BACKGROUND:  Assessment of nystagmus fixation suppression can be used as an additional diagnostic tool for patients with an acute vestibular syndrome to distinguish between a central or peripheral cause. We investigated the ability of physicians to detect fixation suppression using a nystagmus simulation model.
METHODS:  We used a nystagmus simulator to measure the accuracy of the nystagmus fixation suppression test. Fixation suppression was assessed randomly in 6170 trials by 20 otorhinolaryngologists and neurologists, segregated into 2 groups based on their neurootological experience, a beginner and an experienced group. The simulator presented random nystagmus slow velocity (SPV) reductions and presented 3 conditions with either changed nystagmus frequency, amplitude, or both.
RESULTS:  The cutoff for the discernment of fixation suppression ranged from 1.2 to 14°/s nystagmus velocity difference. The more intense the baseline nystagmus was, the more difficult was the detection of fixation suppression. There was not significant difference (P >.05) in the cutoff values in the experts group compared to the novices for all 3 different conditions. Both, novices and experts, detected frequency changes easier than differences of the nystagmus amplitude. Test sensitivity was very low (19%-65%) for discernment of small nystagmus velocity differences of <2°/s by experts.
CONCLUSIONS:  In our study, there was no difference between experts and novices in detection of nystagmus suppression by visual fixation. The examiners could only detect large suppression effects at low-intensity baseline nystagmus. Overall, the sensitivity and accuracy of a clinical fixation suppression test is low and the assistance with a video-oculography device is highly recommended.

BACKGROUND: Recently, end-point nystagmus, traditionally observed in an upright position, has been identified in the Dix-Hallpike position among healthy subjects, suggesting a physiological origin.However, its characteristics in individuals with vestibular hypofunction remain unexplored.
OBJECTIVE: To elucidate the impact of vestibular hypofunction on the characteristics of positional end-point nystagmus.
METHODS: Thirty-one patients diagnosed with acute unilateral vestibulopathy according to Bárány Society criteria were selected. A video head impulse test was conducted in all participants, followed by McClure and Dix-Hallpike maneuvers with and without gaze fixation, and with the initial position of the eye in the straight-ahead position or in the horizontal end-point position. Nystagmus direction, sense, latency, slow-phase velocity, and duration were recorded. The relationship between these characteristics and video head impulse test values was analyzed.
RESULTS: Positional end-point nystagmus was observed in 92.6% of subjects with vestibular hypofunction, significantly more than in healthy individuals. Nystagmus direction varied depending on the performed positional test and on the vestibulo-ocular reflex gains. Gaze occlusion and the initial horizontal end-point position increased its frequency.
CONCLUSIONS: Vestibular hypofunction influences the manifestation of positional end-point nystagmus. Recognizing this nystagmus can aid in resolving diagnostic uncertainties and preventing the misdiagnosis of benign paroxysmal positional vertigo in subjects with acute unilateral vestibulopathy.

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UNASSIGNED: The upright head roll test (UHRT) is a recently introduced diagnostic maneuver for lateral semicircular canal benign paroxysmal positional vertigo (LSC-BPPV).
UNASSIGNED: This study aimed to evaluate the reliability and validity of the UHRT.
UNASSIGNED: Two separate studies were conducted. Study 1 analyzed 827 results of videonystagmography (VNG) to assess UHRT reliability, and Study 2 analyzed 130 LSC-BPPV cases to evaluate UHRT validity.
UNASSIGNED: The inter-test reliability between UHRT and the supine head roll test (SHRT) showed substantial agreement (Cohen\'s kappa = 0.753) in direction-changing positional nystagmus (DCPN) and almost perfect agreement (Cohen\'s kappa = 0.836) in distinguishing the direction of DCPN. The validity assessment of UHRT showed high accuracy in diagnosing LSC-BPPV (80.0%) and in differentiating the variant types (74.6%). UHRT was highly accurate in diagnosing the canalolithiasis type in LSC-BPPV patients (Cohen\'s kappa = 0.835); however, it showed only moderate accuracy in diagnosing the cupulolithiasis type (Cohen\'s kappa = 0.415). The intensity of nystagmus in UHRT was relatively weaker than that in SHRT (P < 0.05).
UNASSIGNED: UHRT is a reliable test for diagnosing LSC-BPPV and distinguishing subtypes. However, UHRT has a limitation in discriminating the affected side owing to a weaker intensity of nystagmus than SHRT.

OBJECTIVE: To investigate whether a headshake applied during galvanic vestibular stimulation (GVS) can enhance GVS-induced nystagmus in healthy subjects.
METHODS: In nineteen healthy participants, we evaluated an average slow-phase velocity (aSPV) of nystagmus in a head-still and after the headshake conditions, with/out the bitemporal 2 mA GVS. The GVS was applied also with polarity congruent (supporting) or incongruent (suppressing) to any preexisting spontaneous nystagmus.
RESULTS: The orientation of GVS-induced nystagmus depended on GVS polarity. In the head-still condition, the GVS-induced nystagmus in 14 subjects (74%) for congruent and in 12 subjects (63%) for incongruent GVS. During headshake, we recorded nystagmus in 16 subjects (84%) for congruent and 15 subjects (79%) for incongruent GVS. The aSPV of congruent GVS-induced nystagmus was higher (p = 0.0003) by 1.33 (SE 0.26) deg/s for headshake compared to head-still condition. The aSPV of incongruent GVS also induced higher nystagmus (p = 0.0014) by 1.24 (SE 0.28) deg/s for the headshake condition.
CONCLUSIONS: Our study adds a new principle to the knowledge of the central processing of a GVS response in healthy subjects. The GVS-safety profile of current up to 2 mA was sufficient to elicit a significant GVS nystagmus response in a head-still position in 63% and after a headshake in 79%. Compared to the GVS head-still condition, a headshake enhanced the GVS-induced nystagmus more than twice.
CONCLUSIONS: The headshake helps to identify GVS-induced nystagmus, which can be weak or absent during the head-still condition.

