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Pain Management Nursing : Official... Jun 2024Identification of fibromyalgia has been a challenge for healthcare professionals due to the lack of a clinical biomarker. A well-supported integrative hypothesis holds...
BACKGROUND
Identification of fibromyalgia has been a challenge for healthcare professionals due to the lack of a clinical biomarker. A well-supported integrative hypothesis holds that this condition is a chronic pain problem partly caused by long-term dysregulation of stress response. Therefore, stress assessment from a biopsychosocial perspective may be a useful approach to recognizing fibromyalgia.
PURPOSE
A cross-sectional case-control study was conducted to explore stress markers from a multidimensional perspective, including heart rate variability (as a biomarker of stress) as well as psychological distress and social stress.
METHODS
Forty-seven women with fibromyalgia were recruited from support groups and another 47 were recruited as matched pain-free controls. Comparison and discriminant function analyses were performed.
RESULTS
The data support the goodness of biopsychosocial stress markers in women with fibromyalgia, resulting in the identification of between 70% and 74.5% of fibromyalgia cases (sensitivity) and 85%-87% pain-free controls (specificity), with medium-high levels of fit (λ = 0.58 and λ = 0.59; p < .00). Women with fibromyalgia were characterized by high levels of psychological distress, social stress (disorder levels), and autonomic dysregulation. Although distress and social stress had a greater weight in discriminant functions, dysregulation in terms of low parasympathetic activity and high sympathetic activity at rest was also relevant.
CONCLUSIONS
A biopsychosocial approach to stress with an objective biomarker such as heart rate variability may be a useful tool to identify and manage FM.
PubMed: 38862334
DOI: 10.1016/j.pmn.2024.05.008 -
BMJ Neurology Open 2024Dissociative seizures often occur in the context of dysregulated affective arousal and entail dissociative symptoms such as a disintegration of bodily awareness....
INTRODUCTION
Dissociative seizures often occur in the context of dysregulated affective arousal and entail dissociative symptoms such as a disintegration of bodily awareness. However, the interplay between affective arousal and changes in interoceptive processing at the onset of dissociative seizures is not well understood.
METHODS
Using retrospective routine data obtained from video-electroencephalography telemetry in a university hospital epilepsy monitoring unit, we investigate ictal changes in cardiac indices of autonomic arousal and heartbeat evoked potentials (HEPs) in 24 patients with dissociative seizures.
RESULTS
Results show autonomic arousal during seizures with increased heart rate and a shift towards sympathetic activity. Compared with baseline, ictal HEP amplitudes over central and right prefrontal electrodes (F8, Fz) were significantly less pronounced during seizures, suggesting diminished cortical representation of interoceptive information. Significant correlations between heart rate variability measures and HEPs were observed at baseline, with more sympathetic and less parasympathetic activity related to less pronounced HEPs. Interestingly, these relationships weakened during seizures, suggesting a disintegration of autonomic arousal and interoceptive processing during dissociative seizures. In a subgroup of 16 patients, MRI-based cortical thickness analysis found a correlation with HEP amplitudes in the left somatosensory association cortex.
CONCLUSIONS
These findings possibly represent an electrophysiological hint of how autonomic arousal could negatively impact bodily awareness in dissociative seizures, and how these processes might be related to underlying brain structure.
PubMed: 38860229
DOI: 10.1136/bmjno-2024-000665 -
Acta Neuropathologica Communications Jun 2024Synucleinopathies are a group of neurodegenerative disorders characterized by the presence of misfolded α-Synuclein (αSyn) in the brain. These conditions manifest with...
Synucleinopathies are a group of neurodegenerative disorders characterized by the presence of misfolded α-Synuclein (αSyn) in the brain. These conditions manifest with diverse clinical and pathophysiological characteristics. This disease diversity is hypothesized to be driven by αSyn strains with differing biophysical properties, potentially influencing prion-type propagation and consequentially the progression of illness. Previously, we investigated this hypothesis by injecting brain lysate (seeds) from deceased individuals with various synucleinopathies or human recombinant αSyn preformed fibrils (PFFs) into transgenic mice overexpressing either wild type or A53T human αSyn. In the studies herein, we expanded on these experiments, utilizing a panel of antibodies specific for the major carboxyl-terminally truncated forms of αSyn (αSynΔC). These modified forms of αSyn are found enriched in human disease brains to inform on potential strain-specific proteolytic patterns. With monoclonal antibodies specific for human αSyn cleaved at residues 103, 114, 122, 125, and 129, we demonstrate that multiple system atrophy (MSA) seeds and PFFs induce differing neuroanatomical spread of αSyn pathology associated with host specific profiles. Overall, αSyn cleaved at residue 103 was most widely present in the induced pathological inclusions. Furthermore, αSynΔC-positive inclusions were present in astrocytes, but more frequently in activated microglia, with patterns dependent on host and inoculum. These findings support the hypothesis that synucleinopathy heterogeneity might stem from αSyn strains with unique biochemical properties that include proteolytic processing, which could result in dominant strain properties.
