posted
so.. had seizures for 3 days. had 2 in neuro's office. he induced one trying to use the light to check my eyes.
i stay awake, not fully unconsious but not all together with-it either. groggy after and VERY tired....
started in legs then moved up. very tonic/clonic and legs/arms even posturing same with neck. back would hyperextend then draw up...
very painful....
hubby called EMS when lasted 30 min sat. ER did labs/CT and sent me home saying..."well, you are on lots of meds...so, think that is the problem" DR or nurses did NO exam of any kind.
WE did some looking at stuff.. and newest rx was aricept for cognative decline.
the aricept had a PROFOUND effect- i mean like a switch was flipped (did post about it) was like magic.. .felt GREAT.. up, moving around, like last yr had not happened but brain still was in slow grear..lol.. didnt help memory,etc at all BUT helped everything else even pain !!1
so... stoppped aricept went back to 3xday on neruontin for few days and now better...
so.... too much atetylcholine ??? apperently. looks like helped my body at first but by wk 3 was too much of it going on in brain..too much will affect muscles. and not much really known about Ach...neurotransmitter but also prob. a hormone????
any input appreciated and also a heads up to anyone who tries aricpet and may have unusual response
-------------------- i am not a Dr. any info is only for education, suggestion or to think/research. please do not mis-intuprest as diagnostic or prescriptive, only trying to help. **
dx in 08:lyme, rmsf, bart, babs, and m.pneumonia. Posts: 422 | From TX | Registered: Oct 2008
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Marnie
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posted
It is very difficult to determine the interaction of 2 medicines, let alone the interaction of multiple meds.
LOW blood level of SODIUM is a seizure trigger. I know...my own son. I think, genetically, he (and my daughter) have a hard time converting B6 to the active form P5P or also called PLP in their livers.
B6 (and other things) control Na levels.
AND...Bb absolutely NEEDS sodium!
Oh, oh! nACHR = an acetylcholine receptor.
"The nAChR is found at the edges of junctional folds at the neuromuscular junction on the POSTsynaptic side; it is activated by acetylcholine release across the synapse.
The diffusion of Na+ and K+ across the receptor causes depolarization, the end-plate potential,
***that opens voltage-gated sodium channels***,
which allows for firing of the action potential and potentially muscular contraction.
I think Bb exchanges H for Na. Hydrogen for sodium.
(No wonder ACh levels drop.)
When sodium goes INTO the cells...less in the general circulation = hyponatremia (low blood level of sodium) may -> seizure.
Consider trying sublingual B6 (Source Naturals carries it). It is the active form of B6. You have to put it under your tongue because our strong stomach acids destroy much of it. The active form of B6 is called P5P or PLP.
For cognitive decline...consider virgin coconut oil!
*********
For any experts out there:
My son was on Depakote for seizures, but like all anti-seizure meds which cause hyperglycemia, his liver became "fatty" (ultrasound).
Unfortunately I did not know then the link between PLP and ACC2 and how PLP impacts (protectively) the liver.
Lamictal TRIGGERED seizures in him. Getting off was a nightmare!
Now he is doing very well on sub B6 and OmegaBrite. He also takes some theanine. Slowly...these are helping.
Besides seizures triggered by low sodium (which his psychiatrist figured out), he has ADHD, Asperger's and severe learning disabilities (which are directly related to B6 levels).
Since B6 works WITH Mg....now a Mg problem. And Mg gates the NMDA receptors...
Ongoing brain inflammation...glutamate excess...
[ 11-09-2009, 11:33 AM: Message edited by: Marnie ]
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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posted
Read the article on autonomic systems in the link Northstar posted today.
It is possible that the increased acetylcholine in the brain could cause vasoconstriction.
What you are describing sounds a lot like some of hubby's spells. He does not have true seizures, but his seizure-like episodes are often triggered by decreased bloodflow to the brain.
Lumbrokinase has been very helpful for this symptom.
One big problem with all meds is that they impact many different things in the body. Psych drugs especially work on many different neurotransmitters -- there may be only 1 or 2 primary ones involved but many others are also impacted.
So sorry for what you are going thru.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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Keebler
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posted
- Sorry this happened. It's very unsettling.
Even if as a "support" and not a "boost" - anything I take to try to wake up my brain or give me more energy will lower the seizure threshold for me.