BACKGROUND: Benign paroxysmal positional vertigo (BPPV) is a vestibular disease characterized by brief  positional vertigo. When examined, characteristic patterns of positional nystagmus (PN) are found with specific head position changes. Previous studies have shown a high prevalence of PN among vestibular healthy subjects. Considering the current diagnostic criteria of BPPV and the potentially high prevalence of PN in healthy individuals, this raises the question of potential over diagnosing BPPV, if diagnostics are based exclusively upon objective findings. This study aims to determine the prevalence of PN within a healthy, adult population and furthermore include a characterization of the PN observed.
METHODS: This is a prospective cross-sectional study. 78 subjects were included. The subjects underwent four standardized positional tests for BPPV in a mechanical rotational chair while using a VNG-goggle to monitor and record eye movements.
RESULTS: Positional nystagmus was recorded in 70.5% (55/78) of the subjects. Of the 55 subjects, who presented with PN, 81.8% (45/55) had upbeating PN. The 95th percentile of the maximum a-SPV was found to be 10.4 degrees per second, with a median of 4. Five subjects (6.4%) in total presented with PN mimicking BPPV.
CONCLUSIONS: This study found PN to be a common finding within a healthy, adult population based on the high prevalence of PN in the study population. Upbeating PN mimicking posterior canalolithiasis was found in numerous subjects. The authors recommend a cautious approach when diagnosing BPPV, especially in cases of purely vertical PN (without a torsional component) and if no vertiginous symptoms are present during Dix-Hallpike and Supine Roll Test examinations.

A clinical scale fully dedicated to evaluating ocular motor abnormalities is required for now. We investigated the utility of a recently developed Scale for Ocular motor Disorders in Ataxia (SODA) in patients with multiple system atrophy (MSA). We prospectively assessed SODA in consecutive patients with MSA between August 2021 and August 2023 at the Korea University Medical Center. The results of the clinical exam-based SODA were compared with those measured using video-oculography (VOG-guided SODA). We also compared the findings with other established clinical scales targeting patients with MSA, including the Unified Multiple System Atrophy Rating Scale (UMSARS) I-II, Movement Disorder Society-Unified Parkinson\'s Disease Rating Scale motor part (UPDRS-III), Scale for Assessment of Rating of Ataxia (SARA), Composite Autonomic Symptom Score-31 (COMPASS-31), and Composite Autonomic Severity Score (CASS). Twenty patients were enrolled in our study (17 with cerebellar-type MSA and three with Parkinson-type MSA). Scores ranged from 1 to 14 (median [interquartile range (IQR)] = 8 [5-10]). Among the subscales, saccades had a median score of 2.5 (IQR = 1-3), followed by ocular pursuit (1 [0-1]), nystagmus (1 [0-2]), saccadic intrusions (1 [0-1]), vestibulo-ocular reflex (VOR) (0.5 [0-1]), ocular alignment (0 [0-1]), and VOR cancellation (1 [0-1]). The clinical-exam-based SODA (p = 0.020) and VOG-guided SODA (p = 0.034) positively correlated with disease duration. No correlation was found between clinical exam-based SODA and other scales. Skew deviation, gaze-evoked nystagmus, VOR cancellation, and smooth pursuit had the highest precision among the items. Ocular misalignment and spontaneous and positional nystagmus were frequently false positive and were poorly detected with clinical exam-based SODA. Six patients with repeated evaluation exhibited higher scores, along with deterioration documented on other clinical scales. The SODA can reliably predict neurodegeneration as an additional clinical surrogate in MSA.

OBJECTIVE: To investigate adherence, characteristics, and first clinical experiences of capturing ictal nystagmus at home, which can be performed to complement the diagnostic process in patients with episodic vestibular symptoms.
METHODS: Patients were recruited at a tertiary referral center in case capturing ictal nystagmus could contribute to the diagnostic process (e.g., to detect or rule out BPPV). They were asked to capture ictal nystagmus with their own smartphone at home, using a smartphone-based adapter (Nystagmocatcher, Balansdiagnos, Stockholm, Sweden). All recordings were analyzed by the last author (RvdB), and the adherence, characteristics, and first clinical experiences were evaluated.
RESULTS: Seventy patients with vestibular symptoms were asked to participate in this study. Sixty-two (89%) agreed to participate. The median period of participation was 86 days. Fifty-one patients experienced attacks during the study period. Eventually, 51% of them provided eye movement recordings sufficient for analysis. Different types of nystagmus were observed: positional nystagmus related to BPPV, positional nystagmus not related to BPPV, functional eye movements, and the absence of nystagmus or functional eye movements. Capturing ictal nystagmus could contribute to the diagnostic process in several ways, including to detect or rule out BPPV, to detect or rule out vestibular origin of symptoms, to determine the affected side, telemedicine, to monitor attack frequency, and to detect malingering. Furthermore, strict guidance of patients was necessary, which could be time-consuming.
CONCLUSIONS: Capturing ictal nystagmus can contribute to the diagnostic process in several ways, which motivates to rethink current clinical workflow in vestibular medicine. However, strict guidance is necessary and not all patients provide ictal recordings. In an outpatient setting, it would be advised to use ictal nystagmus recordings on indication, to complement the diagnostic process.

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