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Acta Neurologica Belgica Aug 2022Autonomic dysfunction in patients with viral infections has been described before. In this study, we aimed to evaluate autonomic functions in patients with the...
PURPOSE
Autonomic dysfunction in patients with viral infections has been described before. In this study, we aimed to evaluate autonomic functions in patients with the coronavirus infectious disease 2019 (COVİD-19).
METHODS
In this cross-sectional study, we compared 112 patients who had recovered from COVID-19 and 106 healthy controls. Symptoms of autonomic dysfunction were assessed with the SCOPA-AUT scale.
RESULTS
Pupillomotor, urinary and sudomotor subscores of SCOPA-AUT scale were significantly higher in the COVID-19 patient group (p = 0.03, p = 0,006, p = 0.0001, respectively). There were no significant difference in terms of gastrointestinal, cardiovascular, sexual subscores and total SCOPA-AUT scores between the patient and control groups. The presence of fatigue symptom in the acute phase of COVID-19 increased the total SCOPA-AUT score by 2.2 points (p = 0.04) whereas the presence of smell loss (OR = 5.82, p = 0.01) and dyspnea (OR = 5.8, p = 0.03) were significant risk factors for pupillomotor dysfunction. The urinary, cardiovascular, sexual subscores and the total score of SCOPA-AUT scale were positively correlated with the age of the patient group.
CONCLUSION
Our study suggests that many patients might have prolonged symptoms of autonomic dysfunction after the acute phase of COVID-19 that might worsen the clinical recovery.
Topics: Autonomic Nervous System Diseases; COVID-19; Communicable Diseases; Cross-Sectional Studies; Humans; Surveys and Questionnaires
PubMed: 35239131
DOI: 10.1007/s13760-022-01899-z -
Hypertension (Dallas, Tex. : 1979) Oct 2023The prognostic role and the clinical significance of orthostatic hypertension (OHT) remained undefined for long because data were sparse and often inconsistent. In... (Review)
Review
The prognostic role and the clinical significance of orthostatic hypertension (OHT) remained undefined for long because data were sparse and often inconsistent. In recent years, evidence has been accumulating that OHT is associated with an increased risk of masked and sustained hypertension, hypertension-mediated organ damage, cardiovascular disease, and mortality. Most evidence came from studies in which OHT was defined using systolic blood pressure (BP) whereas the clinical relevance of diastolic OHT is still unclear. Recently, the American Autonomic Society and the Japanese Society of Hypertension defined OHT as an orthostatic systolic BP increase ≥20 mm Hg associated with a systolic BP of at least 140 mm Hg while standing. However, also smaller orthostatic BP increases have shown clinical relevance especially in people ≤45 years of age. A possible limitation of the BP response to standing is poor reproducibility. OHT concordance is better when the between-assessment interval is shorter, when OHT is evaluated using a larger number of BP readings, and if home BP measurement is used. The pathogenetic mechanisms leading to OHT are still controversial and may vary according to age. Excessive neurohumoral activation seems to be the main determinant in younger adults whereas vascular stiffness plays a more important role in older individuals. Conditions associated with higher activity of the sympathetic nervous system and/or baroreflex dysregulation, such as diabetes, essential hypertension, and aging have been found to be often associated with OHT. Measurement of orthostatic BP should be included in routine clinical practice especially in people with high-normal BP.
Topics: Adult; Humans; Aged; Reproducibility of Results; Hypertension; Blood Pressure; Blood Pressure Determination; Cardiovascular Diseases; Hypotension, Orthostatic
PubMed: 37417253
DOI: 10.1161/HYPERTENSIONAHA.123.21537 -
International Journal of Molecular... Apr 2020Multiple system atrophy (MSA) is a rare, severe, and rapidly progressive neurodegenerative disorder categorized as an atypical parkinsonian syndrome. With a mean life... (Review)
Review
Multiple system atrophy (MSA) is a rare, severe, and rapidly progressive neurodegenerative disorder categorized as an atypical parkinsonian syndrome. With a mean life expectancy of 6-9 years after diagnosis, MSA is clinically characterized by parkinsonism, cerebellar ataxia, autonomic failure, and poor l-Dopa responsiveness. Aside from limited symptomatic treatment, there is currently no disease-modifying therapy available. Consequently, distinct pharmacological targets have been explored and investigated in clinical studies based on MSA-related symptoms and pathomechanisms. Parkinsonism, cerebellar ataxia, and autonomic failure are the most important symptoms targeted by symptomatic treatments in current clinical trials. The most prominent pathological hallmark is oligodendroglial cytoplasmic inclusions containing alpha-synuclein, thus classifying MSA as synucleinopathy. Additionally, myelin and neuronal loss accompanied by micro- and astrogliosis are further distinctive features of MSA-related neuropathology present in numerous brain regions. Besides summarizing current symptomatic treatment strategies in MSA, this review critically reflects upon potential cellular targets and disease-modifying approaches for MSA such as (I) targeting α-syn pathology, (II) intervening neuroinflammation, and (III) neuronal loss. Although these single compound trials are aiming to interfere with distinct pathogenetic steps in MSA, a combined approach may be necessary to slow down the rapid progression of the oligodendroglial associated synucleinopathy.
