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Parkinson's disease (PD) presents diverse symptoms and comorbidities, complicating its diagnosis and management. The primary objective of this cross-sectional, monocentric study was to assess digital gait sensor data's utility for monitoring and diagnosis of motor and gait impairment in PD. As a secondary objective, for the more challenging tasks of detecting comorbidities, non-motor outcomes, and disease progression subgroups, we evaluated for the first time the integration of digital markers with metabolomics and clinical data. Using shoe-attached digital sensors, we collected gait measurements from 162 patients and 129 controls in a single visit. Machine learning models showed significant diagnostic power, with AUC scores of 83–92% for PD vs. control and up to 75% for motor severity classification. Integrating gait data with metabolomics and clinical data improved predictions for challenging-to-detect comorbidities such as hallucinations. Overall, this approach using digital biomarkers and multimodal data integration can assist in objective disease monitoring, diagnosis, and comorbidity detection. [ABSTRACT FROM AUTHOR]

Introduction: While there is an interest in defining longitudinal change in people with chronic illness like Parkinson's disease (PD), statistical analysis of longitudinal data is not straightforward for clinical researchers. Here, we aim to demonstrate how the choice of statistical method may influence research outcomes, (e.g., progression in apathy), specifically the size of longitudinal effect estimates, in a cohort. Methods: In this retrospective longitudinal analysis of 802 people with typical Parkinson's disease in the Luxembourg Parkinson's study, we compared the mean apathy scores at visit 1 and visit 8 by means of the paired two-sided t-test. Additionally, we analysed the relationship between the visit numbers and the apathy score using linear regression and longitudinal two-level mixed effects models. Results: Mixed effects models were the only method able to detect progression of apathy over time. While the effects estimated for the group comparison and the linear regression were smaller with high p-values (+ 1.016/ 7 years, p = 0.107, -0.056/ 7 years, p = 0.897, respectively), effect estimates for the mixed effects models were positive with a very small p-value, indicating a significant increase in apathy symptoms by + 2.345/ 7 years (p < 0.001). Conclusion: The inappropriate use of paired t-tests and linear regression to analyse longitudinal data can lead to underpowered analyses and an underestimation of longitudinal change. While mixed effects models are not without limitations and need to be altered to model the time sequence between the exposure and the outcome, they are worth considering for longitudinal data analyses. In case this is not possible, limitations of the analytical approach need to be discussed and taken into account in the interpretation. [ABSTRACT FROM AUTHOR]

We present diagnostic criteria for motion sickness, visually induced motion sickness (VIMS), motion sickness disorder (MSD), and VIMS disorder (VIMSD) to be included in the International Classification of Vestibular Disorders. Motion sickness and VIMS are normal physiological responses that can be elicited in almost all people, but susceptibility and severity can be high enough for the response to be considered a disorder in some cases. This report provides guidelines for evaluating signs and symptoms caused by physical motion or visual motion and for diagnosing an individual as having a response that is severe enough to constitute a disorder. The diagnostic criteria for motion sickness and VIMS include adverse reactions elicited during exposure to physical motion or visual motion leading to observable signs or symptoms of greater than minimal severity in the following domains: nausea and/or gastrointestinal disturbance, thermoregulatory disruption, alterations in arousal, dizziness and/or vertigo, headache and/or ocular strain. These signs and/or symptoms occur during the motion exposure, build as the exposure is prolonged, and eventually stop after the motion ends. Motion sickness disorder and VIMSD are diagnosed when recurrent episodes of motion sickness or VIMS are reliably triggered by the same or similar stimuli, severity does not significantly decrease after repeated exposure, and signs/symptoms lead to activity modification, avoidance behavior, or aversive emotional responses. Motion sickness/MSD and VIMS/VIMSD can occur separately or together. Severity of symptoms in reaction to physical motion or visual motion stimuli varies widely and can change within an individual due to aging, adaptation, and comorbid disorders. We discuss the main methods for measuring motion sickness symptoms, the situations conducive to motion sickness and VIMS, and the individual traits associated with increased susceptibility. These additional considerations will improve diagnosis by fostering accurate measurement and understanding of the situational and personal factors associated with MSD and VIMSD. [ABSTRACT FROM AUTHOR]

