Spinal Cord Stimulators – MRI scans never again


.

.

.

Spinal cord stimulators may not help, but once placed, the wire leads can never be removed. People do not realize that they can never have an MRI scan no matter how much they need one. Wire leads are placed on the spinal cord and powerful magnets cannot go near those wires.

.

It’s tragic. Patients say no one told them. People live for decades with useless hardware embedded on their cord. The wires become encased by scar on nerve tissue, the cord itself. Should that person ever develop cancer, stroke, infections, seizures, Multiple Sclerosis, fractures, etc, and need a scan, an MRI is not possible.

..

It’s easy to ignore any future need for MRI scans when all the experts are giving an ultimatum telling you these stimulators can help your pain. With CDC’s lower opioid guidelines in March 2016 that dropped doses for millions, there might even be a huge bonanza for the companies that make these partially tested devices.

.

A list of words in the informed consent is not the same as seeing videos of patients who have had to deal with serious problems from them. It’s very sad, tragic, facing cancer or other conditions that cannot be studied adequately.

.

After billions in profit, there is no long term study showing how effective they are after five years, and even after two. It’s time to know the true cost and benefit analysis. But that will never be known, not once the green light was given and money started rolling in.

.

.

.

.

.

.

 

The material on this site is for informational purposes only.

.

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

.

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

~~

This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

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

..

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

.

..

..

.

.

.

.

.

.

 

Metformin – Nerve Pain & Microvascular Pain (angina)


.

.

.

Metformin & Pain

.

.

A diabetes drug used for many who have no diabetes. Recent discussion on metformin here and here.

.

Metformin “can lead to a long-lasting reversal of pain hypersensitivity even long after treatment cessation, indicative of disease modification.” [ref below]

.

.

References:

.

A successful case of pain management using metformin in a patient with adiposis dolorosa.

International Journal of Clinical Pharmacology and Therapeutics

.

.

In this case report, we describe a patient with Dercum’s disease who was successfully managed with metformin. The administration of metformin reduced pain intensity from 9/10 to 3/10 and favorably affected the profile of inflammatory cytokines (i.e., TNF a, IL-1β, IL-6, and IL-10), adipokines (i.e., adiponectin, leptin, and resistin), and β-endorphin. Because each variable was affected moderately by the drug, in the range of 20 – 30%, it follows that these effects are additive, i.e., they act independently of each other. However, taking into account advances in the pharmacology of metformin, it seems that other phenomena, such as modulation of synaptic plasticity, activation of microglia, and autophagy of the afferents supplying painful lipomas should be taken into consideration. Nonetheless, metformin deserves further exploration in the biology of pain.

.

.

The use of metformin is associated with decreased lumbar radiculopathy pain

Journal of pain [2013], from University of Arizona Tucson, Ted Price’s lab, and USC

.

Abstract:

Lumbar radiculopathy pain represents a major public health problem, with few effective long-term treatments. Preclinical neuropathic and postsurgical pain studies implicate the kinase adenosine monophosphate activated kinase (AMPK) as a potential pharmacological target for the treatment of chronic pain conditions. Metformin, which acts via AMPK, is a safe and clinically available drug used in the treatment of diabetes. Despite the strong preclinical rationale, the utility of metformin as a potential pain therapeutic has not yet been studied in humans. Our objective was to assess whether metformin is associated with decreased lumbar radiculopathy pain, in a retrospective chart review. We completed a retrospective chart review of patients who sought care from a university pain specialist for lumbar radiculopathy between 2008 and 2011. Patients on metformin at the time of visit to a university pain specialist were compared with patients who were not on metformin. We compared the pain outcomes in 46 patients on metformin and 94 patients not taking metformin therapy. The major finding was that metformin use was associated with a decrease in the mean of “pain now,” by −1.85 (confidence interval: −3.6 to −0.08) on a 0–10 visual analog scale, using a matched propensity scoring analysis and confirmed using a Bayesian analysis, with a significant mean decrease of −1.36 (credible interval: −2.6 to −0.03). Additionally, patients on metformin showed a non-statistically significant trend toward decreased pain on a variety of other pain descriptors. Our proof-of-concept findings suggest that metformin use is associated with a decrease in lumbar radiculopathy pain, providing a rational for larger retrospective trials in different pain populations and for prospective trials, to test the effectiveness of metformin in reducing neuropathic pain.

