PREGNANT WOMEN INVOLVE PARENT IN ABORTION WHEN ANTICIPATING SUPPORT

When an adolescent wants to terminate a pregnancy, how does she decide whether to talk to a parent? A recent study from the Section of Family Planning and Contraceptive Research at the University of Chicago found that pregnant teens will turn to parents and adults who are engaged in their lives and who will offer support, regardless of her pregnancy decision. Young women will avoid talking with parents who are less involved or may try to prevent them from seeking care

The study, published online ahead of print in theAmerican Journal of Public Health, explored the factors young women under age 18 consider when deciding to involve a parent. Researchers conducted interviews with 30 minors seeking abortion in Illinois, prior to implementation of the 2013 parental notification law. Currently, there are 38 states with laws requiring a parent to provide consent or receive notification before a minor can access abortion services.

"There's a commonly accepted idea that teens will try to hide their pregnancy or abortion decision. However, pregnant young women actually do turn to parents in the majority of cases," said Section policy researcher Lee Hasselbacher. "In our study, 70% of the young women involved a parent or guardian. They thought carefully about which parents and adults in their lives they could turn to for help in making their decision."

While each young woman's family circumstance was different, there were several common motivations for involving a parent. Factors favoring telling included close and supportive relationships, need for help with logistics like travel or payment, or experiences that made discovery of the pregnancy seem inevitable.

Minors expressed a range of motivations for not telling a parent about their abortion. Some teens worried that if their parent learned of their decision, it would dramatically change their relationship or feared it would even lead to anger or harm. Young women also discussed the lack of a relationship or presence as a reason they did not want to involve a parent.

One of the strongest findings was that among those young women who did not involve either parent, most were concerned that one or both parents would directly interfere with their decision to get an abortion.

"Policymakers should not force communication at the time of pregnancy; instead they should focus on supporting family communication long before a pregnancy or abortion decision," said Dr. Melissa Gilliam, Section Chief of the Section of Family Planning and Contraceptive Research at the University of Chicago and senior author on the study. "This study reveals teenagers will seek adult help."

Shaky Evidence Supporting Amitriptyline For Neuropathy

Today's post from cochrane.org (see link below) looks at the evidence supporting the use of amitriptyline as a treatment for neuropathic pain and as many other serious investigations in the past have done; has found that the drug is of very little benefit to neuropathy sufferers. Or at least, there's just not enough research and evidence to prove otherwise. Yet it is drug number one on the lists of standard treatments for nerve pain...why? It's more of a 'following the logic' sort of reasoning; you begin small and build up. Basically that predicts a trajectory ending with opiates but is of little benefit to patients. Apart from the associated side effects of taking anti-depressants, amitriptyline has not been proved to be of any significant benefit in reducing neuropathy symptoms, yet doctors routinely begin with it, in the hope that what they see as, only a very mild drug, will be enough to quell the symptoms. It's been the standard start-up drug of choice for decades; isn't it about time that the industry looked at the evidence and stopped putting us at risk from unnecessary side effects? The evidence suggests that other drugs are far better for the task but unfortunately we still have to go through the hope and ultimate failure of amitriptyline before any relief can be found by moving on to more effective treatments.
 

Amitriptyline for neuropathic pain in adults  
Published: 1 August 2015 Authors: Moore R, Derry S, Aldington D, Cole P, Wiffen PJ

Neuropathic pain is pain coming from damaged nerves, and can have a variety of different names. Some of the more common are painful diabetic neuropathy, postherpetic neuralgia, or post-stroke pain. It is different from pain messages that are carried along healthy nerves from damaged tissue (for example, a fall, or cut, or arthritic knee). Neuropathic pain is treated by different medicines to those used for pain from damaged tissue. Medicines such as paracetamol or ibuprofen are not usually effective in neuropathic pain, while medicines that are sometimes used to treat depression or epilepsy can be very effective in some people with neuropathic pain.

Amitriptyline is an antidepressant, and antidepressants are widely recommended for treating neuropathic pain. Amitriptyline is commonly used to treat neuropathic pain conditions, but an earlier review found no good quality evidence to support its use. Most studies were small, relatively old, and used methods or reported results that we now recognise as making benefits seem better than they are.

In March 2015 we performed searches to look for new studies in adults with neuropathic pain of at least moderate intensity. We found only two additional small studies that did not provide any good quality evidence for either benefit or harm. This is disappointing, but we can still make useful comments about the drug.

Amitriptyline probably does not work in neuropathic pain associated with human immunodeficiency virus (HIV) or treatments for cancer. Amitriptyline probably does work in other types of neuropathic pain, though we cannot be certain of this. Our best guess is that amitriptyline provides pain relief in about 1 in 4 (25%) more people than does placebo, and about 1 in 4 (25%) more people than placebo report having at least one adverse event, which may be troublesome, but probably not serious. We cannot trust either figure based on the information available.

The most important message is that amitriptyline probably does give really good pain relief to some people with neuropathic pain, but only a minority of them; amitriptyline will not work for most people.

Authors' conclusions:

Amitriptyline has been a first-line treatment for neuropathic pain for many years. The fact that there is no supportive unbiased evidence for a beneficial effect is disappointing, but has to be balanced against decades of successful treatment in many people with neuropathic pain. There is no good evidence of a lack of effect; rather our concern should be of overestimation of treatment effect. Amitriptyline should continue to be used as part of the treatment of neuropathic pain, but only a minority of people will achieve satisfactory pain relief. Limited information suggests that failure with one antidepressant does not mean failure with all.

Background:

This is an updated version of the original Cochrane review published in Issue 12, 2012. That review considered both fibromyalgia and neuropathic pain, but the effects of amitriptyline for fibromyalgia are now dealt with in a separate review.

Amitriptyline is a tricyclic antidepressant that is widely used to treat chronic neuropathic pain (pain due to nerve damage). It is recommended as a first line treatment in many guidelines. Neuropathic pain can be treated with antidepressant drugs in doses below those at which the drugs act as antidepressants.

Objectives:

To assess the analgesic efficacy of amitriptyline for relief of chronic neuropathic pain, and the adverse events associated with its use in clinical trials.