Topics: Adrenergic alpha-1 Receptor Agonists; Animals; Disease Models, Animal; Humans; Induced Pluripotent Stem Cells; Monoamine Oxidase Inhibitors; Multiple System Atrophy; Neuroglia; Peroxidase; alpha-Synuclein
PubMed: 32316335
DOI: 10.3390/ijms21082775 -
European Heart Journal May 2021Head-up tilt test (TT) has been used for >50 years to study heart rate/blood pressure adaptation to positional changes, to model responses to haemorrhage, to assess...
Head-up tilt test (TT) has been used for >50 years to study heart rate/blood pressure adaptation to positional changes, to model responses to haemorrhage, to assess orthostatic hypotension, and to evaluate haemodynamic and neuroendocrine responses in congestive heart failure, autonomic dysfunction, and hypertension. During these studies, some subjects experienced syncope due to vasovagal reflex. As a result, tilt testing was incorporated into clinical assessment of syncope when the origin was unknown. Subsequently, clinical experience supports the diagnostic value of TT. This is highlighted in evidence-based professional practice guidelines, which provide advice for TT methodology and interpretation, while concurrently identifying its limitations. Thus, TT remains a valuable clinical asset, one that has added importantly to the appreciation of pathophysiology of syncope/collapse and, thereby, has improved care of syncopal patients.
Topics: Autonomic Nervous System Diseases; Heart Rate; Humans; Hypotension, Orthostatic; Syncope; Tilt-Table Test
PubMed: 33624801
DOI: 10.1093/eurheartj/ehab084 -
Open Heart Oct 2021Incomplete cardiac revascularisation (ICR) assessed by residual SYNTAX score (rSs) is associated with increased 5-year mortality. Furthermore, in the general population,...
INTRODUCTION
Incomplete cardiac revascularisation (ICR) assessed by residual SYNTAX score (rSs) is associated with increased 5-year mortality. Furthermore, in the general population, our group has demonstrated that impaired autonomic function determined by heart rate recovery time between 10 and 20 s (HRR) following an active stand is associated with increased all-cause mortality.
PURPOSE
We hypothesised that ICR would be associated with impaired autonomic function determined by HRR.
METHODS
After ethical approval and informed consent, consecutive patients attending cardiac rehabilitation in a tertiary referral centre were enrolled. All patients had percutaneous coronary revascularisation. During an active stand, real-time heart rate, blood pressure and ECG recordings were taken using non-invasive digital photoplethysmography and HRR determined. Assessment of autonomic function was performed by determining speed of HRR post-orthostatic challenge.Patients with an rSs >0 were considered incompletely revascularised and those with an rSs of 0 fully revascularised. Demographic data were recorded and statistical analysis performed.
RESULTS
Patients (n=53) comprised those with complete revascularisation (CR) (n=37) and ICR (n=16). In the ICR group, mean rSs was 9.4.HRR was impaired in the ICR group (-3±0.60) compared with the CR cohort (-6.56±0.52) (p<0.0001). Completeness of revascularisation was strongly associated with HRR (Pearson's correlation coefficient 0.529; p<0.0001). Baseline demographics did not differ significantly. Use of rate-limiting medication was similar between cohorts (beta blockers, calcium channel blockers, ivabradine).
CONCLUSIONS
Our data confirm significant correlation between ICR and impaired autonomic function determined by speed of heart rate recovery. Thus, determining autonomic dysfunction post-ICR may identify those at increased mortality risk.
