Joint Pain in Children, Part VI: Bone Infections in Children

By Deborah Pate, DC, DACBR

Osteomyelitis is the generic term for bone infections. The great majority of bone and joint infections in North America are primary, developing as a consequence of direct contamination during trauma and or orthopedic surgery.
The most common pathogens are pyogenic bacteria, mycobacteria, and fungi. These pathogenic microorganisms spread to bone by one of three routes: hematogenous spread; direct extension from a contiguous site of infection; and direct introduction. The most serious bone infections are pyogenic osteomyelitis and tuberculosis; there are also rare cases of syphilis and fungal infections.

Take a moment to review the anatomy of a tubular bone and its vascular supply. The vascular supply will vary depending on the age of the individual. In the infant (0-1 yrs.), diaphyseal and metaphyseal vessels may perforate the bone growth plate. In the child (1-16 yrs.), diaphyseal and metaphyseal vessels do not penetrate the open growth plate. Finally, in the adult (>16 yrs.) diaphyseal and metaphyseal vessels penetrate the closed growth plate.

Acute hematogenous osteomyelitis occurs predominately in children and before the age of epiphysial closure (>21 yrs). The infection typically originates in the metaphysis of the long bones, a highly vascular area. Common sites of involvement are the distal femur, proximal tibia, humerus and radius. Hematogenous osteomyelitis in children sometimes results from the blood-borne spread of infection to the bone from an extraskeletal foci, such as the skin, ear, and pharynx. Often the source of the infection is not readily apparent. An event that at the time seemed trivial may cause a bacteremia, such as an ordinary cut or bruise of the skin (or a human bite -- children have been known to bite each other), can be the source of the infection.

Hematogenous osteomyelitis of children is most often caused by S. aureus, which accounts for 60-90% of cases. Osteomyelitis of neonates is also frequently caused by group B streptococci and E. coli. Children with sickle cell disease are prone to acquire salmonella infections and to develop salmonella osteomyelitis.

Osteomyelitis of children usually begins in the metaphysis of long bones. The blood-borne bacteria are carried to the marrow space by way of the nutrient artery. The initial site of infection within a particular bone is determined by the vascular anatomy as related to the epiphysial growth plate. In children a year and older, the metaphyseal branches of the nutrient artery do not penetrate the growth plate. The vessels turn back upon themselves just proximal to the plate and enter venous sinusoids in the marrow space of the metaphysis.

The venous sinusoids are much larger than the arteries feeding them, have a slower blood flow, and provide a medium favorable for bacterial growth. The bacterial infection causes a fulminant acute inflammation of the marrow space, and an exudation of polymorphonuclear leukocytes. The presence of an inflammatory exudate within the rigid limits of the marrow space causes an increase in intramedullary pressure, reduced blood flow, local vascular occlusion, and thrombosis. Local ischemic injury and cell necrosis of marrow and osseous tissue occur and the bacteria, pus cells, and necrotic debris comprise a septic focus of purulent inflammation. At the early stage of the infection, no specific bone changes are seen radiographically.

The infection may then spread rapidly by way of vascular channels through the medullary cavity and the bone cortex, which is thin in the region of the metaphysis and provides easy access to the periosteum. The purulent material may elevate the periosteum and form abscesses beneath it or penetrate the periosteum as sinus tracts which drain into the soft tissue or extend to the skin surface.

The clinical characteristics of acute osteomyelitis are unique to each age group. Infants usually become abruptly and desperately ill with hectic fever, rapid pulse, vomiting, and occasionally convulsions. Less commonly, an infant will become gradually ill, showing the illness only by loss of appetite, lethargy, fretfulness, and variable fever. Older children will usually become rapidly ill, manifesting hectic fever, rapid pulse, and variable degrees of prostration. They will not appear as desperately ill as infants, however. Adults usually do not appear acutely ill and may complain of migrating arthralgias and myalgias prior to localization of pain in one extremity.

Eventually, all patients will develop signs of inflammation at the site of the infection. The signs at the site of infection usually develop in the following order: 

1. Infants and young children manifest a flaccid extremity, at times so flaccid as to mimic a lower motor neuron paralytic illness. Older children and adults complain of pain and resist passive and active motion.


