Health-Related quality of life in Russian children with inflammatory bowel disease is comparable across disease types and treatment modalities.

Migraine is a disease of the central nervous system also characterized by clinical manifestations secondary to the activation of the peripheral nervous and vascular systems. The pathogenesis of migraine is extremely complex and, for this reason, not yet fully understood. Indeed, the pain component, although representing the most consistent aspect of this pathology, is part of a rich and differentiated symptomatic process which sets in in consecutive temporal phases and which is the result of the activation of cortical and subcortical nervous/brain structures strictly interconnected by multiple neurotransmitter and neuroendocrine systems (). A basic role in the pathogenesis of the migraine attack is played by the trigeminovascular system which operates as a “checkpoint” for sensitive and painful stimuli eliciting from intra- and extracranial anatomical structures. Both peripheral and central nerve fibers originate from the trigeminal ganglion neurons. The former collects and transmit the sensory-painful stimuli from the meninges and intra- and extra-cranial vessels, the latter contact the nucleus of the Trigeminocervical Complex (TCC) in the brainstem. Numerous descending nerve fibers from different cortical areas, hypothalamus and brain stem nuclei, all of them regulating and modulating sensory and pain information, also converge on TCC (, ). Nerve fibers from the TCC projects to the superior pontine salivatory nucleus from which, in turn, parasympathetic fibers reach the sphenopalatine ganglion responsible for lacrimation and cranial arterial vasodilation (trigeminal autonomic reflex arc). The activation of the trigeminal autonomic reflex contributes to pain onset and triggers migraine autonomic symptoms (). This widespread and complicated interneuronal and intersystemic, cortical and subcortical connectivity, which involves nervous structures with specific and different functions, accounts for the complexity of the pathology and for the extreme heterogeneity of both exogenous and endogenous factors possibly inducing the migraine attack. A step forward in the still not fully elucidated pathogenesis of migraine has been made with the discovery of the role of the Calcitonin Gene-Related Peptide (CGRP), a vasoactive peptide which is released following the activation of TCC and is responsible for the migraine attack. This finding has been crucial for the development of new migraine treatments based on CGRP-targeting drugs (). Takotsubo syndrome (TS) (otherwise called “broken-heart” syndrome or stress cardiomyopathy) is characterized by a transient dysfunction of the left ventricle wall, usually of the lower part (apex), resulting in a reduction in the systolic contractile capacity of the myocardium. Due to the shape of the dysfunctional apex, the syndrome is also known as “apical ballooning syndrome.” It mainly affects post-menopausal women possibly as a consequence of the increased sympathetic activation in healthy, aging women (). The pathogenesis is not well known, but the most accredited hypothesis is that, given a favorable genetic predisposition, stressful situations, emotional and/or physical, induce an anomalous activation of the limbic system and the hypothalamic axis, determining a massive release of catecholamines in the organism with consequent damage to the microcirculation and ventricular function (, ).