Restless Legs

In 1999, Dr. William Dement, the nation’s foremost sleep researcher, lamented that 15 to 20 million Americans with Restless Leg Syndrome had fallen into a major knowledge gap in the medical care system. Doctors simply didn’t recognize the symptoms, and, more importantly, didn’t understand the serious effects of restless legs on patients’ lives. Dr. Dement wanted to educate patients and their doctors, but sleep medicine didn’t attract much public attention. Then, in 2006, the pharmaceutical industry waded into the knowledge gap, launching an advertising campaign during the Superbowl for the first drug approved for the treatment of Restless Leg Syndrome, something most of the audience had never heard of. Advertising a disorder to market a drug is not the education Dr. Dement had in mind, but at least it generates interest and curiosity, the first steps toward knowledge.

“Syndrome” means a set of symptoms. Restless Leg Syndrome (RLS) encompasses creepy, crawly sensations in the legs (but occasionally in the trunk muscles or arms), occurring mainly in the evening, getting worse on retiring for the night, and relieved by motion, particularly walking. The best estimates are that 5-15% of the population recognizes these symptoms as their own. More men than women are affected and frequency increases with age. The cause is unknown, but recent research suggests that iron metabolism in a tiny part of the brainstem is at fault.

RLS is also known as “Ekbaum’s Syndrome,” after Karl Ekbaum, who first described the problem in 1940. Jerry Seinfeld’s script writers added “Jimmy Legs” to the RLS lexicon when they had Kramer moan about a girlfriend whose nocturnal leg movements made him crazy. Kramer was actually describing not RLS but the primary sleep disorder that often accompanies it: periodic leg movement disorder (PLMD). In contrast to restless legs, Jimmy Legs often bother bedmates more than they do the afflicted sleeper, who spends much of the night bicycling away with no memory at all of the movements or of the multiple awakenings that accompany them.

More than a sleep disorder

Because restless legs cause insomnia and sleep deprivation, RLS is technically a sleep disorder. However, the sufferer’s waking world is also fraught with difficult situations that demand stillness. Theaters, airplanes, dental chairs – even operating tables- can be intolerable. The course of action taken for relief depends on the frequency and severity of the symptoms, balanced against the risks and side effects of the treatments considered.

The mildest version of RLS occurs in otherwise normal people after extreme physical exertion such as running a marathon, and it responds to time, rest and energy replenishment. At the severe end of the RLS spectrum are people whose trouble falling asleep and disrupted nighttime sleep produce severe daytime sleepiness. They need accurate diagnosis and treatment, by sleep specialists if possible. Between the mild, intermittent end of the spectrum and the severe extreme are all the rest of the RLS sufferers, including some pregnant women. These people are best served by an ongoing relationship with a doctor who understands the syndrome and the complete approach to treatment.

Diagnosis and Treatment

Treatment begins with a good history and physical exam. Restless legs are sometimes symptoms of peripheral nerve or kidney problems, and occur in the setting of diabetes. They can also reflect side effects of drugs such as antidepressants, antihistamines, and anti-nausea medicines. Even in the absence of medical problems, a check of the serum iron is on order since long clinical experience and new research implicate iron metabolism. Iron deficiency should prompt a search for a cause – usually bleeding or dietary insufficiency. Medications to reduce stomach acid, now in widespread use, can also cause iron deficiency.

Assuming there are no underlying medical problems, the next step is the elimination of stimulants from the diet – particularly in the latter half of the day. That means caffeine, cigarettes and alcohol – as well as any over the counter medicines of the types mentioned above. Developing mental alerting strategies to occupy the mind during times of boredom may help. When focused and occupied with games or puzzles the brain seems to suppress restless impulses. Increasing daily physical activity quiets the legs in over 50% of RLS patients.

When sleep suffers and normal life situations such as long automobile rides are intolerable, pharmacologic intervention is often necessary. The drugs that appear to be helpful fall into four classes: the ones that increase the neurotransmitter dopamine or act like dopamine (dopamine agonists); narcotics like codeine; the benzodiazepines like Valium, and the anticonvulsant Gabapentin. All of these are serious drugs with potential side-effects, not the least of which is a phenomenon called augmentation – the worsening of symptoms over time producing the need for more drugs. But the drugs can be true life-savers for people who are severely afflicted and in desperate need of sustained sleep and the ability to remain still.

What of the new drug touted in Superbowl ads in 2006, and a more contenders released since then? They are dopamine agonists, some of which have been around for years – FDA-approved for use in Parkinson’s disease, but also used “off-label” by doctors dealing with RLS patients. Their marketing focuses a light on the obscure world of sleep medicine, where devoted researchers who followed Dr. Dement continue to educate patients and doctors about the troubled sleep that generates many accidents and eats away at productivity and emotional resilience. That is a service to all.

Posted by medical plaintalk

Physician turned medical writer.

One-Footedness: The Key to Balance

Human beings negotiate the world on two legs, a skill mastered in toddlerhood. As children we are well balanced and swift. Then one day in mid-adulthood, we look at our children and realize that they are fast out-performing us in skills that require balance. When did balance become more difficult? Of course we cannot define that point because life sneaks up on us, nibbling away at skills we do not practice because nature works assiduously to conserve energy. Motor and mental tasks we do not practice get put to rest.

What’s involved in balance?

We maintain balance by taking in three types of sensory input and adjusting muscular activity accordingly. The three input systems are vision, messages from hair-like projections in three fluid-filled canals set at right angles to each other in the bone of the middle ear, and continuous reporting from delicately engineered receptors in our muscles and tendons that measure stretch and tension. We can learn to balance without the first two components of the balance system, but not the third. To demonstrate the importance of the input from the muscles and tendons, try getting up and walking after one foot has fallen densely asleep from pressure on the nerves which are the highways for sensory information on its way to the brain. Even if you can wiggle the foot because motor nerves are more resistant to pressure, you cannot use it without knowing where it is.

“Use it or lose it” applies to balance

Much of modern adult life involves little more than moving from one form of sitting to another, which gives the feedback systems in the eyes, ears, and muscles and tendons little exercise. Over time, balance skills deteriorate, and eventually falling happens with simply tripping or changing position or direction. Falling is the cause of many hospitalizations and, often, the injuries incurred lead to death. Living well and independently over the decades depends in no small part on maintaining the ability to walk without falling. Fortunately, balance improves with practice, and we have ample opportunity throughout the day to engage the balance systems and give them a workout.

Waking up the eyes and ears

Eyes are easy. Look around while you walk. Off to the side, up, down, straight ahead. If you are a straight-ahead looker most of the time, looking around may make you feel a bit unsteady at first. But your brain will begin to coordinate the changes with the information coming in from the ears and the muscles, so it will get easier. Once it does you can add more head movement, following your gaze. That will add more movement of the inner ear canals, which can become very accustomed to minimal movement. Young adults taking dance lessons for the first time or grandparents taking grandchildren on park equipment might be surprised to find themselves dizzy because of long unpracticed movements that involve spinning in circles or bending over. The ears are reporting unusual movements but with practice they will re-learn and stop sounding alarms. Deliberate exercises in head tilting and turning, such as the ones widely prescribed for benign positional vertigo, can speed the process.

