When changes in biological and physiological variables occur, an individual might perceive this via symptoms. Symptom status is defined by Wilson and Cleary as a patient’s perception of an abnormal physical, emotional, or cognitive state [
9]. As was mentioned previously, NFAs are usually relatively large at time of diagnosis, giving either compression on the pituitary or the optic chiasm, resulting in headaches, hypopituitarism, visual loss, third nerve palsy, pituitary apoplexy, tiredness, decreased libido, and sometimes even galactorrhoea [
3]. These symptoms tend to improve after surgery, however, extensive longitudinal literature of perioperative HR-QoL is limited. Wolf et al. demonstrated that headache severity and vision related HR-QoL improved significantly up to 6 months after transsphenoidal surgery [
21]. Furthermore, patients may suffer from impaired olfactory function as a complication of the transsphenoidal surgery. Little et al. showed an initial decrease of sinonasal HR-QoL after (both microscopic and endoscopic) surgery, which improved at later follow-up [
22]. Wang et al. demonstrated a decrease in the ability to detect odours up to 4 months after surgery [
23]. Although symptoms improve after biomedical treatment, persistent symptoms are reported after long-term remission. During focus group conversations with patients in a chronic state of their disease, patients reported physical pain, sleeping problems, changes in physical appearance (i.e. weight changes), cognitive problems (i.e. problems in concentration, short-term memory, and executive functioning), decreased libido, physical sexual dysfunction, depressive symptoms, melancholy, mood swings, worries, increased sensitivity to stress, fear of tumour recurrence, decreased self-esteem, loneliness, anger, difficulties in communication about the disease, and a lack of empathy from the environment. The reported sleep problems were characterized by sleeping in blocks of 2–3 h [
24]. Sleep characteristics have also been quantitatively examined, showing sleep alterations in patients treated for a NFA, including decreased subjective sleep quality, disturbed distribution of sleep stages and disturbances in diurnal rhythmicity [
6,
25]. Although it can be postulated that these sleeping problems can be explained by imperfections in hormone replacement therapy (i.e. hydrocortisone replacement) [
26], there is increasing evidence that these problems are caused by hypothalamic dysfunction [
27]. Joustra et al. examined sleep characteristics in patients treated for a NFA and patients with primary adrenal insufficiency treated with hydrocortisone replacement therapy and demonstrated that patients with primary adrenal insufficiency have normal sleep characteristics in contrast to patients with a NFA. These results provided evidence that sleeping problems might be caused by hypothalamic dysfunction [
28]. Furthermore, sleep disturbances and daytime sleepiness were also associated with increased impairment in HR-QoL [
6,
29].