We investigated the basal and dynamic regulation of the hypothalamo-pituitary-adrenal (HPA), hypothalamo-pituitary-thyroid (HPT) and hypothalamo-pituitary-gonadal axes and prolactin secretion in 52 patients with clinically definite multiple sclerosis. These patients also had gadolinium enhanced brain MRI scans and were divided into relapsing-remitting, secondary progressive and primary progressive subgroups. These subgroups were compared with healthy controls and a group of patients with other neurological diseases. The cortisol diurnal rhythm was preserved in all groups of patients. The time-integrated cortisol response to human corticotropin-releasing hormone (CRH) stimulation was lower in the patients with secondary progressive multiple sclerosis, compared with patients with primary progressive multiple sclerosis and healthy subjects. The time-integrated beta-endorphin response to CRH was greater in the patients with relapsing-remitting multiple sclerosis compared with the others. Feedback regulation assessed by dexamethasone suppression was normal. Serum testosterone was low in 24% of male multiple sclerosis patients and oestradiol was low in 25% of pre-menopausal female multiple sclerosis patients, whereas prolactin and the HPT function were normal. Correlations with C-reactive protein (CRP) and MRI suggest that activation of the HPA axis in multiple sclerosis patients is secondary to an active inflammatory stimulus.

Whole-brain MR diffusion histograms may quantitate overall cerebral lesion load in patients with MS and may be able to discern differences between clinical subgroups.

Objectives ‐ We investigated mitogenic response and steroid sensitivity in multiple sclerosis (MS) lymphocytes to establish if MS lymphocytes were less steroid responsive. Material and methods ‐ We compared mitogenic response to phytohaemagglutinin (PHA) and inhibition by dexamethasone (DEX) in circulating lymphocytes from both MS patients and healthy subjects. Results ‐ We found a range of responses in each group but no significant differences between the two groups, nor in patients with and without enhancement on magnetic resonance imaging. The mid‐inhibitory concentration of DEX in response to 1 μg/ml PHA was significantly lower than that for 2.5 μg/ml PHA in the patients. The mid‐inhibitory concentrations of DEX in response to 2.5 μg/ml PHA negatively correlated with endogenous serum Cortisol concentrations. Conclusion ‐ These data imply a spectrum of glucocorticoid response that is similar in normal and MS lymphocytes and can partly explain why response to steroid therapy is variable.