Is Inflammation A Chief Cause Of Chronic Pain

Today's post from ufhealth.org (see link below) talks about the effect of inflammation on older pain patients and this includes people living with nerve damage. The link between neuropathy, auto-immune disease and inflammation is often hinted at but rarely confirmed, yet neuropathy is very often the result of inflammation and damage to the nervous system. This article talks about the fact that older people are more prone to and more often suffer from severe inflammation, leading to more and longer lasting pain. It suggests that anti-inflammatory drugs may be the answer but these are rarely on the list of recommended medications for neuropathy patients. It's a chicken and egg question: does the pain cause the inflammation, or the inflammation cause the pain? Inflammation is more often associated with tissue damage than nerve cells but inflammation in the nervous system most definitely can cause chronic pain (ask any shingles sufferer!) An interesting article requiring more research if you're interested. It may also be worthwhile asking your neurologist whether anti-inflammatory drugs such as diclofenac may be of benefit to you, although they do carry the potential for side-effects of their own.

Study shows pain causes older adults to develop more inflammation over a longer period of time 
Published: May 4, 2016 By: Morgan Sherburne 

When older relatives complain about their pains, show a little empathy, because new research suggests that as we age, we may all become more sensitive to pain. A small, preliminary University of Florida Health study has suggested for the first time that inflammation may occur more quickly and at a higher magnitude — and stays around longer — when older adults experience pain versus when younger adults experience pain.

This could mean that older adults could be at risk for developing chronic pain and may benefit from taking anti-inflammatories soon after an injury or procedure, according to the researchers.

Older adults often have a certain level of chronic inflammation in their bodies. But UF researchers found that when they induced pain in older adults, proteins associated with inflammation increased more than they did in younger participants and stayed in the bodies of older adults longer. The researchers also found that anti-inflammatory cytokines, proteins that soothe inflammation, peaked later for older adults than younger adults. Their results were published in a previous issue of Experimental Gerontology.

“Older people go through painful procedures more often, and we wanted to research whether this accumulation of painful procedures or more acute pain episodes that older people encounter is bad,” said Yenisel Cruz-Almeida, Ph.D., MSPH, an assistant professor in the UF College of Medicine’s department of aging and geriatric research who also is affiliated with the UF Institute on Aging. “If you have enough of those in a shorter period of time, does this predispose you to have chronic pain?”

When older adults have this kind of elevated inflammatory response, they’re more likely to have pain generated in the periphery of the body — their tissue and limbs outside of the spinal cord and brain, said the study’s senior author Joseph Riley, Ph.D., director of the pain clinical research unit in the UF Pain Research and Intervention Center of Excellence.

“If older adults are more likely to have these pain messages sent through the spinal cord to the brain, and the nervous system is being adapted to go through these changes, they may become more pain prone,” said Riley, also a professor in the UF College of Dentistry’s department of community dentistry and the UF College of Public Health and Health Professions’ department of clinical and health psychology.While the study does not establish whether accumulation of acute pain predisposes older adults to chronic pain, the researchers say their findings suggest this is a possibility, and it’s the first step in pain research to further understand the relationship between pain and aging. The researchers said the study’s sample size, though small, was more than adequate to demonstrate large differences between the older and younger adults they tested. The differences in inflammation within each group varied very little compared with the overall difference between the two groups, which suggests the populations they sampled were very different and there was little chance of sampling error, Riley said.

Cruz-Almeida and Riley studied eight healthy older adults, whose average age was 68, and nine healthy younger adults, whose average age was 21. None of the participants had illnesses such as diabetes or hypertension. During an initial visit, researchers induced pain in the participants in two ways, either using heat applied to the feet or a cold ice bath.

The first session determined how sensitive the participants were to pain. Determining a tolerable temperature allowed the researchers to recreate the same amount of pain for each participant in the subsequent sessions.

Participants rated their pain on a scale from 1 to 10. The researchers were aiming to induce pain to a Level 4 — a level that created the painful stimuli the researchers needed, but didn’t dissuade the participants from returning for the other visits required in the study.



With a thermode — a device that looks like a microphone with a copper tip — the UF researchers applied heat to the feet of participants in a study that tested the inflammatory response to pain of older adults versus younger adults.To study inflammation in the blood, the scientists inserted a catheter into each participant before inducing pain. That allowed them to collect the participant’s blood before the pain stimulus and then at three, 15, 30, 45, 60 and 90 minutes after the stimulus. These blood samples allowed the researchers to study inflammatory markers in the blood, finding that older adults had higher levels of inflammation when pain was induced than the younger adults.

Riley said activation of the immune system and increased inflammation are not necessarily harmful, but it’s important to understand how the length of time the immune system is activated affects the body.

“We think that the longer you have the immune system activated, having these elevated inflammatory cytokines, the more this activation can alter the homeostasis of the body. Usually an imbalance like that can be associated with autoimmune disorders, which also increase with age,” Cruz-Almeida said. “But the truth is we don’t know what the direct implications would be. We think low-grade inflammation is related to endocrine abnormalities such as diabetes and the development of heart problems. … We need to keep looking and doing future research.”

Riley said immediate implications of the research for patients could be to attack pain quickly with anti-inflammatory medication.

“Early treatment of an injury even with over-the-counter anti-inflammatories may be a good idea,” Riley said. “It’s those first few days of bombarding the central nervous system with pain signals that has a bigger effect (on the body).”
About the Author

Morgan Sherburne

Science writer for UF Health. Morgan writes about the research of faculty physicians in the College of Medicine. She joined the UF Health staff in 2014. A Michigan native, she...Read More

https://ufhealth.org/news/2016/study-shows-pain-causes-older-adults-develop-more-inflammation-over-longer-period-time

How Vitamin B12 Helps To Reduce Or Prevent Nerve Pain

Today's interesting post from liveitholistic.com (see link below) looks in detail at vitamin B12 and the role it plays in helping with and preventing neuropathy. Many people take vitamin B12 supplements for nerve pain because they've heard or read that it helps but few know why they do. Most neurologists will agree that a vitamin B (and B12 in particular) deficiency can cause nerve damage but it's rare that you see a breakdown of how vitamin B actually works in the body. This is such an article and therefore an important one for neuropathy patients. Well worth a read.

The Importance of B12 and its role in Neuropathy and Anemia. 
Marc Capistrano June 19, 2016
 
The stars have aligned on this post. The topic of B12 keeps coming up lately, and it was a sign that I had to put something up on the blog. The thing about writing is that it’s almost like a personal journal (…here’s what’s on my mind at this point in time and how I feel about it.)

In this case, Vitamin B12 is on my mind!

It’s involved in every metabolic cellular process in our body, DNA production and nerve function to name a few.

A good balance of all b-vitamins is important but B12 tends to get most of the attention because it is not absorbed into the blood stream the same way the other b’s are. B12 is usually more deficient than the other b-vitamins due to a deficiency in Intrinsic Factor. It also binds with “intrinsic factor” (It’s a specialized type of protein produced in the stomach). B12 must be bound to Intrinsic Factor. Then it is absorbed in to the small intestine (There are receptor sites for B12). You need to produce HCL in order to produce intrinsic factor. You also need to produce enough HCL to produce pepsin. Intrinsic (IF) is internally produced. On the other hand, B12 is the extrinsic (outside) factor produced.

Ok Marc. Tell me why B12 vitamins are important.

1. It prevents Peripheral Neuropathy: The myelin sheath acts as an insulating cover over a nerve fiber. It’s through this nerve fiber that conduction impulses are produced and electrical signals are sent and received. Think of it this way, you touch something hot, once the sensation is felt, your nerves send a signal to your brain. This signal works on these conduction impulses. If you don’t know, now you know ***Biggie Voice***.

Well B12 prevents the breakdown of the myelin sheath that covers our nerve fibers (also known as “demyelination”). When we hear myelin sheath, we usually associate this with the brain (MS). But, the myelin is also very important for your spinal cord’s nerve fibers. This damage leads to a condition known as peripheral neuropathy, in which symptoms include loss of coordination, sensory touch and eventual decreased muscle mass.

It’s shown that B12 intake from food and supplementation can improve neuropathy conditions. With issues like tingling, muscular dysfunction and especially neuropathy, it’s best to have a specialist (Chiropractor, Physiotherapist) look at you and make a proper diagnosis. As a nutritional practitioner, my job is to support the physical intervention through nutrition once a person is diagnosed.

2. The effects of B12 deficiency can cause irreversible symptoms: This is seen in Multiple Sclerosis (a degenerative disease of the nervous system). As with any tissue in the body, once it’s damaged, scar tissue forms (also known as Sclerosis).

3. A lack of B12 can lead to Pernicious Anemia: This is a form of anemia caused by a lack of absorption of B12 due to a deficiency in Intrinsic Factor. B12 binds with “intrinsic factor” as I had mentioned earlier. Without B12 and Intrinsic factor, the membranes of immature red blood cells rupture, disintegration of the stomach lining can occur which can lead to autoimmune diseases such as Crohn’s disease.

4. It makes us happy: B12 plays an important role in supporting and assisting with the formation of neurotransmitters such as serotonin and dopamine production. And this, make us happy…

5. B12 helps us recycle Homocysteine: Anyone out there with a history of cardiovascular disease will have some knowledge of homocysteine levels. If you don’t, then just know that homocysteine is created as a by-product of our body’s metabolism of methionine and cysteine.

Homocysteine isn’t all bad, it still gives us things like Cysteine, which is a precursor to glutathione (an amino acid known for its detoxification capabilities) and is important to the synthesis of Neurotransmitters. The only problem is that high levels of homocysteine are indicative of cardiovascular and neurodegenerative diseases. B12 is important in taking homocysteine and converting it back to methionine.

Ok…What do I do?

