Tapentadol A Promising Option For Neuropathic Pain

Today's post from diabetesincontrol.com (see link below) talks about Tapentadol (Nucynta) being effective for diabetes-related neuropathy pain. Earlier articles on this blog (see alphabetical list to the right) have highlighted its efficacy for HIV-related neuropathy and other neuropathies also fall under its benefits (but as yet not approved for all). So why isn't this breakthrough semi-opiate ending up as a front-line treatment? The answer seems to lie in the cost and the competition between drug companies, which disregards the needs of the patients, who have been looking for an efficient chronic pain management drug with less side effects than its competitors. The FDA has approved it, which is the first major step with any new drug but doctors throughout the western world are possibly being pressured into not prescribing it due to pressure from health insurance companies who are always looking for cheaper options. It's symptomatic of a culture where economic cuts are paramount and the power of established drug company lobbies has never been stronger. However, if Tapentadol really is a better option for many patients living with neuropathy, then denying them access is at the very least, morally questionable.

Tapentadol-ER for the Treatment of Diabetes Associated Peripheral Neuropathy (DPN)  This article originally posted 26 June, 2014 and appeared in Medication, Neuropathy, Pain, Issue 735

The FDA recently approved tapentadol-ER (Nucynta ER) for the treatment of peripheral neuropathy in diabetics....

Advertisement With an increasing number of patients being diagnosed with diabetes, complications associated with the disease are becoming more common.  Diabetic peripheral neuropathy (DPN) is the most common neuropathic pain seen in patients with diabetes, affecting up to 50% of patients. It is characterized as a burning or tingling sensation that affects the lower limbs. Painful DPN is associated with increased morbidity, mortality and substantial costs to the healthcare system. Tapentadol-ER is a schedule II opioid analgesic that is commonly used for the treatment of moderate to severe chronic pain. It is unique in its dual acting mechanism in which it works as both a weak mu-opioid receptor agonist and a norepinephrine-reuptake inhibitor. This distinct mechanism is said to represent a new pharmacological class of medications: MOR-NRI. Tapentadol ER is a weak mu-opioid receptor agonist, having an 18 fold decrease in receptor affinity when compared to morphine. Despite this decrease in affinity, tapentadol ER only produces a two to three fold decrease in analgesic effects when studied in animals. It also acts on the alpha-2 receptor located on the noxious nerve fibers in the spinal cord and throughout the central nervous system, inhibiting transmission of pain impulses. The dual acting mechanism of tapentadol-ER works to control the complex pathology that is neuropathic pain. Until this approval the only options for FDA approved medications to treat diabetic peripheral neuropathy (DPN) were pregabalin and duloxetine. Tapentadol ER provides sufficient pain relief with convenient twice daily dosing. The starting dose for opioid-naïve patients is 50mg twice daily and can be titrated to an effective dose of 100mg to 250mg twice daily. The maximum daily dose is 250mg twice daily. The maximum serum concentration is increased by 17% when taken in combination with a high fat breakfast but according to package labeling may be administered without regards to food. Tapentadol-ER undergoes extensive hepatic metabolism and therefore must be adjusted in patients with hepatic impairment. The usual adjustment is extension of administration duration to once every 24 hours in patients with mild to moderate hepatic impairment (Child-Pugh Score of 7 to 9). It is contraindicated in patients with severe hepatic impairment. Tapentadol ER and its metabolites are excreted by the kidneys; however, no dose adjustments are required for patients with renal impairment. The efficacy and safety of tapentadol ER has been studied in two DPN studies. Both studies were placebo controlled randomized studies in which patients had either type 1 or type 2 diabetes and painful DPN for a period of at least six months. Pain intensity was at least a 5 on an 11 point scale. In both studies approximately two-thirds of participants were opioid-naïve. Both studies came to the conclusion that tapentadol ER provided statistically significant improvement of pain intensity as compared to that of placebo. Treatment related adverse effects were reported at 70.9% for those taking tapentadol ER and 51.8% for those taking placebo. The most common side effects were nausea, diarrhea, anxiety and dizziness. Most were mild to moderate and did not lead to discontinuation of the medication. Practice Pearls: The incidence of diabetes is on the rise as is the complication of neuropathy The FDA approval of tapentadol ER for treatment of diabetic peripheral neuropathy provides practitioners an additional therapeutic option with a convenient twice daily dosing regimen. Tapentadol ER has a unique dual mechanism suggesting that it may be particularly useful for complex pain associated with DPN. Consult Pharm. 2013 Oct;28(10):672-5. doi: 10.4140/TCP.n.2013.672 Comment from Dr. Aaron Vinik, Diabetes In Control Advisory Board member, and study author: Pain associated with DPN is a common complication of diabetes affecting 10-26% of patients for which the only approved drugs are Pregabalin and Duloxetine which at best reduce pain by 30% in about half the patients treated leaving a significant portion of the affected population without resort to significant pain relief. A paradox here is that third party payors insist that less expensive drugs such as the tricyclics should be used as first line despite the fact that they have cardiovascular cautions as well as not paying heed to the need for attention to the comorbidities of sleep loss, depression and anxiety as determinants of choice of initial therapies. However, the problem occurs when first line therapies have failed and the need for greater reduction of pain arises wherein a combination of drugs acting through different parts of the pain pathway have proved useful. The problem with this approach is that this increases the burden of drugs patients with diabetes must take with untoward effects, particularly cognitive impairment, which can have a disastrous impact on decision-making and is the cause of induced hypoglycemia and its consequences. Tapendalol represents a proposed new class of centrally acting analgesics combining two mechanisms of action: u-opiod receptor agonism and norepinephrine reuptake inhibition. Tapentadol extended release has been shown to be effective and well-tolerated for the management of severe, chronic pain in randomized, double blind, placebo-controlled and/or active comparator controlled phase 3 studies. Two studies (of which I am first author and coauthor of the second) were designed using a randomized withdrawal multicenter placebo control design and reached their primary endpoint and in August 2012 tapentadol ER received FDA approval for the mangement of pain associated with DPN in adults when a continuous around the clock opiod analgesic was needed for an extended period of time. To determine if subgroups would benefit, the data from the two studies were pooled. The results of this pooled analysis indicated that tapentadol ER is effective and well-tolerated for the management of neuropathic pain associated with DPN, improved measures of health related quality of life and had constent efficacy across different patient subgroups divided by age, gender, race, opiod experience and pain intensity. Sensitivity analyses showed that in the tepentadol arm ( n=360) compared with placebo ( n=342) the drug 54% achieved >30% pain reduction and 38.9%;50% pain reduction and the significant side effects were nausea, vomiting, dizziness, and somnolence. These figures argue in favor of using the drug as a second or third tier drug with the recognition that its effects are modest and there is the potential for habituation. Ultimately, what is needed is a drug that will reverse the pathogenic process and that the need for pain-relieving drugs will be the bandaid to be used in the interval before the damage to the nervous system has been resolved.  http://www.diabetesincontrol.com/articles/diabetes-news/16529-tapentadol-er-for-the-treatment-of-diabetes-associated-peripheral-neuropathy-dpn

Gabapentin Neurontin For Nerve Pain A Risky Option

Today's post from jailmedicine.com (see link below) is a fascinating and enlightening look at Gabapentin (neurontin) as a pain relief drug but from the viewpoint of a prison doctor who has to decide whether to prescribe it, or continue prescription to inmates who have pain problems. It's a well-known anti-seizure/epilepsy drug, which needs careful thought before starting or continuing it. It's relevant to neuropathy patients because Gabapentin (neurontin) is high on the list of prescribed drugs for neuropathic pain and is taken by millions across the world. If you are one such person, or may be prescribed the drug by your doctor for your nerve pain, it may be worth your while reading this article and discussing it with your doctor. I'm not going to say any more; the article is self-explanatory; after that it's up to you what you choose to do about it but it may be worth bearing in mind that, as the article says, pregabalin (Lyrica) is not a sensible alternative!

