Analysis of Downbeat Nystagmus

Vertical nystagmus in normal subjects: Effects of head position, nicotine and scopolamine

“…The second hypothesis that we tested was that any change in vertical gaze stability caused by placing the head upside-down is mediated by modulation of otolithic tone. This proposal is consistent with the suggestion of Gresty and colleagues [10,11] that downbeat nystagmus may be otolithic in origin. Because the otoliths do sense the linear acceleration due to gravity, this hypothesis predicts that head inversion will produce sustained changes in vertical nystagmus.…”

“…Our observations were made on normal subjects, and so they may not account for the underlying mechanism in patients with pathological downbeat nystagmus. In those patients, the hypothesis of B öhmer and Straumann [7] may still operate under certain conditions, as well as an otolithic mechanism [10] or a combined effect [11]. Furthermore, vertical asymmetry of smooth-pursuit signals and instability of the neural integrator for eye movements might contribute in some patients.…”

Vertical nystagmus in normal subjects: Effects of head position, nicotine and scopolamine

“…The second hypothesis that we tested was that any change in vertical gaze stability caused by placing the head upside-down is mediated by modulation of otolithic tone. This proposal is consistent with the suggestion of Gresty and colleagues [10,11] that downbeat nystagmus may be otolithic in origin. Because the otoliths do sense the linear acceleration due to gravity, this hypothesis predicts that head inversion will produce sustained changes in vertical nystagmus.…”

“…Our observations were made on normal subjects, and so they may not account for the underlying mechanism in patients with pathological downbeat nystagmus. In those patients, the hypothesis of B öhmer and Straumann [7] may still operate under certain conditions, as well as an otolithic mechanism [10] or a combined effect [11]. Furthermore, vertical asymmetry of smooth-pursuit signals and instability of the neural integrator for eye movements might contribute in some patients.…”

Vestibulo-spatial navigation: pathways and sense of direction

“…DBN is accompanied by gait ataxia and increased sagittal postural sway ( 80 , 81 ), as well as dizziness ( 82 ) and shortened vestibulo-perceptual time constants ( 21 ), which are best explained by damage to vestibulo-spinal and vestibulo-cortical mechanisms, respectively. Other ocular-motor features of DBN such as its head motion/positioning sensitivity ( 83 – 86 ) and, in particular, the fact that the nystagmus is partly suppressed by fixation (like all vestibular nystagmus do) ( 81 ) also support a vestibular origin and argue against a pursuit/fixation mechanism.…”

Downbeat nystagmus: a clinical review of diagnosis and management

“…Zee et al [2] proposed the pathophysiology of DBN to relate to an imbalance in the smooth pursuit pathway, confirmed with sustained asymmetric upward smooth pursuit tasks among healthy volunteers [14]. Others have proposed an imbalance of vestibular input from the semicircular canals (SCC) [4,6,15]. More recently, some have proposed that DBN is caused by cerebellar damage to the inputs of neural velocity-to-position integrators, changing the integrator time constant and intrinsic coordinate system for orientation [16].…”

Vertical nystagmus in normal subjects: Effects of head position, nicotine and scopolamine

“…The second hypothesis that we tested was that any change in vertical gaze stability caused by placing the head upside-down is mediated by modulation of otolithic tone. This proposal is consistent with the suggestion of Gresty and colleagues [10,11] that downbeat nystagmus may be otolithic in origin. Because the otoliths do sense the linear acceleration due to gravity, this hypothesis predicts that head inversion will produce sustained changes in vertical nystagmus.…”

“…Our observations were made on normal subjects, and so they may not account for the underlying mechanism in patients with pathological downbeat nystagmus. In those patients, the hypothesis of B öhmer and Straumann [7] may still operate under certain conditions, as well as an otolithic mechanism [10] or a combined effect [11]. Furthermore, vertical asymmetry of smooth-pursuit signals and instability of the neural integrator for eye movements might contribute in some patients.…”

Vestibulo-spatial navigation: pathways and sense of direction

“…DBN is accompanied by gait ataxia and increased sagittal postural sway ( 80 , 81 ), as well as dizziness ( 82 ) and shortened vestibulo-perceptual time constants ( 21 ), which are best explained by damage to vestibulo-spinal and vestibulo-cortical mechanisms, respectively. Other ocular-motor features of DBN such as its head motion/positioning sensitivity ( 83 – 86 ) and, in particular, the fact that the nystagmus is partly suppressed by fixation (like all vestibular nystagmus do) ( 81 ) also support a vestibular origin and argue against a pursuit/fixation mechanism.…”

Downbeat nystagmus: a clinical review of diagnosis and management

“…Zee et al [2] proposed the pathophysiology of DBN to relate to an imbalance in the smooth pursuit pathway, confirmed with sustained asymmetric upward smooth pursuit tasks among healthy volunteers [14]. Others have proposed an imbalance of vestibular input from the semicircular canals (SCC) [4,6,15]. More recently, some have proposed that DBN is caused by cerebellar damage to the inputs of neural velocity-to-position integrators, changing the integrator time constant and intrinsic coordinate system for orientation [16].…”

Vertical nystagmus in normal subjects: Effects of head position, nicotine and scopolamine

“…The second hypothesis that we tested was that any change in vertical gaze stability caused by placing the head upside-down is mediated by modulation of otolithic tone. This proposal is consistent with the suggestion of Gresty and colleagues [10,11] that downbeat nystagmus may be otolithic in origin. Because the otoliths do sense the linear acceleration due to gravity, this hypothesis predicts that head inversion will produce sustained changes in vertical nystagmus.…”

“…Our observations were made on normal subjects, and so they may not account for the underlying mechanism in patients with pathological downbeat nystagmus. In those patients, the hypothesis of B öhmer and Straumann [7] may still operate under certain conditions, as well as an otolithic mechanism [10] or a combined effect [11]. Furthermore, vertical asymmetry of smooth-pursuit signals and instability of the neural integrator for eye movements might contribute in some patients.…”

Vestibulo-spatial navigation: pathways and sense of direction

“…DBN is accompanied by gait ataxia and increased sagittal postural sway ( 80 , 81 ), as well as dizziness ( 82 ) and shortened vestibulo-perceptual time constants ( 21 ), which are best explained by damage to vestibulo-spinal and vestibulo-cortical mechanisms, respectively. Other ocular-motor features of DBN such as its head motion/positioning sensitivity ( 83 – 86 ) and, in particular, the fact that the nystagmus is partly suppressed by fixation (like all vestibular nystagmus do) ( 81 ) also support a vestibular origin and argue against a pursuit/fixation mechanism.…”

Downbeat nystagmus: a clinical review of diagnosis and management

“…Zee et al [2] proposed the pathophysiology of DBN to relate to an imbalance in the smooth pursuit pathway, confirmed with sustained asymmetric upward smooth pursuit tasks among healthy volunteers [14]. Others have proposed an imbalance of vestibular input from the semicircular canals (SCC) [4,6,15]. More recently, some have proposed that DBN is caused by cerebellar damage to the inputs of neural velocity-to-position integrators, changing the integrator time constant and intrinsic coordinate system for orientation [16].…”