I don't take any pharmaceuticals anymore but this will happen even with Gingko or Chromium (as that may lower blood sugar too much for me). Caffeine, too, if more than in a cup of green tea, has this effect as well.
For me, it's also as you described: tonic/clonic (and myoclonic) with the hyperextended/arched back and neck. Other than for the first few seconds after a any kind of sensory startle trigger, I, too, am aware but as if in a trance watching myself - unable to control anything my body does. It's as if it's being controlled by a powerful and spastic motor.
I think my brain/body just can't handle the excitement of anything to give me more cognitive or physical power.
I would do as you have done, drop the last med added and see how it goes. It takes me about a month to get back to my normal after one of these but after the first week, you should feel better.
Did your blood sugar drop? That is often the last straw before I go flying. Are you taking enough magnesium? What is your liver and adrenal support? -
Posts: 48021 | From Tree House | Registered: Jul 2007
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Marnie
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posted
Read the posts above and then remember this...
Acetylcholine = REM sleep (I know a lyme patient in Sarasota who was tested in a sleep lab and she has NO REM sleep).
Melatonin = NREM sleep
First melatonin then acetylcholine then melatonin then acetylcholine. The switch between NREM sleep (melatonin) and REM sleep(acetylcholine) happens about 5 times per night.
In lyme, we know acetylcholine levels are low and melatonin is high (fatigue, sleepy).
Melatonin is a powerful anti-oxidant.
If acetylcholine is "available", does it downregulate the anti-oxidant, melatonin?
Melatonin also downregulates dopamine which converts to norepinephrine and then epinephrine (= noradrenaline and adrenaline).
Bb's OspA, not OspB...binds to OUR norepinephrine and epinephrine.
So by increasing melatonin -> less dopamine -> less norepinephrine -> less epinephrine...
Bb's OspA would then (theoretically) have nothing to bind to.
So...WE force Bb to "change clothes"...to go from OspA to OspB.
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Keebler
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posted
- Norepinephrine and then epinephrine (= noradrenaline and adrenaline).
Less or more? Wouldn't the energy-result of aricept increase these hormones? Or - I see - it could deplete them and then drop us like a brick.
Maybe in a non-lyme person it would decrease but, in my experience, it seems like all these adrenal hormones are zoomed to the moon with anything to wake up the brain.
I'm sure the HPA axis hypothalamus/pituitary/adrenal triangle of interaction) is involved. It just can't take any more pushing.
Or, Marnie, are you saying that it might be that the lyme then has a party since the norepinephrine and epinephrine is engaged and maybe it's the lyme that is flaring and causing the seizure? -
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TerryK
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So sorry this has happened to you my3Boys.
One of the things that I have been taking for a number of years in order to increase acetylcholine is Huperzine A.
According to Wikipedia "Huperzine A is an Acetylcholinesterase inhibitor similar to other compounds donepezil, rivastigmine, and galantamine."
Donepezil IS Aricept!!
Perhaps taking something less in strength would be useful?
I also take phosphatidyl choline, choline/inositol and citicoline for acetylcholine. It may be a mix of things that are more useful than just one thing.
That said, I found these things several years ago via muscle testing so maybe it is the mix that is right for me and something else would be right for you.
Terry I'm not a doctor
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Keebler
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. . . the medication may cause side effects, including low blood pressure, seizures, bladder obstruction, and weight loss. . . .
Aricept can interact with certain medications (see Aricept Drug Interactions list at the link).
Some Aricept warnings and precautions to be aware of include:
. . .
Heart disease
Liver disease, such as liver failure, hepatitis, or cirrhosis
Low blood pressure (hypotension)
Seizures or epilepsy
Stomach or intestinal disease, ulcers, or bleeding
If you have severe liver disease, your healthcare provider may choose to start you on a lower dose of Aricept and monitor your condition more closely.
Aricept may cause hypotension (low blood pressure) and make you feel light-headed when you stand. Make sure to rise slowly from a sitting or lying position.
Aricept may make certain heart conditions worse. If you have sick sinus syndrome, heart block, or other heart problems, your healthcare provider may choose to monitor your heart problem more carefully while you are taking Aricept.
Aricept oral solution (but not other forms of Aricept) contains a sulfite as an inactive ingredient. This is important for people with a sulfite allergy.