Taming the Beast—Gabapentin. Ban It or Regulate It?
Jeffrey E. Keller  February 2017

In my last post, I began with a question from Christy. Her facility was considering banning gabapentin from their facility due to rampant abuse and diversion problems. My last post dealt with gabapentin’s interesting history and the evidence base for off-label gabapentin prescribing. This JailMedicine post will deal with the pros and cons of banning gabapentin versus creating rules to regulate gabapentin use and hopefully minimize diversion and  abuse.

The main points from the last post were:
Gabapentin is FDA approved for seizures and post herpetic neuralgia.
However, most of the demand for gabapentin and prescriptions for gabapentin are for “off-label” uses, namely for chronic neuropathic pain. Evidence for gabapentin use for other types of chronic pain is not so good.
Despite the poor evidence base, gabapentin is very widely prescribed for all types of chronic pain. It is also used as a sleeping aid, restless leg syndrome, anxiety and all sorts of other stuff.
Gabapentin has a euphoric and dissociative effect and so is very sought after as a drug of abuse in jails and prisons.
Gabapentin is not DEA regulated and most non-correctional physicians have no clue that it can be—and is—abused.

We correctional physicians need to put this all together in order to make a rational and effective policy regarding gabapentin use in our facilities. Basically, we must balance the potential benefits of gabapentin against the potential harm to the patient and the potential harm to the institution when it is diverted and misused.

Our basic options are:
Ban gabapentin outright.
Restrict its use by defining exactly what use is acceptable and what we will not allow.
Allow unrestricted use as a formulary medication—although I doubt that any correctional facility that has had experienced a gabapentin “feeding frenzy” is going to opt for this last one!

Which of these options you pick depends (in my mind at least) on whether you are a jail or a prison. Let’s look at these two situations in detail.
Gabapentin rules for jails.

One basic goal of jail medicine that makes it different from prison medicine is this: Continuity of Outside Care. The average jail patient had a medical provider before coming to jail and will return to that same medical provider when he leaves jail—in an average of, say, two weeks. Assuming that our patient had competent medical care before coming to jail, to a large degree, our job is to continue that care, hopefully without significant interruption. If the patient takes medications for hypertension, seizures, hyperthyroidism or a host of other problems, I usually will want to continue those medications for the short time that the patient is in jail, even if I myself would not treat the patient in exactly the same way.

If gabapentin has been prescribed for seizures (even though it is a crappy seizure drug), I will not want to discontinue the gabapentin while in jail. However, most of the gabapentin prescriptions that I am going to see in newly booked jail patients are going to be for (yes, you guessed it) chronic pain. If I ban gabapentin for this, I have the following considerations:
Gabapentin should not be abruptly stopped. It needs to be tapered at a rate of no more than 300mg a day. If a patient comes in taking 3600mg a day, it will take a minimum of two weeks to safely taper her off of the gabapentin.
When she is released from jail (in an average of two weeks.), the gabapentin will just be immediately restarted.

My thinking is that I have not accomplished much in this scenario. I didn’t accomplish my goal of not allowing gabapentin in the facility—it was there during the taper. I didn’t win friends. The jail patient will be angry and so probably will his outside physician. I did not improve his overall medical care. So if the patient is only going to be in jail for a short time, and if he supplied the gabapentin in appropriately labeled prescription bottles, I will likely continue the gabapentin for his short jail stay.

However, there are limits to this. First, the gabapentin prescribing by the outside physician must conform to commonly acceptable standards. I once had a patient who arrived at the jail taking a monster dose of 5,400 mg of gabapentin a day. I verified that this jaw-dropping prescription was correct by calling the prescribing doctor’s office. 5,400 mg of gabapentin a day far, far exceeds the maximum dose for gabapentin for any indication, which is 3600mg a day. More investigation led me to believe that this patient had been selling his gabapentin on the street, which is why he had pushed the outside prescriber for more and more gabapentin. Interesting incidental point: gabapentin has street value outside of jails and prisons!

Also, gabapentin prescribed for neuropathic pain has an evidence base in the literature. Gabapentin as a sleeping aid does not. I will view the situation differently if someone arrives at the jail taking, say, 100mg of gabapentin every night as a sleeper.

Finally, I myself do not prescribe gabapentin (well, rarely, anyway). If a patient cannot supply their own prescribed gabapentin, I’m not going to fill in the gap. Once a patient’s outside medication supply runs out, I’m not going to refill it for them. I usually will call their outside practitioner and discuss my plan to taper and discontinue the gabapentin in this patient, who is going to be incarcerated for a while. Almost always, the outside practitioner will have no problem with this. But I should make the call anyway in order to accomplish two goals: first, the outside provider and I are united in this treatment decision. Now, the inmate cannot exploit a perceived difference of opinion: “My outside doctor wants me to be on gabapentin. Who are you to deny it?” Second, I have educated the outside practitioner about the abuse potential of gabapentin. Most of them have no idea.
Gabapentin prescribing in prisons

The situation in prison is different than a short stay in jail. The medical care of the prison patient is being transferred to the prison medical providers lock, stock and barrel. These patients will not be returning to their outside medical provider anytime soon. It is akin to a person moving to another city and finding a new primary care physician to take over their medical care. The physician in the new city is under no obligation to continue therapies (like gabapentin) that she considers to be inappropriate or less than optimal. Same thing in a prison: the prison practitioner can certainly modify a treatment plan to fit the patient’s new prison environment.

Because they feel no pressure to continue outside treatment plans, some prison systems have decided to ban gabapentin entirely. The main driving force for this, of course, is the level of diversion and abuse in that particular prison system. Gabapentin abuse is a bigger problem for some prisons than for others.

But a total ban on gabapentin is not as easy as it seems. Some prison systems have banned gabapentin only to return to allowing controlled use of gabapentin later due to the problems of implementing a total ban. Whether you ban gabapentin entirely or just try to beat it into submission with guidelines of appropriate use, here are the issues you are going to have to address:
What are you going to substitute for gabapentin?

Now, if the gabapentin was prescribed for seizures, it is easy to come up with a list of alternative seizure medications. Ditto restless leg syndrome–there are better and cheaper alternatives. There are also lots of substitutes for gabapentin prescribed for psychiatric conditions like Bipolar disorder.

But all of those will likely represent only a small minority of incoming gabapentin prescriptions. Most of the gabapentin prescriptions will be for The Big Two: diabetic neuropathy and chronic pain. There certainly are other medications that can be used to treat diabetic neuropathy and chronic pain—just not very many. Here is the list:

Duloxetine (Cymbalta). Duloxetine is, in my mind at least, the single best alternative. Its efficacy is just as good as gabapentin in randomized trials. I have not heard any reports of significant abuse or diversion of duloxetine. Perfect!

Venlafaxine. Like duloxetine, venlafaxine has consistently outperformed gabapentin as a treatment of neuropathic pain in blinded trials. However, venlafaxine can itself has been diverted and abused in correctional settings.

