Thursday, 19 October 2017

The Real Worth Of Acupuncture For Pain

Today's post from (see link below) looks at new research on acupuncture as an alternative, or extra treatment for pain conditions such as neuropathy. Acupuncture treatment is thousands of years old, yet somehow it's built up a reputation as being a somewhat vague, hippy-like alternative therapy, with less value than chemical medications that we're all used to. This is more than likely, completely unjust although the research does show that it sometimes doesn't work (but name me a neuropathy pill that works 100% - there aren't any!). Dr Takahiro Takano's research has found that an important natural pain suppressor in the body (Adenosine) is released at acupuncture pressure points, thus reducing pain. He also found that certain enzymes that suppress adenosine itself, can be targeted, so that more is produced, bringing about natural pain relief. This is a fascinating article that attempts to lay out some of the science behind acupuncture and may change your opinion completely. It is however, advisable to choose the right acupuncturist - there are so many fakers out there - and preferably someone also qualified as a medical doctor. P.S. Bad news for coffee lovers - caffeine is an adenosine suppressant! An educative article - worth a read.

Chronic pain and acupuncture: from needles to analgesia
By researchfeatures on August 21, 2017 Research Focus
With millions of people suffering from long-term pain, acupuncture is a popular, but mysterious, alternative to painkilling drugs.

 Research carried out by Dr Takahiro Takano, at the University of Rochester Medical Center, not only sheds light on how acupuncture works – and why it sometimes does not – but may lead to a whole new line of pain-relieving treatments. Chronic (or persistent) pain, often defined as pain lasting for at least twelve weeks, affects huge numbers of people, including over one-third of the American population. Existing treatments for chronic pain heavily depend on opioid drugs, such as morphine, codeine and tramadol. However, these drugs have disadvantages including side effects, addiction and tolerance, which cause many pain sufferers to turn to alternative treatments, such as acupuncture.

While acupuncture has many devotees, its efficacy has proven hard to document and its success is often highly variable. However, ground-breaking research by Dr Takahiro Takano is beginning to shed light on the physiological basis of acupuncture, and opens up new possibilities for chronic pain treatment that may bridge the gap between conventional and alternative medicine.

Peripheral pain relief

Unlike mainstream painkillers, which target the central nervous system (the brain and spinal cord) where pain is perceived, acupuncture targets the peripheral nerves in the rest of the body. Developed in China over 4,000 years ago, it is perhaps the most widely-accepted of all the ‘alternative’ forms of medicine. Over ten million treatments are carried out each year in the US, with the World Health Organization endorsing it for over two dozen medical conditions. Acupuncture is now even available on the UK’s National Health Service.

The solution for those using acupuncture to treat chronic pain?

Lay off the coffee!

A transverse section of mouse leg integumentary tissue showing nuclei (blue), nerve bundle (green) and sensory neurones (red), where acupuncture can induce extracellular adenosine increase. The fluorescence image was taken with a 10x magnification lens. Acupuncture claims to be a side effect-free form of pain relief – when it works. But so far there is no scientific explanation for its action, and its effects vary significantly from patient to patient, and even day to day. Some of acupuncture’s effects are thought to result from the release of opioid chemicals in the central nervous system, but this by no means explains its entire action, particularly at a more peripheral level. This is where Dr Takano’s research comes in. His work at the University of Rochester Medical Center has helped demonstrate not only how acupuncture works, but also why its effects are so unpredictable. His findings may ultimately help improve the efficacy of acupuncture itself, and enable us to exploit its underlying mechanisms in developing new treatments for chronic pain.

Chronic pain may be of two types: inflammatory pain associated with tissue damage, and neuropathic pain associated with nerve damage. Dr Takano’s team developed mouse models to characterise both these situations, and showed that acupuncture suppresses both types of pain in these animals. Simultaneously, they found that a small molecule, adenosine, was released at the site of the acupuncture treatment. They later confirmed that the same ‘neuromodulator’ is released during acupuncture treatment in human patients.

Adenosine was already known to have pain-relieving properties, mediated through receptor molecules called ‘adenosine A1 receptors’, which are found throughout the human body. Dr Takano’s research showed that these A1 receptors are essential for the adenosine released during acupuncture to cause pain relief. He also found that injecting mice with CCPA, a molecule that mimics adenosine’s interaction with A1 receptors, brings relief from pain without the need for acupuncture itself. Finally, he showed that inhibiting certain enzymes that degrade adenosine, thus allowing it to build up in the body, could prolong the effect of acupuncture treatment. These findings offer a fascinating insight into an entirely new form of pain relief based around stimulating A1 receptors in the peripheral nervous system.
Wake up and smell the coffee…

Dr Takano’s research in mice clearly explains how acupuncture works at the molecular level: the insertion and particularly the rotation of acupuncture needles causes localised stretch of tissue, which stimulates the body to produce adenosine. The adenosine interacts with A1 receptors, initiating a pathway of molecular changes resulting in pain relief throughout the peripheral nervous system. But, if this pathway is clear, why does acupuncture produce such variable results in humans?

Ground-breaking research by Dr Takahiro Takano is beginning to shed light on the physiological basis of acupuncture, and open up new possibilities for chronic pain treatment

Acupuncture’s effect on the pain network. Step up one of the most ubiquitous drugs in modern society – caffeine. Present in coffee, tea, chocolate, energy and diet drinks, and some pain medicines, it is estimated that around 90% of the US population consumes caffeine in some form every day. Unfortunately, caffeine also binds to the adenosine A1 receptor, blocking its reception of adenosine and compromising the pain relief pathway. In a paper published last month, Dr Takano and colleagues showed that even very low doses of caffeine interfere significantly with acupuncture’s painkilling action. Thankfully, the effect is transient and usually wears off within 24 hours. This phenomenon may well explain why acupuncture sometimes works and sometimes does not, and suggests an easy solution to those using acupuncture to treat chronic pain: lay off the coffee!

Pathway to pain relief 

Dr Takano’s research does not stop at vindicating acupuncture – he now wants to use his findings to develop new therapies for chronic pain. Aside from further exploring the role of the A1 receptor and the impact of caffeine in mouse models, his latest research project, funded by the US National Institutes of Health, will investigate other ways to manipulate the pain relief pathway that is stimulated during acupuncture treatment.

Acupuncture is not a quick fix therapy: it often provides only a few hours respite, with long-term relief coming only after multiple treatments. However, now that its mechanism of action is known, it may be possible to manipulate the physiological pathways involved to achieve more effective or longer-lasting relief. One potential player in this is an enzyme known as CD73, which can cause the human body to make adenosine from a molecular precursor. Takano’s investigations so far suggest that administration of CD73 may contribute to long-lasting, side-effect-free, analgesia, in cases of both inflammatory and neurological, acute and chronic pain.

There is much still to discover but, through Dr Takano’s research, we could be on the cusp of a new paradigm for pain relief, bringing hope to many millions of sufferers.

Wednesday, 18 October 2017

Lady Gaga And Her Life With Fibromyalgia But It's Also A Privileged Life (Vid)

Today's post from (see link below) is an excellent comparison of the situations of the haves versus the have-nots when it comes to chronic pain conditions like neuropathy. Don't get me wrong: when high profile people such as Lady Gaga come out and admit their health problems, they provide the role models that we desperately need...but Gaga is rich and life in pain for her, is very different to life in pain for someone who's poor. Nevertheless, we can't criticise Gaga for being rich - she's earned that money (and how!) thanks to an enormous talent and an enormous work ethic and even she admits that she's eternally grateful to have enough money to pay for treatment for her fibromyalgia but it does highlight the plight of the author of this article and millions like him. If you're a chronic pain patient, even in the most generous of health systems, you're under financial pressure from the off. It's wrong and unjust but unfortunately it's the reality of being in a society that measures pain against a check list and does it's darnedest to reject reasonable claims. Luckily, Gaga's situation lets us state our case and we should thank her - there's no rich bitch playing to the cameras there - she's as generous as the best of them but this article does show the other side of the coin. Well worth a read!

Lady Gaga on Chronic Pain: 'I Don’t Know What I’d Do If I Didn’t Have the Money to Get Someone to Help Me'
by Max Fisher 10 days ago

Five Foot Two, the documentary that follows the life of Lady Gaga as she delves into her life of music, passion, love, family, performance, and chronic pain. Vanity Fair described it as a “powerful, thrilling portal into Lady Gaga’s life.” I definitely agree, it was a riveting and thought-provoking watch. Beyond the fame and notoriety, her honest and candid portrayal of life with chronic pain was more than just relatable, it was like looking in a mirror.

Unlike many of us warriors though, she experiences her pain from a place of privilege. She openly admits, “I don’t know what I’d do if I didn’t have the money to get someone to help me. I don’t know what I’d fuckin’ do if I didn’t have everybody here to help me.”

