HORMONE THERAPY ATTENUATES MENOPAUSE-RELATED IMPAIRMENTS IN CORTICAL NEUROPLASTICITY

Author(s): ANSDELL, P., SPILLANE, P., OHANLON, M., NÉDÉLEC, E., INNS, T., HAUSMANN, M., PIASECKI, M., GOODALL, S., VINCENT, K., STAGG, C., PIASECKI, J., Institution: NORTHUMBRIA UNIVERSITY, Country: UNITED KINGDOM, Abstract-ID: 1147

INTRODUCTION:
Previous research has demonstrated the neuroactive effects of ovarian hormones across the menstrual cycle [1]; however, it remains less clear how the cessation of hormone production across the menopause influences motor cortical properties. Furthermore, it is currently unknown how nervous system adaptation (neuroplasticity) is mediated by endogenous and exogenous hormones across the human lifespan. Paired associative stimulation (PAS) provides a method of quantifying an individual’s capacity for neuroplasticity and offers insight into the pathology of several neurological disorders [2].
METHODS:
The menopausal status of 33 participants was classified according to NICE guidelines on the diagnosis and management of menopause, with 12 pre-menopausal females (age: 29 ± 7 years), 7 peri-menopausal females (50 ± 4 years), 7 post-menopausal females (59 ± 10 years), and 7 females using hormone therapy (HT, 53 ± 3 years) taking part in the study. Participants underwent a resting baseline neurophysiological assessment in the first dorsal interosseous muscle, including electrical stimulation of the ulnar nerve and transcranial magnetic stimulation (TMS) of the motor cortex to assess corticospinal excitability, intracortical inhibition (SICI), and facilitation (ICF), as well as the maximum compound muscle action potential (Mmax). Subsequently, a PAS protocol was performed with electrical stimulation at 300% perceptual threshold delivered 25 ms prior to TMS at 120% motor threshold; 200 paired stimuli were delivered at 0.2 Hz, followed by repeated neurophysiological assessments immediately, then 10, 20, and 30 minutes after PAS.
RESULTS:
No differences between groups were observed at baseline for corticospinal excitability (~10% Mmax, p = 0.941), SICI (~40% unconditioned MEP, p = 0.829) or ICF (~150% unconditioned MEP, p = 0.204). In response to the PAS protocol, the one-way ANOVA revealed a main effect of group (p = 0.024), whereby pre-menopausal females (+69 ± 67%, p < 0.001) and HRT users (+48 ± 32%, p = 0.020) experienced an increase in corticospinal excitability. In comparison, peri- (+13 ± 19%, p = 0.228) and post-menopausal (+1 ± 30%, p = 0.401) females exhibited no change from baseline.
CONCLUSION:
The menopause appears to blunt motor cortical neuroplasticity, with peri- and post-menopausal females experiencing no facilitation of the corticospinal tract following a PAS protocol, compared to their pre-menopausal counterparts. Hormone therapy appears to mitigate this menopause-induced decline, which has implications for a range of populations in health and disease where cortical neuroplasticity is essential for the (re)learning of motor skills in midlife and beyond.

[1] Piasecki et al. (2024) Exerc Sports Sci Rev 52(2): p54-62
[2] Suppa et al. (2017) Clin Neurophysiol 128(11): p2140-2164