What is the best surgery for trigeminal neuralgia?
My mom is 73 year old and diagnosed with trigeminal neuralgia. She's done with al kinds of pain medication and is now considering surgery. Any suggestion?
It depends on what is pressing on the nerve or where on the nerve the problem is. SHe needs to see a Neuro Surgeon. (+ info
Trigeminal neuralgia: can it involve a constant pain instead of a fleeting pain?
Classic trigeminal neuralgia involves a fleeting pain that is often triggered by an external stimulus. The cause is often found to be a blood vessel pressing on a nerve. Can that same situation (a blood vessel pressing on a nerve) cause a constant pain that is not triggered by an external stimulus? If so, is the blood vessel always apparent on an MRI? Or might an MRI miss it? Thanks for all replies.
Yes, TN can cause constant pain. When it does, it's usually classified as "atypical trigeminal neuralgia."
If a blood vessel is pressing on the nerve, an MRI ordered to focus in tightly on the trigeminal nerve ought to catch it, but sometimes the cause of trigeminal neuralgia isn't as readily apparent as a blood vessel pressing on a nerve. Sometimes (as in my case) there's no visible cause at all to explain why the nerve keeps firing.
There's a useful breakdown of the various types of TN and related facial pain problems here:
(Although bear in mind while reading it that this website is focused on MVD, so it tends to overstate both the probability of a blood vessel pushing on a nerve as the evident cause *and* the efficacy of the MVD operation as a cure for TN. Nonetheless, if you can overlook that, it's still a pretty decent breakdown.) (+ info
Benefits available after losing my job due to neuralgia?
I have been offered the option to be dismissed from work due to ill health,I am a community enabler and my job involves getting out and about supporting adults with learning disabilities.I cannot predict my attacks of neuralgia.
Before you take up this offer you need to check out the benefits available either via the Citizens Advice Bureau or the Job Centre which now covers Works and Pensions and Benefit etc.
They no longer offer much without a medical assessment and they assess what you can do rather than what you cannot do and although you cannot predict the attacks they will assess you on the in between times.
Many of the benefits do not apply with this sort of condition as in between times you are able to manage fairly normally. I suffer from neuropathic pain which despite 'waving' in (a term you will understand) and causing major issues I can when it is just there walk and function normally. I seem to fall between all the benefit categories and just cannot understand how other people manage to get them all.
Just be very careful before you jump ship that you have all the facts and figures in hand and know where you stand and what you may be entitled to in the long term. Also some are affected by existing household income and savings.
Also check with the CAB as what might sound like a good offer may be them side stepping some employment issues with regard to employing people with disabilities. If they are a large enough employer they have an obligation to employ x amount of people and to consider and help people with sickness issue.
Spend a couple of weeks really checking your facts for your and your families sake as the benefit band wagon just seems to be so very hard to get on if you have genuine odd needs. (+ info
Can neuralgia be flared up by the changing of the seasons?
My neighbor suffers from neuralgia and it seems that she is often hit with it in the spring, all winter she has no problem all winter
I don't know what kind she has but I suppose it could. Some types, such as trigeminal neuralgia ,can flare up from almost anything. A change in pressure, temperature, a light touch... (+ info
Can a toothache cause Trigeminal Neuralgia?
I know Trigeminal Neuralgia can cause a "toothache", but can a toothache cause a trigeminal neuralgia flare up in someone predisposed to them?
Please cite sources.
Yes it is possible especially those teeth supplied by the trigeminal nerve (+ info
Can Post-Herpetic Neuralgia be connected to a badly broken wisdom tooth?
I have a very badly broken wisdom tooth. The last week it has been excruiatingly painful, and now think me taking too many painkillers to numb pain.
(Am going to dentist on monday so hopefully sorted out)
Is this just the tooth giving me hell or could it be Post-herpetic Neuralgia?
Wow sa_2006 great answer.
Pain is an unpleasant sensation that occurs as a result of injury to the body or as a manifestation of a diseased state. Pain can be classified in many ways. For example, pain can be classified based on its duration (acute or chronic pain) and by the underlying cause (nociceptive or neuropathic).