Search strategy:

We searched CENTRAL, MEDLINE, and EMBASE to March 2015, together with two clinical trial registries, and the reference lists of retrieved papers, previous systematic reviews, and other reviews; we also used our own hand searched database for older studies.

Selection criteria:

We included randomised, double-blind studies of at least four weeks' duration comparing amitriptyline with placebo or another active treatment in chronic neuropathic pain conditions.

Data collection and analysis:

We performed analysis using three tiers of evidence. First tier evidence derived from data meeting current best standards and subject to minimal risk of bias (outcome equivalent to substantial pain intensity reduction, intention-to-treat analysis without imputation for dropouts; at least 200 participants in the comparison, 8 to 12 weeks' duration, parallel design), second tier from data that failed to meet one or more of these criteria and were considered at some risk of bias but with adequate numbers in the comparison, and third tier from data involving small numbers of participants that were considered very likely to be biased or used outcomes of limited clinical utility, or both.

Main results:

We included 15 studies from the earlier review and two new studies (17 studies, 1342 participants) in seven neuropathic pain conditions. Eight cross-over studies with 302 participants had a median of 36 participants, and nine parallel group studies with 1040 participants had a median of 84 participants. Study quality was modest, though most studies were at high risk of bias due to small size.

There was no first-tier or second-tier evidence for amitriptyline in treating any neuropathic pain condition. Only third-tier evidence was available. For only two of seven studies reporting useful efficacy data was amitriptyline significantly better than placebo (very low quality evidence).

More participants experienced at least one adverse event; 55% of participants taking amitriptyline and 36% taking placebo. The risk ratio (RR) was 1.5 (95% confidence interval (CI) 1.3 to 1.8) and the number needed to treat for an additional harmful outcome was 5.2 (3.6 to 9.1) (low quality evidence). Serious adverse events were rare. Adverse event and all-cause withdrawals were not different, but were rarely reported (very low quality evidence).


http://www.cochrane.org/CD008242/SYMPT_amitriptyline-neuropathic-pain-adults

Full Flower Moon The Little Things Self Care

May is in full flower.

The lilacs are in honey. The honeysuckle's in oil, the dandelion infusion is done. The violets have dried on my work island into tiny little curly blue jewels.

The nettles are getting taller, and the cleavers is celebrating. Celandine spots the roads with yellow, and apple blossoms are everywhere. The Lady's Slipper orchids have begun. The black cherry tree flowers are minutes away from opening. Everything is humming with life.

It's been a busy time for me, but not too busy. I am finding a good rhythm lately and am so grateful for the warmer weather, singing frogs, and time in nature. Things will shift again soon as my kids are almost finished with programming and will launch into summertime spontaneity and short burst camps and such. I can't wait to get myself into the river water.

I'm finding rooting in my not-as-new location (now here 2 1/2 years.) I see people I know at the market, I don't get lost (as often), and I'm finding a sense of belonging and community that I hope will grow and deepen.

The cycles of my plant allies are reliable sources of  daily replenishment, of course. This week I'm putting together my Lady's Slipper Ring membership herbals and they are full of flowers and nectar and the healing that bubbles in our spirit when we experience beauty.

My first Aromatic Muse perfume (FloraLuna) departed to their first new Queens already. I'm incredibly inspired by this journey and have begun concocting something unique for June, while soaking up the glamorous FloraLuna in the meantime. It is so.... womanly. mm

Taking care of ourselves is so important, and having beautiful, earthly, sensory conduits for self-care catalyzes cell-response, sensory pleasure responses, immune system functions, positive memories associated with self-love, and creates a biological connection to feeling good without attachment to collateral. Self care first - then achievement becomes enabled. Although I teach this, I am still a student in daily practice. I must be deliberate and devoted to moments of time carved out for my health and well being.

Here are some snapshots of my pleasure medicine as of late .... 

what beauty and pleasure restores you?

IMPACT OF VIOLENT MEDIA ON THE BRAIN DEPENDS ON EACH INDIVIDUALS BRAIN CIRCUITRY

With the longstanding debate over whether violent movies cause real world violence as a backstop, a study published in PLOS One found that each person's reaction to violent images depends on that individual's brain circuitry, and on how aggressive they were to begin with.

The study, which was led by researchers at the Icahn School of Medicine at Mount Sinai and the NIH Intramural Program, featured brain scans which revealed that both watching and not watching violent images caused different brain activity in people with different aggression levels. The findings may have implications for intervention programs that seek to reduce aggressive behavior starting in childhood.

"Our aim was to investigate what is going on in the brains of people when they watch violent movies," said lead investigator Nelly Alia-Klein, PhD, Associate Professor of Neuroscience and Psychiatry at the Friedman Brain Institute and Icahn School of Medicine at Mount Sinai. "We hypothesized that if people have aggressive traits to begin with, they will process violent media in a very different way as compared to non-aggressive people, a theory supported by these findings."

After answering a questionnaire, a group of 54 men were split by the research team into two groups -- one with individuals possessing aggressive traits, including a history of physical assault, and a second group without these tendencies. The participants' brains were then scanned as they watched a succession of violent scenes (shootings and street fights) on day one, emotional, but non-violent scenes (people interacting during a natural disaster) on day two, and nothing on day three.

The scans measured the subjects' brain metabolic activity, a marker of brain function. Participants also had their blood pressure taken every 5 minutes, and were asked how they were feeling at 15 minute intervals.

Investigators discovered that during mind wandering, when no movies were presented, the participants with aggressive traits had unusually high brain activity in a network of regions that are known to be active when not doing anything in particular. This suggests that participants with aggressive traits have a different brain function map than non-aggressive participants, researchers said.

Interestingly, while watching scenes from violent movies, the aggressive group had less brain activity than the non-aggressive group in the orbitofrontal cortex, a brain region associated by past studies with emotion-related decision making and self-control. The aggressive subjects described feeling more inspired and determined and less upset or nervous than non-aggressive participants when watching violent (day 1) versus just emotional (day 2) media. In line with these responses, while watching the violent media, aggressive participants' blood pressure went down progressively with time while the non-aggressive participants experienced a rise in blood pressure.

