Pathophysiology and Clinical Features of Neuropsychiatric Manifestations of Thyroid Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanism-based reasoning with no primary data or systematic review methodology reported
PubMed 35059548 · doi:10.1210/jendso/bvab194
What was done
This narrative review summarizes the clinical presentations and pathophysiological mechanisms underlying cognitive, affective, and psychotic manifestations associated with adult thyroid dysfunction (hypothyroidism and hyperthyroidism).
What was found
The abstract reports no quantitative data or specific numerical findings. Qualitatively, it notes that overt hypothyroidism is linked to cognitive decline, dysphoria, and depression, with associated dementia potentially reversible by levothyroxine, while levothyroxine's effect on depressive symptoms in subclinical hypothyroidism remains controversial. Hyperthyroidism is associated with agitation, acute psychosis, and apathy, particularly in older adults. Proposed pathophysiological pathways include alterations in central neurotransmission, changes in neuronal and glial gene expression, blood-brain barrier disruption, cerebrovascular disease risk, and cerebral inflammation in autoimmune thyroid disease.
Why it matters
It provides a conceptual framework linking adult thyroid dysfunction to diverse neuropsychiatric phenotypes and highlights mechanistic pathways that may inform future therapeutic strategies.
Limits
The paper is a non-systematic narrative review providing no quantitative synthesis, effect estimates, or primary patient data in the abstract. Search strategies, study selection criteria, and quality assessments of included evidence are not provided.
Cited by
- supports Excess thyroid hormone (hyperthyroidism) causes irritability and cognitive deficits, while deficient thyroid hormone (hypothyroidism) can impair cognition severely enough to mimic dementia.