Topics: Aged; Autonomic Nervous System; Autonomic Nervous System Diseases; Case-Control Studies; Coronary Angiography; Coronary Artery Disease; Female; Humans; Ireland; Male; Middle Aged; Percutaneous Coronary Intervention; Postoperative Complications; Prospective Studies; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome
PubMed: 34635578
DOI: 10.1136/openhrt-2021-001835 -
Clinical Autonomic Research : Official... Aug 2019Parkinson disease has traditionally been classified as a movement disorder, despite patients' accounts of diverse symptoms stemming from impairments in numerous body... (Review)
Review
Parkinson disease has traditionally been classified as a movement disorder, despite patients' accounts of diverse symptoms stemming from impairments in numerous body systems. Today, Parkinson disease is increasingly recognized by clinicians and scientists as a complex neurodegenerative disorder featuring both motor and nonmotor manifestations concomitant with pathology throughout all major branches of the nervous system. Dysfunction of the autonomic nervous system, or dysautonomia, is a common feature of Parkinson disease. It produces signs and symptoms that severely affect patients' quality of life, such as blood pressure dysregulation, hyperhidrosis, and constipation. Treatment options for dysautonomia are limited to symptom alleviation because the cause of these symptoms and Parkinson disease overall are still unknown. Animal models provide a platform to interrogate mechanisms of Parkinson disease-related autonomic nervous system dysfunction and test novel treatment strategies. Several animal models of Parkinson disease are available, each with different effects on the autonomic nervous system. This review critically analyses key dysautonomia signs and symptoms and associated pathology in Parkinson disease patients and relevant findings in animal models. We focus on the cardiovascular system, adrenal medulla, skin/thermoregulation, bladder, pupils, and gastrointestinal tract, to assess the contribution of animal models to the understanding of Parkinson disease autonomic dysfunction.
Topics: Animals; Autonomic Nervous System; Autonomic Nervous System Diseases; Blood Pressure; Brain; Disease Models, Animal; Gastrointestinal Tract; Humans; Parkinson Disease
PubMed: 30604165
DOI: 10.1007/s10286-018-00584-7 -
Seminars in Arthritis and Rheumatism Dec 2023Over the years several lines of evidence have implied a pathological involvement of autonomic nervous system (ANS) in systemic sclerosis (SSc). However, the relationship... (Review)
Review
INTRODUCTION
Over the years several lines of evidence have implied a pathological involvement of autonomic nervous system (ANS) in systemic sclerosis (SSc). However, the relationship between autonomic dysfunction and SSc is not yet fully understood. The aims of this scoping review were to map the research done in this field and inform future research to investigate pathogenic hypotheses of ANS involvement.
METHODS
We performed a scoping review of publications collected through a literature search of MEDLINE and Web of Science databases, looking for dysautonomia in SSc. We included original data from papers that addressed ANS involvement in SSc regarding pathogenesis, clinical presentation and diagnostic tools.
RESULTS
467 papers were identified, 109 studies were selected to be included in the present review, reporting data from a total of 2742 SSc patients. Cardiovascular system was the most extensively investigated, assessing heart rate variability with 24 h HolterECG or Ewing's autonomic tests. Important signs of dysautonomia were also found in digital vasculopathy, gastrointestinal system and SSc skin, assessed both with non-invasive techniques and histologically. Research hypotheses mainly regarding the relationship between sympathetic system - ischemia and the role of neurotrophins were then developed and discussed.
CONCLUSION
We described the currently available evidence on pathogenesis, clinical presentation and diagnostic assessment of dysautonomia in SSc patients. A strong influence of ANS deregulation on SSc clearly emerges from the literature. Future research is warranted to clarify the mechanisms and timing of autonomic dysfunction in SSc.
Topics: Humans; Autonomic Nervous System Diseases; Autonomic Nervous System; Heart Rate; Scleroderma, Systemic; Gastrointestinal Tract
PubMed: 37776665
DOI: 10.1016/j.semarthrit.2023.152268 -
Clinical Autonomic Research : Official... Aug 2023Cardiac autonomic dysfunction is one of the main pillars of cardiovascular pathophysiology. The purpose of this review is to provide an overview of the current state of... (Review)
Review
PURPOSE
Cardiac autonomic dysfunction is one of the main pillars of cardiovascular pathophysiology. The purpose of this review is to provide an overview of the current state of the art on the pathological remodeling that occurs within the autonomic nervous system with cardiac injury and available neuromodulatory therapies for autonomic dysfunction in heart failure.
METHODS
Data from peer-reviewed publications on autonomic function in health and after cardiac injury are reviewed. The role of and evidence behind various neuromodulatory therapies both in preclinical investigation and in-use in clinical practice are summarized.
