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Scientific Reports May 2024Variations in the autonomic nervous system activity during exercise therapy in patients with cardiovascular diseases may lead to adverse events. Aromatherapy may reduce... (Randomized Controlled Trial)
Randomized Controlled Trial
Variations in the autonomic nervous system activity during exercise therapy in patients with cardiovascular diseases may lead to adverse events. Aromatherapy may reduce these adverse events by enhancing parasympathetic nervous activity (PNA). However, the effects of aromatherapy during exercise remain relatively unknown. This study aimed to evaluate the effect of aromatherapy on autonomic nervous activity during exercise and recovery. This randomized crossover study included 20 healthy men subjected to both aroma and placebo conditions which involved rest and moderate-intensity aerobic exercise on a cycle ergometer, followed by recovery. Blood pressure, heart rate variability indices, and SpO were measured during the rest, exercise, and recovery phases. Moreover, aroma preferences and emotional changes in response to the aroma were assessed. Under the placebo condition, high frequency (HF), root mean square of successive differences indices, and heart rate showed delayed recovery (P < 0.05). Furthermore, a moderate positive correlation was identified between aroma preference, pleasant emotions induced by aromatherapy, and the HF index (P < 0.05). These results indicate that aromatherapy facilitates the recovery of PNA after exercise. Furthermore, these effects were more pronounced among individuals who exhibited a stronger preference for and more positive emotions toward aromas.
Topics: Humans; Aromatherapy; Male; Exercise; Autonomic Nervous System; Heart Rate; Adult; Cross-Over Studies; Young Adult; Blood Pressure; Odorants
PubMed: 38755393
DOI: 10.1038/s41598-024-61732-w -
PloS One 2024Several cardiovascular disease (CVD) risk factors (e.g., hypertension, poor glycemic control) can affect and be affected by autonomic nervous system (ANS) activity....
Several cardiovascular disease (CVD) risk factors (e.g., hypertension, poor glycemic control) can affect and be affected by autonomic nervous system (ANS) activity. Since excess adiposity can influence CVD development through its effect on hypertension and diabetes mellitus, it is important to determine how adiposity and altered ANS activity are related. The present study employed structural equation modeling to investigate the relation between adiposity and ANS activity both directly and indirectly through biological variables typically associated with glycemic impairment and cardiac stress in older adults. Utilizing the Atherosclerosis Risk in Communities (ARIC) dataset, 1,145 non-smoking adults (74±4.8 yrs, 62.8% female) free from known CVD, hypertension, and diabetes and not currently taking beta-blockers were evaluated for fasting blood glucose (FBG), insulin, and HbA1c concentrations, waist circumference (WC), blood pressure (BP), and markers of ANS activity. WC was recorded just above the iliac crest and was used to reflect central adiposity. Resting 2-minute electrocardiograph recordings, pulse wave velocity, and ankle-brachial index data were used to assess the root mean square of successive differences in RR intervals (RMSSD) and the pre-ejection period (PEP), markers of parasympathetic and sympathetic activity, respectively. FBG, insulin, and HbA1c inferred a latent variable termed glycemic impairment (GI), whereas heart rate and diastolic BP inferred a latent variable termed cardiac stress (CS). The structural equation model fit was acceptable [root mean square error of approximation = 0.050 (90% CI = .036, .066), comparative fit index = .970, Tucker Lewis Index = 0.929], with adiposity having both significant direct (β = 0.208, p = 0.018) and indirect (β = -.217, p = .041) effects on PEP through GI. Adiposity displayed no significant direct effect on RMSSD. CS displayed a significant pathway (β = -0.524, p = 0.035) on RMSSD, but the indirect effect of WC on RMSSD through CS did not reach statistical significance (β = -0.094, p = 0.137). These results suggest that adiposity's relation to ANS activity is multifaceted, as increased central adiposity had opposing direct and indirect effects on markers of sympathetic activity in this population of older adults.
Topics: Humans; Female; Male; Aged; Adiposity; Autonomic Nervous System; Biomarkers; Blood Glucose; Blood Pressure; Waist Circumference; Insulin; Glycated Hemoglobin; Aged, 80 and over; Cardiovascular Diseases
PubMed: 38753844
DOI: 10.1371/journal.pone.0303117 -
Science Advances May 2024Early and precise diagnosis of α-synucleinopathies is challenging but critical. In this study, we developed a molecular beacon-based assay to evaluate...