Tri-cyclic antidepressants, especially amitriptyline. TCAs have also been successfully used to treat chronic pain. The problem with TCAs is twofold: first, they themselves, especially amitriptyline, can be diverted and abused. Also, TCAs can be deadly in overdose. I myself have personally witnessed two deaths caused by TCA overdose (in my ER days). TCAs also have lots of interactions with other medications. If you do use TCAs, use a low dose. Big doses do not improve efficacy, but do increase the possibility of overdose. Also, I would recommend using a TCA with less diversion potential like nortriptyline.

Other antidepressants. I have seen SSRIs prescribed for chronic pain. I have also not heard of significant abuse or diversion of SSRIs. The problem with them is that they have not been well studied as treatments for neuropathic pain.

Other seizure medications like Keppra, Tegretol and Depakote. These also have been used for chronic pain but, like SSRIs, do not have a great literature base.

Capsaicin cream. Interestingly, capsaicin cream performed just as well as did gabapentin in the trials! A definite possibility.

Pregabulin (Lyrica). The problem with Lyrica in corrections is that it is just as abusable/divertable as is gabapentin. In fact, they both act on the same receptors. In my mind, it basically is the same thing as gabapentin–only worse. Where gabapentin is not a DEA controlled substance, Lyrica is. Lyrica is also expensive. You have accomplished little if you replace gabapentin with Lyrica.

“Nothing Works Except Gabapentin”

The next thing you need to decide is what you are going to do when these substitutions fail. Many patients who are switched to the new agents will do fine. But there will be some who are going to say that nothing else works except gabapentin. Some of these are sincere–gabapentin can be a great drug for some patients. But others who say that only gabapentin works want it to abuse or divert. It often is impossible to tell the difference between these two categories.

If gabapentin is totally banned, some inmates will inevitably file grievances, tort actions and complaints to the state medical board that they are being denied “the only medical therapy that works for me.” They will enlist family members and outside doctors and advocacy groups to lobby for them. I know of a couple of prison systems where complaints like these became such a problem that they reversed their decision to ban gabapentin outright. Be prepared!

If your facility is going to ban gabapentin nevertheless, I would strongly recommend that this be an official decision with the agreement of everyone involved: the Medical Director, the Director of Nursing, a representative of your pharmacy, the security administrator of your facility and your legal representative. Having agreement from this diverse group beforehand will go a long way to deal with the inevitable backlash.
The argument against banning gabapentin in prisons.

One of my mentors in prison medicine argues against a total ban on gabapentin in prisons. His reasoning goes like this:

1. 95% of the inmates prescribed gabapentin do not divert or abuse. Gabapentin can be a useful and effective drug for them. Why ban use in the 95% because of the 5% who abuse it?

2. Also, he says, the 5% who are abusing gabapentin are going to divert and abuse some type of medication no matter what. Since gabapentin is relatively safer in an overdose than, say, tricyclic antidepressants or bupropion, it is better that the inevitable prison black market be for the safer drug–gabapentin.

3. Instead, says my mentor, it is possible to make and enforce rules for rational and sane gabapentin prescribing.
Rules for gabapentin prescribing.

Here are some rules for gabapentin prescribing for neuropathy and chronic pain that I think are reasonable and in line with the literature.

Decide who you will be eligible for a gabapentin prescription. As I discussed last week, gabapentin has been basis in the literature as a treatment for neuropathic pain. It is not a viable treatment for “nociceptive” musculoskeletal pain. So diabetics who complain of painful feet might be proper candidates for a gabapentin prescription, whereas a patient with, say, chronic knee pain due to DJD is not a proper candidate according to the literature.

Decide what medications for neuropathic pain should be tried before gabapentin. Since several other medications work just as well–or better–for neuropathic pain than does gabapentin and do not have the abuse potential that gabapentin does, I would recommend that gabapentin be a drug of last resort. Better agents include duloxetine, venlafaxine, tricyclics and capsaicin cream.

Set the maximum dosages. If you look up maximum gabapentin dosage for neuropathy in one of the many drug compendiums (Tarascon, say), it will give the maximum dosage as 3,600 mg a day. And it is true that doses this high have been used in gabapentin studies. But what Tarascon does not tell you is that the studies showed that high doses of gabapentin were no more effective than low doses–but high doses do increase the incidence of gabapentin side effects and, in our world, availability for diversion, abuse and overdose.

So what should the maximum dosage of gabapentin be for neuropathic pain? Well, interestingly, Pfizer, the original maker of Neurontin, answered this question for us. Remember that Neurontin was FDA approved for one type of neuropathy– post herpetic neuropathic pain. And the Neurontin package insert lists the maximum dose for this neuropathic pain as 1,800 mg a day. So there is your answer. Maximum dose of gabapentin for neuropathy is 1,800 mg a day.

Once again, though, almost all of the benefit from gabapentin is gained at doses much lower than this theoretical maximum dose. The Prescriber’s Letter (which is my favorite pharmacy information source) says this (Here): “gabapentin doses above 900 mg/day don’t provide much more pain relief–but do increase side effects. Keep in mind there’s a diminishing return with higher doses . . . doubling the dose does not double drug concentration.”

So although the theoretical maximal dose is 1,800mg a day, the effective maximum dose is just 900mg a day.

Monitor compliance. It is easy to check compliance with prescribed gabapentin. You just need to draw a gabapentin drug level. Decide how often these will be. Will they be scheduled or random? Will you check levels in all patients or just those who you suspect of diversion?

Decide what you will do with those caught diverting. Since gabapentin is not a “must-have” medication, I would recommend that anyone caught diverting gabapentin have their gabapentin prescription stopped. You will need to decide how long until the inmate will be eligible for another trial. Six months? One year? Whatever it is, it must be consistent.

Uniform prescribing. Whatever rules or guidelines you develop for gabapentin use, it is essential that they be followed by all the prescribers in your system and, if you have multiple facilities in your system, at all facilities. Having even one practitioner who ignores your guidelines will result in grievances, complaints and gaming.

As always, the views I have expressed here are my own opinions and the result of my own training and experience. I could be wrong! You should carefully review the evidence for gabapentin prescribing yourself!
How do you handle gabapentin in your facility? I’d like to hear from those of you who work at facilities where gabapentin is banned. Was the ban successful? I’d also like to hear from those who have tried to regulate gabapentin. What are your rules? What works? What does not work? Please Comment!

http://www.jailmedicine.com/taming-the-beast-gabapentin-ban-it-or-regulate-it/

Is Light Therapy A Realistic Option For Neuropathic Pain

Today's post from townsendletter.com (see link below) presents the case for light therapy as a potential treatment for neuropathic pain and related problems. it does this by illustrating three study cases with different forms of neuropathy. Now the problem with light therapy is that mainstream medicine is by no means firmly in favour; some regarding it as another alternative treatment based on expensive equipment and carried out at expensive clinics. After all, if it were as effective as is claimed, the whole of mainstream neurology would be performing it across the world but that doesn't exclude the possibility that it will work for many people living with nerve pain. You have to make your own mind up and investigate further as thoroughly as possible. Talking it over with regular doctors and specialists is advised, with the expectation that they will probably not be in favour. If that's the case, then you need to ask them why. Their answers, plus your own research should give you a better perspective as to whether this may be something for you to try.

A Breakthrough in Using Light Therapy to Treat Neuropathies
by Len Saputo, MD From the Townsend Letter November 2015

This article describes the successful treatment using light therapy of three patients with peripheral neuropathy. The etiology of neuropathy for each of these patients was different, as were the patients themselves in age, sex, and general condition. All of the patients were significantly disabled and had previously undergone extensive conventional treatment without significant relief.

