Friday, 20 July 2018

The Foundation For Peripheral Neuropathy’s Survey On Chronic Pain And Treatments: Is It Producing Any Results?

Today's post from foundationforpn.org (see link below) relays the results of both a recent public forum with the Federal Drug Administration (FDA) and the results of the Foundation for Peripheral Neuropathy’s own survey of its members and their responses to chronic pain issues. It's pretty much preaching to the converted in that only chronic pain (in this case neuropathy) patients are likely to read it but it is very useful information, affirmation and confirmation, for people living with neuropathy and hopefully the messages contained will trigger a few positive responses from the FDA itself. It it's true that 100 million adults in the USA alone, suffer from chronic pain, then this message and all the conclusions surely need national and international coverage because however many surveys you carry out, you're clearly only touching the tip of the iceberg. The depressing conclusions that very little actually works in reducing nerve pain is therefore, an international scandal because this situation hasn't changed largely since the 2nd World War. Worth a read to confirm what you probably already know.



FDA and FPN survey patients on chronic pain and treatments
July 17, 2018

On July 9, 2018, the Federal Drug Administration (FDA) held a public forum focusing on the patient’s perspective on drug development for chronic pain. The FDA invited members of the public, including the Foundation for Peripheral Neuropathy’s (FPN) President, Lou Mazawey, to attend to give their perspectives on living with chronic pain and treatment approaches currently available to patients with chronic pain. Mr. Mazawey, as a patient with peripheral neuropathy, was able to share his viewpoints as well represent FPN in this important discussion.
The Foundation for Peripheral Neuropathy’s Survey on Chronic Pain and Treatments

The Foundation for Peripheral Neuropathy (FPN) surveyed its members on their experience with chronic pain and its treatment. FPN will submit the survey results to the FDA as a follow up to the public meeting. The results of our survey generally mirror the issues and concerns raised by the 1000 patients in attendance either in person or virtually for the FDA forum. We present our summary of the key points below. 


Is Chronic Pain a Problem in the US?

According to the FDA, chronic pain affects approximately 100 million adults in the US. Chronic pain greatly contributes to national rates of morbidity, mortality and disability. It has a major impact on the livelihoods and well-being of those affected. The economic cost of chronic pain is estimated to be $560-$635 billion a year. The FDA confirmed that the medical needs of patients with chronic pain are largely unmet, representing a large health concern in the US. One of the major types of chronic pain included in these statistics is neuropathic pain, such as peripheral neuropathy. 


Symptoms and Daily Impacts of Chronic Pain that Matter Most to Patients

Chronic pain can manifest itself through a number of symptoms and vary in severity. Of those attending the forum, 74% described their pain as always being present but with intensity that changes over time. Patients indicated that, with medication, they often accept moderate pain levels rather than complete pain elimination. Patients in our survey also said that even with medication their pain was in the moderate to significant pain levels.

Nonetheless, chronic pain has a significant impact on the quality of life for patients overall. In our survey, respondents agreed that chronic pain has had an impact on their day-to-day lives. Many patients find their mobility impacted. They also find that chronic pain affects their overall feeling of well-being. Other impacts described by patients during the meeting included an impact on relationships, the ability to care for oneself and family, and stigma or embarrassment related to chronic pain.

Many patients raised the issue of fatigue as a wide-spread but little recognized impact of chronic pain. Fatigue could be caused by disrupted sleep or the sheer energy it takes to battle chronic pain on a daily basis. One patient described battling chronic pain as a full time job. Another describe chronic pain as ‘stealing’ her life. These comments, sadly, drew applause from the audience at large. 


Current Approaches to Treatment of Chronic Pain

Both the patients at the forum and the respondents of FPN’s survey have tried a wide range of medicinal and non-medicinal therapies to address their pain. According to our survey, 45% of patients took gabapentin and found it somewhat or very effective relative to other treatments. Other popular treatments include lidocaine and other nonprescription creams. In terms of non-medicinal treatments, patients in our survey found diet and exercise to be by far the most utilized and most effective of all treatments.

Nonetheless, our survey indicated that these treatments were only moderately effective in managing pain. It was fairly universally agreed that no one treatment completely managed the chronic pain of patients. In our survey, in some cases, patients chose to give up taking certain medications due to the side-effects being worse than the benefit of the pain relief.


Patient Concerns about Treatment Options

A major concern among the participants of the forum and our survey respondents was the cost of treatments. For those with insurance, the cost of treatments was less of an issue. However, not all insurance plans cover physical therapy or many other potentially useful treatments. For patients who are not able to work full time or do not have insurance, the cost of treatments are often prohibitive. Patients are not able to access the best treatments available due to this cost.

Many patients were concerned about being able to continue to get prescriptions for certain treatments. They were also concerned about the added scrutiny that doctors are under in writing these prescriptions.

In summary, there was a consensus that much more needs to be done to ensure safer, more effective and more affordable treatments for chronic pain. The FDA took note of all comments during the session. The FDA encouraged all patients to submit comments through the public docket on their website. The public docket will be open through September 10, 2018. 


For More Information

A recording, transcripts and slides from the July 9 FDA Patient-Focused Drug Development Meeting on Chronic Pain can be found on the FDA website. This is one of a series of meetings on the subject including a 2016 meeting focused on neuropathic pain.

You can view The Foundation for Peripheral Neuropathy’s patient survey on chronic pain and treatment options here.

More information on available treatment options for chronic pain and other symptoms related to peripheral neuropathy can be found on the Foundation for Peripheral Neuropathy website.

https://www.foundationforpn.org/2018/07/17/fda-and-fpn-survey-patients-on-chronic-pain/

Thursday, 19 July 2018

Cancer Treatment And Neuropathy

Today's post from cancerfightersthrive.com (see link below) is specifically directed at patients receiving chemotherapy treatment for their cancer and discusses the ensuing neuropathic problems that many of these patients end up having. However, remove all references to cancer from the article and you have a standard description of nerve damage which can happen to everybody and from a multitude of other causes. For that reason, this article is useful to cancer patients but also for anyone else who is suffering from neuropathy. That's the problem with this disease:- both doctors and experts tend to concentrate too much on the cause, when in fact if you already have neuropathy, you need to be concentrating on treating and reducing the symptoms. Contrary to what this article suggests, in the vast majority of cases, nerve damage can't be reversed and won't go away just because a particular cause has been stopped or removed. It's a cruel disease, with over 100 causes and over 100 different forms - the medical emphasis should be more on treating the patient's discomfort and less on addressing the cause (a bit like shutting the stable door after the horse has bolted!). That said, if the cause is something like cancer then treating that particular cause naturally needs to be ongoing but unfortunately, curing the cancer is unlikely to cure the nerve damage from the cancer treatment.


Burning, Tingling Pain? It Could Be Peripheral Neuropathy 
By Rachael Bieschke 2018

If you've experienced these symptoms after chemo, here’s what you should know about the condition.

Receiving chemotherapy for cancer treatment can lead to a number of unexpected side effects, including damage to the nerves located outside your brain and spinal cord, known as your peripheral nerves. Peripheral neuropathy, which describes nerve damage that’s often felt in your extremities, including your hands, feet, legs and arms, may be caused by a number of factors, from diabetes to alcohol abuse, but it’s also a common side effect of chemotherapy.

“Most cancer chemotherapies can cause peripheral neuropathy,” explains Glynis Vashi, M.D., chief of medicine and lead physician at Cancer Treatment Centers of America® (CTCA) in Suburban Chicago. “Especially the taxanes,” which may include such chemotherapy drugs as paclitaxel (Taxol®), docetaxel (Taxotere®) and cabazitaxel (Jevtana®). Platinum drugs, epothilones, plant alkaloids and thalidomide (Thalomid®) are examples of additional chemotherapy drugs that are frequently linked to peripheral neuropathy, according to the American Cancer Society (ACS).


What Are the Signs and Symptoms of Peripheral Neuropathy?

Pain, burning, numbness and tingling in the areas where your nerves are damaged are the most common symptoms of peripheral neuropathy. The severity varies from person to person, ranging from mild to debilitating.

“It starts out with pain,” Dr. Vashi says. “Your sensory nerves receive all the sensory stimuli, so usually the pain is a burning kind of pain. Then as it gets more severe the pain can ascend more proximally toward the body, and the most severe form is accompanied by muscle weakness.”

So while the pain may initially only be felt in your toes or fingers, it can progress, moving into your feet, ankles and legs or hands and arms. In the most severe cases, you may have severe pain and difficulty walking or carrying out daily activities, such as buttoning a shirt or writing.

