News Category: General

Lupus, also known by its full name: Systemic Lupus Erythematosus or SLE is a chronic and often debilitating condition. It’s an autoimmune disease with many different signs and symptoms affecting all systems of the body. Autoimmune means the immune (defense) system starts to mistake your own cells as “foreign” and begins attacking them.

The destruction that takes place can affect any part of the body but especially the skin, joints, organs, the nervous system, and the blood. The body produces antibodies against itself (called autoantibodies). These immune cells go throughout the body producing an inflammatory (healing) response when it isn’t needed. The result of chronic inflammation is a breakdown of tissues over time.

The patient may face serious problems like atherosclerosis (clogged arteries), osteoporosis (brittle bones), life-threatening infections, kidney failure, and fluid around the heart and lungs, to name just a few.

What can be done about this? Treatment is really more a matter of management than cure. Medications are the front runner in this area. For a long time, antiinflammatories including steroids have been used. But the long-term side effects of these medications can be very harmful.

More recently, scientists have turned toward finding better ways to target the problem rather than just treating the symptoms. Medications in a new class of drugs referred to as biologics are on the horizon. These agents treat the disease at the cellular level.

The first group of disease modifying anti-rheumatic agents found to be effective started with antimalarial drugs. Physicians found that by using antimalarial medications, patients with lupus (SLE) could manage their disease, reduce flare-ups of symptoms, and take less of the more damaging steroidal antiinflammatories.

Patients with SLE who normally have a lower life expectancy than adults without this disease were living longer with a better quality of life after taking antimalarials. Their cholesterol levels went down, too, which means fewer problems with atherosclerosis and heart disease. Steroidal antiinflammatories are still needed when the disease is severe, but antimalarials work well for mild conditions.

Another disease modifying anti-rheumatic drug (DMARD) that has worked for lupus is methotrexate (MTX). This drug seems most effective for patients who don’t respond to the antimalarials and who have skin or joint problems. Like other DMARDs, methotrexate (MTX) works at the enzymatic and cellular level to alter the inflammatory process.

Other disease modifying drugs used with varying effects on lupus include cyclophosphamide (CYC), mycophenolate mofetil (MMF), and azathioprine (AZA). Each of these agents works in a slightly different way with its own benefits and disadvantages (adverse side effects).

Studies are ongoing to figure out who would benefit the most from each one and how results compare using one drug versus another. Combinations of drugs are also effective but it does take time to work through which combination is best for any individual patient.

That brings us to the most recent research focus: biologic agents. Most of the other drugs used for lupus suppress the immune system. Biologic agents stop the specific biologic steps in the pathway leading to lupus. Most of these agents are in clinical trials but close enough to be released for use soon.

There are half a dozen different biologic approaches being investigated. The first is called B-cell depletion. Specific cell-surface antigens (e.g., CD20 and CD22) are targeted. By stopping the action of these immune cells, the process of lupus can be halted.

The main biologic drug under investigation with these effects is called rituximab. It is a monoclonal antibody. It was first used and approved for non-Hodgkin lymphoma but it seems to be helpful in cases of severe lupus that does not respond to the more standard immune suppressive medications. Data from various studies around the world is being collected on the most effective dose and delivery of this drug for lupus.

Three other classes of biologic agents under investigation include costimulatory interactions, cytokine blockade, and B-lymphocyte stimulator (BlyS). As you might imagine just from their names, the way they interact with the very complex immune system isn’t simple.

Each one targets a different area of the immune system in trying to stop the disease process. Some stop B- and T-cell formation (active immune cells). Others don’t reduce the initiation of B-cells but keep the B-cells out of the bloodstream.

Some interfere with the signaling pathway that keeps the autoimmune cycle of self-destruction from repeating itself. There is a cascade of steps in the pathway. Each drug targets a different step along the chain of command.

Experts in the field aren’t sure one drug (monotherapy) will be found to conquer lupus. We may have to be content to target patients based on their particular expression of the disease. Those with kidney disease will have one drug to stop those processes. Others with skin and joint problems will be given something else.

The use of antimalarials for mild disease and disease modifying anti-rheumatic drugs (DMARDs) early on in the disease process will remain the center of treatment. Saving steroidal antiinflammatories for severe disease manifestations may help reduce the toxic side effects of those medications. It won’t be long now before biologic agents will become a routine part of the drug regimen for lupus.

Dr. Kenneth Brandt, clinical professor of medicine at the Kansas University Medical Center and professor of medicine at New York University has written this article on osteoarthritis as one section of a three-part series. The focus of this second article is diagnosis of this all too common disease.

Part one covered an update on new information about what is (and isn’t) osteoarthritis. The third part hasn’t been published yet. It will review current evidence on effective treatment for this condition.

It’s easy to assume as we get older that any joint pain must be osteoarthritis, often jokingly referred to as “Uncle Arthur” or “Arthur Itis”. But, in fact, there are many other possible causes of joint pain such as tumors, metabolic bone disease, osteomyelitis (infection), neurologic problems, and ligament instability.

How does the physician make the diagnosis? It’s a multi-step process from taking your history to performing a physical exam and then ordering appropriate tests. The physician knows to look for involvement of specific joints including the spine, hips, knees, thumbs, and middle joints of the fingers.

The most common symptoms reported by patients with osteoarthritis are joint pain, joint stiffness, and creaking, snapping, or cracking of the joints with movement, a phenomenon called crepitus. The pain and stiffness eventually cause loss of motion and function. Over time, joint deformity may occur as well. A noticeable limp may develop.

But no one wants a delayed diagnosis when deformities and loss of function could be prevented with early intervention. So the physician looks for other well-known tell-tale clues. For example, pain will full knee flexion (squat position) or with hip internal rotation point to arthritis. With osteoarthritis of the thumb and/or fingers, the patient may report difficulty opening jars, using a pinch grasp to hold a key, or grasping objects in general.

Morning stiffness that gradually gets better with movement in the first 20 to 30 minutes after getting out of bed or after sitting for too long is another red flag. In fact, so many patients experience this symptom, it has been given a name: the gelling effect or sensation.

Although osteoarthritis often affects both joints at the same time (e.g., both knees, both hips), it can develop in a single joint as a result of an accident or trauma some time in the past. The involved joint will start to get tender and the bones enlarge until the joint is clearly bigger looking than the uninvolved joint.

The physician will broaden his or her search for answers by ordering radiographs (X-rays) and lab tests. Blood values can offer information about the level of components in blood normally linked with inflammation.

Erythrocyte sedimentation rate, commonly referred to as ESR will be elevated with inflammation. C-reactive protein (CRP) is also increased. And antinuclear antibodies (ANAs) may rise. But the wise physician also knows these values increase with age or obesity. Careful interpretation of lab values is advised in older adults with joint pain. The presence of any or all of these lab values doesn’t immediately confirm a diagnosis of osteoarthritis.

Dr. Brandt cautions physicians to avoid what he calls diagnostic pitfalls. It is easy to misinterpret patients’ pain, deformity, X-rays, and lab results. An accurate diagnosis depends on the physician having an understanding of similarities (and differences) between signs and symptoms of osteoarthritis and other possible causes of joint pain.

A careful history and examination will aid the physician in making a differential diagnosis — in other words, recognizing osteoarthritis from neurologic conditions, other orthopedic problems (e.g., Dupuytrens disease, psoriatic arthritis or some other form of arthritis), and lung disease accompanied by bone or joint changes.

Joint pain or stiffness as a single symptom isn’t enough to know the patient has osteoarthritis. There is usually a collection of three or more of the common signs and symptoms described in this article along with joint changes seen on X-rays.

Making a correct diagnosis and beginning appropriate treatment early can change the course of this disease for many people. The information in this three-part series (including this second part on diagnosis) will guide all physicians in making clinical decisions regarding osteoarthritis.

Many people support the use of stem cell research but government regulation has slowed the process of study in this area. What’s the evidence so far that stem cell therapy could benefit someone with tendinosis? That is the focus of this meta-analysis.

Let’s define some terms here to help explain what is being studied and the results reported so far. First, tendinosis is a term used to describe tendons that developed a painful tendinitis (acute inflammation) that just didn’t heal and became a chronic condition. The body attempted to organize a healing response. But instead of making new, healthy tendon cells to replace the damaged cells, the tendon tissue became thick with disorganized fibers. The already damaged tendon, now further weakened, fails to heal and may even go on to tear even more.