Gaga is lucky enough to be incredibly talented and driven, to a point where she has built a fantastic empire of love, support, and money. In the documentary, we can see she has a team of supporters around her almost constantly. Her career enables her to have people on hand to help and access to treatments she needs to get by. You see, one of the worst parts of this is the vicious circle of pain and unemployment. A lot of those with chronic pain are unemployed or trapped in low-income jobs. Our pain often gets in the way of working. It’s hard to be good at our jobs when our bodies are screaming at us that something is wrong. Sometimes it’s our treatments: they can suppress our immune systems as a way to treat us, leaving us open to infection, and subsequently time off work. Sometimes it’s our means of getting from A to B, when employers can’t look past a wheelchair or a rollator or even a walking stick. This keeps us without money.

Without money, chronic pain is gruelling, arduous, and burdensome. We don’t have the luxury of choosing private doctors who are experts in our conditions. Even here in the UK, where we have free universal healthcare, where the doctor you see doesn’t depend on how much you can afford, finding a good doctor who listens well, and treats you well, is a very laborious task. We don’t often get a choice. We are too frequently told, “This is the specialist. You will see her and only her.” In the US, where healthcare is cost-dependent, this task is even harder. There may be more choice, but our warriors often end up out of pocket or rejected by insurance companies. We often get stuck with doctors who don’t believe we are sick and are sent on our way, with no follow-ups, no treatment, no diagnosis, and no help. No relief. The more money you have, the more believable you are.

“I have chased this pain for five years.” Gaga, you don’t know how lucky you are that it has only taken you this long to have some answers if not all. You’re trying treatments. You’re getting trigger point injections. You’re getting help. I have personally been chasing my pain for over ten years and I’m only 21. There are too many people who are way older who have been chasing their pain for way longer. Better access to better doctors would give us this. Without money, there is no chance of that.

Without money, even if we are lucky enough to be offered treatment, we cannot always afford it. I know of too many people who cannot afford their medication or often have to choose between eating three meals a day and some relief. In the UK, prescription-only medication costs £8.60 per item. Chronic pain conditions are seldom manageable on only one medication. In my case, for example, I have pain relief, both long and short term, as well as daily medication to regulate my heart beat and nausea and anti-emetic medication for when nausea gets really bad. I am also supposed to take anti-histamines and some supplements but can’t afford them on prescription. Some treatments we are advised to undergo are not even covered by the NHS. Yoga, for example. In the US, treatment can be refused by the insurance company. There are co-pays. There are costs. They aren’t a “one price fits all” like the UK’s prescription service. Then there are over the counter medicines, like Tylenol, Ibuprofen, etc.

Without money, we crowd fund for mobility aids. I crowd funded for my wheelchair, so I can get around from day to day. Wheelchairs are massively overpriced considering the financial situations of the majority of people who need them. A custom wheelchair, designed for a person’s body, is upwards of £2,000. The ones that are a “one size fits all,” that often lead to a worsening of problems, more pain, and bad posture, sit in the £200 ball park. The NHS will partially fund it in some cases, but we often don’t have that sort of cash lying around. We crowd fund for people’s medication, just so they can live. We crowd fund for rent because we lose our jobs to pain. We crowd fund to stay alive in our pain.

Without money, we get told by doctors that the cure all for our pain is a healthy diet, yet all I have in my fridge is one-third of a tin of peeled baby potatoes and a variety of sauce. There are so many fad diets out there that claim to cure us. We are often made to try them all before actual, real treatment is offered. The no starch diet is bollocks. Going vegan, while good for the planet, will not cure your chronic pain. Some of these alternative remedies are downright dangerous.

That being said, there are a lot of things about chronic pain that money can’t change. We are often so isolated from friends and family for many reasons. Sometimes our pain makes us unable to go out and meet people, or we simply can’t afford to. We understand that it is not fair for them to come to us whenever we want to see each other. Sometimes we cut ourselves off for fear of upsetting the ones we love, or because chronic pain goes hand in hand with things like depression and anxiety. Not everyone can handle a personal relationship with someone with chronic pain. Lovers leave when the going gets tough. Family don’t understand. Friends meet new friends and move on.

Gaga’s career brings with it the company of other people, whether it’s her colleagues or her fans, but as she touches on in the documentary, “I have people touching me all day, but then when the night comes who’s there? I’m alone.” Regardless of fame or wealth, as a chronic pain warrior, you will never be alone. We will always have your back. We understand each other, we understand pain, and as such we are a family. 

See the trailer for the documentary below.

Tuesday, 17 October 2017

The Dangers Of Nerve Damage From Toxic Substances All Around Us

Today's longer post from (see link below) is an important one for anyone seeking the cause(s) of their neuropathy problems and covers an area that is widely and probably dangerously underestimated, especially in poorer areas of the world where controls on toxic substances are less thorough. Toxic neuropathy is so difficult to diagnose because the possibilities are almost endless and many doctors will not invest the time or energy in finding out if it's a potential cause. Nevertheless, in this day and age, the possibility of nerve damage caused by toxic substances is greater than ever. The problem is as already mentioned - most doctors (if they test at all) will order a series of standard tests for neuropathy and if they can't immediately identify the cause, then send the patient away with medication and a diagnosis of idiopathic neuropathy (basically meaning the can't find the root cause). The importance of being able to identify toxicity as a cause of the nerve damage is vitally important because it's a public health issue and one case may just be the tip of the iceberg. This is a long article but well worth a read and you may be shocked to learn how much we're exposed to toxic environments in our daily lives and work. You'll need to refer to the original article for a full list of references.

Toxic Neuropathy Clinical Presentation
Updated: Feb 03, 2016
Author: Jonathan S Rutchik, MD, MPH, FACOEM; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...


Patients with neuropathy typically present with symptoms of pain, tingling, or numbness in their feet, consistent with dysfunction affecting the longest and largest fibers of the PNS. In some cases, they may have weakness (distal more than proximal) or difficulty with gait. In other cases, patients may also present with symptoms of pain. This may suggest a small fiber neuropathy, which exists when small myelinated and unmyelinated fibers are involved. Clinically, pain may be accompanied by restless leg syndrome, a condition in which disagreeable leg sensations and an irresistible urge to move occur prior to sleep onset.

Additionally, other forms of autonomic dysfunction may be present such as hypohidrosis or hyperhidrosis, diarrhea or constipation, urinary incontinence or retention, gastroparesis, sicca syndrome, blurry vision, facial flushes, orthostatic intolerance, or sexual dysfunction. Autonomic dysfunction may present as cramping. In these cases, the examination reveals normal proprioception, vibration, power or bulk, reflexes, and normal findings on electromyography (EMG) or nerve conduction studies (NCS). [3]

The clinician needs to exercise a high index of suspicion to uncover toxic etiologies. A patient beginning a new medication in the last few weeks or months should raise a red flag. Certainly, the search for an underlying chronic disease is the most common workup ordered; however, new medications are commonly a culprit.

Toxic neuropathy due to recreational drug or chemical abuse may be more difficult to uncover than occupational or environmental exposures, since direct questioning of the patient may lead to incorrect information. In some cases, a dramatic systemic reaction leads to an emergency department (ED) visit because of an acute alteration of consciousness, heralding the diagnosis of drug abuse. The challenge for the ED clinician at this point is to uncover the agent of ingestion or inhalation. Neuropathy, in these cases, may present over a few days to weeks since the dose is often higher than in prescribed-medication settings.

Occupationally induced neuropathies may be secondary to low-level, long-term exposures. The differential diagnosis may not include a work-related exposure, since physicians often are not trained to ask questions about patients' work practices or environment. The presentation may coincide with other lifestyle and medication changes and recent medical diagnoses. After a high-level acute exposure, an occupational etiology for toxic neuropathy may be easier to consider.

Environmental exposure–induced neuropathies follow the same pattern as those from occupational exposures; however, they are omitted even more commonly from the differential diagnosis. For example, a physician is even less likely to ask questions about the patient's use of groundwater, proximity to pesticides, or household use of organic solvents than about occupational exposures. As with occupational exposure, environmental exposures often are very low level, but they are long term and more intensive than occupational exposures, lasting longer than a 40-hour workweek for the duration of employment. Patients who have had high-concentration acute exposure from an environmental accident may present with more obvious clinical symptoms. A differential diagnosis ruling out more common causes of neuropathy is mandatory to establish the cause of neuropathy. [4, 5]

Prior to appearance of symptoms, subclinical findings on EMG or NCV studies may be apparent and consistent with axonal or demyelinating abnormalities. Occupational or environmental exposure at doses approaching regulatory levels for duration or intensity may warrant such an evaluation. Often these are performed in field studies with the use of portable apparatus. Dysfunction associated with environmental exposure to TCE, mainly subclinical, is revealed by electrodiagnostic techniques.

Pain or numbness in the distribution of the trigeminal nerve suggests a disorder of that nerve.