Meredith Boudreau, PT, DPT, physical therapist at CTCA® in Suburban Chicago, notes that there are a variety of symptoms that can occur, but many patients describe peripheral neuropathy as a feeling of “walking on gravel” and says sometimes people also have a sensitivity to temperatures, such as cold or heat. “There’s a wide range on severity of symptoms, some people experience only slight numbness while others can barely feel anything, which can lead to trouble with balance,” she says. ACS lists additional symptoms, including:


Loss of feeling, including less ability to sense pressure, touch and temperatures
Trouble picking things up or holding things
Difficulty walking
Sensitivity to touch or pressure

Less common symptoms may include:


Shrinking muscles
Trouble swallowing
Constipation
Trouble passing urine
Changes in blood pressure
Decreased or no reflexes


Is It Possible to Prevent Peripheral Neuropathy?

Research is ongoing looking into possible tools to prevent chemotherapy-induced peripheral neuropathy (CIPN), but so far results have been mixed. More research is needed, but depending on the type of chemotherapy, the following nutraceuticals have shown some evidence that they could have a protective effect on peripheral neuropathy:


Vitamin E
Glutathione
Vitamin B6
Omega-3 fats

However, according to a review in Critical Reviews in Food Science and Nutrition, “Currently no agent has shown solid beneficial evidence to be recommended for the treatment or prophylaxis of CIPN.” As such, typically when peripheral neuropathy occurs during chemotherapy treatment it’s dealt with by altering the treatment.

“Most oncologists, if the neuropathy seems to be getting more debilitating, would decrease the dose of chemotherapy or stop the therapy,” Dr. Vashi says. Sometimes the chemotherapy would then be restarted once the neuropathy has a chance to subside. Because peripheral neuropathy can also be caused by factors other than cancer treatment, it’s important to address these as well. Dr. Vashi adds:

“We don’t see the patients until they’re having chemotherapy and develop the neuropathy, but in general practice we would want to make sure patients deal with other causes of neuropathy such as poor dietary choices, abusing alcohol, diabetes or the use of certain medications. All of these can cause or add to neuropathy even before the cancer treatment. That way we can help them to start at a better place.”


Treatment Options for Peripheral Neuropathy

Treatments depend on your particular symptoms and their severity. In the mild forms, you can use over-the-counter medications for pain relief. If the pain is severe, prescription pain relievers are the next step. From there, there are specific medications available to treat neuropathy, such as gabapentin (Neurontin®) and antidepressants may also be offered.

“Antidepressants may help increase a patient’s tolerance to pain,” Dr. Vashi says. “When patients are depressed, their pain tolerance is decreased and symptoms are exaggerated.” She also notes that vitamins and nutritional supplements, including vitamin B12 and folate, can be helpful, and for patients who are having trouble walking, physical therapy is recommended.

“If the patient cannot walk and it’s accompanied by muscle weakness, we use physical therapy to help. To help people walk, you can also use specialized footwear,” she says. Boudreau, the physical therapist, often works with patients on balance exercises and grip-strengthening activities, while doing sensory exercises to help patients learn to live with the condition.

Topical neuropathy creams are also available, which may work by temporarily numbing the pain, and there’s also an electrical stimulation unit that helps recreate normal nerve signaling. “It won’t cure the condition,” Boudreau says, “but patients have expressed reduced pain and symptoms with use of electric stimulation.” The prescription-based device is designed to be used at home two to three times a day and can also be administered by a physical therapist. Some people also find relief using acupuncture and essential oils, including aromatherapy massage.


Learning to Live With Peripheral Neuropathy

For some, peripheral neuropathy resolves once chemotherapy is complete. For others, symptoms may persist for years after. “As long as the treatment is ongoing, the neuropathy will be there,” Dr. Vashi says, which is why taking steps to live safely with the condition is so important. “Some people can’t feel the ground, which can result in falls, so education helps patients to know what to expect from having it.”

Boudreau also recommends taking precautions, especially with numbness and pain. “Get your skin checked often and wear proper footwear,” such as closed-toe shoes, to avoid injuries, she says. You may also want to wear gloves to protect your hands and take extra precautions to avoid being harmed by extreme temperatures, such as setting your water heater to a safe temperature to avoid scalding.

If you’re having trouble with muscle weakness, you may need to use the support of a cane or walker, and installing handrails in your home can help you avoid falls. If the symptoms of peripheral neuropathy are persistent and significantly interfering with your quality of life, be sure to let your health care providers know so they can create a treatment plan that addresses your individual needs and provides adequate relief.

http://www.cancerfightersthrive.com/burning-tingling-pain-peripheral-neuropathy/

Wednesday, 18 July 2018

The Pressure On Doctors To Write A Prescription For Pain And Call In The Next Patient

Today's post from wbur.org (see link below) is a fascinating look at the so-called opioid epidemic from the viewpoint of a doctor, who convincingly explains the dilemmas that doctors face when deciding whether to prescribe strong pain killers or not. There are many pressures on modern doctors, not least of which is to serve their patient's needs when it comes to pain relief and yet follow guidelines that are draconian in some cases. Doctors have the patient's best interests at heart but are under enormous pressure to 'succeed' and part of that is to have the patient walk happily out of the practice and that means...giving them the drugs they need to subdue their pain. Every day it's a question of taking each case as it comes and the easiest option is to write a prescription while there are 50 other patients waiting outside but as this doctor explains, it's by no means as easy as that. This article puts the home doctor's case and adds a whole new side to the story. It's a subject that unfortunately is going to run and run!
 


Now We See: How The Opioid Crisis Has Laid Bare Deep Flaws In American Medicine
June 15, 2018 Dr. Elisabeth Poorman

I now know that everything that I was taught about opioids was wrong.

My thinking began to change after meeting a patient I’ll call Danny. A man in his 50s, overweight and over 6 feet tall, he was an imposing physical presence. I could tell he had once been handsome before years of living on the streets; even in his hospital bed, his dark brown hair was impeccably groomed.

Danny had recently left a physical rehab center where he had been given the largest doses of opioids I had ever seen for his chronic back pain. Eventually, he was sent out onto the streets with a week’s prescription and no followup plan. He ran out of pills in a few days.

He walked into our emergency room demanding that we give him opioids. When the ER doctors hesitated, he screamed and threatened them.

This was 2013, two years after the Centers for Disease Control and Prevention had declared that America was in the midst of a prescription drug epidemic. Yet most physicians continued to write prescriptions for opioid medications at record levels.

We had been taught that patients were either in pain or they were drug-seeking addicts -- never both. Patients with chronic pain who started to show addictive behaviors, we were told, were not addicted but “pseudo-addicted,” suffering because we were not giving them enough opioids.

"Pseudoaddiction can be distinguished from true addiction in that the behaviors resolve when pain is effectively treated,” according to a statement in 2001 from the American Pain Society and the American Society of Addiction Medicine. Even illicit drug use was to be seen as a sign that we were not giving enough opioids.

In other words, don’t question your patient’s behavior: Prescribe more pain pills.

The concept of pseudoaddiction, I recently learned, was coined by David Haddox, now a longtime employee of opioid-maker Purdue Pharma and former chairman of the American Pain Society.

Beyond that single 2001 statement, there has never been empirical evidence that pseudoaddiction is a legitimate diagnosis. Yet, in spite of its questionable assumptions, the term was doctrine in pain treatment while I was in medical training, spread throughout the medical community by pharma-sponsored lectures and educational materials.

It was this line of thinking that guided me when I was taking care of Danny. I did not want to give him the opioids. But I worried that I was acting out of bias -- that I didn’t want to give Danny opiates because he was living on the streets, he was unpleasant, and he intimidated me. With all this in my head, and my desire to win Danny’s trust, I decided to give him the medications. My training taught me that it was the right thing to do.

All of us who continued to prescribe these pills closed our eyes to his intensifying addiction.

For the next few days, I walked into Danny’s room every morning to check on his progress. After each dose of opioids, I saw his head drop, his pupils shrink, his breath slow -- early signs of an opioid overdose.

I had followed all the guidelines, but I knew then that I hadn’t given Danny the care he needed. All of us who continued to prescribe these pills closed our eyes to his intensifying addiction. After about a week, I sent Danny back out onto the streets.

Why Didn't We See?


It’s hard to understand now why I couldn’t recognize that Danny was suffering from chronic pain and addiction, or that the two commonly coexisted. It is even more painful to acknowledge that during most of my medical training, the teaching I received was so thoroughly dominated by corporate interests pushing pain prescriptions that we let it blind us to flimsy data and even our own clinical experience.

When some physicians were reluctant to prescribe opioids, hospitals pointed out their importance in increasing patient satisfaction scores. When it was noted that racial minorities received fewer pain pills, hospitals encouraged physicians to prescribe more opioids to everyone in the name of reducing disparities. We accepted teaching from pharmaceutical companies that opioids caused addiction in less than 1 percent of patients with “legitimate” pain, and that they were effective for chronic pain.

While opioids certainly have a role in acute pain, there was never any hard evidence that they were effective or safe for chronic pain conditions. When OxyContin, Purdue’s blockbuster opioid, received FDA approval, the company had conducted no studies on how often longer-term consumers developed an addiction. And studies that were used to justify prescription opioids for chronic pain lasted just six to 12 weeks.