Abstract Background Cognitive impairment and Alzheimer’s disease (AD) are increasingly considered a major public health problem. The MemoVie cohort study aims to investigate the living conditions or risk factors under which the normal cognitive capacities of the senior population in Luxembourg (≥ 65 year-old) evolve (1) to mild cognitive impairment (MCI) – transitory non-clinical stage – and (2) to AD. Identifying MCI and AD predictors undeniably constitutes a challenge in public health in that it would allow interventions which could protect or delay the occurrence of cognitive disorders in elderly people. In addition, the MemoVie study sets out to generate hitherto unavailable data, and a comprehensive view of the elderly population in the country. Methods/design The study has been designed with a view to highlighting the prevalence in Luxembourg of MCI and AD in the first step of the survey, conducted among participants selected from a random sample of the general population. A prospective cohort is consequently set up in the second step, and appropriate follow-up of the non-demented participants allows improving the knowledge of the preclinical stage of MCI. Case-control designs are used for cross-sectional or retrospective comparisons between outcomes and biological or clinical factors. To ensure maximal reliability of the information collected, we decided to opt for structured face to face interviews. Besides health status, medical and family history, demographic and socio-cultural information are explored, as well as education, habitat network, social behavior, leisure and physical activities. As multilingualism is expected to challenge the cognitive alterations associated with pathological ageing, it is additionally investigated. Data relative to motor function, including balance, walk, limits of stability, history of falls and accidents are further detailed. Finally, biological examinations, including ApoE genetic polymorphism are carried out. In addition to standard blood parameters, the lipid status of the participants is subsequently determined from the fatty acid profiles in their red blood cells. The study obtained the legal and ethical authorizations. Discussion By means of the multidisciplinary MemoVie study, new insights into the onset of cognitive impairment during aging should be put forward, much to the benefit of intervention strategies as a whole.

This paper describes the diagnostic criteria for "Vestibular Migraine of Childhood", "probable Vestibular Migraine of Childhood" and "Recurrent Vertigo of Childhood" as put forth by the Committee for the Classification of Vestibular Disorders of the Bárány Society (ICVD) and the Migraine Classification subgroup of the International Headache Society. Migraine plays an important role in some subgroups of children with recurrent vertigo. In this classification paper a spectrum of three disorders is described in which the migraine component varies from definite to possibly absent. These three disorders are: Vestibular Migraine of Childhood, probable Vestibular Migraine of Childhood and Recurrent Vertigo of Childhood. The criteria for Vestibular Migraine of Childhood (VMC) include (A) at least five episodes with vestibular symptoms of moderate or severe intensity, lasting between five minutes and 72 hours, (B) a current or past history of migraine with or without aura, and (C) at least half of episodes are associated with at least one migraine feature. Probable Vestibular Migraine of Childhood (probable VMC) is considered when at least three episodes with vestibular symptoms of moderate or severe intensity, lasting between five minutes and 72 hours, are accompanied by at least criterion B or C from the VMC criteria. Recurrent Vertigo of Childhood (RVC) is diagnosed in case of at least three episodes with vestibular symptoms of moderate or severe intensity, lasting between 1 minute and 72 hours, and none of the criteria B and C for VMC are applicable. For all disorders, the age of the individual needs to be below 18 years old. It is recommended that future research should particularly focus on RVC, in order to investigate and identify possible subtypes and its links or its absence thereof with migraine. [ABSTRACT FROM AUTHOR]