Early and precise diagnosis of α-synucleinopathies is challenging but critical. In this study, we developed a molecular beacon-based assay to evaluate microRNA-containing extracellular vesicles (EVs) in plasma. We recruited 1203 participants including healthy controls (HCs) and patients with isolated REM sleep behavior disorder (iRBD), α-synucleinopathies, or non-α-synucleinopathies from eight centers across China. Plasma miR-44438-containing EV levels were significantly increased in α-synucleinopathies, including those in the prodromal stage (e.g., iRBD), compared to both non-α-synucleinopathy patients and HCs. However, there are no significant differences between Parkinson's disease (PD) and multiple system atrophy. The miR-44438-containing EV levels negatively correlated with age and the Hoehn and Yahr stage of PD patients, suggesting a potential association with disease progression. Furthermore, a longitudinal analysis over 16.3 months demonstrated a significant decline in miR-44438-containing EV levels in patients with PD. These results highlight the potential of plasma miR-44438-containing EV as a biomarker for early detection and progress monitoring of α-synucleinopathies.
Topics: Humans; Extracellular Vesicles; Male; Biomarkers; Female; Middle Aged; Circulating MicroRNA; Parkinson Disease; Aged; Synucleinopathies; alpha-Synuclein; Case-Control Studies; MicroRNAs; Multiple System Atrophy
PubMed: 38748787
DOI: 10.1126/sciadv.adl6442 -
Frontiers in Immunology 2024Anti-NMDA receptor encephalitis is an autoimmune disorder caused by autoantibodies (abs) against the conformational epitope on GluN1 subunits. GluN1-abs have been...
INTRODUCTION
Anti-NMDA receptor encephalitis is an autoimmune disorder caused by autoantibodies (abs) against the conformational epitope on GluN1 subunits. GluN1-abs have been determined with cell-based assay (CBA) co-expressing GluN1/GluN2 subunits. However, commercial fixed CBA expressing only GluN1 subunit has increasingly been used in clinical practice. The ab titers can be determined with serial dilutions, but its clinical significance remains unclear. We aimed to develop an H-intensity scale (HIS) score to estimate GluN1-ab titers in cerebrospinal fluid (CSF) with one-time immunostaining using both commercial CBA and immunohistochemistry and report its usefulness. "H" is the initial of a patient with high CSF GluN1-ab titers (1:2,048).
METHODS
We first determined the reliability of CBA in 370 patients with suspected autoimmune encephalitis by comparing the results between commercial CBA and established assay in Dalmau's Lab. Then, we made positive control panels using the patient H's CSF diluted in a fourfold serial dilution method (1:2, 1:8, 1:32, 1:128, 1:512, and 1:2,048). Based on the panels, we scored the intensity of ab reactivity of 79 GluN1-ab-positive patients' CSF (diluted at 1:2) on a scale from 0 to 6 (with ≥1 considered positive). To assess inter-assay reliability, we performed immunostaining twice in 21 patients' CSF. We investigated an association between the score of CSF obtained at diagnosis and the clinical/paraclinical features.
RESULTS
The sensitivity and specificity of CBA were 93.7% (95% CI: 86.0-97.3) and 98.6% (95% CI: 96.5-99.5), respectively. Linear regression analysis showed a good agreement between the scores of the first and second assays. Patients with a typical spectrum, need for mechanical ventilation support, autonomic symptoms/central hypoventilation, dyskinesias, speech dysfunction, decreased level of consciousness, preceding headache, ovarian teratoma, and CSF leukocyte count >20 cells/µL had a higher median HIS score than those without, but HIS score was not associated with sex, age at onset, or seizure. HIS score at diagnosis had a significant effect on 1-year functional status.
DISCUSSION
The severity of disease and four of the six core symptoms were associated with higher GluN1-ab titers in CSF at diagnosis, which may play a role in poor 1-year functional status. An incomplete phenotype can be attributed to low CSF GluN1-ab titers.
Topics: Humans; Female; Autoantibodies; Middle Aged; Adult; Male; Receptors, N-Methyl-D-Aspartate; Aged; Anti-N-Methyl-D-Aspartate Receptor Encephalitis; Young Adult; Adolescent; Child; Immunohistochemistry; Child, Preschool; Nerve Tissue Proteins; Reproducibility of Results; Biomarkers; Aged, 80 and over
PubMed: 38745654
DOI: 10.3389/fimmu.2024.1350837 -
Cureus Apr 2024Catatonia is a psychomotor syndrome predominantly associated with mental illness disorders, most commonly bipolar disorder and schizophrenia. Catatonia is classified as...
Catatonia is a psychomotor syndrome predominantly associated with mental illness disorders, most commonly bipolar disorder and schizophrenia. Catatonia is classified as malignant when, in addition to catatonic symptoms, dysautonomia is present. Autonomic abnormalities can include changes in temperature, labile blood pressure, and changes in heart and respiratory rates. Because malignant catatonia is life-threatening, prompt recognition and management are essential to prevent mortality. We present a severe case of catatonia with malignant features that highlight the importance of early diagnosis and treatment.