Next, a meta-analysis study tells us the authors found every article possible on the topic and reviewed them for design, quality, and content. Those articles that passed a pre-established set of criteria were then analyzed and summarized. And finally, just exactly what are stem cells?

Stem cells are the basic cells that can form any other type of cell such as bone cells, tenocytes (tendon cells), myocytes (muscle cells), brain cells and so forth. In humans, there are two basic types of stem cells: 1) embryonic stem cells taken from the umbilical cord of newborns or cells of fetuses that have died before being born and 2) adult stem cells that are found in adult tissues. In a developing embryo, stem cells are designed so they can form all the different tissues in the body. In adults, stem cells act as a repair system for the body when something wears out or is damaged due to injury or disease.

Scientists have figured out a way to harvest stem cells from fat, skin, tendon, and muscle then take it to the lab where they can multiply the sample and grow more cells. When there are enough cells to do the repair job needed, they are injected into the damaged area (e.g., tendon). That sounds simple enough but in fact, there are major barriers to the process.

For example, it takes time to generate more tissue in a lab setting. The lab has to have expensive, specialized equipment to do this type of work. Meanwhile, the injured athlete or other patient is waiting and the window of opportunity for healing is getting smaller and smaller. Transporting the cells comes with a lot of potential problems. No one is quite sure how well the cells travel from lab to patient. Questions have been asked about the need to freeze the cells in order to keep them preserved for use. If they could be frozen ahead of time and ready at a moment’s notice, the donor cells could be used right away at the time of injury.

None of these problems can be solved easily or quickly with the current government regulations in place. That’s why some scientists have started looking elsewhere for solutions to the problem (e.g., whole blood, platelet-rich plasma). But for those who have stuck with stem cell therapy, here’s what the authors have found reported in the literature:

Are you having constant muscle aches and joint pain? Perhaps headaches on top of that or trouble sleeping? Not sure why you can’t sleep at night? You may have a condition called fibromyalgia or fibromyalgia syndrome (FMS). How can you find out?

The October 2010 supplemental issue of The Journal of Musculoskeletal Medicine is all about Fibromyalgia. The authors of the first article tell us that your primary care physician is the best place to start. Physicians understand the basic science behind fibromyalgia and know how to create a plan of care that’s just right for you.

Fibromyalgia isn’t really a disease. It’s a group of symptoms that tend to occur together either at the same time or in close proximity to one another. You may experience tension headaches that seem to come and go even when you aren’t stressed. Sometimes there’s joint pain that travels from one joint to the next. Or you feel like a truck ran over you every morning when you wake up.

Scientists haven’t been able to unlock all of the secrets behind fibromyalgia syndrome (FMS). Right now, the main theory is that FMS occurs when something goes hay wire in the nervous system. That something may be what’s called central sensitization syndrome. It means your nervous system is ramped up to react too soon, too often, and for too long. Pain signals are sent when ordinary sensations of light (or other pleasurable) touch occurs.

Your doctor can sort out all the symptoms, select the best tests, and rule out other reasons for your physical distress. Physicians are trained to take a good patient history and interview patients about psychosocial stressors. It turns out that psychologic, emotional, and social stresses are linked with a higher rate of FMS in the general population.

The information gleaned from the medical intake examination will help your physician identify any risk factors you may have for fibromyalgia syndrome. Some of the more common risk factors include traumatic injury, heavy lifting or pulling, and mood disorders. Anxiety, depression, and post-traumatic stress disorder also seem to be linked with FMS. Having a bipolar illness increases the risk of developing fibromyalgia syndrome (FMS) dramatically.

What causes this condition to develop? Sometimes FMS occurs as a result of some other medical condition. For example, patients with rheumatoid arthritis (an inflammatory disease), metabolic dysfunction (e.g., thyroid problems), or cancer often develop a type of FMS referred to as reactive fibromyalgia. It’s important to identify whether or not the FMS is primary (the main problem) or secondary (caused by other problems).

Folks who have fibromyalgia syndrome (FMS) often have certain triggers that seem to bring on (or increase) symptoms. The triggers vary from person to person but may include degenerative (spinal) disc disease, headaches (all kinds), irritable bowel syndrome, reflux (heart burn), trigger points of the muscles, and poor posture.

What can the physician do to treat your fibromyalgia? Getting a good and accurate diagnosis is half the battle. A good physician who is thorough and knowledgeable in his or her interview and examination skills is worth their weight in gold.

Early recognition, diagnosis, and treatment can provide a faster resolution of symptoms and much improved prognosis. In fact, half of all adults diagnosed with fibromyalgia early in the development of their disease (and who are adequately treated) no longer have this problem two years later.

There are different modalities (tools) that can be used to gain control of the main symptoms. Physical therapy, exercise, nutrition, trigger point injection, and medications form the core program used for this condition. Exercise is getting a lot of support right now because of the wide range of evidence showing that any form of exercise but especially isometrics can be helpful.

The physical therapist will prescribe the optimal mode (type), frequency, intensity, and duration of exercise for each patient on an individual basis. There isn’t a one-size-fits-all type of program because of the wide range of physical abilities and disabilities among adults with this condition.

Pilates-based stretching, yoga, and low-impact aerobic exercise have the greatest benefit. Anyone with fibromyalgia syndrome (FMS) must be very careful when trying weight-lifting, rowing, or jogging. In fact, these are not really recommended during painful flare-ups. Many people with FMS don’t have any real trouble during exercise. It’s the painful joint and muscle “after shock” that is the worst. Some can barely get out of bed the next day after what seems like a mildly strenuous work out.

Sometimes several medications are combined to get the most relief of symptoms with the fewest adverse effects. Some medications address the pain or sleep issues, while others deal with the anxiety, depression or other psychologic disorders.

It is expected that treatment will continue to improve as scientists make new discoveries about fibromyalgia syndrome (FMS), its causes, triggers, and responses to different therapies. This article highlights five key areas of understanding right now including fibromyalgia as a primary vs. secondary problem, the role of psychosocial stressors, pain patterns associated with FMS, type of exercise best suited to this problem, and type of medications to prescribe.

There have been some significant breakthroughs in our understanding (and therefore treatment) of fibromyalgia syndrome (FMS). Today’s modern approach to is multimodal, meaning many different treatment options are pursued at the same time. Combining medications with exercise, behavioral counseling, and alternative medicine have made it possible to live a more normal life for those who suffer with this condition.

What exactly is fibromyalgia syndrome (FMS)? FMS is a group of symptoms that tend to occur together either at the same time or in close proximity to one another. The most common symptom is widespread pain throughout the body, with especially tender spots near certain joints.

Pain and stiffness concentrate in spots such as the neck, chest, shoulders, elbows, knees, buttocks, and lower back. The tender spots don’t seem to be inflamed. The pain stops people with fibromyalgia from functioning normally, partly because they feel exhausted most of the time. Most tests show nothing out of the ordinary in the anatomy of people with fibromyalgia.

At one time, there was a strong suspicion that the symptoms of fibromyalgia were psychosomatic — the result of stress and “all in the head” of affected individuals. But scientists have come a long way since then in unraveling the mystery behind this complex condition.

Right now, the main theory is that FMS occurs when something goes hay wire in the nervous system. That something may be what’s called central sensitization syndrome. It means the nervous system is ramped up to react too soon, too often, and for too long.

With a dysregulation of the central nervous system, there appears to be some kind of mistake within the nervous system in how it recognizes and transmits pain messages. Somehow, the nervous system seems to think even the simplest touch is a noxious (painful) stimulus. It’s like a ten-alarm fire signal is sent to the brain when a breeze blows by the barn.

Nervous system dysregulation of this type is likely caused by biochemical abnormalities, altered brain blood flow, and problems with the pain processing mechanisms. Sufferers have lower pain thresholds and lower levels of serotonin, a brain chemical involved in pain, sleep, and mood.

Many people with fibromyalgia also have anxiety disorders, depression, panic disorders, and phobias that are chemically induced and/or the result of abnormal central (nervous system) processing. It’s these chemical changes that have prompted drug companies to look for a way to treat the problem with pharmaceuticals (medications).

