Tag: autonomic dysfunction

A case series of cutaneous phosphorylated α-synuclein in Long-COVID POTS

Dear Editors,

As case numbers of coronavirus disease 19 (COVID-19) increase, chronic symptoms, including those of autonomic dysfunction, are being reported with increasing frequency [], leading to the diagnosis of post-acute sequelae of COVID-19 (PASC), or Long-COVID. In addition, small fiber neuropathy (SFN) has been reported after viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) []. These associations have prompted our group to systematically perform autonomic testing and skin biopsies in a cohort of patients who have developed postural tachycardia syndrome (POTS) as a consequence of PASC (Long-COVID POTS). As part of this evaluation, all skin biopsy samples undergo immunohistochemical analysis of both intraepidermal nerve fiber density (IENFD) and phosphorylated α-synuclein (p-syn) [], the pathological form of α-synuclein associated with the neurodegenerative diseases of Parkinson’s disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF), as well as isolated REM sleep behavior disorder (iRBD), a prodromal manifestation of synucleinopathy for the majority of patients.

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Source: Miglis MG, Seliger J, Shaik R, Gibbons CH. A case series of cutaneous phosphorylated α-synuclein in Long-COVID POTS. Clin Auton Res. 2022 May 16:1–4. doi: 10.1007/s10286-022-00867-0. Epub ahead of print. PMID: 35570247; PMCID: PMC9108014. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9108014/ (Full text)

Risk factors and multidimensional assessment of long COVID fatigue: a nested case-control study

Abstract:

Background: Fatigue is the most prevalent and debilitating long COVID symptom, however risk factors and pathophysiology of this condition remain unknown. We assessed risk factors for long COVID fatigue and explored its possible pathophysiology.

Methods: Nested case-control study in a COVID recovery clinic. Individuals with (cases) and without (controls) significant fatigue were included. We performed a multidimensional assessment evaluating various parameters, including pulmonary function tests and cardiopulmonary exercise testing, and implemented multivariable logistic regression to assess risk factors for significant long COVID fatigue.

Results: Total of 141 individuals were included. Mean age was 47 (SD 13) years; 115 (82%) were recovering from mild COVID-19. Mean time for evaluation was 8 months following COVID-19. Sixty-six (47%) individuals were classified with significant long COVID fatigue. They had significantly higher number of children, lower proportion of hypothyroidism, higher proportion of sore throat during acute illness and long COVID symptoms, and of physical limitation in daily activities. Individuals with fatigue had poorer sleep quality and higher degree of depression. They had significantly lower heart rate [153.52 (22.64) vs 163.52 (18.53), p=0.038] and oxygen consumption per Kg [27.69 (7.52) vs 30.71 (7.52), p=0.036] at peak exercise. The two independent risk factors for fatigue identified in multivariable analysis were peak exercise heart rate (odds ratio [OR] 0.79 per 10 beats/minute, 95% confidence interval [CI] 0.65-0.96, p=0.019); and long COVID memory impairment (OR 3.76, 95% CI 1.57-9.01, p=0.003).

Conclusions: Long COVID fatigue may be related to autonomic dysfunction, impaired cognition and decreased mood. This may suggest a limbic-vagal pathophysiology. Clinical Trial registration: NCT04851561.

Source: Margalit I, Yelin D, Sagi M, Rahat MM, Sheena L, Mizrahi N, Gordin Y, Agmon H, Epstein NK, Atamna A, Tishler O, Daitch V, Babich T, Abecasis D, Yarom Y, Kazum S, Shitenberg D, Baltaxe E, Elkana O, Shapira-Lichter I, Leibovici L, Yahav D. Risk factors and multidimensional assessment of long COVID fatigue: a nested case-control study. Clin Infect Dis. 2022 Apr 11:ciac283. doi: 10.1093/cid/ciac283. Epub ahead of print. PMID: 35403679.  https://pubmed.ncbi.nlm.nih.gov/35403679/

Autonomic dysfunction and post-COVID-19 syndrome: A still elusive link

Editorial:

Infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the long-lasting pandemic coronavirus disease 2019 (COVID-19), with dramatic clinical, social, and economic implications. Importantly, evolving experience consistently shows that, in addition to issues related to the acute phase, patients who recover from COVID-19 may present a wide variety of bothersome symptoms, which may be debilitating and significantly impair their quality of life. This condition, when it persists beyond 12 weeks after recovery, is defined as “post–COVID-19” or “long COVID-19” syndrome.