.

.

The anti-diabetic drug metformin protects against chemotherapy-induced peripheral neuropathy in a mouse model.

PLoS One [2014] from MD Anderson Cancer Center

 .

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) characterized by loss of sensory sensitivity and pain in hands and feet is the major dose-limiting toxicity of many chemotherapeutics. At present, there are no FDA-approved treatments for CIPN. The anti-diabetic drug metformin is the most widely used prescription drug in the world and improves glycemic control in diabetes patients. There is some evidence that metformin enhances the efficacy of cancer treatment. The aim of this study was to test the hypothesis that metformin protects against chemotherapy-induced neuropathic pain and sensory deficits. Mice were treated with cisplatin together with metformin or saline. Cisplatin induced increased sensitivity to mechanical stimulation (mechanical allodynia) as measured using the von Frey test. Co-administration of metformin almost completely prevented the cisplatin-induced mechanical allodynia. Co-administration of metformin also prevented paclitaxel-induced mechanical allodynia. The capacity of the mice to detect an adhesive patch on their hind paw was used as a novel indicator of chemotherapy-induced sensory deficits. Co-administration of metformin prevented the cisplatin-induced increase in latency to detect the adhesive patch indicating that metformin prevents sensory deficits as well. Moreover, metformin prevented the reduction in density of intra-epidermal nerve fibers (IENFs) in the paw that develops as a result of cisplatin treatment. We conclude that metformin protects against pain and loss of tactile function in a mouse model of CIPN. The finding that metformin reduces loss of peripheral nerve endings indicates that mechanism underlying the beneficial effects of metformin includes a neuroprotective activity. Because metformin is widely used for treatment of type II diabetes, has a broad safety profile, and is currently being tested as an adjuvant drug in cancer treatment, clinical translation of these findings could be rapidly achieved.

.

.

Proteomic and functional annotation analysis of injured peripheral nerves reveals ApoE as a protein upregulated by injury that is modulated by metformin treatment

from Mol Pain [2013], from University of Arizona

.

Abstract

BACKGROUND:

Peripheral nerve injury (PNI) results in a fundamental reorganization of the translational machinery in the injured peripheral nerve such that protein synthesis is increased in a manner linked to enhanced mTOR and ERK activity. We have shown that metformin treatment, which activates adenosine monophosphate-activated protein kinase (AMPK), reverses tactile allodynia and enhanced translation following PNI. To gain a better understanding of how PNI changes the proteome of the sciatic nerve and ascertain how metformin treatment may cause further change, we conducted a range of unbiased proteomic studies followed by biochemical experiments to confirm key results.

.

CONCLUSIONS:

These proteomic findings support the hypothesis that PNI leads to a fundamental reorganization of gene expression within the injured nerve. Our data identify a key association of ApoE with PNI that is regulated by metformin treatment. We conclude from the known functions of ApoE in the nervous system that ApoE may be an intrinsic factor linked to nerve regeneration after PNI, an effect that is further enhanced by metformin treatment.

.

.

Volume 107 of the series Experientia Supplementum [2016] from University of Texas Dallas

.

Abstract:

Chronic pain is a major clinical problem that is poorly treated with available therapeutics. Adenosine monophosphate-activated protein kinase (AMPK) has recently emerged as a novel target for the treatment of pain with the exciting potential for disease modification. AMPK activators inhibit signaling pathways that are known to promote changes in the function and phenotype of peripheral nociceptive neurons and promote chronic pain. AMPK activators also reduce the excitability of these cells suggesting that AMPK activators may be efficacious for the treatment of chronic pain disorders, like neuropathic pain, where changes in the excitability of nociceptors is thought to be an underlying cause. In agreement with this, AMPK activators have now been shown to alleviate pain in a broad variety of preclinical pain models indicating that this mechanism might be engaged for the treatment of many types of pain in the clinic. A key feature of the effect of AMPK activators in these models is that they can lead to a long-lasting reversal of pain hypersensitivity even long after treatment cessation, indicative of disease modification. Here, we review the evidence supporting AMPK as a novel pain target pointing out opportunities for further discovery that are likely to have an impact on drug discovery efforts centered around potent and specific allosteric activators of AMPK for chronic pain treatment.