There isn’t one magic pill patients can take to wipe away the pain, improve sleep, improve brain function, or restore energy. Instead, a wide range of medications are available that can act on the nervous system in a variety of ways. These include tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors (SSNRIs), and anticonvulsants (also known as antiepileptics).

And for the first time, there are some medications now FDA approved from these categories specifically for fibromyalgia (e.g., pregabalin, duloxetine, milnacipran). In the past, many of the medications were used off-label. This means the medications were intended for something else (like seizures or depression) but were found to be effective for fibromyalgia.

Two of the drugs now approved in the U.S. for fibromyalgia are antidepressants (duloxetine and milnacipran). Studies have shown that these medications don’t work because they improve the person’s mood (reduce depression). The chemical pathway of the drug seems to impact pain signals directly.

Neither one of these drugs works to improve sleep. They do improve energy levels, physical functioning, and cognitive function — probably because they reduce pain, a symptom that can level a person in all these areas.

Pain relievers, whether over the counter or prescription, are generally not effective by themselves. Many pain medications are addictive and should be used with caution. Mild pain medications may help in combination with other treatments. Opioid (narcotic) pain relievers, corticosteroids, and nonsteroidal antiinflammatories (NSAIDs) are no longer recommended.

Other drugs under continued investigation for the treatment of fibromyalgia include tizanidine (normally used to control muscle spasticity in patients with multiple sclerosis or stroke), growth hormone, 5-HTP, and tropisetron. The last two drugs seem to improve tenderness, stiffness, anxiety, and sleep.

Medications are only used in conjunction with other treatment such as exercise, meditation, hypnosis, acupuncture, nutritional counseling, biofeedback, massage, and behavioral counseling. A new treatment approach involving electromagnetic wave therapy is being tested for pain control by modifying brain activity in a noninvasive way without drugs or surgery.

If you are someone with fibromyalgia, it can be easy to feel overwhelmed by all of these choices. Which one is right for you? In what order should you try them? Who can help you manage all your symptoms and improve function on a day-to-day basis? It takes a team of specialists to accomplish this but working together, your physician, pharmacist, physical therapist, and counselor can form a powerful support team to guide you along the way.

If you’ve ever seen a photograph of Abraham Lincoln you know he had a long, thin face. He was thin and tall, and he had long arms and long fingers. There has been some thought that he might have had a genetic disorder of the connective tissue called Marfan syndrome. All of these physical features are typical with Marfan syndrome. Newer evidence suggests he had a different (but very similar) disorder. But the association of Abraham Lincoln’s name with Marfan Syndrome has forever put this condition on the map.

New information and improved diagnostic testing has spurred the authors of this article to write about improving the recognition of Marfan Syndrome. It is a genetically inherited condition, so genetic testing is one way to prove someone has Marfan syndrome. But genetic testing is expensive and doctors have to identify who might have this disorder before sending anyone and everyone to the genetics expert.

The most serious complications are the defects of the heart valves and aorta. It can also affect the lungs, eyes, the dural sac surrounding the spinal cord, the skeleton, and the hard palate. A family history is helpful but sometimes it doesn’t come until a family member dies of heart complications from Marfan syndrome. Early diagnosis and treatment can prevent such a serious outcome.

Physicians from The Johns Hopkins University (Orthopedic and Pediatric departments) studied two groups of people (those with known Marfan syndrome and those without) to see if they could identify any features that would tell them for sure who had Marfan syndrome. Since Marfan syndrome is fairly uncommon, there were only 183 patients in the Marfan group. Over 1200 people were in the nonMarfan (comparison) group.

Since the skeletal features are the most obvious, they started with those first. These include the long, thin face, a deformity called craniofacial dolichocephaly. Scoliosis (curvature of the spine), a high-arched palate (roof of the mouth), and chest deformities (caved in or protruding out) are other physical signs of Marfan syndrome. Severe flat feet called hindfoot valgus is another common feature of Marfan syndrome.

There are a couple of physical tests that can be helpful in identifying Marfan syndrome. One is the positive thumb or Steinberg sign. The other is the positive wrist or Walker-Murdoch sign. If the patient puts the thumb across the palm and closes the fingers and the thumb pokes out the other (little finger) side, there’s a positive thumb sign. If the patient can circle the forearm with the thumb and little finger of the other hand and cover the entire nail of the little finger with the thumb, there is a positive wrist sign.

X-rays are an easy and fairly inexpensive way to look for evidence of Marfan syndrome. Besides the skeletal features already mentioned, the presence of acetabular protrusio is diagnostic. Aceatbular protrusio means the acetabulum or hip socket is too deep and may protrude into the pelvis. But again, not every child needs hip X-rays. So how does the pediatrician know who might have Marfan syndrome in need of diagnostic test to confirm the suspicion?

Well, that’s the dilemma these authors faced because on the one hand, many children (people) have one or even more of the telltale characteristics of Marfan syndrome — but they don’t actually have this connective tissue disorder. And just as many folks who actually have the syndrome have invisible signs (like heart problems) that could lead to their premature death.

After analyzing all the data, looking at which tests were specific and sensitive enough to be counted on, the authors offered pediatricians the following steps to take:

It makes sense that chronic back pain limits physical activity and exercise. But it has never been proven that a lack of daily activity and exercise contributes to the onset of back pain. And there isn’t convincing evidence that people with chronic low back pain become deconditioned from a lack of physical activity and exercise.

To help focus what we do know and summarize the evidence, researchers from the Netherlands put together this report on deconditioning and chronic low back pain. They raised some interesting questions like is exercise being done for the wrong reasons by patients with chronic low back pain? That’s an important question because intense physical training is often a major part of the rehab program for chronic low back pain.

They took a look at all the studies done on chronic low back pain sufferers with two things in mind: physical activity levels and physical fitness. Physical activity included daily activities of living like cooking, walking, working, bathing, driving, brushing teeth, and so on. Physical fitness included muscle strength, endurance, postural control, and cardiorespiratory function.

Two interesting results were observed. First, the physical activity level of patients with chronic low back pain wasn’t that different from healthy individuals. And second, the risk of developing long-term back pain was highest among sedentary (inactive) people and those who participate in strenuous activities.

Several studies have shown that the disability associated with chronic low back pain really starts in the mind. Patients who perceived that they were losing function and became fearful of moving experienced more disability than those who worked and played despite their pain.

Patients who see their pain as threatening become afraid that movement will increase the pain, so they stop moving. This phenomenon has been labeled catastrophizing and may be a factor in deconditioning but that hasn’t been proven yet. Two other results of inactivity are weight gain and loss of bone density.

As far as physical fitness goes, we know that laying around (either being a couch potato or immobilized by bed rest or paralysis) does lead to muscle atrophy and loss of strength. This type of muscle wasting affects all muscles (legs, arm, trunk, back) from large to small. But whether or not the loss of muscle mass is directly related to low back pain is also unclear.

Researchers who have studied the differences between men and women and by age in patients with chronic low back pain versus controls (adults without back pain) haven’t found links between these factors and level of physical activity. What they did find was that people who continued working despite their back pain had better physical fitness and conditioning. The conclusion of the studies was that people should be encouraged to stay active at work. They were unable to say for sure that working prevents deconditioning.

In summary, current research has not been able to show that low activity or fitness levels in healthy adults is a risk factor for developing chronic low back pain. In the opposite vein, we don’t know that having low back pain for months to years results in deconditioning. There just hasn’t been enough studies done evaluating physical (muscle strength, postural control) and physiologic changes (fat metabolism, oxygen saturation) in patients with chronic low back pain.

That leads to the authors’ final conclusion that future research is clearly needed around the topics of physical activity levels, deconditioning, and low back pain. They suggest that both sides of the equation should be considered: does low back pain cause deconditioning or does deconditioning contribute to low back pain?

There is also a need to consider the role of catastrophizing, fear-avoidance behaviors, motivation, and attitude on physical activity and deconditioning. High-quality studies will need to use valid and reliable tools to measure physical activity, activities of daily living and fitness. Carefully matched controls are essential. Patients should be matched with healthy adults of similar age, sex, work status, and sports activity.

An Australian physical therapist (they are called physiotherapists down under) won The American Journal of Sports Medicine’s annual competition in 2009. It was for the best systematic review with meta-analysis on the subject of leg injuries in athletes who are hypermobile.

