Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (801 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Myeloencephalitis; Myeloencephalitides; Encephalomyelitis, Inflammatory; Inflammatory Encephalomyelitis.
Where it fits in the MeSH classification
- Broader topics
- Central Nervous System Infections; Neuroinflammatory Diseases
- Narrower topics
- Encephalomyelitis, Equine; Fatigue Syndrome, Chronic
- See also
- Encephalitis
Related concepts
Research landscape
PubMed indexes 12,699 records tagged with the MeSH heading “Encephalomyelitis” (counts retrieved 2026-10-29). 1,721 of them (13.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,919 records.
Reviews account for 1,635 records (12.9%) and meta-analyses for 74. Randomized controlled trials number 336 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,919 |
| 2000-2009 | 2,480 |
| 2010-2019 | 2,579 |
| 2020 onward | 1,721 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,635 | 12.9% |
| Meta-analyses | 74 | 0.6% |
| Randomized controlled trials | 336 | 2.6% |
Method: PubMed query "Encephalomyelitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome | 2024 | Research article Design not recorded in structured metadata | 122 | cc by PMID 38383456 · DOI · PMC10881493 |
| Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease | 2024 | Review article Design not recorded in structured metadata | 93 | cc by PMID 38887284 · DOI · PMC11180809 |
| Metabolomic and immune alterations in long COVID patients with chronic fatigue syndrome | 2024 | Research article Design not recorded in structured metadata | 72 | cc by PMID 38304426 · DOI · PMC10830702 |
| Skeletal muscle properties in long COVID and ME/CFS differ from those induced by bed rest | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42649155 · DOI · PMC13518852 |
Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available.
- Closing excerpt
- Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit PI-ME/CFS participants with matched controls to conduct deep phenotyping. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical conditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38383456 · DOI · PMC10881493
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, debilitating disease characterised by a wide range of symptoms that severely impact all aspects of life.
- Closing excerpt
- By integrating these disparate elements, our work emphasises the necessity of a holistic approach to diagnosing, researching, and treating ME/CFS, urging the scientific community to reconsider the disease's complexity and the multifaceted approach required for its study and management.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (203 words)
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, debilitating disease characterised by a wide range of symptoms that severely impact all aspects of life. Despite its significant prevalence, ME/CFS remains one of the most understudied and misunderstood conditions in modern medicine. ME/CFS lacks standardised diagnostic criteria owing to variations in both inclusion and exclusion criteria across different diagnostic guidelines, and furthermore, there are currently no effective treatments available. Moving beyond the traditional fragmented perspectives that have limited our understanding and management of the disease, our analysis of current information on ME/CFS represents a significant paradigm shift by synthesising the disease's multifactorial origins into a cohesive model. We discuss how ME/CFS emerges from an intricate web of genetic vulnerabilities and environmental triggers, notably viral infections, leading to a complex series of pathological responses including immune dysregulation, chronic inflammation, gut dysbiosis, and metabolic disturbances. This comprehensive model not only advances our understanding of ME/CFS's pathophysiology but also opens new avenues for research and potential therapeutic strategies. By integrating these disparate elements, our work emphasises the necessity of a holistic approach to diagnosing, researching, and treating ME/CFS, urging the scientific community to reconsider the disease's complexity and the multifaceted approach required for its study and management.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38887284 · DOI · PMC11180809
Metabolomic and immune alterations in long COVID patients with chronic fatigue syndrome [3]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionA group of SARS-CoV-2 infected individuals present lingering symptoms, defined as long COVID (LC), that may last months or years post the onset of acute disease.
