Central sensitivity syndromes (CSSs) represent a heterogeneous group of disorders like fibromyalgia [FM], irritable bowel syndrome [IBS], chronic headache, temporomandibular disorders [TMDs] or pelvic pain syndromes that share many common symptoms, with persistent pain being the most prominent feature.
Although the etiology and pathophysiology of CSSs are currently incompletely understood, central sensitization has emerged as one of the significant mechanisms.
Given that there are currently no known cures for CSSs, people living with these disorders must learn to cope with and manage their symptoms throughout their lives.
Medical interventions alone have not proven to be sufficient for helping people with CSSs manage their symptoms.
A biopsychosocial perspective that considers the ways that biological, psychological, and social factors work independently and jointly to affect a person’s experience is the most effective conceptualization and guide for effective treatment.
We need to know a several psychological and social features that may influence the experience of a person with CSS and their symptom management, regardless of their specific diagnosis.
We highlight the longitudinal aspect of adjustment to illness, the distinction between psychosocial factors as causes of symptoms versus modifiers and perpetuators of symptoms, dispel the notion that all patients with the same diagnosis are a homogeneous group the patient uniformity myth, and acknowledge the importance of environmental and situational context on symptom management for individuals with any CSS.
The hypothesis that central sensitization like allodynia is the common final mechanism responsible for the progression of migraine pain is supported by the possibility of tracing back to allodynic mechanisms the action of the main risk factors for chronic migraine validated by the recent literature.
The comorbidity between migraine and idiopathic intracranial hypertension without papilledema is emerging as a new, commonly overlooked risk factor for migraine progression whose putative mechanism might also converge on the sensitization of central pain pathways.
If headache progression always occurs at the end of a pathogenetic sequence typical of an individual susceptibility to allodynia, then the primary character of chronic migraine might be debated.
Allodynia is not specific to migraine but is implied in the progressive amplification of pain after repeated stimuli, a universal adaptive phenomenon.