. . . . Cont'd at link abvove.
================
Liver disease? The liver is stressed in every lyme patient. Next, to find out if this is uses Cytochrome P-450 liver detox pathway. If so, that would likely cause even more liver stress for lyme patients. And, if so, a result would be increase in toxic porphyrins which can trigger seizures.
Also the drop in blood pressure can trigger seizures - as can the vertigo. -
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Keebler
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Journal of Neurology, Neurosurgery, and Psychiatry 1999;66:410; doi:10.1136/jnnp.66.3.410
J Neurol Neurosurg Psychiatry 1999;66:410 ( March )
Letters to the editor
Convulsions induced by donepezil . . .
We report on a patient with mild Alzheimer's disease who presented with convulsions during treatment with donepezil.
The patient was a highly educated, ApoE4 homozygous, 72 year old man, who was diagnosed with dementia of probable Alzheimer's type (NINCDS-ADRND criteria) 14 months previously.
His medical history, with the exemption of non-familiar dementia, was unremarkable and
his only medication was 100 mg aspirin daily. . .
He was treated with 5 mg donepezil once daily for 2 weeks, and then 10 mg a day for 23 days when he was . . . .
(subscription required for full text). -
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Pinelady
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posted
I agree. I think this plays a big part of Lyme.
But is it the pineal gland we need to fix or the melatonin?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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One article cited a trial of drinking first urine in am for replacement of melatonin. LOL Not me.
Could this malfunction be what causes low body temp in most lyme patients?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Marnie
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posted
No...keep this in mind...
Bb absolutely needs sodium to go into the cells it is infecting.
When sodium comes out of the blood and goes into the cells, this causes a temporary drop in the circulating blood level of sodium = hyponatremia.
That is one of the seizure triggers.
Acetylcholine opens Na channels.
Repeating...Bb needs Na. Acetylcholine opens Na channels.
Lamictal triggered seizures in my son. One use for Lamictal is to stop seizures.
A long time ago, the head of pediatric neurology at Children's Hospital in Chicago told me:
Kids with ADHD are not getting enough GLUCOSE to the frontal lobe.
In a jam, to substitute for low glucose, we can and do use KETONES.
In AD...it is believed the cells are also starved of glucose so the idea is...switch to ketones.
Our brain and our heart LIKE KETONES, but too many are harmful to our kidneys (which maintain our pH), so we have to be careful not to use too many ketones.
But we can survive a long time on simply ketones (burn our fat) and water.
We have to flip the switch between using fatty acids OR using glucose for energy.
We are shutting off fats and turning on glucose.
Which is HOW virgin coconut oil is working.
Bb is starving our cells of oxygen (the biofilm blocks oxygen) AND it is starving the cells of glucose...glucose IS also needed for "oxidative phosphorylation" which happens in the MITOCHONDRIA - powerhouses of our cells.
Think back...ICHT...speeding up glycolysis...heating the cells...rapid weight loss...fat is BURNED -> KETONES.
Dangerous...but we can do it slowly...
And we have to figure out another way to simultaneously reduce the inflammation.
It appears EPA helps. NOT DHA!!!
Glucose = fat builds up.
When my son was on Depakote to prevent seizures, because all of the anti-seizure meds cause HYPERGLYCEMIA...this -> a fatty liver (not good), but I didn't know then the relationship between
PLP (also called P5P) which is the ***active form of B6*** and ACC2.
When ACC2 is inhibited, mice can eat so much more and NOT GAIN WEIGHT.
This is under neurohormonal control.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Marnie
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posted
Chances are...your body is already doing this.
Since it is likely your B6->PLP levels are low and B6 helps control Na levels, the body will...
Upregulate aldosterone to control Na levels.
Which -> more testosterone and more estrogen.
Dominant. Testosterone dominant and estrogen dominant which of course increases the risk of ...
Valletta's patent "Magnesium for Autoimmune:
Mg pyrophosphate and sublingual B6 (= PLP/P5P).
Pyrophosphate is PPi which is an analogue of ...get this...ATP...our energy carrier.
You see the infected cells are NOT MAKING ENOUGH ATP.
So...we're going to speed up the process...
