Head position during resting modifies spontaneous daytime decrease of  downbeat nystagmus

Spiegel, Rainer; Kalla, Roger; Rettinger, N.; Schneider, Erich; Straumann, Dominik; Marti, Sarah; Glasauer, Stefan; Brandt, Thomas; Strupp, Michael

doi:10.1212/wnl.0b013e3181feb22f

Cited by 23 publications

(26 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here, the flocculus is known to integrate vestibular signals [32] for the adaptation of vertical smooth pursuit and gaze holding. Moreover, ocular motor deficits of DBN patients have been shown to depend on gravity (and thereby on vestibular signals) and a model of a disturbed otolith-ocular interaction in DBN patients was established [33], [34].…”

Section: Discussionmentioning

confidence: 99%

The Gait Disorder in Downbeat Nystagmus Syndrome

et al. 2014

View full text Add to dashboard Cite

BackgroundDownbeat nystagmus (DBN) is a common form of acquired fixation nystagmus with key symptoms of oscillopsia and gait disturbance. Gait disturbance could be a result of impaired visual feedback due to the involuntary ocular oscillations. Alternatively, a malfunction of cerebellar locomotor control might be involved, since DBN is considered a vestibulocerebellar disorder.MethodsInvestigation of walking in 50 DBN patients (age 72±11 years, 23 females) and 50 healthy controls (HS) (age 70±11 years, 23 females) using a pressure sensitive carpet (GAITRite). The patient cohort comprised subjects with only ocular motor signs (DBN) and subjects with an additional limb ataxia (DBNCA). Gait investigation comprised different walking speeds and walking with eyes closed.ResultsIn DBN, gait velocity was reduced (p<0.001) with a reduced stride length (p<0.001), increased base of support (p<0.050), and increased double support (p<0.001). Walking with eyes closed led to significant gait changes in both HS and DBN. These changes were more pronounced in DBN patients (p<0.001). Speed-dependency of gait variability revealed significant differences between the subgroups of DBN and DBNCA (p<0.050).Conclusions(I) Impaired visual control caused by involuntary ocular oscillations cannot sufficiently explain the gait disorder. (II) The gait of patients with DBN is impaired in a speed dependent manner. (III) Analysis of gait variability allows distinguishing DBN from DBNCA: Patients with pure DBN show a speed dependency of gait variability similar to that of patients with afferent vestibular deficits. In DBNCA, gait variability resembles the pattern found in cerebellar ataxia.

show abstract

Section: Discussionmentioning

confidence: 99%

The Gait Disorder in Downbeat Nystagmus Syndrome

et al. 2014

View full text Add to dashboard Cite

show abstract

“…In regular clinical visits it should be decided on a case-by-case basis if a patient benefits from treatment or not. If eye recording is performed to support this decision it is important that the measurements are done in the same position and at the same time of day at each visit 30 32…”

Section: Discussionmentioning

confidence: 99%

“…Based on prior work,30 32 a 30-second eye movement recording was carried out with 3-D video-oculography (Munich: GN Otometrics Hortmann Vestlab 100; London: Senso-Motoric Instruments Berlin; sampling rate=50 Hz, resolution 0.1° in horizontal and vertical direction, accuracy=0.6°, range= ±30° in horizontal and vertical directions). The recording order was (1) calibration with targets 8.5° apart, (2) gaze straight ahead with fixation and (3) gaze straight ahead in darkness.…”

Section: Methodsmentioning

confidence: 99%

A randomised double-blind, cross-over trial of 4-aminopyridine for downbeat nystagmus—effects on slowphase eye velocity, postural stability, locomotion and symptoms

Claaßen

Spiegel

Kalla

et al. 2013

J Neurol Neurosurg Psychiatry

View full text Add to dashboard Cite

“…The vertical integrator receives signals from the utricle via an indirect otolith-ocular pathway, which is responsible for static otolith-driven changes in eye position [21,22]. The same cerebellar dysfunction that causes the increase in utricular responses also explains the well-known strong dependence of DBN on head position relative to gravity: in supine position the upward drift and intensity of DBN are smallest and in prone position the upward drift and DBN are largest [23]. In line with our theory, cVEMP amplitudes in DBN did not increase suggesting that vestibulo-collic reflexes remain unchanged, probably caused by different pathways conveying the ascending utricular and descending saccular projections.…”

Section: Discussionmentioning

confidence: 99%

Downbeat nystagmus: evidence for enhancement of utriculo-ocular pathways by ocular vestibular evoked myogenic potentials?

Bremova-Ertl¹,

Glasauer

Strupp

2015

Eur Arch Otorhinolaryngol

View full text Add to dashboard Cite

Downbeat nystagmus (DBN) is caused by an impairment of Purkinje cells in the flocculus. The decreased cerebellar inhibitory input affects otolith pathways. Since ocular and cervical vestibular evoked myogenic potentials (o-/cVEMP) test the otoliths, the VEMP were measured in DBN patients and in controls. Sixteen patients with DBN, 14 cerebellar oculomotor disorder patients without DBN (COMD), and 16 healthy controls were examined with o-/cVEMP. Computational modeling was used to predict VEMP differences between groups. DBN patients had significantly higher oVEMP peak-to-peak (PP) amplitudes than COMD patients without DBN and controls. Cervical VEMP did not differ. The computational model of DBN predicted a twofold oVEMP increase for DBN patients. These findings suggest an enhancement of the utriculo-ocular response. The unchanged cVEMP indicate no effect on the otolith-cervical reflex in DBN. Computational modeling suggests that the utriculo-ocular enhancement is caused by an impaired vertical neural integrator resulting in the increased influence of utricular signals. This also explains the gravitational dependence of DBN.

show abstract

Head position during resting modifies spontaneous daytime decrease of downbeat nystagmus

Abstract: This study provides Class II evidence that for patients with DBN 2 hours of rest in the upright position decreases nystagmus more than 2 hours of rest in the supine or prone positions (relative improvement 79% upright, 33% supine, and 38% prone: p < 0.05).

Cited by 23 publications

References 8 publications

The Gait Disorder in Downbeat Nystagmus Syndrome

The Gait Disorder in Downbeat Nystagmus Syndrome

A randomised double-blind, cross-over trial of 4-aminopyridine for downbeat nystagmus—effects on slowphase eye velocity, postural stability, locomotion and symptoms

Downbeat nystagmus: evidence for enhancement of utriculo-ocular pathways by ocular vestibular evoked myogenic potentials?

Contact Info

Product

Resources

About