I have used light therapy to treat over 2000 patients with a variety of painful health conditions since 1999, when I first met Maurice Bales, who had extensive experience with the development and manufacturing of infrared light devices, beginning in the 1970s with his work at NASA and the Lawrence Livermore Lab. Maurice trained me to treat a wide range of painful conditions that included neuropathy, neck and back pain, TMJ disorders, headaches, fractures, and sports injuries. I have found that if something hurts, chances are that treatment with light will help.

Despite its remarkable effectiveness, safety profile, and affordability, light therapy remains for the most part underappreciated and underused. This lack of utilization of light therapies is not just by mainstream medicine but also by the alternative and integrative medical communities. This situation exists despite the fact that more than 70,000 peer-reviewed articles have been published on light therapy and listed on PubMed going back to 1899. Since then light therapy has been documented to relieve pain, increase circulation, reduce inflammation, speed up wound healing by an average of 40%, increase lymphatic drainage, attract stem cells, and stimulate mitochondrial production of ATP – among other things.1-15 This sounds a bit like Star-Trek medicine!

I have selected three case histories that demonstrate the range of peripheral neuropathies that can be treated using light therapy.

Case #1: Chemotherapy-Induced Peripheral Neuropathy

J. K. is a 69-year-old female referred by her oncologist for treatment of advanced peripheral neuropathy caused by chemotherapy. She was diagnosed in 2010 with colon cancer and was treated with surgery, chemotherapy, and radiation. She felt well and remained in remission until December 2014, at which time she was found to have stage IV disease based on diagnosing metastases to her lungs. She was started on chemotherapy with Erbitux.

Her cancer responded to this treatment, but within a few months she developed progressively worsening numbness in her hands and feet. By June 2015, she had such dense numbness that she could not feel the accelerator or brake in her car and was unable to button her clothing. She became depressed because she was for the most part confined to her home. Her oncologist referred her to me for treatment of her neuropathy because it had become so severe that chemotherapy had to be discontinued.

She was treated with 11 15-minute light treatments to her feet, legs, and hands from July 29, 2015, through August 20, 2015. She regained enough sensation in her fingers and feet that she can now drive, walk normally, and button her clothing without assistance. She is now much more active socially and is back on her chemotherapy treatment. She remains in remission and is enjoying life once again.
 
Pre-Tx Plantar Feet



Post-Tx Plantar Feet



Pretreatment thermographic image of soles of feet show lack of circulation as blue and green colors. Posttreatment shows significantly increased circulation as red and orange.

Case #2: Trauma-Induced Neuropathy

T. S. is a 39-year-old woman who was in a tornado three years ago, when a large uprooted tree fell on her geodesic dome and crashed her to the ground. Ever since that event, she could not raise her arms above her neck; has been walking with a wide-based gait to maintain her balance; has been weak in both legs; tires easily; and developed numbness, burning pain, and tingling in her feet and lower legs.

Her podiatrist referred her to me to treat her peripheral neuropathy with light therapy.

The patient's examination revealed dense numbness extending from the bottoms of her feet to the midcalf. She had normal pedal pulses and no Babinski sign, but her knee and ankle reflexes were absent. Her lumbar spine had very significant bilateral pain to direct pressure from L3 to S1. The range of motion of her neck was restricted to 45 degrees bilaterally and there was moderate tenderness to palpation in the suboccipital portion of her neck. She also suffered from both lumbar disc disease and neuropathy.

She received seven treatments on her feet, low back, neck, and TMJ with light from July 15 through August 21, 2015. The patient reported, "Photonic stimulation has been a miracle for me. I no longer have pain when I stand or walk, and am able to straighten my knees. I walk with balance and at a normal speed, which I never imagined I would be able to do again. I am dreaming of getting a bike and returning to yoga and dance."

Posterior pre_Tx




Posterior post-Tx



Pretreatment image shows inflammation in orange and red from a posterior radiculopathy. The posttreatment image shows a reduction in inflammation and more symmetrical pattern of heat distrubution. (The white spot is an artifact of the BioPhoton treatment.)

Case #3: Diabetic Neuropathy

R. S. is a 56-year-old male with a history of type 2 diabetes, hypertension, obesity, hyperlipidemia, and being a "wine connoisseur." He was referred by his chiropractor for treatment of his neuropathy with infrared light. His symptoms began in 2008 and included numbness and mild burning nighttime pain that had been progressive and assumed to be caused by type 2 diabetes. It is noteworthy that he was being treated with glipizide, amlopidine, hydrochlorothiazide, pravastatin, and nortriptyline, all of which have an association, albeit weak, with peripheral neuropathy. Odds are that the most likely cause in this case was a combination of diabetes and alcohol.

He was treated from January 2014 through June 2015 with 31 infrared light therapy treatments to his feet. The combination of gradually reducing his alcohol consumption and employing light treatments had a major effect on improving his neuropathy symptoms. At the present time has no pain and only mild numbness in his feet. His gait is normal. In addition to using light therapy, we have successfully focused on improving his lifestyle factors including stress, insomnia, diet, exercise, weight management, and reduction in alcohol consumption. Because of his compliance we have been able to discontinue all of his medications.

Pain management has become a very sophisticated discipline that tends to be complicated and often associated with challenging side effects. Light therapy is another story, because it is simple, effective, safe, and affordable. In contrast, in mainstream clinical practice, it is typical for patients with severe pain to be treated with a polypharmacy that usually includes drugs for pain, anxiety, depression, insomnia, and a wide range of additional drugs to manage their side effects. Many people take 10 or more drugs and, not unexpectedly, simply cannot function very well. These are often those patients who come to my office!

For some neuropathies, light treatment alone is sufficient to relieve even the most severe pain. I have been able to wean more than a thousand patients off their medications. For other painful conditions, it can be helpful to use an integrative team approach that can include chiropractic, Chinese medicine, bodywork, imagery, psychotherapy, pulsed electromagnetic field therapy, and so on.

I have found that the safest and most effective way to use light therapy is to use the right device under the guidance of infrared imaging in real time. The Bales Thermal Image Processor (TIP) that we employ is a high-resolution infrared camera which is highly stable and sensitive. It allows us to use light devices that can deliver the right wavelengths with enough power that we usually get impressive clinical improvement in just a single 15-minute office visit. This approach also allows patients to observe their infrared images in real time and see for themselves the impressive changes that occur during a treatment. So patients get great clinical results not only from the effects of light itself, but also from the effects of visualizing how the treatment changes the thermal patterns on their skin.

We have learned that with certain conditions, it is critical to follow the thermal effects of light during treatment so that we visualize what we're doing and also minimize any chance of making symptoms worse. This is especially important in people with fibromyalgia and other forms of neuropathic pain such as complex regional pain syndromes, shingles, certain vascular headaches, and several other conditions.

There are hundreds of light therapy devices available, greatly varying in their respective prices, mechanisms, and efficacy. The device that I began using in 1999 was the Bales Scientific Photonic Stimulator, in conjunction with the Bales TIP camera. When its inventor, Bales, worked for NASA and the Lawrence Livermore Labs, he was developing equipment used for the space shuttle. Starting in 1985, he began to adapt his work to the medical field, creating his thermographic camera in 1990 and the Photonic Stimulator, which was approved by the FDA as a medical device to treat pain in 1997. Bales has made dozens of incremental improvements to photonic stimulators over the past two decades. What is especially noteworthy about the three cases I discuss in this article is that I used a revolutionary new model introduced only this year, now called the BioPhoton 100. This device is significantly more powerful than its predecessors, offers variable wavelengths and frequencies, is considerably smaller, and costs less.