We now know that having a diagnosis isn’t a magical safeguard against the dangers of these drugs. A quarter of those who are prescribed opioids for chronic pain will misuse them, and about one in 10 will develop an opioid addiction. And the first-ever study of opioids for chronic pain to last at least 12 months, published this year in JAMA, found that opioids were less effective than other medications for arthritis and chronic back pain, and had twice as many adverse effects.

Some doctors also believed that they could accept all-expense-paid trips to places like Boca Raton and Scottsdale funded by pharmaceutical companies, free lunches and free samples from pharma reps, follow guidelines written by doctors with multiple conflicts of interest, and still make the right decisions for patients. We ignored — and continue to ignore — research that suggests as little as $20 in food changes doctors’ prescribing practices.

Looking back, it is clear that opioid manufacturers offered an easy answer to the difficult problem of chronic pain, allowing doctors to feel like we had done something to help our patients. As Dr. Anna Lembke, program director for the Stanford University Addiction Medicine Fellowship, said in a talk last year, “There’s tremendous pressure on doctors to palliate pain, to prescribe pills and perform procedures because that’s what pays, and to please patients because patients have become customers. Guess what? Opioids are a pretty good solution to that problem.”

Patients mistakenly think that I can write a prescription to safely wipe all their pain away -- and it’s uncomfortable for me and other doctors to admit that we can’t.

Colleague And Patient Challenges

Now, even when I try to do the right thing by limiting opioids, my efforts are often undermined by other doctors with freer prescription pads.

Recently, I was unable to convince one of my patients of the dangers of opioids. We talked about it over several visits. I knew that she had an anxiety disorder, a huge risk factor for abuse. I knew that she had little social support. I knew that the opioids might provide her short-term relief, but were unlikely to help with her chronic nerve pain, which she would probably live with for the rest of her life.

But even though I talked to her about the risks, she still kept asking for pain pills. One day, I gave in. I gave her a few weeks of pills until her scheduled surgery for chronic pain. After her surgery, I got a note from her surgeon: She had been discharged from the hospital with 30 days of high-dose, round-the-clock opioids with no followup plan. I haven’t seen her since.

Dr. Andrew Chambers, director of addiction psychiatry training at Indiana University School of Medicine in Indianapolis, shares my frustration.

“The biggest cause of relapse in my [opioid-addicted] patients is getting health care from a dentist, a surgeon, a primary care doctor or an ER doctor," he told me. "How do I treat addiction that’s being caused by two other doctors? If I want to, then I need to track them down and convince them what they’re doing is wrong, and I don’t get reimbursed for that."

Moving forward with patients means starting with honesty about our limitations as providers. Lembke says she breaks the truth to patients this way: “There’s a possibility that there’s nothing that modern medicine has that will help your pain, and I’m very sorry about that. But at the very least we can try to not make things worse.” Lembke explains to them that opioids may help in the short-term, but the only safe solution is “to harness your creativity to find how to make your life worth living, even while we may not be able to stop your pain.”

Pills alone aren’t the solution, Lembke tells her patients, and I’ve started telling mine. Medications all have potential side effects whose consequences multiply the longer they’re used. Safer, more effective therapies long term include things like physical therapy, psychotherapy and mindfulness, which, unlike opioids, have all been shown to improve quality of life.

When our goal is primarily palliative care, opioids are an important treatment option, including for frail elderly patients who cannot safely take alternative medications. And for many patients who are on high doses of opioids and have not shown any signs of addiction, it may be safer to continue them, or discontinue at a very slow pace and only with the patient’s buy-in.

For many, however, this option is no longer available, as some physicians refuse to prescribe opioids under any circumstances, or to take on patients on chronic opiate therapy. These patients are left without support as they abruptly discontinue medications they have been taking for years, and may be physically dependent on.

We have failed to come to grips with the scale of destruction we have created ... and the work we have to do to combat this epidemic and prevent future ones.

When patients show signs of an addiction, many physicians opt to simply sever ties with the patient. Few offer treatment. Buprenorphine, a drug used to treat opioid addiction like methadone that also helps prevent overdose, is an important option I’ve seen work in practice. Buprenorphine and methadone reduce mortality for patients with opioid addiction by half. But only 3 percent of doctors are certified buprenorphine providers, and fewer than a quarter of residency programs offer training. How can we interpret these statistics except as a lack of seriousness about addressing a crisis we helped create?

Things have changed since I was an intern. Some physician groups, including the American Medical Association, are eager to tout successes such as decreasing numbers of prescription opioids. These efforts are important, but they are belated to say the least, and woefully anemic. We have failed to come to grips with the scale of destruction we have created, the ways our clinical decision-making was and still is vulnerable to corporate greed, and the work we have to do to combat this epidemic and prevent future ones.

Patients have a right to be angry with us for the way we’ve (mis)treated them with opioids. We need to give each patient the time they need, make changes slowly, and understand that some will not be able to get off of these medications. We need to ask for help from colleagues and demand that our institutions support safe opioid prescribing and addiction treatment.

Every generation of physicians has to work to undo the mistakes of its predecessors. It is the nature of working in a constantly evolving field. But the physician-fueled opioid epidemic is something different: the result of an effective marketing campaign that has killed hundreds of thousands of people.

As a medical community, we continue to play fast and loose with the corrupting influence of money on our clinical decision making. We allow it into our guidelines, our most prestigious societies, our medical education, our patient advocacy groups, our offices and operating rooms. Important progress has been made. We are exposing fewer patients to these dangerous and largely ineffective drugs. But the fundamental weaknesses in American medicine that led to this crisis remain unchanged: short time with patients; a customer-service mindset that prioritizes satisfaction over good medicine; the largely unchecked influence of money on our providers and health care leaders; and an unwillingness of physicians to diagnose and treat addiction.

The opioid epidemic has laid bare the flaws of American medicine. We should be willing to look at them. Otherwise, this will not be the last epidemic we create.

Elisabeth Poorman is a primary care doctor in Everett, Massachusetts, and a clinical instructor at Harvard Medical School. She is on Twitter at @DrPoorman.

http://www.wbur.org/commonhealth/2018/06/15/opioid-medicine-flaws-physician

Tuesday, 17 July 2018

The Demon Drink Can Wreck Your Nervous System

Topics like that of today's alcoholic neuropathy post from indydetox.com (see link below) always run the risk of sounding 'preachy' when 'experts' advise you to change your lifestyle, or else the sicknesses of the world will rain down on you. However, there are lots of reasons to back up the theory that neuropathy caused by over-indulgence in alcohol, is one of the fastest-growing forms of nerve damage. Add to the fact that people turning to drink as an escape from all the ills of this troubled and dangerous world, are being boosted by the growing numbers of patients who are substituting alcohol for pain relievers that are being denied to them, is an indication of a real social problem that leads to a real medical problem. A massive drinking culture among the youth is fuelling the fire for later years and yet alcoholic nerve damage is rarely spotted on time and often too late to bring about any major changes. This article doesn't preach but it does provide the facts. Everything in moderation eh folks!!
 

Consequence of Alcoholism: Alcoholic Neuropathy
Posted By admin - Posted In Alcohol 15 Jul 2018

Alcoholism or alcohol addiction is compulsive and excessive use of alcoholic drinks. Many symptoms of alcoholism remain hidden for a long time until they manifest as something significant. Alcoholism itself goes undiagnosed most of the times. It harms not only the individual but the whole family. Alcohol is usually initially excessively consumed by someone to counter his/her hardships. What they don’t understand at that time is that it will convert into an addiction becoming another hardship later on.

Introduction to Alcoholic Neuropathy:

Alcoholic neuropathy is one of many complications down the road of consumption of excessive alcohol. In an alcoholic, it’s only a matter of time, when they start getting symptoms of neuropathy. Neuropathy occurs because alcohol deprives the nervous system from some major nutrients like thiamine which are required for nerve conduction. Mostly, peripheral nervous system is affected. All in all, signals between the body, brain and spinal cord are badly disrupted leading to abnormal sensations.

Alcoholic Neuropathy Symptoms:

Chronic alcohol consumption brings about varied symptoms associated with nerve damage.

Sensory symptoms:
Numbness in extremities
Pins and needle sensation
Tingling and burning
Loss of vibration sense
Increased pain sensitivity
Lack of co-ordination
Loss of position sense leading to unsteady gait

Motor symptoms:

Muscle atrophy
Muscle cramping
Non-functioning muscle

Urinary symptoms:

Urinary incontinence
Incomplete bladder emptying
Problems initiating urination

Gastrointestinal symptoms:
Difficulty in swallowing
Constipation
Diarrhea
Nausea
Vomiting

Miscellaneous symptoms:
Sexual dysfunction
Impotency
Dizziness
Speech problems
Intolerance to variation in temperature

Diagnosing Alcoholic Neuropathy:

After taking a detailed history and doing a full neurological examination, there is a need of lab investigations to figure out the cause of neuropathy.
Nervous system symptoms that usually occur due to deficiency of some vitamins and so, first their deficiency has to be rule out. These vitamins are vitamin A, B1, B6, B12, biotin and pantothenic acid, Vitamin E and folic acid.