.

.

Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic pain.

Mol Pain [2011] from University of Arizona

.

Abstract

Neuropathic pain is a debilitating clinical condition with few efficacious treatments, warranting development of novel therapeutics. We hypothesized that dysregulated translation regulation pathways may underlie neuropathic pain. Peripheral nerve injury induced reorganization of translation machinery in the peripheral nervous system of rats and mice, including enhanced mTOR and ERK activity, increased phosphorylation of mTOR and ERK downstream targets, augmented eIF4F complex formation and enhanced nascent protein synthesis. The AMP activated protein kinase (AMPK) activators, metformin and A769662, inhibited translation regulation signaling pathways, eIF4F complex formation, nascent protein synthesis in injured nerves and sodium channel-dependent excitability of sensory neurons resulting in a resolution of neuropathic allodynia. Therefore, injury-induced dysregulation of translation control underlies pathology leading to neuropathic pain and reveals AMPK as a novel therapeutic target for the potential treatment of neuropathic pain.

.

.

Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice.

Age [20124, from University of Arizona

.

Abstract:

The chronic and systemic administration of rapamycin extends life span in mammals. Rapamycin is a pharmacological inhibitor of mTOR. Metformin also inhibits mTOR signaling but by activating the upstream kinase AMPK. Here we report the effects of chronic and systemic administration of the two mTOR inhibitors, rapamycin and metformin, on adult neural stem cells of the subventricular region and the dendate gyrus of the mouse hippocampus. While rapamycin decreased the number of neural progenitors, metformin-mediated inhibition of mTOR had no such effect. Adult-born neurons are considered important for cognitive and behavioral health, and may contribute to improved health span. Our results demonstrate that distinct approaches of inhibiting mTOR signaling can have significantly different effects on organ function. These results underscore the importance of screening individual mTOR inhibitors on different organs and physiological processes for potential adverse effects that may compromise health span.

..

.

Two Weeks of Metformin Treatment Enhances Mitochondrial Respiration in Skeletal Muscle of AMPK Kinase Dead but Not Wild Type Mice

.PLoS One from University of Copenhagen [2013].

.

Abstract:

Metformin is used as an anti-diabetic drug. Metformin ameliorates insulin resistance by improving insulin sensitivity in liver and skeletal muscle. Reduced mitochondrial content has been reported in type 2 diabetic muscles and it may contribute to decreased insulin sensitivity characteristic for diabetic muscles. The molecular mechanism behind the effect of metformin is not fully clarified but inhibition of complex I in the mitochondria and also activation of the 5′AMP activated protein kinase (AMPK) has been reported in muscle. Furthermore, both AMPK activation and metformin treatment have been associated with stimulation of mitochondrial function and biogenesis. However, a causal relationship in skeletal muscle has not been investigated. We hypothesized that potential effects of in vivo metformin treatment on mitochondrial function and protein expressions in skeletal muscle are dependent upon AMPK signaling. We investigated this by two weeks of oral metformin treatment of muscle specific kinase dead α2 (KD) AMPK mice and wild type (WT) littermates. We measured mitochondrial respiration and protein activity and expressions of key enzymes involved in mitochondrial carbohydrate and fat metabolism and oxidative phosphorylation. Mitochondrial respiration, HAD and CS activity, PDH and complex I-V and cytochrome c protein expression were all reduced in AMPK KD compared to WT tibialis anterior muscles. Surprisingly, metformin treatment only enhanced respiration in AMPK KD mice and thereby rescued the respiration defect compared to the WT mice. Metformin did not influence protein activities or expressions in either WT or AMPK KD mice.

.