Waken the muscle receptors by paying attention to walking

The stretch and strain receptors in the muscles are active whenever we are upright, but also lose function – even in walking, which is the most frequent and complex motor function we perform. Walking involves the subconscious coordination of over 300 muscles in a series of controlled falls that move the 200 bones of the skeleton forward or backwards in space, sometimes with the addition of upward or downward travel on stairs or ramps. Walking requires one-footed balance, with one foot bearing the body’s entire weight while the other foot swings forward. Landing the forward moving foot prevents the body from falling as it moves forward.

As the years pass, the body’s motor system tries to conserve energy by allowing you to use fewer, large muscles rather than more numerous small ones to accomplish the task of walking. Balance suffers and it is harder to adjust quickly to uneven terrain or surprises that throw you off balance. Learning to re-engage and strengthen all the smaller muscles devoted to one-legged balance re-awakens a lot of the sensory input and improves stability in all your upright activities.

Exercises for one-footedness

A good exercise for developing one-footed balance involves standing on one foot while barefoot (elevated heels throw the center of gravity forward), lifting the other knee in front of you and using a countertop for support. The gluteal muscles in the buttock on the side of the weight bearing leg will be forced to contract to keep the pelvis from dropping on the other side. The entire foot, powered by the lower leg muscles, is the stable platform that supports the rest of the body and the big toe stays in active contact with the ground. As strength and balance improve, try moving away from the support of the counter, getting the free knee up to a right angle in front of you and then swinging it down and back and a little behind you, concentrating on keeping the pelvis level and stable and the trunk upright. Adding toe lift exercises on stairs – dropping the heels a little below the stair level and pushing up from there – adds to the strength and flexibility of the ankles and to sensory input from the many intrinsic foot muscles and lower leg muscles.

Taking the exercises out for a walk

Once you get the feel of the muscle contractions necessary for one-legged balance, then try to feel the same sequences of activity while walking. Good, upright posture helps. Your head weighs 10-14 pounds when directly over your spine, but the weight doubles, triples and even quadruples in proportion to how far in front of the body it is. If you have the habit of jutting your head forward with a curve in the back of the neck, or looking at the ground while you walk, the work of balancing increases proportionately. Keep the chest lined up over the pelvis and engage the trunk muscles – the so-called core – by trying to lift the pubic bone upward with the front of the abdomen. The core muscles maintain proper pelvic tilt. Then, while walking, try to feel the one-footedness you practiced while standing next to the kitchen counter and the ankle motion you felt doing toe lifts.

The action in walking is at the hip, ankle, and foot. The role of the knee is to let the leg bend as necessary. As you shift your weight to one foot, the gluteals contract in the buttock to hold the pelvis and prevent the released side from dropping. In the brief phase before the supporting leg begins to push you forward, notice the entire sole of the foot. Its connection with the ground begins with the heel planting down and continues as the body weight rolls forward. The knee will be straightest when you push through and are about to plant the new foot.

Do not neglect the feeling coming from the toes – especially the big one as you push off and begin to move the other leg through. Toes add a significant amount of surface area, increasing the available sensory information fed into the motor system and they contribute to the push phase of the gait. Notice also how the ankle moves as the heel lifts off the ground. Notice all of it as your other leg is swinging through and really try to relate the sensations to the one footed balance exercises you have done to practice.

Notice other gaits

And while you are out walking and noticing your own one-footedness, take a look at some of the gaits you see. You will begin to learn the risk factors for falling. You’ll see people using only large muscle groups, initiating the leg swing by lifting the entire side of the body, from the shoulder down. They are already off balance. Their bodies must tip to the opposite side to allow the advancing leg to clear the ground. When the new leg lands and the weight shift begins again, the gluteals are not engaged, there is no push off from the hip and the foot, and the other side begins to lift from the shoulder. On a sunny day you will see such a walker’s shadow shift from side to side. Sometimes there are physical problems that impair walking balance, but for someone in good health, without neurological disorders like neuropathy, working to make the shadow move in a straight line pays off in a longer functional life.

Posted by medical plaintalk

Physician turned medical writer.

Morning Foot Pain: Plantar Fasciitis

“.as we know, there are known knowns; there are things we know we know. We also know there are known unknowns; that is to say we know there are some things we do not know. But there are also unknown unknowns—the ones we don’t know we don’t know.” Donald Rumsfeld former US Secretary of Defense

In medicine, what we “know” changes regularly as long as curiosity keeps opening doors. For many decades, the complaint of pain in the bottom of the foot, just in front of the heel bone and always worse with the first few steps of the morning or after prolonged periods of inactivity, fell into the “known known” category. Doctors and physical therapists confidently made diagnoses of plantar fasciitis, certain there was inflammation in the plantar fascia, the band of tough fibrous tissue that spans the bottom of the foot. The condition was common, especially in runners, in people who spend a lot of time standing on hard surfaces and in post-menopausal women. Most of the time it resolved but there were enough prolonged and vexing cases that did not get better with anti-inflammatory medications and rest that some practitioners began to suspect that plantar fasciitis was a “known unknown” – maybe the cause was not so simple as the inflammation that they postulated. After all, no one had actually looked at the troublesome tissue under a microscope before.

Plantar fascia gets an inspection

In 2003, a Philadelphia podiatrist and pathologist, Harvey Lemont, took microscopic samples of the plantar fascia from patients undergoing surgical release of their presumably inflamed connective tissue. In all 50 samples he found no evidence of inflammation. But the tissue was not normal. The collagen structure was disorganized and degenerated, as if it had been deprived of sufficient blood flow. Some samples contained crystals from prior cortisone injections, common treatment for plantar fasciitis, but by 2000 known to carry significant risk of causing the plantar fascia to separate from the heel bone. Degeneration of plantar fascial structure, a previously unknown unknown, was discovered, and that prompted a change in the name plantar fasciitis to plantar fasciosis, a term which indicates chronic structural disruption but not inflammation.

Lack of inflammation prompts new thinking

Lack of inflammation in Dr. Lemont’s pathologic examinations explained the failure of conventional treatment many cases of plantar fasciitis. And his work raised significant questions about the cause of the problem. Why does the plantar fascia begin to degenerate? What exactly hurts? Is it the bone where the connective tissue attaches? Is it the connective tissue itself? Study of the feet of non-shoe wearing cultures in which our most common foot problems are practically non-existent, and more attention to foot, leg and gait biomechanics began to yield some different ideas, not only about the heel pain syndrome, but about bunions and hammertoes.

Are shoes the problem?