Let’s back up a bit and explain a few things. First, what’s the big deal about the competition? Well, a systematic review involves sifting through 1000s (4841 to be exact in this study) of studies on a particular topic. Meta-analysis means the researchers had to find studies that were similar enough in data collection and analysis that the results could be pooled together.

In the case of this review, no one had ever performed a meta-analysis and all previous systematic reviews had not been able to answer the question. And what was the question again? Are athletes with generalized joint hypermobility (GJH) more likely to injure knees and/or ankles compared with sports participants who have “normal” joint motion.

Generalized joint hypermobility (GJH) is defined as a condition in which most, if not all, of a person’s joints are super flexible. They move past the range of motion that the normal, average person has. This type of connective tissue flexibility is sometimes referred to as being “double jointed”.

The person really only has one joint at each location. It’s just that those joints move too far, too easily. Sprains, strains, subluxations (partial dislocations), and complete dislocations are common. It seems like athletes with generalized joint hypermobility (GJH) actively involved in sports injure the joints of the legs more often than those players who don’t have GJH. But does it just seem that way or is it a true observation?

The results of this systematic review with meta-analysis suggest there is a direct link between GJH and leg injuries. One of the challenges the authors faced was the fact that most of the studies they found only looked at one type of leg injury (just the knee or just the ankle). There was very little information on hip injuries (only one study and only three hip injuries).

There was a wide range of athletes included from ballet dancers and divers to military recruits and football players, the last group was from the college and professional level. Some of the injuries were from contact activity with high-impact collisions (with another body or with the ground). Others were from overuse (e.g., diving, dancing). Overall, there were significantly more injuries among the contact or collision sports participants.

As for the joints injured most often — that distinction goes to the knees. Individuals with generalized joint hypermobility (GJH) were much more likely to injure the knee (much moreso than the ankle) compared with athletes who had normal joint motion.

These findings are consistent with what other studies show about ankle injuries — namely, that loss of ankle motion is the key risk factor in ankle injuries (not hypermobility). Likewise, when it comes to knee injuries, when the foot is planted on the ground and the body twists or rotates above, the lack of restraint on the knee joint in someone with GJH contributes to knee injuries. Without stiff ligaments, there’s no tension keeping the joint from sliding too far.

So whether it’s ballet or grid iron, male or female, amateur or professional, there is an increased risk of leg (knee) injury among people with generalized joint hypermobility. No recommendations were made based on these findings. Just coming to some conclusions about this issue based on a systematic review and meta-analysis is a major step forward in sports orthopedics.

Platelet-rich plasma (PRP) (also known as blood injection therapy)) is a medical treatment being used for a wide range of musculoskeletal problems. Platelet-rich plasma refers to a sample of serum (blood) plasma that has as much as four times more than the normal amount of platelets. This treatment enhances the body’s natural ability to heal itself and is used to improve healing and shorten recovery time from acute and chronic soft tissue injuries.

Blood injection therapy of this type has been used for knee osteoarthritis, degenerative cartilage, spinal fusion, bone fractures that don’t heal, and poor wound healing. This treatment technique is fairly new in the sports medicine treatment of musculoskeletal problems, but gaining popularity quickly.

Patients with chronic tendinitis (e.g., tennis elbow, patellar tendinitis or jumper’s knee, Achilles tendinitis) have also benefited from this treatment. It’s even being tried on hernias, labral (shoulder cartilage) tears, meniscal tears of the knee, and ankle sprains. Some surgeons are using it more and more with any orthopedic surgery involving the soft tissues to augment (reinforce) bone or ligamentous graft materials already being used.

As with any new treatment, over time it is possible to see more clearly the pros and cons of treatment. Data can be collected on long-term results and more information published to guide surgeons in using this treatment tool. In this article, research on the subject of platelet-rich plasma to augment connective tissue healing is offered by the Orthopaedic Research Society (ORS).

Taking a look back over the past few years, we now see there are some inconsistencies in results with this treatment. Some studies have shown no benefit from the use of platelet-rich plasma (PRP) for tissue healing. Why is that? The authors propose several reasons for the variable results reported in the literature.

First, not all PRP is the same. The product may vary based on how much whole blood was taken and how quickly platelets recover during the injection. The presence of other blood parts such as red or white blood cells can make a difference. And any other substances that might have been added (e.g., thrombin, calcium chloride) can affect how the PRP functions.

Second, the potency (strength) of each PRP preparation varies — again, this depends on what’s in the product. Too little or too much of any component part can change how quickly and how effectively the body responds to the product. Then there is what’s called biologic variation — everyone responds a little differently to the same PRP. Individual body chemistry, metabolism, and reactivity can vary significantly.

Along these same lines, getting the right mix of product for each person is a challenge. Clearly, one formulation does not fit all. The amount of PRP to achieve the best result for each person is called the dose-response. This goes back to how the body responds to each substance within the PRP (e.g., growth factors, cytokines, proteins, clotting factors).

And finally, even with the right mix of elements within the PRP, using it at the exact right time for best results may make a difference. The best timing for the use of PRP has not yet been determined. Likewise, the way in which the PRP is delivered (e.g., injected, brushed on) might make a difference in results.

The authors conclude that any future research done using PRP will have to pay attention to which PRP product was used and how it was used. The early enthusiasm about PRP may be still warranted but since not all results have been positive, it’s time to take a closer look before continuing as if this product is fail-proof.

Aches, pains, sprains, strains — these are everyday problems for sports athletes. But there’s one particular condition that may seem to be a minor problem but can cause debilitating sidelining. And that’s something called exercise-associated muscle cramps or EAMC.

Exercise-associated muscle cramps presents with acute pain, muscle stiffness, and soreness. The muscles affected most often include the hamstrings, quadriceps, and calf. The muscles on both sides of the body are often involved. And on visual examination, it’s possible to see a knotted up ball of muscle.

The symptoms don’t occur at the time of exercise. The athlete is most likely to notice the muscle cramps after exercise. It can even be hours later. The tendency to develop these exercise-associated muscle cramps after exercise is referred to as the cramp prone state.

What causes exercise-associated muscle cramps? Who’s at risk? What can be done to prevent them? Or treat them once they get started? Those are questions physical therapists who are also certified as athletic trainers are trying to answer. Although the problem has been recognized for the last 50 years, there has been no formal study/testing to find evidence-based answers to these questions.

That’s why this group of physical therapists/athletic trainers performed a review of the literature to summarize what we do know and where to go from here. They searched all of the major publications from 1955 to 2008 looking for high-quality studies on this topic. In this article, they summarized what they found.

First, it’s still not known what causes exercise-associated muscle cramps. Athletes of all kinds experience them — including recreational and high-level competitive players. It doesn’t seem to matter what type of sport the player is involved in. Climate (hot and humid) may be a factor. Dehydration and electrolyte imbalances are more likely during hot, humid outdoor activities.

The dehydration theory is the most commonly used explanation. But why does dehydration trigger exercise-associated muscle cramps? Sweat loss without replacing fluids adequately alters the balance of fluids and electrolytes (chemicals) in the body. Without the proper mix of calcium, potassium, sodium, magnesium, chloride, and others, the nerve endings attached to the muscles can’t work properly.

When the nerve terminals are too sensitive, they set off a series of events that leave the muscles in a chronic state of contraction, unable to relax. That’s when the muscle cramps become unbearable.

But this is just a theory based on observations of athletes suffering from muscle cramps in hot environments. The fact is, the same problem has been seen in athletes exercising in cool or temperature controlled arenas and gyms. So maybe it’s something else — like some athletes are just more susceptible because of the way their bodies function. Maybe there are crampers and noncrampers and that’s just the way it is!

Some other interesting observations have been made about exercise-associated muscle cramping. Stretching the muscle seems to help relieve the cramp. Stretching doesn’t affect the fluid and electrolyte balance. Replacing fluids is ineffective as well. So that leaves scientists scratching their heads trying to come up with reasonable alternative theories.

The next theory proposed is the neuromuscular theory. In this model, muscle overload during exercise results in an imbalance within the motor firing mechanism of the muscle. The feedback loop that tells a muscle when to contract and when to relax gets off-balance. An imbalance of impulses results in messages to the muscle to contract getting stuck. Stretching the muscle overrides the system and is like hitting the reset button.