We conclude that two weeks of in vivo metformin treatment enhances mitochondrial respiration in the mitochondrial deficient AMPK KD but not WT mice. The improvement seems to be unrelated to AMPK, and does not involve changes in key mitochondrial proteins.

.

.

Effects of metformin on microvascular function and exercise tolerance in women with angina and normal coronary arteries

.

Journal of the American College of Cardiology [2006], from University of Glasgow Cardiovascular Research Centre
.

Abstract:

We conducted an 8-week double-blind, randomized, placebo-controlled study of metformin 500 mg twice a day in 33 women with a prior history of normal coronary angiography but 2 consecutive positive (ST-segment depression ≥1 mm) exercise tolerance tests. Women randomized to metformin (n = 16) showed significant improvements in endothelium-dependent microvascular function (p < 0.0001) and maximal ST-segment depression (p = 0.013), and a trend (p = 0.056) toward reductions in chest pain incidence relative to placebo recipients. Hence, metformin may improve vascular function and decrease myocardial ischemia in nondiabetic women with chest pain and angiographically normal coronary arteries. Larger controlled trials of longer duration are warranted.

.

.

.
.
.
.
.
.
.

.

The material on this site is for informational purposes only.

.

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

.

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

~~

This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

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

..

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

.

.

.

.

.

 

March for Science – SCIENCE, NOT SILENCE April 22 & 29


.

.

.

SCIENCE, NOT SILENCE

.

.

March for Science on Earthday April 22.

.

“The March for Science champions robustly funded and publicly communicated science as a pillar of human freedom and prosperity. March with us April 22, 2017.”

.

Find a march near you.

And register to attend your local march.

.

Washington, DC

marchforscience.com

.

.

.

 

On April 29th, the People’s Climate March Join the march for climate, justice, and jobs.

.

We need more science.

.

Volunteer to help in any way you can.

.

.

.

.

.

.

.

.

The material on this site is for informational purposes only.

.

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

.

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

~~

This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

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

..

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

.

.

.

.

 
 

Cannabis risk, death from fungal infection, demanding peer reviewed science. Not even billions can buy CBD if it is classed as Schedule I


.

.

.

“IMPROVING MICROBIAL DETECTION STANDARDS FOR CANNABIS”

.

The full article in O’Shaunessy’s is recommended. I’ve extracted a few parts.

.

.

“If the government is going to tax us, in return they’ve got to provide us with needed services. And that means well-equipped analytic test labs run by disinterested technicians.” [emphasis mine]

.

“Let’s make measured changes before another patient is harmed while demanding peer reviewed science is used to guide the regulatory process. In an era of fake news, science by press release with “beliefs” derived from companies that have a vested interest in seeing more cannabis safety testing should be hyper scrutinized.”

.

“I think the cannabis-testing labs should be operated by the Department of Public Health, overseen by Commissioner Raber (and equally proficient chemists in every city and state) and staffed by well trained and well paid technicians whose pensions are secure.”

.

The importance is that many patients who are immunosuppressed use medical marijuana, and need to use it safely because nothing else helps as well, including those who are immunosuppressed and don’t know it. For example, many do not know that diabetics are immunosuppressed. Those with autoimmune diseases, chronic renal disease, may be using medical cannabis and should demand testing be done with their taxed dollars as should we all. This has been one of the most useful herbs in history, for thousands of years, and can give balm and relief even to shattered nerves, especially now that healthcare insurers are denying to pay for pharma’s gobsmacking overnight billious costs.

.

.

gobsmacking billious costs

vs

getting up to speed on legal cannabis &

 research on endocannabinoid systems

.

.

.

This is a timely issue. Discuss with your doctor, get your representatives to help to legalize it nationwide. It may be the only thing that can help, or the only one that doesn’t constipate or cause erectile dysfunction or interact with other drugs. We don’t want our medication infected, even if we want to use cannabis for relaxation and pleasure. The Xanax’s and Ativan’s could be improved upon if only the right science is funded.

.

“On February 7, the Daily Mail reported a cancer patient in northern California died from a fungal infection that authorities suspect was caused by the inhalation of contaminated medical cannabis.”