When we are babies and young children, our feet are widest at the tips of the toes. By the time we wear conventional shoes for decades, with shallow, narrow and tapered toe boxes and elevated heels (even running shoes have a 1-1.5” heel elevation), the big toe begins to curve toward its mates, which begin to curl under. The muscle that normally pulls the big toe away from the other toes is pulled inward and weakens because of inactivity. What does this have to do with the plantar fascia? The big toe muscle runs from heel to toe on the foot’s inside edge, right over the artery near the heel that supplies blood to the plantar fascia. Pulling it inward narrows the artery and decreases blood flow to the plantar fascia. It is possible that morning heel pain is ischemic pain, from lack of sufficient blood flow while the foot is dropped down during sleep. Gradual Improvement in the pain with walking may reflect better blood flow with activity, but over time insufficient blood flow takes a toll on the integrity of the tissue in the plantar fascia, adding pain from stressed attachment to the heel bone.

Wimpy foot muscles

For many years people with plantar fasciitis were told they had collapsed arches and flat feet. Or high arches and no flexibility. Or that they pronated – walking on the inside of their feet. Or supinated, walking on the outside of their feet. The treatment was external support with rigid orthotics. But feet are very individual in their structure, and there is little solid evidence that arch height causes problems. Much more evidence implicates weakness at the ends of the arch – the toes and the heels, which bear the weight of the body and are supported by muscles in the feet and in the lower legs.

A shift in treatment plans

Treatment of the heel pain syndrome is shifting to restoration of strength and flexibility in the foot. The plantar fascia functions as a windlass, a pulley that adds to the arch strength when the foot lifts at the heel and bends at the big toe joint to propel the body forward. The goal of therapy is not to stretch that windlass, but to realign the big toe and strengthen the not only the foot muscles that flex the toes and the sole, but also the muscles of the lower leg, the knee and the hip. The toes are coaxed to flatten out and spread by stretching the top of the foot and the front of the ankle and wearing toe spacers. (Useful resource below.)

In the acute phase of plantar heel pain, some external support of the foot under the arch often helps, as does a boot that keeps the foot from dropping down in bed at night. But these aids are temporary while the work of regaining foot strength and flexibility gets under way. It can be difficult to transition from elevated heels to flat shoes, and that process is almost like training for a new physical activity – short bouts at first, gradually increasing over time.

Improvement takes patience, persistence and consistency. All footwear needs to change to shoes with wide, deep toes boxes, flexible soles at the forefoot, and no elevation between heel and toe. Perhaps we will find more unknown unknowns and a way to combine healthy feet with fashionable shoes, but at the moment, the known knowns suggest that changing fashion norms to align them with natural foot function is more likely to be successful.

Resources:

https://naturalfootgear.com

Foot Conditions

Posted by medical plaintalk

Physician turned medical writer.

Thin Bones

Osteoporosis is an equal opportunity disease. Everyone is at some risk for age- related thinning of the bones. Prevention is the best treatment, and understanding how osteoporosis happens is the key to prevention.

Bone is alive

Bone may resemble concrete, but it is vibrant, living tissue that is perpetually under reconstruction. From the time of birth, when bones are composed mostly of soft, pliable cartilage, they shape and reshape themselves. Cells called osteoblasts appear in the cartilage and begin to lay down a protein matrix, spinning it into flexible tendrils like fine rope. A mixture of minerals, mostly calcium and phosphorus, hardens the matrix, creating the blend of strength and flexibility needed for the forces the skeleton has to bear. Throughout life the bones restore, remodel and repair themselves in response to the stresses of life on a planet governed by gravity.

Bones are storage depots for calcium

The bones also store calcium for the rest of the body and respond to its constant demands for the mineral. Cells called osteoclasts break bone down to free calcium for use elsewhere, and to remodel bone where changes are needed. So there is a constant interplay of bone construction and bone destruction throughout life, with the material of you skeleton renewing itself completely every ten years or so.

Bones build, remodel and breakdown

In youth, bone construction goes full blast. Once maturity hits, the process evens out. In older age, breakdown begins to exceed construction. Just another sign of inevitable decline? Yes, but don’t give up hope. You control some things that influence how fast bone loss occurs, and science is making strides to help.

You are the general contractor

You are in charge of the building material that your bones use. A healthy balance of food, including protein, fat, calcium and Vitamin D makes healthy, well-mineralized bones. You need 1200 milligrams of calcium a day, the amount in about three glasses of milk, and 400 IU of Vitamin D, which is made in the skin when it is exposed to sunlight (10-15 minutes of sun on hands arms and face, or back, twice a week). Vitamin D deficiency is common in the elderly because of indoor lifestyles, and in northern climates. Many foods are fortified with Vitamin D, and cod liver oil and fish are excellent natural sources.

Childhood habits matter

The bone density that you achieve in youth is important because it is the starting point for the gradual losses that come later. Maximal bone density for life is achieved in the early twenties The generations of children that have opted for pop over milk are at a disadvantage, arriving at adulthood with less calcium than past generations have. and pediatricians are already seeing more children with fractures than in the past. The cost of neglecting childhood nutrition is bound to rise as time passes.

Gravity and exercise matter

You are also in charge of the activity that stimulates bone formation. When you are upright and fighting gravity, the osteoblasts lay down more bone matrix where it is needed to bear weight, particularly in the pelvis, lower spine and hip. But as soon as the stresses diminish, the osteoclasts start their breakdown work. Just a few days of bed rest sets them in motion. Astronauts in the space lab, under minimal gravity, lose as much bone in a month as a post- menopausal woman loses in a year. Even the impaired movement of a bone under a cast causes localized osteoporosis.

The more you exercise against gravity – as in walking, running, doing yoga or calisthenics, or weight lifting – the more you will call osteoblasts into action. Sit out life, and your osteoclasts will dominate.

Who does osteoporosis affect?

Youth compensates for deficits in diet and activity, but as growth-related hormones fall with age, the cost comes due. Genetic makeup counts too. Women lose more bone than men, smaller-framed people more than larger-framed people, and Caucasians,and Asians more than dark-skinned people. Smokers and heavy drinkers are also at higher risk for osteoporosis, as are people who are confined to bed or taking steroid medications.

The cost of thin bones

Thin bones break and fractures are costly, about $10 billion for the 1.5 million fractures a year in the USA. Spinal fractures, the most common breaks, are very painful and cause spinal deformity and loss of height. Of all the people who fracture hips, 50% are permanently disabled, and twenty percent are dead within a year, from the consequences of immobility. This mortality rate is even greater in men, who are 20% of the 44 million people who have or are at risk for osteoporosis.

Prevention of osteoporosis and fractures

The best treatment for osteoporosis is prevention, starting in childhood. Prevention means solid diet and habitual weight bearing exercise throughout life, and, as the risk of falling increases, exercises to maintain speed and balance. Canes, walkers, hip protectors (padded garments worn over the hips), and attention to the living environment (clear walkways, even surfaces, handrails, etc.) are forms of external prevention.

