4-AP, Symptom relief, personal experience. Wow!

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4-AP, Symptom relief, personal experience. Wow!

Postby CureOrBust » Fri Feb 02, 2007 8:56 pm

Hi all, just wanted to let people know about this stuff. I know I would of wanted to know about this earlier.

A few months ago I came accross the study Acordia are doing on a substance called 4-Aminopyridine (ie Fampradine, 4-AP). I followed some threads here, and found that a few people are actually getting it compounded, now. I thought it wouldnt be available

Anyway, I did more research, and eventually found out that the place that compounds my LDN, could also do 4-AP. So I got my GP to give me a script, and got the pills (5mg x 30, dosage is 30-40mg/day ie 6-8 capsules a day).

On the first day I took a single 5mg tablet just to check I didnt have any adverse reaction to it (after all, it is bird poison). The next day I took around 30mg spread over the day in 5mg doses (yeah, I know your suppose to build up over a week).

Anyway, on that second day, by the time I was just about to go to bed, the clonus in my knees had faded about 50-80%! It was a definite improvement. Thats the best effect I have had, but I do still notice that my clonus is definitely reduced while on this medication (say 20-70%).

Its a little wierd in that the results are not consistent. Additionally, it supposedly only has a plasma half life of 4hrs, but Its not till the end of the day that I notice the most benefits. Which fadde somewhat over the 8hrs I am in bed; but still better than when I take none the day before.

For those in Sydney, the pharmacy is fairly famous for LDN and also compunds prokarin. It just cost me $65AUD for 100x 10mg capsules. You can PM me to get more details of their location.

It really feels like a tiny bit of a holiday from some MS symptoms. But I guess anyone who would want to consider this, would be someone comfortable with chemical relief.
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Postby marcstck » Fri Feb 02, 2007 11:38 pm

I too take 4-AP, and do notice that it helps increase my limb strength. The effects, for me, are not overly dramatic, but even subtle help is welcome. Be careful about the dosage though, as my understanding is that 40 mg is the absolute maximum you can take without running the risk of seizures. Seizures are fairly common at doses above that. Also, you should be ramping up to the maximum dosage, but since you jumped ahead anyway I guess there was no harm done. Do not exceed the 40 mg dosage, as the side effects can be very harmful. As you mentioned, the industrial use for this drug is as an extremely effective aviary poison...
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Postby Brainteaser » Wed May 16, 2007 11:18 pm

I've been using 4ap at different times, commencing about 5 years ago. I find it helps with spasticity. Lately I've been taking a 10mg cap in the mornings and maybe another late afternoon, if I need it.

Recently I was talking to a friend in the US who also has used it but decided to stop as he has learned it adversely affects remyelination. I've looked around the web but can't see anything to support such concerns.

I know COB went 'ape-droppings' about the positive effects of 4ap a few months back, so I'd be interested to learn if he's still on it or stopped for this or another reason...Thanks.

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Re: 4ap

Postby CureOrBust » Mon May 21, 2007 6:02 am

Brainteaser wrote:Recently I was talking to a friend in the US who also has used it but decided to stop as he has learned it adversely affects remyelination. I've looked around the web but can't see anything to support such concerns.
Please if you can.

Voltage-gated potassium channels in multiple sclerosis: Overview and new implications for treatment of central nervous system inflammation and degeneration, pg. 111

In multiple sclerosis (MS), various immune cells are mistakenly triggered to orchestrate an attack against the myelin wrapping on nerve fibers, which leads to impaired nerve function. This review discusses how drugs that block proteins known as potassium channels in the outer membranes of T cells, macrophages, microglia, and dendritic cells may help regulate the detrimental inflammatory immune response underlying MS. Two potassium channels are primary potential therapeutic targets: the Kv1.3 potassium channel that is expressed in each of the fully activated immune cells and the Kv1.5 channel that appears only in activated microglia and dendritic cells. Research in this field focuses on the role of immune cell potassium channels in inflammation and on better drugs for blocking these channels, which will lead to new or improved clinical treatments for MS patients

Conduction studies indicate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduction. However, during remyelination, 4-AP profoundly increased both compound action potential amplitude and duration. The level of this effect matched closely the nodal presence of these voltage-dependent K+ channels. Our results suggest that K+ channels may have a significant effect on conduction during remyelination and that Schwann cells are important in K+ channel redistribution and clustering.
http://www.jneurosci.org/cgi/content/abstract/18/1/36 HUH?

Pharmacologic blockade of these potassium channels can increase the safety factor for conduction in demyelinated axons. Restoration of conduction in demyelinated axons, so that action potentials can traverse the zone without myelin, appears to underly clinical remissions in patients with multiple sclerosis and may occur in some patients with spinal cord injury.

In contrast to the demyelinated plaques, all remyelinated lesions are characterized by the detection of aggregates of Nav channels, paranodin/Caspr, Kv channels and Caspr2. Our data suggest that these aggregates precede remyelination, and that Nav channel aggregation is the initial event, followed by aggregation of paranodal and then juxtaparanodal axonal proteins.


Does the following one have a sentence that ends a little too quickly.
<shortened url>

and this one is pretty clear...
The adult CNS has the capacity to remyelinate following metabolic, toxic and autoimmune demyelinating insults. In cuprizone-induced demyelination, spontaneous remyelination occurs after the cessation of cuprizone diet. We used the cuprizone model to investigate the role of glial K+ channels in oligodendroglial (OLG) regeneration and remyelination in vivo. We found that treatment with 4-aminopyridine (4-AP), a broad-spectrum K+ channel antagonist, results in: (1) decreased number of oligodendroglial progenitors (OP) and OLGs; (2) diminished astrogliosis; and (3) decreased remyelination in the corpus callosum based on the immunoreactivity to myelin basic protein (MBP), Rip monoclonal antibody, and by electron microscopy. Our findings support the concept that glial K+ channels play an important role during OLG regeneration and remyelination, a crucial factor to be considered during the development of therapeutic strategies to facilitate recovery in demyelinating diseases and spinal cord injury. © 2004 Wiley-Liss, Inc.

<shortened url>

No smoking guns here (unless your on a copper diet), i think? I found these by using "potassium channels Multiple sclerosis remyelination" in google. there were more.

The way I look at it was that I would see how I go. I thought it could go one of two ways.
1. The leaking Potasium channels are what trigger remylination, and hence 4-AP would hinder remylination
2. The leaking Potassium channels mean that an electrical charge didnt make it down the full length of the nerve fibre, and hence the end of the axon slowly died.

I felt better about believing option 2.

I found it hard not to go without it when I strarted, and I am pretty certain that I have improved since being on it (while off it ... if you know what I mean...)

So for now, its a win win for me, and I will continue till I recover more, or more is known.
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