The underlying physiological processes that manifest subjectively as reduced cognitive clarity, often characterized by impaired executive function, slowed processing speed, and difficulty with memory retrieval. Clinically, it represents a state of suboptimal neuronal network efficiency across cortical areas. This subjective experience correlates with measurable changes in brain metabolic activity.
Origin
The term originates from descriptive patient language (“fog”) applied to a constellation of cognitive symptoms, which modern science seeks to map onto concrete physiological substrates. It describes a functional state rather than a discrete pathology identifiable by a single marker. The origin emphasizes the patient’s lived experience of cognitive impairment.
Mechanism
Physiology suggests this state involves neuroinflammation, altered cerebral blood flow, or dysregulation of key neurotransmitter systems, such as GABA or glutamate balance. Hormonal perturbations, particularly involving cortisol or sex steroids, can significantly influence these inflammatory and metabolic states within the CNS. Restoring euthyroid status or optimizing HPA axis function often reverses these detrimental physiological changes leading to symptom resolution.
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