- Closing excerpt
- Finally, our study reveals that LC disproportionally affects females more than males, as evidenced by nearly 70% of our LC patients being female.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (299 words)
IntroductionA group of SARS-CoV-2 infected individuals present lingering symptoms, defined as long COVID (LC), that may last months or years post the onset of acute disease. A portion of LC patients have symptoms similar to myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS), which results in a substantial reduction in their quality of life. A better understanding of the pathophysiology of LC, in particular, ME/CFS is urgently needed.MethodsWe identified and studied metabolites and soluble biomarkers in plasma from LC individuals mainly exhibiting ME/CFS compared to age-sex-matched recovered individuals (R) without LC, acute COVID-19 patients (A), and to SARS-CoV-2 unexposed healthy individuals (HC).ResultsThrough these analyses, we identified alterations in several metabolomic pathways in LC vs other groups. Plasma metabolomics analysis showed that LC differed from the R and HC groups. Of note, the R group also exhibited a different metabolomic profile than HC. Moreover, we observed a significant elevation in the plasma pro-inflammatory biomarkers (e.g. IL-1α, IL-6, TNF-α, Flt-1, and sCD14) but the reduction in ATP in LC patients. Our results demonstrate that LC patients exhibit persistent metabolomic abnormalities 12 months after the acute COVID-19 disease. Of note, such metabolomic alterations can be observed in the R group 12 months after the acute disease. Hence, the metabolomic recovery period for infected individuals with SARS-CoV-2 might be long-lasting. In particular, we found a significant reduction in sarcosine and serine concentrations in LC patients, which was inversely correlated with depression, anxiety, and cognitive dysfunction scores.ConclusionOur study findings provide a comprehensive metabolomic knowledge base and other soluble biomarkers for a better understanding of the pathophysiology of LC and suggests sarcosine and serine supplementations might have potential therapeutic implications in LC patients. Finally, our study reveals that LC disproportionally affects females more than males, as evidenced by nearly 70% of our LC patients being female.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38304426 · DOI · PMC10830702
Skeletal muscle properties in long COVID and ME/CFS differ from those induced by bed rest [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Patients with long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suffer from post-exertional malaise.
- Closing excerpt
- As skeletal muscle characteristics differ between patients and healthy individuals after bed rest, physical inactivity cannot solely explain the lower exercise capacity and skeletal muscle adaptations in long COVID and ME/CFS patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Patients with long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suffer from post-exertional malaise. The accompanying physical inactivity may contribute to a lower aerobic capacity and may explain skeletal muscle adaptations in these patients. Here, we compare whole-body exercise responses and skeletal muscle adaptations after strict 60-day bed rest in healthy people with those in long COVID and ME/CFS patients, and healthy age- and sex-matched controls. Bed rest alters respiratory and cardiovascular responses to maximal exercise, which are dissimilar in patients. Bed rest causes muscle atrophy without altering fiber type. Both patient groups have more glycolytic fibers, and ME/CFS patients display type I-specific atrophy. Only after bed rest is oxidative phosphorylation capacity associated with maximal oxygen uptake. As skeletal muscle characteristics differ between patients and healthy individuals after bed rest, physical inactivity cannot solely explain the lower exercise capacity and skeletal muscle adaptations in long COVID and ME/CFS patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42649155 · DOI · PMC13518852
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article MOG encephalomyelitis: international recommendations on diagnosis and antibody testing [5]
- Research article Unexplained post-acute infection syndromes [6]
- Research article Systematic review and meta-analysis of the prevalence of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) [7]
- Research article Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) [8]
- Research article Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Essentials of Diagnosis and Management [9]
- Research article Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - Evidence for an autoimmune disease [10]
References
- Walitt B, Singh K, LaMunion SR, Hallett M, Jacobson S, Chen K, et al.. Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome. . 2024. PMID 38383456 · DOI · PMC10881493
- Arron HE, Marsh BD, Kell DB, Khan MA, Jaeger BR, Pretorius E. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease. . 2024. PMID 38887284 · DOI · PMC11180809
- Saito S, Shahbaz S, Luo X, Osman M, Redmond D, Cohen Tervaert JW, et al.. Metabolomic and immune alterations in long COVID patients with chronic fatigue syndrome. . 2024. PMID 38304426 · DOI · PMC10830702
- Charlton BT, Slaghekke A, Appelman B, Eggelbusch M, Huijts JY, Noort W, et al.. Skeletal muscle properties in long COVID and ME/CFS differ from those induced by bed rest. . 2026. PMID 42649155 · DOI · PMC13518852
- Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J, et al.. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflammation. 2018. PMID 29724224 · DOI · PMC5932838
- Choutka J, Jansari V, Hornig M, Iwasaki A. Unexplained post-acute infection syndromes. Nat Med. 2022. PMID 35585196 · DOI
- Lim EJ, Ahn YC, Jang ES, Lee SW, Lee SH, Son CG. Systematic review and meta-analysis of the prevalence of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). J Transl Med. 2020. PMID 32093722 · DOI · PMC7038594
- Rasa S, Nora-Krukle Z, Henning N, Eliassen E, Shikova E, Harrer T, et al.. Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). J Transl Med. 2018. PMID 30285773 · DOI · PMC6167797
- Bateman L, Bested AC, Bonilla HF, Chheda BV, Chu L, Curtin JM, et al.. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Essentials of Diagnosis and Management. Mayo Clin Proc. 2021. PMID 34454716 · DOI
- Sotzny F, Blanco J, Capelli E, Castro-Marrero J, Steiner S, Murovska M, et al.. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - Evidence for an autoimmune disease. Autoimmun Rev. 2018. PMID 29635081 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.