.

snip

.

“Furthermore, molecular techniques can be used to assess whether this cancer patient’s infection was actually cannabis derived. This is possible by using PCR and sequencing as performed by Remington et al. on the cannabis material and on the patient to confirm such an event.”

.

“Rather than jumping to conclusions from a news story about cannabis contamination (which may in fact be the case), officials should confirm, via molecular methods, that a fatal infection occurred from the consumption of contaminated Cannabis or from another source, such as a hospital acquired infection. Once confirmed, the scientific data can help drive the appropriate regulations forward to ensure patient safety.  Unfortunately, most regulations passed to date for microbial detection do not appropriately address patient safety and often suggest the use of antiquated, inaccurate technologies.  For instance, we have peer-reviewed evidence that the currently accepted 48-hour Petrifilm-based method currently in use fails to detect some of the most harmful microbes found on cannabis. The State of Colorado has recently come to similar conclusions and has moved their Petrifilm detection times from 48 hours to 60-72 hours while referencing a paper suggesting 120 hours may be required.  And even with these adjustments to the regulations, Petrifilms will never give as accurate results as PCR.” [emphasis mine]

.

“All technologies used to ensure product quality and patient safety should be peer reviewed. DNA-based methods are imperative to patient safety, as they are accepted, peer reviewed, and have been used for decades in other industries for similar purposes.”

.

Kits to perform qPCR-based microbial testing on cannabis are commercially available at medicinalgenomics.com. We hold the largest sequence database of microbes found on cannabis and have kits that perform these tests in hours as opposed to days.”
[emphasis mine]

.
“The technology exists to ensure safer cannabis for patients. Let’s make measured changes before another patient is harmed while demanding peer reviewed science is used to guide the regulatory process. In an era of fake news, science by press release with “beliefs” derived from companies that have a vested interest in seeing more cannabis safety testing should be hyper scrutinized. This extends to our own work at Medicinal Genomics and underscores our publication history in this space.”

.

.

snip

.

O’Shaughnessy’s retro message:

.

Medicinal Genomics’s qPCR technology is undoubtedly superior and would have picked up the aspergillus that may have been fatal to the California  patient. But how widespread is the danger, really? In San Francisco in the ’90s, many thousands of AIDS patients whose immune systems were beyond “compromised” smoked untested crude herb, and I only heard of one rumored instance in which aspergillus may have been involved in a death. Donald Abrams, MD, might be able to confirm or correct my reassuring recollection.”

.
.
“That said, of course the labs testing cannabis should employ the best available technology. The question, is who should pick up the tab?” [emphasis mine]

.
.
“When I was working for the San Francisco District Attorney in ’01 or ’02 I called on Josh Bamberger at the city health department on Grove Street and asked if their lab would take on the testing of cannabis being sold at dispensaries. He said he didn’t have the budget or the personnel.  In the years ahead I was surprised that nobody from the movement/industry ever made the demand —not even the request— that a government agency take responsibility for testing medical cannabis. No patient advocate declared, “If the government is going to tax us, in return they’ve got to provide us with needed services. And that means well-equipped analytic test labs run by disinterested technicians.” [emphasis mine]

.
.
“All around the world, PRIVATIZATION is the overwhelming socioeconomic trend of our time.  The Power Elite have done such a thorough job of selling off the commons and undermining the public sector that everybody now simply assumes that for-profit labs can and should take on the responsibility of protecting public health. “

.
.
“I think the cannabis-testing labs should be operated by the Department of Public Health, overseen by Commissioner Raber (and equally proficient chemists in every city and state) and staffed by well trained and well paid technicians whose pensions are secure. And while we’re at it, how about free public education and single-payer medical care?”

.

.

 

.

I keep getting the suspicion billions are being funneled rapidly down new rabbit holes using fear to prevent science. We must be able to do more than just prescribe  opioids for severe pain. Opioids cause inflammation which causes more pain. Cannabis is anti-inflammatory, analgesic, etc etc etc, and not allowed in hospitals, SNFs, or in facilities that seniors can only dream of retiring to when they can no longer manage at home. We need medical better choices.