Before we get into the details of B12 intake, it’s important to note that all b vitamins including B12 are depleted in the body by things like stress, birth control pills and high intake of sugars.

1. Some people can’t produce Intrinsic Factor. If this is the case, B12 shots are available. You’ll want to buy Methylcobalamin (the active form), not Cyanocobalamin.

2. HCL (stomach acid) is required in order to take B12 from its protein carrier Intrinsic Factor. Refrain from antacids and supplement with Hydrochloric acid with betaine to improve stomach pH.

3. If you’re simply deficient and looking for the next best thing to a shot, then a sublingual (under the tongue) is another alternative option. This skips the digestion process and gets right into the bloodstream. People looking to simply optimize or increase B12 intake can take a Vitamin B complex with a higher B12 content.

4. B12 food sources: Liver, Meat Protein, Dairy, and Seafood (particularly shellfish).

5. The liver has to activate B-vitamins. If you have an under functioning liver, then B-vitamins are not being absorbed. Support the liver, and the b-vitamins will follow!

6. Supplements and B12 aside, it’s important to look at the root cause of demyelination (breakdown of the nerve fiber). In some cases, autoimmune conditions cause the self-destruction of the myelin sheath. Eliminating triggers that cause chronic inflammation (high sugar, poor diet etc.…) can prove to be your best prevention and early treatment. The entry of pathogens through the blood brain barrier affects the CNS, which in turn affects the peripheral system. Boosting your immune system can also be a great way to properly limit the amount of sclerotic tissue that forms.

http://www.liveitholistic.com/blog/2016/6/19/the-importance-of-vitamin-b12-and-its-role-in-neuropathy

Pelvic Bone Pain During Pregnancy

Pubic Bone Pain Pregnancy

Are you pregnant and having difficulty rolling in bed, getting in and out of your car, climbing stairs, or walking due to pelvic pain? You may be suffering from a .When you enlist in the pregnancy corps, your tour of duty is sure to include at least some activity on the pelvic front. But it sounds like you're experiencing more .Veronica's Story: During the third trimester of my first pregnancy, I started to have debilitating pain in my pubic region. I told my OB about my symptoms and she .One of the issues we treat regularly at our clinics is prenatal and postnatal pain. Although discomfort or pain during and after pregnancy is an extremely common .Pelvic pain, also referred to as PPGP pregnancy-related pelvic girdle pain , is a normal symptom associated with pregnancy. It can result from a wide range of .Early in pregnancy, many women have pelvic pain. Pelvic pain refers to pain in the lowest part of the torso, in the area below the abdomen and between the hipbones .Symptoms of pregnancy-related pelvic pain. PPGP is a collection of uncomfortable symptoms caused by a misalignment or stiffness of your pelvic joints at either the .IStockphoto. Pelvic pain or discomfort is common during pregnancy. After all, ligaments are stretching, hormone levels are changing, and organs are shifting around to .Pelvic joint instability is a leading cause of pelvic pain in women, especially after pregnancy. A look at the diagnosis and treatment of pelvic joint pain..Pubic bone pain in pregnancy is also known as Symphysis Pubic Diastasis SPD . This is where, usually in later pregnancy, the hormone relaxin causes the pelvis .

Pubic Bone Pain Pregnancy

Types Of Back Pain Causes

Pelvic pain, also referred to as PPGP pregnancy-related pelvic girdle pain , is a normal symptom associated with pregnancy. It can result from a wide range of .IStockphoto. Pelvic pain or discomfort is common during pregnancy. After all, ligaments are stretching, hormone levels are changing, and organs are shifting around .Are you pregnant and having difficulty rolling in bed, getting in and out of your car, climbing stairs, or walking due to pelvic pain? You may be suffering from a .Early in pregnancy, many women have pelvic pain. Pelvic pain refers to pain in the lowest part of the torso, in the area below the abdomen and between the hipbones . Pelvic joint instability is a leading cause of pelvic pain in women, especially after pregnancy. A look at the diagnosis and treatment of pelvic joint pain..When you enlist in the pregnancy corps, your tour of duty is sure to include at least some activity on the pelvic front. But it sounds like you're experiencing more .Veronica's Story: During the third trimester of my first pregnancy, I started to have debilitating pain in my pubic region. I told my OB about my symptoms and she .One of the issues we treat regularly at our clinics is prenatal and postnatal pain. Although discomfort or pain during and after pregnancy is an extremely common .Symptoms of pregnancy-related pelvic pain. PPGP is a collection of uncomfortable symptoms caused by a misalignment or stiffness of your pelvic joints at either the .Pubic bone pain in pregnancy is also known as Symphysis Pubic Diastasis SPD . This is where, usually in later pregnancy, the hormone relaxin causes the pelvis .

Sciatica relief leg pain

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Chest Pain During Pregnancy

Chest Pain Heart

Live a healthier life with TODAY's health tips and find the latest news for personal wellness, fitness,t and relationships..Whether you're looking to lose weight or just want a way to get rid of that nasty cold, eHow has all the answers you're looking for..TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..Prepare for Your Procedure. Get the facts on what to expect during your procedure as well as your recovery..Diabetes Scandals For Feet Diabetes Scandals For Feet :: what is the cause of type 1 diabetes - The 3 Step Trick that Reverses Diabetes Permanently in As .Chest pain can be caused by anything from muscle pain to a heart and should never be ignored..Chest pain angina . Taking L-carnitine by mouth seems to improve exercise tolerance in people with chest pain. Taking L-carnitine along with standard treatment also .

Chest Pain Heart

Right Rib X Ray Technique

Chest pain can be caused by anything from muscle pain to a heart and should never be ignored..Prepare for Your Procedure. Get the facts on what to expect during your procedure as well as your recovery..TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..Whether you're looking to lose weight or just want a way to get rid of that nasty cold, eHow has all the answers you're looking for..Chest pain angina . Taking L-carnitine by mouth seems to improve exercise tolerance in people with chest pain. Taking L-carnitine along with standard treatment also .Live a healthier life with TODAY's health tips and find the latest news for personal wellness, fitness,t and relationships..Diabetes Scandals For Feet Diabetes Scandals For Feet :: what is the cause of type 1 diabetes - The 3 Step Trick that Reverses Diabetes Permanently in As .

Neuropathic Pain For Health Professionals

Today's post from journals.lww.com (see link below) written for Nursing magazine, is a comprehensive article about neuropathy, its causes and treatments for health professionals. It's often interesting to read about how professionals are taught to approach the disease. We can then better understand the reasons for their decisions on our behalf. It also can give us some insights that the doctors don't tell us, either because they don't have time, or because they consider the subject matter too complex for the patient to understand. Definitely worth a read on a day when you don't have to rush off to work. The reference links referred to by the numbers throughout the article can be followed in the original article (see link below).

Living with the nightmare of neuropathic pain
D'Arcy, Yvonne MS, CRNP, CNS Nursing 2014

PATIENTS LIVING WITH a neuropathic pain syndrome will tell you that this vicious pain can ruin quality of life and spoil dreams. Some neuropathic pain, such as that from diabetic neuropathy, has a gradual onset, but other types, such as complex regional pain syndrome (CRPS), can develop suddenly. Some patients with neuropathic pain who have difficulty getting a diagnosis can experience increased pain and anxiety from the uncertainty of their pain condition.

To get a better understanding of this pain, let's look at a patient who had an accident that resulted in a neuropathic pain syndrome that changed her life.
 
Meet the patient

Mrs. S, age 65, is a retired teacher who went to bed one night free from pain. During the night, she got up to use the bathroom without turning on the light and ran into a table leg quite hard, injuring her right foot. Because the pain was so severe, her husband drove her to the ED. There she rated her pain as an 8 on a pain intensity rating scale of 0 (no pain) to 10 (worst pain imaginable).

The healthcare provider (HCP) obtained an X-ray of her foot, which revealed no fractures. Believing that Mrs. S had only soft-tissue damage, the HCP prescribed an opioid-acetaminophen combination medication for moderate pain, and told her to elevate, ice, and rest her foot for several days.

Although Mrs. S very diligently rested her foot, used ice packs, and took her medications as needed, the pain didn't resolve. In fact, it increased and became constant. Over the next 6 weeks, Mrs. S was evaluated by many HCPs, but none could give her a concrete diagnosis. Her pain was 7/10 at best and none of the pain medications she'd been given significantly relieved it; instead, they just made her sleepy. Because she had trouble putting weight on her foot, she started to use crutches. Her foot often felt cold, so she tried to put a sock on for warmth, but she couldn't stand the pressure it put on her foot.

Her husband was concerned about her unrelieved pain, loss of function, and lack of sleep due to pain. At 3 months, Mrs. S was referred to the local pain management specialist, who diagnosed her with CRPS, a neuropathic pain syndrome where the injury is located in the peripheral nerves but can also include changes in the central nervous system.1 (See Focusing on CRPS.)

When Mrs. S asked about treatment, she was told the pain would most likely persist and that the best approach was to try medications designed to treat neuropathic pain to help reduce it. At this point, she broke into tears and told the specialist, “This can't be! I just retired after teaching for 30 years. I planned to travel the world and now I'm in constant pain. How could this have happened to me?”

What we know about neuropathic pain

Neuropathic pain is chronic pain caused by damage in the peripheral or central nervous system. It's been defined as pain that's the direct consequence of a lesion or disease affecting the somatosensory system.2 (See The language of pain.)

This distinct type of pain encompasses a wide variety of neuropathic pain conditions. Unlike acute pain, it has absolutely no protective function and doesn't require any nociceptive input; that is, it exists independent of a stimulus. In contrast, nociceptive pain results from damage to tissue that's nonneural, such as surgical tissue damage or a tissue injury. Nociceptive pain is caused by activation of thermoreceptors, chemoreceptors, and mechanoreceptors, depending on whether the pain is caused by burns or muscle or tendon damage.3

Clinically, a patient such as Mrs. S doesn't have to move or walk on her affected foot to have pain. This type of pain persists without any pressure or sensory input.

