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 for a wide (and getting wider) range of condtions.
Lyrica Prescribed for neuropathic pain
Tizanidine Prescribed for stress and insomnia
Gabapentin Prescribed for neuropathic pain.
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).
The science behind 4-Aminopyridine (4-AP) is reassuringly simple. Though with a different list of side effects to CNS depressants. 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.
But, how do potassium channel blockers work?
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 very well to treat spasticity, albeit with attendant side-effects. It does, though, have a narrow therapeutic range, meaning, the difference between an effective and a toxic dose can be extremely close. This isn’t as dangerous as it may sound, as you long as you stick to the dosing regimen, most people have few problems with 4-AP.
Are you interested in spasticity medication?
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