I am continuing to worsen and am starting to think my only hope is surgery. I had botox a few times but not with much success. Does anyone know why botox doesn't work? Does it not do the same thing as LIS, it's just that LIS is more localized? I had bad urgency with the botox and am really afraid the LIS would do that too. Is it less likely to do that because it IS more localized? Thanks for any input

Most know my opinion, Botox has higher success rates when given in large amounts, placed properly. I also believe that other complications make it less successful, IBS, chronic constipation, multiple fissures etc. Botox is supposed to replicate the effect of LIS, but for a limited time. If people have adverse effects on Botox I would assume it effects the healing process and then the botox wears off. With LIS even if there are complications after surgery you have still weakened the sphincter and healing can occur. Just an opinion, not a doctor.

Bear in mind that repeated botox injections can lead to permanent paralysis.
As Apes says, the skill of the surgeon is absolutely crucial to the success of botox.

Scientist, where have you heard that repeated botox can have a permanent effect? I have been looking for literature on the subject...

Hmm, well, of course I go looking and I can't find what I thought I saw a couple of weeks ago. So I may have to eat my words.

It's interesting. If you remove a nerve, or inactivate it long term, the muscle will atrophy (well known). So paralysis was not the right word to use - sorry. Atrophy is more appropriate. I would expect loss of muscle function due to atrophy, especially with repeated botox. However, it's possible that as the botox wears off, the recovery of nerve function is enough to re-invigorate the muscle.

I did find one paper http://www.ncbi.nlm.nih.gov/pubmed/25130293
that says that patients who had repeated botox found that over time, the effects started sooner and lasted longer. The changes were not great though. And it was not in the anus.

The other thing about the internal anal sphincter is that much of its tone does not require input from the nerves. It is "myogenic", meaning that it maintains contraction without neural input. That being the case, botox could never have a huge effect on anal tone (just as well - you don't want the internal anal sphincter to relax completely).
So again, perhaps the myogenic properties of the sphincter prevent it from atrophying when paralysed by botox.
I got the info about myogenic properties from this paper, which is very technical.
file:///C:/Documents%20and%20Settings/Owner/My%20Documents/Downloads/15836455.pdf

For people who are having botox for pelvic floor dysfunction, I don't know what kind of muscles are involved, but if they are not myogenic muscles, I do think that repeated botox could lead to atrophy. Of course in some cases that's what you want - the muscles are the problem. In other cases, maybe you don't want it.

It's all rather difficult to understand. For example, botox could technically inactivate the nerves that cause the sphincter to relax, as well as the ones that cause it to tighten. I truly doubt the doctor can inject one kind of nerve vs the other.

Sorry if this is rambling. I am a neuroscientist, but I'm quite a bit out of my field here. I work on fruit flies, and their nervous systems are somewhat different.

Very cool thank you. I am interested because I had 370 units of botox injected into my IAS in less than a year, in addition to having a LIS, and I was very concerned that the botox did some long term damage...Everything I've read says that botox's effects are temporary, but most of the literature is on people's faces, where muscle tone isn't so crucially important.

Thanks Apes and Scientist.

Wow Scientist! Thanks for the input. That is so interesting. In all my research and education I have sadly not heard of a myogenic muscle contraction. Well, maybe that explains when the botox doesn't work if used in smaller doses. I have never got more than 25 units at once due to my weak pelvic floor, and he wanted to give me 50 units(I had a lot of urgency at 25 units)! Yes, I do believe I have an atrophied pelvic floor and have to be very careful how much botox I get as a result. What is interesting is I have found many studies in which people healed with only 5-10 units of botox...that is a BIG difference!

Do you think then that for one to optimize their success in treatment that those who get botox should also use one of the ointments as well. That way both methods of muscle contraction are addressed?

"botox could technically inactivate the nerves that cause the sphincter to relax, as well as the ones that cause it to tighten. I truly doubt the doctor can inject one kind of nerve vs the other. "

Yes! I came across this too and I swear that my butthole always feels tighter when I get botox into the internal sphincter! Like it is hard to the touch and really burning right now! I wonder why I react this way...It made me afraid that LIS would do the same but based on this info it in fact may not. I also think I finally understand why botox seems to flare hemmies up. It's probably because the smooth muscle in the walls of blood vessels also relax and the hemmies can then swell easier. Does that make sense?

Sorry for the ramble!

Hey Scientist, in this article (http://onlinelibrary.wiley.com/doi/10.1 ... 0995.x/pdf) it states that nitric oxide donation is the main mechanism of myogenic internal sphincter muscle relaxation.

"Nitric oxide donors.The discovery that nitric oxide is the principal non-adrenergic non-cholinergic inhibitory transmitter mediating relaxation in the internal anal sphincter led on to research into exogenous organic nitrates as a source of nitric oxide to pharmacologically manipulate the internal anal sphincter."