Scientists have found it difficult to study this problem. Animal models (cats, rabbits) can’t be used because they have different neuromuscular signaling mechanisms that don’t match humans.

Working backwards (find a solution, then figure out why it’s working) hasn’t panned out either. People have used a wide variety of sports drinks, massage, electrical stimulation, changing exercise/workout intensity, and even drinking pickle juice! None of these seems to work equally for all people prone to muscle cramps or in the midst of an attack.

The one prevention and treatment technique that has consistently had the most successful results has been stretching. Keeping up on fluids and salt intake for athletes who seem prone to this problem is also still recommended — even though direct evidence is lacking for this advice. And along with the recommendation to take in fluids and electrolytes is the reminder that these substances aren’t absorbed right away. Athletes are frequently reminded to eat before you are hungry; drink before you are thirsty.

Finally, it’s likely that exercise-associated muscle cramping is the result of a combination of factors. Until evidence-based experiments can sort out who should do what to prevent the problem, a multi-strategy approach is advised. Stretching, replacing fluids and electrolytes, and conditioning muscles affected most often are all advised. Strength-training, endurance, and plyometrics may help prevent neuromuscular imbalances and fatigue that set off inappropriate signals.

Platelet-rich plasma (PRP) (also known as blood injection therapy)) is a medical treatment being used for a wide range of musculoskeletal problems. Platelet-rich plasma refers to a sample of serum (blood) plasma that has as much as four times more than the normal amount of platelets.

Platelets are like the emergency medical technicians (EMTs) of the body. When there’s an injury, they are the first one on the scene of the accident, so-to-speak. Platelets have a large number of available growth factors and other bioactive molecules that signal the body to start the tissue-healing process. This treatment enhances the body’s natural ability to heal itself and is used to improve healing and shorten recovery time from acute and chronic soft tissue injuries.

It has been used for years after plastic surgery and surgery on the mouth, jaw, and neck. It seems to promote bone graft healing. Researchers have found a way to combine this substance with other chemicals to make it into a putty or gel that can be painted on a surgical site to speed up healing.

Blood injection therapy of this type has been used for knee osteoarthritis, degenerative cartilage, spinal fusion, bone fractures that don’t heal, and poor wound healing. This treatment technique is fairly new in the sports medicine treatment of musculoskeletal problems, but gaining popularity quickly.

Patients with chronic tendinitis (e.g., tennis elbow, patellar tendinitis or jumper’s knee, Achilles tendinitis) have also benefited from this treatment. It’s even being tried on hernias, labral (shoulder cartilage) tears, meniscal tears of the knee, and ankle sprains. Some surgeons are using it more and more with any orthopedic surgery involving the soft tissues to augment (reinforce) bone or ligamentous graft materials already being used.

New treatments are always welcomed, especially if they speed up the healing process. But the question is: how well are platelet-rich plasma treatments really working for muscle, tendon, ligament, and labral repairs? The authors of this report performed a search of all related studies published over the last 10 years on this topic.

They found that the basic science behind this technique is sound. Animal studies have shown very favorable results. But the number and type of studies using platelet-rich plasma in humans is very limited. And the way the different studies were conducted makes it difficult to compare or combine the results.

There are also different growth factors released and different concentrations of platelets in samples used from study to study. It’s not really clear yet just how much platelet-rich plasma is needed for each type of injury or even how many platelets are needed for the best response.

The idea that platelet-rich plasma treatment could heal a tendon tear is appealing. Most tendon tears just fill in with scar tissue. The result is often more tears later or even chronic pain. A complete and natural healing of tendon tissue would benefit many people, especially athletes involved in repetitive activities that stress tendons where they attach to the bone.

Of the studies that have been done in humans, there have been good results. For example, athletes who had surgery to repair ruptured tendons or rotator cuff tears and then received platelet-rich plasma regained joint motion faster. They had fewer complications from the surgery. And they were able to get back to training sooner than patients who did not receive the platelets.

One study on the use of platelets to heal cartilage lesions showed improved function and less pain compared with the group who did not receive this treatment. Currently, there are no reported studies using platelets with muscle injuries in humans. This is an area for future research.

The authors conclude that platelet-rich plasma at the site of soft tissue injury has the ability to create an ideal healing environment. This has been shown in animal studies and now in a limited way in humans. The treatment is simple, easy to do, and inexpensive.

There are very few side effects and most of these are very minor. For example, there is always the risk of infection. A small number of patients have reported increased pain, redness, and swelling at the injection site but this response didn’t last long.

The lack of high-quality, randomized controlled trials points to the need for attention in this area. Before expanding its use to an even wider array of musculoskeletal problems, it should be proven that the treatment has a positive benefit for each type of injury or trauma.

Whether you use a manual wheelchair, power wheelchair, or any one of the many scooters available, managing corners, turning around, and general maneuvering of the chair/scooter can be a real challenge. If you’ve been thinking you are the problem, this study might help set the record straight.

Guidelines were set in the 1970s to make buildings accessible to wheelchair users. But in the 40 years since then, mobility equipment sizes and designs have changed. However, building codes have not changed to accommodate the wide assortment of power wheelchairs, manual (push-type) wheelchairs, and now the newer scooters many of the older adults are using.

Some of this equipment is pretty heavy and bulky while others are light-weight. The wheel base varies as does the length of the chair and placement of the wheel axes. Some chairs have a front wheel set up while others have a mid-wheel drive or rear-wheel drive. Each one of these designs has its own space requirements for turns.

Not everyone can sit up straight. Individuals in wheelchairs who have to be reclined have an even harder time managing U-turns, L-turns, or other pathways. Maneuverability becomes even more difficult when the legs have to be elevated.

People using the newer scooters are usually able to sit up straight. They have good trunk control and can operate the hand controls. But even the compact scooters are fairly large when it comes to navigating narrow hallways in older homes and small living spaces (not to mention public bathrooms).

In order to find out just what kind of space is needed, these researchers set up a lab with cardboard walls to mimic turns and tasks often faced by people in mobility equipment. Over 200 people in mobility equipment participated. The reason for their chair/scooter use ranged from spinal cord injuries to cerebral palsy, multiple sclerosis, arthritis, brain injury, diabetes, and other diseases and injuries.

Their task was to maneuver the set up course without touching the walls. They could go at their own pace. Anyone who could not pass through the standard size doorway or hallway was considered unsuccessful. Anyone who touched the walls was also considered unsuccessful (failed trial). Measurements were taken to find out just how wide the area had to be for successful wheelchair/scooter navigation.

It might seem obvious that spaces too small for mobility equipment are a problem. But it’s a bigger problem than you might think. It limits accessibility, of course. But banging into walls can cause bodily harm to the person in the chair/scooter. The equipment can get damaged and so can the structure.

The results showed that the minimum Wheelchair Turning Space recommended by the Accessibility Guidelines for Buildings and Facilities (ADAAG) wouldn’t be enough for anyone in the study to make some of the turns. Ninety-degree turns were easier than smooth U-turns.

Only the ultralight wheelchairs with the compact design and rear-wheel drive could handle small spaces. These types of chairs are mainly used by individuals who can sit up, who are not overweight, and who have full use of their arms.

The authors came to three conclusions with this study. First, anyone needing a specialized wheelchair should be evaluated carefully by a therapist specifically trained in mobility equipment. A wheelchair prescription of this type will make sure the person gets the right kind of chair for his or her needs and use.

Second, the home should be modified to allow for easy use of the mobility equipment (chair or scooter). Expecting the person who needs the chair/scooter to manage tight spots without hitting walls may not be realistic.

And finally, current guidelines and standards for buildings (e.g., door and hallway widths, bathrooms) should be updated. The goal is to make sure today’s current wheelchair and scooter users can get in and out of public areas easily. With almost two million Americans in wheelchairs or scooters, this recommendation has the potential to affect the daily lives of many people.

We are starting to see more and more older adults out and about in the community in power wheelchairs or scooters. It’s not so uncommon to see someone motoring down the grocery store aisle or attending a sporting event in one of these power mobility devices (PMDs).

You might wonder — how did disabled adults get around before these units were available? Good question and most likely the answer is that they were shut-ins (unable to leave home). You might wonder — is an expensive, motorized wheelchair really necessary? Whatever happened to the old-fashioned manual wheelchairs?