The role – and the problems – of pharmacologic attempts at prevention

Doctors often recommend bone density tests and sometimes they prescribe drugs to slow the loss of bone. At menopause, bone loss accelerates, and estrogen supplements for a few years have been common practice. Newer drugs such as Evista mimic estrogen’s effects on bone alone and may be safer than the older hormone supplements, which are associated with increased risks of strokes and some cancers, especially when used for many years. The biphosphanates, like Fosamax, slow the work of the osteoclasts by attaching to bone to block breakdown. But they bond to the bone and cannot be released. Some unusual and serious side effects such as sudden, unprovoked leg bone fractures and death of jaw bone after dental procedures. Fortunately these have been fairly rare occurrences. Calcium and Vitamin D supplements improve bone-building supplies, but calcium absorption is not as good from pills as it is from whole foods, and sunlight exposure produces much more Vitamin D than pills can provide. More severe osteoporosis warrants more unusual treatments like shots of calcium-regulating hormones.

You job

Your skeleton will outlast you. Your job is to do your best to make sure it supports you while you are here, and to pass the word to the younger generations who are still building their bones.

Posted by medical plaintalk

Physician turned medical writer.

Lyme Disease: A Whodunit Tale

Some medical advances begin with old-fashioned detective work. Lyme disease, which was unknown in this country prior to 1975 is a good example. That fall, two mothers from Old Lyme, Connecticut convinced the state Department of Public Health and Yale University to explore a mysterious outbreak of cases of inflammatory arthritis among the town’s children, because they were unsatisfied with the explanations they had been given for the cause. The investigation that winter centered on thirty-nine children and twelve adults from Old Lyme, all of whom had developed painful swelling of one or more joints between June and September.

Clues in clinical histories

Although blood tests and physical exams of the affected people had not previously revealed any known cause for the painful, swollen joints, investigators noted that there were striking similarities in the patients’ histories. Especially notable was a peculiar spreading rash that appeared about a month prior to the development of the arthritis and resembled an archer’s bull’s eye target. The affected people also lived close to one another, all in heavily wooded areas. The researchers concluded that the area where the cases clustered and the time of year in which they occurred were both crucial clues to the mystery. They believed that the illness could be an unknown type of infection but would have to await the next disease “season” for confirmation of this theory.

More clues in old European medical literature

In the meantime, investigators began combing through European medical literature, where they discovered similar descriptions of rashes going back to 1909. Over time, the Europeans had named the skin lesion erythema migrans and associated it with an illness that was similar to the one being reported in Connecticut, although without the arthritis. Some European reports mentioned tick bites in conjunction with the rashes, as well as successful treatment with antibiotics. Back in Connecticut, the next summer produced thirty more cases of what was by then being called “Lyme arthritis,” which investigators now believed was some kind of infection transmitted during outdoor activity.

Figuring out the tick relationship

The next pieces of evidence came from field studies of ticks. The distribution of a particular type of tick called Ixodes scapularis (variously known as the blacklegged tick, deer tick, or bear tick) near Old Lyme matched the distribution of local arthritis cases. Tick autopsies conducted in New York on Shelter Island, another hot spot for this mystery arthritis, showed that most of the ticks carried a spiral-shaped bacterium called Borrelia burgdorferi. Blood tests on affected individuals for antibodies to this organism tied it to the clinical cases of arthritis. Over the next two decades, the explosion of the deer population carrying the tick made the disease more common and widely known.As knowledge about and experience with the new disease accumulated, Lyme arthritis was renamed Lyme disease.

Early Lyme disease symptoms

Lyme disease symptoms include an early stage of fatigue, muscle and joint pains, swollen glands, and headaches and fever that begin days to weeks after the infected tick bite. These symptoms represent the immune system’s response to the bacterial invasion. If a bull’s eye rash at the site of a former tick bite is present, diagnosis is easy. If not, diagnosis depends on a clear history of a tick bite and on the development of antibodies to the organism, which usually occurs later than the first few weeks of the illness.

Later symptoms

Left untreated, some, but not all infected patients develop symptoms within the next few weeks to months after the infected tick bite. Symptoms include arthritis, nerve pains, facial nerve paralysis, heart palpitations, shortness of breath, and chest pains. An even less common late phase that can occur up to two years after an infected tick bite might include migrating joint pains, muscle aches, abnormal muscle movements, weakness, heart arrhythmias, and cognitive complaints such as memory problems. These symptoms are not well understood and may represent a combination of the body’s ongoing fight against persistent bacteria and an autoimmune response that they trigger.

Treatment

Treatment of Lyme disease with oral antibiotics, either doxycycline or amoxicillin, is usually curative. If an infected tick is attached for more than thirty-six hours (the least amount of time it takes for transmission of the infection) and was encountered in an area where more than 20 percent of the deer tick population carries Borrelia burgdorferi, most patients are given a prophylactic one-time dose of doxycycline. Otherwise, treatment with antibiotics for two to four weeks begins as soon as the diagnosis of Lyme disease is made. The earlier the treatment, the faster the disease responds and symptoms subside. Late-phase treatment of neurological, cardiac, or arthritic symptoms may require intravenous delivery of antibiotics over longer periods. Although rare cases of persistent symptoms after treatment exist, no study has yet shown enough benefit from very long-term antibiotic use to justify the potential adverse effects of such a treatment.

Prevention of tick bites

Prevention of Lyme disease is the best way to deal with the illness, and there are things you can do to protect yourself. In the states where most cases occur (the New England states and New York, New Jersey, Maryland, Virginia, Wisconsin, and Minnesota), be aware that ticks tend to cling to high grasses and shrubbery in areas where deer roam. By hiking in the center of paths, away from tall grasses and shrubs, and wearing protective clothing, such as long sleeves and pants, you can reduce the chances of a tick bite. Shirt tails should be kept tucked in at the waist, sleeves should be kept closed at the wrists, and pants cuffs should be kept tucked into socks at the ankles. Additionally, spraying with insect repellent containing 20 to 30 percent DEET can help.

Self-examination is very important after potential tick exposure

The type of tick that transmits Lyme disease is Ixodes scapularis. It may be either a six-legged, immature tick nymph the size of a poppy seed or the slightly larger, eight-legged mature tick. Both forms excrete an anesthetic in their saliva that prevents you from feeling their bite, so close examination of your body is necessary after potential exposure. Bathe within two hours of coming inside and do a full body exam, with the aid of a mirror, paying close attention to areas covered with hair. Inspect all gear, clothing, and pets for ticks, and tumble clothing in a dryer at high heat to kill any hidden ticks.

Tick removal

Should you find an attached tick on your body, to remove it place the tip of a clean, fine-tipped tweezer as close to the skin as possible and pull gently, in a straight line. Dispose of all ticks in a toilet or drown them in alcohol and then seal them in a plastic bag for disposal. Clean bites with alcohol or iodine. Because the transmission of an infection from a tick to a human requires thirty-six to forty-eight hours of attachment, ridding yourself of ticks in the first twenty-four hours is effective prevention. Longer attachments that occur in high-risk parts of the country merit a single dose of doxycycline within seventy-two hours of a bite. Otherwise, be alert for symptoms or a rash, and seek treatment as soon as possible if they occur. (See blow for a link to an interesting tick removal tool.*)

Research continues

The detective work surrounding the unraveling of the Lyme disease mystery continues today in the laboratory. Now researchers tend to focus on the rare people who, despite receiving adequate antibiotic treatment after contracting Lyme disease, experience persistent, unexplained, or recurring symptoms. These people remain almost as much of a mystery to researchers today as the initial thirty-nine children and twelve adult with arthritis were to researchers in the mid-1970s.