Kimura, in Electrodiagnosis in Diseases of Nerve and Muscle, notes that polyneuropathy presents clinically as a "triad of sensory changes in a glove and stocking distribution, distal weakness, and hyporeflexia." The sensory changes include sensory loss in a stocking-glove distribution. Often, progression is distal to proximal. This is consistent with the commencement of axonal degeneration. Early loss of symmetrical ankle jerk is noted. In severe cases, motor dysfunction such as abnormal gait and foot drop also may occur. In some patients with exclusively small fiber neuropathy, the motor and reflexes examination may be normal.

Spencer and Schaumberg emphasized a gradual insidious onset, as well as slow recovery. Recovery proceeds at a rate of 2 mm/day and may take months or several years, or may never be complete. Function is restored in reverse order to the sequence of loss. Coasting may be noted, that is, intensification may occur for weeks before improvement. This often reflects continued axonal degeneration and reconstitution.

Signs of CNS disease also may be present at examination. This occurs in some patients recovering from certain toxic neuropathies. Dorsal column or corticospinal tract degeneration may be present. These clinical signs of degeneration are not prominent early in the illness; however, the patient may manifest hyperreflexia, Babinski responses, and stiff-leg ataxic gait with corticospinal tract disease or diffusely decreased proprioceptive and vibratory sensations and gait ataxia with dorsal column degeneration.

Involvement of the autonomic nerves may lead to a different clinical presentation–miosis, anhydrosis, orthostatic hypotension, sphincter symptoms, impotence, and vasomotor abnormalities. These may occur with or without evidence of a peripheral neuropathy. Tachycardia, rapid alterations in blood pressure, flushing and sweating, and abnormalities in gastrointestinal motility may be present.

Spencer and Schaumberg reported the association of sensory ganglion cell loss in pyridoxine-associated sensory neuropathy with 9 clinical features; they are as follows:

Rapid or subacute onset may occur following massive intravenous administration.

Initial sensory loss may occur anywhere; the gasserian ganglion often is affected simultaneously with the dorsal root ganglion, and thus facial numbness may be noted.

Diffuse sensory loss with ataxia and preservation of motor power may be present. Proprioceptive deficit is noted to be greater than the loss of pain or temperature sensation.

Tendon reflexes may be absent.

NCV results usually are normal; sensory nerve potentials may be abnormal or absent. Recovery is variable, reflecting the death of nerve cell bodies and consequent permanent loss of axons. Collateral sprouting from surviving axons may account for the extent of recovery in these conditions.

No signs of CNS disease are present.

Cholinergic symptoms follow (see Organophosphates and disorders of neuromuscular transmission).


A variety of drugs and industrial chemicals cause distal axonopathy. In 1989, Kimura listed the following as potential causes of toxic neuropathy [6, 7] :










Nitrous oxide

Perhexiline maleate




In August 2013, the US Food and Drug Administration (FDA) announced that oral or injected fluoroquinolone antibiotics can cause permanent peripheral neuropathy and that labels on the drugs will be updated to reflect this finding. (Topical fluoroquinolones have not been associated with this condition.) [8, 9]

The change strengthens the FDA’s previous warning, first added to fluoroquinolone labels in 2004, that oral and injectable fluoroquinolones carry a risk of peripheral neuropathy. The 6 FDA-approved fluoroquinolone antibiotics on the market are ciprofloxacin, gemifloxacin, levofloxacin, moxifloxacin, norfloxacin, and ofloxacin. [8, 9]

Industrial chemicals causing toxic axonal neuropathy also are listed by Kimura; they include the following [6, 7] :


Carbon disulfide

Inorganic mercury

Methyl n -butyl ketone


Polychlorinated biphenyl


Triorthocresyl phosphate

Vinyl chloride

In 1999, Feldman added the heavy metals arsenic and lead, as well as the solvents n -hexane, perchloroethylene (PERC), and TCE to this list. [10] In 1995, Albers and Bromberg summarized the literature on toxic neuropathy caused by the solvents ethylene oxide (EtO), styrene, toluene, and mixed solvents. [11]

Spencer and Schaumberg listed agents that commonly are associated with peripheral neuropathy (see Table 2 in Schaumberg, 2000 [12] ).

Toxic neuropathy may be the result of exposure to numerous agents and is related to dose and duration of exposures and to host factors. Most syndromes are subacute, progressing to chronic as already described. Chemicals such as thallium, dimethylaminopropionitrile (DMAP), and organophosphates (eg, parathion) produce specific syndromes associated with peripheral neuropathy; however, all of these may lead to systemic abnormalities as well.

Thallium is used in glass and in metal alloys. It had been used therapeutically to treat venereal disease, tuberculosis, and ringworm. It has also been used as a rodenticide. Accidental or homicidal abuse is a common reason for toxicity.

Acute thallium intoxication leads to pain and paresthesias in the distal extremities followed by weakness and eventual atrophy. Preservation of peripheral reflexes is a useful physical finding to differentiate thallium toxicity from Guillain-Barré syndrome. Alopecia is a clinical hallmark of thallium toxicity that may develop weeks after intoxication. Mee lines, nephropathy, anemia, and hepatotoxicity are systemic manifestations. Autonomic dysfunction also may be a part of the clinical syndrome. Thallium toxicity may be mistaken for porphyria, arsenic toxicity, or botulism. Serum thallium levels typically are elevated.

DMAP is used as a catalyst in the manufacture of polyurethane foam and in an acrylamide grouting compound. It is used as a waterproofing agent in tunnels and sewer lines. Industrial exposure has led to prominent urinary and sexual dysfunction as well as to distal sensory neuropathy.

Alcohol, by itself, is toxic to the PNS. Individuals who consume alcohol also may become nutritionally compromised. Studies have found that alcohol impairs axonal transport and that this can occur in the setting of normal nutrition. Since it may affect both the cerebellum and the autonomic nervous system, ataxia and other systemic symptoms may accompany symptoms of dysesthesia and weakness of the lower extremities. In the patient with occupational exposure to other peripheral neurotoxic agents, alcohol may act either to slow metabolism and increase toxicity or, in the case of a habitual alcohol user, promote metabolism and reduce toxicity from the agent. This is observed most clearly with toluene exposure.

A number of studies have attempted to address the type of neuropathy that occurs with alcohol exposure, as well as what amount of exposure is required before neuropathy occurs. A sensorimotor axonopathy with secondary demyelination that was not necessarily related to a deficit in thiamine was described by Mellion et al in 2011. [13] Ten ounces of whiskey per day in a 70-kg man for several years was mentioned to cause alcohol neuropathy. [14] Three liters of beer per day for 3 years was described as another threshold. [15] Wine in combination with other forms of ethanol was deemed worse, possibly due to impurities with lead. [16]

Other organic solvents have been associated with peripheral neuropathy on the basis of cross-sectional studies and animal data. Prospective data are unavailable. Solvent mixtures have been noted to be responsible for toxic neuropathies in many studies. Identifying the culpable agent has been difficult. Often, no chemical with a clear association with neuropathy is listed, suggesting that organic solvents themselves, either in mixture or individually, may cause neuropathy. Studies that have found subclinical abnormalities further support this hypothesis.

Often, study designs have been criticized for their definition of neuropathy. NCV and EMG findings in many of these studies are difficult to categorize. To ascertain whether a toxic etiology is a possibility for a patient, a clinician may need to search the literature for the agent as well as the industry. Many agents are used in many different industries. The industrial agents and some of the industries that utilize them are listed in Table 3. For information on toxic neuropathy caused by organophosphates, refer to the article Organophosphates

Carbon disulfide and peripheral neuropathy

Carbon disulfide is an agent used in the viscose rayon industry. Refer to Table 3 for its other uses.

Carbon disulfide has been deemed a peripheral neurotoxin in both animals and humans by the Agency for Toxic Substances and Disease Registry (ATSDR). Consistency has been established for effect (ie, neurophysiological impairment and pathologic changes) but not for dose. The pathophysiology for toxic neuropathy is an axonal neuropathy in a distal dying back pattern. Reduced or absent sensory nerve action potentials (SNAPs) are common. Conduction velocities are usually normal, but they may be borderline low owing to selective involvement of large fibers. Metabolic abnormalities from coexisting diseases may be associated with reduced conduction velocities and may contribute to electrophysiologic abnormalities.