Most of the wheelchair users in this country are 65 years old or older. They are in a mobility device because they have a disabling condition. It’s often the case that they live alone or with someone who can’t push a self-propelled chair. And the disabled adult may be able to push the wheels forward with their arms and hands a bit but not enough to go everywhere.

Given that background, it’s time to take a closer look at how these power mobility devices (PMDs) impact peoples’ lives. Just how effective are they? Do the benefits outweigh the cost? How long does it take before older adults get the hang of using it? And does that learning curve translate into functional mobility?

These are some of the questions addressed by this study. Adults between the ages of 50 and 89 years of age who use some type of powered mobility device (PMD) were included in the study. The goal was to see how stage of PMD affected what they called life-space mobility (getting around). The researchers divided patients up into two groups based on stage of usage.

One group consisted of people who had been using their first PMD for less than six months. This group was called the initial users group. The second group (the long-term users) had been using their PMDs for more than six months. As a little peek into their results, we will tell you that by the end of the study they had identified a third group: expert users (stage beyond the first year).

The data was collected over the phone in interviews with all the participants. Questions were asked to determine each person’s usage of their wheel chair or scooter. Use was measured inside the home, outside just around the house, in the neighborhood, in town, and outside of town. Information was gathered about how much time the mobility device was used and how much help the person needed from someone else.

While analyzing the data, factors that might affect power mobility device usage were also examined. These variables included things like sex (male or female), diagnosis, walking ability, type of device used, training to use the device, living status (alone, partner, assisted living), and overall activity level.

The group was made up of 60 per cent women, 40 per cent men. Most were power chair users (52 per cent) with 48 per cent scooter users. Half the group had some kind of neurologic problem such as a stroke, Parkinson’s, multiple sclerosis, or brain injury. They could walk indoors (independently or with a walker or cane) and get in and out of their wheelchair or scooter without help.

They found that men were more likely to travel distances farther away from home in their powered mobility device compared with women. Men and women who used scooters were able to go farther more often than those in a wheelchair.

Participants who had a trial usage at home before purchasing the device made greater use of it compared with those who did not have a trial run. And it was observed that those individuals who still drove their own car were able to experience a greater and wider Life-space (i.e., they went more places more often).

In summary, power mobility devices (whether a powered wheelchair or scooter) give older adults the ability to get out more in their own neighborhood. Having a powered mobility device didn’t mean the user would increase the distance to his or her outings — just the frequency (how often) they got out. People who had specific reasons for wanting a powered mobility device called participation objectives (e.g., go shopping, eat out, take the dog out) did increase their Life-space mobility.

The authors recommend training for anyone considering a power mobility device. Training specifically geared for women is advised. A trial use of any device but especially the scooters is recommended for everyone of either sex and of any age. When considering the prescription and purchase of these devices, participation objectives are a good idea and helpful to create first.

Scientists are slowly uncovering the mysteries of fibromyalgia syndrome (FMS). Instead of seeing this condition as a painful musculoskeletal problem, it’s looking more and more like a complex nervous system disorder affecting (in part) how pain messages are processed.

Pain has always been a key feature of fibromyalgia. For a long time, diagnosis has been based on the number and location of tender points. But with the presence of anxiety, depression, and sleep problems, there’s been a shift away from diagnosis by tender points to a more whole person approach.

Besides the typical physical symptoms that characterize fibromyalgia syndrome, there’s also a common past history (e.g., abuse, prematurity, growing pains as a child) and possibly some environmental factors. But since the past can’t be changed, treatment is now what we call multimodal management. That means the many problem areas are addressed all at the same time instead of just treating the painful symptoms.

Patient education is first and foremost for a successful outcome. Affected individuals must understand that their pain, depression, and fatigue can be improved but it may take weeks to months. Patients must be patient with the process.

Moderately intense exercise is prescribed and supervised by a physical therapist. Having a therapist guide individual patients to find the optimum program that works for them is essential. Exercise will help reduce pain and depression, as well as improve sleep. Getting good sleep at night also improves muscle pain and boosts mood.

High-intensity aerobic activity is not the goal. In fact, patients are advised to avoid intense exercise. It’s far better to establish a consistent program of 20 to 30 minutes of physical activity and exercise four to five times each week than to start off at a pace patients can’t keep up with.

There are many things patients with fibromyalgia syndrome can do to manage their own symptoms, In addition to regular exercise, attending a local support group can give patients a place to vent their frustrations and worries, meet other people with similar symptoms and challenges, and find out what others are doing that’s working. Support groups help everyone stay on target with their program and are considered a very valuable part of disease management.

So, is fibromyalgia syndrome a disease? If the term disease is used to describe a condition in which the body-mind complex is not at ease, then yes, fibromyalgia syndrome can be considered a disease. We have certainly moved away from seeing this condition as one defined (and diagnosed) just by tender points of the muscles.

Recognizing the diagnosis requires more than identifying tender points, new tools are being used to objectively assess patients. A new scale called the symptom intensity scale (SIS) charts regional areas of pain, measures pain levels, and monitors fatigue. Other ways to assess mood, quality of life, and function include the Mood Disorder Questionnaire (MDQ), Patient Health Questionnaire (PHQ), Sleep Scale, and Fibromyalgia Impact Question (FIQ).

What’s next for patients with fibromyalgia syndrome? Until more is known about how pain is processed and what goes wrong, we can’t fix or cure this condition. The focus will remain on examining different treatment approaches and objectively measuring results. There may be one best treatment method that can be used with all fibromyalgia patients. But for now, it looks like management will remain multimodal and individualized for each patient.

We hear about how often adults suffer from low back pain but with more and more jobs requiring repetitive motions like typing, scanning product labels, or grasping tools, arm pain is starting to move from the back seat to the front. Treatment tends to be conservative with antiinflammatories, physical therapy, and sometimes, steroid injections. In this study, the use of an antidepressant (Amitriptyline) for persistent arm pain associated with repetitive arm motions is examined.

The goal of the study was to see if Amitriptyline worked better than a placebo (sugar pill). Amitriptyline is often used successfully for patients with chronic low back pain. It has also been used for patients with headaches, nerve pain, and fibromyalgia. So, it makes sense that it might be equally effective in treating chronic arm pain.

The measures used to test how well Amitriptyline worked compared to a placebo pill were pain intensity and function. Function was measured using tests of grip strength, mood, and sleep. When researchers want to compare one specific treatment to another like this, they perform a double-blind, random-controlled trial. Double-blind means no one (patients or researchers) knew which type of pill each patient was given. Patients were randomly selected for each group using a computer program.

Only adults with overuse or strain of the muscles and/or tendons were included in the study. Many of them had been diagnosed with wrist or elbow tendonitis or carpal tunnel syndrome. Types of repetitive tasks linked with arm, wrist, or hand symptoms included computer work (keyboarding, using a mouse), playing a musical instrument, construction or assembly work, arts and crafts, house cleaning, or handwriting. Results were compared for Amitriptyline versus the placebo based on type of task causing the initial symptoms.

Anyone who had a known neurologic problem, arthritis, or specific injury to the arm was not included. Pills (Amitriptyline or placebo) were taken once daily at bedtime for eight weeks. Taking the pills at bedtime was advised because the Amitriptyline does tend to make people drowsy. The Amitriptyline pills given contained 25 mg of the drug, which is considered a low-dose.

Participants were tested at the start of the program and retested after three weeks, six weeks, and finally four weeks after the treatment was completed. They used a wide range of self-report questionnaires to assess sleep, pain, mood (anxiety or depression), and sense of well-being. Each person gave a report of any side effects from the “medication”. A handheld device called a dynamometer was used to test hand grip and finger pinch strength.

In the end what they found was that there wasn’t a difference in the effect on arm pain for either pill. The patients taking the Amitriptyline did gain strength and function compared with the placebo group. And the Amitriptyline group improved in their sense of well-being.

Despite taking the pill at bedtime, persistent drowsiness (into the morning upon waking up) remained the single most reported side effect. Almost half of the Amitriptyline group reported being affected by drowsiness, whereas only 15 per cent of the placebo group experienced this particular side affect. The longer the group took the Amitriptyline, the less daytime drowsiness bothered them.