*Tick removal tool

https://www.thegrommet.com/tickease?utm_campaign=20180626&utm_content=49931&utm_medium=email&utm_source=CC&trk_msg=77TUPK4NDPL4R992MUGHP52NOS&trk_contact=4ACPOO38FT83AKKO084SUBGRPC&trk_sid=ICRD996NV2C3PQ9D216CFKVDLG

Posted by medical plaintalk

Physician turned medical writer.

New Knees and Hips: Making the Leap

In these days of angst about health care and its costs, I am reminded of a medical school professor who told his students that all surgery was optional. Without surgery, he said, some people would die prematurely and some would have miserable lives, but the human race would survive. He was right. Surgery benefits individuals, not populations, and all surgery falls into one of two categories – those procedures, like appendectomies and C-sections, which rescue individuals from premature death, or those like joint replacements, which improve individual quality of life.

Artificial joints

The forerunners of joint replacements were wooden legs – the crude mechanical approximations of limbs torn asunder by accidents and war. Fast forward a few hundred years, through remarkable developments in materials science, anesthesia and infection control, and we have slick titanium or ceramic implants that replace joints worn down by modern life. Hip and knee replacements, procedures which began in earnest in the 1960s, are safe and effective. Currently it is estimated that over 300,000 hips are replaced in the United states alone each year. In most people, even the very elderly, they return mobility and help maintain independence.

Costly and difficult substitutes for nature

As good as these artificial parts are, they are still less than perfect substitutes for your native joints. Joint replacement is irreversible, initially painful, and potentially risky. Good results require serious commitment to rehabilitation – more exercise than some people have ever engaged in. Already major consumers of the health care dollar, hip and knee replacements are set to explode budgets as our obese population ages and wears out weight bearing joints. Between 1997 and 2004, private insurance layouts climbed from $1.1 billion to $3 billion for new hips and from $1.46 billion to $4.64 billion for new knees. These figures don’t include Medicare expenditures, which are the principle source of payment, and constitute over 20% of Medicare outlays. Limits may be imposed by available surgeons trained to do these procedures, a number already in decline and not expected to increase over the next decade. If you are in possession of good joints, try to hang on to them for as long as possible. Maintain normal weight, don’t smoke, and work on strength and flexibility of trunk and limbs.

Deciding to replace a joint

The decision to replace a hip or knee usually comes after years of declining physical activity and escalating anti-inflammatory and pain medication use. At times a decision is forced on a patient as treatment for a hip fracture, but ideally the surgery is an elective procedure decided upon by a patient, along with a doctor who knows him well and understands all his other medical problems. Time spent researching surgeons and hospitals and settling upon those with good results is worthwhile. Sometimes a decision can be delayed by opting for steroid injections, but they weaken connective tissue and cannot be repeated indefinitely. Delaying too long, however, might influence results. Some studies show worse functional outcomes after knee or hip replacements in more debilitated patients.

On the replacement road

Whatever way it happens, once the road to hip or knee replacement is undertaken, the orthopedic team and patient travel as close companions. Careful adherence by the patient to all instructions and advice insures the best possible outcome, and good communication from the doctors, nurses and therapists encourages patient cooperation. Work starts well before the surgery. Painful knees and hips are often housed in bodies that are overweight and out of shape. The difficult job of getting a new joint moving is easier if muscles have been in training pre-operatively. And the more weight that can be shed ahead of time, the less the strain on bone and muscle as they attempt to hold a new joint in place.

Immediately after surgery, mobilization begins. First comes sitting up, getting out of bed, and walking with assistance – as soon as tolerable and with whatever restrictions needed to protect the new joint. Supervised therapy sessions, starting within the first few days, aim at moving the new joint through larger ranges of motion without endangering its stability. Every encouragement to move and every caution about how one moves (such as the prohibition against leg crossing) is important.

Potential problems

The push to get patients moving and the precautions about how they move are important for preventing two of the biggest complications of lower extremity joint replacement: blood clots in the legs (with potentially catastrophic migration to the lungs) and dislocation of the hip (slipping of the ball of the new hip out of the socket). The most feared complication, infection, prompts meticulous wound care and surveillance for other infections. A brief stay in a transitional care facility, if recommended, is beneficial. Therapy occurs in well-equipped spaces several times a day and gets the long-term recovery off to a good start, and medical supervision is close at hand. Most people will also need home help for a month or more, as well as continued outpatient physical therapy.

The long run

If joint replacements are so advanced and helpful, why suffer with bad knees and hips at all? There are many joint replacements being done at younger and younger ages, but the fact remains that artificial joints have a limited – though quite long – life span, in the range of 15-20 years, though as advances are made, these figures may stretch out. Some people are still walking well on their first new joints at the 25 year mark. But artificial materials will eventually suffer wear, and there is an additional problem of the prosthesis loosening in the bone, a process that is not entirely understood. Replace a joint at age 65 and it may well last until life’s end. Replace one at 45 and you may be looking at a second period of disabling pain followed by a redo of the replacement, but this time in an older bone already altered by the first procedure. Opting for a new knee or hip is a decision that warrants careful, educated and open-eyed assessment of short and long-term risks and benefits, but as quality of life surgery goes, these procedures are among the most useful.

Posted by medical plaintalk

Physician turned medical writer.

Osteoarthritis – Time’s Marker

The garden-variety arthritis that afflicts millions of people is the great humbler – the nagging messenger that tells the truth about age. Joints are the junctions between bones that allow movement of the skeleton. Over time joints suffer from wear, tear and imperfect repair and the result is “osteo(bone)arthr(joint)itis(inflammation).”

The structure of joints: cartilage, synovial membranes, tendons and ligaments

You have 206 bones and over 230 joints. The more movement required at a junction between bones, the more complex the joint. In freely moveable joints the ends of the bones are covered with cartilage, a smooth, tough and pliable tissue that lacks a blood supply. In some joints there are also cushions of cartilage – menisci or discs – between the bones. Cartilage is the weak link in joints – the part that thins out and breaks down with age. Bone stripped of cartilage slides poorly and painfully over other bone. Old, dried out discs and menisci fragment and hurt. Inflammation and more pain accompany the body’s attempts to repair the damage.

The synovial membranes lining joints make a thick, lubricating fluid that seeps into crevasses in cartilage, where it forms reservoir pools that keep the thin film of fluid between the bones even during movement. This synovial fluid carries nutrients and waste products and depends on joint movement for its circulation.

