Saccadic lateropulsion and upbeat nystagmus: Disorders of caudal medulla

@article{Tilikete2002SaccadicLA,
  title={Saccadic lateropulsion and upbeat nystagmus: Disorders of caudal medulla},
  author={Caroline Tilikete and Marc Hermier and Denis P{\'e}lisson and A. Vighetto},
  journal={Annals of Neurology},
  year={2002},
  volume={52}
}
Key ResultA patient developed a primary position upbeat nystagmus and a left saccadic lateropulsion. Magnetic resonance imaging demonstrated a probable cavernoma at right caudal paramedian medullary level. Anatomical correlations are discussed. Saccadic lateropulsion is attributed to olivocerebellar pathway impairment but usually is described in more rostral medullar lesions. Our case would still support this hypothesis because the lesion could have involved the olivocerebellar pathway at its very caudal…
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The pathophysiology of spontaneous upbeat (UBN) and downbeat (DBN) nystagmus is reviewed in the light of several instructive clinical findings and experimental data and it is hypothesized that the excitatory SVN‐VTT pathway, along with its specific floccular inhibition, has developed to counteract the gravity pull.
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Nystagmus and saccadic intrusions.
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References

SHOWING 1-10 OF 25 REFERENCES
Upbeat nystagmus: clinicoanatomical correlation
TLDR
The conjunction of a vestibular pattern of nystagmus with this focal lesion runs contrary to a previous suggestion that the nucleus intercalatus may act as a neural integrator for vertical conjugate eye movements.
Lateropulsion and upbeat nystagmus are manifestations of central vestibular dysfunction.
TLDR
An elderly man presented with acute onset of gait instability, characterized by leaning to the left while walking, vertigo, diplopia, and transient facial numbness, which illustrates that lateropulsion can occur in Cerebellar lesions, but that it may be contralateral to the cerebellar hemisphere involved.
Lateropulsion and Upbeat Nystagmus Are Manifestations of Central Vestibular Dysfunction
TLDR
The examination of an elderly man with acute onset of gait instability, characterized by leaning to the left while walking, vertigo, diplopia, and transient facial numbness, illustrated that lateropulsion can occur in cerebellar lesions, but that it may be contralateral to the Cerebellar hemisphere involved.
Upbeat nystagmus in a patient with a small medullary infarct.
TLDR
Ocular motor studies showed that the nystagmus slow phase decayed exponentially, suggesting a failure of integration for vertical eye movements, and vertical integration might, therefore, be performed partly in the nucleus intercalatus, possibly involving the most caudal of the perihypoglossal nuclei.
Primary position upbeat nystagmus due to unilateral medial medullary infarction
TLDR
It is proposed that a unilateral lesion of the nucleus intercalatus is sufficient to cause primary position upbeat nystagmus (ppUBN) and that the nuclei of this structure are a part of the vertical position‐to‐velocity neural integrator in the human ocular–motor system.
Saccadic dysmetria is similar in patients with a lateral medullary lesion and in monkeys with a lesion of the deep cerebellar nucleus.
Some of the clinical hallmarks of lateral medullary infarction--Wallenberg's syndrome--are saccadic dysmetria, smooth pursuit deficit, and lateropulsion of the body. Similar movement disorders are
Pathophysiology of saccadic contrapulsion in unilateral rostral cerebellar lesions
TLDR
It is proposed that a lesion of the efferent pathways from the caudal fastigial nucleus to the direct premotor structures for saccades in the brainstem which cross within the cerebellum, causes the contrapulsion seen in the patient.
Saccadic lateropulsion in Wallenberg's syndrome may be caused by a functional lesion of the fastigial nucleus
TLDR
It is hypothesize that saccadic lateropulsion in lateral medullary infarction is essentially identical with cerebellar saccic dysmetria and results from a disruption of afferent olivocerebellar climbing fibres that gives rise to functional disinhibition of the Cerebellar cortex and to increased inhibition of the deep cerebellare nuclei of monkeys.
Saccadic dysmetria induced by transient functional decortication of the cerebellar vermis
TLDR
The oculomotor abnormalities associated with the bicuculline treatment (in effect, functional as well as reversible, unilateral decortication of the vermis) were hypometric saccades toward the injection side and gaze deviation toward the opposite side.
Primary position upbeating nystagmus. A variety of central positional nystagmus.
TLDR
Modification of the amplitude of upbeat nystagmus by tilt of the head with respect to gravity in the majority of patients implies an otolith-related component in the genesis of the ny STG, which supports previous reports that primary position upbeat nnagmus occurs predominately with intra-axial brainstem lesions.
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