Research shows that migraines are more common in women with MS. Here is some information on a study that looked at nearly 117,000 U.S. women and found that women with a migraine diagnosis were 47% more likely to develop MS. http://news.health.com/2010/02/16/migra ... osis-risk/
Following is some info from my book.
"Compared with the general population, people with lupus may be twice as likely to experience migraine headaches, commonly known as lupus headaches. The paper entitled “A study of headaches and migraine in Sjögren’s syndrome and other rheumatic disorders” reported that nearly half (46%) of Sjögren’s patients and 32% of patients with scleroderma suffer from migraines as well (Pal, 1989). It concluded that, “There was a significant association between occurrence of Raynaud’s phenomenon and migraine. Small vessel pathology may underlie both migraine and Raynaud’s phenomenon in these connective tissue disorders--as has been suggested in systemic lupus erythematosus.”
In Headache: The Journal of Head and Face Pain, author Cris S. Constantinescu M.D., Ph.D., states, “Migraine and Raynaud phenomenon often coexist and may reflect similar vascular reactions. Both have been associated with vascular endothelial cell dysfunction,” (Constantinescu, 2002).
The following study found that homocysteine levels were significantly higher in patients with migraine with aura (MA) than in healthy controls.
Homocysteine Plasma Levels in Patients With Migraine With Aura
Moschiano. F., D. D’Amico, S. Usai, L. Grazzi, M. Di Stefano, E. Ciusani, N. Erba, G. Bussone. 2008, Neurol Sci 29(Suppl. 1):S173-5.
Abstract: We investigated homocysteine plasma levels in 136 MA sufferers and in 117 sex-and age-matched controls. Mean homocysteine plasma levels - as well as the proportion of subjects with hyperhomocysteinaemia - were significantly higher in patients with MA than in healthy controls. Hyperhomocysteinaemia may be a link between MA and ischaemic stroke.
The next study, done in Japan, is notably and appropriately titled, “Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells.”
Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells Through Activation of the Unfolded Protein Response
Zhang, C, Y. Cai, M.T. Adachi, S. Oshiro, T. Aso, R.J. Kaufman, S. Kitajima. 2001. J Biol Chem 276(38):35867-74.
Severe hyperhomocysteinemia is associated with endothelial cell injury that may contribute to an increased incidence of thromboembolic disease. In this study, homocysteine induced programmed cell death in human umbilical vein endothelial cells as measured by TdT-mediated dUTP nick end labeling assay, DNA ladder formation, induction of caspase 3-like activity, and cleavage of procaspase 3. Homocysteine-induced cell death was specific to homocysteine, was not mediated by oxidative stress, and was mimicked by inducers of the unfolded protein response (UPR), a signal transduction pathway activated by the accumulation of unfolded proteins in the lumen of the endoplasmic reticulum. Dominant negative forms of the endoplasmic reticulum-resident protein kinases IRE1alpha and -beta, which function as signal transducers of the UPR, prevented the activation of glucose-regulated protein 78/immunoglobulin chain-binding protein and C/EBP homologous protein/growth arrest and DNA damage-inducible protein 153 in response to homocysteine. Furthermore, overexpression of the point mutants of IRE1 with defective RNase more effectively suppressed the cell death than the kinase-defective mutant. These results indicate that homocysteine induces apoptosis in human umbilical vein endothelial cells by activation of the UPR and is signaled through IRE1. The studies implicate that the UPR may cause endothelial cell injury associated with severe hyperhomocysteinemia.
The previous studies on Raynaud’s and migraines, in addition to the study from Japan, show the damage homocysteine can do to the vascular endothelial cells. Endothelial cells line the entire circulatory system, from the heart to the smallest capillary.