The ligaments that connect bone to bone, and the tendons that attach the muscles to bone form the joint capsule. Tendons and ligaments are tough and gristly and have poor blood supplies. They heal slowly, repairing themselves with stiff scar tissue. Time marks its progress in these structures by making them less flexible and more prone to damage.

Joint symptoms

The pain of joint inflammation, the stiffness of ligaments and tendons, and the resulting limitation of joint movement are the cardinal symptoms of osteoarthritis. Excessive bone formation, narrowing of joint spaces and irregularity of bony margins, seen mainly on X-rays are signs of the ailment. In contrast to other more inflammatory joint problems, such as rheumatoid arthritis and gout, osteoarthritis produces no blood or joint fluid abnormalities.

Why are some people more affected than others by osteoarthritis?

If osteoarthritis is a result of age, then why are some people crippled at 60 and others still dancing at 90? As usual, genetic makeup counts. Some families pass arthritis down. Others pass along bowed legs and other skeletal builds that result in early joint deterioration. Osteoarthritis also creeps into joints injured long ago and into joints damaged by inflammation from infectious and immune system diseases. Obesity contributes to the load on weight-bearing joints, subjecting them to more damage.

Use joints or lose them: underactivity ages joints

While overuse at times predisposes joints to arthritis, under use is also a threat. There is ample evidence in laboratory animals that joint immobility produces degeneration. Zookeepers have long known that elephants in captivity, deprived of their need to walk thirty miles a day in search of food, develop debilitating arthritis in their hips and feet. Joint cartilage gets nutrients from the surrounding tissues by diffusion through the joint fluids. Movement helps that diffusion, so optimal joint health depends in part on regular movement through a full range of motion.

Limited joint motion sets up a process of uneven wear that precedes arthritic change. In Eastern cultures, where squatting is frequent, thinning of cartilage in the hip joint occurs with age just as it does in the West, but hip degeneration is far less common. Squatting puts the ball-and-socket joint of the hip through the rotational movement for which it is designed, while walking and sitting in chairs requires flexion and extension in only one plane, wearing cartilage unevenly.

Treatment

Osteoarthritis develops over many years. There is no cure. Medical treatment focuses on maintaining the mobility that pain and stiffness reduce. Reduced movement causes muscle weakness, tightens tendons and ligaments, and deprives cartilage of synovial fluid circulation. Intervening in this cycle requires relief of pain and maintenance of activity.

Anti-inflammatory agents such as aspirin and ibuprofen are helpful – but often osteoarthritis involves little real inflammation and the potential hazards of chronic use of these medications (kidney damage) have to be weighed against their pain-relieving benefits. Ice, heat, massage and topical agents like Ben Gay are substitutes. Supplements such as glucosamine and chondroitin – the building blocks of cartilage – are thought by some to be helpful. While there is no proof of their efficacy, there is also no indication that they are harmful. External devices such as knee braces and back supports are useful for stability in exercise.

Exercise is treatment

Exercise is crucial for joints. Properly carried out, exercise strengthens muscles and maintains range of motion. Stiffness improves as a joint “warms up.” With time, patience and the proper exercises, range of motion can be increased and symptoms greatly reduced. Exercise promotes weight loss, which relieves the load on hips, knees, ankles and feet. Because it reduces gravitational forces, water is a wonderful medium for exercise for arthritic patients.

Alternative treatments and joint replacement

Acupuncture might help some people. Cortisone injections provide transient relief, but weaken tissues further. Because osteoarthritis is common and often debilitating, patients are easy targets for sales pitches guaranteeing relief. Therapies like magnets and copper bracelets and a host of pain relieving supplements beckon everywhere. At the end of the line for a joint, there is the prospect of replacement. Artificial joints restore mobility and improve life significantly for many arthritis sufferers – but they are to be approached with the care and caution. Joint replacement is a major surgical procedure in which the original joint is permanently removed. The recovery process is arduous and the new joint surfaces are also subject to wear and tear. Time marches on in titanium as well as in bone.

Useful Websites

http://www.arthritis.org/default.asp – Arthritis Foundation homepage

http://www.rheumatology.org/public/factsheets/index.asp – American College of Rheumatology – patient education page

http://www.arthritis.com/ – Animated graphic representations of joints and arthritic processes.

Posted by medical plaintalk

Physician turned medical writer.

Carpal Tunnel Syndrome

Wrist splints are common sights. You see them on cashiers and typists, on hairdressers and bank tellers. They reflect the frequency of a problem called carpal tunnel syndrome. The carpal tunnel is an anatomical structure inside the palm of the hand at its base, and the syndrome is a collection of symptoms related to the nerve that passes through the tunnel on its way from the forearm to the hand. The nerve is the median nerve, and it is accompanied by nine tendons that connect the muscles of the forearm to the fingers. At times, lack of space puts pressure on the median nerve, causing aching pain in the wrist, forearm and even upper arm, and numbness or tingling in the thumb, index, third and the half of the ring finger closest to the thumb. With enough pressure the thumb muscles weaken and shrink. Any combination of these symptoms, when caused by pressure on the median nerve in the hand, adds up to carpal tunnel syndrome.

Nerves tell you they are in trouble

Pressure on nerves that run close to the surface of the body slows conduction of the electrical impulses that carry sensory information about pain, temperature, position and touch. When your foot or arm “falls asleep,” the culprit is pressure on the nerves that carry sensory information. Pressure symptoms from the median nerve in the base of the hand are so common that many people experience them transiently when they grip a steering wheel tightly over a long period of time, or pound or push with the base of the hand. Instinctively, they respond to the feeling of fingers tingling or going to sleep with re-positioning or shaking of the hand. Only when pressure is sustained do nerves become damaged enough to cause the muscles they supply to weaken. The median nerve is a common site of chronic pressure because of the anatomy of the tunnel it must pass through to the hand.

Tunnel anatomy

The roof of the carpal tunnel is an arch of bones at the base of the hand. The floor is a horizontal span of several tendons and ligaments between the bones on the thumb side and the little finger side of the hand. The bony arch changes shape with hand movements, especially with bringing the thumb across to the little finger side, flexing the wrist and extending the wrist.

Who gets carpal tunnel syndrome?

Because the carpal tunnel is smaller in women than in men, they are more frequently affected by symptoms from pressure on the median nerve, particularly during pregnancy when hands commonly swell. Some medical conditions like heart or kidney failure, diabetes and growth hormone producing brain tumors may cause pressure to increase in the carpal tunnel. Inflammatory conditions like rheumatoid arthritis may also bring out symptoms. While carpal tunnel syndrome seems common in people whose occupations involve repetitive hand motions or hand pressure, such as hairdressers, typists, bakers, and jackhammer operators, rigorous studies do not fault the activities alone, but the activities combined with the individual anatomic structure, and with underlying medical conditions, if present.