Nerve conduction studies

Electromyography
Nerve biopsy
Renal function test
Liver function test
Thyroid function test
Complete blood count
Esophagogastroduodenoscopy

Prevention is Better Than Cure!


It is better to control the drinking habit from the very start to prevent complications like alcoholic neuropathy. Such a disease may be irreversible and may lead to poorer quality of life. As per the Dietary Guidelines for Americans, moderate consumption for men and women is 2 and 1 drinks per day respectively but most exceed the recommended limit leading to alcohol use disorders. In any case, people should be advised to drink within safe limits and observe a healthy lifestyle. Regular exercise and healthy diet with minerals and vitamins are the basics of a good living. If one fails to handle the amount of alcohol consumption, they should immediately consult professional help which will supervise them while tapering off their alcohol.

Treating Alcoholic Neuropathy:

If prevention doesn’t help and the disease progresses to become a full-blown alcoholic neuropathy, there are some treatment options for symptomatic relief because most injuries to the nerve are permanent and thus incurable. The first thing alcoholic should do now is stop drinking and for that they might need help of rehabilitation centers. They should also keep a check for any injuries which will go unnoticed because of loss of sensation. Apart from that, other measures that can be taken are: 


Pain relief medications to manage increased sensitivity to pain
Tricyclic anti-depressants prescribed as a pain reliever medication and to look after any co-occurring disorder
Anti-convulsants as a pain killer
Multivitamins rich in vitamin A, B3, B6, B12, E, biotin, pantothenic acid and folic acid
Medication to improve urinary function. For some, medication would not be a good idea and catheterization would have to be done
Walking aid in the form of stabilizing footwear to prevent trauma
Orthopedic devices for proper functioning of extremities
Physiotherapy to improve the muscle mass and reduce the rate of atrophy
Stockings to avoid episodes of dizziness. Also, consuming more salt and putting a pillow beneath the head also helps to counter symptoms of dizziness.

Alcoholism is a serious disorder with complicated consequences. If a loved one is consuming alcohol in excessive amounts, do not turn a blind eye. It can be easier to heal the person and reverse the symptoms if treatment is sought soon after the alcoholism is developed. Reach out for help today!

http://www.indydetox.com/consequence-of-alcoholism-alcoholic-neuropathy/

Monday, 16 July 2018

How Does Marijuana Work For Neuropathy? (Vid)

Today's YouTube video (51 minutes) is an extensive look at pain, how it works and the various medications used to treat It's an excellent source of information about cannabinoids and how they work to reduce pain symptoms and as such is an invaluable resource for those considering using cannabis products to alleviate their symptoms. Many people see cannabis and cannabinoids as an alternative to opioids in the current climate because it's a plant-based product and in many ways, it is. However, it's worth bearing in mind that opioids are also a plant-based product, so the most important factors are addiction possibilities and side effects. Using CBD oil for instance, will remove the addiction and side-effect elements (no THC) and measured against opioids, there's no contest really in customer friendliness. However, everything hangs on what works best for you (with the benefit of doctor's advice and careful research). This video will give you much of the background information you need - well worth a watch.

Marijuana for Pain and Neuropathy 
July 14, 2018 admin 

National Conference 2018 - Presented by Dr Zeid Mohamedali For more information about multiple myeloma, visit, myeloma.ca.



 

https://youtu.be/JsL--trSNb4

Sunday, 15 July 2018

Fluoroquinolone Antibiotics Even More Dangerous Than Previously Thought

Today's short post from webmd.com (see link below) reinforces a message often covered here on the blog and that is that the antibiotics covered by the type name, fluoroquinolones, are even more dangerous than we already knew. This especially applies to people living with nerve damage! As has been said here many times before: if your doctor prescribes fluoroquinolones (see the brand names below) for you, ask him or her if they could possibly prescribe an alternative (there are several available), to avoid the risk of worsening existing neuropathy problems, or prevent any in the future. The FDA has increased their demand for severe warnings on packaging - it's time that doctors followed their advice and stopped giving in to persuasive pharmaceutical reps. Many more posts on the same subject can be found here on the blog - just type in fluoroquinolones in the Search box.


FDA Adds Stronger Warnings to Fluoroquinolones
By Robert Preidt HealthDay Reporter WEDNESDAY, July 11, 2018 (HealthDay News) -- 


A powerful class of antibiotics will now come with stronger safety warnings about dangerous drops in blood sugar and neurological side effects that can include delirium and memory problems, the U.S. Food and Drug Administration said Tuesday.

Called fluoroquinolones, these drugs include levofloxacin (Levaquin), ciprofloxacin (Cipro), ciprofloxacin extended-release tablets, moxifloxacin (Avelox), ofloxacin, gemifloxacin (Factive) and delafloxacin (Baxdela). There are more than 60 generic versions of fluoroquinolones.


"The use of fluoroquinolones has a place in the treatment of serious bacterial infections -- such as certain types of bacterial pneumonia -- where the benefits of these drugs outweigh the risks," Dr. Edward Cox, director of the FDA's Office of Antimicrobial Products, said in an agency news release.



What kinds of infections should not be treated with these antibiotics?
According to the agency, the risks generally outweigh the benefits of fluoroquinolone treatment for patients with acute sinusitis, acute or chronic bronchitis and uncomplicated urinary tract infections.


Fluoroquinolones already carried warnings about a number of neurological side effects, but those warnings differed by drug.


Fluoroquinolone labels must now list the blood sugar warning and all potential neurological side effects associated with this class of antibiotics -- such as attention problems, disorientation, agitation, nervousness, memory impairment and delirium.

The FDA said the decision to require stronger safety warnings came after a review of reports of side effects it had received, as well as case reports published in medical journals.
Fluoroquinolones also carry warnings about disabling and potentially permanent side effects involving tendons, muscles, joints, nerves and the central nervous system.

WebMD News from HealthDay

https://www.webmd.com/cold-and-flu/news/20180711/fda-adds-stronger-warnings-to-fluoroquinolones

Saturday, 14 July 2018

Will The FDA Acknowledge The Needs Of Current Chronic Pain Patients?

Today's post from nationalpainreport.com (see link below) follows on from yesterday's post about the nature of pain and how it is assessed and reports on a recent important meeting on drug development for chronic pain, hosted by the FDA and where countless testimonies were heard from people in chronic pain who's access to their medications has been denied or made difficult due to the current panic reactions to the so-called opioid crisis. The question now is, will the FDA take these people's situations into consideration and bring out a statement designed to tackle their problems; or will the focus lie only on new drug development, with the inevitable result that current chronic pain patients will become collateral damage along the way? It's acknowledged by the FDA that people living with serious chronic pain or coping with pain at the end of life face serious challenges if their doctors and pharmacists bow to pressure to refuse them medication but there needs to be firm and unequivocal action to protect what are basically human rights (that patients in serious pain must receive available medications to relieve their symptoms). Whether the FDA will take the sensible route and refuse to bend the knee to the conservatives and the media, remains to be seen. In the meantime, in America and increasingly across the world, people living with daily pain will be holding their breath.


FDA Hearing Draw Chronic Pain Community – So What Now?

 
Posted on July 10, 2018 in Government with 25 Comments By Ed Coghlan.

The FDA Public Meeting on Drug Development for Chronic Pain heard from an audience of chronic pain advocates and patients in Washington D.C. this week.

The FDA meeting was part of what the agency said is an effort to seek a balance on opioid access.

“While we work to ensure appropriate and rational prescribing of opioids, we won’t lose sight of the needs of Americans living with serious chronic pain or coping with pain at the end of life,” Dr. Scott Gottlieb, the FDA commissioner, said before the meeting. “They too face significant challenges.”

Here is Commissioner Gottlieb’s entire statement.

For chronic pain advocates, like Terri Lewis Ph.D. who shared the results of an extended survey that the National Pain Report promoted, the meeting Monday was a start.

“Now we find out if they listened,” she said. “The FDA heard from the people who have been caught in the federal government crackdown on opioids–the patients. It’s a voice not often heard, but it was today.

There is an unmet medical need experienced by patients with chronic pain.

“Collecting information from the patient’s experience provides an opportunity for the FDA to enhance regulatory decision-making”, she added.

For Cindy Steinberg of the US Pain Foundation—the nation’s largest pain patient advocacy group, the theme of what the FDA heard and what the agency will do now is also important.