 Nociceptive pain results directly from local tissue injury whereas neuropathic pain follows nerve injury. Key features of nociceptive pain are that it can be experienced as sharp, dull, or aching, and that there may be radiation of the pain, or the perception of pain in a different area than where the nerves are being stimulated. For example, when a person experiences a heart attack, pain may radiate from the chest down the arms or up the neck, even though there is no tissue damage in these areas. Examples of nociceptive pain include pain from surgical incisions, bone pain from fractures or metastatic cancer, and pain from joint diseases such as osteoarthritis and rheumatoid arthritis.
 Neuropathic pain occurs as a result of damage to, or dysfunction, of the nervous system. Neuropathic pain is frequently described as burning, tingling or having an electrical shock-like feeling. Another key feature of this type of pain is its paradoxical occurrence upon stimulation that otherwise would not be expected to cause pain. For example, a condition called trigeminal neuralgia may cause patients to feel extreme pain upon a light touch on the cheek. Examples of neuropathic pain include the pain resulting from diabetes and HIV infection, and postherpetic neuralgia, commonly called zoster, which is a painful condition caused by the chicken pox virus long after the initial infection has healed, in many cases years later. Neuropathic pain frequently coexists or follows nociceptive pain, as for example when a patient that has had a surgical procedure continues to experience pain long after the wound has healed.
 Pain is a worldwide problem with serious health and economic consequences. The medical effort to treat pain, known as pain management, addresses a large and under-served market. According to IMS Health, the worldwide prescription market for pain drugs totaled over $23 billion in 2003, of which nearly $18 billion was spent in the United States. For example, in the United States medical economists estimate that pain results in approximately $100 billion of costs annually, as reported by the National Institutes of Health (NIH). Pain in the hospital is associated with increased length of stay, longer recovery times and poorer patient outcomes, all of which have health care quality and cost implications. Approximately 40 million Americans are unable to find relief from their pain, according to the NIH and more than 30 million Americans suffer chronic pain for which they visit a doctor.
 Drugs are the principal means of treating pain. The pain management market is anticipated to grow at a compounded annual growth rate of 10% through 2010 due to a number of factors, including a rapidly aging population with an increasing need and desire to address pain-related ailments; longer survival times for patients with painful chronic conditions, such as cancer and AIDS; patients' increased demand for effective pain relief; and increasing recognition of the therapeutic and economic benefits of effective pain management by physicians, health care providers and payers.
 Drugs that treat pain are referred to as analgesics. The type of analgesic selected for treatment depends upon the severity of the pain. For mild pain, the type of pain associated with many headaches or joint pain, weak analgesics such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and Celebrex.RTM. (Pfizer) are used. For moderate pain, the type of pain associated with wisdom tooth extraction, other minor surgery and some arthritis pain, NSAIDs, weak opioids such as codeine or short-acting formulations of strong opioids such as Percocet.RTM. (Endo) may be used. Severe pain, which may occur following major surgery, advanced arthritis or cancer, requires strong opioids such as morphine, oxycodone, hydrocodone or fentanyl.
 Despite widespread clinical use of drugs for pain, pain management remains less than optimal due to a variety of factors including: i) insufficient efficacy (NSAIDs are effective in treating only minor pain. Narcotics, the current standard of care for severe nociceptive pain, reduce pain less than 50% in most situations. Neuropathic pain is poorly treated by all existing analgesics); ii) side effects (NSAIDs often cause gastrointestinal ulcers, and more than 20,000 patients die each year from gastrointestinal bleeding induced by NSAIDs. One of the COX 2-selective NSAIDs, Vioxx.RTM. (Merck), has been shown to cause increased risk of heart attacks and possibly stroke. Use of narcotics is associated with nausea and vomiting in most patients. High-dose narcotics cause sedation and may also cause respiratory depression, or a decreased ability to breathe spontaneously. Narcotics used chronically can cause severe constipation that leads many patients to stop using them, and narcotics may sometimes cause severe itching. All of the drugs used to treat neuropathic pain frequently cause problems with coordination and sedation); iii) frequent dosing (Drugs used to treat neuropathic pain require frequent dosing that makes their use inconvenient, often leading to reduced patient compliance); iv) physical dependence (Narcotics, when used chronically, can cause physical dependence. Fear of physical dependence often influences clinicians to prescribe less than adequate doses of narcotic analgesics. Similar fears lead many patients to refuse narcotic analgesics); and v) diversion potential (Narcotics are often used by drug abusers, leading to considerable potential for diversion of legitimate narcotic analgesics for illicit uses. In fact, many pharmacies have removed high-dose narcotic analgesics from their inventories because of the risk of theft).