"How an individual responds to their environment depends on the brain of the beholder," said Dr. Alia-Klein. "Aggression is a trait that develops together with the nervous system over time starting from childhood; patterns of behavior become solidified and the nervous system prepares to continue the behavior patterns into adulthood when they become increasingly coached in personality. This could be at the root of the differences in people who are aggressive and not aggressive, and how media motivates them to do certain things. Hopefully these results will give educators an opportunity to identify children with aggressive traits and teach them to be more aware of how aggressive material activates them specifically."

Spinal Electro Stimulation For Neuropathy

Today's short article from poz.com discusses a recent small trial of electrical spinal stimulation procedures to help severe neuropathic symptoms. It is an operative procedure wherein permanent electrodes are inserted into a segment of the spine. It sounds slightly scary and is a relatively new method for neuropathy but is a well-established technique used for treating other conditions. You do wonder if it's a one size fits all approach or if it is only effective for specific forms of nerve damage. More information and larger trials are sure to follow but it sounds promising. It may be worth discussing the possibility of joining a trial, with your doctor or neurologist, especially if you haven't had any success with the medications. However, there may be cost issues, or plain lack of knowledge to deal with.

Spinal Cord Stimulation Shows Potential for Peripheral Neuropathy
February 7, 2012

Electrical stimulation of the spinal cord markedly reduced peripheral neuropathy (PN)–associated pain in a man living with HIV who didn’t respond to more conventional PN therapies, according to a February 5 presentation at the 6th World Congress of the World Institute of Pain in Miami and reported by Medscape.

Data involving another five patients enrolled in the study, being conducted by Kenneth Candido, MD, of the Advocate Illinois Masonic Medical Center in Chicago and his colleagues, are awaited, but the researchers are encouraged by the results they’ve seen thus far. “We believe that it is not only a new indication, but it offers relief for individuals who were previously left to the devices of primary care physicians who really only have at their disposal the ability to prescribe narcotic analgesics,” Candido said.

Treatment initially involved temporary placement of two leads, each containing eight electrodes, into a segment of the spine. Once the electric stimulation proved safe and effective, permanent electrodes were placed by the study investigators.

The study volunteer highlighted by Candido’s group at the Miami conference was a 50-year-old man who had been living with HIV for 20 years and had an eight-year history of “excruciating” neuropathic pain and burning sensations, notably on the soles of his feet. He had not responded to other available neuropathy treatments, such as narcotic and non-narcotic pain relievers, anti-seizure drugs and nerve blocks.

The results thus far have been encouraging, Candido told Medscape. “He has now had almost two years of reduction in his pain, from a constant level of about 8 out of 10 down to about 1 or 2 out of 10, and we’ve been able to wean him off his [narcotic pain relievers],” he said.

Spinal cord stimulation is a well-established technique currently indicated for the management of failed back surgery syndrome, complex regional pain syndrome, inoperable peripheral vascular disease, and refractory angina pectoris.

http://www.poz.com/articles/hiv_spinal_neuropathy_761_21869.shtml

MODIFIED VITAMIN D SHOW PROMISE AS TREATMENT FOR PANCREATIC CANCER

A synthetic derivative of vitamin D was found by Salk Institute researchers to collapse the barrier of cells shielding pancreatic tumors, making this seemingly impenetrable cancer much more susceptible to therapeutic drugs.

The discovery has led to human trials for pancreatic cancer, even in advance of its publication today in the journal Cell. By attacking a wound repair mechanism called fibrosis, the findings may also have implications for other tough-to-treat tumors, such as lung, kidney and liver cancer.

"While the success of this drug in humans with pancreatic cancer is still unclear, the findings in animal studies were strong, raising hope that ongoing clinical trials will give people with this terrible disease hope for a truly new type of therapy," says Ronald Evans, director of Salk's Gene Expression Laboratory and senior author of the new paper.

Pancreatic cancer is one of the deadliest forms of cancer, a fact highlighted in recent years by the deaths of well-known figures such as Steve Jobs and Patrick Swayze. About 46,000 people are diagnosed in the United States each year and about 40,000 people die from the disease, according to the National Institutes of Health.

"For pancreatic cancer, the five-year survival rate is the lowest of all cancers," says Evans, holder of Salk's March of Dimes Chair and a Howard Hughes Medical Institute investigator. "Part of the problem is that the science of pancreatic cancer and its renowned resistance to therapy has not been understood and that's why the work that we're doing is so important."

Evans and his colleagues knew that the ability of the pancreatic tumor to communicate with nearby cells -- called the tumor microenvironment -- is key to its growth. Tumor cells send out signals that make the microenvironment inflamed and dense; this "living shield" around a tumor not only helps the cancer grow, but blocks the access of immune cells and chemotherapeutic drugs, making the cancer particularly hard to treat.

Evans -- in collaboration with researchers around the country involved in an interdisciplinary initiative supported by Stand Up to Cancer -- wanted to figure out how to restore this inflamed microenvironment to its normal or "quiescent" state and weaken the wall around the tumor.

"There was evidence that the activation of the microenvironment was theoretically reversible, but nobody knew exactly what was responsible for the activation, making it hard to turn off," says Salk postdoctoral research fellow Mara Sherman, first author of the new paper.

Sherman, Evans and their collaborators focused their attention on one component of this wall: pancreatic stellate cells, which usually respond to small injuries by briefly switching to an activated state, spurring new cell growth. In the case of cancer, however, the stellate cells near a tumor -- in response to signals from the tumor -- are constantly turned on. This chronic activation of the stellate cells provides the tumor cells with extra growth factors and therefore helps them proliferate, but also forms a wall-like barrier around the tumor that protects it from chemotherapeutics and other cancer-fighting drugs.

In 2013, Evans' group discovered that stellate cells in the liver could be inactivated by a chemically modified form of vitamin D. They wondered whether the same could hold true in the pancreas, despite the fact the vitamin D receptor was not thought to be present in pancreatic tissue.

But indeed, when the group of researchers examined the differences between activated and inactivated stellate cells in the pancreas, they found that activated stellate cells near a tumor had high levels of the vitamin D receptor. And when the researchers then added modified vitamin D to activated stellate cells the cells quickly reverted back to a healthy, inactivated state, stopping production of signals that spur growth and inflammation.

"This was a big surprise because vitamin D has been tried multiple times as a therapy for pancreatic cancer and never worked," says Evans.