In humans, neurophysiological effects have been demonstrated at low levels of occupational exposure. In 1974, Seppalainen and Tolonen demonstrated a decrease in maximal motor NCV in the median, ulnar, peroneal, and posterior tibial nerves in 118 viscose rayon workers who had exposure to an average of 10-20 parts per million (ppm) of carbon disulfide for an average of 15 years. No improvement was noted after removal from exposure, but a follow-up study by these authors demonstrated that fewer workers who had retired 10-15 years prior had decreased NCVs than those who had been removed from their work 0-4 years prior to the study. (These abnormalities were in workers who had no subjective complaints.) [17]

In 1990 and 1993, Ruitjen et al demonstrated that 44 viscose rayon workers exposed to 1-30 ppm of carbon disulfide for at least 10 years had somewhat slower slow motor fiber conduction velocities than 31 controls, based on the antidromic collision technique. Symptoms of clinical neuropathy related to cumulative exposures were absent in the patients in this study. This study revealed that a decrease in the conduction velocity occurs at low levels of exposure to carbon disulfide. Extrapolation of these results suggests that small effects may occur after a mean cumulative exposure of 165 ppm-years, which would be equivalent to a concentration of 4 ppm over an 8-hour time-weighted average (TWA). At this exposure level over a lifetime of employment, the observed effects would be expected.

The authors explained that the significance of these effects on health would be that these observed changes might reduce reserve capacity to cope with other noxious influences. They concluded that these changes are undesirable until they are shown to be not detrimental to health in the long term.

The second study to verify these findings reexamined these workers 4 years later and found a statistically significant decrease in velocities in the slow as well as the fast motor nerve fibers of the peroneal nerve. Weighted cumulative exposures correlated less well with the peripheral nerve indices and revealed no evidence that the effects were reversible. The authors reiterated their concerns for the neurotoxic effects of carbon disulfide at these exposure levels. [18, 19]

In 1983, Johnson et al examined 189 workers from a viscose rayon plant; 245 workers in polyester-nylon filament and staple plants were used as controls. [20] Confounding exposures were hydrogen sulfide, tin oxide, zinc oxide and sulfate, sodium hydroxide, and sulfuric acid. At no point in time did hydrogen sulfide levels exceed 1 ppm.

Carbon disulfide exposure was divided into high (median >7.1 ppm), medium (median 3-7.1 ppm), and low (median < 3 ppm). Exclusion criteria were alcohol consumption >35 U, blood glucose >110 mg/dL, or blood lead >40 mcg/L. Mean duration of exposure for all exposed subjects was 12.1 years; for the high-exposure group it was 13.6 years; for the medium-exposure group it was 12.3 years; and for the low-exposure group it was 10.5 years. The average age of exposed individuals was 38.5 years and of controls, 33.9 years.

The study assessed NCV of motor (ie, peroneal, ulnar) and sensory (ie, sural) nerves. A reduction in peroneal nerve mean conduction velocity (MCV) was found to be related, in a dose-response sense, to cumulative exposure to carbon disulfide. 

Ethylene oxide and peripheral neuropathy

EtO is a sterilizing agent with an epoxide structure often used in hospital settings. Refer to Table 3 to review other industrial uses of EtO. Symptoms suggestive of neuropathy, such as numbness and weakness of extremities, leg cramps, and gait difficulties, are reported mostly after long-term EtO exposures. In 1979, Gross et al reported 4 cases of peripheral neuropathy caused by EtO resulting from a large EtO sterilizer leak that was not noticed for 2 months. [21] These patients were working as sterilizer operators and had exposures of 3 weeks to 8 years. One operator was asymptomatic; 3 had headaches; and 2 developed fatigue, numbness, and muscle weakness in the extremities. In 1983, 5 of 6 sterilizer operators of a factory producing medical appliances were poisoned by EtO gas.

In 1986, Fukushima et al examined 4 operators who had exposures to the chemical ranging in duration from 20 days to 8 months. Gait disturbance was noted in all 4 operators. All 4 complained of numbness and muscle weakness in the feet and numbness of the fingers. Two operators had pain in the calf muscles and 3 had muscle weakness of the fingers. A 23-year-old man had been exposed 2-3 times a day for 5 months to high levels of EtO, up to 500 ppm, while working in a food and medical supply sterilization factory prior to his admission to a hospital. He complained of increasing weakness in his lower extremities. [22]

Schroder and Kuzuhara reported 2 patients with long-term EtO exposure. Both had difficulty in walking. One had been an operator of a sterilizer for 3 months before noting paresthesias and weakness in the distal limbs with staggering. After he returned to work, his symptoms worsened, and 3 months later he was admitted to a local hospital. His symptoms cleared entirely after 2 months. The second patient noted paresthesias in his feet 6 months after he had started to load and unload the sterilizers with medical supplies. Staggering followed the numbness and tingling of both hands and feet. Symptoms cleared 1 month later. [23, 24]

Finelli et al reported another case series of 3 males with toxicity from EtO. Two of these had been operators of sterilizers. One worked for a year and the other worked part-time for 1.5 years before developing symptoms. Both had difficulties with their gait after developing numbness and weakness in their lower extremities. One operator reported numbness in his feet and buckling of his right leg, and the other complained of cramps in his calf muscles. Both reported an odor; the part-time operator also reported headaches, burning eyes, and nausea. [25]

The third patient worked for 6 days a week at a plastic manufacturing company, where several times a day he worked in a sterilizing tank for about 40 minutes; he also unloaded materials in a decontamination area for half an hour each day. His chief complaints were leg cramps and a sense of heaviness of the feet. He first noted difficulty with sleeping, nervousness, and cramps in his hands and calf muscles. One month later, he noted poor balance and repeated stumbling. He also was aware of odd tingling sensations in both feet that had been present for longer than 3 months.

Two women workers developed symptoms referred to the PNS after chronic EtO exposure. Both had been part of a group of 12 sterilizer workers in a hospital in Italy who were tested 2 years after the commencement of this exposure. Four of these 12 women complained of paresthesias and fatigue. Two were found to have peripheral neuropathy. Complete remission of these symptoms was reported for most of these women approximately 6 months after removal from exposure.

Mercury (inorganic and organic) and peripheral neuropathy

Inorganic mercury is used in the chloralkali industry. Other uses are noted in Table 3. Neuropathy and PNS dysfunction, often motor more than sensory, were noted in the cases summarized here.

Albers et al reported 138 chloralkali plant workers with long-term exposure to inorganic mercury vapor who were found to have elevated urine mercury levels and reduced sensation on quantitative testing. Subjects exposed to mercury for 20-35 years who had urine mercury levels greater than 0.6 mg/L demonstrated significantly less strength, poorer coordination, more severe tremor, more impaired sensation, and higher prevalence of Babinski and snout reflexes than controls. Subjects with polyneuropathy had higher peak levels of mercury than healthy subjects. [11]

In another study by Andersen et al, chloralkali workers exposed to inorganic mercury vapor for an average of 12.3 years revealed a higher prevalence of reduced distal sensation, postural tremor, and impaired coordination than controls. [26] Barber reported 2 employees of a chloralkali plant who had findings suggestive of amyotrophic lateral sclerosis (ALS). Signs, symptoms, and laboratory findings returned to normal 3 months after withdrawal from exposure. [27] Adams et al reported a 54-year-old man with a brief but intense exposure to mercury vapor, which led to a syndrome resembling ALS that resolved as urinary mercury levels fell. [28] Ross reported that prolonged application of an ammoniated ointment to the skin was a cause of motor polyneuropathy, with cerebrospinal fluid (CSF) findings suggestive of Guillain-Barré syndrome. [29]

Warkany and Hubbard reported the association of acrodynia and symmetrical flaccid paralysis with mercury toxicity. [30]

Organic mercury was deemed the culprit in a number of historic environmental accidents. One noted catastrophe, reported by Yoshida et al, occurred in Minimata Bay, Japan, and involved organic mercury. The majority of Minimata patients with methylmercury intoxication had elevated pain thresholds but suffered from glove and stocking hyperesthesia in the extremities. [31] 

Lead and neuropathy

A review of the literature reported that acute, high-level lead exposure has been described to cause motor neuropathy with minimal sensory involvement and rarely the textbook-described wrist drop. Chronic, lower-level exposures lead to axonal dying back neuropathies that appear similar to neuropathies from diabetes or alcohol. Chronic exposures, depending on the length of exposure, may have poorer prognoses but may present with a slower and more gradual onset. High–level, acute exposures are more likely to cause motor neuropathies, and recovery may be complete if termination of exposure is prompt. Because neuropathies have not seemed to correlate with blood lead levels, interference with porphyrin metabolism has been proposed as the etiology. [32]
Xylene and neuropathy

Xylene often is a component of paints and other industrial processes (see Table 3 for other uses of xylene). A literature search using Medline uncovered 11 epidemiologic studies of painters or other subjects with occupational exposure to organic solvents, including xylene, that found positive associations between exposure and PNS dysfunction. Two studies reported that vibration sensation was significantly less acute in 102 painters than in 102 age- and sex-matched controls. Four studies utilized quantitative sensory test (QST) methods.

