Migraine attacks the Basal Ganglia

<p>Abstract</p> <p>Background</p> <p>With time, episodes of migraine headache afflict patients with increased frequency, longer duration and more intense pain. While episodic migraine may be defined as 1-14 attacks per month, there are no clear-cut phases defined, and those patients with low frequency may progress to high frequency episodic migraine and the latter may progress into chronic daily headache (> 15 attacks per month). The pathophysiology of this progression is completely unknown. Attempting to unravel this phenomenon, we used high field (human) brain imaging to compare functional responses, functional connectivity and brain morphology in patients whose migraine episodes did not progress (LF) to a matched (gender, age, age of onset and type of medication) group of patients whose migraine episodes progressed (HF).</p> <p>Results</p> <p>In comparison to LF patients, responses to pain in HF patients were significantly lower in the caudate, putamen and pallidum. Paradoxically, associated with these lower responses in HF patients, gray matter volume of the right and left caudate nuclei were significantly larger than in the LF patients. Functional connectivity analysis revealed additional differences between the two groups in regard to response to pain.</p> <p>Conclusions</p> <p>Supported by current understanding of basal ganglia role in pain processing, the findings suggest a significant role of the basal ganglia in the pathophysiology of the episodic migraine.</p

Neuroimaging functional pain networks in health and disease

Chronic pelvic pain (CPP) is considered a significant public health problem. In the United Kingdom, it has been estimated that 24&percnt; of women suffer from CPP. Using neuroimaging, this dissertation aims to characterise the pain experience by examining functional changes in critical pain networks. I begin by examining the functional correlates of capsaicin-induced central sensitisation in healthy individuals. Most of the results did not reach significance, largely due to the use of early 7T data and small sample sizes. In an exploratory analysis, amygdala - anterior insula connectivity is positively correlated with pain intensity. The remaining experimental chapters examine mechanisms of pain in women with CPP. I begin by attempting to better characterise this diverse patient population. I demonstrate correlations between measures of the pain experience and psychological scores. Following this, I examine clinically-relevant changes in functional connectivity. I demonstrate that there are potentially different underlying modulatory mechanisms in women with neuropathic components to their pelvic pain. Furthermore, women who experience pain for longer than 24 months have increased functional connectivity between the hippocampus and periaqueductal gray, suggesting pain-related alterations in central circuitry. The final experimental chapters explore surgical and pharmaceutical treatments for CPP and endometriosis; however, due to small sample sizes and nonsignificant findings, limited conclusions can be drawn from the results. In this dissertation, I found changes in important pain networks that could either represent the maintenance of the pain state or are consequence of the pain itself. These findings may serve as an indicator of underlying central changes that relate to relevant components of the clinical pain experience.</p