Spontaneous baroreflex sensitivity and heart rate variability (HRV) are different in migraine patients selleckchem compared to healthy controls (Nilsen et al., 2009). Neural systems, including the prefrontal cortex, control parasympathetic control of the heart via the vagus nerve and also regulate inflammation (Thayer, 2009); in addition, decreases in heart rate variability are associated with a variety of changes (e.g., increased proinflammatory cytokines, acute phase protein, increased cortisol, increased fasting glucose), all of which relate to increased allostatic load.

Migraine is associated with alterations in sleep (Rains et al., 2008). In chronic migraine, altered hormone secretion has been reported for prolactin (decreased nocturnal peak), melatonin (delayed nocturnal peak), and cortisol Selleck PARP inhibitor (increased concentrations) (Peres et al., 2001), suggesting that the condition has produced changes in circadian regulation. Sleep deprivation and circadian disruption is itself a source of stress and allostatic load (Spiegel et al., 1999). “The way sleep impacts next day mood/emotion is thought to be affected particularly via REM-sleep, where we observe a hyperlimbic and hypoactive dorsolateral prefrontal functioning

in combination with a normal functioning of the medial prefrontal cortex, probably adaptive in coping with the continuous stream of emotional events we experience” (Vandekerckhove and Cluydts, 2010). Indeed, migraine (along with disorders such as depression and gastric ulcers) is an independent predictor of excessive daytime sleepiness (Stroe et al., 2010). The basis for this may be an abnormal (reduced) arousal index in rapid eye movement (REM) sleep, which implicates dysfunction in hypothalamic and brainstem regions (Della Marca et al., 2006). Abnormal sleep or sleep restriction can have negative consequences for brain

function and peripheral physiology (Kim et al., 2007), including increased appetite and energy expenditure, increased levels of proinflammatory cytokines, decreased parasympathetic and increased sympathetic tone, increased blood pressure, increased evening cortisol levels, and elevated insulin and blood glucose (McEwen, 2006b). Clearly, sleep disturbances already and migraine (both allodynic and nonallodynic) have complex interactive effects on each other (Lovati et al., 2010) that suggest that implementing congruent therapeutic approaches may be of significant importance. Medications may be allostatic moderators or exacerbators. In migraine, the overuse of triptans and opioids seems to induce or contribute to chronification of migraine (Bigal, 2009). Corticotrophic and somatotrophic functions are significantly impaired in chronic migraine medication overuse (CM-MOH) patients: after human corticotrophin-releasing hormone (hCRH) administration, ACTH and cortisol concentrations are significantly higher in CM-MOH cases than in controls (Rainero et al., 2006).