.

Medicinal cannabis is a healing plant with cannabinoids like ones that your body makes that helps you feel healthy and somehow influences the immune system more than any other system, while also lifting mood. Wouldn’t it be nice to know? It has 400 chemicals, not just two synthetic ones pharma makes. An exciting new cosmos in the body’s realm of more than just neuroscience. We have more cannabinoid receptors than any other kind in our body. We need to learn.
.
Stop this Schedule I nonsense. Legalize cannabis. Privatize and regulate it like big alcohol, but keep it apart from big pharma, and endow strong university ties. For pete’s sake, fund the research immediately. We need it. The immune system needs it. The pain matrix needs it. Why should we allow euthanasia when we can treat pain and symptoms. Grandmothers used to know how. We are living in the dark ages with cannabinoid systems science. It is in starving infancy, Israel’s Mechoulam lab pioneering this blossoming for decades.
.

Don’t forget to tell your representatives that you hear you may benefit from medical marijuana. Cannabis, marijuana, just may help, as it helped so many little children having hundreds of seizures each day, helped by just one of the cannabinoids in the plant: CBD.  It has been reported to almost completely stop the hundreds of daily seizures in possibly 50% —wouldn’t it be important to do research on it?

.

CBD  has no psychoactive power. There is no high, no hallucinations. It actually blocks the psychoactive power of THC. It should be legal. The plant should be legal. It helps many medical conditions. I have posted an astonishing case months ago 100% relief with CBD. Instead it, just the other day, CBD got clearly classified as Schedule I. This must go to the courts. This insanity about a healing plant can be sanely managed, just like alcohol is managed. Without privatized prison systems that waste taxpayer dollars.

.

We see new funnels of big money going down the rabbit hole. The urgency to privatize. We have a lot of people who cannot afford the American medical system, cannot afford doctors, who may get some relief even as a muscle relaxant or for sleep or anxiety.

.

How can anyone respect a legal system that does not even allow research on a healing plant so important to the immune system?

 

.

No amount of billions can buy CBD if it is classed as Schedule I.

.

.

.

.

.

.

.