Objectives/hypothesis: To aggregate symptoms reported by patients with superior canal dehiscence syndrome (SCDS) and to develop an evidence-based symptom set by performing a systematic review of the literature.Study Design: Database search and critical assessment of research studies.Methods: Medline and PubMed databases were searched for articles that reported the preoperative symptoms of adult and pediatric patients with unilateral and bilateral SCDS. Articles were excluded if they reported on associated diseases or did not report symptoms.Results: Of the 397 articles retrieved, 66 were retained for quantitative analysis. Among 431 patients with SCDS, 91 symptom terms were reported. After combining synonymous terms, 22 symptoms were derived by consensus. Of the raw total number of reported symptoms, 92.5% can be attributed to five common symptoms: spontaneous dizziness (51%), autophony (42.5%), pressure-induced vertigo (37.4%), hearing loss (39.9%), and sound-induced vertigo (42.7%).Conclusions: This systematic review of symptoms reported by patients with SCDS identified a 22-item common symptom set. These items can be used to create an evidence-based patient-reported outcome measure to evaluate health-related quality of life in SCDS. Laryngoscope, 1932-1938, 2018. [ABSTRACT FROM AUTHOR]

DOI: 10.3233/VES-200701] On page 215, under section 3, "VI-implantation criteria", where it reads: Reduced horizontal angular VOR gain<=0.1 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/sec) and a phase lead > 68° (time constant < 5 sec) Should be changed to: Reduced horizontal angular VOR gain<=0.1 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/sec) and a phase lead>=15° (time constant<=6 sec). [Extracted from the article]

Previous studies of anatomical changes associated with tinnitus have provided inconsistent results, with some showing significant cortical and subcortical changes, while others have found effects due to hearing loss, but not tinnitus. In this study, we examined changes in brain anatomy associated with tinnitus using anatomical scans from 128 participants with tinnitus and hearing loss, tinnitus with clinically normal hearing, and non-tinnitus controls with clinically normal hearing. The groups were matched for hearing loss, age and gender. We employed voxel- and surface-based morphometry (SBM) to investigate gray and white matter volume and thickness within regions-ofinterest (ROI) that were based on the results of previous studies. The largest overall effects were found for age, gender, and hearing loss. With regard to tinnitus, analysis of ROI revealed numerous small increases and decreases in gray matter and thickness between tinnitus and non-tinnitus controls, in both cortical and subcortical structures. For whole brain analysis, the main tinnitus-related significant clusters were found outside sensory auditory structures. These include a decrease in cortical thickness for the tinnitus group compared to controls in the left superior frontal gyrus (SFG), and a decrease in cortical volume with hearing loss in left Heschl's gyrus (HG). For masked analysis, we found a decrease in gray matter volume in the right Heschle's gyrus for the tinnitus group compared to the controls. We found no changes in the subcallosal region as reported in some previous studies. Overall, while some of the morphological differences observed in this study are similar to previously published findings, others are entirely different or even contradict previous results. We highlight other discrepancies among previous results and the increasing need for a more precise subtyping of the condition. [ABSTRACT FROM AUTHOR]

This paper describes the diagnostic criteria for vestibular paroxysmia (VP) as defined by the Classification Committee of the Bárány Society. The diagnosis of VP is mainly based on the patient history and requires: A) at least ten attacks of spontaneous spinning or non-spinning vertigo; B) duration less than 1 minute; C) stereotyped phenomenology in a particular patient; D) response to a treatment with carbamazepine/oxcarbazepine; and F) not better accounted for by another diagnosis. Probable VP is defined as follows: A) at least five attacks of spinning or non-spinning vertigo; B) duration less than 5 minutes; C) spontaneous occurrence or provoked by certain head-movements; D) stereotyped phenomenology in a particular patient; E) not better accounted for by another diagnosis. Ephaptic discharges in the proximal part of the 8th cranial nerve, which is covered by oligodendrocytes, are the assumed mechanism. Important differential diagnoses are Menière's disease, vestibular migraine, benign paroxysmal positional vertigo, epileptic vestibular aura, paroxysmal brainstem attacks (in multiple sclerosis or after brainstem stroke), superior canal dehiscence syndrome, perilymph fistula, transient ischemic attacks and panic attacks. Current areas of uncertainty in the diagnosis of VP are: a) MRI findings of vascular compression which are not diagnostic of the disease or predictive for the affected side because they are also observed in about 30% of healthy asymptomatic subjects; and b) response to treatment with carbamazepine/oxcarbazepine supports the diagnosis but there are so far no randomized controlled trials for treatment of VP. [ABSTRACT FROM AUTHOR]