| Summary: | Chronic pain is a complex experience that involves sensory, emotional, and cognitive aspects. The neurobiological mechanisms are therefore expected to be complex, widespread and largely maladaptive. Recent research of neuroimaging in chronic pain suggests cerebral re-organization on a structural level as a consequence of chronic pain. However, a combined and large-scale brain morphological profile in chronic pain to investigate its neural substrates has not been elucidated. The research presented aims to investigate morphological brain correlates and putatively related behavioural and cognitive aspects of chronic pain due to primary nociceptive knee osteoarthritic disorder using advanced imaging techniques for manual, voxel-based, and surface-based analysis, and questionnaire-based participants’ characterization. 31 participants with chronic painful knee osteoarthritis (age= 64.6± 8.4 years, 15 females, mean duration of pain=9.6 years) and 22 healthy controls (age= 61.3± 7.5, 13 females) underwent high-resolution anatomical MRI at 3 Tesla, and detailed pain characterization and psychometric assessment. Findings from this thesis challenge the common belief that chronic pain leads to hippocampal volume reduction and allegedly cognitive dysfunction. Indeed, general cognitive function and delayed recall memory were normally preserved in the studied cohort, and moreover the hippocampal volume was significantly enlarged. The volume of the rostral part (emotional) of anterior cingulate showed significant positive correlation with pain catastrophizing behaviour suggesting that it may underlie the pain catastrophizing tendency in patients with chronic knee pain. Higher scores of mechanical pain sensitivity correlated with reduced cortical thickness in the anterior cingulate indicating its potential key role in the process of central pain sensitization. Sufferers of chronic knee OA pain exhibited less grey matter volume in the left dorsolateral prefrontal cortex, which has a modulatory role in nociceptive transmission namely, pain perception inhibitory effect. Although the mechanism of this reduction is unknown, such a change may suggest functional disturbance with subsequent aberrant contribution to pain sustainability and chronification. Whole brain cortical thickness was investigated in patients and results revealed wide spread cortical thinning progresses with pain duration, preferentially in females, and in areas largely outside the known pain matrix, but including the posterior default mode network. Finally, preliminary results from investigating the potential mechanism of chronic pain related neocortical plasticity will be presented that may provide framework for future studies.
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