the bottom of the fourth ventricle. Accordingly it is mostly a druginduced dysfunction or congenital (Arnold-Chiari malformation), 20% have
cerebellar degeneration and more seldom lesions of the medulla oblongata, and
by MS, haemorrhage, infarctionor tumour for example. A downbeat nystagmus
due to a lesion in the upper medulla at the level of the rostral nucleus
praepositus hypoglossi has so far only been reported in monkeys, not in human.
Upbeat nystagmus is rarer than downbeat nystagmus. It is also a fixation
induced nystagmus that beats upward in primary gaze position and is combined
with a disorder of the vertical smooth-pursuit eye movements, a visual and
vestibulospinal ataxia with a tendency to fall backward, and past pointing
downward.
On the one hand, the pathoanatomic location of most acute lesions is
paramedian in medulla oblongata in neurons of the paramedia tract, close the
caudalpart of the perihypoglossal nucleus, which is responsible for vertical gaze
holding. On the other hand, lesions have been reported paramedian paramedian
in tegmentum of the pontomescencephalic junction, the brachium conjunctivum
and probably in the anterior vermis. The symptoms persist as a rule for several
weeks but are not permanent. Because the eye movement generally have larger
amplitudes, oscillopsia in upbeat nystagmus is very distressing and impairs
vision. Upbeat nystagmus due to damage of the pontomesencephalic brainsteam
is frequently combined with a unilateral or bilateral internuclear ophtalmoplegia,
indicating that the MLF is affected. The main aetiologies are bilateral lesions in
MS, brainsteam ischemia or tumour, wernickes encephalopathy cerebellar
degeneration and dysfunction of the cerebellum due to intoxication.
The course and prognosis depend on the underlying illness. It is
therapeutically expedient to attempt treatment of the symptoms of persisting
downbeat or upbeat nystagmus syndrome by administering 4-aminopiridine,
gabapentin, baclofen, clonazepam.
Vestibular syndromes in the vertical (roll) plane
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These syndrome indicate an acute unilateral deficit of the graviceptive


vestibular pathways, which run from the vertical canals and otoliths over
the ipsilateral (medial and superior) vestibular nuclei and the contralateral
MLF to the ocular motor nuclei and integration centres for vertical and
torsional eye movements (INC and riMLF) in the rostral mid-brain.

Most rostral to the midbrain, only the vestibular projection of the VOR for
perception in the roll plane (determination of the subjective visual vertical,
SVV) runs over the vestibular nuclei in the posterolateral thalamus to the
parietoinsular vestibular cortex in the posterior insula. The crossing of
these pathways at pontine level is especially important for topographic
diagnosis of the brainsteam.

All signs of lesions in the roll plane-single components or a complete


ocular tilt reaction (head tilt, vertical divergence of the eyes, ocular
torsion, SVV deviation).

Setiap individu dapat berbeda, karena mungkin ada patogenesis selain


masalah vestibular dengan ketidakseimbangan dalam VOR graviceptive
(penurunan proyeksi otolithic).

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