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Carol in PA
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posted
Well darn, seizures after three weeks of Aricept. I saw the recommendations were to start the med at 5 mg daily, then go up to 10 mg.
I want to talk to my doc about trying this, but now I'm leary.
Were you still on 5 mg?
Carol
Posts: 6947 | From Lancaster, PA | Registered: Feb 2004
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Pinelady
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posted
* Ginkgo Biloba 120 mg/day o acetylcholinesterase inhibitor o anti-oxidant * Vitamin E 2000 IU? * Melatonin & Aricept study * Upcoming I found this interesting but I can't find the study.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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ok- NO hyponatremia. actual blood levels for all my electrolytes where normally, wnl... ok, that sounds confusing?? all were good. Na level very normal.
and yes-- VERY bummed that my lil miracle med crashed me out..
so... been off it since sat and have had decreased "episodes" since. sat. had about 3 bouts of "uh-oh, my eyes are doing IT again" which has been the pre-cursor. i get a little light show, or circles,etc..
then sunday, very tired. muscles hurt like all get out. got a massage. drank tons of water. and bit of twictching freq. to arms/legs and head bobbeling off/on
then yest. NO funny eye episodes. just very, very cranky. muscles hurt and joints hurt.. BAD.
so.. pain is back. that is huge bummer.
I do supp. with Mg, the lactate-dehydrate one recommended by Dr B. and on bio-identicals for estrogen dominance.
do take B-12 complex by jarrow but have NOT tried just the B-6 .. thanks Marnie will look at that.
Funny how NONE of the lit. we got listed seizures, nor does thier website. we figured it out doing research and looking at meds.
ER Dr was very dissapointing IMO. PCP-oncall wanted me to hit ER and be admitted and monitored but just treat/street was it. no assessment even ... AT ALL.
another thing -- been off the IV rocehpin for month now..ins. deciceded not med. ness. so neruo said not the prob. but i think when add up ALL of it is just one reciepe for disaster.
just got letter from ins. and looks like may let me do another month ???? lol, the letter is so confusing I cant understand what they are reversing the decision OF ?? and i am ususally good to go on uderstnading all that, would help patients understand it..geez
also- gaining wt. like CRAZY. was adding the VCO to diet and backed it up when up 25 lbs. in only few mo. time. on the normal thyroid meds and body temp still 97 or high 96's. LLMD not wanting to up thyroid either. so not sure what to do for that.
i did try ginko.. do not recall the exact but is the one recommended..a specific chinease version...anyway made me VERY jittery, twitchy, headache, pressure,etc... body was NOT happy so stopped it.
do take omega 3 supp and zyflamend too.
still no IgG's after 1 yr and NK cells low.. several of em.
just..... blah !!!!!!! oh, and thanx but think i will pass on drinking own first urine...will let someone else play with that one...lol.. not me !!
-------------------- i am not a Dr. any info is only for education, suggestion or to think/research. please do not mis-intuprest as diagnostic or prescriptive, only trying to help. **
dx in 08:lyme, rmsf, bart, babs, and m.pneumonia. Posts: 422 | From TX | Registered: Oct 2008
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TerryK
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Huperzine a improves chronic inflammation and cognitive decline in rats with cerebral hypoperfusion.
Wang J, Zhang HY, Tang XC.
State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Chronic cerebral hypoperfusion has been suggested to contribute to the progression of dementia.
Inflammation and white matter lesion (WML) are involved in the pathologic process. This study investigated whether huperzine A, a natural acetylcholinesterase (AChE) inhibitor, has beneficial effects on long-lasting inflammation as well as cognitive impairment in a rat model of cerebral hypoperfusion and how it plays these roles.
Chronic cerebral hypoperfusion was induced by occlusion of bilateral common carotid arteries (two-vessel occlusion; 2VO). Huperzine A was initially given 150 min after 2VO and daily for 3, 7, 14, and 28 days.
Learning and memory dysfunction as tested by Morris water maze performance was observed in 2VO-operated rats and was significantly improved by huperzine A treatment.
WML and activation staining of immune cells were evaluated by Kl�ver-Barrera (KB) and immunohistochemistry, respectively. Myelin damage and increased immunostains were found in optic tract at all indicated days. Huperzine A treatment significantly ameliorated all these phenomena.