Some of the symptoms, including tachycardia/palpitations, chest pain, fatigue, and dyspnea with reduced effort tolerance, suggest a possible cardiovascular cause, whereas others (eg, muscle and/or joint pain, headache, memory loss, nausea, mood disturbances) suggest involvement of other systems. Symptoms may occur independently of the severity of COVID-19, although patients with more severe symptoms in the acute phase experience a higher rate of symptom persistence during follow-up. , 

Importantly, careful diagnostic assessment usually fails to identify specific causes of post–COVID-19 syndrome. However, it has been suggested that at least some post–COVID-19 symptoms, including those of potential cardiovascular origin, might be related to abnormalities of the autonomic nervous system (ANS). The pathophysiological mechanisms responsible for ANS impairment remain speculative and might include direct damage of the ANS (ganglia and/or nerve terminations) by the virus, a toxic effect of inflammatory cytokines released during the acute infection, and an immune-mediated response triggered by some viral component(s). ,  Independent of the mechanism, the possibility of ANS involvement in SARS-CoV-2 infection is supported by the frequent occurrence of neurologic symptoms (eg, anosmia, dysgeusia) as well as the sporadic occurrence of clinical conditions typically related to ANS dysfunction (eg, orthostatic hypotension, orthostatic tachycardia) in post–COVID-19 syndrome. Furthermore, patients with COVID-19, compared to healthy subjects, have been found to show reduced heart rate variability (HRV) parameters 20 weeks after recovery from the illness. However, a pathogenetic relationship between dysautonomia and post–COVID-19 syndrome remains to be demonstrated. Establishing such a relationship would be of importance because it might help guide the management of this clinical condition.

The study by Ladlow et al in this issue of Heart Rhythm Journal is welcome because it attempts to clarify whether any association exists between dysautonomia and symptoms, as well as objective evidence of exercise intolerance, in patients with post–COVID-19 syndrome. In their study, Ladlow et al enrolled 205 patients referred to a post–COVID-19 clinic who fulfilled specific eligibility criteria (hospitalization and desaturation ≤95% on a Harvard step test or chest pain with electrocardiographic [ECG] changes during acute illness and life-limiting symptoms persisting for >12 weeks). All patients underwent bicycle cardiopulmonary exercise testing (CPET) and were divided into 1 of 2 groups according to evidence or no evidence of dysautonomia.

Dysautonomia was diagnosed based on 3 heart rate (HR) parameters that Jouven et al found to be associated with total mortality and sudden death in a population of asymptomatic subjects: (1) resting HR >75 bpm; (2) increase in HR during exercise <89 bpm; and (3) HR reduction <25 bpm during the first minute of recovery from peak exercise. HRV was also assessed by calculating the root mean square of the squared differences of adjacent RR intervals (RMSSD) on a 1-minute 12-lead ECG at rest and on 30-second ECGs during the first 3 minutes of recovery after peak exercise.

Patients were studied 183 ± 77 days (∼6 months) from COVID-19 disease, and dysautonomia was found in 51 patients (25%). Per definition, these patients had higher HR at rest (95 ± 12 bpm vs 81 ± 12 bpm; P <.001) and lower HR increase during CPET (75 ± 12 bpm vs 96 ± 13 bpm; P <.001) and HR recovery after peak exercise (17 ± 4 bpm vs 31 ± 17 bpm; P <.001) compared to those without dysautonomia.

Patients with dysautonomia were older, had a higher body mass index (BMI) (P = .013) and waist circumference (WC) (P = .003), and had a lower basal RMSSD (P <.001). Furthermore, at rest, dysautonomic patients showed a higher breathing rate (P = .006) and lower forced vital capacity (P = .031), forced expiratory volume in 1 second (P = .036), and ventilatory efficiency (Ve/Vco 2) (P = .036).