In 1991, Bleecker found a correlation between increasing exposure dose and elevated vibration sensation thresholds in 187 workers from 2 paint-manufacturing plants. [33] A second study noted higher vibration thresholds in 80 exposed painters than in controls. [34] Demers et al noted statistically significant differences in vibrotactile measurements by QST of upper and lower extremities between 28 painters and 20 nonexposed controls. [35] In 1989, Bove et al compared 93 painters to a nonexposed control population of 105 construction workers. [36] Subjects were tested by 2 QST devices, a vibrometer and a temperature sensitivity tester. Painters had significantly higher temperature sensation thresholds, and exposure intensity and cumulative exposure over the past month and year were associated positively with vibration thresholds.

In 1989, Padilla et al performed an important animal study in which axonal transport was noted to be decreased by 30-50% in the rat optic nerve system immediately and 13 hours after inhalation exposure to xylene. Exposure was subacute; 800 and 1600 ppm for 6 hours/day, 5 days a week for 8 days led to these abnormalities. The authors concluded that the decreased supply of cellular materials to the axon and nerve-ending regions could initiate the neuronal malfunction reported in solvent-exposed animals and humans. [37] As axonal transport is a process common to all nerves, any perturbation in these processes may disrupt the structure and functional integrity of the neuron. This mechanism has been used to explain both the CNS and PNS toxicity from organic solvents.

Seven men aged 17-22 years developed severe distal symmetrical polyneuropathy after repeatedly inhaling a commercially available brand of lacquer thinner that was composed predominantly of xylene. All 7 were disabled permanently with motor weakness. One man died, 3 remained wheelchair bound, and 3 could walk but demonstrated varying degrees of weakness. Pathologic specimens revealed evidence of peripheral neuropathy. 

Perchloroethylene and neuropathy

PERC is an agent used in the dry-cleaning industry. Its various other uses are listed in Table 3. Peripheral neuropathy is a clinical diagnosis that is listed as secondary to chronic PERC exposure by Feldman. [38, 39] Neither article refers to specific study results. Spencer and Schaumberg list neuropathy with a question mark as an effect of tetrachloroethylene (ie, perchloroethylene) toxicity. This article refers to 2 articles by Antti-Poika and Juntunen et al that reported sensory trigeminal (fifth cranial nerve) defects in those exposed to mixed solvents. A 1978 National Institute for Occupational Safety and Health (NIOSH) publication on PERC remarked that "various disturbances of the peripheral nervous system such as tremors and numbness have also been associated with exposure to tetrachloroethylene."

Juntunen et al studied 87 patients from Finland diagnosed as having chronic intoxication caused by exposure to a mixture of solvents or to TCE and PERC between 1970 and 1974. Of these, 14 had been exposed to TCE or PERC alone, 53 to solvent mixtures, and 13 to all of them. Disturbances of cutaneous sensation and the sense of vibration were encountered frequently as clinical signs. [40]

The Antti-Poika article of the same year (1982) discussed the EMG findings of this same group. Electroneuromyography ([ENMG], including NCV and EMG) revealed 64 patients with signs positive for PNS disease and 34 patients with subjective symptoms. Signs of polyneuropathy were reported in 13 subjects. In the discussion, the author remarked that the number of patients with clinical polyneuropathy was so small that a trend could not be evaluated definitively. [41]

A publication the following year (1983) by Seppalainen and Antti-Poika categorized the specific ENMG findings of each of the 3 groups in the previously mentioned 2 studies. Of 18 patients in the group exposed to either TCE or PERC alone, 9 (50%) were deemed to have neuropathy on the first ENMG examination. On the second ENMG, 15 of 21 (71%) patients had this diagnosis. For those exposed to TCE or PERC or a mixture, 10 of 11 (91%) patients and 11 of 13 (85%) patients had this diagnosis, as opposed to 26 of 44 (59%) and then 38 of 53 (72%) of those exposed only to a mixture excluding chlorinated hydrocarbons (ie, TCE or PERC). The authors concluded that those patients with exposure to a mixture of solvents and to TCE or PERC tended to have neuropathic findings more often than patients exposed to either TCE or PERC alone or to a solvent mixture that did not include TCE or PERC. Findings on ENMG in these patients suggested axonal changes rather than segmental demyelination. [42]

One toxicology text remarked that neuropathy may present following solvent exposures because the solvent (ie, PERC) often is mixed with amines, epoxides, and esters to protect it from moisture and light. Some of these compounds are known to cause neuropathy. Two European articles report PERC as being associated with neuropathy. In 1989, Herruzo-Perez et al described one case in which the authors suspected that a sensitive painful polyneuropathy probably was caused by poisoning with PERC. [43] In 1989, Muller et al found slight derangements in neural functions in 130 dry-cleaning workers with long-term exposure to PERC during a 5-year follow-up study.

Baker reported in a review from 1994 that recent studies suggested that mild subclinical disruption of PNS function does occur in workers exposed to solvent mixtures. [44] In 1988, Orbaek et al studied patients with long-term exposures to organic solvents and found evidence of PNS dysfunction and slowing of the median nerve that was more pronounced in follow-up testing 22-72 months later. Slowing in the peroneal nerve was observed only at the follow-up NCV examination. Sensory conduction studies showed substantially reduced amplitudes in median and sural nerves with a prolongation of the distal latency in comparison with a control group; sensory conduction velocity in the median nerve also was slowed in the follow-up examination. [45]

Whether this and other studies of mixed organic solvent exposures suggesting neuropathy with various neurophysiological tests can implicate PERC is not clear, since PERC, its metabolites, or chemicals of similar structure may or may not have been a component of the solvent mixture. Maizlish et al refer to chlorinated aliphatic and chlorinated hydrocarbon solvents as components of paint vehicles and glues to which their subject population was exposed [46] ; other authors do not specify the composition of the substances to which their subjects were exposed. 

Trichloroethylene and neuropathy

TCE is used as degreaser in many industrial processes (refer to Table 3 above to review its other industrial uses). Bernad et al evaluated 22 persons in a cohort of Michigan residents exposed for 5-20 years to well water with a low level of TCE contamination; 8-14 ppm of TCE was measured in the well water. Questionnaire, examination, and computer current perception-threshold testing (CPT) was performed. Results revealed hyperesthesia in 21 of 22 persons by CPT. Fatigue, lack of energy, somnolence, numbness, and tingling were reported by all 10 adults.

Feldman et al evaluated 21 residents of a Massachusetts community with alleged long-term exposure to TCE through drinking water and laboratory controls. The wells in question had 256 and 111 parts per billion (ppb) mean concentrations of TCE (maximum contaminant level [MCL] recommended by the Environment Protection Agency [EPA] is 0.5 ppb) and 26 and 24 ppb mean concentrations of PERC; duration of exposures was less than 1 to 12 years. Blink reflexes revealed differences in conduction latency of the reflex for the exposed population versus the controls, suggesting a subclinical alteration in the function of the fifth cranial nerve. [47]

In 1994, Feldman et al published a study that compared this population to 2 other populations that had been exposed to environments contaminated with TCE and PERC and included more details of the population's neurologic examinations. The Massachusetts group was found to have sensory impairment and reflex abnormalities as evidence of peripheral neuropathy.

The second group was 12 residents from an Ohio community who had been exposed to well water contaminated by wastewater deposited in a nearby creek by a company that fabricated sheet metal and precision-formed metal tubes. Their exposure was 3.3-330 ppb of TCE for 5-17 years. PERC also was found in the contaminated water. Nerve conduction studies (including blink reflexes) were performed. Reflex abnormalities were the most prevalent examination finding. Abnormal ulnar sensory latencies were noted in 81% of the group.

The third group comprised 14 residents from a Minnesota community who had been exposed to well water contaminated by a nearby army ammunitions plant. Exposure to TCE was between 261 and 2440 ppb in wells. 1,1-dichloroethane (DCE), 1,2-DCE, and 1,2-trans -DCE were identified in some wells. Questionnaires, examinations, and nerve conduction studies (including blink reflexes) were performed. Reflex abnormalities were the most common finding on neurologic examination. Approximately 70.6% had abnormal ulnar sensory latency, while 21% had abnormal blink reflex studies. [47]

Table 3. Industrial Uses of Common Organic Solvents and Metals (Open Table in a new window)

Compound Industrial Uses
Acrylamide Mining and tunneling, adhesives, waste treatment, ore processing, paper, pulp industry, photography, dyes
Arsenic Pesticides, pigments, antifouling paint, electroplating, seafood, smelters, semiconductors, logging
Carbon disulfide Viscose rayon, explosives, paints, preservatives, textiles, rubber cement, varnishes, electroplating
Ethylene oxide Instrument sterilization, chemical precursor
n -hexane Glues and vegetable extraction, components of naphtha, lacquers, metal-cleaning compounds
Lead Solder, lead shot, illicit whiskey, insecticides, auto body shops, storage batteries, foundries, smelters, lead-based paint, lead stained glass, lead pipes
Mercury Scientific instruments, electrical equipment, amalgams, electroplating, photography, felt making, taxidermy, textiles, pigments, chloroalkali industry
Methyl n -butyl ketone Paints, varnishes, quick-drying inks, lacquers, metal-cleaning compounds, paint removers
Organochlorine Insecticides
Organophosphates Insecticides
Perchloroethylene Dry cleaning, degreaser, textile industry
Styrene Fiberglass component, ship building, polyester resin
Thallium Rodenticides, fungicides, mercury and silver alloys, lens manufacturing, photoelectric cells, infrared optical instruments
Toluene Paint, fuel oil, cleaning agents, lacquers, paints and paint thinners

Trichloroethane (methyl chloroform)

Degreaser and propellant 

Trichloroethylene Cleaning agent, paint component, decaffeination, rubber solvents, varnish
Vinyl chloride Intermediate for polyvinyl chloride (PVC) resins for plastics, floor coverings, upholstery, appliances, packaging
Xylene Fixative for pathologic specimens, paint, lacquers, varnishes, inks, dyes, adhesives, cements

Monday, 16 October 2017

Personal Experience Of A Pain Management Clinic - Food For Thought?

