Migraine is a common disorder, characterized by recurrent episodes of headache 
and associated symptoms. The full pathophysiology of migraine is incompletely 
delineated. Current theories suggest that it is a neurovascular disorder 
involving cortical depression, neurogenic inflammation and vasodilation. Various 
neuropeptides and cytokines have been implicated in the pathophysiology of 
migraine including calcitonin gene-related peptide, interleukin (IL)-1, IL-6 and 
tumour necrosis factor (TNF)-alpha. There is evidence demonstrating an 
association between migraine and processes associated with inflammation, 
atherosclerosis, immunity and insulin sensitivity. Similarly, adiponectin, an 
adipocytokine secreted by adipose tissue, has protective roles against the 
development of insulin resistance, dyslipidaemia and atherosclerosis and 
exhibits anti-inflammatory properties. The anti-inflammatory activities of 
adiponectin include inhibition of IL-6 and TNF-induced IL-8 formation, as well 
as induction of the anti-inflammatory cytokines IL-10 and IL-1 receptor 
antagonist. Adiponectin levels are also inversely correlated with C-reactive 
protein (CRP), TNF-alpha and IL-6 levels. Likewise, recent studies have shown a 
possible correlation between CRP, TNF-alpha and IL-6 and migraine attacks. In 
addition, insulin sensitivity is impaired in migraine and obesity is a risk 
factor for the transformation from episodic to chronic migraine. In this review 
we discuss the basic science of adiponectin and its potential connection to the 
pathophysiology of migraine. Future research may focus on how adiponectin levels 
are potentially altered during migraine attacks, and how that information can be 
potentially translated into migraine therapy.