Summary Headache is very common in pituitary disease and is reported to be present in more than a third of all patients with pituitary adenomas. Tumour size, cavernous sinus invasion, traction or displacement of intracranial pain‐sensitive structures such as blood vessels, cranial nerves and dura mater, and hormonal hypersecretion are implicated causes. The present review attempts to systematically review the literature for any combination of headache and pituitary or hormone overproduction or deficiency. Most data available are retrospective and/or not based on the International Headache Society (IHS) classification. Whereas in pituitary apoplexy a mechanical component explains the almost universal association of the condition with headaches, this correlation is less clear in other forms of pituitary disease and a positive impact of surgery on headaches is not guaranteed. Similarly, invasion into the cavernous sinus or local inflammatory changes have been linked to headaches without convincing evidence. Some studies suggest that oversecretion of GH and prolactin may be important for the development of headaches, and treatment, particularly with somatostatin analogues, has been shown to improve symptoms in these patients. Otherwise, treatment rests on general treatment options for headaches based on an accurate clinical history and a precise classification which includes assessment of the patient's psychosocial risk factors.

No stress after 24-hour on-call shifts? : Birgit HARBECK, et al. Department of Medicine I, University of Luebeck, Germany-Objectives: Irregular sleep patterns can adversely affect physiological functions and have been associated with increased physiological and psychological stress. Nocturnal work of physicians during 24-hour on-call shifts (OCS) disrupts the sleep/wake cycle. Chronic exposure to distress has been shown to affect cardiovascular homeostasis and to impair performance in neurocognitive and simulated clinical tasks. Methods: In a prospective cohort study, biochemical and physiological stress parameters were assessed in 11 female and 9 male physicians (median age: 32 years, range 26−42 years) before a normal working day and after a 24-hour OCS in internal medicine. In addition, various tests of attentional performance (TAP) were conducted. Results: The levels of thyroid stimulating hormone (TSH) were significantly higher after a 24-hour OCS, while there were no significant changes in cortisol, epinephrine, and norepinephrine levels. Heart rate variability and skin resistance increased following an OCS, although the differences were not statistically significant. Intrinsic alertness was comparable, while phasic alertness was significantly improved following a 24-hour OCS. Focused attention tended to be better following a night shift. There was no correlation with age or medical working experience; however, men experienced more stress than women. Conclusions: Following a 24-hour OCS, (i) TSH may be an early and sensitive biochemical predictor of stress; (ii) other classical biochemical stress parameters do not depict the psychological stress perceived by physicians; (iii) there may be a mismatch between experienced and objective stress levels; (iv) neurocognitive functions are not impaired, while performance may even be improved; and (v) men might be more sensitive to distress.

Cortisol replacement in patients with adrenal insufficiency usually consists of hydrocortisone (HC) given orally during day time. Due to the short half-life of hydrocortisone, cortisol levels between midnight and early morning are very low in contrast to the physiological rise of cortisol serum levels during this time. We investigated whether short-term cortisol replacement during the night improves cognitive function and well-being in these patients. Fourteen patients with adrenal insufficiency were put on HC infusion between midnight and 8 a.m. They subsequently underwent neurocognitive testing to measure intellectual functioning, concentration, memory and fine motor skills. Quality of life and mood were also evaluated. All tests were repeated after 2-4 weeks during usual oral glucocorticoid replacement therapy. Blood samples were taken for cortisol, epinephrine and norepinephrine measurement. With the exception of the digit symbol test with better scoring in the oral group (p = 0.005) there were no significant differences in neurocognitive testing, vegetative functions and quality of life on the two occasions. However, a higher cortisol level was associated with a worse performance in short-term memory. Plasma epinephrine concentration was subnormal in both groups, but increased only after intravenous hydrocortisone replacement. Mimicking the physiological rise in cortisol secretion during the night in this pilot study did neither significantly affect quality of life nor cognitive performance and vegetative functions. There was no improvement in general well being. Hydrocortisone infusion during night time might improve adrenomedullary reserve in patients with adrenal insufficiency.

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Cardiovascular disease (CVD) is the most common cause of death in the world. Recent studies have shown an association between adrenal insufficiency (AI) and increased cardiovascular risk (CVR). Patients with AI receive glucocorticoid (GC) replacement therapy which can lead to varying levels of blood cortisol. It was shown that these imbalances in blood cortisol may lead to a higher prevalence of coronary heart disease, major adverse coronary events, and increased mortality. GC substitution is essential in the treatment of AI without which the disease has been shown to be fatal. The most frequently used GC formula for replacement therapy is hydrocortisone (HC). There is no uniform opinion on hydrocortisone replacement therapy. Alternative GC such as prednisolone is also in use. Overreplacement of GC may lead to adverse effects including obesity, high blood pressure, and hyperglycaemia. Outcome may vary between primary and secondary AI mainly due to differences in the renin-angiotensin-aldosterone system (RAAS). Furthermore, decreased blood levels of cortisol may lead to a compensatory secretion of inflammatory mediators such as Interleukin-1 (IL-1), Interleukin-6 (IL-6), and/or tumor-necrosis factor (TNF). Physicians and patients should be properly educated about the increased risk of CVD in patients with AI.

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