Today's post from (see link below) is a personal account of one person's experience of a pain management program. More and more neuropathy patients (and other chronic pain conditions) have gone through the entire list of medications and have emerged feeling frustrated and unsatisfied by the results. They're often dependent on the pain killers but have no other avenues to explore and are pretty much left to their own devices. Recently, the idea of a more varied therapy philosophy has been developed, including attending pain management courses and clinics. However, unless those courses and clinics are up to date with their information, people can feel bullied into doing things they're not comfortable with and are not tailored to their own needs. Pain management clinics can end up making the situation worse but they're probably the right way forward as part of a holistic treatment of chronic pain issues. This article is an account of one person's experiences and is naturally, not true for all but it may make you think about what's involved and what's best for you. The key issue is trust - it shouldn't be seen as a sort of punishment. If that's the feeling you get, then you need to find a better one.

What is a Pain Management Clinic?
Posted by theworldinmywords17 on September 21, 2017 Pain Management.

To some pain management may seem like the worst thing. To others pain management may seem like the best thing; (although honestly I don’t think I’ve ever heard anyone say that). To me? pain management is a pain in the arse!

Pain Management can be extremely beneficial to somebody like myself i.e. someone with chronic pain. It helps someone with chronic pain to better manage the pain and the symptoms to live their life as best as they can alongside their pain. Personally I have had a long relationship with pain management, I have had some great results, I’ve had some alright results and then I have felt let down despite all my work I’ve had some fairly devastating results (please do continue reading as this does get brighter!). However, despite my mixed results through pain management there are definitely things I can take away from it. I do feel that most people don’t take much away from pain management as I think they expect too much and don’t make the most of what they get out of it; but the clue is in the title pain management. It is to help you manage your pain not to cure it.

Pain Management is a tool that can be used by those with chronic pain. It is essentially there to teach you how to live your life the best you can with your pain.

There are several steps within pain management and you may try some of these before you reach a pain management clinic. In my experience the one thing I can always guarantee you will have tried before reaching a pain management clinic is cognitive behaviour therapy also known as CBT, or at least something like it i.e. some form of psychology sessions. Again these techniques are used to help you learn to live with your pain and to learn how it impacts your daily life but it’s mainly there to teach you to think about your pain in a specific way. However, and this is a big however… I disagree with a lot of these approaches. Anyone who knows me well will be nodding with a little laugh right now because they know how strongly I personally feel about this. As I said I have found some benefits, which goes to show that even the most dubious can find benefit… if done correctly. I do not nor do I believe that anyone else will benefit from being told that if they think positively about their pain it will go away or be less problematic – I wont go any further because this is a WHOLE other topic and blog post.

When dealing with pain I can almost guarantee that you’ve tried every over-the-counter medication/Painkiller there is and inevitably when they don’t work because they are not strong enough to go up against your pain so, you seek advice from your GP. Some people may speak to their rheumatologist or consultant but more often than not you go through your GP first.

A GP will quite often encourage you to try something like paracetamol which you have probably already done (and it stood no chance against your chronic pain). As well as an anti-inflammatory the most common thing being ibuprofen. Depending on how well your GP knows you, your conditions and how long you’ve been suffering they may prescribe you something such as codeine or a medication that contains codeine. However, no matter what combination they try they never really touch your pain and when it does the relief you get doesn’t last very long. When I say your relief doesn’t last very long I’m talking about the relief you get between each dose but also the relief you get overtime. As overtime your body often becomes too used to the medication and you no longer get relief from it.

Eventually your GP, rheumatologist or consultant will advise that they will refer you to a pain management clinic. If like me, you will be very surprised when this referral is offered as you never knew a pain management clinic existed. Plus given the fact that you suffer from chronic pain you would have assumed that your doctor would have mentioned or referred you sooner. I should say here that pain management clinics are slightly more common now compared to what they were 10 years ago.

Again in my experience a pain management clinic was offered when I was most desperate. This does not necessarily mean this is where my pain was at its worst but this is when we were getting the least success with any other treatment and were running out of treatment options. Therefore, for some people, including myself pain management clinics are a last resort.

When you attend a pain management clinic, they may offer CBT or some form of psychological therapy. Although you have usually covered this basis before they like to make sure that you have covered all possible roots before you are offered anything else. This does make sense as you wouldn’t want to take on a new medication or heavy treatment on if there’s something you can do beforehand.

Some pain management consultants will offer you other forms of medication. When I first saw a pain management consultant I was about 15 we discussed a few options however these weren’t anything I looked into until I was around 18. These medications quite often include things such as tramadol, gabapentin and pre-gabalin. However, depending on your circumstances and your pain these medications may not always be the best form of treatment. Despite being in severe amounts of pain there was a lot of thought that had to go into whether or not I wanted to try these types of medications. Therefore, if you are thinking of trying a higher more impacting type of medication I would urge you to really think about the side-effects and weigh up the pros and cons first. This is something the consultant should do with you and it’s probably done on your behalf before the medication is offered. However, if they don’t, do make sure this is a discussion you have. You may even decide that this is something you need to think about personally before you make the decision. As most things when it comes to health and medications always make sure you have as much information as possible.

A consultant may not always offer medication straightaway and for me the medication wasn’t what we are looking to try first. In a lot of cases your local pain management clinic can offer an outpatient course that runs over a number of weeks. You work with the consultant, physiotherapists, occupational therapists and other medical professionals along with other people like you with chronic pain to learn how to deal with your pain on a daily basis and to how to live your life the best you can.

Sometimes this isn’t always an option or there is not an appropriate group for you to be a part of. This was the case for me therefore I was offered a three-week inpatient pain rehab course. This is similar to an outpatient course however, less hospitals run this and it is much more intense although the aim remains the same. I don’t want to go into too much detail about this now as this is something I’d like to do later on in my blog but most people do this again as a last resort hoping for answers and it is a very intense program but some people can get some real benefits from it.


Taken August 2015 during my time at a 3 week inpatient pain rehab course – I was much better physically then than I am now Bare in mind that pain management clinics are specifically for those with chronic pain. Although many people with chronic pain have many other conditions they have to deal with, this is specifically set up to help you learn to live daily life to the best of your ability with pain. The service and clinics have been set up by great doctors that really understand chronic pain therefore they are some of the best treatment a sufferer of chronic pain can receive.

If you live with chronic pain or know somebody that does you will know the stigma that is attached to it. Therefore, personally I feel that even when things are really tough and you are at your lowest point remember, these doctors and clinics can’t cure you but these are the people that really care and really want to help you live a better life with pain.



These views are my own, based on my own experience of Pain Management as well as my view on other cases I have heard about or seen. Others may have had different experiences and any individual looking to be seen by Pain Management Clinics/Consultants may have a different experience to me. These services may not be open to all chronic pain suffers depending on your own circumstances and/or your location/local services.

Sunday, 15 October 2017

The Puffer Fish Joins The Neuropathy Zoo

Today's post from (see link below) returns to the Puffer fish as being the source of a potential new neuropathy drug. Along with spiders, snakes, zebra fish, scorpions and others, the Puffer fish is joining the list of animals whose venom may be turned into a drug to treat nerve pain. It's completely logical if you think about it - paralysing venoms that  anaesthetise nerve pain signals, seem to be obvious candidates for research. However, it has to be said that very year a new creature joins the neuropathy zoo but we don't seem to see the results on our chemist's shelves. FDA approval for trials is always a promising step so maybe we need to give the researchers more time but even that statement is becoming a bit of a cliche for neuropathy patients.

Could a pufferfish be the next big thing for neuropathy treatment? Posted: 4:27 PM, October 10, 2017 Updated: 6:36 PM, October 10, 2017 
Researchers are testing new non-addictive treatment
NEW YORK, N.Y. (Ivanhoe Newswire) - Thirty percent of all Americans will be affected by peripheral neuropathy, a condition that impacts nerves leading to the arms and legs.

