Mouth-Opening-Induced Vertigo and Downbeat Nystagmus.
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ABSTRACT:
SUBMITTER: Lee SU
PROVIDER: S-EPMC8490893 | biostudies-literature | 2021 Oct
REPOSITORIES: biostudies-literature
Publications
Mouth-Opening-Induced Vertigo and Downbeat Nystagmus.
Lee Sun Uk SU Na Seunghee S Yu Sungwook S Lee Tae Kyeong TK Lee Eek Sung ES
Journal of clinical neurology (Seoul, Korea) 20211001 4
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Project description:We report the case of a 76-year old lady under lithium carbonate for a bipolar disorder who presented with a suspected optic neuritis. A typical lithium-induced downbeat nystagmus was observed. Discontinuation of lithium therapy resulted in frank improvement in visual acuity and disappearance of the nystagmus.
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Project description:Cerebellar nodulus and uvula and their connections with the vestibular nuclei form the so-called velocity-storage circuit. Lesions involving the velocity-storage circuit give rise to positional vertigo and nystagmus. Herein, we present a 32-year-old man with cerebellar nodulus and uvular hemorrhage who showed periodic vertigo and downbeat nystagmus in the supine position. To explain this unusual pattern, we adopted velocity-storage model with a lesion on the neural connection between the gravity and inertia estimators, resulting in periodic neural impulses and a gravity bias in a specific position. This report expands the spectrum of central positional nystagmus due to dysfunction of the velocity-storage mechanism.
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Project description:The aim of this study was to investigate the clinical characteristics and underlying pathogenesis of episodic vestibular syndrome (EVS) with hyperventilation-induced downbeat nystagmus (HV-DBN).
2020-05-14 | GSE150453 | GEO
Project description: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.
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Project description:Episodic vestibular syndrome with hyperventilation-induced downbeat nystagmus
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Project description:Downbeat nystagmus (DBN) observed in head-hanging positions, may be of central or peripheral origin. Central DBN in head-hanging positions is mostly due to a disorder of the vestibulo-cerebellum, whereas peripheral DBN is usually attributed to canalolithiasis of an anterior semicircular canal. Here, we describe an atypical case of a patient who, after head trauma, experienced severe and stereotypic vertigo attacks after being placed in various head-hanging positions. Vertigo lasted 10-15 s and was always associated with a robust DBN. The provocation of transient vertigo and DBN, which both showed no decrease upon repetition of maneuvers, depended on the yaw orientation relative to the trunk and the angle of backward pitch. On a motorized, multi-axis turntable, we identified the two-dimensional Helmholtz coordinates of head positions at which vertigo and DBN occurred (y-axis: horizontal, space-fixed; z-axis: vertical, and head-fixed; x-axis: torsional, head-fixed, and unchanged). This two-dimensional area of DBN-associated head positions did not change when whole-body rotations took different paths (e.g., by forwarding pitch) or were executed with different velocities. Moreover, the intensity of DBN was also independent of whole-body rotation paths and velocities. So far, therapeutic approaches with repeated liberation maneuvers and cranial vibrations were not successful. We speculate that vertigo and DBN in this patient are due to macular damage, possibly an unstable otolithic membrane that, in specific orientations relative to gravity, slips into a position causing paroxysmal stimulation or inhibition of macular hair cells.
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Project description:Positional downbeat nystagmus (pDBN) represents a relatively frequent finding. Its possible peripheral origin has been widely ascertained. Nevertheless, distinguishing features of peripheral positional nystagmus, including latency, paroxysm and torsional components, may be missing, resulting in challenging differential diagnosis with central pDBN. Moreover, in case of benign paroxysmal positional vertigo (BPPV), detection of the affected canal may be challenging as involvement of the non-ampullary arm of posterior semicircular canal (PSC) results in the same oculomotor responses generated by contralateral anterior canal (ASC)-canalolithiasis. Recent acquisitions suggest that patients with persistent pDBN due to vertical canal-BPPV may exhibit impaired vestibulo-ocular reflex (VOR) for the involved canal on video-head impulse test (vHIT). Since canal hypofunction normalizes following proper canalith repositioning procedures (CRP), an incomplete canalith jam acting as a "low-pass filter" for the affected ampullary receptor has been hypothesized. This study aims to determine the sensitivity of vHIT in detecting canal involvement in patients presenting with pDBN due to vertical canal-BPPV. We retrospectively reviewed the clinical records of 59 consecutive subjects presenting with peripheral pDBN. All patients were tested with video-Frenzel examination and vHIT at presentation and after resolution of symptoms or transformation in typical BPPV-variant. BPPV involving non-ampullary tract of PSC was diagnosed in 78%, ASC-BPPV in 11.9% whereas in 6 cases the involved canal remained unidentified. Presenting VOR-gain values for the affected canal were greatly impaired in cases with persistent pDBN compared to subjects with paroxysmal/transitory nystagmus (p < 0.001). Each patient received CRP for BPPV involving the hypoactive canal or, in case of normal VOR-gain, the assumed affected canal. Each subject exhibiting VOR-gain reduction for the involved canal developed normalization of vHIT data after proper repositioning (p < 0.001), proving a close relationship with otoliths altering high-frequency cupular responses. According to our results, overall vHIT sensitivity in detecting the affected SC was 72.9%, increasing up to 88.6% when considering only cases with persistent pDBN where an incomplete canal plug is more likely to occur. vHIT should be routinely used in patients with pDBN as it may enable to localize otoconia within the labyrinth, providing further insights to the pathophysiology of peripheral pDBN.
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Project description:Paroxysmal positional nystagmus frequently occurs in lesions involving the cerebellum, and has been ascribed to disinhibition and enhanced canal signals during positioning due to cerebellar dysfunction. This study aims to elucidate the mechanism of central positional nystagmus (CPN) by determining the effects of baclofen on the intensity of paroxysmal positional downbeat nystagmus due to central lesions. Fifteen patients with paroxysmal downbeat CPN were subjected to manual straight head-hanging before administration of baclofen, while taking baclofen 30 mg per day for at least one week, and two weeks after discontinuation of baclofen. The maximum slow phase velocity (SPV) and time constant (TC) of the induced paroxysmal downbeat CPN were analyzed. The positional vertigo was evaluated using an 11-point numerical rating scale (0 to 10) in 9 patients. After treatment with baclofen, the median of the maximum SPV of paroxysmal downbeat CPN decreased from 30.1°/s [interquartile range (IQR) = 19.6-39.0°/s] to 15.2°/s (IQR = 11.2-22.0°/s, Wilcoxon signed rank test, p < 0.001) with the median decrement ratio at 40.2% (IQR = 28.2-50.6%). After discontinuation of baclofen, the maximum SPV re-increased to 24.6°/s (IQR = 13.1-34.4°/s, Wilcoxon signed rank test, p = 0.001) with the median increment ratio at 23.5% (IQR = 5.2-87.9%). In contrast, the TCs of paroxysmal downbeat CPN remained unchanged at approximately 3.0 s throughout the evaluation. The positional vertigo also decreased with the medication (Wilcoxon signed rank test, p = 0.020), and remained unchanged even after discontinuation of medication (Wilcoxon signed rank test, p = 0.737). The results of this study support the prior presumption that paroxysmal CPN is caused by enhanced responses of the semicircular canals during positioning due to cerebellar disinhibition. Baclofen may be tried in symptomatic patients with paroxysmal CPN.
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Project description:Background and objectivesLesions of the cerebellar flocculus cause enduring downbeat nystagmus (DBN) with unrelenting oscillopsia. Unlike most patients with DBN, the flocculus is structurally spared in nonalcoholic Wernicke encephalopathy (nWE) with chronic DBN. The objective was to study the effects of alcohol in nWE.MethodsWe recorded eye movements of a unique patient with nWE under controlled alcohol consumption who said his oscillopsia disappeared with a few drinks of alcohol.ResultsHis DBN was markedly diminished by alcohol (by 77.4%), although he remained alert with normal saccades.DiscussionThis striking observation may be caused by the differential effect of alcohol on the perihypoglossal complex and the paramedian tract neurons, which control the level of activity in the flocculus, with opposite (inhibition and excitation, respectively) effects. The finding suggests new ideas about the treatment and pathophysiology of DBN with a structurally intact cerebellum.
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Project description: Not available
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