Sorting out neuropathic pain

Of the many different types of neuropathic pain, some are caused by chronic diseases such as diabetes or HIV infection. Others, such as postmastectomy pain syndrome, result from surgery or treatments such as chemotherapy. Overall, neuropathic pain is thought to affect 1,765,000 people in the United States, not including those with back pain neuropathy.4 (See Sorting out common neuropathic pain conditions.)

Neuropathic pain has many sources and causes. For example, the continued inflammatory process of osteoarthritis may create neuropathic pain. Fibromyalgia is now considered a disease caused by dysregulation of pain inhibition pathways and amplification of central pain.5
 
Pathophysiology: Getting to the root

Generation of neuropathic pain involves both the peripheral nervous system and the central nervous system, and both the ascending and descending neural pathways. It's maladaptive: Neuropathic pain promotes abnormal functioning of nerves in one or both systems leading to a difficult-to-treat chronic pain condition.6 As the nerves change function, a phenomenon called neural plasticity occurs. These changes are responsible for heightened pain sensitivity and unpredictable, sudden pain exacerbations.

If the source of the neuropathic pain is in the periphery, continued pain stimuli from the peripheral nerve injury create sensitization that over time creates abnormal neural activity along the afferent nerve pathways leading to the central nervous system.7 This sensitization causes the release of what's commonly called an “inflammatory soup” of pain-promoting substances such as cytokines, tumor necrosis factors, bradykinin, and substance P. This in turn leads to hypersensitivity of the nerves, allowing them to crosstalk with each other, release pain-facilitating substances, activate higher level pain-generating functions such as N-methyl-D-aspartate receptors, and fire faster.

Sodium channels on nerve fibers play a part in the creation of neuropathic pain. In normal neural functioning, nerve depolarization occurs when the stimulus reaches the activation point and the nerve is forced to fire. When neuropathic pain is created, more primary and secondary sodium channels are activated, allowing for an ectopic neural discharge.4

Pain that originates from the central nervous system is even more difficult to manage. Pain that's centrally controlled can be created by a continued barrage of pain stimuli to the peripheral neurons, causing central neurons to become hyperexcitable. This hyperexcitability has been transferred to the central nervous system through the synaptic junction between the two nervous systems. As a result of this central sensitivity, synaptic connectivity reorganizes, causing lower activation thresholds and increased responses to stimuli.8

Additionally, collateral neurons may sprout and create larger fields of effect with the ability to crosstalk with each other and recruit additional neurons for pain creation. This phenomenon, called wind-up, causes an increased response to painful stimuli.6 Meanwhile, the descending pathway inhibition potential used to block pain is adversely affected, letting more pain reach the patient.

This explains the pain that Mrs. S is continuing to have. Continual pain stimuli from the periphery have created central sensitization and the wind-up effect has been created related to neuronal plasticity. Because the pain had continued at high levels for so long, the central nervous system pain-facilitating process was activated, which will make her pain much harder to manage.
 
Signs and symptoms

When assessing neuropathic pain, the nurse must ask the patient to describe the pain. Aside from the numeric pain intensity scale, the descriptors the patient uses are the best means of identifying the pain. If the patient uses words such as burning, shooting, electric, painful numbness, or tingling, the pain has a neuropathic source. After a mastectomy, some patients complain of strange painful sensations or painful pruritus in the ipsilateral axilla or upper arm. This is also classified as neuropathic pain.

Using fiber wisps for sensation testing or alcohol to create a cool sensation and touching the painful areas can determine just how large an area is affected. Ask patients if they experience hyperalgesia, increased pain from a stimulus that's normally painful, such as a pinprick, or allodynia, a painful response to a stimulus that isn't normally painful, such as touch from clothes or bedsheets.6 Assess for other signs of neuropathic pain. Other common types of neuropathic pain include paresthesia, an abnormal sensation that isn't unpleasant, such as numbness or tingling, and dysesthesia, an unpleasant sensation such as painful pruritus or feeling as though bugs are crawling under the skin.6

In the acute phase, patients who are developing CRPS after an injury continue to report high-intensity pain despite escalating doses of opioids. As the condition develops, besides allodynia, patients report edema, skin discoloration due to changes in blood flow, temperature differences between the affected and nonaffected extremity, changes in hair and nail growth, weakness, and tremor.9

Mrs. S is having difficulty with severe pain and she can't put any pressure on her foot. She has allodynia, and she's started to use descriptors indicative of CRPS, such as painful coldness.
 
Treatment options

One of the best ways to manage neuropathic pain is to use a stepwise approach. To adequately assess and diagnose a patient with neuropathic pain, the HCP will need to perform a focused physical exam. If possible, the HCP will identify the source, make a diagnosis, and examine any contributing comorbidities such as diabetes. Remember that the patient may not understand that pain descriptors may be the key to adequate management.

Besides explaining the diagnosis to the patient and discussing treatment options, the HCP will set realistic achievable goals. Many patients with neuropathic pain have seen multiple HCPs with no success; receiving a diagnosis may end the uncertainty that these patients have experienced and give them some hope for reducing the pain. Although complementary techniques such as relaxation or yoga may be beneficial for adjunct pain relief, the mainstay is pharmacologic management.

Stepping up to medications

Using the stepwise approach to treatment includes using first-line medications with the highest level of evidence for success in controlling neuropathic pain. (See Lining upmedications for neuropathic pain.)

After patients begin drug therapy, nurses need to reassess the efficacy of the therapeutic regimen. If the first medication chosen doesn't provide pain relief or increase functionality, the HCP may try titrating the dose upward. If that doesn't provide adequate pain relief, the HCP may consider combining two first-line medications.

If careful drug choices in the first-line category don't provide adequate pain relief, trialing second-line options may be a way of optimizing pain relief. As always, adding nonpharmacologic therapies, such as yoga, pool therapy, or meditation, can help with pain relief and relaxation.

For Mrs. S, our patient with CRPS, using one or more first-line therapies should provide some level of pain relief. Her current medication is an opioid, which is a second-line option. Using first-line medications either alone or in conjunction with the opioid may optimize her pain relief, and a consultation with physical medicine and rehabilitation professionals to work on increasing functionality is highly recommended. Mrs. S may never be pain free—that isn't a reasonable goal for her—but she should be able to move to a higher level of physical activity and perhaps begin to take short trips to see some of the places she's been dreaming about.

New options on the horizon

Research evidence supports the use of some antiepileptic drugs for certain types of neuropathic pain such as painful diabetic neuropathy. However, lacosamide, an antiepileptic drug, was trialed for managing neuropathic pain and fibromyalgia but failed to show significant benefit. The FDA has declined to approve its use for neuropathic pain.10 Another therapy that produced better outcomes is topical application of high-dose capsaicin, 8% patch, which is thought to produce desensitization. It's indicated for a particularly difficult-to-treat neuropathic pain syndrome called postherpetic neuralgia. In six studies involving 2,073 patients, a small number of participants with postherpetic neuralgia and HIV neuropathy with high pain levels benefited.11 Pain relief lasted for up to 12 weeks. In studies, 11 or 12 patients had to be treated to get 1 positive outcome of reduced pain (this is known as numbers needed to treat and is considered high).11 However, some patients did benefit, and their pain was significantly reduced.

Although single medications used alone can positively affect neuropathic pain, combination therapy demonstrates superior pain relief. Some agents caused problematic sedation.12 Unfortunately, there weren't enough comparative or replication studies to identify particular combinations of drugs that had improved pain relief. In a meta-analysis with 386 patients, gabapentin plus an opioid was superior to gabapentin alone, according to a modest but clinically significant finding.12

One of the most exciting ideas for managing neuropathic pain is attempting to use molecular approaches. Chromaffin cells release a combination of pain-reducing neuroactive compounds, including catecholamines and opioid peptides.13 Encapsulating the cells and implanting them in the subarachnoid space has relieved pain in both animal and human studies.13

In these cell transplantation studies, encapsulated cells with permeable membranes turn into cellular pumps that create and dispense analgesic compounds.13 Future research targets include astrocyte cells that are genetically modified to secrete enkephalin and genetically engineered cells designed to secrete gamma-aminobutyric acid, a pain inhibitory substance.13 Patients thought to be good candidates for study include those with low back pain and knee pain; these can have neuropathic elements. Understanding the pathways and physiology of neuropathic pain transmission can help researchers look for ways to use these specialized cells to reduce pain right at the source of pain generation.

Other options for managing neuropathic pain include using autologous bone marrow-derived progenitor cells to repair damaged neurons in patients with diabetic peripheral neuropathy and gene transplants applied to peripheral nerves, injected into dorsal root ganglia, or introduced into the intrathecal space of the spine via lumbar puncture or injected directly into the brain.13 Gene transplants have been tested only in animals using the herpes simplex virus.13

Stem cell transplantation also provides promise for pain research. Mesenchymal stem cells can be harvested from bone marrow, are fairly stable, and can, once transplanted, migrate to injured tissue and have immunosuppressive characteristics.14 They can also differentiate into astrocytes and neurons and migrate to injured neuronal areas to mediate functional recovery.14 Although many of the finer points of the process are yet to be discovered, studies of mice have shown that the transplanted stem cells relocated themselves into key areas for neuropathic pain generation in the brain.14

Although many new management options are still being studied in animals, they hold promise for human use in the future. Researchers are attacking the pain process from many different directions and using the known pain pathophysiology to direct the therapy to targets that may yield good results.

