Objectives: Neuropsychological investigations have shown a degree of cognitive dysfunction in a proportion of non-demented patients with ALS. Respiratory muscle weakness in ALS can lead to nocturnal hypoventilation, resulting in sleep disturbance and daytime somnolence. Sleep deprivation of this type may cause impairments in cognitive function, but this has not been formally evaluated in ALS.
Methods: Cognitive functioning was evaluated in nine patients with ALS with sleep disturbance caused by nocturnal hypoventilation (NIPPV group), and in a comparison group of 10 similar patients without ventilation problems (control group). The NIPPV group then started non-invasive positive pressure ventilation (NIPPV) at night. After about 6 weeks, change in cognitive function was evaluated.
Results: Statistically significant improvement in scores on two of the seven cognitive tests was demonstrated in the NIPPV group postventilation, and a trend towards significant improvement was found for two further tests. Scores in the control group did not improve significantly for these four tests, although an improvement was found on one other test.
Conclusions: Nocturnal hypoventilation and sleep disturbance may cause cognitive dysfunction in ALS. These deficits may be partially improved by NIPPV over a 6 week period. This has important implications for investigations of both cognitive dysfunction in non-demented patients with ALS, and the effect of ventilation on quality of life.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1763518 | PMC |
http://dx.doi.org/10.1136/jnnp.71.4.482 | DOI Listing |
J Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFAge Ageing
January 2025
Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Background: A mobile cognition scale for community screening in cognitive impairment with rigorous validation is in paucity. We aimed to develop a digital scale that overcame low education for community screening for mild cognitive impairment (MCI) due to Alzheimer's disease (AD) and AD.
Methods: A mobile cognitive self-assessment scale (CogSAS) was designed through the Delphi process, which is feasible for the older population with low education.
Appl Neuropsychol Adult
January 2025
Department of Psychology and Logopedics, University of Helsinki, Helsinki, Finland.
Cognitive impairment in patients with COVID-19 has been reported, but findings are inconsistent. This study assessed cognitive functioning 6 months post-infection across three COVID-19 severity groups compared to non-COVID controls. Seventy-two ICU-treated, 49 ward-treated, and 44 home-isolated patients with COVID-19, along with 48 controls, underwent neuropsychological evaluation and assessment of subjective cognitive symptoms, depressive symptoms, and fatigue.
View Article and Find Full Text PDFParkinsonism Relat Disord
January 2025
Department of Nuclear Medicine, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea. Electronic address:
Introduction: In isolated REM sleep behavior disorder (iRBD), the evidence of cognitive impairment and co-existing amyloid pathology suggests that mild behavioral impairment (MBI) may be associated with disease progression. In this study, we investigated MBI and its association with cognitive function, brain amyloid load and glucose metabolism in iRBD patients to evaluate the utility of MBI as a predictive marker of disease progression.
Methods: Patients with iRBD underwent a neuropsychological evaluation, F-florbetaben (FBB) PET, and F-fluorodeoxyglucose (FDG) PET.
Cell Rep
January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!