The reason for those wrist splints

Since the anatomy of the hand is responsible for carpal tunnel syndrome, relief comes from maximizing the space between the ligaments and bones. When symptoms begin, the first line of treatment is a splint that keeps the wrist aligned in a neutral position – neither flexed nor extended. It also keeps the thumb from falling in toward the ring finger. The splint’s design allows for use of the fingers and thumb and it can be worn during most activities. The crucial time for keeping it on is during sleep. When we sleep our hands naturally fall into a posture of wrist and finger flexion, and some people exaggerate this pose by tucking their hands beneath them, and even unconsciously clenching them. Hand position at night often brings carpal tunnel symptoms to light, especially aching in the forearm, and tingling in all the fingers except the pinky.

Stretching the tunnel

Stretching the base of the hand during the day is also helpful. One good stretch is accomplished by placing the hand flat on a wall at about shoulder height, turning the body perpendicular to the wall and stepping far enough away to straighten the elbow as much as possible. Then rotate the “eye” of the elbow, its inner bend, up to face the ceiling as much as possible. Hold the stretch for up to thirty seconds at a time.

Advil doesn’t change the anatomy

Anti-inflammatory drugs like Advil can help reduce swelling of tendon sheaths if the problem with the hand is related to injury or an underlying inflammatory condition like rheumatoid arthritis, but chronic use of anti-inflammatory drugs has not been shown to help typical, uncomplicated carpal tunnel syndrome.

When conservative measures fail

If conservative measures like splinting and stretching do not resolve carpal tunnel symptoms, surgery to expand the canal is generally successful. Some surgeries are performed through a small incision, using a scope and tools inserted directly onto the tunnel to cut away the connective tissue surrounding the nerve and tendons. Other cases require an open incision in the palm.

Diagnosis

Diagnosis of carpal runnel syndrome is relatively easy from the history alone. Conservative measures can be attempted without any other tests, provided that there are no underlying medical conditions suspected to be causing the symptoms. However, if conscientiously applied conservative measures fail, or if there is muscle weakness at the time of diagnosis, then a test called a nerve conduction study and electromyogram (EMG) will almost always confirm the diagnosis. The pressure on the nerve in the carpal tunnel causes a current applied to the nerve to be delayed in its passage to the hand, easily picked up in the nerve conduction study. Tiny needles that measure activity in the palm of the hand pick up signs of loss of nerve supply to muscles. Muscle nerve loss does not respond as well to conservative measures as sensory symptoms like numbness and tingling do, so if the EMG demonstrates muscle nerve loss, surgery is usually recommended.

Posted by medical plaintalk

Physician turned medical writer.

Your Discs Are Bulging—Does it Matter?

Have you been told that you have bulging, degenerated discs in your spine? If so, you are not alone. Millions of Americans undergo X-rays, CT scans, and MRI scans of their backs and necks each year and receive the same news. As a result, multiple millions of dollars are spent on medications, physical therapies, surgical procedures, and spinal manipulations in an effort to treat back pain. The people undergoing all this diagnosis and treatment might imagine that other, luckier people have normal spinal discs, but they might be surprised to learn that bulging discs are so common that they may be considered a normal part of aging. Most often, they cause no symptoms or problems, and it pays to be cautious about embarking on courses of investigation and treatment based simply on these “degenerative changes.” But it also pays to know when and why discs do cause trouble.

What and where are spinal discs?

The spine is a column of thick, circular bones—also called vertebral bodies—that in terms of anatomy is divided into three major sections: the cervical (neck) spine, thoracic (mid-back) spine, and lumbar (lower back) spine. The vertebral bodies have flat tops and bottoms, and they sit atop one another, separated by discs that cushion the spine and allow for the compression, rotation, and bending of the entire spinal column. The arches of bone on the back sides of each of the vertebral bodies line up with each other to form a bony tunnel, which surrounds the spinal cord and the nerves that connect it to the body. Pairs of these nerves exit from the sides of this canal below each vertebral body.

Spinal discs are a lot like flattened cream-filled doughnuts, with a soft center called the nucleus pulposus and a tougher perimeter called the annulus. Each annulus is attached to the ligaments that run the length of the spine and hold it together. Every day, gravity squeezes so much water out of each disc that an average adult shrinks by more than one-half inch between morning and night. As a disc loses water and flattens, it may protrude beyond the edges of the vertebral bodies located above and below it. Under these conditions, the ligaments bounding the disc tend to bow outward to accommodate the flattening, and the result is the classic “bulging” discs often seen on back scans. Is such bulging a cause of pain?

When bulging becomes cracking and herniation

Judging by the number of people who have bulging discs and no pain, the answer to this question is, not very often. But discs can cause pain if they are damaged. Cracks can develop in the back part of the annulus, especially in the lower neck and lower back, and are sometimes caused by sudden movement or excessive loading of the neck or back or sometimes with no readily identifiable cause. Risk factors for the development of cracks include age, smoking, and heavy weight lifting. When cracks form in the annulus, nerve fibers send out distress signals which feel like deep back pain that sometimes radiates down the legs. Symptoms usually improve over a period of six to eight weeks, but if the tear is extensive enough, it may open a path for part of the soft nucleus pulposus of the disc to work its way through, becoming a so-called herniated or “slipped” disc.

Location determines symptoms

Extruded far enough, a herniated disc bulges straight backward into the bony tunnel that houses the spinal cord or off to either side, where it squeezes into the narrow canal that should hold only a spinal nerve root passing out to the body. Depending on the location and the extent of the disc herniation, pain in the back or neck might be accompanied by a set of neurological symptoms including numbness, tingling, and a sense of weakness in an arm or a leg. Symptoms may improve over time with no treatment or with relatively modest treatments, like physical therapy or cortisone injections, as the disc shrinks. But there is potential for the worsening of symptoms, so careful physical evaluation and follow-up are important.

More than 95 percent of disc problems occur in the lumbar spine. Here, as in the neck, discs tend to slip off to the side, compressing single nerves and causing pain to run down a leg or arm or weakness in corresponding muscles. Definite loss of strength in a muscle group controlled by the nerve under pressure most often calls for surgery to decompress the nerve. Sometimes scans indicate that a fragment of disc has broken off and lodged itself under a nerve. Unlike nonfragmented disc herniations, which may gradually shrink and relieve symptoms, symptoms caused by fragmented discs tend to be persistent unless the fragment is removed.

Disc herniation in the upper spine

When discs slip straight back into the central spinal canal, symptoms can range from none to neurological deficits that require immediate decompression surgery. Serious central disc herniations are uncommon in the neck and quite rare in the thoracic spine but in both locations may cause symptoms from the spinal cord itself that include pain, balance problems, weakness in the legs, and an inability to control the bladder.

Disc herniation in the lumbar spine

In the lumbar spine, because the spinal cord does not reach down this far, central disc herniations put pressure on the so-called cauda equine, or “horse’s tail” of nerves that travel down the spinal canal from the spinal cord to their exit points at different lumbar levels. Symptoms here often consist of a confusing array of pain, numbness around the groin and legs in a pattern that traces an area where a saddle would make contact with the body, leg weakness, fecal incontinence, and trouble initiating urination. This combination of symptoms requires immediate surgical decompression.

