I don't know, but I do know that my spasticity has increased significantly over the last three months and for some reason it just won't go back to its normal condition: some muscle spasms, but not enough to cause me great difficulties.
I've been on the same medication level for more than three years now, so it have to think something's going on which is causing the spasms. Unfortunately I've had two UTIs over the last three months after going a significant period of time without any. I am one of the ones taking baclofen, dantrolene and 5 mg of diazepam a day. I would like to get off the dantrolene, but I have recently switched doctors (not my idea) and I'm not at all confident in the two doctors I see most of the time. It's going to be difficult, but I'm going to try to get my other doctor back. Quadius On Sat, Sep 26, 2009 at 8:18 AM, <[email protected]> wrote: > THANKS TODD! You are correct. And hope many members here didn't know > that, lol. How many members here forgot about 4-AP? > > Best Wishes > > In a message dated 9/25/2009 9:37:16 P.M. Central Daylight Time, > [email protected] writes: > > OH I should mention that I didn't write the post. I am busy making > marijuana butter with crushed Viagra...lol. > > I don't know what any of this means but.... > > 4-AP works as a potassium channel blocker. Electrophysiologic studies of > demyelinated axons show that augmented potassium currents increase > extracellular potassium ion concentration which decreases action potential > duration and amplitude which may cause conduction failure. Potassium channel > blockade reverses this effect. > > MS patients treated with 4-AP exhibited a response rate of 29.5% to 80%. A > long-term study (32 months) indicated that 80-90% of patients who initially > responded to 4-AP exhibited long-term benefits. Although improving symptoms, > 4-AP does not inhibit progression of MS. > Spinal cord injury patients have also seen improvement with 4-AP therapy. > These improvements include sensory, motor and pulmonary function, with a > decrease in spasticity and pain > > > On Fri, Sep 25, 2009 at 9:31 PM, <[email protected]> wrote: > >> ok smarty pants... what about 4AP? I've always wonder about that drug >> during trials. Anyone know? >> (just kidding Todd) >> Best Wishes >> >> In a message dated 9/25/2009 7:17:16 P.M. Central Daylight Time, >> [email protected] writes: >> >> Just wanted to pass along a forum post...I am trying Tizanidine for the >> first time. >> >> Let me add another perspective from the viewpoint of mechanisms. When you >> mix drugs, it is useful to know the mechanisms by which the drugs act, >> whether they are pushing the same buttons or different buttons on the >> neurons. >> >> Baclofen is what is called a GABA-B receptor agonist. In other words, it >> turns on GABA-B receptors. GABA and glycine are the two major inhibitory >> neurotransmitters of the central nervous system. GABA plays a more important >> role in motor systems and particularly in the spinal cord. GABA presses two >> buttons (receptors) on neurons: the GABA-A and GABA-B receptors. GABA-A >> turns on chloride channels that makes the membrane more negative and reduces >> the excitability of neurons. GABA-B turns on intracellular messengers that >> tell the neurons to activate cellular programs that reduce their >> excitability. >> >> Diazepam is a GABA receptor enhancer. In other words, it enhances the >> effects of GABA. It is called a tranquilizer because it calms people down by >> reducing neuronal excitability. It is also a "muscle relaxant" because it >> reduces the excitability of spinal reflexes. The problem is that diazepam >> has effects on the brain. Two of its most important side effects are >> short-term memory loss and sleepiness. It is also addictive in the sense >> that the brain becomes dependent on it and sudden withdrawal of the drug may >> result in unpleasant hyperexcitability states. >> >> Tizanidine is an alpha-2 adrenergic receptor agonist. It reduces >> excitatory amino acid release by spinal interneurons. It also seems to have >> an anti-nociceptive (anti-pain) and anti-convulsant (anti-seizure) activity. >> It has relatively mild or transient cardiovascular side-effects. While high >> doses may depress the central nervous system, there is sufficient separation >> of its CNS depressive effects and its anti-spasticity activity so that this >> is not usually a problem. Its main side effects are dry mouth, flushing, >> tiredness, and weakness. >> >> Dantrolene is a muscle relaxant that acts directly on the >> excitation-contraction coupling in muscle cells, through the ryanodine >> receptor. It is the specific and high effective treatment of a condition >> called malignant hyperthermia (which results from overactivity of muscle) >> and neuroleptic malignant syndrome (which also causes overactivity of >> muscle) that may occur with a variety of drug (or anesthesia) overdose and >> intoxication. Before baclofen, dantolene was the most popular >> anti-spasticity drug. Today, it is rarely prescribed alone for spasticity >> because its main side-effect is muscle weakness. Dantrolene should not be >> used in people who have pre-existing liver disease, compromised lung >> function, severe cardiovascular impairment, or weak muscles whose function >> is crucial for activity of daily living. >> >> Thus, when you take diazepam along with baclofen, both drugs press the >> same GABA button, enhancing each other's side-effects. Tizanidine acts on a >> different mechanism, directly affecting spasticity by reducing glutamate >> neurotransmitter release and excitability of spinal circuits. Dantrolene >> reduces spasticity by inhibiting muscle, which is not desirable particularly >> in people cervical spinal cord injury with compromised lung function and >> weak hand muscles but it might be useful for people with paraplegia for whom >> baclofen plus tizanidine are insufficient to control spasticity. >> >> >> Todd C6 >> >> >
