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In the grand pantheon of spasticity drugs, it isn’t so, errr, grand.

In fact, your choices are decidedly slim. Shall I adumbrate them? It isn’t a long list, won’t take too long. Here we go:

Tranquilisers. Usually Diazepam (Valium) or Clonazepam. Essentially sleeping pills. The former two have a half-life of around ten hours. This means, obviously, that after ten hours, you’ll still have half the dose still working it’s way through your system.

Tranquilisers are prescribed for the, so called, umbrella effect. That being, on account of their long action of duration, they’ll provide spasticity relief for the best part of the day.

Spasticity relief can be a relative term, because tranquilisers are CNS depressants. They are prescribed for a wide range of conditions. Stress, Aspergers, insomnia, and, of course, our old friend, spasticity.

They depress your Central Nervous System. This will calm you down, likely send you to sleep, say goodbye to any worries, and relax your muscles. The price? Well, obviously, you’ll be tired. Alcohol is a CNS depressant. Plenty of others, all with varying degrees of efficacy.

Baclofen Prescribed (generally) for spasticity.

Lyrica Prescribed, generally for neuropathic pain.

Tizanidine Prescribed for spasticity.

Gabapentin Prescribed for a wide (and getting wider) range of condtions.

What the above drugs have in common is that they do nothing to affect the underlying cause of spasticity. That being, the action messages from your brain aren’t reaching the intended location. More than likely a muscle in your leg(s).

Often, the cause of spasticity is because of some sort of spinal cord damage.

This could be because of chemicals, a physical damage to your spine because of an accident, or, more often in the case of diseases like Adrenomyeloneuropathy and Multiple Sclerosis, demyelination..

The outer surface of the spinal cord is encased in a sheath of a fatty substance called myelin. The action of different diseases can degrade this myelin, causing demyelination.

The inner part of the spine contains cells called axons. It is the job of axons to carry action signals from the brain to the muscles, but because of demyelination, these signals can leak out through the myelin. By the time the signals reach the muscle, they are either severely degraded of next to non existent.

CNS depressants can remedy one symptom of spasticity, that being the tense, painful muscles. So that when the action signal reaches your muscle, the muscle will respond to the signal, moving to a greater extent than if no medicine had been taken.

But CNS depressants don’t address the other cause of the spasticity, the weakened signal that reaches the muscle.

This is where the other class of spasticity drugs comes into play.

Potassium Channel Blockers.

Because of demyelination, the action signals can leak through the potassium channels in the myelin.

Potassium Channel Blockers can help to block these holes in the myelin, thereby allowing the action signals to continue traveling through the axons, to eventually reach the muscle.

The most commonly prescribed Potassium Channel Blocker is 4-Aminopyridine (4-AP).

But, how do potassium channel blockers work?

The science behind 4-Aminopyridine (4-AP) is reassuringly simple. Though with a different list of side effects. These include dizzyness, nausea and a tingling on the skin.

Everything has a price with spasticity. It’s either the symptom,or the drugs. Take your pick.

If you recall the above description about demyelination, the action messages from the brain leak through the holes in the myelin. Potassium channel blockers work to plug the holes in the myelin, thereby enhancing conduction in injured and demyelinated axons.

And, 4-AP works, and works well, albeit with attendant side-effects. It also has a narrow therapeutic range, meaning, the difference between an effective and a toxic dose can be extremely close. Tat said, 5mg seems to be the generally accepted therapeutic dose of 4-Aminopyridine. Any more, in one dose, will produce side effects.

What about other Potassium Channel Blockers?

Other Potassium Channel Blockers have been developed, 3,4-diaminopyridine, N-(4-pyridyl) methyl carbamate, N-(4-pyridyl) ethyl carbamate, N-(4-pyridyl) t-butyl carbamate and 4-AP-3-Me-OH.

We will come to 3,4-diaminopyridine very soon, but for now, let’s take a look at 4-AP-3-Me-OH.

4-AP-3-Me-OH (4-Aminopyridine-3-methanol) was developed at Perdue University.

4-aminopyridine-3-methanol is safer drug than 4-AP, it is also more effective at closing the potassium channels )at least 50 percent more effective), and the effects last for a much longer time than 4-AP.

4-aminopyridine-3-methanol has also has been shown to reduce neuropathic pain to a greater degree than 4-AP.

Whereas 4-AP has a narrow therapeutic range, 4-aminopyridine-3-methanol has been demonstated to have a broader therapeutic dosing range. The minimum effective dose of 4-AP-3-Me-OH can be as low as 10 times less than 4-AP, but it can also be applied at a level that is five times as high.”

This means that the minimum, effective dose of 4-AP-3-Me-OH would be 0.5mg, as opposed to a minimum dose of 5mg for 4-AP.

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4-AP, as a Potassium Channel Blocker, aids the conduction of action messages through the axons to a certain extent, but 4-AP-3-MeOH also restores conduction of injured axons in a manner similar to normal, uninjured uninjured, healthy axons

Nerves transmit signals through a series of rapid electrical pulses, or “action potentials.” For proper nerve function, the time gap between pulses must be as brief as possible. However, 4-AP has been shown to lengthen the gap, or “refractory period,” between pulses. 4-AP-3-MeOH restores function without affecting the refractory period. As a result, the damaged nerves perform more like healthy nerves than those treated with other drug.

Or, to put it simply:

With 4-AP, after an action message reaches the muscle, there is a waiting period (a refractory period) before the next action message can be conducted through the axons. This can make repetitive actions difficult. People can walk better on 4-AP, but they tend to lumber about. Fine motor-skills are difficult.

In 4-AP-3-MeOH-restored axonal conduction, refractory periods are not changed, compared with that of the normal axons. Similarly, those axons rescued by 4-AP-3-MeOH retained the normal ability to conduct repetitive messages.

So, the axons that are rescued by 4-AP-3-MeOH can conduct action messages in a manner that is similar to normal axons and superior to those rescued by 4-AP.

All this translates to 4-AP-3-MeOH being a more effective medicine that conducts allows your spine to conduct signals better, more frequently and at a much lower dose than 4-AP. 4-AP-3-MeOH can also be taken at a much higher dose than 4-AP, with less side effects.

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One of the exciting things about the newer types of Potassium Channel Blockers is that they have been shown to help not just people with spasticity caused by diseases like Multiple Sclerosis, they can also help people with spinal cord injuries caused by accidents.

Accoding to Riyi Shi, a professor in Purdue University’s Department of Basic Medical Sciences, School of Veterinary Medicine, Center for Paralysis Research and Weldon School of Biomedical Engineering “The compound could make it possible to sidestep spinal cord damage by enabling axons to transmit signals as though they were still sheathed in myelin”.

4-AP-3-MeOH isn’t yet approved as a prescription medication yet, but it is available from various compounding pharmacies, and it has been prescribed in various countries, and taken by numerous patients for eight years now.

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