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Background Current evidence on chronic conditions favors promotion of health behaviors as a mean to positively impact health outcomes. In Parkinson’s disease, performing health behaviors is indicated as a means to fight the long-lasting burden of the disease. Understanding actual engagement in health behaviors and patient activation and their association to function and health-related quality of life is therefore important. Our objectives were, among people with Parkinson’s disease: (1) to characterize health behaviors including utilization of rehabilitative treatments, physical activity, and patient activation levels, and (2) to test the associations between these health behaviors and health outcomes. Methods A cross-sectional study of 88 people with Parkinson’s disease (age 66.84 ± 8.8) was conducted. Participants answered questionnaires measuring health behaviors including utilization of health professions treatments, physical activity, patient activation, and health outcomes consisting of function and health-related quality of life. Linear regression models were conducted to test associations between measured health behaviors, function and health-related quality of life. Results Participants rarely engage in rehabilitative treatments, but showed high levels of patient activation. Controlled by demographics and disease severity, physical activity and patient activation were associated with function (b = 0.41, p  < .001; b = 0.2, p  = .02, respectively) and physical activity but not patient activation, which was associated with health-related quality of life (b = 0.19, p  = .03). There was also interaction effects of physical activity and non-motor symptoms, and physical activity and motor symptoms on health-related quality of life (b = 0.19, p  = .02 and b = − 0.22, p  = .01, respectively). Conclusions In respect to their potential health-related benefits for people with Parkinson’s disease, health professionals’ treatments are underutilized. Findings supported the importance of health behaviors for maintaining function and health-related quality of life among people with Parkinson’s disease. They also show a differential contribution of motor and non-motor symptoms to the association between physical activity and quality of life. It is suggested that policy makers encourage opportunities for physical activity tailored for people with Parkinson’s disease and adopt a proactive stance towards enhancing awareness and use of rehabilitation services. Trial registration NCT05211700, ClinicalTrials.gov ID: NCT05211700 first release 12/30/2021, https://classic.clinicaltrials.gov/ct2/show/NCT05211700

The coronavirus (COVID-19) pandemic is still evolving, causing hundreds of millions of infections around the world. The long-term sequelae of COVID-19 and neurologic syndromes post COVID remain poorly understood. The present study aims to characterize cognitive performance in patients experiencing cognitive symptoms post-COVID infection. Patients evaluated at a post COVID clinic in Northern Israel who endorsed cognitive symptoms were referred for neurologic consultation. The neurologic work-up included detailed medical history, symptom inventory, neurological examination, the Montreal Cognitive Assessment (MoCA), laboratory tests and brain CT or MRI. Between December 2020 and June 2021, 46 patients were referred for neurological consultation (65% female), mean age 49.5 (19–72 years). On the MoCA test, executive functions, particularly phonemic fluency, and attention, were impaired. In contrast, the total MoCA score, and memory and orientation subscores did not differ from expected ranges. Disease severity, premorbid condition, pulmonary function tests and hypoxia did not contribute to cognitive performance. Cognitive decline may affect otherwise healthy patients post-COVID, independent of disease severity. Our examination identified abnormalities in executive function, attention, and phonemic fluency. These findings occurred despite normal laboratory tests and imaging findings.

Background: The reason some diabetic polyneuropathy (DPN) patients develop neuropathic pain while others present with painless symptoms is unknown. Altered central pain processing has been associated with neuropathic pain. Previous EEG studies found unique cortical patterns in patients with neuropathic pain however these studies were limited to univariate analysis of locally activated areas of cortex. It has been proposed that pain is encoded by complex activity and connectivity patterns which can be explored by application of Machine Learning techniques on the EEG signal. We aimed to investigate whether EEG based functional connectivity can be a potential biomarker for distinction between painful and non-painful DPN. Methods: We recorded contact-heat pain evoked potentials (CHEPs) of 120 painful DPN patients (33F, 63.2 ± 9.9 yrs) and 38 non-painful DPN patients (7F, 64.3 ± 9.5 yrs). Connectivity analysis was conducted based on a measure of synchrony (Phase Locking Value) between the recording sites. We then applied a data-driven analysis scheme to identify the most differentiating functional connections in each frequency band. These connections were validated and used to predict neuropathic pain. Results: We found overall higher cortical functional connectivity between areas of the pain matrix among painful DPN patients. In alpha and theta bands, the connectivity values were significantly different, and differentiated between the two groups with fair-to-excellent specificity (0.797) and sensitivity (0.9). Conclusion: Patients with DPN can be successfully classified into painful and non-painful based solely on EEG functional connectivity data. Increased connectivity between areas of the pain matrix in alpha and tetha band might be a biomarker for neuropathic pain.