It turns out that activated stellate cells rapidly break down normal vitamin D, preventing the vitamin from binding to the receptor, Evans explains. But systematic analysis of vitamin D analogues allowed the team to discover a modified form of vitamin D that is more stable, resilient and effective in vitro.

To see whether this new vitamin D-like compound could halt the growth of a tumor, Evans and the team next studied its effectiveness in mice. The researchers found that combining the drug with existing chemotherapeutics gave a 50 percent increase in lifespan compared to chemotherapy alone.

"It's really remarkable considering that vitamin D itself is not attacking the cancer cells," says Michael Downes, a senior staff scientist at Salk and co-corresponding author of the new work. "It's changing the environment to a more favorable setting needed for the chemotherapy drugs to work."

Studies have shown that people deficient in vitamin D are more likely to develop pancreatic cancer. Based on the new results, Evans thinks that healthy levels of vitamin D may help keep vitamin D receptor signaling in stellate cells normal and squash a cancer's growth -- at least until a tumor itself forces the stellate cells to "turn on."

"Recently, other research groups have explored the idea of destroying the microenvironment altogether to weaken a tumor," says Downes. "Our approach is very different. Instead of destroying, we simply want to reprogram the tumor microenvironment to a healthy state. This has the dual effects of delivering more drugs to the tumor as well as replenishing the tissue with normal stellate cells."

Evans group has already teamed up with clinicians at the University of Pennsylvania to launch a clinical trial testing the effectiveness of using their vitamin D-like drug in cancer patients before pancreatic surgery. "Previous trials with vitamin D failed because they didn't understand the need for a special form of vitamin D and that for pancreatic cancer it must be used in combination with chemotoxic drugs," Evans says. "So, by re-thinking the problem, have been able to open up a new route to the treatment of pancreatic cancer and, looking forward, hopefully other diseases as well."

Inflammation And Neuropathy

Today's post from glendaleneuropathydoctor.com (see link below) looks at the role inflammation plays with neuropathy. Although it uses the example of post-injury inflammation; inflammation affecting various organs of the body can cause or make your neuropathy worse. HIV patients may wonder how this is relevant to them but tests have shown that even if your immune system (T4-Cells) is healthy, HIV can bring about unseen inflammation in your major organs. See more information here. The point is that inflammation can be treated in various ways and by doing that may reduce the need for stronger pain killers, or other drugs used to treat neuropathy. Treating the cause rather than the symptoms (which most often happens with neuropathy) should always be the preferred way and inflammation can be treated once identified.

Inflammation: The Role Of Inflammation in Peripheral Neuropathy
February 12, 2013

An article published in 2011 in the prestigious Regional Anesthesia and Pain Medicine Journal points out an important, yet often overlooked, aspect of peripheral neuropathy.

In the article they follow the case of a young boy who develops neuropathy after undergoing hip surgery.

Usually neuropathy that develops after surgery is attributed to things like anesthesia toxicity, mechanical trauma, or ischemic nerve damage.

In this case study the doctors ruled out all of these causes but the boys neuropathy continued to progress.

Why Is This Important?

A thorough neurological evaluation was performed and he was diagnosed with post-surgical inflammatory neuropathy.

This is important because we know that inflammation is an important component of neuropathy. In fact there is usually an inflammation component in most of the cases of neuropathy we treat in our office.

The problem is most neuropathy patients have never had a doctor that has really investigated and treated the inflammation.

In the case study presented in the journal article the cause of the inflammation was apparent, it was caused by surgery.

But in other neuropathy patients the inflammation can be secondary to diabetes, chemotherapy, food sensitivities … and a number of other causes. In other words the source of the inflammation is not always obvious and is therefore commonly overlooked.

The important thing is to know that inflammation is an important component of neuropathy and make sure that the initial evaluation includes an investigation of various inflammation sources.

Once inflammation is ruled in as a contributing factor we must then provide treatments that can help lower the inflammation.

This type of approach deals with root causes and ensures that a long lasting reduction in symptoms can occur.

Source:

Reg Anesth Pain Med. 2011 Jul-Aug;36(4):403-5. doi: 10.1097/AAP.0b013e31821e6503

http://glendaleneuropathydoctor.com/neuropathy-inflammation/

The Right Insoles For Neuropathic Feet

Today's post comes from jfootankleres.com (see link below) and looks at a specific problem for people trying to find the best sorts of footware to support feet with neuropathy (especially those prone to foot ulcers). Many people pay for expensive custom-made insoles but the trial described here comes to the conclusion that there's little to no difference with ordinary shop-bought insoles. It may mean trying on every shoe in the shop and then trying out various insoles to give further support but if you have neuropathic foot problems, you know it's worth taking the greatest care of your feet.

A comparison of customised and prefabricated insoles to reduce risk factors for neuropathic diabetic foot ulceration:
a participant-blinded randomised controlled trial
Joanne S Paton, Elizabeth A Stenhouse, Graham Bruce, Daniel Zahra and Ray B Jones
Journal of Foot and Ankle Research 2012, Published: 5 December 2012

Abstract (provisional)
Background
Neuropathic diabetic foot ulceration may be prevented if the mechanical stress transmitted to the plantar tissues is reduced. Insole therapy is one practical method commonly used to reduce plantar loads and ulceration risk. The type of insole best suited to achieve this is unknown. This trial compared custom-made functional insoles with prefabricated insoles to reduce risk factors for ulceration of neuropathic diabetic feet.
Method
A participant-blinded randomised controlled trial recruited 119 neuropathic participants with diabetes who were randomly allocated to custom-made functional or prefabricated insoles. Data were collected at issue and six month follow-up using the F-scan in-shoe pressure measurement system. Primary outcomes were: peak pressure, forefoot pressure time integral, total contact area, forefoot rate of load, duration of load as a percentage of stance. Secondary outcomes were patient perceived foot health (Bristol Foot Score), quality of life (Audit of Diabetes Dependent Quality of Life). We also assessed cost of supply and fitting. Analysis was by intention-to-treat.
Results
There were no differences between insoles in peak pressure, or three of the other four kinetic measures. The custom-made functional insole was slightly more effective than the prefabricated insole in reducing forefoot pressure time integral at issue (27% vs. 22%), remained more effective at six month follow-up (30% vs. 24%, p=0.001), but was more expensive (UK 6.56 pounds vs. 5.54 pounds, p=less than 0.001). Full compliance (minimum wear 7 hours a day 7 days per week) was reported by 40% of participants and 76% of participants reported a minimum wear of 5 hours a day 5 days per week. There was no difference in patient perception between insoles.