BioPhoton

Photonic Stimulator

Here are some of the specific differences:

Power: Output power has been increased from 0.250 watts to 8.9 watts. Output power is a very important factor for permeation depth. While lower-powered devices may benefit cells at the superficial level, they fail to penetrate deeper tissue, which is often the root problem of a chronic disease. The BioPhoton can target tissues deep within the body and penetrate the skull to reach the brain. More power equates to more photon energy being transmitted to the cells, which also reduces the duration and number of treatments.

Spectrum wavelengths: The previous model had a fixed wavelength of 850 to 880 nm, while the BioPhoton 100 has mixed-spectrum blue light at wavelengths from 450 nm and red and far-infrared light up to 940 nm. Blue light only penetrates superficial tissues but can treat cutaneous conditions such as traumatic injuries such as burns, cuts, contusions, and even infections such as MRSA.16-18 Increasing the power of blue light can deliver substantial amounts to the deeper tissues. It should be noted that blue light has greater ability than red or infrared in releasing nitric oxide to cause vasodilation.19,20 Infrared wavelengths include 850 nm and 940 nm and have the actions mentioned earlier.

Modulation (waveform) options: The BioPhoton 100 Professional model can accept external input from other devices. This provides the practitioner with the ability to replicate other frequency protocols that can be customized to meet individual treatment goals. These protocols may include square, triangular, sine, or audio waveforms at varied frequencies. It has been theorized that different waveforms are beneficial in the treatment of various diseases.

Smaller size and lower price: The size of the device has gone from 14.5² × 10² × 6² down to 5.5² × 2.5² × 2.75.² The price of the original Photonic Stimulator was $9320 (in today's dollars), while models of the BioPhoton 100 range from $2200 to $7000. These improvements make it possible for practitioners to devise a treatment protocol and then rent the device to patients to use in their homes for a specified period. This allows for daily use, which equates to faster healing, and more satisfied patients. Home treatment allows for more regular treatments at a lower cost while freeing up more time for other patients.

I believe that the BioPhoton 100 is a significant breakthrough not just in light therapy in particular but in medicine in general. We are now involved in research in conjunction with the National Institutes of Health at UCSF. Light therapy often provides superior results than do conventional treatments for a variety of illnesses and is completely noninvasive and, used correctly, free of side effects. The clinical applications of photon therapy are expanding at the speed of light!

I'm even more enthusiastic today than when I was first introduced to light therapy by Maurice Bales. It has been very rewarding to see the surprised look on the faces of so many of my patients after just a short 15-minute treatment. Because the word spreads fast when there's an effective, quick, safe, and affordable solution to managing painful conditions, I've had to devote more than half of my practice to light treatment. The vast majority of my patients come to me through word of mouth from other patients. I encourage my medical brethren to see how they might incorporate light therapy into their practices. They will not only be able to help a lot of patients who don't need to suffer, but can also make it a profitable undertaking.

BioPhoton

Light Emitter



Len Saputo, MD, is a graduate of Duke University Medical School and board certified in internal medicine. He was in private practice in affiliation with John Muir Medical Center in the San Francisco Bay Area for more than 30 years. His approach to healing has evolved from mainstream medicine into "Health Medicine" – an integrative, holistic, person-centered, and preventive style of practice. drlen@doctorsaputo.com

Notes

1. Branco K, Naeser MA. Carpal tunnel syndrome: clinical outcome after low-level laser acupuncture, microamps transcutaneous electrical nerve stimulation, and other alternative therapies--an open protocol study. J Altern Complement Med. 1999;5:5–26.

2. Irvine J, Chong SL, Amirjani N, Chan KM. Double-blind randomized controlled trial of low-level laser therapy in carpal tunnel syndrome. Muscle Nerve. 2004; 30:182–187.

3. Weintraub MI. Noninvasive laser neurolysis in carpal tunnel syndrome. Muscle Nerve. 1997;20:1029–1031.

4. Ehrreich SJ, Furchgott RF. Relaxation of mammalian smooth muscles by visible and ultraviolet radiation. Nature. 1968;218:682–684.

5. Chaudhry H, Lynch M, Schomacker K, Birngruber R, Gregory K, Kochevar I. Relaxation of vascular smooth muscle induced by low-power laser radiation. Photochem Photobiol. 1993;58:661–669.

6. Mittermayr R, Osipov A, Piskernik C, et al. Blue laser light increases perfusion of a skin flap via release of nitric oxide from hemoglobin. Mol Med. 2007;13:22–29; Passarella S. He-Ne laser irradiation of isolated mitochondria. J Photochem Photobiol B. 1989;3:642–643.

7. Alves ACA, Vieira R, Leal-Junior ECP, et al. Effect of low-level laser therapy on the expression of inflammatory mediators and on neutrophils and macrophages in acute joint inflammation. Arthritis Res Ther. 2013;15:R116. doi:10.1186/ar4296.

8. Whelan HT, Smits RL Jr, Buchman EV, et al. Effect of NASA light-emitting diode irradiation on wound healing. J Clin Laser Med Surg. 2001 Dec;19(6):305–314. Review PMID: 11776448.

9. Chaves ME, de Araujo AR, Piancastelli ACC, Pinotti M. Effects of low-power light therapy on wound healing: Laser vs LED. An Bras Dermatol. 2014 Jul–Aug;89(4):616–623. doi:10.1590/abd1806-4841.20142519.

10. Pereira AN, Eduardo Cde P, Matson E, Marques MM. Effect of low-power laser irradiation on cell growth and procollagen synthesis of cultured fibroblasts. Lasers Surg Med. 2002;31:263–267.

11. Shimotoyodome MD. Effects of IR light on lymph flow. Lasers Surg Med. 2001;29(5):442–447.

12. Hou J, Zhang H, Yuan X, Li J, Wei Y, Hu S. In vitro effects of low-level laser irradiation for bone marrow mesenchymal stem cells: Proliferation, growth factors secretion and myogenic differentiation. Lasers Surg Med. December 2008;40(10):726–733. doi:10.1002/lsm.20709.

13. Pastore D, Greco M, Passarella S. Specific helium-neon laser sensitivity of the purified cytochrome c oxidase. Int J Radiat Biol. 2000;76:863–870.

14. Yu W, Naim JO, McGowan M, Ippolito K, Lanzafame RJ. Photomodulation of oxidative metabolism and electron chain enzymes in rat liver mitochondria. Photochem Photobiol. 1997;66:866–871.

15. Passarella S. He-Ne laser irradiation of isolated mitochondria. J Photochem Photobiol B. 1989;3:642–643.

16. Kim SW et al. In vitro bactericidal effects of 625, 525, and 425 nm wavelength light-emitting diode irradiation. Photomed Laser Surg. November 2013;31(11):554–562. doi:10,1089/pho.2012.3343.

17. Dai T et al. Blue light eliminates community-acquired methicillin-resistant Staphylococcus aureus in infected mouse skin abrasions. Photomed Laser Surg. November 2013;331(11):531–538. doi:10.1089/pho.2012.3365.

18. Bumah VV et al. Wavelength and bacterial density influence the bactericidal effect of blue light on methicillin-resistant Staphylococcus aureus (MRSA). Photomed Laser Surg. November 2013;31(11):547–553. doi:10.1089/pho.2012.3461.