PubMed: 38741865
DOI: 10.7759/cureus.58142 -
BMC Neurology May 2024Multiple system atrophy (MSA) is a progressive, incurable, life-threatening neurodegenerative disease uniquely characterized by the risk of sudden death, which makes...
BACKGROUND
Multiple system atrophy (MSA) is a progressive, incurable, life-threatening neurodegenerative disease uniquely characterized by the risk of sudden death, which makes diagnosis delivery challenging for neurologists. Empirical studies on breaking a diagnosis of MSA are scarce, with no guidelines currently established. This study aimed to investigate neurologists' current practices and experiences in delivering the diagnosis of MSA.
METHODS
We conducted a multicenter online survey and employed a mixed-methods (quantitative and qualitative) study design in which responses to open-ended questions were analyzed qualitatively using critical incident technique.
RESULTS
Among the 194 neurologists surveyed, 166 opened the survey (response rate = 85.6%), of whom 144 respondents across various Japanese regions completed the survey. Accordingly, 92.3% and 82.8% of the participating neurologists perceived delivering the diagnosis of MSA and explaining the risk of sudden death as difficult, respectively. Factors independently associated with difficulties in diagnosis delivery included explaining the importance of the family decision making process in life-prolonging treatment, perceived difficulties in delivering information regarding the risk of sudden death, and perceived difficulties in differential diagnosis of MSA.
CONCLUSIONS
Our findings showed that the majority of neurologists perceived delivering the diagnosis of MSA and explaining the risk of sudden death as difficult, which could have been associated with the difficulty of breaking the diagnosis of MSA. Difficulty in conveying bad news in MSA are caused by various factors, such as empathic burden on neurologists caused by the progressive and incurable nature of MSA, the need to explain complex and important details, including the importance of the family decision-making process in life-prolonging treatment, difficulty of MSA diagnosis, and communication barriers posed by mental status and cognitive impairment in patients or their family members. Neurologists consider various factors in explaining the risk of sudden death (e.g., patient's personality, mental state, and degree of acceptance and understanding) and adjust their manner of communication, such as limiting their communication on such matters or avoiding the use of the term "sudden death" in the early stages of the disease. Although neurologists endeavor to meet the basic standards of good practice, there is room for the multiple aspects for improvement.
Topics: Humans; Multiple System Atrophy; Neurologists; Japan; Male; Female; Middle Aged; Surveys and Questionnaires; Attitude of Health Personnel; Adult; Death, Sudden; East Asian People
PubMed: 38741055
DOI: 10.1186/s12883-024-03666-4 -
Cureus Apr 2024Malignant catatonia is a rare, life-threatening variant of catatonia requiring prompt treatment. Malignant catatonia is characterized by typical catatonia symptoms of...
Malignant catatonia is a rare, life-threatening variant of catatonia requiring prompt treatment. Malignant catatonia is characterized by typical catatonia symptoms of psychomotor, neurologic, and behavioral changes complicated by autonomic instability, with an estimated mortality rate of 50% or more when untreated. Electroconvulsive therapy (ECT) is considered the definitive and most effective treatment for malignant catatonia, with minimal literature on the efficacy of pharmacological interventions alone. Timely access to life-saving ECT may be limited in some hospitals due to restrictive laws on the use of ECT when the patient is incapacitated or due to lack of treatment availability. This case report describes the successful pharmacologic treatment of a patient with malignant catatonia where ECT was unobtainable due to legal restrictions and lack of access to treatment. The patient was initially commenced on lorazepam but continued to deteriorate, subsequently developing complications of aspiration pneumonia and colitis. The patient's malignant catatonia resolved with a combination of lorazepam, memantine, and a one-time dose of dantrolene. This complex case highlights the challenges of treating malignant catatonia in under-resourced systems or jurisdictions with restrictive ECT laws and adds additional data on the successful use of pharmacologic interventions for malignant catatonia where ECT is impractical or delayed.
PubMed: 38737995
DOI: 10.7759/cureus.58071 -
Tremor and Other Hyperkinetic Movements... 2024Opsoclonus is a rare disorder characterized by conjugate multidirectional, horizontal, vertical, and torsional saccadic oscillations, without intersaccadic interval,...
BACKGROUND
Opsoclonus is a rare disorder characterized by conjugate multidirectional, horizontal, vertical, and torsional saccadic oscillations, without intersaccadic interval, resulting from dysfunction within complex neuronal pathways in the brainstem and cerebellum. While most cases of opsoclonus are associated with autoimmune or paraneoplastic disorders, infectious agents, trauma, or remain idiopathic, opsoclonus can also be caused by medications affecting neurotransmission. This review was prompted by a case of opsoclonus occurring in a patient with Multiple System Atrophy, where amantadine, an NMDA-receptor antagonist, appeared to induce opsoclonus.