In the foreseeable future, patients like Mrs. S won't be limited to medications or interventions for intractable pain syndromes such as spinal cord stimulators. Instead, they'll have options that include stem cell transplants for nerve repair or genetically engineered cells that will enhance the production of pain-reducing substances. Using these new techniques will help many patients leave the nightmare of neuropathic pain behind and fulfill their dreams.

Focusing on CRPS

CRPS, or complex regional pain syndrome, was formerly called causalgia or reflex sympathetic dystrophy.3 It's usually the result of a crush injury or repeated tissue trauma. Continuing pain or abnormal sensation is out of proportion to the event that initiated it. At some time, the patient experiences edema, skin blood flow changes, or abnormal sudomotor activity in the region of pain. No other condition is identified that could explain the pain or dysfunction.15

The International Association for the Study of Pain defines two types of CRPS:

CRPS I, which doesn't require the presence of a nerve lesion.
CRPS II, which includes the presence of a nerve lesion.
Although the true cause of CRPS hasn't been determined, the most accepted rationales include the following:
enhanced peripheral neurogenic inflammation
sympathetic nervous system dysfunction
structural reorganization in the central nervous system.

Source: Fechir M, Geber C, Birklein F. Evolving understandings about complex regional pain syndrome and its treatment. Curr Pain Headache Rep. 2008;12(3):186–191.


The language of pain

Allodynia: painful response to a stimulus that isn't normally painful, such as touch from clothes or bed sheets.
Crosstalk: new communication, or neural sprouts, between nerves that don't normally synapse with one another.
Dysesthesia: an unpleasant sensation, such as painful pruritus or feeling as though bugs are crawling under the skin.
Hyperalgesia: increased pain from a stimulus that's normally painful.
Neural plasticity: continued noxious stimuli and inflammation causing an elevation of nociceptive input from the periphery to the central nervous system, which then creates an increased response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.
Neuropathic pain: chronic pain caused by damage in the peripheral or central nervous system that's the direct consequence of a lesion or disease affecting the somatosensory system.
Nociceptive pain: pain that results from nonneural damage to tissue.
Paresthesia: an abnormal sensation that isn't unpleasant, such as numbness or tingling.
Wind-up: an increased response to painful stimuli. Add, on a new line as source format:

Source: Chou R, Fanciullo GJ, Fine PG, et al. Clinical guidelines for the use of chronic opioid therapy in chronic noncancer pain. J Pain. 2009;10(2):113–130.

Sorting out common neuropathic pain conditions

Peripheral syndromes and U.S. patients affected

Painful diabetic neuropathy; 600,000
Postherpetic neuralgia; 500,000
Cancer associated; 200,000
HIV associated; 100,000
Phantom limb pain; 50,000

Central syndromes and U.S. patients affected
 
Spinal cord injury; 120,000
CRPS I and II; 100,000
Poststroke; 30,000

Source: Irving GA. Contemporary assessment and management of neuropathic pain. Neurology. 2005;64(12 suppl 3):S21-S27.

http://journals.lww.com/nursing/Fulltext/2014/06000/Living_with_the_nightmare_of_neuropathic_pain.12.aspx

A Great Letter About Chronic Pain

This post comes from a FaceBook site (see link below) and is unapologetically, a repeat of an earlier post on this blog. It's a letter that is obviously still doing the rounds on the internet but it is so well-written, also for people with severe neuropathy, that it has to be worth repeating once more. It is self explanatory but may just be worth printing out for friends and family if you suffer from neuropathic pain. The author is anonymous but he or she has my thanks.

Letter to People without Chronic Pain

 Posted by guest on May 22, 2006

Having chronic pain means many things change, and a lot of them are invisible. Unlike having cancer or being hurt in an accident, most people do not understand even a little about chronic pain and its effects, and of those that think they know, many are actually misinformed.

In the spirit of informing those who wish to understand …… These are the things that I would like you to understand about me before you judge me…

Please understand that being sick doesn’t mean I’m not still a human being. I have to spend most of my day in considerable pain and exhaustion, and if you visit, sometimes I probably don’t seem like much fun to be with, but I’m still me– stuck inside this body. I still worry about school, my family, my friends, and most of the time – I’d still like to hear you talk about yours, too.

Please understand the difference between “happy” and “healthy”. When you’ve got the flu, you probably feel miserable with it, but I’ve been sick for years. I can’t be miserable all the time. In fact, I work hard at not being miserable. So, if you’re talking to me and I sound happy, it means I’m happy. That’s all. It doesn’t mean that I’m not in a lot of pain, or extremely tired, or that I’m getting better, or any of those things. Please don’t say, “Oh, you’re sounding better!” or “But you look so healthy!¨ I am merely coping. I am sounding happy and trying to look normal. If you want to comment on that, you’re welcome.

Please understand that being able to stand up for ten minutes doesn’t necessarily mean that I can stand up for twenty minutes, or an hour. Just because I managed to stand up for thirty minutes yesterday doesn’t mean that I can do the same today. With a lot of diseases you’re either paralyzed, or you can move. With this one, it gets more confusing everyday. It can be like a yo-yo. I never know from day to day, how I am going to feel when I wake up. In most cases, I never know from minute to minute. That is one of the hardest and most frustrating components of chronic pain.

Please repeat the above paragraph substituting, “sitting”, “walking”, “thinking”, “concentrating”, “being sociable” and so on … it applies to everything. That’s what chronic pain does to you.

Please understand that chronic pain is variable. It’s quite possible (for many, it’s common) that one day I am able to walk to the park and back, while the next day I’ll have trouble getting to the next room. Please don’t attack me when I’m ill by saying, “But you did it before!” or Oh, come on, I know you can do this!” If you want me to do something, then ask if I can. In a similar vein, I may need to cancel a previous commitment at the last minute. If this happens, please do not take it personally. If you are able, please try to always remember how very lucky you are–to be physically able to do all of the things that you can do.

Please understand that “getting out and doing things” does not make me feel better, and can often make me seriously worse. You don’t know what I go through or how I suffer in my own private time. Telling me that I need to exercise, or do some things to get my mind off of it¨ may frustrate me to tears, and is not correct if I was capable of doing some things any or all of the time, don’t you know that I would? I am working with my doctor and I am doing what I am supposed to do. Another statement that hurts is, “You just need to push yourself more, try harder…” Obviously, chronic pain can deal with the whole body, or be localized to specific areas. Sometimes participating in a single activity for a short or a long period of time can cause more damage and physical pain than you could ever imagine. Not to mention the recovery time, which can be intense. You can’t always read it on my face or in my body language. Also, chronic pain may cause secondary depression (wouldn’t you get depressed and down if you were hurting constantly for months or years?), but it is not created by depression.

Please understand that if I say I have to sit down/lie down/stay in bed/or take these pills now, that probably means that I do have to do it right now – it can’t be put off or forgotten just because I’m somewhere, or am right in the middle of doing something. Chronic pain does not forgive, nor does it wait for anyone.

If you want to suggest a cure to me, please don’t. It’s not because I don’t appreciate the thought, and it’s not because I don’t want to get well. Lord knows that isn’t true. In all likelihood, if you’ve heard of it or tried it, so have I. In some cases, I have been made sicker, not better. This can involve side effects or allergic reactions. It also includes failure, which in and of itself can make me feel even lower. If there were something that cured, or even helped people with my form of chronic pain, then we’d know about it. There is worldwide networking (both on and off the Internet) between people with chronic pain. If something worked, we would KNOW. It’s definitely not for lack of trying. If, after reading this, you still feel the need to suggest a cure, then so be it. I may take what you said and discuss it with my doctor.
If I seem touchy, it’s probably because I am. It’s not how I try to be. As a matter of fact, I try very hard to be normal. I hope you will try to understand. I have been, and am still, going through a lot. Chronic pain is hard for you to understand unless you have had it. It wreaks havoc on the body and the mind. It is exhausting and exasperating. Almost all the time, I know that I am doing my best to cope with this, and live my life to the best of my ability. I ask you to bear with me, and accept me as I am. I know that you cannot literally understand my situation unless you have been in my shoes, but as much as is possible, I am asking you to try to be understanding in general.

In many ways I depend on you – people who are not sick. I need you to visit me when I am too sick to go out… Sometimes I need you help me with the shopping, cooking or cleaning. I may need you to take me to the doctor, or to the store. You are my link to the normalcy of life. You can help me to keep in touch with the parts of life that I miss and fully intend to undertake again, just as soon as I am able.
I know that I have asked a lot from you, and I do thank you for listening. It really does mean a lot.

AUTHOR UNKNOWN**********************************

TIPS FOR DEALING WITH PEOPLE IN PAIN

1. People with chronic pain seem unreliable (we can’t count on ourselves). When feeling better we promise things (and mean it); when in serious pain, we may not even show up.

2. An action or situation may result in pain several hours later, or even the next day. Delayed pain is confusing to people who have never experienced it.

3. Pain can inhibit listening and other communication skills. It’s like having someone shouting at you, or trying to talk with a fire alarm going off in the room. The effect of pain on the mind can seem like attention deficit disorder. So you may have to repeat a request, or write things down for a person with chronic pain. Don’t take it personally, or think that they are stupid.

4. The senses can overload while in pain. For example, noises that wouldn’t normally bother you, seem too much.
5. Patience may seem short. We can’t wait in a long line; can’t wait for a long drawn out conversation.

6. Don’t always ask “how are you” unless you are genuinely prepared to listen it just points attention inward.

7. Pain can sometimes trigger psychological disabilities (usually very temporary). When in pain, a small task, like hanging out the laundry, can seem like a huge wall, too high to climb over. An hour later the same job may be quite OK. It is sane to be depressed occasionally when you hurt.

8. Pain can come on fairly quickly and unexpectedly. Pain sometimes abates after a short rest. Chronic pain people appear to arrive and fade unpredictably to others.