The authors concluded that low-dose Amitriptyline is not more effective than a placebo pill in terms of pain control in the treatment of arm pain from repetitive overuse. But it does improve function and mood quickly. Amitriptyline has both analgesic (pain relieving) properties and acts as an antidepressant. Once the antidepressant took effect, the person felt better and could do more. When the study ended, arm function got worse again for the Amitriptyline group. That’s called a reversal of positive treatment effects and points to Amitriptyline being more effective than a placebo.

More study is needed to investigate the effectiveness of different dosages of Amitriptyline and over longer periods of time. Higher doses of the drug might reduce pain but there’s always the risk of worse side effects with more active drug ingredient. Still, this is the first study comparing Amitriptyline with a placebo for chronic arm pain caused by repetitive motion. Having another tool for treatment of this persistent pain may benefit some patients who do not respond to conservative care otherwise.

Most of us who are 50 years old or older are acutely aware of the many changes we see in our bodies. The mirror shows us everyday that we ain’t what we used to be. But there are some things we can’t see that may need your attention. One of those is a condition called osteoporosis. You’ve probably already heard about it but may not think it applies to you.

Osteoporosis is a decrease in bone mass. The bone is less dense, a concept referred to as a decrease in bone mineral density (BMD) — a thinning of the bone, so-to-speak. Left untreated, bones can become brittle and break causing bone fractures and other problems.

You may not think this applies to you, but half of all adults over the age of 50 are affected. How can you tell if you have osteoporosis? Your primary care physician is the best person to evaluate and advise you. But educating yourself about this skeletal disease, recognizing your risk factors, and practicing some prevention is a very good idea.

First, who is at risk? Are you? According to the National Osteoporosis Foundation (NOF), there are two categories of risk factors: lifestyle factors and medical risk factors. Lifestyle factors include things like too much alcohol, tobacco, caffeine, and antacids (aluminum). Not enough calcium, vitamin D, and physical activity add to your risk. These are all considered modifiable risk factors, meaning you can do something about them to reduce your risk.

Some of the medical risk factors are nonmodifiable. For example, there’s not much you can do about your age or sex (women are at greater risk than men). A previous fracture, poor vision (contributing to falls), poor balance, and some medications also increase your medical risk of decreased bone mass. Some of these are modifiable, while others are not. Your physician will help you sort out which are your risk factors and how to reduce your risk as much as possible.

Although older Caucasian (white) women (especially after menopause) are the group affected most often, anyone of either sex (male or female) and of any color (racial or ethnic background) can develop osteoporosis. In fact, there is evidence now that not enough calcium and having diabetes mellitus has bumped up the number of Hispanic women affected by osteoporosis.

Men can also develop osteoporosis. This is especially true if they are over 70 years old or have low levels of testosterone hormone and any of the other risk factors already mentioned. Caucasian men are affected most often (seven per cent), followed by African American men (five per cent), and Hispanic men (three per cent). Those figures compare with 20 per cent for both Caucasian and Asian women.

If you have any of these risk factors, you should be evaluated. The next question is what kind of testing is available to see if you do have osteoporosis? The gold standard (number one tool used) is still dual-energy X-ay absorptiometry (DXA, pronounced Dex-uh) scanning. It’s painless, noninvasive, and easy to do. Not only that but it is precise (accurate). In some cases, ultrasound or MRI may be used instead of DXA scans, but the DXA test measure is the most reliable and the most widely used.

The National Osteoporosis Foundation along with the World Health Organization (WHO) recommends the use of another assessment tool. This one is called the fracture risk assessment tool or FRAX. The FRAX measures your risk of fragility fractures and gives the probability of a major osteoporosis fracture (spine, wrist, shoulder, hip) over the next 10 years. You can access the FRAX questionnaire yourself at www.sheffield.ac.uk but you will need your DXA scan results in order to complete the formula.

Many older adults who need osteoporosis testing may be concerned about how to pay for it. Medicare coverage is available for women who have low estrogen and qualify for Medicare and anyone on Medicare who is taking corticosteroids (usually used for chronic inflammatory conditions). Patients on Medicare who are already on medication for osteoporosis are covered for repeat testing to monitor response to therapy.

The important thing is to recognize your risk factors, take precautions when necessary, and see your physician for testing and treatment if you are 50 years old or older. This is one condition for which a small amount of prevention can go a long way. And these days, anything that keeps us healthy, active, free of fractures, and out of the hospital or nursing home is worth paying attention to!

If you’ve had gout for a long time or you are a new patient with gout, this report will be of interest to you. After years without new hope for treatment, safer and more effective medications are now available.

Gout is a form of arthritis with joint inflammation. It’s caused by too much urate (uric acid) in the body because of a missing enzyme (uricase). Excess uric acid causes needle-shaped crystals to form in the synovial (joint) fluid. One of the most distressing symptoms of gout is painful, inflamed, hot, and tender joints. The big toe is affected most often but other joints can become symptomatic, too.

For the last 40 years, treatment has focused on diet to reduce urate levels. Painful inflammation is managed with nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids. But not everyone can take these medications. These drugs are often off-limits for some patients with gout who also have diabetes, high blood pressure, or kidney problems.

Despite the need for an alternative approach to gout, no new medications have been developed until just recently. In 2009, the Food and Drug Administration (FDA) approved a group of new drugs for the treatment of gout. These new medications are the subject of today’s review and include colchicine, anti-interleukin (IL)-1 beta therapy, urate transporter (URAT1) inhibitors, febuxostat, and uricase replacement.

The first drug mentioned (colchicine) isn’t really new. It’s been used for gout for 200 years. But the FDA has never formally approved it. As a result of reviewing the effectiveness and safety of this drug, a new nongeneric drug (Colcrys) has been developed, approved, and is now available. Colcrys has the advantage of stopping the gouty attack quickly but it only worked for half the people who tried it.

Anti-interleukin therapy is a biologic approach designed to prevent the inflammation associated with gout. These medications can also be used to treat inflammation once it begins. Three of these anti-interleukins (Anakinra, Rilonacept, and Canakinumab) are being tested and studied in humans.

So far, Anakinra has been effective in reducing 50 per cent of the painful symptoms associated with gout and it does so within 48 hours. Rilonacept provided 75 per cent pain relief for half of the patients who took it and prevented symptoms in three-fourths of the patients who took it prophylactically (to prevent joint inflammation). Canakinumab is faster in delivering relief from pain (within 24 hours) and seemed to be able to prevent recurrent attacks later.

Besides treating the symptoms of a gouty attack, modern treatment now has new agents to reduce urate levels. This can be done by helping the body get rid of the excess urate or by keeping the body from making so much urate in the first place.

Febuxostat is a new drug that does both at the same time. Compared with the drug that’s been in use since 1963 (Allopurinol), Febuxostat is almost twice as effective. And Febuxostat can be used by patients who have kidney problems if they don’t already have severe kidney failure.

You might think that if gout is caused by a lack of uricase enzyme, why not just replace the missing ingredient? Good idea! But uricase replacement isn’t that easy. It requires intravenous (IV) delivery and the effect doesn’t last. And in some people, infusion (IV drug delivery) causes an immune reaction to the drug. The IV drug is also very expensive and inconvenient. For now, this approach is used with a small number of patients who can’t take Allopurinol or who have not responded to other treatment.

In summary, drug companies have turned their attention to finding better, safer ways to prevent, treat, and manage gout. Successful elimination of painful joint symptoms will be appreciated by the increasing number of adults who suffer from this on again/off again condition. Studies are in the early phases with human trials right now. Results look promising, but time will tell.

More people are involved in weight training than ever before! We’re talking kids to seniors from age six to 100! Naturally, there has been a corresponding increase in the number of injuries. These injuries occur whether free weights or weight machines are used. In this article, a composite picture is made from data taken from 100 emergency departments where weight-training injuries were examined and treated.

There’s been a huge increase in weight training-related injuries since the last time a survey of this type was done. With over 25,000 injuries reported in these 100 hospitals, it’s estimated that almost one million weight training-related injuries are seen every year in other hospitals across the United States — and that doesn’t include injuries that are never reported or evaluated.

So who’s getting hurt? Why? What kind of injuries are being reported? And what can be done about it? Let’s start with who — mostly men (82.3 per cent) but that’s also because many more men than women lift weights. The breakdown by age was also reported in terms of area of the body injured. For example, women were more likely to injure their foot, whereas children (12 and younger) had more hand and foot injuries.

