Chronic fatigue syndrome (CFS) is a symptom defined illness with persistent relapsing and recurring fatigue. Among the cardinal symptoms and often a chief complaint is a form of cognitive impairment described by patients as “brain fog” This often signifies neurocognitive impairment of concentration, working memory, and information processing speed, and may be used to describe forms of lightheadedness or dizziness often posturally driven. Neither a complete description of the neurocognitive deficits nor a pathophysiological origin for neurocognitive impairment have been found. Some investigators have hypothesized that impaired or otherwise altered cerebral perfusion contributes to neurocognitive dysfunction in CFS. However, to date there is evidence that either supports or refutes this hypothesis. Cognitive defects may only appear under conditions of physical or mental stress, and may be environmentally sensitive. There may also be a need for novel, illness-specific testing tools to uncover pathophysiology.
Neuronal activity and cerebral blood flow are tightly coupled in both the resting and the task-activated brain such that increased neuronal activity increases cerebral blood flow a process known as “functional hyperemia”. Recent data suggest that defects in neurovascular coupling and in cognitive performance co-vary in CFS, as it does in diabetes, depression, hypertension, stroke and Alzheimer’s disease.
Our purpose is to summarize knowledge concerning neurocognitive and neurovascular dysfunction in chronic fatigue syndrome in a “state of the art” reference publication which will present and review data and hypotheses that pertain to neurovascular or cerebral blood flow pathogenetic models of central fatigue and cognitive loss. Appropriate topics might include, but are not limited to, a synopsis of cognitive defects in CFS, abnormalities or even interesting normalities in cerebral blood flow or autoregulation in CFS during mental or physical stress, connections between cognition and cerebral metabolism and blood flow, and potential therapies for cognitive loss, especially as they relate to cerebral vascular properties. Studies may include in-vivo and in-vitro investigations of humans with CFS, experimental animal models of CFS, or their tissues.
Chronic fatigue syndrome (CFS) is a symptom defined illness with persistent relapsing and recurring fatigue. Among the cardinal symptoms and often a chief complaint is a form of cognitive impairment described by patients as “brain fog” This often signifies neurocognitive impairment of concentration, working memory, and information processing speed, and may be used to describe forms of lightheadedness or dizziness often posturally driven. Neither a complete description of the neurocognitive deficits nor a pathophysiological origin for neurocognitive impairment have been found. Some investigators have hypothesized that impaired or otherwise altered cerebral perfusion contributes to neurocognitive dysfunction in CFS. However, to date there is evidence that either supports or refutes this hypothesis. Cognitive defects may only appear under conditions of physical or mental stress, and may be environmentally sensitive. There may also be a need for novel, illness-specific testing tools to uncover pathophysiology.
Neuronal activity and cerebral blood flow are tightly coupled in both the resting and the task-activated brain such that increased neuronal activity increases cerebral blood flow a process known as “functional hyperemia”. Recent data suggest that defects in neurovascular coupling and in cognitive performance co-vary in CFS, as it does in diabetes, depression, hypertension, stroke and Alzheimer’s disease.
Our purpose is to summarize knowledge concerning neurocognitive and neurovascular dysfunction in chronic fatigue syndrome in a “state of the art” reference publication which will present and review data and hypotheses that pertain to neurovascular or cerebral blood flow pathogenetic models of central fatigue and cognitive loss. Appropriate topics might include, but are not limited to, a synopsis of cognitive defects in CFS, abnormalities or even interesting normalities in cerebral blood flow or autoregulation in CFS during mental or physical stress, connections between cognition and cerebral metabolism and blood flow, and potential therapies for cognitive loss, especially as they relate to cerebral vascular properties. Studies may include in-vivo and in-vitro investigations of humans with CFS, experimental animal models of CFS, or their tissues.
