The findings of a study suggest that plasma and cerebrospinal fluid (CSF) lipid metabolism are associated with chronic migraine (CM) pathology. The results appeared in Frontiers in Molecular Neurosciences.

To conduct this study, data were obtained on plasma and CSF from healthy controls (n = 10) or CM subjects (n = 15). The researchers then measured unesterified fatty acid (UFA) and esterified fatty acids (EFAs) using gas chromatography–mass spectrometry. Glycerophospholipids (GP) and sphingolipid (SP) levels were determined using liquid chromatography–mass spectrometry, and phospholipase A2 (PLA2) activity was determined using fluorescent substrates, the researchers noted.

According to the results, unesterified fatty acid levels were significantly higher in CM plasma but not in CSF. The researchers found that unesterified levels of five saturated fatty acids (SAFAs), eight monounsaturated fatty acids (MUFAs), five ω-3 polyunsaturated fatty acids (PUFAs), and five ω-6 PUFAs were higher in CM plasma in the CSF, while PLA2 activity was similar. In addition, the plasma UFA to EFA ratio is higher in CM.

“Plasma and CSF lipid changes are consistent with abnormal lipid metabolism in CM. Since plasma UFAs correspond to diet or adipose tissue levels, higher plasma fatty acids and UFA/EFA ratios suggest enhanced adipose lipolysis in CM. Differences in plasma and CSF desaturases and elongases suggest altered lipid metabolism in CM. A lower plasma ceramide level suggests reduced de novo synthesis or reduced sphingomyelin hydrolysis. Changes in CSF PAF suggest differences in brain lipid signaling pathways in CM,” the researchers concluded. “(Taken together) this pilot study shows lipid metabolic abnormality in CM corresponding to altered energy homeostasis. We propose that controlling plasma lipolysis, desaturases, elongases, and lipid signaling pathways may relieve CM symptoms.”

 

Source: https://pubmed.ncbi.nlm.nih.gov/34531722/

 

Keywords: chronic migraine, insulin resistance, lipases, lipid signaling, lipolysis, metabolic syndrome, phospholipase A2, platelet-activating factor