Statistics show an upward trend for injuries among three distinct groups: teens under the age of 13, women in general, and older men (55+). Men of all ages injure their backs and upper trunk most often. They are also more likely to overexert themselves (lift too much, too many times) leading to an injury. There have even been deaths reported from heart attacks among men lifting weights.

Why are these injuries occurring? Well, believe it or not, the largest proportion of injuries occurred while using free weights, which the individuals dropped on themselves or hit themselves with. There were some cases of getting smashed or crushed under weights and losing balance and falling while holding onto weights. Older adults (55 and older) tend to use free weights more often than weight machines. Of the injuries reported in patients using machines, the majority of individuals hurt were 55 or older.

As for type of injuries, the possibilities are strains or sprains; bruising, crushing, or scratching skin and other soft tissues; cuts and punctures; fractures and/or dislocations; burns; bleeding; and tendon/muscle avulsions (complete tears and pulling away from the bone).

The information gained from this study is very useful for several reasons. First, it is an estimate of injuries among the general population — boys, girls, men, and women of all ages. Previous studies were more focused on power lifters. Second, the fitness craze is catching on! More and more people really are getting active and participating in weight training. That means we can expect even more of these kinds of injuries. Which leads us to the third point: efforts must be made to target injuries prevention.

More studies are needed to help identify when each age group suffers injuries. Is there supervision available by trained fitness instructors? Are these injuries occurring early on in the training period? Is it a simple matter of teaching everyone who lifts weight how to maintain control of the free weights?

And finally, could it be that older adults can’t accept limitations as they age? If they refuse to see that their decreased abilities can lead to injuries, they are less likely to modify their activities and approaches to weight training.

Educating young to old about the proper use of weights is important. Anyone starting a weight-training program of any age or sex should start with lighter weights and work up over time. This is called progressive resistance exercise or PRE. Having a knowledgeable trainer to guide beginners of all ages is not just a good idea — it could make the difference between success and painful injuries.

The use of machines also requires some tips on training. It’s just as easy to overdo on weight machines as it is with free (handheld or dumbbell) weights. Most of the commercially available weight machines used in home gyms and fitness centers are designed for the average sized adult. They are not proportioned for short or tall, small or large people.

No matter what type of weights are used, a safe training program under the supervision of a knowledgeable health care professional or fitness trainer is advised. Proper instruction may reduce injuries and help all interested individuals advance at their own pace for a successful injury free outcome.

This group of researchers have been studying patients with complex regional pain syndrome (CRPS) for a long time. They’ve been trying to figure out what causes the symptoms these patients suffer in order to find better ways to treat CRPS (or even prevent it).

Complex regional pain syndrome (CRPS) is a group of symptoms usually affecting the arm and hand on one side but it can affect the leg and foot (and even other parts of the body). After trauma, injury, or surgery, the person develops pain and changes in skin temperature and circulation to the affected area(s). The involved body part can become very cold and clammy or very hot and sweaty. Patches of dark hair might form on the back of the hand or forearm. The pain that accompanies CRPS can be very excruciating.

Scientists think the changes that occur develop because normal function of the sympathetic nervous system (SNS) has been interrupted or disrupted. The automatic portion of the nervous system that keeps you breathing and your heart beating is broken down into two parts: the parasympathetic and the sympathetic nervous systems.

The sympathetic nervous system is the get up and go guy. This part of the nervous system makes sure you can run fast and jump high when being chased by a tiger (or during any stressful situation). The sympathetic nervous system is balanced by the parasympathetic nervous system (PNS).

The parasympathetic nervous system is the rest and digest part of the automatic nervous system. It’s the parasympathetic nervous system that brings calm and order back into balance after any kind of stress (physical, mental, emotional). It helps bring your pulse and blood pressure back down, relaxes your muscles, and turns your bowel and bladder functions back on.

Previous studies have shown that some people with complex regional pain syndrome eventually get better. Their nervous systems seem to recover and return to normal functioning. Others end up with a permanent set of changes that reduce their hand function for the rest of their lives.

In this study, the authors take a look at the status of the sympathetic nervous system over time in patients with a diagnosis of upper extremity complex regional pain syndrome (CRPS). Using the Michigan Hand Outcome Questionnaire (a measure of pain and hand function) and a Doppler study (measure of skin blood-flow), the scientists compared early to late results. Subjects in the study all had CRPS for at least three years before becoming a part of this study. Men and women adults were both included.

As part of the tests of sympathetic nervous system responses, skin blood-flow was measured in both hands under two separate conditions. In the first one, skin blood flow was monitored as the patient took a deep breath in and let it out fully. During the second provocative test (meant to provoke the sympathetic nervous system into responding), an ice pack was applied to the uninjured upper arm. Skin blood-flow was measured continuously as the cold pack was put on and taken off (looking for a normal response to the cold and return to normal).

Results were compared to values measured in normal adults of the same ages. They found pathologic results in response to both tests — and in both hands! That means the uninjured hand also showed some deterioration of the sympathetic nervous system function, too.

The most interesting result was that hand function was no different between patients who had complex regional pain syndrome (CRPS) plus sympathetic nervous system impairment and those patients who only had CRPS (without sympathetic nervous system dysregulation). Hand function refers to activities of daily living, pain, and work performance. But it also includes the patient’s perception of appearance, and overall patient satisfaction.

They also found that some people developed greater impairments of the sympathetic nervous system function over time. Half of the patients who tested with normal nervous system function at first later developed measurable sympathetic nervous system dysfunction.

The reason for the lack of sympathetic nervous system recovery in some CRPS patients and the deterioration in others has not been explained. The fact that function isn’t always affected by changes in sympathetic nervous system function may be because there is some other (as yet unknown) factor at work here.

The authors propose the theory that people with CRPS who lose their automatic nervous system reflex responses might have a faulty nervous system to begin with. It’s possible that’s why they develop complex regional pain syndrome after trauma when others with similar injuries recover normally. One way to find out is to measure the sympathetic nervous system function in many normal, healthy adults and follow them their whole lives to see who develops CRPS. That’s a major undertaking but could be done in conjunction with other lifelong studies already underway.

Recent research has suggested the effectiveness of Tai Chi in
developing and maintaining balance an older populations, and thereby
decreasing the incidence of falls. It has been noted that in the
absence of a training program, aging will result greater postural sway
and lower walking speeds. However, little has been published
concerning the specific ability of Tai Chi relative to other forms of
balance training in producing these outcomes. That is, while Tai Chi
has proven effective in this area, the question remains whether this
is a characteristic exclusive to Tai Chi, or if other forms of
training can produce equivalent results. This article will examine the
findings of a recent study which attempted to test the merits of Tai
Chi against those of basic balance training in a 12-week training
period.

The study concluded that at the end of the 12-week training period, no
significant differences were present in the two groups’ upright
standing control, walking ability, or walking speed. At first glance
it seems that there exists no tangible difference between balance
training programs and Tai Chi programs in maintaining functionality in
older people.

Many explanations have been offered for why this study failed to
replicate similar experiments’ findings. First, the researchers note
that this 12-week training program required far less extensive
training than the typical 6 times a week for 4-8 weeks commonly
employed in other studies. Also, the sample population was comprised
of individuals who all regarded themselves as physically active, prior
to enrollment in the program. As such, these individuals did not
experience an increase in their baseline ability in either postural
control or walking speed. Taken together, these two factors may
explain why these finding represent such a departure from findings
concerning the merits of Tai Chi compared to inactivity.

While the study failed to demonstrate any significant difference
between the two training programs in predetermined statistical
measures, it did spot a noticeable difference between the two in terms
of a tertiary statistic, the Romberg quotient. It seems that although
Tai Chi did not directly improve statistical outcomes any more than
balance training, it can aid in limiting the eye closure effects on
postural control. Thus, Tai Chi may prove effective in limiting the
negative impact of aging on sway perception. While this did not
manifest itself in the test group’s walking speed or standing control,
it is theorized that under a longer or more intense training program
this benefit might begin to reveal itself.

As yet, it is uncertain whether Tai Chi possesses any unique ability
to limit postural sway and maintain one’s movement and walking
functionality. What is certain is the ability for training programs
like these, aimed at developing and maintaining balance, to make
improvements in older populations’ daily living.