Endocrine Abstracts (2015) 38 P216 | DOI: 10.1530/endoabs.38.P216

Enhanced orbitofrontal cortex activation following sympathetic neural stimulation in young women with polycystic ovary syndrome: an fMRI study

Andrew Lansdown1, Esther Warnert2, Richard Wise2 & Aled Rees1


1Institute of Molecular and Experimental Medicine, Cardiff University, Cardiff, UK; 2Cardiff University Brain Research Imaging Centre, Cardiff, UK.


Introduction: Polycystic ovary syndrome (PCOS) is associated with increased cardiovascular risk, which may relate to enhanced sympathetic nervous system (SNS) activation. The cerebral pathways involved in this process are not known.

Aims: i) To compare SNS activation in response to isometric forearm contraction (IFC) in patients with PCOS and controls. ii) To identify and compare the neuronal signatures of this response.

Methods: 15 PCOS (age 30.6 years, BMI 24.7 kg/m2) and 15 matched controls (age 29.1 years, BMI 25.7 kg/m2; P=NS) were studied. Out-of-scanner tests: measurement of mean blood pressure (MAP) and heart rate (HR) responses to 30% IFC for 180 seconds; baseline and post-task catecholamines. In-scanner: Blood oxygen level dependent (BOLD) fMRI using an identical block paradigm design for IFC. BOLD signal changes were measured during the task and a general linear model (www.fmrib.ox.ac.uk/fsl FEAT) was used to identify BOLD signal correlating to MAP responses, (threshold Z>2.3, corrected cluster threshold P=0.05).

Results: IFC elicited an increase in HR and MAP in PCOS and controls but these did not differ between groups (P=0.45 (HR) and P=0.41 (MAP)). Adrenaline increased significantly post-IFC in PCOS (0.8–1.4 ng/ml P=0.01) but not in controls (0.7–0.8 ng/ml P=0.3). Brain activation indexed by the BOLD signal in response to IFC was significantly greater in the PCOS group compared to the control group in the right orbitofrontal cortex (P<0.0001), left angular gyrus and lateral occipital cortex (P=0.04).

Conclusions: PCOS is associated with enhanced SNS activation and increased regional brain activation in response to IFC. These observations may explain some of the increased cardiovascular risk evident in this patient group, and may offer new cerebral targets for intervention associated with enhanced SNS activity.

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