Topics: alpha-Synuclein; Animals; Humans; Mice, Transgenic; Mice; Brain; Disease Models, Animal; Synucleinopathies; Antibodies, Monoclonal; Multiple System Atrophy; Prions; Female
PubMed: 38858742
DOI: 10.1186/s40478-024-01805-z -
The Egyptian Heart Journal : (EHJ) :... Jun 2024Myeloproliferative disorders, including monoclonal gammopathy of undetermined significance (MGUS), are often associated with amyloid light-chain (AL)-type cardiac...
BACKGROUND
Myeloproliferative disorders, including monoclonal gammopathy of undetermined significance (MGUS), are often associated with amyloid light-chain (AL)-type cardiac amyloidosis (CA) but occasionally with wild-type transthyretin (ATTR) CA. In recent years, ATTR amyloidosis has attracted necessity for its reliable diagnosis with the addition of new treatments. Usually, both wild-type ATTR CA and AL-type CA present with marked cardiac hypertrophy, but renal dysfunction is milder in wild-type ATTR amyloidosis than in AL-type amyloidosis. Peripheral neurologic and autonomic symptoms such as numbness and dysesthesia are moderately present in AL-type amyloidosis, but less so in wild-type ATTR amyloidosis. Furthermore, the prognosis of ATTR-type amyloidosis is better than that of AL-type amyloidosis.
CASE PRESENTATION
A 72-year-old man with cardiac hypertrophy presented with New York Heart Association functional class III dyspnea and leg edema. He had no history of carpal tunnel syndrome. An electrocardiogram showed atrial fibrillation and low voltage. The N-terminal pro-B-type natriuretic peptide level was 3310 pg/mL, and troponin T was elevated to 0.073 ng/mL. However, the glomerular filtration rate was only slightly decreased at 69.0 mL/min/1.73 m. The serum free light-chain assay revealed a significant increase in the kappa chain, with positive results in Bence Jones proteins and serum immunoelectrophoresis. Bone marrow examination confirmed the diagnosis of monoclonal gammopathy of undetermined significance (MGUS). AL-type amyloidosis associated with a myeloproliferative disorder was suspected, and the prognosis was initially predicted to be poor, classified as Mayo stage IV. Contrary to this prognosis, the patient showed a slow progression of heart failure. Further imaging modalities and cardiac tissue findings confirmed the diagnosis as transthyretin type amyloidosis, and a favorable prognosis was established with the use of tafamidis.
CONCLUSIONS
MGUS occasionally coexists with wild-type ATTR CA. Scant autonomic symptoms, mild renal dysfunction, and slow progression of heart failure might be clues that the CA associated with the myeloproliferative disease is wild-type ATTR amyloidosis.
PubMed: 38856864
DOI: 10.1186/s43044-024-00499-x -
Cureus May 2024Introduction Epilepsy is a complex prevalent seizure disorder impacting a significant number of individuals worldwide. Those with epilepsy face the possibility of...
Introduction Epilepsy is a complex prevalent seizure disorder impacting a significant number of individuals worldwide. Those with epilepsy face the possibility of experiencing sudden unexpected death in epilepsy (SUDEP). When examining the relationship between epilepsy and SUDEP, cardiac-related deaths (CRD) may be considered a driving force. We hypothesize that patients with epilepsy are at higher risk of CRD than those without epilepsy. While utilizing the National Institutes of Health (NIH) All of Us Researcher Program (AoU) database, we also explored the relationship between epilepsy and cardiac-related deaths and propose potential connective mechanisms between the two conditions. Methods Baseline data from the National Institutes of Health All of Us Researcher Program was used to evaluate the relationship between cardiac-related deaths and epilepsy. A retrospective cohort study was conducted where individuals with epilepsy and without epilepsy were matched by inclusion and exclusion criteria including death, cardiac-related death, and epilepsy. Additionally, the prevalence of cardiac-related deaths was compared to neurological, respiratory, and hepatic-related deaths for patients with epilepsy to identify emerging causes of SUDEP. Results Among patients with a history of epilepsy, the prevalence of CRD was 45 (17.3%) compared to 305 (11%) in the control group. This difference was statistically significant by p<0.0042 with an odds ratio (OR)=1.698, 95%CI 1.214-2.379. Additionally, there was the highest number of significant cardiac-related deaths amongst patients with epilepsy compared to patients without epilepsy as opposed to different mechanisms of death such as acute respiratory failure, acute hepatic failure, and hypoxic brain injury. Conclusion This study indicates that epileptic patients have a statistically significant higher prevalence of cardiac-related deaths. Additionally, cardiac-related deaths constitute a significantly higher proportion of fatalities amongst patients with epilepsy compared to other causes of SUDEP. Potential mechanisms for these findings may include seizure-induced arrhythmias, hypoxia-induced cardiac arrest, autonomic dysregulation, and neurotransmitter disequilibrium. The results of our study suggest promising directions for future research in identifying predictors of cardiac-related deaths with proposed cardiac monitoring protocols as preventative strategies for epileptic patients in efforts to reduce the prevalence of SUDEP.