2. The area over the infected metaphysis becomes tender.


3. The area over the infected metaphysis becomes reddened, indurated, and swollen.


4. If the infection erodes into overlying soft tissue, the area will become fluctuant and may eventually develop a draining sinus.


5. The neighboring joint may develop an aseptic hydrarthrosis as it participates in the inflammation surrounding the bone infection.


6. If the infection erodes into a neighboring joint, the joint will develop all the signs of septic arthritis (joint will be very painful, hot, red and fluctuant; joint fluid when aspirated will be cloudy or frankly purulent).

Radiographic signs associated with osteomyelitis and joint infection will vary depending on the stage of development of the infection the films are taken. Radiographs are remarkably normal during the first 1-2 weeks of infection, although bone scans quickly demonstrate an increase uptake in the zone of infection. As the infection develops, the following changes will appear: 

1. An initial break in the bony trabeculae of the metaphysis will appear and will progress to become larger areas of lytic destruction which appear as radiolucent areas in the metaphyseal region.


2. Periosteal new bone formation will appear at the epiphyseal end of the metaphysis.


3. The cartilage of the growth plate and/or joint surface may show multiple areas of scalloped erosion.

In children (>1 yr) who have an intact epiphysial plate without capillary penetration, a sterile "sympathetic" effusion may occur, indicating a barrier between the infection and the joint space. The pathological picture in hematogenous osteomyelitis may occasionally differ from the spreading and destructive pattern previously described. The initial focus of bone infection may become circumscribed by a fibrous capsule and bone sclerosis to form a localized abscess (Brodie's abscess), which may undergo sterilization or become a chronic focus of infection.

The course of acute hematogenous osteomyelitis is age-dependent. In neonates (<3 months), bone infections are often fulminant but rarely necrotizing, because the spongy bone and thin cortex adapt to increase intraosseous pressure without compromising the blood supply. In infants (3-12 months) and adults, capillaries extend from the metaphysis to the epiphysis and can spread the infection to the adjacent joint, causing suppurative arthritis and septic joint effusion.

Prompt clinical diagnosis and the institution of a potent and protracted regimen of antibiotic therapy have greatly decreased the mortality, which at one time was as high as 40% in the pre-antibiotic era. Even now, occasionally bone infections may be undiagnosed or inadequately treated. In chronic osteomyelitis, the avascular dead tissue, pus and bacteria may remain isolated within an area of bone fibrosis and sclerosis and give rise to recurrent episodes of acute osteomyelitis. The treatment of chronic bone infections usually requires, in addition to antimicrobial therapy, surgical intervention to drain abscesses and remove necrotic tissue.

Other less common fungal infections, mycobacterium tuberculosis, coccidioidomycosis, and actinomycosis, are likely to spread from antecedent lung and skin infections to bone and joint. Tuberculous osteomyelitis is almost always caused by the hematogenous spread of organisms from an active focus of tuberculosis elsewhere in the body, usually the lung and occasionally some other site. The bone infection may occur at any age but is most commonly seen in children. The vertebrae and long bones of the extremities are most frequently involved. In many cases the infection also spreads to contiguous joints such as the hip and knee or contiguous intervertebral joints.

Whenever an indolent arthritis fails to clear or a bone aches relentlessly without evidence of other causes, granulomatous infection must be included in the differential diagnosis along with chronic septic arthritis, rheumatoid arthritis and persistent synovial disorders.

Joint Pain in Children, Part V: Juvenile Chronic Arthritis

By Deborah Pate, DC, DACBR

The most common cause of chronic joint disease in children is juvenile rheumatoid arthritis. Arthritis affects approximately one child in 1,000 in a given year. Fortunately, most of these cases are mild, however, approximately one child in 10,000 will have more severe arthritis that doesn't just go away. 
Many children have what is called an acute reactive arthritis following a viral or bacterial infection. This arthritis is often quite severe for a brief period, but usually disappears within a few weeks or months. For both children with arthritis and the doctors who care for them, public education is one of the greatest challenges. Most lay people and many doctors fail to realize that the problem exists. Many children suffer for months or years before the diagnosis of arthritis is thought of the proper treatment begun.¹

There are three major forms of juvenile rheumatoid arthritis: systemic, pauciarticular, and polyarticular. These types are distinguished from one another by their distinct modes of onset and characteristic features (see Table).