When assessing symptoms that showed prevalence >25%, a significant association with dysautonomia was found for low mood (P = .007), headache (P = .026), and poor attention (P = .047). However, other symptoms, including some of potential cardiovascular origin (eg, shortness of breath, fatigue), showed no significant association with dysautonomia.

Patients with dysautonomia, however, showed a lower performance on CPET. In particular, HR at peak exercise (170 ± 13 bpm vs 177 ± 15 bpm; P = .003), maximal work rate (219 ± 37 W vs 253 ± 52 W; P <.001), and maximal oxygen consumption (V⋅O2) (30.6 ± 5.5 mL/kg/min vs 35.8 ± 7.6 mL/kg/min; P <.001) all were significantly lower in patients with dysautonomia than in those without dysautonomia, suggesting a role of ANS dysfunction in their physical limitation.

Ladlow et al should be congratulated for performing this large study on post–COVID-19 syndrome. However, possible alternative interpretations of the data suggest caution in deriving definitive conclusions from their results.

Although the study shows the lack of significant relationship between dysautonomia and most post–COVID-19 symptoms, including, in particular, some symptoms of possible cardiovascular origin, the method applied to identify patients with an impairment of ANS function presents some limitations. Both higher HR at rest and lower HR recovery after exercise suggest an imbalance of sympathovagal tone toward adrenergic predominance in their patients with dysautonomia. However, rather than reflecting a primary impairment of the ANS, these findings simply might have been related to differences between the 2 groups with regard to some basal clinical characteristics, including higher BMI/WC, lower efficiency in respiratory function, and lower mood in dysautonomic patients. In addition, the lower increase in HR during maximal exercise in patients with dysautonomia might have been a mere consequence of their having a higher HR at rest and, given their older age, a lower maximal theoretical HR for age. The percent of predicted maximal HR for age achieved during CPET, in fact, did not differ between the 2 groups. The possibility that the differences in HR behavior might have not been related to a primary abnormality of the ANS is also suggested by the fact that, despite the basal difference, RMSSD values were similar during exercise recovery in the 2 groups of patients, suggesting a similar ANS response to exercise interruption in the 2 groups.

Future studies should clarify whether different results regarding the relationship between ANS dysfunction and post–COVID-19 symptoms might be obtained using more comprehensive and better validated methods for the diagnosis of ANS dysfunction, such as standard tests of autonomic function and HRV assessed from its multiple (short-term and long-term) components.

Of note, although the results of CPET in the study by Ladlow et al suggest lower performance by patients classified with dysautonomia, exercise tolerance was largely normal in these subjects, who achieved >100% of the predicted maximal oxygen consumption and an average maximal work rate of 219 W, with only small differences compared to patients without dysautonomia, possibly explained, again, and at least in part, by some demographic (age) and clinical (BMI, respiratory function) differences.

In conclusion, the study by Ladlow et al provides interesting data on the clinical characteristics and objective physical performance of patients with post–COVID-19 syndrome. However, the role of ANS in determining symptoms (particularly those of potential cardiovascular origin) and physical limitation in these patients still has not been fully elucidated by their data, making necessary further studies applying more comprehensive and valuable methods for the assessment of ANS function.

Source: Lanza GA. Autonomic dysfunction and post-COVID-19 syndrome: A still elusive link. Heart Rhythm. 2022 Apr;19(4):621-622. doi: 10.1016/j.hrthm.2021.12.027. Epub 2021 Dec 28. PMID: 34968741; PMCID: PMC8712711. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712711/ (Full study)

Non-improvement in chronic fatigue syndrome: relation to activity patterns, uplifts and hassles, and autonomic dysfunction

Abstract:

Objective: To test a model of non-improvement in chronic fatigue syndrome (CFS) utilizing self-report activity patterns (e.g., “push-crash”), uplifts and hassles, and a biological measure of cardiac autonomic function. Activity pattern impacts on symptoms and objective measures of autonomic and physical activity were also examined.

Methods: This prospective study in CFS collected all data remotely, including six months of weekly web diaries that recorded symptom ratings, activity patterns, and hassles and uplifts. In addition, six months of weekly heart monitoring and three months of daily waking actigraphy data were collected. Improvement or non-improvement status was assessed using semi-structured interviews at 6 months follow-up.