It also states that, "Calcium channel antagonists. Calcium is known to be important for both agonist-induced contraction of the internal anal sphincter and myogenic tone. Calcium channel antagonists have therefore been used in an attempt to modulate resting anal pressure. "

Do you think this means that the calcium channel blockers (nifedipine and diltiazem) work on both mechanisms and that they would be better that Nitro because they can relax the muscle by both mechanisms? This is so confusing.

Yes, msimon, I did see that, and also remember reading something similar in a different article several months ago.
I agree that nitro and Ca channel blockers should therefore be more effective than botox.......what I find confusing is that the IAS doesn't completely relax when Ca channels are blocked. I think it could be a question of how well the drugs are absorbed?

So I have read more, and found that botox only blocks stimulatory motorneurons.
The more I read, the more I realise how little I know. Sigh.

This may be interesting: (from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856357/ )

Botulinum toxin, also called “miracle poison,” is one of the most poisonous biological substances known.[1] It is a neurotoxin produced by the bacterium Clostridium botulinum, an anaerobic, gram-positive, spore-forming rod commonly found on plants, in soil, water and the intestinal tracts of animals. Scott[2] first demonstrated the effectiveness of botulinum toxin type A for the management of strabismus in humans. Subsequently, botulinum toxin was approved for the treatment of numerous disorders of spasticiy[1] and a host of other conditions. Currently it is used in almost every sub-specialty of medicine. In 2002, the FDA approved the use of Botox®
(Botulinum toxin-A) for the cosmetic purpose of temporarily reducing glabeller forehead frown lines.
Biochemical aspects
C. botulinum elaborates eight antigenically distinguishable exotoxins (A, B, C1
, C2, D, E, F and G). Type A is the most potent toxin, followed by types B and F toxin. Types A, B and E are commonly associated with systemic botulism in humans.[3] All botulinum neurotoxins are produced as relatively inactive, single polypeptide chains with a molecular mass of about 150 kDa with a high degree of amino acid sequence homology among the toxin types. The polypeptide chain consists of a heavy (H) chain and a light (L) chain of roughly 100 and 50 kDa respectively, linked by a disulfide bond.[4] The botulinum toxin neurotoxin complex is also associated with various other nontoxic proteins, which may also have hemagglutinating properties.[5]
How botulinum toxin works
All the serotypes interfere with neural transmission by blocking the release of acetylcholine, which is the principal neurotransmitter at the neuromuscular junction. Intramuscular administration of botulinum toxin acts at the neuromuscular junction to cause muscle paralysis by inhibiting the release of acetylcholine from presynaptic motor neurons.[6] Botulinum toxins act at four different sites in the body: The neuromuscular junction, autonomic ganglia, postganglionic parasympathetic nerve endings and postganglionic sympathetic nerve endings that release acetylcholine.[5] The heavy (H) chain of the toxin binds selectively and irreversibly to high affinity receptors at the presynaptic surface of cholinergic neurones, and the toxin-receptor complex is taken up into the cell by endocytosis. The disulphide bond between the two chains is cleaved and the toxin escapes into the cytoplasm. The light (L) chain interact with different proteins (synaptosomal associated protein (SNAP) 25, vesicle associated membrane protein and syntaxin) in the nerve terminals to prevent fusion of acetylcholine vesicles with the cell membrane.[5,7] The peak of the paralytic effect occurs four to seven days after injection. Doses of all commercially available botulinum toxins are expressed in terms of units of biologic activity. One unit of botulinum toxin corresponds to the calculated median intraperitoneal lethal dose (LD50) in female Swiss-Webster mice.[8] The affected nerve terminals do not degenerate, but the blockage of neurotransmitter release is irreversible. Function can be recovered by the sprouting of nerve terminals and formation of new synaptic contacts; this usually takes two to three months.
Botulinum toxin induces weakness of striated muscles by inhibiting transmission of alpha motor neurones at the neuromuscular junction. This has led to its use in conditions with muscular overactivity, such as dystonia. Transmission is also inhibited at gamma neurones in muscle spindles, which may alter reflex overactivity.[9] The toxin also inhibits release of acetylcholine in all parasympathetic and cholinergic postganglionic sympathetic neurons. This has generated interest in its use as a treatment for overactive smooth muscles (for example, in achalasia) or abnormal activity of glands (for example, hyperhidrosis).[1]
The toxin requires 24-72 hours to take effect, reflecting the time necessary to disrupt the synaptosomal process. In very rare circumstances, some individuals may require as many as five days for the full effect to be observed. Peaking at about 10 days, the effect of botulinum toxin lasts nearly 8-12 weeks.