Surgery or not?

While surgery for severe symptoms is an easy decision and while many disc removals are done with microsurgical techniques and small incisions and are less invasive than in the past, the decision to try to improve back pain alone by operating on a bulging disc is not as easy. To improve the likelihood of good results, studies like disc injections are sometimes done. The dye used helps visualize the disc, and, if the injection reproduces the patient’s pain, confidence that the disc is the source of the back pain increases. Injections can be helpful in determining which of several bulging discs might be the source of pain.

Caution in the decision

Disc removal for pain alone or for pain combined with sensory symptoms that come and go should be approached with caution. First, every attempt should be made to improve the strength of the muscles that support and move the spine, to improve overall posture, and to lose excess weight that the spine is asked to support. Back and neck pain arise from many different structures—muscles, ligaments, tendons, bones, and nerves—and can improve dramatically with improved strength, flexibility, and posture—bulging discs or not.

Posted by medical plaintalk

Physician turned medical writer.

The Latest on Charley Horse: How Muscle Cramps Work

No one knows for certain how “charley horse” became a name for muscle cramps. Baseball lore from the late 1800s links the term to a player named Joe Quest, who may or may not have compared his cramp-prone teammates to an old, stiff-legged white horse named Charley who pulled heavy loads in his father’s machine shop in New Castle PA. The first newspaper story using the term charley horse in the context of players who pulled up with thigh cramps was allegedly the Chicago Tribune, during Quest’s 1879-1882 stint with the Chicago White Stockings. The first retrievable story using the term, in the Boston Globe in 1886, referred to the Tribune story as the origin of the name. By that time, Quest was with the Philadelphia Athletics and at the end of his career, but the off-hand description he may or may not have coined has become a household word, spread far beyond the world of baseball.

What is a muscle cramp?

Muscle cramps of are involuntary, intense and painful contractions which harden the muscle and last seconds to minutes. Aching pain and even chemical indications of muscle damage may persist much longer. Electrical recording of muscle activity during cramping and between bouts of cramping indicates that the baseline or normal amount of electrical activation of the muscle is increased – maybe a measurable correlate of the feeling that a muscle is “about to cramp.”

Theories about cramps

Long-held theories have blamed muscle cramps on dehydration, electrolyte losses from sweating, extreme environmental conditions of heat and cold, or inherited problems of energy production. In addition, cramps happen more in people taking some medications some medications such as cholesterol lowering drugs and diuretics. While these factors may play supporting roles, they do not explain the mechanism of cramping. Nor do they explain why stretching, as well as folklore-based remedies like the Amish combination of vinegar, ginger and garlic, or consumption of pickle juice, mustard or hot peppers help cramps. Newer, “neural” theories about the mechanism of cramping, which implicate feedback loops between muscle and the spinal cord, might account not only for exercise related cramps but also for and the kind that grab hold of a leg as you roll over in bed. And they might explain the seeming success of peculiar remedies. To understand the neuromuscular feedback loops we must diverge briefly into a little muscle anatomy and physiology.

How your muscles move things

When you decide to lift this magazine, your brain sends a message to motor nerve cells in the spinal cord, the alpha motor neurons, which then fire signals down nerves to the biceps muscle and to all the other muscles are involved in the task, telling some to contract and others to relax. That is the simple part. The complex part, which goes on in the background at all times, is the feedback from two types of specialized muscle receptors which act much like strain gauges used in civil engineering to detect forces deforming land and buildings.

Strain gauges in every muscle: moderators of muscle tone

One type of muscle receptor strain guage is a muscle spindle. It calculates stretching forces in the belly of a muscle. The other is a Golgi tendon organ, which calculates the stretch in the tendon, the fibrous end of the muscle that attaches to bone. Muscle spindles send messages to the spinal cord motor cells to fire up and contract the muscle when the muscle lengthens too much. Golgi organs send the opposite message to prevent the tendon from becoming too tight as the muscle contracts. All of this occurs rapidly and constantly, in a balance that keeps your muscles at the right degree of tone for all your movements.

In 1997, researchers suggested that unbalanced feedback from these little muscle strain gauges was the primary cause of cramping. In fatigued muscle, at least in animal studies, the spindles were more active than normal, and the Golgi tendons less active. The net result caused alpha motor neurons to fire up the muscle fibers than they usually do. Passive stretching of the muscles, which stretches tendons, woke the Golgi receptors back up, prompting them to send more cease and desist orders to the motor neurons. The cause of cramping thus appeared to be too much spindle input.

Regulation from above

Motor neuron feedback loops also receive input via pathways that originate higher in the nervous system. Swallowing liquids with striking tastes stimulates sensory cells in these spinal pathways, sending messages up to the brain and down through the spinal cord. Cramp researchers speculate that stimulation of these pathways tamps down some of the incoming messages from the muscle spindles, providing an explanation for the efficacy of some old-fashioned cramp remedies.

The well-known tendency of baseball players to suffer cramps might also bolster the neuromuscular feedback theory. Baseball players wait to explode into motion from crouches, get up from slides to race back to safety after failed base stealing attempts, and stop, start and reverse direction abruptly. It is easy to imagine some Golgi tendon organs and muscle spindles lulled into altering their feedback and then lagging in adjusting to the abrupt new actions.

Cramps in bed

But what about the cramps that are not associated with the fatigue of exercise? Shortening of the muscle in certain positions, such as lying in bed, may set them up for the same imbalance in input from the stretch receptors. The increasing frequency of cramp problems with age could be a result of general loss of strength and flexibility in muscles that are not used as much as in the past. The ideal input from muscle stretch receptors occurs in the rested muscle which has maintained its youthful length and flexibility.

Practical application of the latest theory

Practical application of the neuromuscular feedback theory of cramping applies not only to charley horses, but also to musculoskeletal injury prevention in general. Maintenance of flexibility and balance of strength in opposing muscle groups such as the quadriceps and the hamstrings keeps the spindles and Golgi tendon organs in balance, and muscles which are less stiff and prone to cramping allow movement with less discomfort as life moves on. Such maintenance requires regular work, especially if you want to avoid some of the creeping stiffness of old age.

Note: the muscle receptors and their connections may well play roles or even be the culprits in some mysterious muscle disorders that are associated with cramping or decreased muscle tone. Muscle research is a blossoming field in this new age of genetic research. All muscles bear the stamp of their genetic makeup in their differing structural proteins. Some people have big bulky muscles, some long slender ones; some have more fast twitch fibers that make them speedy, others more slow twitch fibers that endure for marathons. And some people are relatively inflexible, others loose and prone to twisting ankles. You get what you get from the usual complement of both parental versions of DNA, in the nucleus of the cells. (But if you want to complain about your speed, blame your mother- she provided all the DNA in the mitochondria which power the cells.)

Posted by medical plaintalk

Physician turned medical writer.

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