Results: 148 individuals (87.2% female) were enrolled and 12.2% were lost to follow-up. Participants reporting non-improvement (n = 92), as compared to improvement (n = 38) showed greater autonomic dysfunction (lower heart rate variability [HRV], group difference = 5.93 (SE = 2.73) ms; p = .032) and lower mean intensity of behavioral uplifts (group difference = 0.14 (SE = 0.16); p = .043), but no significant differences in any activity pattern, including push-crash, limiting activity, and healthy pacing.

Conclusions: This study provided evidence for linking patient-reported non-improvement to a biological variable indexing autonomic dysfunction and a behavioral measure indicating a deficit in psychological uplifts. These findings suggest a possible marker of illness trajectory that could potentially advance the biomedical underpinnings of CFS.

Source: Friedberg F, Adamowicz JL, Bruckenthal P, Milazzo M, Ramjan S, Quintana D. Non-improvement in chronic fatigue syndrome: relation to activity patterns, uplifts and hassles, and autonomic dysfunction. Psychosom Med. 2022 Apr 15. doi: 10.1097/PSY.0000000000001082. Epub ahead of print. PMID: 35420586. https://pubmed.ncbi.nlm.nih.gov/35420586/

Reduced Parasympathetic Reactivation during Recovery from Exercise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Abstract:

Although autonomic nervous system (ANS) dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) has been proposed, conflicting evidence makes it difficult to draw firm conclusions regarding ANS activity at rest in ME/CFS patients. Although severe exercise intolerance is one of the core features of ME/CFS, little attempts have been made to study ANS responses to physical exercise. Therefore, impairments in ANS activation at rest and following exercise were examined using a case-control study in 20 ME/CFS patients and 20 healthy people.

Different autonomous variables, including cardiac, respiratory, and electrodermal responses were assessed at rest and following an acute exercise bout. At rest, parameters in the time-domain represented normal autonomic function in ME/CFS, while frequency-domain parameters indicated the possible presence of diminished (para)sympathetic activation. Reduced parasympathetic reactivation during recovery from exercise was observed in ME/CFS.

This is the first study showing reduced parasympathetic reactivation during recovery from physical exercise in ME/CFS. Delayed HR recovery and/or a reduced HRV as seen in ME/CFS have been associated with poor disease prognosis, high risk for adverse cardiac events, and morbidity in other pathologies, implying that future studies should examine whether this is also the case in ME/CFS and how to safely improve HR recovery in this population.

Source: Van Oosterwijck J, Marusic U, De Wandele I, Meeus M, Paul L, Lambrecht L, Moorkens G, Danneels L, Nijs J. Reduced Parasympathetic Reactivation during Recovery from Exercise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. J Clin Med. 2021 Sep 30;10(19):4527. doi: 10.3390/jcm10194527. PMID: 34640544; PMCID: PMC8509376. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8509376/ (Full text)

Autonomic dysfunction post-acute COVID-19 infection

Introduction:

SARS-CoV-2 infection which causes the disease COVID-19 is most known for its severe respiratory complications. However, a variety of extrapulmonary effects have since been described, with cardiovascular complications being amongst the most common [ 1 ]. Those who recover from the acute phase of COVID-19 may be left with residual symptoms such as chest pain and dyspnea, resulting in a decreased quality of life and a syndrome sometimes described as “long COVID”[ 2 ].

Recent evidence suggests that survivors with some of these chronic symptoms may have autonomic dysfunction with features of postural orthostatic tachycardia syndrome (POTS) and/or inappropriate sinus tachycardia (IST)3 , 4. POTS is characterized by symptoms that occur with standing, an increase in heart rate of ≥30 beats per minute (or heart rate >120 bpm) when moving from a supine to a standing position, and the absence of orthostatic hypotension[ 5 ]. IST is defined as a sinus heart rate >100 beats per minute at rest without an identifiable cause of sinus tachycardia[ 6 ]. Cardiac manifestations of autonomic dysfunction lie on a wide spectrum and can therefore be classified as either POTS, IST, or other unspecified symptoms such as tachycardia and palpitations without a clear, single underlying pathological mechanism.[ 7 ]

The treatment of these arrhythmias includes nonpharmacologic management, such as increasing salt and fluid intake, as well as the use of oral medications. Beta-blockers or off label use of ivabradine have used reported to be used in both syndromes with the goal of controlling heart rate to reduce the symptoms 8 , 9. Other therapies more common in POTS include fludrocortisone, midodrine, pyridostigmine, and alpha-2 agonists[ 8 ].