ConclusionThe custom-made insoles are more expensive than prefabricated insoles evaluated in this trial and no better in reducing peak pressure. We recommend that where clinically appropriate, the more cost effective prefabricated insole should be considered for use by patients with diabetes and neuropathy.

Trial registration
Clinical trials.gov (NCT00999635). Note: this trial was registered on completion.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

http://www.jfootankleres.com/content/5/1/31/abstract

Just Saying That Exercise Helps Neuropathy Doesnt Necessarily Make It So

Today's post from nursing.onclive.com (see link below) again promotes exercise as a way of reducing neuropathy symptoms but in this case, the evidence seems a little thin. By testing a group of cancer patients with neuropathy as a side effect, they found that walking and other general exercise prevented the symptoms from worsening, especially in older patients. I would suggest that moderate exercise will help older patients feel generally better anyway than sitting or lying for long periods of time but they'll need to provide much more specific evidence to prove that neuropathic symptoms can be reduced by a graduated walking course. In this case, I would suggest that with this sort of patient, there are far too many variables to come to the conclusion that exercise is more effective in reducing or limiting nerve damage symptoms in older people. That said, there is a general consensus among doctors that regular exercise will improve neuropathy, or at least stop it getting worse but in this case, I feel too much is being assumed from too little data.

Walking and Resistance Training Eases CIPN, Especially Among Older Patients
LAUREN M. GREEN @OncNurseEditor Wednesday, July 20, 2016

Patients undergoing chemotherapy prescribed a formal exercise program experienced less chemotherapy-induced peripheral neuropathy (CIPN), and the finding held true across all chemotherapy regimens tested. The effect was strongest in older patients, according to findings from a nationwide randomized controlled trial reported at the 2016 ASCO Annual Meeting.

CIPN is a highly prevalent and severe side effect of certain chemotherapy types, such as platinums, taxanes, and vinca alkaloids, affecting more than 50% of patients receiving these therapies. Nevertheless, “there are currently no established treatments for CIPN—despite 50 randomized clinical trials—testing the efficacy of drugs to prevent or treat it,” explained lead study author Ian Kleckner, PhD.

Kleckner, a research assistant professor at the University of Rochester Medical Center, and colleagues performed a secondary analysis of a subset of 314 sedentary patients receiving taxane-, vinca alkaloid-, or platinum-based chemotherapy derived from a larger, phase III, national, randomized controlled trial (N = 619).

The majority of patients were women (92%), and 78% had breast cancer. They were randomized to chemotherapy alone or chemotherapy plus exercise. Patients randomized to the EXCAP arm (Exercise for Cancer Patients) which is a personalized, 6-week, home-based, moderate-intensity progressive program, were prescribed a daily walking regimen (eg, steps per day), supplied with pedometers, and also given a set of resistance bands to perform specific exercises.

Walking and resistance exercises were recommended for the control group. They did not receive any formalized support; however, control participants were given the exercise kit at the end of the study.

The investigators used patient self-report of tingling and numbness at baseline and after the intervention, rated on a 0-10 scale with 10 being the worst level of CIPN. In the EXCAP arm, CIPN was reduced compared with controls, with an effect size of 0.26 (P = .06), and the finding was independent of other variables, such as gender, BMI, and cancer stage. However, age was a moderating variable.

“We found that exercise was more effective for older patients,” said Kleckner. “Older patients in the control arm experienced a large increase in CIPN after 6 weeks of chemotherapy, whereas older patients in the experimental exercise arm had a very small, if any, increase in CIPN.”

Kleckner said that based on these findings, he and colleagues hope to expand their research. “What we’d like to do now is design a randomized clinical trial testing exercise against chemotherapy alone, where CIPN is the primary outcome. Only one trial to date has looked at this, and it was very small—60 patients.”

He hopes researchers can identify biomarkers in the brain circuitry or signals of the role inflammation may play to help better identify who is most at risk for CIPN.

Over the next few years, Kleckner would like to see this research continue to “scale up, so we can better learn about the effectiveness of exercise, understand what dose/intensity of exercise is important, what type of exercise, and who responds best to exercise … we’re hoping for an exercise prescription, instead of the generic ‘please exercise.’”

Kleckner I, Kamen CS, Peppone LJ, et al. A URCC NCORP nationwide randomized controlled trial investigating the effect of exercise on chemotherapy-induced peripheral neuropathy in 314 cancer patients. J Clin Oncol. 2016; 34 (suppl; abstr 10000).

http://nursing.onclive.com/web-exclusives/walking-and-resistance-training-eases-cipn-especially-among-older-patients

Spinal Manipulation For Chronic Pain

Today's post from sciencedaily.com (see link below) looks at spinal manipulative therapy (SMT) as a means of reducing chronic pain in the back. central spinal sensitization is also a factor in peripheral neuropathic problems and SMT may also be able to play a role in lessening neuropathic pain too. The post is generally aimed at low back pain sufferers but it's an interesting read for all those living with chronic pain.

Spinal manipulative therapy reduces central pain sensitization 
Date:
February 25, 2014
Source:
American Pain Society

The lessening of pain sensitivity achieved with spinal manipulation therapy (SMT) occurs as a result of the treatment and not as much from a placebo effect caused by the expectation of receiving SMT. Chronic low back pain is associated with altered pain processing, suggesting a mechanism related to central sensitization of pain. Central sensitization is considered a factor in the progression of acute pain to chronic pain and in the maintenance of chronic pain.

The lessening of pain sensitivity achieved with spinal manipulation therapy (SMT) occurs as a result of the treatment and not as much from a placebo effect caused by the expectation of receiving SMT, according to a study published in The Journal of Pain.

Spinal manipulative therapy has been shown to reduce the severity of low back pain in some patients. Improved understanding of its pain-relieving mechanisms could enhance clinical effectiveness.