PubMed: 38854242
DOI: 10.7759/cureus.59921 -
BioRxiv : the Preprint Server For... Jun 2024Recent research emphasizes the intricate interplay of genetics and epigenetics in neurological disorders, notably Multiple Sclerosis (MS) and Guillain-Barre Syndrome...
Recent research emphasizes the intricate interplay of genetics and epigenetics in neurological disorders, notably Multiple Sclerosis (MS) and Guillain-Barre Syndrome (GBS), both of which exhibit cardiovascular dysregulation, with GBS often featuring serious bradyarrhythmias requiring prompt recognition and treatment. While cardiovascular autonomic dysfunction in MS is typically less severe, orthostatic intolerance affects around half of MS patients. Their distinction lies in their autoimmune responses, MS is an autoimmune disease affecting the central nervous system, causes demyelination and axon damage, leading to cognitive, ocular, and musculoskeletal dysfunction. In contrast, GBS primarily affects the peripheral nervous system, resulting in paralysis and respiratory complications. Despite their differences, both diseases share environmental risk factors such as viral infections and Vitamin D deficiency. This study aims to explore shared gene expression pathways, functional annotations, and molecular pathways between MS and GBS to enhance diagnostics, pathogenesis understanding, and treatment strategies through molecular analysis techniques. Through the gene expression analysis, five significant genes were found UTS2, TNFSF10, GBP1, VCAN, FOS. Results shows that Common DEGs are linked to apoptosis, bacterial infections, and atherosclerosis. Molecular docking analysis suggests Aflatoxin B1 as a potential therapeutic compound due to its high binding affinity with common differentially expressed proteins.
PubMed: 38853933
DOI: 10.1101/2024.05.29.595759 -
Alzheimer's Research & Therapy Jun 2024Higher order regulation of autonomic function is maintained by the coordinated activity of specific cortical and subcortical brain regions, collectively referred to as...
BACKGROUND
Higher order regulation of autonomic function is maintained by the coordinated activity of specific cortical and subcortical brain regions, collectively referred to as the central autonomic network (CAN). Autonomic changes are frequently observed in Alzheimer's disease (AD) and dementia, but no studies to date have investigated whether plasma AD biomarkers are associated with CAN functional connectivity changes in at risk older adults.
METHODS
Independently living older adults (N = 122) without major neurological or psychiatric disorder were recruited from the community. Participants underwent resting-state brain fMRI and a CAN network derived from a voxel-based meta-analysis was applied for overall, sympathetic, and parasympathetic CAN connectivity using the CONN Functional Toolbox. Sensorimotor network connectivity was studied as a negative control. Plasma levels of amyloid (Aβ, Aβ), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) were assessed using digital immunoassay. The relationship between plasma AD biomarkers and within-network functional connectivity was studied using multiple linear regression adjusted for demographic covariates and Apolipoprotein E (APOE) genotype. Interactive effects with APOE4 carrier status were also assessed.
RESULTS
All autonomic networks were positively associated with Aβ ratio and remained so after adjustment for age, sex, and APOE4 carrier status. Overall and parasympathetic networks were negatively associated with GFAP. The relationship between the parasympathetic CAN and GFAP was moderated by APOE4 carrier status, wherein APOE4 carriers with low parasympathetic CAN connectivity displayed the highest plasma GFAP concentrations (B = 910.00, P = .004). Sensorimotor connectivity was not associated with any plasma AD biomarkers, as expected.