19. Chaudhry H, Lynch M, Schomacker K, Birngruber R, Gregory K, Kochevar I. Relaxation of vascular smooth muscle induced by low-power laser radiation. Photochem Photobiol. 1993;58:661–669.

20. Mittermayr R, Osipov A, Piskernik C, et al. Blue laser light increases perfusion of a skin flap via release of nitric oxide from hemoglobin. Mol Med. 2007;13:22–29.

http://www.townsendletter.com/Nov2015/break1115.html

Is Ketamine An Option For Neuropathic Pain

Today's post from zen-haven.com (see link below) is a realistic look at the reality of neuropathic pain but becomes subjective when considering the use of ketamine to control it. Ketamine has a bad rap. It's widely known as a party drug and is on many countries' banned lists. It is used under controlled conditions in hospital situations after surgery but many mainstream doctors will raise their eyebrows at the idea of it as a neuropathic pain controller. Yet the article is correct in that theoretically, the way ketamine works it could well help reduce chronic nerve pain. The suggestion is that a hospital administered infusion may give reasonably long lasting relief but the conclusion that this will then give the nervous system time 'to repair itself' is optimistic at best. The drug may well play a part in reducing neuropathic pain but the nerve damage can't logically be 'repaired' due to its administration - so far, no drug can repair nerve damage.

Navigating the Murky World of Neuropathic Pain
Posted on August 11, 2013 by Soren Dreier
Author: Christine Lin

As human beings, we instinctively avoid pain—the sting of nettles, the burn of a hotplate, the pinching of door hinges. Pain is useful because it communicates immediate danger and helps us keep out of it. However, some pain is chronic, as neuropathic pain often is.

Neuropathic pain derives from the central nervous system or peripheral nervous system. It is pain that comes from the nerves, as opposed to common muscular aches and arthritic pain. Sometimes it is triggered by traumatic accidents.

In support forums, patients suffering from neuropathic pain describe their symptoms as “burning all over,” “shooting pains in the arms and legs,” “agony,” and “unbearable.” Many of them recount their experiences in seeking relief “frustrating,” that they’ve “tried everything,” or that “not one doctor can give me an answer.”

Neuropathic pain, as a broad category of conditions that include neuralgia, phantom limb syndrome, complex regional pain syndrome (CRPS), and central pain syndrome, is a little-understood realm in medicine. We don’t always know its causes. And current treatment methods are mediocre at best.

Even its occurrence rate among the general population is hard to discern.

In 2008, a study of neuropathic pain incidences in the Dutch population found it has an annual incidence of almost 1 percent of the general population and affects women and middle-aged persons more often.

A 2005 survey of three U.K. cities puts the rate at 8 percent, while a 2006 one conducted in France came up with 5 percent.

Chronic pain affects more than day-to-day functioning. A study last year published in the Journal of Neuroscience found that people with chronic back pain or CRPS have smaller hippocampi than healthy people.

The hippocampus plays a crucial role in processing information, memory, and spatial navigation.

Current Treatments Hit-or-Miss

While researchers are slowly forming a better idea of what causes neuropathic pain, the research has been hard to translate into medical practice, leaving many patients feeling hopeless. Part of the reason is that there are likely a variety of causes that depend on the patient’s history of injury, lifestyle, and drug history.

Tricyclic antidepressants and anticonvulsants are the common, first-line drugs used to treat neuropathic pain.

According to a 2005 study, tricyclic antidepressants will give relief to one in every two to three patients with peripheral neuropathic pain, which is superior to serotonin noradrenaline reuptake inhibitors (SNRIs), which are successful in one in every four to five, and selective serotonin reuptake inhibitors (SSRIs), good for one in every seven patients.

Anticonvulsants have not been found to be more effective than tricyclic antidepressants with an efficacy rate about the same as that of SNRIs.

Emerging Treatment

Patients who fail to find relief may have a new treatment option to turn to.

A 2006 study in the American Journal of Therapeutics found that 85 percent of neuropathic pain patients who underwent outpatient ketamine infusion saw improvements in their conditions. Just over half of the study participants reported continued relief one month after discontinuing treatment.

Known more popularly for its abuse as a club drug, ketamine has been recognized and used for several decades as an anesthetic. It works to stop the transmission of pain by blocking N-methyl-D-aspartate (NMDA) receptors. Recent research has identified hyperactivity of these receptors as a possible factor in generating neuropathic pain.

Few medical establishments in the United States administer ketamine infusions. While it does not cure neuropathic pain conditions, treatment can put the patient into remission long enough to give the nervous system a chance to repair itself.

Read More: Here

http://zen-haven.com/navigating-the-murky-world-of-neuropathic-pain/

Is Acupuncture An Option For Your Nerve Damage

Today's post from time.com (see link below) follows on from yesterday's post and adds a little more information to the argument as to whether acupuncture may help relieve your neuropathic symptoms or not. It's a sensibly written and short description of how acupuncture works and offers no guarantees but as the acupuncturist points out at the end; “...if you’re being prescribed opioids, or you’re considering surgery, you lose very little by trying acupuncture first.” Worth a quick read if you're worried about the amount of chemicals you're swallowing in order to keep the pain down.

You Asked: Does Acupuncture Work? 
Markham Heid @markhamh June 29, 2016

For certain conditions—particularly pain—there’s evidence it works. Exactly how it works is an open question.

You hear the term “acupuncture,” and visions of needles may dance in your head. But the 3 million Americans (and counting) who have tried it know there’s a lot more to the treatment than pokes and pricks.

A typical visit to an acupuncturist might begin with an examination of your tongue, the taking of your pulse at several points on each wrist and a probing of your abdomen. “They didn’t have MRIs or X-rays 2,500 years ago, so they had to use other means to assess what’s going on with you internally,” says Stephanie Tyiska, a Philadelphia-based acupuncture practitioner and instructor.

These diagnostic procedures inform the placement of the needles, Tyiska says. But a visit to an acupuncturist could also include a thoughtful discussion of your diet and personal habits, recommendations to avoid certain foods or to take herbal supplements and an array of additional in-office treatments—like skin brushing or a kind of skin suctioning known as “cupping”—that together fall under the wide umbrella of traditional Chinese medicine.

But does it work? Figuring out whether each one of these practices may be therapeutically viable is a challenge, and determining how all of them may work in concert is pretty much impossible. Combine them with acupuncturists’ frequent references to “qi,” or energy flow, and it’s easy for a lot of people to dismiss the practice as bunk.

Not so fast, though. A recent meta-analysis, which examines existing research on a topic, compared acupuncture treatment to standard medical treatment (the kind involving a doctor’s exam and drugs) for musculoskeletal pain, chronic headaches, and osteoarthritis. It also compared real acupuncture to “sham” acupuncture, a procedure where needles are inserted at random to make patients believe they were receiving acupuncture when they were not. “There are many poorly designed acupuncture studies out there, so we tried to include only the best trials,” says Andrew Vickers, a biostatistician at Memorial Sloan Kettering Cancer Center who coauthored the meta-analysis.

When comparing legit acupuncture to standard care, there was a statistically significant benefit to acupuncture, Vickers says. “We saw a measurable effect there,” he explains. “If acupuncture were a drug, we’d say the drug works.”

When Vickers and his team compared legitimate acupuncture to sham acupuncture, that benefit persisted, but shrank. There are a lot of ways to interpret this, Vickers says. “It could be acupuncture has a large placebo effect, or it could be that pressure points”—the precise locations at which needles are inserted—“are less important than acupuncturists claim,” he explains.

