Memantine for Neuropathic Pain & Complex Regional Pain Syndrome, CRPS


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Neuropathic pain syndromes show an over-expression of NMDA receptors in the brain in animal models. Ketamine blocks the NMDA receptor. Another medication with the same mechanism, but in pill form is memantine. This report on six patients of the use of memantine for Complex Regional Pain Syndrome (CRPS) from 2007 in the Clinical Journal of Pain, six months after treatment with memantine, showed significant decrease in pain, improved motor symptoms and autonomic changes, and fMRI changes on the affected side improving, comparable to the unaffected side of the brain.

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It was approved for Alzheimer’s dementia gradually titrating to a dose of 28 mg/day, but for decades has been very useful off label for neuropathic pain including but not limited to CRPS, at a dose of 55 mg/day, and in recent years often prescribed for migraine.

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Ketamine is highly successful also for treatment resistant depression, and one patient, a psychiatrist disabled from the unfortunate triad of intractable neuropathic pain, migraine and treatment resistant depression, while slowly titrating to a dose of 55 mg/day, a process that takes almost 3 months, found depression relieved for the first time in decades at the dose of 35 mg. It was highly effective as one component of the multi-pronged approach for all three conditions.

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This life is a hard fact. We all need all the help, encouragement and positive attitudes we can get. Complex intractable pain and/or depression requires rational polypharmacy, selectively chosen based upon well known mechanisms, neurotransmitters, receptors, hormones, stress reduction, cognitive behavioral therapy, physical therapy, occupational therapy, nerve blocks, etc. Several choices were summarized almost two years ago here.

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In my experience, memantine is very well tolerated with few if any side effects but covered by insurance only for mild to moderate dementia. Thus, not only is it highly challenging to treat neuropathic pain, but important to creatively meet the challenges of our backwards medical system that barely recognizes the needs of those with chronic pain.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Opioids increase risk of chronic pain – potentiate pain – faster, stronger, longer. Activate TLR4 receptor on microglia, blocked by low dose naltrexone (LDN)


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Professor Linda Watkins was the distinguished keynote speaker at the May 2015 American Pain Society annual meeting and gave the NIH 2015 Kreshover Lecture:

“Targeting Glia to Treat Chronic Pain: Moving from Concept to Clinical Trials.”

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The University of Colorado at Boulder describes her work

She has authored or co-authored over 190 book chapters, review articles and journal articles.

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Dr. Watkins’ research focuses on 3 inter-related areas. Her primary research interest is understanding how to control clinically relevant pathological pain states. Her group’s research points to a novel reason that clinical pain has been impossible to successfully control. That is, pathological pain is being created and maintained by a surprising cell type, namely glia. These cells, upon activation, dysregulate normal pain processing by the spinal cord neurons.

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Medical News Today published news of her recent study April 19, 2018

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“Opioids may increase risk of chronic pain.” They potentiate pain “faster, stronger, longer” and activate the TLR4 receptor on microglia. That receptor is blocked by low dose naltrexone (LDN).

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Opioids trigger inflammation in the brain and spinal cord. This is an elegant study by renowned Prof. Linda Watkins at the University of Colorado Boulder, with Peter Grace. His early work on LDN brought him from Australia to postdoc at her lab and now research at MD Anderson Cancer Center.

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“Having been used in one form or another for millennia, opioids beat pain into submission, quickly making the patient more comfortable. The latest study, which was carried out at the University of Colorado Boulder, turns this firmly held notion on its head.

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Senior author Prof. Linda Watkins, from the Department of Psychology and Neuroscience, says, ominously, “[…] there is another dark side of opiates that many people don’t suspect.”

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In this case, it is not addiciton issues that Prof. Watkins is referring to. Paradoxically, opioids may actually prolong pain following surgery. The results were published recently in the journal Anesthesia and Analgesia.

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Postsurgical pain and opioids examined

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For the study, Prof. Watkins and colleague Peter Grace, of MD Anderson Cancer Center in Houston, TX, carried out laparotomies on male mice. This procedure involves making an incision through the abdominal wall to access the interior of the abdomen, and it is done on tens of thousands of U.S. individuals each year.

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“Opiates are really effective for acute pain relief. There is no drug that works better. But very little research has been done to look at what it is doing in the weeks to months after it’s withdrawn.”