9. Knowing where a refuge is, such as a couch, a bed, or comfortable chair, is as important as knowing where a bathroom is. A visit is much more enjoyable if the chronic pain person knows there is a refuge if needed. A person with chronic pain may not want to go anywhere that has no refuge (e.g.no place to sit or lie down).

10. Small acts of kindness can seem like huge acts of mercy to a person in pain. Your offer of a pillow or a cup of tea can be a really big thing to a person who is feeling temporarily helpless in the face of encroaching pain.

11. Not all pain is easy to locate or describe. Sometimes there is a body-wide feeling of discomfort, with hard to describe pains in the entire back, or in both legs, but not in one particular spot you can point to. Our vocabulary for pain is very limited, compared to the body’s ability to feel varieties of discomfort.

12. We may not have a good “reason” for the pain. Medical science is still limited in its understanding of pain. Many people have pain that is not yet classified by doctors as an officially recognized “disease”. That does not reduce the pain, – it only reduces our ability to give it a label, and to have you believe us.

AUTHOR UNKNOWN

http://www.facebook.com/notes/neuropathy-talk-on-line/a-letter-to-people-without-chronic-pain/10150525210097821

How Spinal Cord Neurons Control Pain

Today's post from sciencedaily.com (see link below) is a very interesting look at a study which has identified nerve cells in the spine that regulate pain signals and determine whether they should be forwarded to the brain - like a sort of central sorting office for mail. It's called a 'gate control theory'. It's a fascinating read but it will take some considerable time before scientists will be able to manipulate these neurons by use of specifically delivered viruses and actively control pain in humans. Even itching may be able to be controlled by manipulating these nerve cells in the spine. Fascinating read.
 

Spinal cord neurons that control pain and itch
Date: March 19, 2015 Source:University of Zurich
 
Summary:

The spinal cord transmits pain signals to the brain, where they are consciously perceived. But not all the impulses arrive at their destination: Certain neurons act as checkpoints and determine whether a pain signal is relayed or not. Researchers from UZH identified these neurons and their connections. Moreover, they developed means to specifically activate these neurons, which reduces not only pain -- but astonishingly also alleviates itch.

Sensing pain is extremely unpleasant and sometimes hard to bear -- and pain can even become chronic. The perception of pain varies a lot depending on the context in which it is experienced. 50 years ago, neurobiologist Patrick Wall and psychologist Ronald Melzack formulated the so-called "Gate Control Theory" of pain. The two researchers proposed that inhibitory nerve cells in the spinal cord determine whether a pain impulse coming from the periphery, such as the foot, is relayed to the brain or not. A team headed by Hanns Ulrich Zeilhofer from the Institute of Pharmacology and Toxicology at the University of Zurich did now reveal which inhibitory neurons in the spinal cord are responsible for this control function: As the study published in the science journal Neuron shows, the control cells are located in the spinal dorsal horn and use the amino acid glycine as an inhibitory messenger.

The pain gate can be manipulated with viruses

With the aid of genetically modified viruses, the research group from UZH managed to specifically interfere with the function of these neurons in mice. They discovered that disabling the glycine-releasing neurons leads to an increased sensitivity to pain and signs of spontaneous pain. Moreover, Zeilhofer's team developed viruses that enable these specific pain-control cells to be activated pharmacologically. Mice treated with these viruses were less sensitive to painful stimuli than their untreated counterparts. Activating these nerve cells also alleviated chronic pain. And the surprising additional result: "Evidently, the neurons don't just control pain, but also various forms of itch," explains Zeilhofer.

How light touch controls pain

One key aspect of the Gate Control Theory is that various influences can modulate the pain-controlling neurons' activity. Based on our experience from everyday life, for instance, we know that gently rubbing or holding an injured extremity can alleviate pain in this area. According to the theory, non-painful contact with the skin is supposed to activate the inhibitory cells. Sure enough, the UZH researchers were able to verify this hypothesis and confirm that the inhibitory, glycine-releasing neurons are innervated by such touch-sensitive skin nerves.

Moreover, the pharmacologists were able to demonstrate that neurons on the superficial layers of the spinal cord, where the relay of the pain signals takes place, are primarily inhibited by glycine signals. "These three findings identify for the first the neurons and connections that underlie the Gate Control Theory of pain," sums up Zeilhofer.

Targeted therapy in humans not yet possible

Can these findings be used to treat pain? "The targeted stimulation or inhibition of particular types of neurons in humans is still a long way off and might only be possible in a few decades' time," says Zeilhofer. Another way may well reach the target sooner -- namely via the receptors that are activated by the inhibitory neurons: "As these receptors are located on the neurons that relay pain signals to the brain, their specific pharmacological activation should also block pain," says Hanns Ulrich Zeilhofer. His group has already achieved promising initial results in this field, too.

Story Source:

The above story is based on materials provided by University of Zurich. Note: Materials may be edited for content and length.

Journal Reference:
Edmund Foster, Hendrik Wildner, Laetitia Tudeau, Sabine Haueter, William T. Ralvenius, Monika Jegen, Helge Johannssen, Ladina Hösli, Karen Haenraets, Alexander Ghanem, Karl-Klaus Conzelmann, Michael Bösl, Hanns Ulrich Zeilhofer. Targeted Ablation, Silencing, and Activation Establish Glycinergic Dorsal Horn Neurons as Key Components of a Spinal Gate for Pain and Itch. Neuron, 2015; 85 (6): 1289 DOI: 10.1016/j.neuron.2015.02.028

http://www.sciencedaily.com/releases/2015/03/150319075826.htm 

Antibodies For Neuropathic Pain

Today's post comes from painresearchfoorum.org (see link below) and discusses in some detail, one of the stories currently appearing across the 'neuropathy net' and that is the use of intravenous immunoglobulin and other antibodies to control neurological pain. The article is both long and scientific in nature and may make tricky reading but we need to know about any new developments in the search for an effective neuropathy treatment for all and is thus worth a read (or at least a 'skim')

An Autoimmune Basis for Chronic Pain?
Antibodies to potassium channel complex implicated in pain
by Megan Talkington on 4 Sep 2012

In people, autoantibodies to neuronal voltage-gated potassium channel (VGKC) complexes are associated with diverse neurologic disturbances, including seizures, encephalitis, and muscle cramps and twitching. The symptoms, many of which are attributed to antibody-induced neuronal hyperexcitability, often respond to immunotherapy. Now, researchers led by Christopher Klein at the Mayo Clinic, Rochester, Minnesota, US, have shown that the autoantibodies frequently associate with another condition: pain. In a paper published August 15 in Neurology, Klein and colleagues report pain, often chronic, in half of a group of 316 patients with VGKC-complex autoreactive antibodies. Patients with pain showed signs of hyperexcitability in sensory pathways, and, among the few who received immunotherapy, pain improved for most.

The results bolster the emerging concept that autoimmune reactions can contribute to some forms of chronic pain. In an accompanying editorial, David Bennett of King’s College London, UK, and Angela Vincent of John Radcliffe Hospital, Oxford, UK, write, “We may … be entering an exciting phase in which autoantibodies to neural antigens are recognized as having a role in the etiology of a number of hitherto poorly understood chronic pain states, opening new avenues for treatment.”

An unusual case

Klein, a neurologist, said the investigation started with one patient, a healthy 80-year-old professor who suddenly developed disabling pain in his hands and lower legs that kept him out of the classroom and home in bed. The doctors suspected neuropathy, but nerve conduction studies, and even nerve biopsy, showed no signs of damage. The physicians considered a diagnosis of psychogenic pain. But tests revealed VGKC-complex antibodies, so Klein initiated immunotherapy with an intravenous steroid. The treatment rapidly relieved the man’s pain, and the patient eventually discontinued narcotic pain relievers and returned to his normal activities.

The finding of pain with no apparent cause, coupled with the presence of VGKC antibodies and the success of immunotherapy, was unexpected, Klein said, and intriguing. VGKC autoantibodies had been linked to pain previously, but there was little information about the scope of pain symptoms in seropositive patients. To fill the gap, Klein and his colleagues embarked on a systematic review of pain symptoms in the records of 316 seropositive patients who had undergone neurologic evaluation at the Mayo Clinic. The results were surprising: 159 (50 percent) of the patients studied had pain that was not explained by other causes. In contrast, among 167 patients with one of several other neural autoantibodies, only 9 percent reported pain.

Remarkably, 45 of the patients with VGKC-complex immunoglobulin (IgG) reported pain as their only symptom. Many, like Klein’s patient, were evaluated for neuropathy or CNS disease, but no abnormalities turned up. The discovery of isolated, unexplained pain in so many “was kind of a shock to us,” Klein said.

Examination of patient records revealed that, in most cases, pain reached maximal severity within two weeks of onset, and often became chronic. The pain took a variety of forms: In half of patients, pain was isolated to extremities, while others reported total body pain, head or face pain, abdominal visceral pain, or pain in multiple locations. Patients’ descriptions suggested the pain was either neuropathic or nociceptive.

In support of an autoimmune source of pain, Klein and colleagues found that, of 16 patients in the pain group who had been treated with immunotherapy (usually for other neurologic issues), 14 showed reduced or eliminated pain symptoms. “Many of these patients were on multiple [pain] medications including narcotics, and were able to come off of them with immunotherapy,” Klein said.

Laying the blame

Were the VGKC antibodies the cause of pain? On average, titers of VGKC-complex IgG were no different in the pain group and the patients without pain. However, VGKC-complex IgG is heterogeneous: Antibodies that react with different proteins in the channel complex are thought to be associated with different clinical symptoms (Irani et al., 2010). When the Mayo group checked for antigen specificity, they detected reactivity to one accessory protein, contactin-associated protein-2 (CASPR2), more frequently in the pain group than the non-pain patients. That finding agreed with previous work by Vincent (coauthor of the accompanying editorial), who found a high incidence of pain in VGKC-complex IgG-positive patients with CASPR2 autoimmunity (Irani et al., 2010; Irani et al., 2012).