Moreover, huperzine A also suppressed overexpression of the inflammatory factor tumor necrosis factor-alpha (TNF-alpha) and overphosphorylation of JNK and p38 mitogen-activated protein kinases (MAPKs) in a cell model of chronic hypoxia.
Preincubation with mecamylamine (MEC), a nicotinic acetylcholine receptor (nAChR) antagonist, for 30 min before hypoxia notably reversed the effects of huperzine A on TNF-alpha production and MAPKs phosphorylation.
In conclusion, delayed and chronic administration of huperzine A could protect against 2VO-induced cognitive impairment, which might be related to its beneficial effects on WML, and the nAChR-dependent cholinergic anti-inflammation pathway plays an important role. (c) 2009 Wiley-Liss, Inc.
PMID: 19795377 [PubMed - as supplied by publisher]
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TerryK
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posted
Nutr Neurosci. 2009 Aug;12(4):142-8.
Green tea polyphenol (-)-epigallocatechin-3-gallate enhances the inhibitory effect of huperzine A on acetylcholinesterase by increasing the affinity with serum albumin. Zhang L, Cao H, Wen J, Xu M.
Research Institute for Molecular Pharmacology and Therapeutics, Central South University, Changsha, Hunan, People's Republic of China.
The green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) was investigated for its enhancement effect of huperzine A on inhibiting acetylcholinesterase (AChE).
The inhibitory effect of huperzine A on acetylcholinesterase is quite weak in the whole phase. EGCG hardly inhibits the AChE activity within the range 10-300 mg/kg. However, upon addition of EGCG to the huperzine A groups, a remarkably enhanced inhibitory effect was observed. The EGCG also can largely prolong the inhibitory time.
These results indicate that addition of EGCG to huperzine A can reduce the dose of huperzine A required compared with huperzine A alone. The enhancement and complementary effect of EGCG on huperzine A activity may partly be due to the antioxidant property of EGCG.
One of the beneficial effects of green tea is to induce a feeling of relief. It is conceivable that this function may be regulated by EGCG in the central nervous system since EGCG is distributed in the brain after oral administration.
EGCG can be used as an enhanced supplement for huperzine A to treat Alzheimer's disease.
PMID: 19622237 [PubMed - indexed for MEDLINE]
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TerryK
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Clinical use of an herbal-derived compound (Huperzine A) to treat putative complex partial seizures in a dog.
Schneider BM, Dodman NH, Faissler D, Ogata N.
Clinical Sciences Department, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA, USA.
A Bernese mountain dog was diagnosed with complex partial seizures that were supported by electroencephalographic findings. Clinical signs of the problem included "star gazing," fly snapping, licking, vacuous chewing, and ongoing anxiety.
Treatment with Huperzine A, a compound isolated from Chinese club moss with NMDA receptor blocking activity, anticholinesterase activity, and anticonvulsant properties, produced useful suppression of the abnormal behavior for more than months.
A relapse occurred when the dog was treated with tramadol for joint pain and the improvement that had been made was not recaptured with Huperzine A. At this stage, phenobarbital therapy was instituted and the dog improved greatly. The role of Huperzine A in controlling seizures is discussed.
PMID: 19616481 [PubMed - indexed for MEDLINE]
Posts: 6286 | From Oregon | Registered: Jan 2006
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TerryK
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I haven't done a huge amount of searching but not a lot of safety info on huperzine a. Looks to be safe but it is an over the counter supplement so it is considered a food.
The level of safety testing for pharmaceuticals is not required for over the counter supplements so please be careful with this product just like you would with any medication.
Terry I'm not a doctor
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Keebler
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- Pinelady,
If you have the energy, it would be helpful to replace that long link with a tiny URL so that the width of the thread's page goes back to normal?
"Moreover, huperzine A also suppressed overexpression of the inflammatory factor tumor necrosis factor-alpha (TNF-alpha) and overphosphorylation of JNK and p38 mitogen-activated protein kinases (MAPKs) in a cell model of chronic hypoxia."
WOW.
Bb is triggering MAPK(K) and cleaving the phosphates.
Yes phosphatidylserine is really taking a beating. HPA axis...
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Carol in PA
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quote:Originally posted by Keebler: ...it would be helpful to replace that long link with a tiny URL so that the width of the thread's page goes back to normal?
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