ReviewJournal of clinical medicine2025
The Brain Fatigue Syndrome-Symptoms, Probable Definition, and Pathophysiological Mechanisms.
Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Brain fatigue in Graves' disease: symptoms and presentation of a possible mechanism at the cellular level.European thyroid journal · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatigue is a common consequence of traumatic brain injury, neurological diseases or developmental disorders, and systemic inflammatory diseases, including autoimmune conditions that affect the brain. This condition is characterized by reduced endurance for cognitive tasks, diminished quality of life, and impaired work capacity. In addition to cognitive difficulties, individuals often experience disproportionately long recovery times after demanding tasks, emotional instability, stress sensitivity, sensory sensitivity, impaired ability to initiate activities, and sleep disturbances. Tension headaches frequently occur when the brain is excessively activated by mental activity. In this paper, we propose the term "Brain Fatigue Syndrome" (BFS) as a collective name for the symptoms closely associated with this pathological fatigue resulting from brain impact. BFS can be identified through interviews and measured using the self-assessment instrument, the Mental Fatigue Scale (MFS). We suggest potential underlying mechanisms at the cellular level for the BFS symptom complex, including astrocyte dysfunction with impaired glutamate signaling and glucose uptake, mitochondrial dysfunction, blood-brain barrier dysfunction, and the activation of microglia and mast cells. In conclusion, BFS suggests a general brain impact. The symptoms associated with BFS typically resolve when the injury or disease heals. However, in some individuals, BFS persists even after the injury or illness has ostensibly healed.
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Registered trials
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