RESULTS
A harmonic interplay between the heart and the autonomic nervous system exists at multiple levels of the neuraxis. This interplay becomes disrupted in the setting of cardiovascular disease, resulting in pathological changes at multiple levels, from subcellular cardiac signaling of neurotransmitters to extra-cardiac, extra-thoracic remodeling. The subsequent detrimental cycle of sympathovagal imbalance, characterized by sympathoexcitation and parasympathetic withdrawal, predisposes to ventricular arrhythmias, progression of heart failure, and cardiac mortality. Knowledge on the etiology and pathophysiology of this condition has increased exponentially over the past few decades, resulting in a number of different neuromodulatory approaches. However, significant knowledge gaps in both sympathetic and parasympathetic interactions and causal factors that mediate progressive sympathoexcitation and parasympathetic dysfunction remain.
CONCLUSIONS
Although our understanding of autonomic imbalance in cardiovascular diseases has significantly increased, specific, pivotal mediators of this imbalance and the recognition and implementation of available autonomic parameters and neuromodulatory therapies are still lagging.
Topics: Humans; Autonomic Nervous System; Heart; Arrhythmias, Cardiac; Heart Failure; Cardiovascular Diseases; Primary Dysautonomias; Ventricular Function
PubMed: 37166736
DOI: 10.1007/s10286-023-00948-8 -
Cardiology in Review 2020Cardiovascular disorders, such as orthostatic hypotension and supine hypertension, are common in patients with neurodegenerative synucleinopathies such as Parkinson... (Review)
Review
Cardiovascular disorders, such as orthostatic hypotension and supine hypertension, are common in patients with neurodegenerative synucleinopathies such as Parkinson disease (PD), and may also occur in other conditions, such as peripheral neuropathies, that result in autonomic nervous system (ANS) dysfunction. Dysfunction and degeneration of the ANS are implicated in the development of orthostatic and postprandial hypotension and impaired thermoregulation. Neurogenic orthostatic hypotension (nOH) results from sympathetic failure and is a common autonomic disorder in PD. Supine hypertension may also occur as a result of both sympathetic and parasympathetic dysfunction in conjunction with nOH in the majority of patients with PD. Management of supine hypertension in the setting of nOH can be counterintuitive and challenging. Additionally, the presence of other noncardiovascular comorbidities, such as diabetes mellitus and peripheral edema, may further contribute to the burden of disease. ANS dysfunction thus presents major healthcare implications and challenges for neurology and cardiovascular practices, necessitating an integrated neurology and cardiology management approach.
Topics: Autonomic Nervous System; Cardiovascular Diseases; Humans; Hypotension, Orthostatic; Parkinson Disease
PubMed: 31764015
DOI: 10.1097/CRD.0000000000000280 -
Cerebellum (London, England) Oct 2023Multiple system atrophy (MSA) is a rare, adult-onset, progressive neurodegenerative disorder with major diagnostic challenges. Aiming for a better diagnostic accuracy... (Review)
Review
Multiple system atrophy (MSA) is a rare, adult-onset, progressive neurodegenerative disorder with major diagnostic challenges. Aiming for a better diagnostic accuracy particularly at early disease stages, novel Movement Disorder Society criteria for the diagnosis of MSA (MDS MSA criteria) have been recently developed. They introduce a neuropathologically established MSA category and three levels of clinical diagnostic certainty including clinically established MSA, clinically probable MSA, and the research category of possible prodromal MSA. The diagnosis of clinically established and clinically probable MSA is based on the presence of cardiovascular or urological autonomic failure, parkinsonism (poorly L-Dopa-responsive for the diagnosis of clinically established MSA), and cerebellar syndrome. These core clinical features need to be associated with supportive motor and non-motor features (MSA red flags) and absence of any exclusion criteria. Characteristic brain MRI markers are required for a diagnosis of clinically established MSA. A research category of possible prodromal MSA is devised to capture patients manifesting with autonomic failure or REM sleep behavior disorder and only mild motor signs at the earliest disease stage. There is a number of promising laboratory markers for MSA that may help increase the overall clinical diagnostic accuracy. In this review, we will discuss the core and supportive clinical features for a diagnosis of MSA in light of the new MDS MSA criteria, which laboratory tools may assist in the clinical diagnosis and which major differential diagnostic challenges should be borne in mind.
Topics: Adult; Humans; Multiple System Atrophy; Diagnosis, Differential; Parkinsonian Disorders; Magnetic Resonance Imaging; Levodopa
PubMed: 35986227
DOI: 10.1007/s12311-022-01453-w