“Anyone listening today heard a clear and resounding message from patients who traveled great distances to deliver it and will undoubtedly pay a cruel price in days of increased pain for doing so,” she said. “Their message was clear – we are sick with devastating pain conditions yet doctors will no longer treat us. We have been forced off opioid medications we have used appropriately that have helped us to function. We are suffering to the point that many of us are losing the will to live. Why don’t you hear our pleas and take action to stop this inhumane treatment?”

“My question now is what action the FDA will take to demonstrate that they care?” she told the National Pain Report.

Commissioner Gottlieb said the FDA is seeking a balance on opioid access and seemed to acknowledge the chronic pain patient has often been caught in the crossfire.

“As we consider new policy steps to address the opioid addiction crisis, the FDA remains focused on striking the right balance between reducing the rate of new addiction by decreasing exposure to opioids and rationalizing prescribing, while still enabling appropriate access to those patients who have legitimate medical need for these medicines,” he said.

For Lauren Deluca, who is President and Founder of the Chronic Illness Awareness Advocacy Group, the hearing was a good opportunity for the chronic pain patients to make their case, but she also is wary about the focus of the government hearing.

“I am so proud of hearing so many passionate advocates speak out against these egregious human right abuses. But I have my reservations about the FDA’s focus on drug development rather than the delivery of essential medical services that are clearly need right now,” she told the National Pain Report. “Drug Development is fine and good for the future but our community needs immediate action. I am hopeful to see some steps from the FDA and other regulatory bodies to ensure access as this is a consumer rights issue as well.”

For more on what the survey of chronic pain patients revealed, click here.

http://nationalpainreport.com/fda-hearing-draw-chronic-pain-community-so-what-now-8836702.html

Friday, 13 July 2018

The Pain Puzzle: How On Earth Do You Assess It?

Today's lengthy but fascinating article from newyorker.com (see link below), should really be required reading for people living with neuropathy. The pain (and other sensations) that neuropathy brings, are as difficult to quantify, assess and measure as pain can possibly be for doctors; yet that's precisely what they're asked to do. Similarly, patients can't be expected to put a number on their pain because it can't really be compared to anything else. We know what headaches, toothaches, cuts and burns feel like but trying to measure nerve pain against those experiences, is extremely difficult because it's both different and similar and in so many ways. Nevertheless, everyone demands a self-assessment from the neuropathy patient and if that's not forthcoming, then the doctor basically guesses to confirm diagnoses and choose a level of treatment. Now a long article about the science of pain may not seem an attractive proposition but this article from the New Yorker is extremely well-written and easy to understand and will give you a significant insight into how your pain works and the various ways both you and the doctors can evaluate it. Absolutely worth a read - you'll have a much greater understanding of how your pain works in your body and then maybe you won't feel so bad about giving it an 8, or a 10, or a 3 when a frustrated doctor demands it of you.



The Neuroscience of Pain:-Brain imaging is illuminating the neural patterns behind pain’s infinite variety.
By Nicola Twilley 
July 2, 2018 Issue

Research is illuminating the neural patterns behind pain’s infinite variety.Illustration by Anna Parini

On a foggy February morning in Oxford, England, I arrived at the John Radcliffe Hospital, a shiplike nineteen-seventies complex moored on a hill east of the city center, for the express purpose of being hurt. I had an appointment with a scientist named Irene Tracey, a brisk woman in her early fifties who directs Oxford University’s Nuffield Department of Clinical Neurosciences and has become known as the Queen of Pain. “We might have a problem with you being a ginger,” she warned when we met. Redheads typically perceive pain differently from those with other hair colors; many also flinch at the use of the G-word. “I’m sorry, a lovely auburn,” she quickly said, while a doctoral student used a ruler and a purple Sharpie to draw the outline of a one-inch square on my right shin.

Wearing thick rubber gloves, the student squeezed a dollop of pale-orange cream into the center of the square and delicately spread it to the edges, as if frosting a cake. The cream contained capsaicin, the chemical responsible for the burn of chili peppers. “We love capsaicin,” Tracey said. “It does two really nice things: it ramps up gradually to become quite intense, and it activates receptors in your skin that we know a lot about.” Thus anointed, I signed my disclaimer forms and was strapped into the scanning bed of a magnetic-resonance-imaging (MRI) machine.

The machine was a 7-Tesla MRI, of which there are fewer than a hundred in the world. The magnetic field it generates (teslas are a unit of magnetic strength) is more than four times as powerful as that of the average hospital MRI machine, resulting in images of much greater detail. As the cryogenic units responsible for cooling the machine’s superconducting magnet clicked on and off in a syncopated rhythm, the imaging technician warned me that, once he slid me inside, I might feel dizzy, see flashing lights, or experience a metallic taste in my mouth. “I always feel like I’m turning a corner,” Tracey said. She explained that the magnetic field would instantly pull the proton in each of the octillions of hydrogen atoms in my body into alignment. Then she vanished into a control room, where a bank of screens would allow her to watch my brain as it experienced pain.

During the next couple of hours, I had needles repeatedly stuck into my ankle and the fleshy part of my calf. A hot-water bottle applied to my capsaicin patch inflicted the perceptual equivalent of a third-degree burn, after which a cooling pack placed on the same spot brought tear-inducing relief. Each time Tracey and her team prepared to observe a new slice of my brain, the machine beeped, and a small screen in front of my face flashed the word “Ready” in white lettering on a black background. After each assault, I was asked to rate my pain on a scale of 0 to 10.

Initially, I was concerned that I was letting the team down. The capsaicin patch hardly tingled, and I scored the first round of pinpricks as a 3, more out of hope than conviction. I needn’t have worried. The patch began to itch, then burn. By the time the hot-water bottle was placed on it, about an hour in, I was surely at an 8. The next set of pinpricks felt as if I were being run through with a hot metal skewer.

“You’re a good responder,” Tracey told me, rubbing her hands together, when I emerged, dazed. “And you’ve got a lovely plump brain—all my postdocs want to sign you up.” As my data were sent off for analysis, she pressed a large cappuccino into my hands and gently removed the capsaicin with an alcohol wipe.

Tracey didn’t need to ask me how it had gone. The imaging-analysis software, designed in her department and now used around the world, employs a color scale that shades from cool to hot, with three-dimensional pixels coded from blue through red to yellow, depending on the level of neural activity in a region. Tracey has analyzed thousands of these “blob maps,” as she calls them—scans produced using a technique called functional magnetic resonance imaging (fMRI). Watching a succession of fiery-orange jellyfish flaring up in my skull, she had seen my pain wax and wane, its outlines shifting as mild discomfort became nearly unbearable agony.

For scientists, pain has long presented an intractable problem: it is a physiological process, just like breathing or digestion, and yet it is inherently, stubbornly subjective—only you feel your pain. It is also a notoriously hard experience to convey accurately to others. Virginia Woolf bemoaned the fact that “the merest schoolgirl, when she falls in love, has Shakespeare or Keats to speak her mind for her; but let a sufferer try to describe a pain in his head to a doctor and language at once runs dry.” Elaine Scarry, in the 1985 book “The Body in Pain,” wrote, “Physical pain does not simply resist language but actively destroys it.”

The medical profession, too, has often declared itself frustrated at pain’s indescribability. “It would be a great thing to understand Pain in all its meanings,” Peter Mere Latham, physician extraordinary to Queen Victoria, wrote, before concluding despairingly, “Things which all men know infallibly by their own perceptive experience, cannot be made plainer by words. Therefore, let Pain be spoken of simply as Pain.”

But, in the past two decades, a small number of scientists have begun finding ways to capture the experience in quantifiable, objective data, and Tracey has emerged as a formidable figure in the field. By scanning several thousand people, healthy and sick, while subjecting them to burns, pokes, prods, and electric shocks, she has pioneered experimental methods to survey the neural landscape of pain. In the past few years, her work has expanded from the study of “normal” pain—the everyday, passing experience of a stubbed toe or a burned tongue—to the realm of chronic pain. Her findings have already changed our understanding of pain; now they promise to transform its diagnosis and treatment, a shift whose effects will be felt in hospitals, courtrooms, and society at large.


The history of pain research is full of ingenious, largely failed attempts to measure pain. The nineteenth-century French doctor Marc Colombat de l’Isère evaluated the pitch and rhythm of cries of suffering. In the nineteen-forties, doctors at Cornell University used a heat-emitting instrument known as a “dolorimeter” to apply precise increments of pain to the forehead. By noting whenever a person perceived an increase or decrease in sensation, they arrived at a pain scale calibrated in increments of “dols,” each of which was a “just-noticeable difference” away from the adjacent dols. Last year, scientists at M.I.T. developed an algorithm called DeepFaceLIFT, which attempts to predict pain scores based on facial expressions.