CASPR2 antibodies are not the whole answer, though. Overall, CASPR2-specific antibodies were found in just 16 percent of the seropositive patients with pain. That means that for most patients, “we still don’t know what the primary antigen is,” said Klein.

In light of the new findings, Bennett and Vincent ask in their editorial, “Should we be testing patients with chronic pain for VGKC-complex antibodies, and if so, which patients?” For patients with other telltale signs of VGKC autoimmunity, they say, the answer is yes. “The more problematic issue is those patients whose sole complaint is pain.... Larger focused studies and more detailed pain phenotyping will be required to determine the true prevalence of VGKC-complex antibodies in chronic pain cohorts.”

Klein, too, wants to know how often, and in which patients, VGKC autoantibodies might explain chronic pain. To address that question, he and his colleagues are investigating the frequency of neural autoimmunity in patients being treated at a chronic pain center.

Meanwhile, the mechanism by which the autoantibodies could cause pain remains unclear. VGKCs, also known as Kv channels, cooperate with other neuronal channels to set resting membrane potentials and regulate neuronal excitability, and some family members have already been linked to nociceptor excitability and pain (for a review, see Takeda et al., 2011). Antibodies that block VGKC function could render sensory neurons hyperexcitable, as previously seen for motor neurons. Indeed, Klein and colleagues did see evidence of abnormal sensory excitability: Excessive sweating and quantitative heat-pain hyperalgesia (C fiber allodynia) were reported only in the pain group, supporting the idea that hyperexcitability of nociceptive pathways leads to pain in patients with VGKC antibodies.

Also in support of that idea, the Mayo team recently implicated VGKC-complex autoimmunity in an unusual instance of job-related pain. They found the autoantibodies in workers at two slaughterhouses; the workers developed painful neuropathy after exposure to aerosolized brain tissue from pigs (Lachance et al., 2010; Meeusen et al., 2012). In those cases, the workers showed signs of neuronal hyperexcitability.

But Klein is cautious. “It’s an attractive theory” that the antibodies alter neuronal VGKC-complex function, “but maybe it’s more complicated than that.” In fact, the current finding “simply helps us to tell if there’s an autoimmune component,” he said. He noted that VGKCs are located on immune cells as well as neurons, so that VGKC-specific antibodies might affect neuronal excitability indirectly via cytokines, rather than targeting neurons directly. Moreover, it is possible that the VGKC-complex IgG is what Klein calls a “sentinel finding,” meaning that other—as-yet undetected—antibodies may be the real culprits.

Other labs are also providing evidence that autoantibodies play a role in pain. Recent clues point to an autoimmune basis for chronic regional pain syndrome (CRPS), where researchers have reported autoantibodies against autonomic neuron proteins in patients, including the β2 adrenergic receptor and M2 muscarinic acetylcholine receptor (Kohr et al., 2011). And, in an encouraging preliminary study, a small, randomized, placebo-controlled trial of immunotherapy with intravenous immunoglobulin reduced pain in patients with refractory CRPS (Goebel et al., 2010).

References:
Editors' Pick
Autoimmune pain: An emerging concept.
Bennett DLH, Vincent A
Neurology. 2012 Aug 15.
PMID: 22895596.
See related: An Autoimmune Basis for Chronic Pain?
Editors' Pick
Chronic pain as a manifestation of potassium channel-complex autoimmunity.
Klein CJ, Lennon VA, Aston PA, McKeon A, Pittock SJ
Neurology. 2012 Aug 15.

http://www.painresearchforum.org/news/19697-autoimmune-basis-chronic-pain

Writing A Free Distraction From Chronic Pain

Today's post from paincommunity.org (see link below) talks about a form of therapy that won't reduce the painful symptoms of neuropathy but may serve as a distraction and therefore lessen its impact. Not only that but it may help you put into writing (and therefore words) how long-term neuropathy affects your personality and quality of life. The article urges you to start writing! I don't need to say any more than that but if you do start writing and are looking for an outlet, or an audience, this blog will be happy to publish your work. Let me know that you're intending to write something and I'll provide an email address to which you can send your word file, or whatever. Fiction or non-fiction - it's all good and you may be surprised how much positive energy the simple act of writing can give. If while you're doing it, you don't notice your discomfort as much, then it's a win-win situation.

Writing as a Form of Therapy
by The Pain Community | Apr 21, 2017 | Daily Living
by Guest Blogger – Maria Miguel

All of us encounter stressful and traumatic experiences in our lives. We could be fighting everyday battles of anxiety, depression and other mental health disorders. For me, I find a special comfort in the written word. I can read countless novels and teleport myself into the writer’s worlds. The characters come alive on the pages, and I can visit faraway places conjured up in the minds of the author.

As a writer, I use words to relay emotions and thoughts I can’t exactly form orally. Over the years, writing has been the consistent and most therapeutic method to ease my stress. As someone with obsessive compulsive personality disorder, this is sometimes a challenging task. When I am writing, either about my life or creating my own characters and stories, I am able to work through the best — and worst — times in my life. Through this introspection, I find some of my greatest strength. For me, it’s easier to write about how I am feeling versus talking about every single rumination. Writing allows me to collect my thoughts.

Even if you aren’t a seasoned writer, give it a shot. After all, you don’t have to share your musings with anyone but yourself. Writing can help you assess patterns in your behaviors, increase your sense of self-identity and determine goals and objectives. For example, if you have been struggling with depression, writing about your feelings could help you determine that you are depressed because you are in a failing relationship, don’t enjoy your current job or feel overwhelmingly hopeless because you see the world through a loved one’s sickness.

Here are some tips to use writing as a form of therapy in your own life:

Keep a journal.

Write in this journal as often as needed. I recommend writing every day. It’s OK if your journal writing isn’t structured and is more stream of consciousness. Make your journal an extension of your personality. I write all of my dates in French and tend to purchase journals that are vintage, Parisian or “Wizard of Oz” themed.

Write a letter to yourself or someone else.

If you’re in the midst of letting go of something or someone, writing a “goodbye” letter could work for you. If you weren’t able to say what you wanted to say, then this could be a way to get your feelings out in the open without ever sending the letter or email. You will tell your truths in your internal narrator’s voice, which can be extremely therapeutic. You won’t be bottling up your emotions.

Detail your emotions in poetry.

We all probably had to read and write poetry in high school. For some of us, we didn’t understand the stanzas in front of us; however, poets draw from their own experiences and emotions to pen their poetry. If you feel overwhelmed and don’t know where to start, make a list of images, such as in your bedroom, from your childhood days, from a stressful situation, etc. Then, write a list of senses you experienced associated with these images. Write down your emotions related to the images and senses. After this process, write a poem containing these words and images. You will be able to show yourself — and potential readers — how you are feeling without having to put blatant labels on your emotions.

Be prepared to uncover good and bad memories.

During the writing process, your mind could rediscover thoughts and emotions associated with something bad that happened in your life. For example, if you are writing about lost loves, you may think of a former significant other who wasn’t faithful. You may feel helpless as you write about your parents’ divorce. However, you could also relive the best parts of your life, such as the birth of your child, achieving a goal, traveling to your favorite location and more. Using writing as therapy can help you forgive yourself and others. You can reflect on situations and improve into your best self because you have learned from your successes and mistakes.

Write fiction based on your nonfiction experiences.

Often, when we use writing as therapy, we talk about our personal journeys. Use your own story and craft your own characters. If you are uncomfortable writing about a traumatic experience of your own, have your character experience the event. Writing about specific emotions can help you in the healing process. If you decide to share your writings with someone else — or even a mass audience — the works centered on your experiences and emotions could help others going through the same type of situation. This gives you a new role and gives your writings even more meaning that is greater than you.

To figure out if writing could be therapeutic for you and to find more therapy options, seek out a licensed professional to talk with you about your mental health disorder and its effects and solutions.

Marie Miguel is an avid internet researcher. She is fueled by her determination to answer the many questions she hasn’t been able to find the answer to anywhere else. When she finds these answers she likes to spread the knowledge to others seeking help. She is always looking for outlets to share her information, therefore she occasionally has her content published on different websites and blogs. Even though she doesn’t run one for herself she loves contributing to others.

http://paincommunity.org/writing-form-therapy/

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All You Need To Know About HIV And Pain

Well not quite all and despite this being an earlier article, updated in June 2012,  they still don't issue any information about the fact that Lyrica (Pregabalin) has been withdrawn for HIV-related pain by the company that makes it. However, for the rest, this comprehensive article from aidsetc.org (see link below) is about as good an overview as you can find. As they say, 30% to 60% of HIV patients experience some degree of pain related to their condition, so well-explained articles like this are essential for people trying to put two and two together and not come up with five. If, for instance, you've just realised that your neuropathic symptoms are not just a temporary irritation, you may be looking for information that gives a solid framework to what you're feeling - this article will help you make sense of what's happening.

Pain Syndrome and Peripheral Neuropathy

Guide for HIV/AIDS Clinical Care, HRSA HIV/AIDS Bureau

June 2012

Background

The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage." Pain is subjective, it is whatever the patient says it is, and it exists whenever the patient says it does. Pain is a common symptom in people with HIV infection, especially those with advanced disease. It occurs in 30-60% of HIV/AIDS patients and can diminish their quality of life significantly. Like cancer patients, HIV patients experience an average of 2.5 to 3 types of pain at once. Pain in HIV-infected patients may have many causes (as discussed below).