CONCLUSION
The present study findings suggest that CAN function is associated with plasma AD biomarker levels. Specifically, lower CAN functional connectivity is associated with decreased plasma Aβ, indicative of cerebral amyloidosis, and increased plasma GFAP in APOE4 carriers at risk for AD. These findings could suggest higher order autonomic and parasympathetic dysfunction in very early-stage AD, which may have clinical implications.
Topics: Humans; Female; Alzheimer Disease; Aged; Male; Biomarkers; Amyloid beta-Peptides; Magnetic Resonance Imaging; Brain; Peptide Fragments; Autonomic Nervous System; Glial Fibrillary Acidic Protein; Aged, 80 and over; Neurofilament Proteins; Autonomic Nervous System Diseases
PubMed: 38851772
DOI: 10.1186/s13195-024-01486-9 -
Frontiers in Neuroscience 2024Vagus nerve stimulation (VNS) improves diseases such as refractory epilepsy and treatment-resistant depression, likely by rebalancing the autonomic nervous system (ANS)....
BACKGROUND
Vagus nerve stimulation (VNS) improves diseases such as refractory epilepsy and treatment-resistant depression, likely by rebalancing the autonomic nervous system (ANS). Intradermal auricular electro-acupuncture stimulation (iaES) produces similar effects. The aim of this study was to determine the effects of different iaES frequencies on the parasympathetic and sympathetic divisions in different states of ANS imbalance.
METHODS
We measured heart rate variability (HRV) and heart rate (HR) of non-modeled (normal) rats with the treatment of various frequencies to determine the optimal iaES frequency. The optimized iaES frequency was then applied to ANS imbalance model rats to elucidate its effects.
RESULTS
30 Hz and 100 Hz iaES clearly affected HRV and HR in normal rats. 30 Hz iaES increased HRV, and decreased HR. 100 Hz iaES decreased HRV, and increased HR. In sympathetic excited state rats, 30 Hz iaES increased HRV. 100 Hz iaES increased HRV, and decreased HR. In parasympathetic excited state rats, 30 Hz and 100 Hz iaES decreased HRV. In sympathetic inhibited state rats, 30 Hz iaES decreased HRV, while 100 Hz iaES decreased HR. In parasympathetic inhibited rats, 30 Hz iaES decreased HR and 100 Hz iaES increased HRV.
CONCLUSION
30 Hz and 100 Hz iaES contribute to ANS rebalance by increasing vagal and sympathetic activity with different amplifications. The 30 Hz iaES exhibited positive effects in all the imbalanced states. 100 Hz iaES suppressed the sympathetic arm in sympathetic excitation and sympathetic/parasympathetic inhibition and suppressed the vagal arm and promoted the sympathetic arm in parasympathetic excitation and normal states.
PubMed: 38846714
DOI: 10.3389/fnins.2024.1367266 -
Neurologia I Neurochirurgia Polska 2024
Topics: Humans; Flushing; Hypohidrosis; Autonomic Nervous System Diseases; Thermography; Male; Adult; Female
PubMed: 38845593
DOI: 10.5603/pjnns.100534 -
Neurological Research and Practice Jun 2024The aim of this German national guideline is to optimize the clinical care of patients with Parkinson's disease (PD) in terms of diagnostics, drug and surgical treatment...
INTRODUCTION
The aim of this German national guideline is to optimize the clinical care of patients with Parkinson's disease (PD) in terms of diagnostics, drug and surgical treatment and care. This guidance was prepared for the German Society of Neurology (DGN) in collaboration with the Austrian Society of Neurology (ÖGN) and the Swiss Neurological Society (SNG) for German-speaking countries. The guidelines for the diagnosis and treatment of PD have been revised by a national expert group and the guideline commission of the DGN at S2k level. The main objective of these guidelines is to optimize the clinical care of PD patients regarding diagnosis, including early detection, technical diagnostic examinations, and pharmacological as well as invasive treatment options.
RECOMMENDATIONS
The updated PD diagnosis and treatment guidelines are emphasizing optimized clinical care. Key revisions include preferring the name "Parkinson's disease" over previous terms and adopting International Parkinson and Movement Disorder Society (MDS) diagnostic criteria. Recommendations cover genetic and imaging diagnostics, initial pharmacotherapy considering efficacy and patient factors, and tailored pharmacological combinations for complications. Guidelines extend to managing cognitive, affective, psychotic, and autonomic symptoms, along with non-oral therapies like pump therapy and deep brain stimulation. Special situations like akinetic crisis, driving ability, and care concepts are addressed, ensuring comprehensive management for PD patients at various stages and conditions.
CONCLUSIONS
This guidance reflects the state of the art at the beginning of 2024.
PubMed: 38845028
DOI: 10.1186/s42466-024-00325-4