In many cases, doctors prescribe medicines to help manage the pain, burning and tingling. Now, researchers are testing a new non-addictive treatment inspired from a surprising source.

Joseph Malkevitch has been a math enthusiast for most of his adult life. Ironically, for years Joseph has been battling a medical condition that is highly unpredictable.

Malkevitch explained, “I noticed it in the form of tingling in my feet and toes and initially it went away and so I just tossed it aside as a glitch.”

Joseph’s doctors diagnosed him with peripheral neuropathy; damage to the nerves in the peripheral system which lead from the brain to the extremities. But they could not determine a cause.

Medical experts say that’s not uncommon.

David M Simpson, MD, FAAN, Professor of Neurology; Director, Clinical Neurophysiology Laboratories; Director, Neuromuscular Division; Director, Neuro-AIDS Program, Icahn School of Medicine at Mount Sinai said, “In upwards of 30 percent of patients with peripheral neuropathy one can’t identify a cause.”

Now, researchers are testing a drug to treat neuropathy pain. Right now it’s known only as CC8464. Inspired by the toxin found in Japanese pufferfish, the drug copies how the fish toxins disrupt signals to the body.

How it works in the body is by targeting those peripheral nerve fibers and not penetrating the brain,” said Heikki Mansikka, MD, PhD, VP Clinical Development at Chromocell.

Researchers say since the drug candidate bypasses the brain and works directly on the peripheral nerves, it may not be addictive.

While Joseph chooses to manage his neuropathy without medication, he knows others with this condition may be searching for serious pain relief.

The potential new drug is being developed by the New Jersey-based company, Chromocell. The FDA granted the drug “fast-track” status based on need. It is currently in phase one clinical trials.

Saturday, 14 October 2017

Neuropathy And Sex: One Doesn't Have To Exclude The Other

Today's post from (see link below) revisits a subject that's sensitive for both men and women living with nerve damage and that interrupted sexual function. It's 2017 and yet people still find it difficult to talk about sexual problems, even to their doctors. When these arise from neuropathy, it's a sort of double blow - it's bad enough being in constant pain and/or discomfort but you're also denied those intimate moments that make life worthwhile - not fair! However, it's a reality for many people but very often not an insurmountable one. First you really need to talk to your doctor and if you feel you can't do that with your home doctor, there are sexual health clinics, often attached to hospitals, that will be only too happy to help you. It's not between your ears, it's a real problem caused by nerve malfunction - why wouldn't you get help! This article helps you understand what's going on when this happens and you may be surprised to know that it affects women just as much as men.

Sexual Side Effects of Peripheral Neuropathy 
by MATTHEW BUSSE Last Updated: Aug 14, 2017

Damage to the nerves of the peripheral nervous system is referred to as peripheral neuropathy. The peripheral nervous system is a network of neurons that connect the spinal cord and the brain to the rest of the body. Peripheral neurons are responsible for transmitting physical sensations, like touch and heat, from the skin to the brain. The peripheral neurons also allow the brain to control many processes throughout the body, such as movement, digestion, heart rate and sexual response. Damage to the peripheral neurons resulting from peripheral neuropathy can cause sexual side effects in both men and women. 

Damage to Nerves Controlling the Sex Organs

The sexual organs in both men and women are connected to the brain by peripheral neurons. Sexual arousal occurs when the brain registers an excitatory signal and transmits that signal to the sex organs, explains the Boston University School of Medicine. When the sexual organs receive the excitatory signal, neurotransmitters are released that increase blood flow to the sex organs, causing erections in men and labial, vaginal and clitoral engorgement in women, in addition to stimulation of vaginal secretions. If the nerves that connect to the sex organs become damaged, these signals required for sexual arousal cannot reach the sex organs. 

Sexual Side Effects in Men

In men affected by peripheral neuropathy, the neurons that connect the penis to the brain may become damaged. As a result, when the brain experiences sexually stimulating input, it cannot transmit that signal to the penis. An erection results from signals reaching the penis that cause its smooth muscles to relax and allow in increased blood flow. Without the signals from the brain, blood flow to the penis cannot be increased, and there is no erection. However, sex drive in men with peripheral neuropathy may remain unchanged. Alternatively, men with peripheral neuropathy may be able to achieve an erection, but they may experience sexual climax without normal ejaculation. 

Sexual Side Effects in Women

Similar to men, women require signal transmission through peripheral neurons between the brain and the sex organs to induce the sexual response. When the brain receives a sexually stimulating signal, that signal is transmitted to the vagina. Similar to men, the signal induces the smooth muscles surrounding the vagina to relax and increase blood flow to the vagina, clitoris and labia. In addition to causing engorgement of these organs, the increased blood flow also stimulates vaginal secretions that lubricate the vagina. Women with peripheral neuropathy may not experience physical sexual arousal, leading to vaginal dryness. Women with damage to the peripheral nerves may also have difficulty achieving orgasm.

Friday, 13 October 2017

Fluoroquinolone Antibiotics: A Serious Threat To Your Nerves

Today's post from (see link below) returns to an old 'chestnut' here on the blog and that is fluoroquinolone antibiotics, which are a common form of antibiotics that need to be taken with the greatest care, especially if you have, or are prone to, nerve damage. The evidence is so overwhelming that these drugs have invidious side-effects that despite an FDA warning on every box, they remain one of the most commonly prescribed antibiotics across the world. You can only conclude that the drug companies producing them have extremely powerful lobbyists in their retail teams. However, saying all this is easy...just why are they so dangerous? This article attempts to explain objectively why they need to be the prescribed antibiotic when all else has failed and even then with monitoring and caution. For recognition purposes, common fluoroquinolones are: Levofloxacin‎:(Levaquin) Ciprofloxacin‎: (Cipro)Moxifloxacinand other antibiotics ending in '...oxacin'. Please talk seriously to your doctor if he or she proposes administering these drugs.

A prescription for fluoroquinolones: Cure-all or curse? 
By Michael Raj and Dr. Janice Mann October 2017

Most of us, at some point in our lives, have been prescribed an antibiotic to treat an infection. And we’re lucky to have medications so readily available to treat infections that just a few generations ago were often fatal. But like most things in our modern lives, when it comes to antibiotics, we want them to act fast and be easy to take so we can get back to our busy routines. In fact, for antibiotics, we may think “the quicker, the stronger, the better” to cure what ails us, but there may be something amiss with that logic.

There are many different classes of antibiotics used to treat different types of bacterial infections. One class, called fluoroquinolones, is able to successfully treat a wide variety of infections and includes ciprofloxacin, moxifloxacin, levofloxacin, norfloxacin, and ofloxacin. They are often prescribed in Canada to treat urinary tract infections (also sometimes called bladder infections or UTIs) as well as to treat common respiratory infections like bronchitis or sinusitis. Fluoroquinolones are generally easy to take — requiring less frequent dosing than some other antibiotics — and they work well to clear these infections, making them a popular choice for health care providers. In fact, prescribing of this drug class increases each year.

But because a drug is easy to take and works well to treat an infection doesn’t always mean it’s the best choice. It’s also important to consider any potential harms that could result from taking the medication. And when it comes to fluoroquinolones, the list of possible side effects is lengthy, with a recent safety review by Health Canada finding that some of the side effects can even lead to disability long after the medication is finished. Side effects of fluoroquinolones can include tendonitis (inflammation of the tendons that join muscle to bone) or rupture of a tendon (a partial or complete tear of a tendon); effects on the nerves of the body, leading to symptoms such as chronic pain, anxiety, dizziness and confusion; an overly sensitive immune system; phototoxicity (a sunburn like reaction of the skin in response to light); and abnormal heart rhythms. These side effects can occur within hours to weeks after taking a fluoroquinolone and in rare cases may be permanent. Those most at risk appear to be children under the age of 18, adults over 60, and pregnant and nursing women.

So with these risks, and with other antibiotics available, why are fluoroquinolones still so widely used? To better understand this issue, CADTH — an independent agency that finds, assesses, and summarizes the research on drugs, medical devices, tests, and procedures — recently conducted a review to understand and explain the experiences and decision-making processes around the prescribing of antibiotics for specific types of infections. CADTH carefully searched the medical literature, reviewed clinical practice guidelines, and conducted a survey of primary care practitioners, including family physicians, nurse practitioners, and pharmacists.