Peripheral Neuropathy

Pain from HIV-associated peripheral neuropathy is particularly common, and may be debilitating. Peripheral neuropathy is clinically present in approximately 30% of HIV-infected individuals and typically presents as distal sensory polyneuropathy (DSP). It may be related to HIV itself (especially at CD4 counts of <200 cells/µL), to medication toxicity (e.g., from certain nucleoside analogues such as stavudine or didanosine), or to the effects of chronic illnesses (e.g., diabetes mellitus). Patients with peripheral neuropathy may complain of numbness or burning, a pins-and-needles sensation, shooting or lancinating pain, and a sensation that their shoes are too tight or their feet are swollen. These symptoms typically begin in the feet and progress upward; the hands may be affected. Patients may develop difficulty walking because of discomfort, or because they have difficulty feeling their feet on the ground. Factors associated with increased risk of peripheral neuropathy include the following:

• Previous peripheral neuropathy
• Low CD4 count (<200 cells/µL)
• Previous AIDS-defining opportunistic infection or neoplasm
• Vitamin B12 deficiency
• Exposure to stavudine or didanosine
• Use of other drugs associated with peripheral neuropathy (e.g., isoniazid, dapsone, metronidazole, hydroxyurea, thalidomide, linezolid, ribavirin, vincristine)
• Use of other neurotoxic agents (e.g., alcohol)
• Diabetes mellitus

Patients should be assessed carefully before the introduction of a potentially neurotoxic medication (including stavudine or didanosine), and the use of these medications for patients at high risk of developing peripheral neuropathy should be avoided.

Pain is significantly undertreated, especially among HIV-infected women, because of factors ranging from providers' lack of knowledge about the diagnosis and treatment of pain to patients' fear of addiction to analgesic medications. Pain, as the so-called fifth vital sign, should be assessed at every patient visit.

S: Subjective

Self-report is the most reliable method to assess pain.

The patient complains of pain. The site and character of the pain will vary with the underlying cause. Ascertain the following from the patient:

• Duration, onset, progression
• Distribution, symmetry
• Character or quality (e.g., burning, sharp, dull)
• Intensity
• Severity (using the 0-10 scale; see Figure 1)
• Neurologic symptoms (e.g., weakness, cranial nerve abnormalities, bowel or bladder abnormalities)
• Exacerbating or relieving factors
• Response to current or past pain management strategies
• Past medical history (e.g., AIDS, diabetes mellitus)
• Psychosocial history
• Substance abuse and alcohol use history (amount, duration)
• Medications, current and recent (particularly zalcitabine, didanosine, stavudine, and isoniazid)
• Nutrition (vitamin deficiencies)
• Meaning of the pain to the patient

Measuring the severity of the pain: Have the patient rate the pain severity on a numeric scale of 0-10 (0 = no pain; 10 = worst imaginable pain), a verbal scale (none, small, mild, moderate, or severe), or a pediatric faces pain scale (when verbal or language abilities are absent). Note that pain ratings >3 usually indicate pain that interferes with daily activities. Use the same scale for evaluation of treatment response.

Figure 1. Faces Pain Rating Scale (0-10)

Quick screen for peripheral neuropathy: Ask about distal numbness and check Achilles tendon reflexes. Screening for numbness and delayed or absent ankle reflexes has the highest sensitivity and specificity among the clinical evaluation tools for primary care providers. For a validated screening tool, use the ACTG Brief Peripheral Neuropathy Scale (BPNS) to scale and track the degree of peripheral neuropathy.

O: Objective

Measure vital signs (increases in blood pressure, respiratory rate, and heart rate can correlate with pain). Perform a symptom-directed physical examination, including a thorough neurologic and musculoskeletal examination. Look for masses, lesions, and localizing signs. Pay special attention to sensory deficits (check for focality, symmetry, and distribution [such as "stocking-glove"]), muscular weakness, reflexes, and gait. Patients with significant motor weakness or paralysis, especially if progressive over days to weeks, should be evaluated emergently.

To evaluate peripheral neuropathy: Check ankle Achilles tendon reflexes and look for delayed or absent reflexes as signs of peripheral neuropathy. Distal sensory loss often starts with loss of vibratory sensation, followed by loss of temperature sensation, followed by onset of pain. Findings are usually bilateral and symmetric.

A: Assessment

Pain assessment includes determining the type of pain, for example, nociceptive, neuropathic, or muscle spasm pain.

Nociceptive pain occurs as a result of tissue injury (somatic) or activation of nociceptors resulting from stretching, distention, or inflammation of the internal organs of the body. It usually is well localized; may be described as sharp, dull, aching, throbbing, or gnawing in nature; and typically involves bones, joints, and soft tissue.

Neuropathic pain occurs from injury to peripheral nerves or central nervous system structures. Neuropathic pain may be described as burning, shooting, tingling, stabbing, or like a vise or electric shock; it involves the brain, central nervous system, nerve plexuses, nerve roots, or peripheral nerves. It is associated with decreased sensation and hypersensitivity.

Muscle spasm pain can accompany spinal or joint injuries, surgeries, and bedbound patients. It is described as tight, cramping, pulling, and squeezing sensations.

Although pain in HIV-infected patients often results from opportunistic infections, neoplasms, or medication-related neuropathy, it is important to include non-HIV-related causes of pain in a differential diagnosis. Some of these other causes may be more frequent in HIV-infected individuals. A partial list for the differential diagnosis includes:

• Anorectal carcinoma
• Aphthous ulcers
• Appendicitis
• Arthritis, myalgias
• Candidiasis, oral or esophageal
• Cholecystitis
• Cryptococcal disease
• Cytomegalovirus colitis
• Dental abscesses
• Gastroesophageal reflux disease (GERD)
• Ectopic pregnancy
• Herpes simplex
• Herpes zoster
• Kaposi sarcoma
• Lymphoma
• Medication-induced pain syndromes (e.g., owing to growth hormone, granulocyte colony-stimulating factor)
• Medication-induced peripheral neuropathy (e.g., owing to didanosine, stavudine, isoniazid, vincristine)
• Other causes of peripheral neuropathy: diabetes, hypothyroidism, B12 deficiency, syphilis, cryoglobulinemia (especially in patients with hepatitis C coinfection)
• Mycobacterium avium complex
• Myopathy
• Pancreatitis
• Pelvic inflammatory disease
• Toxoplasmosis

P: Plan

Perform a diagnostic evaluation based on the suspected causes of pain.

Treatment

Treatment should be aimed at eliminating the source of pain, if possible. If symptomatic treatment of pain is needed, begin treatment based on the patient's pain rating scale, using the least invasive route. The goal is to achieve optimal patient comfort and functioning (not necessarily zero pain) with minimal medication adverse effects, negotiated with the patient. Use the three-step pain analgesic ladder originally devised by the World Health Organization (WHO); see Figure 2.

Nonpharmacologic interventions

The following interventions can be used at any step in the treatment plan:

• A therapeutic provider-patient relationship
• Physical therapy
• Exercise
• Relaxation techniques
• Guided imagery
• Massage
• Biofeedback
• Reflexology
• Acupuncture
• Thermal modalities (hot and cold compresses or baths)
• Transcutaneous electrical nerve stimulation (TENS)
• Spiritual exploration
• Prayer
• Deep breathing
• Meditation
• Enhancement of coping skills
• Self-hypnosis
• Humor
• Distraction
• Hobbies

Pharmacologic interventions

Principles of pharmacologic pain treatment

• The dosage of the analgesic is adjusted to give the patient adequate pain control.
• The interval between doses is adjusted so that the pain control is uninterrupted. It can take 4-5 half-lives before the maximum effect of an analgesic is realized.
• Chronic pain is more likely to be controlled when analgesics are dosed on a continuous schedule rather than "as needed." Sustained-release formulations of opioids should be used whenever possible.
• For breakthrough pain, use "as needed" medications in addition to scheduled-dosage analgesics. When using opiates both for scheduled analgesia for breakthrough pain, a good rule of thumb is to use 10% of the total daily dosage of opiates as the "as needed" opiate dose for breakthrough pain.
• Oral administration has an onset of analgesia of about 20-60 minutes, tends to produce more stable blood levels, and is cheaper.
• Beware of the risk of prolonged analgesic half-lives in patients with renal or hepatic dysfunction.
• Caution when using combination analgesics that are coformulated with ingredients such as acetaminophen, aspirin, or ibuprofen. Determine the maximum daily dosage of all agents.

The following three steps are adapted from the WHO analgesic ladder. Agents on higher steps are progressively stronger pain relievers but tend to have more adverse effects.

Figure 2. Pharmacologic Approaches to Pain Management: WHO Three-Step Ladder

Adapted from World Health Organization. Cancer Pain Relief and Palliative Care, Report of a WHO Expert Committee. Geneva: World Health Organization; 1990.

Note: "Adjuvants" refers either to medications that are coadministered to manage an adverse effect of an opioid or to so-called adjuvant analgesics that are added to enhance analgesia.

Step 1: Nonopiates for mild pain (pain scale 1-3)

• The most common agents in this step include acetaminophen (650-1,000 mg PO Q6H as needed) and nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen 600-800 mg PO TID with food, and cyclooxygenase-2 (COX-2) inhibitors such as celecoxib and rofecoxib.
• A proton-pump inhibitor (such as omeprazole) can decrease the risk of gastrointestinal bleeding when using NSAIDs.
• Acetaminophen has no effect on platelets and no antiinflammatory properties; avoid use in patients with hepatic insufficiency, and in general limit to 4 g per day in acute use (or 2 g per day for patients with liver disease). Monitor liver function tests in chronic use.
• NSAIDs and acetaminophen can be used together for synergism.
• Note that COX-2 inhibitors have been associated with an increased risk of cardiovascular events and should be used with caution.

