Memory formation largely depends on normal function of the temporal lobes (particularly the hippocampal complex) and prefrontal cortex. Evidence from animal studies suggests abnormal hippocampal function in hypothyroidism1. We hypothesized that specific defects in hippocampal-dependent memory would be observed in hypothyroid patients. Patients with overt (n=17) and subclinical (n=17) hypothyroidism underwent neuropsychological testing at baseline, 3 and 6 months following l-thyroxine replacement. Matched normal subjects were studied at the same time-points. Spatial (Rey-Osterrieth Figure), verbal (Rivermead Short Stories), associative (Face-Name Learning) and working (n-Back Working Memory task) memory were assessed.
|Verbal memory (arbitrary units)||Baseline||3 months||6 months|
|Mean±S.D., *P<0·05 vs normal, †P<0·05 vs baseline (within group difference). ANOVA with Tukey post-hoc testing|
At baseline, deficits in spatial and verbal memory (which both rely upon the integrity of the hippocampal-complex) were identified in patients with overt hypothyroidism (P<0.05) while patients with SCH showed impairment in verbal memory only (see Table). Following treatment, verbal memory normalised in both patient groups (see Table) but spatial memory deficits persisted in the hypothyroid group. Impaired working memory (P<0.05) was observed in the hypothyroid group only and normalised with treatment. Measures of attention and response inhibition were not affected in either group.
Cognitive impairment occurs in subclinical and more markedly in overtly hypothyroid patients. These impairments appear specific to hippocampal- and frontally-driven memory processes, suggesting that the aetiology is not indicative of general cognitive slowing.
1. Alzoubi KH, Gerges NZ, Alkadhi KA Levothyroxin restores hypothyroidism-induced impairment of LTP of hippocampal CA1: electrophysiological and molecular studies. Exp. Neurol. 2005 195 330341.