Background An accurate clinico‐biological diagnosis of cognitive decline is crucial for identifying neurodegenerative diseases from disorders with similar clinical presentations and administration of appropriate treatments. Recent biotechnological advancements have enabled the measurement of protein biomarkers associated with Alzheimer's Disease (AD) pathology and the assessment of paraneoplastic and non‐paraneoplastic antibodies indicative of autoimmune processes. Since June 2020, our service has conducted comprehensive assessments, incorporating neurological, cognitive evaluations, imaging and CSF biomarker workups. Our aim was to assess the effectiveness of our approach in achieving an accurate clinic‐biological diagnosis of the underlying etiology of cognitive impairment in individuals evaluated at our center. Method Consenting patients presenting with cognitive and/or behavioral deterioration underwent lumbar puncture (LP) for cerebrospinal fluid (CSF) analysis, tailored according to the clinical differential diagnosis. The analysis included cell count, protein, glucose, chloride, cytology, AD biomarkers—total tau, 181‐phosphorylated tau, amyloid‐β42—and panels for paraneoplastic and non‐paraneoplastic antibodies. Result A total of 131 patients presenting with cognitive and/or behavioral deterioration (mean age 63.4 ± 9.4 years; 60 females, 45%) underwent LP for CSF evaluation. AD biomarkers were assessed in 120 subjects, with 59 (49%) testing positive. Antibodies associated with autoimmune encephalitis were tested in 92 subjects, revealing positive paraneoplastic antibody profiles in 14 (15%) subjects (8 with biomarker‐confirmed AD and 6 with non‐AD pathology). Two patients with positive both AD‐biomarkers and paraneoplastic antibodies passed away 34 and 77 months after the evaluation, 6 received immune treatment, and 5 were diagnosed with an oncological condition. Conclusion Our study highlights the significant value of biomarkers in diagnosing cognitive and behavioral impairments, helping to prevent misdiagnosis or inappropriate labeling of Alzheimer's Disease and guiding the appropriate treatment. We suggest that it is essential to include autoimmune encephalopathy in the differential diagnosis for patients presenting with cognitive decline, as appropriate treatment can be life‐saving.

An accurate clinico-biological diagnosis of cognitive decline is crucial for identifying neurodegenerative diseases from disorders with similar clinical presentations and administration of appropriate treatments. Recent biotechnological advancements have enabled the measurement of protein biomarkers associated with Alzheimer's Disease (AD) pathology and the assessment of paraneoplastic and non-paraneoplastic antibodies indicative of autoimmune processes. Since June 2020, our service has conducted comprehensive assessments, incorporating neurological, cognitive evaluations, imaging and CSF biomarker workups. Our aim was to assess the effectiveness of our approach in achieving an accurate clinic-biological diagnosis of the underlying etiology of cognitive impairment in individuals evaluated at our center. Consenting patients presenting with cognitive and/or behavioral deterioration underwent lumbar puncture (LP) for cerebrospinal fluid (CSF) analysis, tailored according to the clinical differential diagnosis. The analysis included cell count, protein, glucose, chloride, cytology, AD biomarkers-total tau, 181-phosphorylated tau, amyloid-β42-and panels for paraneoplastic and non-paraneoplastic antibodies. A total of 131 patients presenting with cognitive and/or behavioral deterioration (mean age 63.4 ± 9.4 years; 60 females, 45%) underwent LP for CSF evaluation. AD biomarkers were assessed in 120 subjects, with 59 (49%) testing positive. Antibodies associated with autoimmune encephalitis were tested in 92 subjects, revealing positive paraneoplastic antibody profiles in 14 (15%) subjects (8 with biomarker-confirmed AD and 6 with non-AD pathology). Two patients with positive both AD-biomarkers and paraneoplastic antibodies passed away 34 and 77 months after the evaluation, 6 received immune treatment, and 5 were diagnosed with an oncological condition. Our study highlights the significant value of biomarkers in diagnosing cognitive and behavioral impairments, helping to prevent misdiagnosis or inappropriate labeling of Alzheimer's Disease and guiding the appropriate treatment. We suggest that it is essential to include autoimmune encephalopathy in the differential diagnosis for patients presenting with cognitive decline, as appropriate treatment can be life-saving.