Chronic low back pain is associated with altered pain processing, suggesting a mechanism related to central sensitization of pain. Central sensitization is considered a factor in the progression of acute pain to chronic pain and in the maintenance of chronic pain.

Researchers from the University of Florida investigated whether lessening of pain sensitivity attributed to SMT is specific to the procedure itself or occurs as a placebo effect from treatment expectation. Studies have shown that placebo is associated with robust analgesia produced by anticipation of pain relief.

Subjects for the study had low back pain and were recruited from the University of Florida campus. Participants underwent baseline pressure and thermal pain testing and were randomly assigned to SMT, placebo SMT, enhanced placebo SMT (same as placebo SMT except subjects were informed they would get SMT or a placebo intervention) or no intervention. The 110 study subjects had repeat mechanical and thermal pain sensitivity testing to measure immediate, within session, change in pain sensitivity.

Results showed that significantly more participants receiving the enhanced placebo SMT indicated good to excellent outcomes than those receiving standard placebo SMT or no treatment. A significant difference was not found between subjects receiving SMT and the enhanced placebo.

The authors concluded their findings reveal a mechanism of SMT unrelated to the expectation of receiving SMT, but from modulation of dorsal horn excitability and lessening of central sensitization. This suggests potential for SMT to be a clinically beneficial intervention.

Story Source:

The above story is based on materials provided by American Pain Society. Note: Materials may be edited for content and length.

Journal Reference:
Joel E. Bialosky, Steven Z. George, Maggie E. Horn, Donald D. Price, Roland Staud, Michael E. Robinson. Spinal Manipulative Therapy–Specific Changes in Pain Sensitivity in Individuals With Low Back Pain (NCT01168999). The Journal of Pain, 2014; 15 (2): 136 DOI: 10.1016/j.jpain.2013.10.005
 
http://www.sciencedaily.com/releases/2014/02/140225122220.htm

Treatment for sciatica pain in the leg

Treatment for sciatica pain in the leg is the trend of today's popular content, we all know in the evaluation from the internet search engine so they can present reputable knowledge we tend to make an effort to look for imagery based on a Treatment for sciatica pain in the leg . and the results you can see below you should be aware many of the photographs can be a powerful example.

Some images on Treatment for sciatica pain in the leg

Treatment for sciatica pain in the leg - it has long been circulated aided by the expectation of which you may invigorate expected to any one. The next few paragraphs might offer for a a blueprint remember when you are mystified to choose the best suited lead This Treatment for sciatica pain in the leg content articles may just be your own preference that they are put on to the repair system, considering that it comes with its own arrange should look and feel a great deal more completely satisfied Treatment for sciatica pain in the leg - Handy available for you subsequently we tend to making the effort see a reliable form which inturn will help uou find inspiration without confusion. do not forget to bookmark this page, as its possible in the future you have to pick the software lower back since the inspirational tips.

STRATEGIC OR RANDOM HOW THE BRAIN CHOOSES

Many of the choices we make are informed by experiences we've had in the past. But occasionally we're better off abandoning those lessons and exploring a new situation unfettered by past experiences. Scientists at the Howard Hughes Medical Institute's Janelia Research Campus have shown that the brain can temporarily disconnect information about past experience from decision-making circuits, thereby triggering random behavior

In the study, rats playing a game for a food reward usually acted strategically, but switched to random behavior when they confronted a particularly unpredictable and hard-to-beat competitor. The animals sometimes got stuck in a random-behavior mode, but the researchers, led by Janelia lab head Alla Karpova and postdoctoral fellow Gowan Tervo, found that they could restore normal behavior by manipulating activity in a specific region of the brain. Because the behavior of animals stuck in this random mode bears some resemblance to that of patients affected by a psychological condition called learned helplessness, the findingsmay help explain that condition and suggest strategies for treating it. Karpova, Tervo and their colleagues published their findings in the September 25, 2014, issue of the journal Cell.

The brain excels at integrating information from past experiences to guide decision-making in new situations. But in certain circumstances, random behavior may be preferable. An animal might have the best chance of avoiding a predator if it moves unpredictably, for example. And in a new environment, unrestricted exploration might make more sense than relying on an internal model developed elsewhere. So scientists have long speculated that the brain may have a way to switch off the influence of past experiences so that behavior can proceed randomly, Karpova says. But others disagreed. "They argue that it's inefficient, and that it would be at odds with what some people call one of the most central operating principles of the brain -- to use our past experience and knowledge to optimize behavioral choices," she notes.

Karpova and her colleagues wanted to see if they could create a situation that would force animals to switch into this random mode of behavior. "We tried to create a setting that would push the need to create behavioral variability and unpredictability to its extreme," she says. They did this by placing rats in a competitive setting in which a computer-simulated competitor determined which of two holes in a wall would provide a sugary reward. The virtual competitor, whose sophistication was varied by the experimenters, analyzed the rats' behavior to predict their future choices.

"We thought if we came up with very sophisticated competitors, then the animals would eventually be unable to figure out how to outcompete them, and be forced to either give up or switch into this [random] mode, if such a mode exists," Karpova says. And that's exactly what happened: When faced with a weak competitor, the animals made strategic choices based on the outcomes of previous trials. But when a sophisticated competitor made strong predictions, the rats ignored past experience and made random selections in search of a reward.

Now that they had evidence that the brain could generate both strategic and random behavior, Karpova and her colleagues wanted to know how it switched between modes. Since that switch determines whether or not an animal's internal model of the world influences its behavior, the scientists suspected it might involve a brain region called the anterior cingulate cortex, where that internal model is likely encoded.

They found that they could cause animals to switch between random and strategic behavior by manipulating the level of a stress hormone called norepinephrine in the anterior cingulate cortex. Increasing norepinephrine in the region activated random behavior and suppressed the strategic mode. Inhibiting release of the hormone had the opposite effect.

Karpova's team observed that animals in their experiments sometimes continued to behave randomly, even when such behavior was no longer advantageous. "If all they've experienced is this really sophisticated competitor for several sessions that thwarts their attempts at strategic, model-based counter-prediction, they go into this [random mode], and they can get stuck in it for quite some time after that competitor is gone," she says. This, she says, resembles the condition of learned helplessness, in which strategic decision-making is impaired following an experience in which a person finds they are unable to control their environment.