The material on this site is for informational purposes only.
.
It is not legal for me to provide medical advice without an examination.
.
It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.
~~
This site is not for email and not for appointments.
If you wish an appointment, please telephone the office to schedule.
~~~~~
For My Home Page, click here:  Welcome to my Weblog on Pain Management!

.

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

.

.

.

 
 
 

Avoid opioid use in surgery to reduce postop pain


.

.

.

Science for years has confirmed that opioids trigger inflammation and that creates pain. Trauma and surgery also create inflammation that leads to pain. How logical is it then to continue use of sufentanil for anesthesia when it is the most highly potent opioid 500 to 1,000 times stronger than morphine. Where is the logic in creating pain by using sufentanil as the anesthetic? A new one on the market will be 10,000 times stronger than morphine. Inflammation is not always easy to reset after you strafe the innate immune system with an opioid.

.

Why is ketamine not used more often for surgical anesthesia when we know ketamine profoundly lowers the inflammatory response thus reducing pain more than ever. Studies for years have shown that even a small dose of ketamine reduces postop pain. This is not new.

.

A study needs to be done comparing patients who receive no opioids. At least this study showed that when fewer opioids are used, pain scores are 37% lower than if more had been given. Patients given higher doses of opioid, had higher analgesic requirements postop. That increases the risk of persistent chronic pain and the tragic risk of addiction.

.

Opioids inflict known lasting harm, pain and suffering, perhaps disability and addiction.

.

.

Reduced opioid use in surgery linked to improved pain scores
Written by Brian Zimmerman

.

After anesthesiologists at the University of Virginia Health System in Charlottesville began administering fewer opioids to patients during surgeries, patients’ self-reported pain levels dropped, according to a study led by three UVA anesthesiologists.
.
For the study, the team examined 101,484 surgeries that took place in the UVA Health System from March 2011 to November 2015. During this time period, the amount of opioids administered via general anesthesia at the system was reduced by 37 percent.
.
For the same time period, self-assessed patient pain scores recorded in post-op recovery units dropped from an average of 5.5 on a 10-point scale to an average of 3.8, marking a 31 percent improvement.

.
One of the study’s leaders, UVA anesthesiologist Marcel Durieux, MD, PhD, said the impetus behind the pain score improvements is likely attributable to several factors. One, previous research has indicated opioids can ultimately make people more sensitive to pain. And two, the increased use of non-opioid painkillers like lidocaine and acetaminophen during surgeries at UVA was likely effective.

.

….”There is very clear evidence that people can become opioid-dependent because of the drugs they get during and after surgery,” said Dr. Durieux. “I think that by substantially limiting opioids during surgery, we’ve made an important step in addressing that problem.”

.

.

.

.

The material on this site is for informational purposes only.
.
It is not legal for me to provide medical advice without an examination.

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

~~
This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

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

.

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

.

.

.

.

 

 

 

 

Medical Marijuana – Cannabis for Pain


.

.

.

These references include links to peer reviewed journal articles on cannabinoids. They are taken from the Reference Library of the outstanding RSD Association in Connecticut, whose mission is to help relieve pain. They have grouped the articles in helpful folders by subject, and this is one of many folders on the immense subject of pain. Please donate to them as their research helps everyone with pain, not just nerve pain or CRPS. May the references help enrich your lives and help support congress and regulators in legalizing cannabis across the country — the attorney general just now voted in by congress opposes medical marijuana.

.

Be aware that states should monitor the plant for bacteria, fungus, pesticides, and heavy metals as discussed in this Smithsonian article:

.

“Washington, the second state to legalize recreational marijuana, does require such testing for microbial agents like E. coli, salmonella and yeast mold, and officials there rejected about 13 percent of the marijuana products offered for sale in 2014.”

.

Concentrates may be made with toxic butane or heptane. If you have cancer or are immunosuppressed – cancer and autoimmune diseases fall into that category – it is safer not to inhale. Cannabis can be used on the skin or swallowed but be aware when swallowed, it takes 60 to 90 minutes before you feel the effect. It is easy to overdose when swallowed. Check your blood pressure and pulse before use and again while you feel its effect.

.

The article also points out that on testing, many of the plants have high THC but no longer have CBD, one of the 86 known cannabinoids, the one that blocks the psychoactive side effects of THC. On its own, CBD has many medical benefits.

.

For those who have allodynia, the most intense form of nerve pain, pain that is triggered by a light touch or breath of air:

.

.

Keep in mind that chronic pain is much harder to treat than cancer pain and acute pain. Chronic nerve pain is the hardest of all to treat. We need to be able to prescribe anything that helps. Pain can lead to suicide in these extreme pain conditions.

.

Watch out for the munchies – do not get fat.

.

O’Shaunessy’s today published articles that may be useful for your Senators, healthcare insurers and states:

..

“some additional articles published by cannabis clinicians in O’Shaughnessy’s showing the strength of aggregated case reports. We hope the MBC Marijuana Task Force will give them serious consideration.”

 

.

 

Cannabinoids

.

Medications denied for pain today – Celebrex, Skelaxin, Morphine, Oxycodone, Methadone, Suboxone


.

.

.

Happy New Year. Medications are denied for pain one month after you sign onto new insurance based on medications they cover:

 

Celebrex, a generic NSAID, less risk of GI bleed which is an increased in seniors day by day as we age.

 

Skelaxone, generic muscle relaxant

 

Lorzone, muscle relaxant

 

Morphine 30 mg ER, generic, denied 3 per day, well within CDC guidelines

 

Methadone 10 mg 3/day, well within CDC guidelines

 

Oxycodone 5 mg 3/day, well within CDC guidelines

 

Suboxone generic,  FDA approved for addiction in US but not for pain; approved for pain and for addiction in EU.

 

Does insurance cover cost of medication?

 

 .

.

.

.

.

.

.

.

.

.

%d bloggers like this: