Gravity dependence of ocular drift in patients with cerebellar downbeat nystagmus

Marti, Sarah; Palla, Antonio; Straumann, Dominik

doi:10.1002/ana.10370

Cited by 115 publications

(106 citation statements)

References 29 publications

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“…VOR and pursuit pathways converge at the brainstem level by additive combination, as has been confirmed experimentally and suggested previously (e.g., Schweigart et al 1999 Apart from an influence on static eye position, otolith input also causes small but detectable gravity-dependent positional nystagmus in darkness (Bisdorff et al 2000). Gravitydependent modulation of nystagmus becomes evident in cerebellar disease, probably due to overacting otolith-ocular reflexes (Marti et al 2002).…”

Section: Vor Pathwayssupporting

confidence: 69%

A model-based theory on the origin of downbeat nystagmus

et al. 2008

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A model-based theory on the origin of downbeat nystagmus AbstractThe pathomechanism of downbeat nystagmus (DBN), an ocular motor sign typical for vestibulo-cerebellar lesions, remains unclear. Previous hypotheses conjectured various deficits such as an imbalance of central vertical vestibular or smooth pursuit pathways to be causative for the generation of spontaneous upward drift. However, none of the previous theories explains the full range of ocular motor deficits associated with DBN, i.e., impaired vertical smooth pursuit (SP), gaze evoked nystagmus, and gravity dependence of the upward drift. We propose a new hypothesis, which explains the ocular motor signs of DBN by damage of the inhibitory vertical gaze-velocity sensitive Purkinje cells (PCs) in the cerebellar flocculus (FL). These PCs show spontaneous activity and a physiological asymmetry in that most of them exhibit downward on-directions. Accordingly, a loss of vertical floccular PCs will lead to disinhibition of their brainstem target neurons and, consequently, to spontaneous upward drift, i.e., DBN. Since the FL is involved in generation and control of SP and gaze holding, a single lesion, e.g., damage to vertical floccular PCs, may also explain the associated ocular motor deficits. To test our hypothesis, we developed a computational model of vertical eye movements based on known ocular motor anatomy and physiology, which illustrates how cortical, cerebellar, and brainstem regions interact to generate the range of vertical eye movements seen in healthy subjects. Model simulation of the effect of extensive loss of floccular PCs resulted in ocular motor features typically associated with cerebellar DBN: (1) spontaneous upward drift due to decreased spontaneous PC activity, (2) gaze evoked nystagmus corresponding to failure of the cerebellar loop supporting neural integrator function, (3) asymmetric vertical SP deficit due to low gain and asymmetric attenuation of PC firing, and (4) gravity-dependence of DBN caused by an interaction of otolith-ocular pathways with impaired neural integrator function.

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Section: Vor Pathwayssupporting

confidence: 69%

A model-based theory on the origin of downbeat nystagmus

et al. 2008

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“…Quantitative VOR gains were assessed with search coil head impulse testing. Static ocular counterroll in sustained whole-body roll positions and gravity-dependent modulation of DBN along the pitch plain were assessed using the same experimental protocols as described in Marti et al (in press) and Marti et al (2002), respectively. RESULTS VOR gains measured by head impulse testing were reduced in all five patients (Table 1, (Wagner et al, 2007) or a peripheral vestibulopathy, one would need to explain the selective impairment of SCC function.…”

Section: Methodsmentioning

confidence: 99%

Preserved otolith function in patients with cerebellar atrophy and bilateral vestibulopathy

Marti¹,

Tarnutzer²,

Palla³

et al. 2008

Progress in Brain Research

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“…The upward drift of DBN consists of a gaze-evoked drift, which is hypothesised to be due to an impaired neural integrator function, and a spontaneous upward drift during gaze straight ahead [Glasauer et al 2003a;Straumann et al 2000]. Three different pathomechanisms are thought to cause the spontaneous upward drift: first, a tone imbalance of the central vestibular pathways of the vertical eye movements [Bohmer and Straumann, 1998;Dieterich and Brandt, 1995;Halmagyi et al 1983;Baloh and Spooner, 1981], including otolith pathways as suggested by the finding that DBN is gravity-dependent [Sprenger et al 2006;Marti et al 2002]; second, an imbalance …”

Section: Downbeat Nystagmus (Dbn)mentioning

confidence: 99%

Review: Current treatment of vestibular, ocular motor disorders and nystagmus

Strupp

Brandt²

2009

Ther Adv Neurol Disord

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Vertigo and dizziness are among the most common complaints with a lifetime prevalence of about 30%. The various forms of vestibular disorders can be treated with pharmacological therapy, physical therapy, psychotherapeutic measures or, rarely, surgery. In this review, the current pharmacological treatment options for peripheral and central vestibular, cerebellar and ocular motor disorders will be described. They are as follows for peripheral vestibular disorders. In vestibular neuritis recovery of the peripheral vestibular function can be improved by treatment with oral corticosteroids. In Menière's disease a recent study showed long-term high-dose treatment with betahistine has a significant effect on the frequency of the attacks. The use of aminopyridines introduced a new therapeutic principle in the treatment of downbeat and upbeat nystagmus and episodic ataxia type 2 (EA 2). These potassium channel blockers presumably increase the activity and excitability of cerebellar Purkinje cells, thereby augmenting the inhibitory influence of these cells on vestibular and cerebellar nuclei. A few studies showed that baclofen improves periodic alternating nystagmus, and gabapentin and memantine, pendular nystagmus. However, many other eye movement disorders such as ocular flutter opsoclonus, central positioning, or see-saw nystagmus are still difficult to treat. Although progress has been made in the treatment of vestibular neuritis, downbeat and upbeat nystagmus, as well as EA 2, stateof-the-art trials must still be performed on many vestibular and ocular motor disorders, namely Menière's disease, bilateral vestibular failure, vestibular paroxysmia, vestibular migraine, and many forms of central eye movement disorders.

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Gravity dependence of ocular drift in patients with cerebellar downbeat nystagmus

Cited by 115 publications

References 29 publications

A model-based theory on the origin of downbeat nystagmus

A model-based theory on the origin of downbeat nystagmus

Preserved otolith function in patients with cerebellar atrophy and bilateral vestibulopathy

Review: Current treatment of vestibular, ocular motor disorders and nystagmus

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