The most widely adopted tools rely on the subjective reports of sufferers. In the nineteen-fifties, a Canadian psychologist named Ronald Melzack treated “an impish, delightful woman in her mid-seventies” who suffered from diabetes and whose legs were both amputated. She was tormented by phantom-limb pain, and Melzack was struck by her linguistic resourcefulness in describing it. He began collecting the words that she and other patients used most frequently, organizing this vocabulary into categories, in an attempt to capture pain’s temporal, sensory, and affective dimensions, as well as its intensity. The result, published two decades later, was the McGill Pain Questionnaire, a scale comprising some eighty descriptors—“stabbing,” “gnawing,” “radiating,” “shooting,” and so on. The questionnaire is still much used, but there have been few surveys of its efficacy in a clinical setting, and it’s easy to see how one person’s “agonizing” could be another person’s “wretched.” Furthermore, a study by the sociologist Cassandra Crawford found that, after the questionnaire’s publication, clinical descriptions of phantom-limb pain shifted dramatically, implying that the assessment device was, to some extent, informing the sensations it was intended to measure.

Meanwhile, as the historian Joanna Bourke has shown, in her book “The Story of Pain,” attempts to translate the McGill Pain Questionnaire into other languages have revealed the extent to which cultural context shapes language, which, in turn, shapes perception. In mid-century Montreal, Melzack’s talkative diabetic might have described a migraine as lacerating or pulsing, but the Sakhalin Ainu traditionally rated the intensity of pounding headaches in terms of the animal whose footsteps they most resembled: a bear headache was worse than a musk-deer headache. (If a headache was accompanied by a chill, it was described with an analogy to sea creatures.)


By far the most common tool used today to measure pain is the one I employed in the scanner: the 0-to-10 numerical scale. Its rudimentary ancestor was introduced in 1948, by Kenneth Keele, a British cardiologist, who asked his patients to choose a score between 0 (no pain) and 3 (“severe” pain). Over the years, the scale has stretched to 10, in order to accommodate more gradations of sensation. In some settings, patients, rather than picking a number, place a mark on a ten-centimetre line, which is sometimes adorned with cheerful and grimacing faces.

In 2000, Congress declared the next ten years the “Decade of Pain Control and Research,” after the Supreme Court, rejecting the idea of physician-assisted suicide as a constitutional right, recommended improvements in palliative care. Pain was declared “the fifth vital sign” (alongside blood pressure, pulse rate, respiratory rate, and temperature), and the numerical scoring of pain became a standard feature of U.S. medical records, billing codes, and best-practice guides.

But numerical scales are far from satisfactory. In Tracey’s MRI machine, my third-degree burn felt five points more intense than the initial pinpricks, but was it really only two points less than the worst I could imagine? Surely not, but, having never given birth, broken any bones, or undergone serious surgery, how was I to know?

The self-reported nature of pain scores leads, inevitably, to their accuracy being challenged. “To have great pain is to have certainty,” Elaine Scarry wrote. “To hear that another person has pain is to have doubt.” That doubt opens the door to stereotyping and bias. The 2014 edition of the textbook “Nursing: A Concept-Based Approach to Learning” warned practitioners that Native Americans “may pick a sacred number when asked to rate pain,” and that the validity of self-reports will likely be affected by the fact that Jewish people “believe that pain must be shared” and black people “believe suffering and pain are inevitable.” Last year, the book’s publisher, Pearson, announced that it would remove the offending passage from future editions, but biases remain common, and study after study has shown shocking disparities in pain treatment. A 2016 paper noted that black patients are significantly less likely than white patients to be prescribed medication for the same level of reported pain, and they receive smaller doses. A group of researchers from the University of Pennsylvania found that women are up to twenty-five per cent less likely than men to be given opioids for pain.

In addition, once pain assessment became a standard feature of American medical practice, doctors found themselves confronted with an apparent epidemic of previously unreported agony. In response, they began handing out opioids such as OxyContin. Between 1997 and 2010, the number of times the drug was prescribed annually grew more than eight hundred per cent, to 6.2 million. The disastrous results in terms of addiction and abuse are well known.

Without a reliable measure of pain, physicians are unable to standardize treatment, or accurately assess how successful a treatment has been. And, without a means by which to compare and quantify the dimensions of the phenomenon, pain itself has remained mysterious. The problem is circular: when I asked Tracey why pain has remained so resistant to objective description, she explained that its biology is poorly understood. Other basic sensory perceptions—touch, taste, sight, smell, hearing—have been traced to particular areas of the brain. “We don’t have that for pain,” she said. “We still don’t know exactly how the brain constructs this experience that you absolutely, unarguably know hurts.”


Irene Tracey has lived in Oxford almost all her life. She was born at the old Radcliffe Infirmary, went to a local state school, and studied biochemistry at the university. Her husband, Myles Allen, is an Oxford professor, too, in charge of the world’s largest climate-modelling experiment, and they live in North Oxford, in a semidetached house comfortably cluttered with their children’s sports gear and schoolwork. In 1990, Tracey embarked on her doctorate at Oxford, using MRI technology to study muscle and brain damage in patients with Duchenne muscular dystrophy. At the time, the fMRI technique that she used to map my brain in action was just being developed. The technique tracks neural activity by measuring local changes associated with the flow of blood as it carries oxygen through the brain. A busy neuron requires more oxygen, and, because oxygenated and deoxygenated blood have different magnetic properties, neural activity creates a detectable disturbance in the magnetic field of an MRI scanner.

In 1991, a team at Massachusetts General Hospital, in Boston, showed its first, grainy video of a human visual cortex “lighting up” as the cortex turned impulses from the optic nerve into images. Captivated, Tracey applied for a postdoctoral fellowship at M.G.H., and began working there in 1994, using the MRI whenever she could. When Allen, at that time her boyfriend, visited from England one Valentine’s Day, she cancelled a trip they’d planned to New York to take advantage of an unexpected open slot on the scanner. Allen spent the evening lying inside the machine, bundled up to keep warm, while she gazed into his brain. He told me that he had intended to propose to Tracey that day, but saved the ring for another time.

It was toward the end of her fellowship in Boston that Tracey first began thinking seriously about pain. Playing field hockey in her teens, she’d had her first experience of severe pain—a knee injury that required surgery—but it was a chance conversation with colleagues in a pain clinic that sparked her scientific interest. “It was just one of those serendipitous conversations that you find yourself in, where this whole area is opened up to you,” she told me. “It was, like, ‘God, this is everything I’ve been looking for. It’s got clinical application, interesting philosophy, and we know absolutely nothing.’ I thought, Right, that’s it, pain is going to be my thing.”

By then, Tracey had been recruited to return home and help found the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain. Scientists had already largely given up on the idea of finding a single pain cortex: in the handful of fMRI papers that had been published describing brain activity when a person was burned or pricked with needles, the scans seemed to show that pain involved significant activity in many parts of the brain, rather than in a single pocket, as with hearing or sight. Tracey’s plan was to design a series of experiments that picked apart this larger pattern of activity, isolating different aspects of pain in order to understand exactly what each region was contributing to the over-all sensation.

In 1998, while her lab was being built, she took her first doctoral student, a Rhodes Scholar named Alexander Ploghaus, to Canada, their scientific equipment packed in their suitcases, to use a collaborator’s MRI machine for a week. Their subjects were a group of college students, including several ice-hockey players, who kept bragging about how much pain they could take. While each student was in the scanner, Tracey and Ploghaus used a homemade heating element to apply either burns or pleasant heat to the back of the left hand, as red, green, and blue lights flashed on and off. The lights came on in a seemingly random sequence, but gradually the subjects realized that one color always presaged pain and another was always followed by comfortable warmth. The resulting scans were striking. Throughout the experiment, the subjects’ brain-activity patterns remained consistent during moments of pain, but, as they figured out the rules of the game, the ominous light began triggering more and more blood flow to a couple of regions—the anterior insula and the prefrontal cortices. These areas, Tracey and Ploghaus concluded, must be responsible for the anticipation of pain.

Showing that the experience of pain could be created in part by anticipation, rather than by actual sensation, was the first experimental step in breaking the phenomenon down into its constituent elements. “Rather than just seeing that all these blobs are active because it hurts, we wanted to understand, What bit of the hurt are they underpinning?” Tracey said. “Is it the localization, is it the intensity, is it the anticipation or the anxiety?” During the next decade, she designed experiments that revealed the roles played by various brain regions in modulating the experience of pain. She took behavioral researchers’ finding that distraction reduces the perception of pain—as when a doctor tells a child to count backward from ten while receiving an injection—and made it the basis of an experiment that showed that concentrating on a numerical task suppressed activity in several regions that normally light up during pain. She examined the effects of depression on pain perception—people suffering from depression commonly report feeling more pain than other people do from the same stimulus—and demonstrated that this, too, could change the distribution and the magnitude of neural activity.

One of her most striking experiments tested the common observation that religious faith helps people cope with pain. Comparing the neurological responses of devout Catholics with those of atheists, she found that the two groups had similar baseline experiences of pain, but that, if the subjects were shown a picture of the Virgin Mary (by Sassoferrato, an Italian Baroque painter) while the pain was administered, the believers rated their discomfort nearly a point lower than the atheists did. When the volunteers were shown a secular painting (Leonardo da Vinci’s “Lady with an Ermine”), the two groups’ responses were the same. The implications are potentially far-reaching, and not only because they suggest that cultural attitudes may have a neurological imprint. If faith engages a neural mechanism with analgesic benefits—the Catholics showed heightened activity in an area usually associated with the ability to override a physical response—it may be possible to find other, secular ways to engage that circuit.

Tracey’s research had begun to explain why people experience the same pain differently and why the same pain can seem worse to a single individual from one day to the next. Many of her findings simply reinforced existing psychological practices and common sense, but her scientific proof had clinical value. “Countless people who work in cognitive behavioral therapy come up at the end of talks or write to me,” Tracey told me. “They say how helpful it has been to empower their education of the patient by saying that, if you’re more anxious about your pain, or more sad, look, here’s a picture telling you it gets worse.”

These early experiments repeatedly demonstrated that pain is neurologically complex, involving responses generated throughout the brain. Nonetheless, by identifying regions that control ancillary factors, such as anticipation, Tracey and her team were gradually able to zero in on the regions that are most fundamental. In 2007, Tracey published a survey of existing research and identified what she called “the cerebral signature of pain”—the distinctive patterns produced by a set of brain regions that reliably act in concert during a painful experience. Some of these regions are large, and accommodate many different functions. None are specific to pain. But, as we stared at the orange blobs of an fMRI scan on her laptop screen, Tracey rattled off the names of half a dozen areas of the brain and concluded, “With a decent poke, you’d activate all of that.”

In 2013, Tor Wager, a neuroscientist at the University of Colorado, Boulder, took the logical next step by creating an algorithm that could recognize pain’s distinctive patterns; today, it can pick out brains in pain with more than ninety-five-per-cent accuracy. When the algorithm is asked to sort activation maps by apparent intensity, its ranking matches participants’ subjective pain ratings. By analyzing neural activity, it can tell not just whether someone is in pain but also how intense the experience is. “What’s remarkable is that basic pain signals seem to look pretty much the same across a wide variety of people,” Wager said. “But, within that, different brain systems are more, or less, significant, depending on the individual.”

Among the brain’s many pain-producing patterns, however, there is only one region that is consistently active at a high level: the dorsal posterior region of the insula. Using a new imaging technique, Tracey and one of her postdoctoral fellows, Andrew Segerdahl, recently discovered that the intensity of a prolonged painful experience corresponds precisely with variations in the blood flow to this particular area of the brain. In other words, activity in this area provides, at last, a biological benchmark for agony. Tracey described the insula, an elongated ridge nestled deep within the Sylvian fissure, with affection. “It’s just this lovely island of cortex hidden in the middle, deep in your brain,” she said. “And it’s got all these amazing different functions. When you say, ‘Actually, I feel a bit cold, I need to put a sweater on,’ what’s driving you to do that? Probably this bit.”

The importance of the dorsal posterior insula had previously been highlighted in a somewhat horrifying experiment conducted by Laure Mazzola, a neurologist at the Lyon Neuroscience Research Center, in France. It is common for surgeons treating patients with drug-resistant epilepsy to disable the portions of the brain in which the seizures are occurring. Before surgery, neurologists often stimulate the area and its surroundings with an electrical probe, to make sure they’re on target. Taking advantage of this opportunity, Mazzola stimulated various parts of the posterior insula in pre-surgical patients and recorded their responses. When she reached the dorsal region, Tracey told me, the patients “were leaping off the bed.” The presence of a probe in the brain shouldn’t in itself hurt, because there are no pain receptors there. Yet activating this area was apparently enough to create a brutally convincing synthetic pain.


The day after my fMRI scan, Tracey took me to her department’s Clinical Pain Testing lab, a room that she refers to as her “torture chamber.” A red illuminated sign blinked “Do Not Enter,” and Tracey removed a retractable belt blocking the door. Inside were all the devices that she and her team use to hurt people scientifically. As I reclined in a blue dentist-style chair under the room’s lone fluorescent light, she and a couple of her colleagues burned the back of my hand with a laser. Someone pressed a device about the size of a camera’s memory card against my forearm. It was rippled with heating elements, which were covered with a thin layer of gold foil to conduct the heat to the skin. “We can raise the temperature by thirty degrees in under a second,” Tracey said.

Each of the methods has a particular use. Lasers and electrodes can deliver precise increments of pain in experiments requiring a quick transition between different levels of stimulation. Capsaicin, because it sensitizes the central nervous system, is best for simulating chronic pain. Inflatable rectal balloons mimic the distinctive pain caused by damage to internal organs. All of them have been designed with the aim of reliably producing in laboratory conditions sensations that hurt enough to mirror real life but don’t cause lasting harm, which would be unethical. A scientist hoping to gather publishable data can’t just hit someone with a hammer and hope that each blow is as hard as the last one, even if an institutional ethics committee would permit such a thing.

Tracey has developed protocols to inflict the maximum amount of pain with the minimum amount of tissue damage. Using psychological tricks and carefully choreographed shifts in intensity, she has also devised ways of heightening a subject’s perception of pain. At the same time, research identifying the regions most crucial to the experience of pain has inadvertently pointed the way to the creation of artificial pain purely through targeted neurostimulation. It does not take much imagination to discern the potential for misuse of this kind of knowledge. For this reason, the International Association for the Study of Pain (I.A.S.P.) has a code of ethics, and its members are pledged not to inflict or increase pain except in an experimental setting.

A more nuanced ethical issue involves the potential use of neuroimaging as a sort of lie detector—to expose malingerers or increase payouts in injury-compensation suits. “Pain is enormously important in law,” Henry Greely, the director of the Center for Law and the Biosciences, at Stanford University, told me. “It’s the subject of hundreds of thousands of legal disputes every year in the United States.” Many are personal-injury cases; others involve Social Security and private-insurance disability. Greely pointed out that the lack of an objective test for pain means not only that people who deserve compensation miss out (and vice versa) but also that millions of billable hours are spent on these suits. With an agreed-upon empirical metric for pain, he estimates, the vast majority of cases would be settled rather than litigated.

Greely believes that the routine use of fMRI evidence in court is likely a decade away, but there are already signs that it is coming. In 2008, a colleague of his, Sean Mackey, was asked to serve as an expert witness in the case of a man who was suing an asphalt manufacturer after suffering first- and second-degree burns. The man’s lawyers were planning to use brain-imaging data to show that the injuries had left him in chronic pain. The company’s legal team wanted to put Mackey on the stand to argue that the current state of pain science could not justify this as an objective assessment. The case was eventually settled out of court, but the judge ruled that, despite a demurring opinion from Mackey, the scans were admissible as evidence.

All the scientists I spoke to were careful to stress that they think the field is not far enough advanced for an fMRI scan to be used as legal evidence of pain, or to overrule a subjective report. Some are convinced that it will never reach that point. Karen Davis, a researcher at the Krembil Brain Institute, in Toronto, told me, “Pain is, literally by definition, a subjective experience. That makes self-report the only true measure.” Greely is less sure: “I’m willing to agree that it’s still truly a subjective state, but there are objective things that can give you more or less confidence in the reality of that subjective state.”

Davis is sufficiently worried about the legal ramifications of pain neuroimaging that she recently chaired an I.A.S.P. task force to consider the subject. Researchers who have spent their careers investigating the ways that pain is altered by mood, context, and suggestion are naturally skeptical of the idea that personal testimony can be proved or disproved by making someone spend an hour lying horizontal and immobile in a rigidly controlled, socially isolated, loud, boring, and claustrophobic environment. Although fMRI is often taken to be a transparent window into brain function, Davis told me that it would be more accurate to think of it as a low-resolution, somewhat out-of-synch set of stills from a black-and-white movie. While electrical impulses that travel along neurons last only about a millisecond, blood, which fMRI measures as a proxy, arrives on the scene slightly after the fact, and dissipates slowly.


Most brain imaging has been carried out in 3-Tesla MRI scanners, which cannot resolve detail below a scale of two millimetres. Neurons are so tiny that a cube of brain tissue that size will contain tens of thousands of them. Even the 7-Tesla that scanned my brain had only a maximum resolution of one millimetre. Tracey cautions against overestimating how much “blob maps” can explain. “Underneath that blob there’s an awful lot of nuance, and there’s an awful lot of anatomy,” she said. To help validate her findings, she often combines magnetic imaging with other techniques, such as measurements of electrical activity using an EEG.