Step 2: Mild opiates with or without nonopiates for moderate pain (pain scale 4-6)

• Most agents used to treat moderate pain are combinations of opioids and Step 1 agents. The most common agents are acetaminophen combined with codeine, oxycodone, or hydrocodone. Codeine can be dosed as codeine sulfate, separately from acetaminophen. Beware of acetaminophen toxicity in these combination drugs.
• Other agents include buprenorphine (partial opiate agonist).
• Tramadol (Ultram) is a centrally acting nonopiate that can be combined with NSAIDs. As with opiates, it is prone to abuse. Tramadol lowers the seizure threshold; avoid use for patients with a seizure history. Avoid coadministration with selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) because of the risk of serotonin syndrome.

Step 3: Opioid agonist drugs for severe pain (pain scale 7-10)

• Morphine is the drug of choice in this step. Start with short-acting morphine and titrate the dosage to adequate pain control, then divide the 24-hour total in half to determine the dosing for the sustained-release morphine, given Q12H. When converting from IV to PO morphine, PO dosage is about two to three times the parenteral dose.
• Other agents used are oxycodone, hydromorphone, fentanyl, levorphanol, methadone, codeine, hydrocodone, oxymorphone, and buprenorphine.
• Avoid meperidine because of the increased risk of delirium and seizures.
• Around-the-clock, sustained-release PO dosing will achieve optimum pain relief.
• Patients unable to take PO therapy may use transdermal fentanyl patches or do rectal administration of sustained-release tablets such as long-acting morphine. Note that the onset of analgesia with fentanyl patches can take more than 12 hours, and the analgesic effect can last more than 18 hours after the patch is removed.
• Anticipate and treat complications and adverse effects of opioid therapy, such as nausea, vomiting, and constipation. Constipation often leads to nausea and can be prevented with prophylactic stool softeners (such as docusate) and stimulant laxatives (such as senna).

Adjunctive treatments

The addition of antidepressant medications can improve pain management, especially for chronic pain syndromes. These agents, and anticonvulsants, usually are used to treat neuropathic pain (discussed in more detail below), but should be considered for treatment of other chronic pain syndromes as well.

Treatment of neuropathic pain

Assess the underlying etiology, as discussed above, and treat the cause as appropriate. Review the patient's medication list for medications that can cause neuropathic pain. Discontinue the offending agents, if possible. For patients on stavudine or didanosine, in particular, switch to another nucleoside analogue if suitable alternatives exist, or at least consider dosage reduction of stavudine to 30 mg BID (consult with an HIV expert). For patients on isoniazid, ensure that they are taking vitamin B6 (pyridoxine) regularly to avoid isoniazid-related neuropathy.

Nonpharmacologic interventions for neuropathic pain

The nonpharmacologic interventions described above can be useful in treating neuropathic pain.

Pharmacologic interventions for neuropathic pain

Follow the WHO ladder of pain management described above. If Step 1 medications are ineffective, consider adding antidepressants, anticonvulsants, or both before moving on to opioid treatments.

Antidepressants

Antidepressant medications often exert analgesic effects at dosages that are lower than those required for antidepressant effects. As with antidepressant effects, optimum analgesic effects may not be achieved until several weeks after starting therapy.

• Tricyclic antidepressants (TCAs): Note that ritonavir and other protease inhibitors may increase the level of TCAs, so start at the lowest dosage and titrate up slowly. Dosages may be titrated upward every 3-5 days, as tolerated. In general, use lower dosages for elderly patients, up to 100 mg QHS.
  • Nortriptyline (Pamelor): Starting dosage is 10-25 mg QHS. Usual maintenance dosage is 20-150 mg QHS.
  • Desipramine (Norpramin): Starting dosage is 25 mg QHS. Usual maintenance dosage is 25-250 mg QHS.
  • Imipramine: Starting dosage is 25 mg QHS. Usual maintenance dosage is 25-300 mg QHS.
  • Amitriptyline (Elavil): Starting dosage is 10-25 mg QHS. Usual maintenance dosage is 25-150 mg QHS. Amitriptyline has the highest rate of adverse effects among the TCAs, so other agents typically are preferred.
  Adverse effects include sedation, anticholinergic effects (e.g., dry mouth, urinary retention), QT prolongation, arrhythmias, and orthostatic hypotension. Monitor TCA levels and EKG at higher dosage levels. There is a risk of overdose if taken in excess.
• SSRIs: See chapter Major Depression and Other Depressive Disorders for dosing, side effects, and drug interactions associated with this class of agents. SSRIs are less effective than TCAs in treating chronic pain.
• Venlafaxine (Effexor): Starting dosage is 37.5 mg daily. Usual maintenance dosage is 75-300 mg daily in divided doses or by extended-release formulation (Effexor XR). Note that there are limited data on using venlafaxine for patients with HIV infection.
• Duloxetine (Cymbalta): Starting dosage is 30-60 mg daily. Dosages of >60 mg per day are rarely more effective for either depression or pain treatment. Note that there are limited data on using duloxetine for patients with HIV infection.

Anticonvulsants

The following agents may be effective for neuropathic pain:

• Gabapentin (Neurontin): Considered first-line for HIV sensory neuropathy for its tolerability. Starting dosage is 100-300 mg QHS; may be increased every 3-5 days to BID or TID to achieve symptom relief. Monitor response and increase the dosage every 1-2 weeks by 300-600 mg/day. Usual maintenance dosage is 1,200-3,600 mg/day in divided doses. Adverse effects include somnolence, dizziness, fatigue, weight gain, and nausea. To discontinue, taper over the course of 7 or more days.
• Pregabalin (Lyrica): Starting dosage is 25-50 mg TID; may be increased by 25-50 mg per dose every 3-5 days as tolerated to achieve symptom relief. Maximum dosage is 200 mg TID. Adverse effects are similar to those of gabapentin. To discontinue, taper over the course of 7 or more days.
• Lamotrigine (Lamictal): Starting dosage is 25 mg QOD; titrate slowly to 200 mg BID over the course of 6-8 weeks to reduce the risk of rash (including Stevens-Johnson syndrome). Adverse effects include sedation,dizziness, ataxia, confusion, nausea, blurred vision, and rash. Note that lopinavir/ritonavir (Kaletra) may decrease lamotrigine levels; higher dosages may be needed. To discontinue, taper over the course of 7 or more days.
• Although phenytoin and carbamazepine have some effectiveness in treating neuropathy, they have significant drug interactions with protease inhibitors and nonnucleoside reverse transcriptase inhibitors, and their use with HIV-infected patients is limited. Topiramate and valproic acid have been used for migraine prophylaxis and anecdotally may be useful for treating peripheral neuropathy, but have not been well-studied in HIV-related neuropathies.

Treatment of Muscle Spasm Pain

Stretching, heat, and massage may help the pain of muscle spasm. This pain also can respond to muscle relaxants such as baclofen, cyclobenzaprine, tizanidine, benzodiazepines, as well as intraspinal infusion of local anesthetics for spinal injuries.

Substance Abuse, HIV, and Pain

Some health care providers hesitate to treat pain in patients with current or past substance abuse because of concern about worsening these patients' dependence on opioids or suspicion that such patients are seeking pain medications for illicit purposes. However, the following points should be considered:

• Many patients with current or past substance abuse do experience pain, and this pain should be evaluated by care providers and treated appropriately.
• Failure to distinguish among addiction, tolerance, and dependence can lead to undertreatment of chronic pain by health care providers.
• Addiction (substance abuse) is a complex behavioral syndrome characterized by compulsive drug use for the secondary gain of euphoria.
• Pharmacologic tolerance refers to the reduction of effectiveness, over time, of a given dosage of medication.
• Physical dependence is the consequence of neurophysiologic changes that take place in the presence of exogenous opioids.
• Aberrant use of pain medications, if it develops, is best managed by an interdisciplinary team of providers from HIV clinical care, psychiatry, psychology, pharmacy, social services, and drug addiction management.
• Drug-drug interactions between certain antiretroviral medications and methadone can decrease methadone serum concentrations (see chapter Drug-Drug Interactions with HIV-Related Medications). If this occurs, methadone dosages may need to be increased to prevent opiate withdrawal.
• As part of chronic pain management in patients with substance abuse, consider establishing a written pain-management contract to be signed by the clinician and the patient. The contract should:
  • Clearly state limits and expectations for both the patient and provider.
  • Identify a single clinician responsible for managing the pain regimen.
  • Tell the patient what to do if the pain regimen is not working.
  • Describe the procedure for providing prescriptions (e.g., one prescription given to the patient, in person, for a limited period of time, such as 1 month).
  • List the rules for dealing with lost medications or prescriptions.

Patient Education

• Pain management is part of HIV treatment, and patients should give feedback to allow the best treatment decisions. If pain persists for more than 24 hours at a level that interferes with daily life, patients should inform their health care provider so that the plan can be changed and additional measures, if needed, can be tried.
• Patients should not expect full pain relief in most cases, but enough relief that they can perform their daily activities.
• "Mild" pain medications (e.g., NSAIDs, aspirin, acetaminophen) usually are continued even after "stronger" medications are started because their mechanism of action is different from that of opiates. This combination of pain medication has additive effects, so that pain may be controllable with a lower narcotic dosage.
• Patients taking "around-the-clock" medications, should take them on schedule. Those taking "as needed" medications should take them between doses only if they have breakthrough pain.
• Opiates may cause severe constipation. Patients must remain hydrated and will likely need stool softeners, laxatives, or other measures. They should contact their health care provider promptly if constipation occurs.
• Patients should avoid use of recreational drugs and alcohol when taking opiates because opiates can interact with them or cause additive adverse effects, possibly resulting in central nervous system depression, coma, or death.
• Patients taking opiates should avoid driving and operating machinery.

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