Peter Grace

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Following surgery, one group of rats received the equivalent of a moderate dose of morphine for the next 7 days, while another group received morphine for 8 days, and the dosage was tapered off by day 10.

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Another group was given morphine for 10 days, after which point treatment stopped abruptly. A final group was given saline injections rather than morphine as a control.

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And, in another experiment, a group of rats received a 7-day course of morphine that ended 1 week before surgery was carried out.

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Before the morphine regimes commenced, and after they had been completed, the rats’ sensitivity to touch was measured, as was the activity of genes related to inflammation in the spinal cord.

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Compared with rats given saline, those that received morphine endured postoperative pain for over 3 additional weeks. Also, the longer the morphine was provided, the longer the rats’ pain lasted.

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The study also revealed that tapering of morphine dosage makes no difference. As Grace explains, “This tells us that this is not a phenomenon related to opioid withdrawal, which we know can cause pain. Something else is going on here.”

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How can morphine raise postoperative pain?

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The next question to ask, of course, is what drives this counterintuitive effect. Prof. Watkins calls it the result of a “one-two hit” on glial cells.

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In the brain, glial cells are more numerous than neurons. They protect and support nerve cells and, as part of their role as protector, they direct the brain’s immune response, including inflammation.

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The first “hit” occurs when surgery activates glial cells’ toll-like receptor 4 (TLR4). Prof. Watkins calls these “not me, not right, not O.K.” receptors; they help to orchestrate the inflammatory response. This first hit primes them for action when the second hit occurs.

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The second hit is morphine, which also stimulates TLR4. As Prof. Watkins explains:

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“With that second hit, the primed glial cells respond faster, stronger, and longer than before, creating a much more enduring state of inflammation and sometimes local tissue damage.”

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Although the study is in an animal model and will need replicating in humans, it does line up with previous findings.

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For instance, in 2016, the same scientists published another animal study, which found that a few days of opiate treatment for peripheral nerve pain exacerbated and prolonged pain. In that study, the activation of inflammatory pathways was also implicated.

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“An unusually high number of people end up with postoperative chronic pain,” explains Prof. Watkins. In fact, millions of U.S. individualssuffer with chronic pain. “This new study lends insight into one explanation for that.”

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Interestingly, the rats that received a course of morphine that ended a week before surgery did not experience prolonged postsurgical pain, leading the study authors to conclude that there is “a critical window for morphine potentiation of pain.”

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Because opioids are currently considered the best course of action to deal with postoperative pain, if these results are replicated in humans, it leaves medical science in a difficult situation.

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This is why Prof. Watkins is focusing much of her energy on designing drugs that could be given alongside opioids to dampen down the inflammatory response. She is also exploring alternative painkillers, such as cannabinoids.”

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Spinal Cord Stimulation, Current Status 2017


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One of the top read articles in 2017 from the journal Pain (free pdf).

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Click title below:

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Current status and future perspectives of spinal cord stimulation in treatment of chronic pain

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Geurts, José W.a,*; Joosten, Elbert A.a,b; van Kleef, Maartena

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3. Complications and side effects

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“Complications and side effects (adverse events) acquiring reinterventions often occur during treatment with SCS.6,8,16,20,37 Complications include deep and superficial infections or equipment-related side effects like hardware malfunction, lead migration, fractured electrode, pulse generator discomfort, and battery replacements. Localized pain over the implanted hardware occurs regularly, on average in 6% of cases.6 This pain, for instance, can present as pain around the implanted pulse generator or over the lead. Such pain typically leads to replacement of the lead and therefore an additional surgery. Removal of the SCS system may be necessary in cases of deep infection or treatment failure. A prospective study performed over 12 years8 showed adverse events in 61% of patients. However, the complication rate was significantly reduced during the last 4 years of the study from an annual mean of 30% to 22%. The authors concluded that this was likely due to technological developments and improvements in the SCS hardware. Another explanation for this reduction is that the physicians treating patients gradually gain experience in a particular implant technique.22 New implantation techniques like DRG-STIM have been reported to cause more complications and it has been concluded that refinement and optimization of the technique are needed to minimize adverse events.22

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5. Future perspectives of spinal cord stimulation

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….”A point of concern is that, at present, cost-effectiveness of SCS is impeded by the high cost of the device and the high incidence of complications and side effects requiring reintervention and surgery. Consequently, SCS treatment is not accessible for everyone in the world and up to now is only available for selected indications.”….

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Among problems from spinal cord stimulators that I have seen in those with CRPS, the procedure has created a new pain that is now #1 most severe, often at the battery pack that is placed at the low back. Several patients reported units were explanted with difficulty due to severe scar formation.   

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Reference

[8]: Geurts JW, Smits H, Kemler MA, Brunner F, Kessels AG, van Kleef M.

Spinal cord stimulation for complex regional pain syndrome type I: a prospective cohort study with long-term follow-up.

Neuromodulation 2013;16:523–9; discussion 529.

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Objectives: Spinal cord stimulation (SCS) is an effective treatment for intractable complex regional pain syndrome type I pain. Long-term data are scarce on effectiveness, degree of pain relief, predictors, and complications.

Materials and methods: From 1997 to 2008, 84 consecutive patients who received an implanted SCS system after positive test stimulation were included in the prospective study. Treatment effectiveness was assessed annually as measured by mean visual analog scale pain scores and with the Patients Global Impression of Change scale. Treatment success was defined as at least 30% mean pain relief at end point and treatment failure as explantation of the system. A Cox regression determined if baseline factors were associated with both these outcomes.

Results: During 11 years, 41% (95% CI: 27-55) of the patients experience at least 30% pain relief at assessment end point. During 12 years of follow-up 63% (95%CI: 41-85) of the implanted patients still use their SCS device at measured end point. Pain relief of at least 50% one week following test stimulation is associated with a higher probability of long-term treatment success. In 51 patients, 122 reinterventions were performed over 12 years; 13 were due to complications, 44 to battery changes, and 65 reinterventions were equipment related.

Conclusion: SCS provides an effective long-term pain treatment for 63% (95%CI: 41-85) of implanted patients. Forty-one percent (95%CI: 27-55) of SCS treated patients have at least 30% pain reduction at measurement end point. The number of reinterventions after implantation due to equipment-related problems, battery changes, and complications is 122 over 12 years of follow-up. Sixty-one percent (N = 51) of the patients had at least one reintervention. Mean pain relief of at least 50% (visual analog scale) one week after the test stimulation is associated with long-term treatment success.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~

Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

~~~~~

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Spinal Cord Stimulators – Not Allowed to Sue Medtronic – Supreme Court Ruling 2008


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More than any other topic  readers seem to read and comment more about serious problems with the Medtronic spinal cord stimulator than anything else on this site, yet they overlook this post last week: 

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Supreme Court ruling 2008

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Riegel v Medtronic

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Patients Who are Implanted with High-Risk Devices

 

Not Allowed to Sue

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And the problems never get addressed. There is no accountability for the damage to spinal cord that so many experience—the spinal cord for Pete’s sake —and no research on the incidence of the many different problems. If complications were not severe, thousands would not care to search the subject.

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Perhaps a person with a legal background would discuss how that case was won.

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How can this possibly be right? 

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~

Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

~~~~~

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Cannabis That Can Stop the Munchies? What is THCV?


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MEDICAL MARIJUANA

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Cannabis is legal in California for adult use as of January 1, 2018. This may be helpful to someone you know. It is a most important drug. Below you can find a few pointers that are basic to understanding what strains to try. Distributors are swamped with ten times as many buyers as last week, prices are doubled, taxes are very high, it is very expensive and you will need to test many strains before you find what works for you without making you stupid with euphoria that lasts 12 hours. Do be warned of turning the body into sofa-size obesity overnight. Munchies occur with high THC strains. To discuss below how to avoid that torture and still relieve pain or muscle spasm.

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Horvath et al at Yale in 2015 found cannabis stimulates hunger and arousal in hypothalamic neurons. Here’s the YaleNews on the multi-authored work.

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Horvath is the Jean and David W. Wallace Professor of Neurobiology and of Obstetrics, Gynecology, and Reproductive Sciences, director of the Yale Program in Cell Signaling and Neurobiology of Metabolism, and chair of the Section of Comparative Medicine.

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To orient you in the quote below, cannabinoid receptor 1 (CB1R) is one of the two known cannabinoid receptors in the brain. Others are located outside brain, throughout the body.

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“The Pomc gene encodes both the anorexigenic peptide α-melanocyte-stimulating hormone, and the opioid peptide β-endorphin. Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake. CB1R activation selectively increases β-endorphin but not α-melanocyte-stimulating hormone release in the hypothalamus, and systemic or hypothalamic administration of the opioid receptor antagonist naloxone blocks acute CB1R-induced feeding.

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Interesting. Low dose naltrexone, which is essentially long acting naloxone, may block munchies in humans? At what dose? Please comment if you take naltrexone 4.5 mg or 15 mg (anti-inflammatory doses) or 28 mg (weight loss dose) or 50 mg and above doses of naltrexone (high doses for addiction).

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One strain that is better at stopping or reducing the munchies, and that is believed due to a cannabinoid in the strain called THCV. You can always do a search for THCV.

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Cannabis is one of the few medications that can relieve some of the worst side effects of opioid withdrawal. Many patients find they need to use fewer opioid pills for pain or can stop them altogether; they need to use fewer muscle relaxants; and they can eat or sleep better if they use cannabis. Once cannabis became legal, many alcoholics were able to give up alcohol because their first preference is cannabis.

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Get a low cost recommendation for medical marijuana in minutes at home from your mobile phone. The best source for recommendation is : HelloMD.

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Cannabis may be legal in all states once tobacco companies toss some money at Congress. Could cannabis be related to the vow of Phillip Morris and a wave of big tobacco companies to stop selling cigarettes this year?

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It is dreadfully expensive and heavily taxed. All states should adopt New Mexico’s law that allows healthcare insurers to reimburse patients who have paid for medicinal cannabis. Voters…

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Cannabis is made by the body and the brain makes two of the endogenous cannabinoids. If is highly anti-inflammatory, and profoundly important mainly in the immune system but also in bone turnover. You have more cannabinoid receptors in your body than any other kind. It is as old as sponges, an ancient medicine.

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A WORTHY READ

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Mr. X – by Carl Sagan who describes his experience with marijuana at length and used it creatively for decades opening his brain to experiences he was otherwise not oriented to at all.

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MUNCHIES

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Fear the munchies. Cannabis, medical marijuana, can cause the munchies, an overwhelming desire to eat nonstop, usually all the most high calorie things your desperately fevered brain can dream of cramming in.

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Certain strains of cannabis can be life saving for those who have loss of appetite from conditions such as cancer, HIV/AIDS, depression, inflammatory conditions, etc. But the munchies can be disastrous when you cannot afford to gain weight due to pain or disability or simply wish to develop an important standard to maintain best health which means good lean body weight. The best way to reduce inflammation is to avoid obesity, avoid sugar, avoid diabetes, heart attacks, strokes. Remember inflammation is the root cause of 90% of the conditions we die of: diabetes, cancers, Alzheimer’s, Parkinson’s, autoimmune disease, atherosclerosis, etc.

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Those with an eating disorder should scrupulously avoid those strains that are highly rated for helping anorexia, loss of appetite.

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CHOOSE STRAINS THAT STOP THE MUNCHIES

STRAINS WITH HIGH THCV  OR HIGH CBD 

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If needing high THC for pain or appetite, for example, then a strain with high THC and high THCV is Durban Poison. Read in detail about strains on leafy.com using the search function and it will find dispensaries in your area.

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If low THC is all you need, then Leafly discusses high CBD strains with low THC currently available. Google it or ask the dispensary.

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I am not going to do more than mention these three cannabinoids: THC, CBD, THCV. You can google them but do glance at my outdated 2009 cannabis website – CBD has vastly changed since then, available even at farmer’s markets and nutrition departments of groceries.

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The cannabis plant has 400 chemicals of which about 86 are known cannabinoids but we focus on just a few and hybrids have been bred to display many qualities and various percentages of cannabinoids.

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THC

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THC, tetrahydrocannabinol, can cause euphoria and is the principal psychoactive ingredient useful for pain, depression, appetite, multiple sclerosis, fatigue, stress, and many conditions including just to have fun, be giggly or creative. For the California Medical Board, a strain with 18% THC is considered high, but some strains such as Holy Grail have 27% or more THC. Some strains are noted for causing more anxiety or paranoia due to THC content. It is widely said THC is necessary for pain relief but… see CBD below.

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CBD

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CBD, cannabidiol, a non-psychoactive cannabidiol that blocks the psychoactive component of THC so that you may be able to mix with THC in order to use a stronger dose of THC for the underlying condition —  find your best ratio of CBD to THC. Or use 100% CBD. Among strains of flower sold at dispensary, I’m not sure what % CBD

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Some people are highly sensitive to THC (paranoia, panic attacks, anxiety) and cannot use any THC or only very tiny amounts of THC with higher percentage CBD.

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Some use pure 100% CBD which is said to be useful for Crohn’s Disease, PTSD, multiple sclerosis and certain seizure disorders, the severe childhood Dravet Syndrome. There is a recent single report of an adult who failed all anticonvulsants and responded to CBD alone. I have seen a patient with depression after 2 years of severe disability from 4 major chronic pain conditions, surprisingly all pain 100% relieved by CBD. It is widely said that THC is essential for pain relief but for this case not needed.

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Some dispensaries will mix liquid CBD:THC in ratios of 15mg/mL CBD to 0.1 mg/mL CBD all the way up to ratio of 15:15 or more. Use topically, under tongue or swallow. One patient dilutes and uses topically. Very expensive!!! It is the only thing helping his extremely painful autoimmune neuropathy.

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THCV

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Leafly discusses ten strains that will not make you (as) hungry

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After discussing high CBD strains, then turn to high THCV:

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High THCV Sativa Strains

“By now you know what THC and CBD is, but you may not be familiar with the less ubiquitous THCV, a related chemical that suppresses appetite. While most strains on the market today tend to test anywhere between 10-20% THC, what’s considered a high THCV content might only hit a high-water mark of 5%. THCV tends to be more abundant in sativa strains, and it’s possible you’ve noticed that sativas tend to provoke hunger less than indica strains. The unique metabolic effects of THCV even have researchers considering its utility in treating obesity and diabetes.”

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Durban Poison is the name of the strain with highest THC and THCV, and a good profile detailed on Leafly: Maximal effect is Energetic > happy > uplifted >> focused >> euphoric. Not everyone may have all these effects.

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Always check Leafly’s negatives for each strain and look at the bar graphs — how severe are the side effects? Note that always worst is dry mouth. Half as bad are dry eyes for this strain – at least not as bad as dry mouth; and much lower in incidence is dizzy, anxious, paranoid. Overall a very good profile for a high THC strain.

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RISKS

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Note, those with Sjogren’s Syndrome who have dry eyes are at risk for corneal transplants and who have dry mouth are at risk for all teeth crumbling, so choose and treat accordingly.

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Cannabis can increase pulse and blood pressure which can be a risk of heart attack and stroke for any age. It is especially likely if you are naive to the drug, i.e. have never used it or have not introduced it to your system for decades. Check blood pressure and pulse before use and after you feel the peak effect.

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The youngest person I found on the internet who died of heart attack caused by cannabis was a healthy 17 year old male, possibly a false report, but cardiac arrhythmias can be fatal and there are undiagnosed cardiac conditions in young athletes who may be likely to use cannabis.

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Cannabis can interfere with memory.

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The adolescent developing brain may be vulnerable to harmful effects.

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HOW TO USE IT

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Vaporize it. Avoid 4 toxins. Rapid onset, short duration of effect.

If smoking, you will inhale 4 major toxins.

Use under tongue or topically on skin.

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If you swallow cannabis, you will not feel effect for 90 to 120 minutes so allow 2 hours before you add more or you may seriously overdose. Duration of effect may be 4 to 12 hours or more – overdosing can last days.

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5 mg oral THC may be too much for a starter dose for some people, but may be average for many, and some may need 10 mg. But heavy users need far, far more: TOLERANCE DEVELOPS!!! Money down the drain. Use only as much as you need or you will develop tolerance and require more frequent and higher and higher doses to reach same effect. That can be unaffordable for the average middle class person. 

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And yes, it may appear in urine for 30 to 60 days, possibly more.

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Cannabis is still a schedule I drug. The Emperor has no clothes. Do not take it onto planes or attempt to mail it.

