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OBJECTIVE: Patient-centered studies have shown that several patients on thyroid hormone replacement therapy for hypothyroidism exhibit persistent symptoms, including “brain fog.” Here, we aimed to determine which of these specific symptoms are associated with brain fog, identify patient-reported factors that modify these symptoms, and identify patient concerns related to brain fog not included in thyroid-specific questionnaires. METHODS: A survey on brain fog symptoms adapted from thyroid-specific patient-reported outcome was distributed online. Textual data analysis was performed to identify common areas of concern from open-ended survey responses. RESULTS: A total of 5170 participants reporting brain fog while being treated for hypothyroidism were included in the analysis. Of these, 2409 (46.6%) participants reported symptom onset prior to the diagnosis of hypothyroidism, and 4096 (79.2%) participants experienced brain fog symptoms frequently. Of the symptoms listed, participants associated fatigue and forgetfulness most frequently with brain fog. More rest was the most common factor provided for improving symptoms. The textual data analysis identified areas of concern that are not often included in thyroid-specific quality of life questionnaires, including a focus on the diagnosis of hypothyroidism, the types and doses of medications, and the patient-doctor relationship. CONCLUSION: Brain fog in patients treated for hypothyroidism was associated most frequently with fatigue and cognitive symptoms. Several additional areas of patient concern were found to be associated with brain fog, which are not typically addressed in thyroid-specific questionnaires.

Early-life status epilepticus produces deficit in social interaction and vocalization, enhances anxiety, no cognitive impairment and alters functional connectivity within the hippocampus (CA3-CA1) and between the hippocampus and prefrontal cortex [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], but the underlying mechanisms remain unknown. This data article contains behavioral and molecular data of the adult male Wistar rats subjected to early life pilocarpine-induced seizures. Animal's behaviors were assessed to social memory and social motivation, working and reference memories and cognitive flexibility. The brain tissues (hypothalamus, hippocampus, amygdala, and striatum) were probed to gene and protein expression of molecules related to social behavior, reward system and synaptic function.

Early-life status epilepticus produces deficit in social interaction and vocalization, enhances anxiety, no cognitive impairment and alters functional connectivity within the hippocampus (CA3-CA1) and between the hippocampus and prefrontal cortex [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], but the underlying mechanisms remain unknown. This data article contains behavioral and molecular data of the adult male Wistar rats subjected to early life pilocarpine-induced seizures. Animal's behaviors were assessed to social memory and social motivation, working and reference memories and cognitive flexibility. The brain tissues (hypothalamus, hippocampus, amygdala, and striatum) were probed to gene and protein expression of molecules related to social behavior, reward system and synaptic function.