TLDR: partial TLE seizures since the onset of ME, nimodipine stopped them. Inositiol and oxaloacetate provoke them.
Just posting here to see if this ties in with anyone else's experiences or research really. Calcium channels would seem to be key. All theories and tidbits welcome!
I've suffered from simple partial temporal lobe seizures since the onset of ME, which was most likely EBV-induced, but I also suspect some mito issues since birth. I've always had visibly low muscle mass and was unable to do normal kid things like climbing, monkey bars or opening heavy doors. Though nothing showed up in mtDNA testing.
The seizures weren't diagnosed until 2015 but they're 'textbook': 30 secs+ of nausea, rising sensation, nose sensation and unusual odour and deja vu, with right-sided face and arm tingling, right-sided vision loss plus hissing in ears. I'd get clusters ranging from 1-10+ per day, usually only a few days per month. Bad days would be accompanied by a constant nauseous migrainous state. There didn't seem to be a cyclical/hormonal pattern.
I found that taking 2-4g/day of inositol would provoke these seizures and leave me in the constant nauseous state having multiple seizures every day.
I then discovered nimodipine for ME and to my amazement this stopped the seizures completely, I've not had one in about 3 or 4 years, save for the odd hint of an aura a few times a year. I re-challenged with inositol and have since been able to take it without issue now I'm on nimodipine.
I couldn't figure out if the nimodipine worked by dilating a structural issue in the brain vasculature that was causing hypoperfusion, or whether the calcium channel-blocking effects were responsible independently of vasodilation.
Fast forward to last week when I began oxaloacetate/Benagene at 300mg AM and 200mg PM. Within days I was hit by sudden nausea and headache about 30 mins after taking it in the morning which persisted all day, though I didn't make the connection. Today, I was hit with a seizure about 30 mins after taking.
I feel like these things are potentially huge clues to the underlying pathology but I lack the depth of knowledge of biology to make more sense of it, I'm rather hoping someone here might know something or have made similar discoveries of their own.
I was able to find that "Inositol trisphosphate is a second messenger that controls many cellular processes by generating internal calcium signals."
And this, which links oxaloacetate to mitochondrial calcium efflux- can anyone with a better understanding of cell biology tie any of this in, maybe?
Thanks for reading!
Just posting here to see if this ties in with anyone else's experiences or research really. Calcium channels would seem to be key. All theories and tidbits welcome!
I've suffered from simple partial temporal lobe seizures since the onset of ME, which was most likely EBV-induced, but I also suspect some mito issues since birth. I've always had visibly low muscle mass and was unable to do normal kid things like climbing, monkey bars or opening heavy doors. Though nothing showed up in mtDNA testing.
The seizures weren't diagnosed until 2015 but they're 'textbook': 30 secs+ of nausea, rising sensation, nose sensation and unusual odour and deja vu, with right-sided face and arm tingling, right-sided vision loss plus hissing in ears. I'd get clusters ranging from 1-10+ per day, usually only a few days per month. Bad days would be accompanied by a constant nauseous migrainous state. There didn't seem to be a cyclical/hormonal pattern.
I found that taking 2-4g/day of inositol would provoke these seizures and leave me in the constant nauseous state having multiple seizures every day.
I then discovered nimodipine for ME and to my amazement this stopped the seizures completely, I've not had one in about 3 or 4 years, save for the odd hint of an aura a few times a year. I re-challenged with inositol and have since been able to take it without issue now I'm on nimodipine.
I couldn't figure out if the nimodipine worked by dilating a structural issue in the brain vasculature that was causing hypoperfusion, or whether the calcium channel-blocking effects were responsible independently of vasodilation.
Fast forward to last week when I began oxaloacetate/Benagene at 300mg AM and 200mg PM. Within days I was hit by sudden nausea and headache about 30 mins after taking it in the morning which persisted all day, though I didn't make the connection. Today, I was hit with a seizure about 30 mins after taking.
I feel like these things are potentially huge clues to the underlying pathology but I lack the depth of knowledge of biology to make more sense of it, I'm rather hoping someone here might know something or have made similar discoveries of their own.
I was able to find that "Inositol trisphosphate is a second messenger that controls many cellular processes by generating internal calcium signals."
And this, which links oxaloacetate to mitochondrial calcium efflux- can anyone with a better understanding of cell biology tie any of this in, maybe?
Thanks for reading!
