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Spinocerebellar ataxias are progressive neurodegenerative disorders primarily affecting the cerebellum. Although the first disease-causing gene was identified nearly 30 years ago, there is no known cure to date, and only a few options exist for symptomatic treatment, with modest effects. The recently developed tools in molecular biology, such as CRISPR/Cas9 and antisense oligonucleotides, can directly act on the disease mechanisms at the genomic or RNA level in disease models. In a nutshell, we are finally just one step away from clinical trials with therapies targeting the underlying genetic cause. However, we still face the challenges for rare neurodegenerative diseases difficulty in obtaining a large cohort size for sufficient statistical power and the need for biomarkers and clinical outcome assessments (COA) with adequate sensitivity to reflect progression or treatment responses. To overcome these obstacles, ataxia experts form research networks for clinical trial readiness. In this review, we retrace our steps of the collaborative efforts among ataxia researchers in the United States over the years to study and treat these relentless disorders and the future directions of such research networks.Introduction Cognitive impairment and orthostatic hypotension (OH) are common, disabling Parkinson disease (PD) symptoms that are strongly correlated. Whether the relationship is causative or associative remains unknown. OH may occur without classic orthostatic symptoms of cerebral hypoperfusion (i.e., lightheadedness or dizziness). Whether longitudinal differences in cognition occur between symptomatic and asymptomatic OH patients has not been explored. Objectives We characterized the prevalence of OH, orthostatic symptoms, and cognitive impairment among PD patients and compared cognition between patients with and without OH, and between patients with symptomatic and asymptomatic OH. Methods Our cross-sectional, retrospective, observational study included 226 clinically diagnosed PD patients who underwent repeated standardized evaluations. Among these, 62 had longitudinal follow-up of > 3.5 years. We compared longitudinal Montreal Cognitive Assessment (MoCA) scores between patients remaining OH-free (n = 14) and those without baseline OH that developed OH (n = 28), matched for age, sex, education, and PD duration. We also compared MoCA scores between groups with asymptomatic OH (n = 13) and symptomatic OH (n = 13) matched for the same factors. Selleckchem RO5126766 Results In the cross-sectional analysis, OH patients had worse cognition. In the longitudinal analysis (mean follow-up = 5.3 years), OH patients had worse cognitive decline (p = 0.027). Cognitive impairment was similar between asymptomatic and symptomatic OH patients in the cross-sectional and longitudinal analyses. Conclusions OH is associated with cognitive impairment in PD. Further studies are needed in larger cohorts to expand our findings and to determine whether treating OH can prevent or delay cognitive dysfunction.Background Coronavirus disease 2019 (COVID-19) is a new viral respiratory disease and has become a pandemic. Fever, weakness, and dry cough are the main clinical manifestations. However, little is known about neurological symptoms of non-critically ill COVID-19 patients. Objective To investigate the neurological symptoms and implications of patients with non-critically ill COVID-19 patients. Materials and Methods This retrospective cohort study investigated all COVID-19 patients admitted to Wuhan East-West Lake Fangcang shelter hospital. Demographic data, clinical manifestations, comorbidities, radiological data, the result of nucleic acid test, and treatments were collected and analyzed. Results Among 1,682 patients with confirmed non-critically ill COVID-19, 509 patients (30.3%) had neurological symptoms, including myalgia (311, 18.5%), headache (216, 12.8%), fatigue (83, 4.9%), and dizziness (15, 0.9%). One hundred and fourteen patients (6.8%) were the expansion of pulmonary infection according to their chest CT images and medical history. Compared with patients without neurological symptoms, patients with neurological symptoms had a significantly longer length of hospital stay, time of nucleic acid turning negative, and the mean time from onset of symptom to hospital admission (p less then 0.05). Patients with neurological symptoms were more likely to occur the expansion of pulmonary infection compared with the patients without neurological symptoms (46/509 [9.0%] vs. 68/1,173 [5.8%]). Conclusions Non-critically ill COVID-19 patients commonly have neurological symptoms. Neurological symptoms are significantly associated with the processes of COVID-19. Early identification and aggressive treatment are particularly important for COVID-19 patients with neurological symptoms.The functional integrity of the inferior vestibular nerve (IVN) may be evaluated by the cervical vestibular evoked myogenic potential (cVEMP) response, which requires signal transmission via the nerve. As functional integrity of the IVN innervating the posterior semicircular canal is required to produce the typical positioning vertigo and nystagmus characterizing posterior canal benign paroxysmal positional vertigo (PCBPPV), we hypothesized that normal cVEMPs would be found in most PCBPPV patients. Twenty-four PCBPPV patients participated in a prospective cohort study. All were treated by canal repositioning maneuver and had air-conduction cVEMP and videonystagmography (VNG). Follow-up evaluations including history and otoneurological bedside examination were carried out 1, 3, 6, and 12 months after the initial treatment. At the last follow-up, the patients filled the Dizziness Handicap Inventory (DHI) questionnaire. Normal cVEMPs were recorded in 19 (79%) and were absent in 5 (21%) of the subjects. The averating the role of IVN functional integrity. The absent cVEMPs in the minority of patients, although having similar clinical presentation, raise the possibility that the ipsilateral saccule is affected by the same pathology causing degeneration of the utricle macula. Alternatively, lacking inhibitory stimuli from the involved ipsilateral utricle or partial degeneration of the IVN and ganglion could explain the diminished cVEMP response. Clinical Trial Registration The study was registered in ClinicalTrials.gov Internet site (study ID-NCT01004913; https//clinicaltrials.gov/ct2/show/NCT01004913?cond=BPPV&cntry=IL&draw=2&rank=3).
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