The scientists could release the animals from this "stuck" state by suppressing the release of norepinephrine in the anterior cingulate cortex. "Just by manipulating a single neuromodulatory input into one brain area, you can dramatically enhance the strategic mode. The effect is strong enough to rescue animals out of the random mode and successfully transform them into strategic decision makers," Karpova says. "We think this might shed light on what has gone wrong in conditions such as learned helplessness, and possibly how we can help alleviate them."

Karpova says that now that her team has uncovered a mechanism that switches the brain between random and strategic behavior, she would like to understand how those behaviors are controlled in more natural settings. "We normally try to use all of our knowledge to think strategically, but sometimes we still need to explore," she says. In most cases, that probably means brief bouts of random behavior during times when we are uncertain that past experience is relevant, followed by a return to more strategic behavior -- a more subtle balance that Karpova intends to investigate at the level of changes in activity in individual neural circuits.

Autonomic Neuropathy Vid

Today's post is a very short YouTube video about Autonomic Neuropathy originally from focusappsstore.net. As you probably know, autonomic neuropathy affects the involuntary functions of the body but in the beginning is difficult to diagnose, especially if you have other health problems clouding the picture. See description from ncbi.nlm.nih.gov (see link below) under the video clip.

A.D.A.M. Medical Encyclopedia.

Autonomic neuropathy

Neuropathy - autonomic; Autonomic nerve disease

Last reviewed: October 3, 2012.

Autonomic neuropathy is a group of symptoms that occur when there is damage to the nerves that manage every day body functions such as blood pressure, heart rate, sweating, bowel and bladder emptying, and digestion.

 

Causes, incidence, and risk factors

Autonomic neuropathy is a group of symptoms, not a specific disease. There are many causes.
Autonomic neuropathy involves damage to the nerves that carry information from the brain and spinal cord to the heart, bladder, intestines, sweat glands, pupils, and blood vessels.
Autonomic neuropathy may be seen with:

• Alcohol abuse
• Diabetes (diabetic neuropathy)
• Disorders involving scarring of tissues around the nerves
• Guillain Barre syndrome or other diseases that inflame nerves
• HIV and AIDS
• Inherited nerve disorders
• Multiple sclerosis
• Parkinson's disease
• Spinal cord injury
• Surgery or injury involving the nerves
•  
• http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001780/

SCIENTISTS DISCOVER DIMMER SWITCH FOR MOOD DISORDERS

Researchers at University of California, San Diego School of Medicine have identified a control mechanism for an area of the brain that processes sensory and emotive information that humans experience as "disappointment.

The discovery of what may effectively be a neurochemical antidote for feeling let-down is reported Sept. 18 in the online edition of Science.

"The idea that some people see the world as a glass half empty has a chemical basis in the brain," said senior author Roberto Malinow, MD, PhD, professor in the Department of Neurosciences and neurobiology section of the Division of Biological Sciences. "What we have found is a process that may dampen the brain's sensitivity to negative life events."

Because people struggling with depression are believed to register negative experiences more strongly than others, the study's findings have implications for understanding not just why some people have a brain chemistry that predisposes them to depression but also how to treat it.

Specifically, in experiments with rodents, UC San Diego researchers discovered that neurons feeding into a small region above the thalamus known as the lateral habenula (LHb) secrete both a common excitatory neurotransmitter, glutamate, and its opposite, the inhibitory neurotransmitter GABA.

Excitatory neurotransmitters promote neuronal firing while inhibitory ones suppress it, and although glutamate and GABA are among two of the most common neurotransmitters in the mammalian brain, neurons are usually specialists, producing one but not both kinds of chemical messengers.

Indeed, prior to the study, there were only two other systems in the brain where neurons had been observed to co-release excitatory and inhibitory neurotransmitters -- in a particular connection in the hippocampus and in the brainstem during development of the brain's auditory map.

"Our study is one of the first to rigorously document that inhibition can co-exist with excitation in a brain pathway," said lead author Steven Shabel, a postdoctoral researcher with Department of Neurosciences and neurobiology section of the Division of Biological Sciences. "In our case, that pathway is believed to signal disappointment."

The LHb is a small node-like structure in the epithalamus region of the brain that is critical for processing a variety of inputs from the basal ganglia, hypothalamus and cerebral cortex and transmitting encoded responses (output) to the brainstem, an ancient part of the brain that mammals share with reptiles.

Experiments with primates have shown that activity in the LHb increases markedly when monkeys are expecting but don't get a sip of fruit juice or other reward, hence the idea that this region is part of a so-called disappointment pathway.

Proper functioning of the LHb, however, is believed to be important in much more than just disappointment and has been implicated in regulating pain responses and a variety of motivational behaviors. It has also been linked to psychosis.

Depression, in particular, has been linked to hyperactivity of the LHb, but until this study, researchers had little empirical evidence as to how this overstimulation is prevented in healthy individuals given the apparent lack of inhibitory neurons in this region of the brain.

"The take-home of this study is that inhibition in this pathway is coming from an unusual co-release of neurotransmitters into the habenula," Shabel said. Researchers do not know why this region of the brain is controlled in this manner, but one hypothesis is that it allows for a more subtle control of signaling than having two neurons directly counter-acting each other.

Researchers were also able to show that neurons of rodents with aspects of human depression produced less GABA, relative to glutamate. When these animals were given an antidepressant to raise their brain's serotonin levels, their relative GABA levels increased.

"Our study suggests that one of the ways in which serotonin alleviates depression is by rebalancing the brain's processing of negative life events vis-à-vis the balance of glutamate and GABA in the habenula," Shabel said. "We may now have a precise neurochemical explanation for why antidepressants make some people more resilient to negative experiences."

Funding for this project came, in part, from the National Institutes of Health (grant NS047101).

Co-authors include Christophe Proulx, UC San Diego, and Joaquin Piriz, Universidad de Buenos Aires, Argentina.

What it means to me

To be a Wise Woman Herbalist.

Upon preparation for teaching my workshop yesterday (a Wild Medicine Walk) I got inspired to try and articulate this, so I could print it out to include with the handouts.