Many people equate placebo effects with scams. “The term placebo has always had this very negative connotation,” says Vitaly Napadow, director of the Center for Integrative Pain Neuroimaging at Harvard Medical School. But Napadow says our poor opinion of placebo needs revising. The human body has built-in systems for stoking or calming pain and other subjective sensations. “If a placebo can target and modulate these endogenous systems, that’s a good and a real thing,” he says.

But acupuncture may have effects even more profound than placebo. Napadow has conducted dozens of brain imaging studies on acupuncture in an effort to determine just how the treatment may or may not calm pain or related conditions like headache or arthritis. He says there are lots of ways acupuncture might work, and the specific mechanism may depend on the type of condition you’re trying to treat.

One possibility is that being jabbed with a needle induces a tiny injury, causing your immune system to respond by sending inflammatory proteins and other infection-fighting, would-healing chemicals to the source of that injury. “There’s the idea that by inducing many of these very small injuries, you’re ramping up the immune system so that it can deal with bigger problems,” Napadow says.

It’s also possible that the increased flow of blood and immune system chemicals to the poke site could help clear away accumulated cellular byproducts that may trigger or worsen a condition like plantar fasciitis or tendonitis, he says. “Or the needles might activate nerve receptors in the skin, which then pass info up into your spinal cord and brain,” he says. “That information might trigger a change in brain physiology, like the release of endorphins or those sorts of neurotransmitters that could lessen the sensation of pain associated with something like fibromyalgia.”

His research has borne out some of these potential mechanisms. One of his studies showed that after traditional acupuncture, opioid receptors were more available, or receptive, to the body’s natural pain-quelling chemicals. There was no such change after sham acupuncture.

It basically means opioid receptors were more available or receptive to the types of body hormones and chemicals that help quell pain.

Napadow says that more research has looked into the effect of expectancy on acupuncture outcomes—or whether people who believe the treatment will work experience more benefit than those who don’t. The evidence suggests that expectancy doesn’t improve acupuncture’s effectiveness. “Often it’s the guy who says his wife made him try it who has the greatest benefit,” he says.

Couple these promising findings with the fact that acupuncture is a low-cost treatment option with very few side effects, and Napadow says it makes sense to consider it a helpful partner to Western medicine—especially when it comes to chronic pain-related ailments for which Western medicine often relies on painkillers. “It won’t cure cancer,” he says. “But it could be effective for managing side effects of radiation or chemotherapy—things like pain or neuropathy or nausea.”

Tyiska, the Philadelphia-based acupuncturist, makes a similar argument. “I don’t tell people to stop seeing their doctors,” she says. “But if you’re being prescribed opioids, or you’re considering surgery, you lose very little by trying acupuncture first.”

http://time.com/4383611/acupuncture-alternative-medicine-pain/

Cannabis Provides Another Option For Nerve Pain

Today's well-reasoned post is from cannabisnow.com (see link below) and is targeted at people living with cancer and the pain it can bring. As you probably know, neuropathy is often the result of chemotherapy treatments for cancer but this article applies to severe non-cancer neuropathy sufferers as well as cancer patients. It's careful explanation of how cannabis works gives you various options to consider, if your nerve pain is severe and almost everything else has failed. Apart from that, cannabis (and CBD oil) is non-addictive and is a far safer option than most heavy duty drugs normally issued to control neuropathy symptoms. It has to work of course - the proof is in the pudding - but medical cannabis has advanced so far in terms of quality and variety, that it's surely worth a try. Do your research and talk to people and consider all the options.

Cannabis for Cancer 
By Sara Payan on May 30, 2017@cannabisnow


Photo Gabe Perry for Cannabis Now
 
Marijuana has long been known to ease certain cancer symptoms and alleviate the painful side effects of pharmaceutical cancer treatments. With the growing availability of concentrated and refined cannabinoids, treatment options are expanding and improving for patients seeking relief from a disease that touches the lives of billions. Cancer is the great equalizer: it does not discriminate by gender, age, race or socioeconomic background — it touches everyone, whether you have endured it yourself or supported a friend or family member’s journey.

Along with HIV, cancer was one of the first illnesses identified as benefiting from the therapeutic effects of cannabis. Early on the plant was found to be particularly effective for alleviating side effects caused by harsh pharmaceutical treatments like chemotherapy.

The antiemetic properties of cannabis are well known. Even those on the fence about medicinal cannabis generally acknowledge its benefits in terms of appetite stimulation and nausea relief for cancer patients. But when it comes to the effect of cannabis on pain, the general public’s understanding is still developing, even though many cancer patients report major pain relief from cannabis medicine.

Dr. Frank Lucido, a nationally recognized medical cannabis clinical specialist, said that pain is the most common complaint during consultations with patients undergoing cancer treatments.

“Often there are people who haven’t used cannabis before or haven’t used it in years but now they have a serious illness and they’re hoping it’s going to help their pain,” Lucido said.

He added that, while it can provide direct pain relief, the euphoric effects often decrease awareness of the pain.

“[Cannabis] does help pain in some people, some people don’t experience it as pain relief and describe it as ‘I still feel the pain but it’s not a central part of my life, I can still think of other things, it sort of distracts me.’”

Dr. Lucido often recommends high CBD medicine to patients who are afraid of experiencing euphoria, but he also lets them know that the mood-altering effects of THC can be helpful for working with the anxiety and depression that can come during cancer treatment.

Unfortunately, so much of what we know about the effects of cannabis on cancer patients is based on personal testimony and “anecdotal data,” not formal studies. Many medical professionals blame this lack of actionable clinical data on government obstructionism.

Among them, Dr. Donald Abrams. An oncologist who’s been practicing in San Francisco, California, for over three decades, Abrams pinned the lack of research on NIDA’s mandate to study cannabis as a “substance of abuse” instead of exploring its therapeutic effects.

In Cannabis Nurses Magazine’s oncology issue, Abrams outlined the therapeutic effects of cannabis on nausea, its uses for the treatment and prevention of neuropathy, the synergistic effects of opioids and cannabis for pain management and the possibility of cannabis’ anti-cancer properties.

He also said that he believes “the majority” of the patients he’s treated during his career have used cannabis during their treatment.

But for cancer patients who’ve already experienced the potentially life-changing benefits of cannabis firsthand, no clinical data is required — they know it works for them.

Judy is a 65-year-old endometrial cancer patient. She’s been orally ingesting a high-CBD oil to manage her pain and in hopes of slowing the growth of her cancer.

She says that she can tell the difference in her ease of movement. The ability to stand upright without pain when walking was not possible until she started medicating with the oil.

Her most recent tests have shown that the cancer has not spread and has slightly improved since she started her regimen nine months ago.

Judy said the use of CBD has also diminished her anxiety considerably.

“It’s changed my quality of life for the better,” she said.

Nurses working with palliative and hospice care patients are also acutely aware of the quality of life benefits cannabis use can provide those experiencing the often painful effects of cancer treatment.

Marcie Mar of the American Nurses Association said the adverse impacts of cancer treatments can linger for months.

“By the time they get to me they may have been off for a month, they may have been off for 6 months but when they get into hospice they’re not actively taking chemo,” she said. “But they are still suffering from the side effects, whether it’s neuropathy or chronic nausea, insomnia and on top of just the fear of where the cancer has brought them to.”

Mar has seen patients receive great relief from the use of transdermal patches and low dose edibles. Topicals tend to be the most popular way of medicating, especially for her senior patients.

Since her patients live in Colorado, family members can pick up various cannabis products to help mitigate their loved one’s discomfort. Hopefully as more states open to cannabis sales to adults even more people will discover its medical applications.