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Do read more about it on my cannabis website linked above. It is a drug. You will benefit from learning how to use it.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~

Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

~~~~~

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

.

Please IGNORE THE ADS BELOW. They are not from me.

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Editorial from PAIN: Hijacking the endogenous opioid system


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Neuropathic pain responds poorly to opioids, often not at all, and may become worse with treatment.

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I have seen pain improve in many after tapering off.

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Then you must treat pain without opioid; it doesn’t just disappear, but it will not be as intense. This editorial explains some of the reasons opioids become a problem.

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Excerpted from an editorial in the current issue of PAIN

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[emphasis mine]

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[COT = chronic opioid therapy]

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…..This review highlights why we may see some of the more insidious problems that occur with COT, which are summarized below.

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Individuals on COT may continue to “need” opioids to replicate the functions of endogenous opioids that are no longer being released (or are in competition with the exogenous opioids). As the review by Ballantyne and Sullivan states, “a new homeostasis is reached that can only be maintained by continued drug taking”.1 Individuals on COT lose the ability to endogenously improve mood, decrease stress, and socially engage because the endogenous opioid system becomes inherently less responsive. In pain management, we know of this need for increasing opioid dose over time to maintain analgesia as opioid tolerance. But a similar physiological phenomenon likely occurs with any endogenous opioid function. Although we have mainly anecdotal reports from individuals who have been weaned off of opioids, the change in personality, social engagement, motivation, fatigue, and mood is often profound when individuals on COT successfully taper to lower doses or off opioids. These insidious side effects of COT would all be expected to inhibit individuals from maximally engaging in the patient-centric, disease management strategies that are now recommended for all chronic pain states.

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This may also explain why it is often very difficult to taper individuals on COT completely off opioids and underscores the importance of a slow, structured weaning protocol with appropriate psychological support. It may take months or years for endogenous opioid function to return to normal after cessation of opioids, or perhaps this system never returns to normal in some patients (as seems to occur in heroin addicts).5

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This paralysis of the endogenous opioid system by COT could render ineffective many other treatments that are recommended for chronic pain and that work in part via the endogenous opioid system. Many if not most nonpharmacological therapies for pain, such as exercise, acupuncture, and many other mind-body therapies are believed to work in part by engaging endogenous analgesic pathways that are partly opioid dependent.

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Opioids have acute antistress and antidepressant effects, and many of our patients with chronic pain are taking opioids chronically to medicate their co-morbid depression, despair or distress more so than to treat pain. Brain imaging studies indicate that many brain regions typically involved in pain and sensory processing are also involved in affective regulation. Patients having chronic pain who show higher degrees of psychological comorbidity or stress might therefore desire opioids because of their temporary salutary effects on these domains, rather than for their intended analgesic effects. We need to develop better cognitive-behavioral and psychosocial interventions that target the needs of the many patients with pain experiencing more harm than benefit from opioids, but still seek these drugs to reduce their affective symptoms.

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The endogenous opioid system may actually participate in the pathogenesis of some chronic pain conditions making this class of drugs particularly problematic for some patients. Many lines of evidence suggest that individuals with more centralized pain conditions such as fibromyalgia are particularly unresponsive to opioids, and the endogenous opioid system may be participating in the pathogenesis of these conditions.2,7 This has tremendous clinical implications because it means that we may actually make these patients’ pain worse by administering opioids. These same individuals may also be those at highest risk for prolonged use of opioids initially given for acute pain, both because they need higher doses for longer durations, and they are more likely to have the psychological comorbidities that drive unintended use and misuse.

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We clearly need to re-think the focus of opioid education and screening programs in light of some of these observations. After any exposure to an opioid, especially following the very common use in the United States for treating acute pain, patients can become addicted or can misuse these drugs to treat concomitant despair, depression, or pain elsewhere in the body that would not be expected to be responsive to an opioid. As we contemplate risk evaluation and mitigation strategies to curb further opioid misuse and addiction, we need to better appreciate these common alternate paths to unintended uses of opioids.

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We are not the first field to underappreciate the consequences of hijacking a critical endogenous system for one purpose, only to eventually find that there are significant consequences. Following the discovery of the endogenous corticosteroid system, Hench and others found that cortisone was an extremely effective treatment for rheumatoid arthritis, and this revolutionized our treatment of inflammatory processes. But it took several decades to fully appreciate all of the intermediate and long-term side effects of chronic corticosteroid use.4 Nearly all of these under-recognized issues were due to off target effects of exogenous corticosteroids on critical endogenous functions of these hormones. Although the short-term effects of opioids have been understood for centuries, long-term, high-dose opioids have only been advocated for a few decades. It is likely that we are now witnessing a similar clinical phenomenon, and as we increasingly appreciate the off-target effects of repurposing a critical endogenous system, the pendulum needs to rapidly swing back towards caution with prescribing a class of drugs that have a plethora of serious side effects other than addiction and death from overdose.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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Best wishes to all!


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Please ignore the Advertising – has nothing to do with me.

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