How did I do? Did I forget anything?
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

What it means to be a Wise Woman Herbalist

To be a Wise Woman Herbalist means to carry a philosophy of wholeness and inclusion. We view the human body as a self-actualized ecosystem, capable of complete healing and regeneration. We believe that health is innately ever-present and continues through nourishment and love. That health is nourished through whole foods and plant medicine. We believe that illness is the body’s way of bringing information to our conscious selves. It is the language of the body. We do not believe that the body is broken and is in need of fixing. We do not believe the body is filthy and needs cleaning and purging. Illness is our Teacher not our enemy. Herbs are our naturally available healing, nourishing allies.

To be a Wise Woman Herbalist means to use locally available, abundant, sensible resources; to use herbs wisely for food and medicine, ethically harvested or grown, and to ally with them. It means that I am the ultimate authority on my health, happiness and well being and I ask my self first and last before making any choices. I choose to listen to my body’s cues, and to trust my body’s capacity for health. I consciously prepare whole, holographic medicines.

Wise Women Herbalists honor the plant bodies as living beings, and honor their gifts of sacrifice upon harvest. Gifts of food or liquid or something sacred is offered to the plant in gratitude.

Our philosophy or paradigm is manifested as a spiral symbol. Life, death, birth, and rebirth are all an equal experience and a constant. We all grow, change, shed old patterns, and recreate ourselves and our environments. We are part of Mother Earth, therefore we embody her patterns and cellular knowledge. Life includes all expressions and experiences and is in constant flow.

HOMOEOPATHIC PREVENTIVE MEDICINES

Preventive Medicine is the specialty of medical practice that focuses on the health of individuals, communities, and defined populations. Its goal is to protect, promote, and maintain health and well-being and to prevent disease, disability, and death. Preventive medicine specialists have core competencies in biostatistics, epidemiology, environmental and occupational medicine, planning and evaluation of health services, management of health care organizations, research into causes of disease and injury in population groups, and the practice of prevention in clinical medicine. They apply knowledge and skills gained from the medical, social, economic, and behavioral sciences. Preventive medicine has three specialty areas with common core knowledge, skills, and competencies that emphasize different populations, environments, or practice settings: aerospace medicine, occupational medicine, and public health and general preventive medicine.

In this area Homoeopathy medicines can done wonders . Homoeopathic medicines are very effective for preventing for preventing many of the diseases. Some of the important preventive medicines are given below

CHICKEN POX- Give  Variolinum 200 one dose  in the first day and in the second day onwards Rhus toxicodendron 200 daily 3 times for one week

Or

Sarracenia purpurea 6 and Maladrinum 200 alternately  two times daily ( morning and night ) for one week

INFLUENZA –Give in the first day  Influenzinum 200 – eight doses at an interval of 10 minutes . In the second day give Arsenic album 200 two times daily  ( morning and night ) for one week

WEILS’S DISEASE OR RAT FEVER—Give Phosphorus 200  two times daily ( morning and night ) for one week

CHIKUNGUNYA – Polyporus  200- times daily ( morning and night ) for one week

DENGUE FEVER—Eupatorium Perfoliatum 200-  two times daily ( morning and night ) for one week

JAPANESE ENCEPHALITIS -- Give Belladonna 200 one dose at night, after one week give Calcarea carb 200 one dose at night and after two weeks give Tuberculinum 200 one dose at night.

CONJUNCTIVITIS—Belladonna 200- alternately  two times daily ( morning and night ) for one week

MUMPS—Give  Parotidinum  200 one dose  in the first day and in the second day onwards Pilocarpus  200 two times daily ( morning and night ) for one week

TETANUS –Ledum pal 200 and Hypericum 200 alternately every three hours for one week

TONSILITIS –Baryta carb. 1000 one dose every week for four weeks

TUBERCULOSIS— Give Tuberculinum 10M one dose in the first month , Tuberculinum 50 M one dose  in the second month, and Tuberculinum CM one dose in the third month.

TYPHOID—  Typhoidinum 1000- one dose every 10 minutes – maximum 4 doses.

WHOOPING COUGH-Pertrussin 1000 one dose every 10 minutes – maximum 4 doses

POLIO-- Give Lathyrus sativa 200- one dose in the first month , Lathyrus sativa 1000 one dose  in the second month, and Lathyrus sativa 10M - one dose in the third month.

DIPHTHERIA –Diphtherinum 1000, one dose daily for three days

CHOLERA –Cuprum metallicum 30--  two times daily ( morning and night ) for one week

JAUNDICE- Give in the first day  Merc sol  200 – eight doses at an interval of 10 minutes . In the second day give Kali mur 6x  four  times daily   for one week

MALARIA – Give Malaria officinalis 1000 four doses at an interval of 10 minutes.

Or

Natrum muriaticum 200 two times daily ( morning and night ) for one week

MEASLES – Give Pulsatilla nig. 200 --  two times daily ( morning and night ) for one week

Or

Give Morbillinum 1000 four doses at an interval of 10 minutes

Or

Give Malandrinum  1000 four doses at an interval of 10 minutes

MEASLES, MUMPS, CHICKEN POX- Give Pulsatilla nig. 1000 one dose

GERMAN MEASLES OR RUBELLA- Give Rubella  200 four doses at an interval of 10 minutes

DENTAL CARIES and GINGIVITIS –Calcarea renalis 30 two times daily ( morning and night ) for one week.

COMMON COLD–Ammonium carb. 30 three times daily for one week

GALL BLADER STONE – Chionanthus virginica 30 three times daily for one week.

GASTROENTERITIS –Give Arsenic alb. 200 ten doses at an interval of 10 minutes.

CATARACT- Give Calcarea flour. 12x- 4 tablets in morning, Calcarea phos 12x -4 tablets in the evening, Natrum mur 12x and Silicea 12x –each 4 tablets at night after food, Kali phos 12x – 4 tablets at bed time—for one week

Along with this use Cineraria maritime eye drops three times daily.

FILARIA – Give Capsicum 30 – 4 times daily, and Calcarea  flour. 30x -4 times daily for one week

WORM TROUBLES- Give Calcarea carb.1000 – one dose every month  for 3 months.

GOUT-Give  Fragaria vespa  6  -4 times daily for one week