The following material is an extrapolation of data from a paper by Osaka researchers entitled Neuroninflammation in Patients with CFS/ME. It is recommended that you read at least the abstract and discussion and view the images. The paper can be found here- http://jnm.snmjournals.org/content/55/6/945.long#ref-24 I highly recommend watching a couple of Youtube brain function animations to help you orientate regarding the diagrams I have included below. Key points The method targeted activated astrocytes and microglia (cells of the brain's immune system). The immune cells are activated in a situation of neuroinflammation. Nine ME patients and ten healthy controls were scanned. ME patients had 'inflammation scores' between 45% and 199% higher than controls. Degree and localisation of neuroinflammation was correlated positively with severity and nature of symptoms. High value scores in the amygdala, thalamus and midbrain correlated with cognitive impairment score. High values in the cingulate and thalamus correlated with pain score. The PET scan results show that in this cohort of ME patients neuroinflammation is centred on the limbic system, which is critically important for normal brain function. I have attempted to synthesize some of the data form the the Osaka paper into a diagrammatic form for ease of accessibility to PR members. Please excuse my poor graphic work, it is difficult to successfully layer the components of such a complex organ as the brain. Figure 1 Normal brain functions Figure 1 relates normal brain function to specific locations. It is not a comprehensive map, but isolates functional locations which the PET scans proved to be in a neuroinflammatory state and physiologically neighbouring area which may tentatively be affected by adjacent inflammation in my opinion. Figure 2 Confirmed area of neuroinflammation Orange dots marked confirmed localized areas of inflammation and crosses in red indicate associated dysfunction proven in the PET scans. Question marks indicate potential associated deregulation in my opinion only. it is worth noting that this is a generalized diagram encompassing all the scans (9 patients). Different patients have slightly different localized areas of neuroinflammatory process. Figure 3 Correlation of neuroinflammation with ME symptoms Using the Canadian primer and PET scan findings, I have linked damaged brain localities to well established ME symptoms. Greyed out titles are not directly referred to in the Osaka study but again may, in my opinion suffer possible deregulation. Key points Given the success of the Osaka team's methodology why have health authorities failed to consider PET scan as the gold standard technique in ME diagnosis and monitoring? The Osaka team postulates two mechanisms causing neuroinflammation. The first is overactivity of neurons in a compensatory process for functional loss in ME. The second is as a neuroimmune response to infection. (I tentatively covered this model in a blog essay called 'paper' on CFS/me pathogenesis-the brain). This issue of pathogenesis/cause of neuroinflammation needs resolving. Given the fact of neuroinflammation in ME patients, the urgent question is how to address it- how do we best quell inflammation to minimize brain damage? How do we promote healing-neurogenesis etc? I have used nootropics for 4 years with some success but there is (as I have found out!) the contentious issue of anti-inflammatories/steroids. If we conclude that severity of ME symptoms (mild to very severe) correlates with 1-severity of neuroinflammation and 2- localization of neuroinflammation to specific brain structures then can we also infer that fluctuations in symptoms also relate to extent of neuroinflammation I would welcome any revisions/ corrections/ criticism of the post..I am not a neuroscientist.