 Pain management is of particular importance for treating severe post-surgical pain. There are over three million surgeries performed in the United States each year that result in severe post-surgical pain. Morphine and related narcotics, which are presently the standard of care for acute post-surgical pain, have serious side effects including respiratory depression, nausea, itching and sedation. In addition, many currently marketed drugs that treat pain require frequent dosing, which makes usage less convenient for patients.
 As a result of the shortcomings of existing drugs that treat pain, capsaicin has become a front-runner of research and development for it use in treating pain.
 Capsaicin, a pungent substance derived from the plants of the solanaceae family (hot chili peppers) has long been used as an experimental tool because of its selective action on the small diameter afferent nerve fibers C-fibers and A-delta fibers that are believed to signal pain. From studies in animals, capsaicin appears to trigger C-fiber membrane depolarization by opening cation channels permeable to calcium and sodium. Recently one of the receptors for capsaicin effects has been cloned. Capsaicin can be readily obtained by ethanol extraction of the fruit of capsicum frutescens or capsicum annum. Capsaicin is known by the chemical name N-(4-hydroxy-3-methoxybenzyl)-8-methylnon-trans-6-enamide. Capsaicin is practically insoluble in water, but freely soluble in alcohol, ether, benzene and chloroform. Therapeutically capsaicin has been used as a topical analgesic. Capsaicin is available commercially as Capsaicin USP from Steve Weiss & Co., 315 East 68.sup.th Street, New York, N.Y. 10021 and can also be prepared synthetically by published methods. See Michalska et al., "Synthesis and Local Anesthetic Properties of N-substituted 3,4-Dimethoxyphenethylamine Derivatives", Diss Pharm. Pharmacol., Vol. 24, (1972), pp. 17-25, (Chem. Abs. 77: 19271a), discloses N-pentyl and N-hexyl 3,4-dimethoxyphenylacetamides which are reduced to the respective secondary amines.
 Capsaicin is listed in the pharmacopoeias of the United Kingdom, Australia, Belgium, Egypt, Germany, Hungary, Italy, Japan, Poland, Portugal, Spain, and Switzerland and has previously been listed in the United States Pharmacopoeia and the National Formulary. The FDA proposed monographs on analgesic drug products for over-the-counter (OTC) human use. These include capsaicin and capsicum preparations that are regarded as safe and effective for use as OTC external analgesics. Capsaicin is the only chemical entity of Capsicum recognized by the FDA. Capsaicin (USP) contains not less than 110% total capsaicinoids which typically corresponds to 63% pure capsaicin. USP capsaicin is trans-capsaicin (55-60%) and also contains the precursors dihydrocapsaicin and nordihydrocapsaicin.
 Capsaicin mediated effects include: (i) activation of nociceptors in peripheral tissues; (ii) eventual desensitization of peripheral nociceptors to one or more stimulus modalities; (iii) cellular degeneration of sensitive A-delta and C-fiber afferents; (iv) activation of neuronal proteases; (v) blockage of axonal transport; and (vi) the decrease of the absolute number of nociceptive fibers without affecting the number of non-nociceptive fibers.
 Capsaicin works to relieve pain by causing a localized degradation of the C neuron endings, and it is the only analgesic known to relieve pain by this mechanism. The activity of capsaicin results from its binding to, and activating, an ion channel called vanilloid receptor 1, or VR1. Under normal circumstances, when the VR1 ion channel is activated it opens for a short time, causing the C neurons to transmit a pain signal toward the brain. When capsaicin binds to, and activates VR1, it causes a series of events within the cell that degrade the pain-sensing endings, or terminals of the C neuron, thereby preventing the neuron from transmitting pain signals.
 The effects of capsaicin are confined exclusively to the region of application because of low distribution to other areas of the body after capsaicin is administered. For example, after injection into a joint space or after application in a surgical procedure to the cut surfaces of skin, muscle and bone, capsaicin enters the blood slowly by diffusion from its site of initial application. Thereafter, capsaicin is highly metabolized, or broken down, by the liver into various inactive compounds, none of which retain any of the analgesic properties of capsaicin. As a consequence, capsaicin does not usually act at sites in the body distant from its initial application, nor is the body exposed to any derivatives of capsaicin that could act in a similar manner. By contrast, opioids and many other analgesics must be given by mouth or by intravenous injection, thereby subjecting the patient to circulation of high concentrations of drug. These high circulating concentrations may exert undesirable side effects by acting on parts of the body unrelated to pain perception. For example, opioids may cause constipation when used chronically. Opioids also may cause alteration of mood, and alertness, and can cause patients to feel drowsy, euphoric, or sleepy. These effects, when experienced by patients in the hospital, tend to increase rehabilitation time because patients are often sedated and therefore unable to begin the recovery process.