Relatively few people have had their brains scanned while being hurt, and an algorithm like Wager’s, which has correctly predicted pain in the brains of a small cohort of healthy volunteers, cannot be reliably extrapolated to apply to the population as a whole. But Greely believes that overcoming this deficiency is simply a matter of doing more studies. He predicts that, once researchers have collected enough data and developed standardized protocols, neuroimaging will follow in the path of forensic DNA—a scientific breakthrough whose results were eventually considered robust enough to use as evidence in court. Our trust in DNA evidence is increasingly seen as problematic, but Greely is unperturbed. “No evidence is perfect,” he said. “The stuff courts rely on most—eyewitness testimony—is known to be awful, but we use it anyway.”


When I asked Tracey whether she thought her work could eventually rid the world of pain, she snorted in a polite attempt not to laugh. Most pain, she explained, is “the good kind.” Hurting yourself when you touch a hot surface is unpleasant, certainly, but it’s also crucial. While in Oxford, I met one of her frequent collaborators, the neurobiologist David Bennett, whose research involves patients who, because of rare genetic mutations, cannot feel pain. “You might wonder, Why are humans born with this system where they have to feel pain?” Bennett said. “And these patients give you the answer to that very quickly, because not feeling pain is a health disaster.” Often, he told me, such people die young. Historically, they frequently became circus freaks: the earliest clinically documented example was a Czech immigrant to the United States, whose case was described by a Dr. Dearborn in the Bronx, in 1932. According to Dearborn, the patient earned a living on the vaudeville circuit as Edward H. Gibson, the Human Pincushion, inviting audience members to come up onstage and push pins into him.

Bennett said that patients of his have chewed off the tips of their own tongues and scratched their corneas. They suffer hearing loss from untreated ear infections, unwittingly rest their hands on hot surfaces, and walk on broken legs, which leaves their limbs deformed. In an evolutionary context, Bennett explained, it makes sense that we are built in anticipation of pain: we are soft, and the world is a dangerous place. Undergoing an extremely unpleasant response to harm helps us avoid further injury in the moment and teaches us to reduce its likelihood in the future.

But there’s a “bad kind” of pain, too—one that is not the result of any obvious external source. Chronic pain is often defined, somewhat misleadingly, as “pain that extends beyond the expected period of healing.” In reality, once you’ve “gone chronic,” as Tracey puts it, pain is the disease, rather than a symptom. That view represents a shift in understanding, brought about in part by her work. Until recently, chronic pain was thought of merely as prolonged “normal” pain. But neuroimaging has shown that, if a chronic-pain sufferer and an unafflicted person are given the same burn or pinprick, their brains manifest activity differently. Chronic pain, Tracey said, is now understood as “something new, with a life of its own, with its own biology and its own mechanisms, most of which we really don’t understand at all.”

Until a couple of years ago, Tracey, like most researchers in the field, focussed on the good kind of pain; this was crucial to understanding the basic neurobiology involved. Yet the true problem is chronic pain. Estimates suggest that somewhere between ten and thirty per cent of the American population suffers from chronic pain. Its cost to society is some six hundred and thirty-five billion dollars each year—more than that of cancer and heart disease combined. And behind such statistics is the heavy psychic and emotional toll on those who spend every conscious moment suffering. A journalist who was given a diagnosis of fibromyalgia twenty years ago told me that his entire identity is subsumed by his experience of incessant, whole-body agony: “It’s who I am now. I’m broken. I need to be fixed, but I can’t be fixed.”

Tracey’s latest research has investigated a key neural mechanism of chronic pain. It is situated in the brain stem, a hard-to-reach, tube-shaped mass of gray matter at the top of the spinal cord, which functions as the conduit for communication between the brain and the body. Experiments on animals had identified two mechanisms within the brain stem that, respectively, muffle and boost pain signals before they reach the rest of the brain. Since Tracey’s lab first succeeded in imaging the region, more than a decade ago, she has been able to show how these two mechanisms operate. “It can completely block the signals coming in,” she said of one, explaining that it is responsible for situations in which you don’t feel pain even though you should—for instance, when your brain is distracted by the euphoria of crossing the finish line of a marathon. Unfortunately, in some people the mechanism that exacerbates pain is dominant. Scanning the brains of patients with diabetic nerve pain, Tracey and Segerdahl found enhanced communication from the brain stem, via the spine, to the parts of the brain known to contribute to the sensation of pain.

Tracey told me that it seems we may all be predisposed by our brain stems to feel pain more acutely or less, but that in chronic-pain patients it’s as if the volume knob of pain were turned all the way up and jammed there permanently. No one knows why this hypersensitization occurs. Studies of twins suggest that our pain response is, in part, heritable, but there are close correlations between chronic pain and many other factors—gender, age, stress, poverty, and depression. Tracey has begun to study whether recurrent experiences of acute bodily distress early in life trigger brain-stem changes that make chronic pain likelier later on. With colleagues in Oxford, she is involved in a longitudinal study of extremely premature babies and another of teen-age girls who suffer particularly painful periods.

Although the results of this work won’t be known for many years, her brain-stem research is already on its way to a clinical application. A few years ago, in collaboration with the rheumatologist Anushka Soni, Tracey began imaging the brains of osteoarthritis patients before and after knee-replacement surgery. Roughly a fifth of patients who have knee replacements find that the operation doesn’t meaningfully reduce their pain, and, again, no one knows why. But when Tracey analyzed the scans she found that the unlucky patients had increased activity in the mechanism of the brain stem known to amplify pain signals. Their brains revealed that they had “gone chronic”; they were not just ordinary people whose knees hurt.

Although it’s not feasible to give every prospective patient a brain scan, results from fMRI experiments correlate strongly with responses to a questionnaire called painDETECT, which was developed to diagnose nerve malfunction. Such a questionnaire could predict the likely outcome of surgery, so that patients could make an informed decision about whether the procedure was worth it. Tracey is also testing, on a group of twenty-four volunteers, a compound that she hopes could dampen activity in the problematic brain-stem region. In time, patients who seem predisposed to less successful surgical outcomes may be given a drug that makes relief likelier by adjusting their brain-stem biochemistry.

Drug development could be the most influential result of Tracey’s work. Pain medications have become something of a pharmacological graveyard, she told me; their development is often abandoned after patients report no improvement. “But their pain rating might still be up for all these other reasons—they’re anxious, they’re depressed, they’re expecting to be in pain,” Tracey said. “We’ve thrown out drugs that probably had high efficacy because we had the wrong measure—we relied on the subjective rating.” She believes that drug tests will become much more reliable once their efficacy can be measured against an objective target. She is part of an academic consortium that has received a large grant from Europe’s Innovative Medicines Initiative to help establish a set of measurable biological signs that can be used to ascertain whether new drugs are effective at disarming known pain mechanisms, regardless of whether the person taking them experiences any relief. Ultimately, she expects that various combinations of therapies will need to be delivered, in order to quiet the particular neural systems responsible for each individual’s unique experience of suffering.


A few weeks after my ordeal in the MRI machine, Andrew Segerdahl e-mailed me the resulting images. I looked for the brain regions I’d been told were important, but all I could see was a brain on fire. Everything was orange, particularly in the left hemisphere. (The pain was being inflicted on my right leg.)

Over the phone, Segerdahl talked me through my scans. “That map is actually really difficult to make sense of,” he said. “Your brain is really, really, really lit up—there’s just a lot going on.” But then he showed me a sequence of images that had been processed in such a way that the color coding appeared only in regions that had elevated blood flow while I endured the prolonged pain of the capsaicin cream. The characteristic pattern of pain began to emerge, and Segerdahl recited the names of the active regions like old friends.

Then came a set of maps that showed my brain during the exquisite moment of relief when the cooling pack was applied. There were many regions with activity levels—the images looked almost as busy as the heat maps—but the blobs were subtly different in shape and location. In my brain, pain was shading into pleasure, and, curiously, many of the same regions were involved, activated in a slightly different pattern. “There’s quite a lot still to be understood in terms of the relief side of this equation,” Segerdahl said. He hesitated. “It’s, like, I’m super interested in it, but I almost don’t want to touch it yet, because it’s the ultimate goal.”

Tracey has been looking at pleasure for almost as long as she’s been studying pain. “They are two sides of the same coin,” she told me. Many signs of their interrelation crop up in her work. Chronic-pain patients typically also suffer from anhedonia—the inability to experience pleasure—and research suggests that their brains’ reward systems are wired slightly differently from those in other brains. Pain is naturally a more urgent research priority, given that most of us find it intolerable, but fully understanding it will require a better understanding of its opposite. “There’s a Jeremy Bentham quote I like,” Tracey said. “ ‘Nature has placed mankind under the governance of two sovereign masters, pain and pleasure.’ These are the two things that drive us, as animals, to do what we do.” ♦This article appears in the print edition of the July 2, 2018, issue, with the headline “Seeing Pain.”



Nicola Twilley is a contributing writer for newyorker.com. She is the author of the blog Edible Geography and a co-host of the Gastropod podcast. She is working on a book about refrigeration.Read more »

https://www.newyorker.com/magazine/2018/07/02/the-neuroscience-of-pain