About this Research Topic
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a debilitating disorder characterised by medically unexplained, disabling fatigue as well as constitutional and neuropsychiatric symptoms of at least 6 months duration. Despite decades of hypothesis-driven research, the risk factors and pathophysiology of CFS/ME are poorly understood, and effective therapies are not yet available.
The symptoms of CFS/ME can be diverse, exhibiting wide variations both between individuals and in each person over time. Individual symptoms may fluctuate in intensity and severity, with great variability in the symptoms different people experience. These symptoms can include fatigue, malaise, muscle pain, sleep disturbances, headaches, and difficulties with concentration. CFS/ME is characterized by debilitating fatigue that is unlike everyday fatigue and can be triggered by minimal activity.
CFS/ME is poorly understood. At present, there are no physical signs, nor gold standard diagnostic criteria or laboratory tests that specifically identifies CFS/ME. Currently, diagnosis of CFS/ME is made on the foundation of recognizable patterns of characteristic symptoms, whilst excluding other known causes. Hence, mechanistic, and causal understanding is vital if effective treatment paradigms are to be found.
The World Health Organization (WHO) classifies CFS/ME as a neurological illness, and while potential neuroendocrine, immunological, genetic, psychiatric, and infectious causes have been investigated, causal evidence and consensus is lacking. Recent advances in CFS/ME research have explored diverse areas such as autonomic involvement, neuroimaging, and the microbiota (gut/brain axis) among others.
In a significant number of cases the onset of CFS has been noted to occur following exposure to viral infection. One hypothesis posits that CFS is triggered by a viral illness that results in immune mediated brain dysfunction. Indeed, a considerable number of CFS cases may be classed as Post Infective Fatigue (PIFS) - where the patient shows a definitive link to a preceding infection.
With the recent global surge related to the COVID19 pandemic, and with growing reports and concerns of the possibility of CFS related to the pandemic, this edition welcomes manuscripts providing greater insight into the mechanistic relationship between CFS, infection and resultant neuroinflammation:
• Papers exploring the potential mechanistic underpinnings of infectious/inflammatory causes of CFS/ME. These explored mechanisms can be of a diverse nature, e.g. peripheral vs central, effects on autonomic functioning, neuroimaging (fMRI etc.) of inflammation, immunological, neuroendocrine, genetic, and infectious markers as they pertain to CFS/ME.
• Diverse potential treatment approaches including electrophysiological, behavioural and pharmacological and their effects on symptoms. In particular, interventions targeting the reduction of the neuroinflammatory response are encouraged.
The symptoms of CFS/ME can be diverse, exhibiting wide variations both between individuals and in each person over time. Individual symptoms may fluctuate in intensity and severity, with great variability in the symptoms different people experience. These symptoms can include fatigue, malaise, muscle pain, sleep disturbances, headaches, and difficulties with concentration. CFS/ME is characterized by debilitating fatigue that is unlike everyday fatigue and can be triggered by minimal activity.
CFS/ME is poorly understood. At present, there are no physical signs, nor gold standard diagnostic criteria or laboratory tests that specifically identifies CFS/ME. Currently, diagnosis of CFS/ME is made on the foundation of recognizable patterns of characteristic symptoms, whilst excluding other known causes. Hence, mechanistic, and causal understanding is vital if effective treatment paradigms are to be found.
The World Health Organization (WHO) classifies CFS/ME as a neurological illness, and while potential neuroendocrine, immunological, genetic, psychiatric, and infectious causes have been investigated, causal evidence and consensus is lacking. Recent advances in CFS/ME research have explored diverse areas such as autonomic involvement, neuroimaging, and the microbiota (gut/brain axis) among others.
In a significant number of cases the onset of CFS has been noted to occur following exposure to viral infection. One hypothesis posits that CFS is triggered by a viral illness that results in immune mediated brain dysfunction. Indeed, a considerable number of CFS cases may be classed as Post Infective Fatigue (PIFS) - where the patient shows a definitive link to a preceding infection.
With the recent global surge related to the COVID19 pandemic, and with growing reports and concerns of the possibility of CFS related to the pandemic, this edition welcomes manuscripts providing greater insight into the mechanistic relationship between CFS, infection and resultant neuroinflammation:
• Papers exploring the potential mechanistic underpinnings of infectious/inflammatory causes of CFS/ME. These explored mechanisms can be of a diverse nature, e.g. peripheral vs central, effects on autonomic functioning, neuroimaging (fMRI etc.) of inflammation, immunological, neuroendocrine, genetic, and infectious markers as they pertain to CFS/ME.
• Diverse potential treatment approaches including electrophysiological, behavioural and pharmacological and their effects on symptoms. In particular, interventions targeting the reduction of the neuroinflammatory response are encouraged.
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