There is a need to understand the patient characteristics and risk factors for developing AD as a sequela of COVID-19. Furthermore, there is limited management information specific to patients suffering from AD following COVID-19. It is unclear how treatment of these patients and their prognoses may differ from other cases of POTS or IST. In this study, we investigated a small cohort of patients diagnosed with suspected AD post SARS-CoV-2 infection to elucidate possible risk factors and treatment strategies in this population.

Source: Desai AD, Boursiquot BC, Moore CJ, Gopinathannair R, Waase MP, Rubin GA, Wan EY. Autonomic dysfunction post-acute COVID-19 infection. HeartRhythm Case Rep. 2021 Nov 27. doi: 10.1016/j.hrcr.2021.11.019. Epub ahead of print. PMID: 34868880; PMCID: PMC8626157. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8626157/ (Full text)

The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Healthy People

Abstract:

Background: Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are unable to activate brain-orchestrated endogenous analgesia (or descending inhibition) in response to exercise. This physiological impairment is currently regarded as one factor explaining post-exertional malaise in these patients. Autonomic dysfunction is also a feature of ME/CFS.

Objectives: This study aims to examine the role of the autonomic nervous system in exercise-induced analgesia in healthy people and those with ME/CFS, by studying the recovery of autonomic parameters following aerobic exercise and the relation to changes in self-reported pain intensity.

Study design: A controlled experimental study.

Setting: The study was conducted at the Human Physiology lab of a University.

Methods: Twenty women with ME/CFS- and 20 healthy, sedentary controls performed a submaximal bicycle exercise test known as the Aerobic Power Index with continuous cardiorespiratory monitoring. Before and after the exercise, measures of autonomic function (i.e., heart rate variability, blood pressure, and respiration rate) were performed continuously for 10 minutes and self-reported pain levels were registered. The relation between autonomous parameters and self-reported pain parameters was examined using correlation analysis.

Results: Some relationships of moderate strength between autonomic and pain measures were found. The change (post-exercise minus pre-exercise score) in pain severity was correlated (r = .580, P = .007) with the change in diastolic blood pressure in the healthy group. In the ME/CFS group, positive correlations between the changes in pain severity and low frequency (r = .552, P = .014), and between the changes in bodily pain and diastolic blood pressure (r = .472, P = .036), were seen. In addition, in ME/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability.

Limitations: Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations.

Conclusions: Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS, suggesting a role for the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients.

Source: Oosterwijck JV, Marusic U, De Wandele I, Paul L, Meeus M, Moorkens G, Lambrecht L, Danneels L, Nijs J. The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Healthy People. Pain Physician. 2017 Mar;20(3):E389-E399. PMID: 28339438. https://www.painphysicianjournal.com/linkout?issn=&vol=20&page=E389 (Full text)

Chronic Fatigue Syndrome and Cardiovascular Disease: JACC State-of-the-Art Review

Abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medically unexplained illness characterized by severe fatigue limiting normal daily activities for at least 6 months accompanied by problems with unrefreshing sleep, exacerbation of symptoms following physical or mental efforts (postexertional malaise [PEM]), and either cognitive reports or physiological evidence of orthostatic intolerance in the form of either orthostatic tachycardia and/or hypocapnia.

Although rarely considered to have cardiac dysfunction, ME/CFS patients frequently have reduced stroke volume with a significant inverse relation between cardiac output and PEM severity. Magnetic resonance imaging of ME/CFS patients compared with normal control subjects found significantly reduced stroke, end-systolic, and end-diastolic volumes together with reduced end-diastolic wall mass. Another cardiovascular abnormality is reduced nocturnal blood pressure assessed by 24-hour monitoring. Autonomic dysfunction is also frequently observed with postural orthostatic tachycardia and/or hypocapnia. Two consecutive cardiopulmonary stress tests may provide metabolic data substantiating PEM.