The review found that, in general, healthcare providers are aware of the risks posed by fluoroquinolones and the need to carefully balance the potential benefits of the medication with those risks. Family physicians, nurse practitioners, and pharmacists all voiced concern that fluoroquinolones may be over-prescribed and not always the appropriate choice. However, there are some factors that make it more likely for prescribers to choose fluoroquinolones — and patients saying that they are allergic to other antibiotics is an important one. Unfortunately, patients who believe they are allergic to other antibiotics often are not, and instead have experienced side effects of the medication that are normal, albeit unpleasant, such as an upset stomach. Determining whether a patient is truly allergic to other antibiotics can be a difficult and time-consuming task for health care providers, which makes fluoroquinolones seem like an attractive option for these patients. Another key reason for prescribing fluoroquinolones is the awareness of how effective they are in treating a wide variety of bacterial infections and uncertainty about whether the infection they are treating is resistant to other antibiotics. Along the same lines, fluoroquinolones are also chosen when other treatment options have already been tried. Health care providers may also opt for fluoroquinolones if they are concerned that a patient may not be able to successfully take an antibiotic that requires a more demanding schedule (that needs to be taken more often each day and for a longer period of time).

What do the findings of the CADTH review mean for patients, their health care providers and the Canadian health system?

As a patient, it’s important to be aware of the risks and benefits of taking fluoroquinolones if you have an infection and to discuss these with your health care provider. Knowing the difference between side effects and a true allergy to a particular antibiotic is important and can help ensure you’re receiving the antibiotic prescription that is best for you. Ask your health care provider for more information on this important issue. If you are taking a fluoroquinolone and experience any side effects, or if you have taken fluoroquinolones in the past and think you may be experiencing any long-term side effects of the medication, let your health care provider know.

Knowing the factors that may influence fluoroquinolone prescribing can help health care providers and the health care system address them. Health Canada has already reviewed the safety of fluoroquinolones, and is now recommending that the safety information for all fluoroquinolone products be updated and is working with manufacturers to do so. Evidence shows that policy changes, tailored education, and sharing information can all be effective in positively influencing antibiotic prescribing. Strategies to increase awareness of local antibiotic resistance patterns and of local, national, and international clinical practice guidelines may also help support optimal prescribing decisions.

Fluoroquinolones remain an important option for effectively treating some bacterial infections. But taking into consideration all of the important information and evidence before prescribing them will help ensure that we maximize the benefits of this medication while minimizing the risks.

For more information on CADTH and the review of FQ prescribing, visit, follow us on Twitter @CADTH_ACMTS, or contact a CADTH Liaison Officer in your region.

Michael Raj, BSc MHA is a consultant for CADTH’s Knowledge Mobilization and Liaison Program, and, Dr. Janice Mann BSc MD is a Knowledge Mobilization Officer at CADTH.

Thursday, 12 October 2017

What You're Not Often Told About Your Chronic Pain Disease!

Today's post from (see link below) really lays into doctors for what they don't tell us about chronic pain diseases like neuropathy. It's true, all of it but it's also a bit harsh on doctors, who are under time and money pressures to deliver results. The question is - when do they have the time to tell us all these things? However, it's true that many patients generally leave with their diagnoses and prescriptions and have to pretty much get on with it. There is however, a case to be made for patients taking some personal responsibility to ask the right questions and furthermore, do their own research. There's never been as much information on the internet than there is now. Not all of it is valid and it's wise to check a few trusted sites for confirmation but it's there and can save a lot of time - knowledge is most definitely power when it comes to neuropathy for instance. That all said, the points below are very valid and somewhat shocking. That's why it's more important than ever to forge relationships with our medical providers - share the burden a bit so to speak. Our treatment needs to be a balance between medical care and bedside manner - how we achieve that with the doctors is the dilemma we all face. An interesting article and yet another list (which people seem to love) but certainly worth a read.

24 Things Doctors Don’t Tell People About Chronic Pain
July 1, 2017 admin

When the average person gets sick or injured, they often go to the doctor, expecting to be diagnosed, treated and cured within a matter of days or weeks. Doctors are supposed to be the experts – the people you can trust and turn to for answers and relief from symptoms of Chronic Pain.

Unfortunately, this is not always the case when it comes to chronic pain. As with any chronic condition, there are no simple answers or one-size-fits-all treatments. The reality is that there simply isn’t enough research or knowledge of chronic pain conditions available yet, so many doctors are unable to effectively treat or prepare patients for a life with pain.

We asked our Mighty community to share what doctors didn’t tell them about chronic pain. It is difficult to understand how illness or pain can affect every aspect of an individual’s life unless you have experienced it yourself, but hopefully the following will help shed some light on what a patient might be able to expect after receiving a chronic pain diagnosis.

1. “Doctors don’t tell you that chronic pain is not only physical! It causes a lot of mental and emotional turmoil as well, especially when the physical pain greatly affects your quality [of life] and keeps you from being able to do the things you want to.”

2. “My doctors never told me to forgive my body for no longer being able to do what it used to, to never compare myself to non-chronic pain people.”

3. “I think mostly they don’t validate how severe your pain is and how much it impacts your day-to-day living.”

4. “Exercise only works for some people. It’s not a cure-all.”

5. “They often won’t tell you [if] they have no idea how to treat you – even when you have a valid and medically recognized diagnosis, and they won’t tell you they have no intention of learning about your condition or helping you seek out a doctor who does know. They also don’t tell you that your condition [could] bankrupt you financially, no matter what kind of insurance you have, and that your care might be vastly better if you were living in a different state or country.”

6. “Doctors can sometimes make you feel like it’s just one piece of your life and that your relationships and your job, your dreams and goals should be relatively unaffected. That is never true of a chronic health problem.”

7. “Doctors don’t tell you that chronic pain is possible in your early 20s and that it will be lifelong. They [might] tell you it’s ‘in your head.’”

8. “It’s OK to refuse to take medications and treatments they suggest. Sometimes the side effects of medications are worse than our symptoms and it’s ultimately our right to make the decision to continue treatment.”

9. “They usually don’t tell you about the side effects: depression, random symptoms, negative effects on your social and work life, more difficulty focusing, etc. I wish I’d had some warning.”

10. “Doctors don’t tell you that everyone is different in treatment. Some people can and do get better with certain combinations of medications and others don’t. Numbers constantly change, new medications being added or taken away, off label prescriptions. New research is always coming in and a lot of doctors don’t even know about it yet.”

11. “Doctors don’t [often] tell you [if] they reach a point where they no longer know how to help you. They have exhausted all options. Ordering more tests and trying new meds are really just trial and error.”

12. “[They don’t tell you] how isolating and lonely it is. No one understands what being in constant pain is like unless they are in constant pain. And since no one understands, they don’t know what to say or how to treat you, so they stop coming around or reaching out to you as often. The loneliness is almost worse than the pain.”

13. “They [may not] refer you to a therapist. Chronic pain causes a lot of anger and grief over the life changes that go along with it. It took me years to seek one [out] on my own.”

14. “It has nothing to do with not being active or having a proper diet. It’s not being a hypochondriac, and you shouldn’t get shamed for it. When it rains, you hurt. When it’s sunny, you hurt, too. You never know what you’re going to face with another day.”

15. “Doctors don’t tell you that the amount of energy you put into blocking out your chronic pain can also cause you to block out pain you shouldn’t, like not noticing you have a kidney infection until it’s bad enough to put you in the hospital for days.”

16. “Doctors don’t tell you that they don’t really understand what it means to be in pain all day, every day, for the rest of your life (unless they personally deal with it). I once overheard my rheumatologist explain to a health care marketer that it was difficult to treat fibromyalgia patients because they required so much empathy that it was emotionally draining.”

17. “[I didn’t know] I’d be prescribed painkillers by doctors for my chronic pain and then be treated like a drug-seeker by doctors, the media and others.”

18. “[Doctors didn’t tell me] how to tell if the pain is from my chronic condition or something more serious. I end up at urgent care a lot because I will get a ‘new’ pain and I don’t know if it is a new symptom or something more serious. I am constantly [worried] that I am going to ignore it and it ends up being life-threatening.”

19. “Nothing will ever completely ease the pain and some days nothing, not even the strongest painkiller out there, will help it at all. You [often] have to settle for any improvement and adapt your life around pain.”

20. “[Doctors didn’t tell me chronic pain] will exhaust my brain so much I’ll become horribly forgetful. That stress can make it worse (I have fibromyalgia). That any new pain you have [may] be written off as your chronic pain, even if you know it’s something different.”

21. “They don’t tell you that at some point in your journey you have to make decisions based on the lack of true medical knowledge. That you will spend your life researching every aspect of your illness and will know more about your illness than your doctor ever would.”

22. “It’s a hard thing to prove, so a lot of people will think it’s phantom pain. You have to stick to the truth and stick up for yourself through it all.”

23. “They don’t tell you that inflammatory triggers (food, drink) can make pain worse.”

24. “My doctors haven’t given me any information on chronic pain. Only recently did they stop trying to say it was ‘all in my head.’ They still try to refuse to give me painkillers. Luckily the internet has been a huge help. Finding others who are going through the same thing and listening to what they do to cope has been a huge help!”