TELL US, do you use cannabis to treat a medical condition?

Originally published in Issue 25 of Cannabis Now. LEARN MORE

Sara Payan is an award-winning cannabis educator specializing in cancer related therapies. She is the director of education at the Apothecarium, vice-chair of the San Francisco Cannabis State Legalization Task Force, writer, industry consultant, patient advocate and stage-three colon cancer survivor. Sara has presented at Patients Out of Time, Women Grow and The Women's Visionary Congress. Her work has been highlighted in Dope Magazine, Cannabis Now, and Ladybud. 

https://cannabisnow.com/cannabis-for-cancer/

Tapentadol An Opioid Option For Severe Neuropathy

Today's article from medscape .com (see link below) talks about a drug that has been on the market for a short time  but has had displayed good results for patients with severe and painful neuropathy. The problem is that it's an opioid (although one of the better-tolerated opioids) and there are two objections that stand in the way of it being more widely prescribed. It's apparently expensive and insurance companies are reluctant to pay for it and possibly because of that, the moral argument against opioids in general (addiction dangers, public image) is strengthened. Tapendatol (Nucynta) however, has had such good results with less side effects, that many specialists are wondering why it isn't more widely prescribed. You are unlikely to be prescribed opioids unless your pain is severe and chronic and you've already been through the gamut of other options and even then many doctors are also biased against opioids. New evidence has shown however, that if used properly and under supervision, opioids can be extremely useful in reducing nerve pain and improving the quality of life of patients and Tapentadol seems to be step forward in refining opioids for safer use. Maybe worth discussing with your doctor, if the pain is affecting your life badly.

Tapentadol is 'Third-Tier' Drug for Diabetic Neuropathic Pain
Lara C. Pullen, PhD June 04, 2014

The opioid analgesic tapentadol (Nucynta, Janssen Pharmaceuticals) is approved for use in patients with painful diabetic peripheral neuropathy in the United States, but it is expensive, and most insurance companies require physicians to first attempt multiple other drugs before prescribing it, says the lead author of a new paper describing the efficacy and tolerability of this agent.

The agent is also a scheduled narcotic, which further deters doctors; thus, tapentadol is currently a "third-tier" drug for the treatment of diabetic peripheral neuropathy, Aaron I. Vinik, MD, PhD, from East Virginia Medical School in Norfolk, told Medscape Medical News.

Dr. Vinik and colleagues' findings were published online May 21 in Diabetes Care. While the results show tapentadol is an effective treatment for diabetic peripheral neuropathy, "it is not being prescribed as much as I thought it would be," he said.

John D. England, MD, from the department of neurology at Louisiana State University Health Sciences Center School of Medicine in New Orleans, who was not involved with this research, agrees that doctors are uncomfortable prescribing this agent.

"[Tapentadol] is a [Drug Enforcement Administration] schedule II narcotic and has significant potential for abuse and addiction. It is only indicated for moderate to severe pain. For the treatment of neuropathic pain, there are many other drugs that are safer and have fewer adverse effects. This drug, like all opioids, would be a last-tier option for neuropathic pain," he explained in an email.

Dr. Vinik says he also has another reason to hesitate when considering tapentadol for this indication, "I prescribe it in very specific circumstances. I am keen on managing diabetic peripheral neuropathy based on comorbidity," he elaborated.

Tapentadol ER Effective and Well Tolerated

An extended-release (ER) formulation of tapentadol was approved for use in painful diabetic peripheral neuropathy by the Food and Drug Administration in August 2012, and the United States is currently the only country in which this agent is approved for this indication.

In the newly published study by Dr. Vinik and colleagues, adults with moderate to severe diabetic peripheral neuropathy pain were titrated to tapentadol ER 100 to 250 mg twice daily during a 3-week open-label period. Patients with 1-point or more reduction in pain intensity (11-point numerical rating scale) at the end of titration were then randomized to receive placebo or tapentadol ER, at the optimal dose determined from titration, for a 12-week, double-blind, fixed-dose maintenance phase.

The primary end point was mean change in average pain intensity from the start to week 12 of the double-blind maintenance phase.

A total of 358 patients completed the titration period; 318 patients (placebo, n=152; tapentadol ER, n=166) were randomized and received 1 or more doses of double-blind study medication. Mean pain intensity was 7.33 at the start and 4.16 at week 3 of the open-label titration period (mean change, –3.22).

The mean change in pain intensity (a positive value indicates worsening of pain) from start of double-blind treatment to week 12 was 1.30 for placebo vs 0.28 for tapentadol ER (P lt; .001 in favor of tapentadol).

Dr. Vinik said while there was quite a high rate (35%) of gastrointestinal disturbances, such as nausea and vomiting, observed with tapentadol ER, as well as a high rate of dizziness (12%) and headache (4%), the side effects did not stop patients from taking the medication.

"Tapentadol ER (100–250 mg [twice daily]) was effective and well tolerated for the management of moderate to severe chronic pain associated with diabetic peripheral neuropathy," he and his colleagues conclude.

Treating Pain Based on Comorbidity

However, in practice, Dr. Vinik noted that many patients with painful diabetic neuropathy also experience sleep disorders, anxiety, and/or depression. So physicians should ideally prescribe drugs that will treat as many of these comorbidities as possible, looking for the best fit with the total clinical picture of a patient.

If a pharmaceutical treatment can ameliorate sleep disturbance, it may also have a significant effect on pain, he noted. Unfortunately, in the case of tapentadol and many other drugs prescribed for diabetic neuropathy, their effect on sleep has not been well studied, he observed.

While many physicians and patients believe a number of commonly prescribed medications to have a beneficial effect on sleep, research shows that while an agent may make a patient tired, for example, it doesn't necessarily help the patient to sleep. For instance, a commonly prescribed drug for diabetic neuropathy, duloxetine (Cymbalta, Eli Lilly), actually fragments sleep, he explained.

Dr. Vinik suggests that, when treating a patient with diabetic peripheral neuropathy and sleep disturbance, a gabapentinoid may be the best option.

Anxiety is a common comorbidity with diabetic neuropathy, too, but unfortunately, tapentadol is also not particularly effective for anxiety, he added, noting that tricyclic antidepressants may be the best option for these 2 coexisting conditions.

He warns, however, that tricyclics may have cardiac effects, and thus physicians should take care to evaluate the cardiac status of patients before and after prescribing these older antidepressants.

Depression and Diabetic Neuropathy: A Good Fit for Tapentadol?

The other common comorbidity, occurring in approximately half of all patients with diabetic neuropathy is depression. While tricyclics may be an effective treatment for depression alone, they do not appear to ease the pain of patients with both conditions.

While he cautioned that patients who are bipolar do not respond well to either tapentadol or duloxetine, he said that the unique properties of tapentadol — it is a combination of a µ-opioid-receptor agonist and a norepinephrine-reuptake inhibitor in a single molecule — means it is possible for the physician to prescribe 1 drug instead of 2 for patients with diabetic peripheral neuropathy and classic depression.

For this reason, tapentadol is a good addition to the physician arsenal and can be extremely beneficial for the right patient because it not only relieves pain but also has the potential to elevate mood, he concluded.

Editorial support was funded by Janssen Research and; Development and Grünenthal. Dr. Vinik received funding for this study from Janssen; disclosures for the authors are listed in the article. Dr. English has reported no relevant financial relationships.

Diabetes Care. Published online May 21, 2014. Abstract

http://www.medscape.com/viewarticle/826174