 Humans have long been exposed to dietary sources of capsaicin-containing spices and to topical preparations used for a variety of medical indications. This vast experience has not revealed significant or lasting adverse effects of capsaicin exposure. The recent determination of potential therapeutic effects of capsaicin on unmyelinated sensory afferent nerve fibers require diligent consideration of this compound for further pharmaceutical development.
 Because of the ability of capsaicin to desensitize nociceptors in peripheral tissues, its potential analgesic effects have also been assessed in various clinical trials. However, since the application of capsaicin itself frequently causes burning pain and hyperalgesia apart from the neuropathic pain being treated, patient compliance has been poor and the drop out rates during clinical trials have exceeded fifty percent. The spontaneous burning pain and hyperalgesia are believed to be due to intense activation and temporary sensitization of the peripheral nociceptors at the site of capsaicin application. This activation and sensitization occur prior to the desensitization phase. The activation phase could be a barrier to use of capsaicin because of the pain produced.
 Prior publications describe topical administration of capsaicin for the treatment of various conditions. For example, U.S. Pat. No. 4,997,853 (Bernstein) describes methods and compositions utilizing capsaicin as an external analgesic. U.S. Pat. No. 5,063,060 (Bernstein) describes compositions and methods for treating painful, inflammatory or allergic disorders. U.S. Pat. No. 5,178,879 (Adekunle, et al.) describes methods for preparing a non-greasy capsaicin gel for topical administration for the treatment of pain. U.S. Pat. No. 5,296,225 (Adekunle, et al.) describes indirect methods of treating orofacial pain with topical capsaicin. U.S. Pat. No. 5,665,378 (Davis, et al.) describes transdermal therapeutic formulations comprising capsaicin, a nonsteroidal anti-inflammatory agent and pamabrom for the treatment of pain. U.S. Pat. No. 6,248,788 (Robbins, et al.) describes administration of 7.5% capsaicin cream in combination with marcaine epidural injections in patients suffering from long-term persistent foot pain. U.S. Pat. No. 6,239,180 (Robbins) describes combining capsaicin loaded patches with local anesthesia to treat peripheral neuropathy. The use of topical capsaicin has also been described in the art to treat conditions as diverse as post mastectomy pain syndrome (Watson and Evans, Pain 51: 375-79 (1992)); painful diabetic neuropathy (Tandan et al., Diabetes Care 15: 8-13 (1992)); The Capsaicin Study Group, Arch Intern Med 151: 2225-9 (1991); post-herpetic neuralgia (Watson et al., Pain 33: 333-40 (1988)), Watson et al., Clin. Ther. 15: 510-26 (1993); Bernstein et al., J. Am Acad Dermatol 21: 265-70 (1989) and pain in Guillian-Barre syndrome (Morganlander et al., Annals of Neurology 29:199 (1990)). Capsaicin has also been used in the treatment of osteoarthritis (Deal et al., Clin Ther 13: 383-95 (1991); McCarthy and McCarthy, J. Rheumatol 19: 604-7 (1992); Altman et al., Seminars in Arthritis and Rheumatism 23: 25-33 (1994).
 Capsaicin is currently marketed for topical administration in the form of over-the-counter, low dose, non-sterile creams and patches, which tend to be poorly absorbed. There are more than thirty brands of creams and patches, including Capzasin-P.RTM. (Chattem) and Zostrix.RTM. (Rodlen Laboratories). These formulations are generally crude preparations of capsaicin that may contain other chemical entities. These over-the-counter preparations can be purchased widely without a prescription and are used topically by consumers to relieve pain in conditions such as osteoarthritis, shingles (herpes zoster), psoriasis and diabetic neuropathy.