Source: Natelson BH, Brunjes DL, Mancini D. Chronic Fatigue Syndrome and Cardiovascular Disease: JACC State-of-the-Art Review. J Am Coll Cardiol. 2021 Sep 7;78(10):1056-1067. doi: 10.1016/j.jacc.2021.06.045. PMID: 34474739. https://pubmed.ncbi.nlm.nih.gov/34474739/

Reduced heart rate variability predicts fatigue severity in individuals with chronic fatigue syndrome/myalgic encephalomyelitis

Abstract:

BACKGROUND: Heart rate variability (HRV) is an objective, non-invasive tool to assessing autonomic dysfunction in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). People with CFS/ME tend to have lower HRV; however, in the literature there are only a few previous studies (most of them inconclusive) on their association with illness-related complaints. To address this issue, we assessed the value of different diurnal HRV parameters as potential biomarker in CFS/ME and also investigated the relationship between these HRV indices and self-reported symptoms in individuals with CFS/ME.

METHODS: In this case-control study, 45 female patients who met the 1994 CDC/Fukuda definition for CFS/ME and 25 age- and gender-matched healthy controls underwent HRV recording-resting state tests. The intervals between consecutive heartbeats (RR) were continuously recorded over three 5-min periods. Time- and frequency-domain analyses were applied to estimate HRV variables. Demographic and clinical features, and self-reported symptom measures were also recorded.

RESULTS: CFS/ME patients showed significantly higher scores in all symptom questionnaires (p < 0.001), decreased RR intervals (p < 0.01), and decreased HRV time- and frequency-domain parameters (p < 0.005), except for the LF/HF ratio than in the healthy controls. Overall, the correlation analysis reached significant associations between the questionnaires scores and HRV time- and frequency-domain measurements (p < 0.05). Furthermore, separate linear regression analyses showed significant relationships between self-reported fatigue symptoms and mean RR (p = 0.005), RMSSD (p = 0.0268) and HFnu indices (p = 0.0067) in CFS/ME patients, but not in healthy controls.

CONCLUSIONS: Our findings suggest that ANS dysfunction presenting as increased sympathetic hyperactivity may contribute to fatigue severity in individuals with ME/CFS. Further studies comparing short- and long-term HRV recording and self-reported outcome measures with previous studies in larger CFS/ME cohorts are urgently warranted.

Source: Escorihuela RM, Capdevila L, Castro JR, Zaragozà MC, Maurel S, Alegre J, Castro-Marrero J. Reduced heart rate variability predicts fatigue severity in individuals with chronic fatigue syndrome/myalgic encephalomyelitis. J Transl Med. 2020 Jan 6;18(1):4. doi: 10.1186/s12967-019-02184-z. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6943898/ (Full article)

Autonomic dysfunction in myalgic encephalomyelitis and chronic fatigue syndrome: comparing self-report and objective measures

Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) have debilitating impacts on affected individuals. Core symptoms include post-exertional malaise, neurocognitive challenges, and sleep dysfunction [1]. Additionally, a significant minority of patients experience autonomic symptoms, including orthostatic intolerance, gastrointestinal disturbances, and circulation issues [2].

Several case definitions for ME and CFS require the presence of autonomic dysfunction for diagnosis [2], while other researchers have proposed an “autonomic dysfunction” subtype of ME and CFS [3]. Identifying the appropriate measures of autonomic symptomatology for individuals with ME and CFS will further contribute to understanding the role of the autonomic system in this illness.

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Source: Kemp J, Sunnquist M, Jason LA, Newton JL. Autonomic dysfunction in myalgic encephalomyelitis and chronic fatigue syndrome: comparing self-report and objective measures. Clin Auton Res. 2019 May 21. doi: 10.1007/s10286-019-00615-x. [Epub ahead of print]  https://sci-hub.se/10.1007/s10286-019-00615-x (Full article)