METHODS
Case report of a single patient and systematized review of toxic/drug-induced opsoclonus, selecting articles based on predefined criteria and assessing the quality of included studies.
RESULTS
The review included 30 articles encompassing 158 cases of toxic/drug-induced opsoclonus. 74% of cases were attributed to bark scorpion poisoning, followed by 9% of cases associated with chlordecone intoxication. The remaining cases were due to various toxics/drugs, highlighting the involvement of various neurotransmitters, including acetylcholine, glutamate, GABA, dopamine, glycine, and sodium channels, in the development of opsoclonus.
CONCLUSION
Toxic/drug-induced opsoclonus is very rare. The diversity of toxics/drugs impacting different neurotransmitter systems makes it challenging to define a unifying mechanism, given the intricate neuronal pathways underlying eye movement physiology and opsoclonus pathophysiology.
Topics: Humans; Male; Amantadine; Multiple System Atrophy; Ocular Motility Disorders; Aged
PubMed: 38737300
DOI: 10.5334/tohm.832 -
Diagnostics (Basel, Switzerland) Apr 2024The paper presents a system for analyzing cardiac activity with the possibility of continuous and remote monitoring. The created sensor mobile device monitors heart...
The paper presents a system for analyzing cardiac activity with the possibility of continuous and remote monitoring. The created sensor mobile device monitors heart activity by means of the convenient and imperceptible registration of cardiac signals. At the same time, the behavior of the human body is also monitored through the accelerometer and gyroscope built into the device, thanks to which it is possible to signal in the event of loss of consciousness or fall (in patients with syncope). Conducting real-time cardio monitoring and the analysis of recordings using various mathematical methods (linear, non-linear, and graphical) enables the research, accurate diagnosis, timely assistance, and correct treatment of cardiovascular diseases. The paper examines the recordings of patients diagnosed with arrhythmia and syncope recorded by electrocardiography (ECG) sensors in real conditions. The obtained results are subjected to statistical analysis to determine the accuracy and significance of the obtained results. The studies show significant deviations in the patients with arrhythmia and syncope regarding the obtained values of the studied parameters of heart rate variability (HRV) from the accepted normal values (for example, the root mean square of successive differences between normal heartbeats (RMSSD) in healthy individuals is 24.02 ms, while, in patients with arrhythmia (6.09 ms) and syncope (5.21 ms), it is much lower). The obtained quantitative and graphic results identify some possible abnormalities and demonstrate disorders regarding the activity of the autonomic nervous system, which is directly related to the work of the heart.
PubMed: 38732339
DOI: 10.3390/diagnostics14090926 -
Journal of Neuroinflammation May 2024Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant... (Review)
Review
Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack of effective treatments underscore the urgent need for innovative therapeutic strategies. The brain-gut axis has emerged as a crucial bidirectional pathway connecting the brain and the gastrointestinal (GI) system through an intricate network of neuronal, hormonal, and immunological pathways. Four main pathways are primarily implicated in this crosstalk, including the systemic immune system, autonomic and enteric nervous systems, neuroendocrine system, and microbiome. TBI induces profound changes in the gut, initiating an unrestrained vicious cycle that exacerbates brain injury through the brain-gut axis. Alterations in the gut include mucosal damage associated with the malabsorption of nutrients/electrolytes, disintegration of the intestinal barrier, increased infiltration of systemic immune cells, dysmotility, dysbiosis, enteroendocrine cell (EEC) dysfunction and disruption in the enteric nervous system (ENS) and autonomic nervous system (ANS). Collectively, these changes further contribute to brain neuroinflammation and neurodegeneration via the gut-brain axis. In this review article, we elucidate the roles of various anti-inflammatory pharmacotherapies capable of attenuating the dysregulated inflammatory response along the brain-gut axis in TBI. These agents include hormones such as serotonin, ghrelin, and progesterone, ANS regulators such as beta-blockers, lipid-lowering drugs like statins, and intestinal flora modulators such as probiotics and antibiotics. They attenuate neuroinflammation by targeting distinct inflammatory pathways in both the brain and the gut post-TBI. These therapeutic agents exhibit promising potential in mitigating inflammation along the brain-gut axis and enhancing neurocognitive outcomes for TBI patients.
Topics: Humans; Brain Injuries, Traumatic; Brain-Gut Axis; Animals; Anti-Inflammatory Agents; Gastrointestinal Microbiome; Neuroinflammatory Diseases
PubMed: 38730498
DOI: 10.1186/s12974-024-03118-3