 It would therefore be advantageous to provide a topical capsaicinoid gel formulation and methods of use thereof that would be useful in different clinical settings as compared with current over-the-counter and prescription products. Specifically, it would be advantageous to provide a topical capsaicinoid gel formulation for use by physicians in the surgical setting prior to wound closure, e.g., in bunion removal surgery, hernia repair and other surgeries, by orthopedic surgeons and other physicians for the treatment of osteoarthritic knee joint disease and tendonitis, and for certain forms of localized neuropathic pain that are not amenable to treatment with currently marketed topical preparations. (+ info
Does anyone have Neuralgia or Trigeminal Neuralgia and what pain relief and medication are you taking?
Hi, I have Trigeminal Neuralgia and am not fining my pain relief effective or my medication but particularly pain relief i am taking up to 450mg of Codeine a day and Tramadol (not at the same time). It is not even touching the pain! Any advise from others who have this or from professionals who have come across this sort of problem? Any advise at all would be welcome even if it seems really obvious! Thanks, C x
Hi. I'm on Tegretol right now for my TN, and I also have oxycodone for breakthrough pain. The Tegretol isn't working for me at the moment, so I find I'm taking far more oxycodone that I'd like. I'm not in a very good place right now, pain-wise. I have an appointment with my neurologist coming up, but I'm sort of dreading it. I suspect he's going to want to titrate my dosage of Tegretol upwards, and I'm already having a really hard time with the side-effects. I think that it may be time for us to try a different anti-convulsant, but if we do that, then I'm going to need a lot more pain-killers to help me through the transition period, and even with that help, it's still going to be pretty awful.
Are you on an anti-convulsant, like Tegretol, neurontin, or Lyrica? They've only been partially successful for me, but I know they've helped a lot of TN sufferers to live very nearly pain-free. If the one you're on isn't working for you, it may be time to try another and see if it does a better job. There are quite a few of them to choose from, and everybody seems to react differently to them, so it's definitely worth checking to see if another drug might be more effective for you.
Pain-killers usually don't work on neuralgia nearly as well as they do on, for example, post-operative pain or muscle pain. For me, they don't stop the pain altogether; they just knock it down a few notches on the pain chart. But those few notches can make such a huge difference! I'm sorry that they're not even doing that much for you.
Have you been to see a pain management specialist, or gone to a pain management clinic? If not, I very much recommend it. They're experienced in dealing with these problems, and might be able to find a pain management regime that works better for you.
ETA: A good place to talk to lots of other people who suffer from this monstrous problem are the TNA Forums here:
You have to sign up first, but it doesn't cost anything and they won't spam you. The people there are friendly, and even just lurking there can make you feel a lot less alone. It did for me, anyway. (+ info
What caused my trigeminal neuralgia?
I have trigeminal neuralgia, an agonising condition involving pressure on a nerve in my face. I am on epilepsy drugs but am tired and forgetful and still in pain. I really feel my life, which until last year was perfectly happy, isn't worth living. I have no idea why I suddenly got this. I am only 25. It first occured at quite a stressful time. I have also had root canal treatment on the same side of my face. Of course the dentist denies all involvement, but I can't help thinking this could have triggered it. Any ideas? Or remedies?
My mother has suffered from this on and off over the past few years, and I wouldn't wish it on my worst enemy. So I feel really sorry for you. She has had some really effective tablets. I'll find out what they are, but when she was referred to see a consultant, he gave her an injection which gave immediate relief and seemed to have quite a lasting effect. She was also told that if the pain got unbearable again, she could phone up and have another injection. It's worth asking about this, and seeing if you could have the same back up for any future attacks. Good luck. (+ info
What is the success rate of motor cortex stimulation when a person has trigeminal neuralgia?
I'm just wondering the success rate of it, and any other information about it.
It would be very difficult to determine a success rate for an individual person. I have included several sites that might be some help to you.
Good luck with everything.pp (+ info
What causes trigeminal neuralgia? What are the things that triggers the pain? Any suggestion on what to avoid?
My mom suffers from trigeminal neuralgia I just want to know things on how to help her to ease the pain.. Thank You so much..Your info will be much appreciated..
I have suffered this awful condition, i was put on Tegretol (an epilepsy drug) and it went away. Im not sure what triggers it but....its tgh compression of the root of the trigeminal nerve by an abnormally positioned blood vessel is the most common cause of trigeminal neuralgia.
The pressure on the nerve causes it to misfire, resulting in pain. Occasionally, the compression is caused by a tumour, and sometimes there is no obvious cause found. Other, rarer causes of trigeminal neuralgia include multiple sclerosis and strokes affecting the lower part of the brain. (+ info
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