The diagnostic criteria for juvenile rheumatoid arthritis include age of onset 16 years or younger, and the involvement of one or more joints for at least three months. No extraarticular manifestations are diagnostic by themselves. No one laboratory test is diagnostic, thus tests to exclude other disease processes are useful. The test for rheumatoid factor is usually negative, except in older children. The most helpful antibody test is that for antinuclear antibodies, which are commonly positive in younger children, particularly when the mode of onset is pauciarticular. As far as initial x-ray findings, there should be only evidence of soft tissue swelling. X-rays should be taken only to rule out any other pathology, i.e., trauma or developmental anomalies. The type of signs of joint changes associated with rheumatoid are not generally present and, one hopes, will not progressive if properly managed.

Table: The three forms of juvenile rheumatoid arthritis.

Mode of Onset	Features: Articular	Systemic
Systemic	varies, only arthralgia may be present	high fevers, rash, possible pericarditis
Pauciarticular	involves no more than four joints	possible iridocyclitis
Polyarticular	bilateral & symmetric four or more joints	low-grade fever, rash, pericarditis

Pauciarticular JRA is defined by the involvement of less than four joints; it is the most common form of JRA. It often begins in a swollen knee or ankle which appears without a history of injury. There are no systemic manifestations, but there is a high incidence of chronic asymptomatic iridocyclitis associated with this type of JRA. There are two dominant subtypes of pauciarticular JRA. The more common subtype occurs in girls ages 2-3 years. The test for antinuclear antibodies is often positive and iridocyclitis is a common finding. The other subtype is most often seen in older boys. The large joints of the lower extremities are usually involved and heel pain is common. An HLA-B27 antigen test is usually positive. Other conditions should be considered when diagnosing this subtype (i.e., inflammatory bowel disease, psoriatic arthritis, ankylosing spondylitis, infection, etc.).

Aside from the pauciarticular JRA, the greatest concern with this condition is the iridocyclitis. The inflammation is not painful, but if not detected and treated it may lead to scarring of the lens and permanent visual damage. Initially this inflammation cannot be seen except by an ophthalmoscope. Iridocyclitis is more common in children with a positive ANA test; these children should be examined at regular intervals. It is recommended that children with positive ANA test be examined every three months; and all other children with JRA be examined every six months. The etiology for this condition and relationship with JRA is still unknown, but it is important to know there is a high incidence associated with JRA.

Another problem associated with pauciarticular JRA is that it may cause accelerated growth of the symptomatic extremity. This will cause a leg length discrepancy, and may lead to premature arthritis (osteoarthritis/DJD) involving the normal extremity. The accelerated growth is caused by the inflammation; if that is controlled there will be minimal accelerated growth. Most often treatment is successful with controlling the inflammation; however, if there appears to be significant leg length discrepancy, the growth of the extremities should be monitored. Shoe lifts can be used to reduce any limp that child may develop. If, however, the leg with arthritis is on radiographs 3cm or more longer than the other leg, more aggressive intervention may be necessary to prevent any damage to the normal leg.

Polyarticular JRA is the form in which four or more joints are involved. This form is more severe, because of the greater number of joints involved, and the fact that it tends to progress over time. Symptoms generally are bilateral and symmetric. Systemic manifestations include low-grade fever, rash, and pericarditis. Polyarticular JRA can also be divided into two subtypes. The more common subtype can affect either sex but is more common in girls. Small and large joints are affected, and involvement tends to be symmetric. Tests for antinuclear antibodies and rheumatoid factor are usually negative. The other subtype mainly affects older girls. There is symmetric involvement of small and large joints, and the rheumatoid factor test is positive. This is the only subtype that is truly rheumatoid.²

Polyarticular JRA may require fairly aggressive treatment, but it's important to be extremely careful with the use of steroids. In severe cases steroid may be necessary, however the child should be given a short course of treatment with the steroid and taken off as quickly as possible. Steroid treatment for long periods of time will cause short stature and osteoporotic bones, along with other systemic side affects.

The worst form of JRA is systemic juvenile rheumatoid arthritis (Still's disease). It is characterized by high fever, rash, anemia, leukocytosis, and elevated ESR, and sometimes pericarditis. Articular symptoms are variable and arthralgia may be the only such symptoms that are present. It is very important to rule out an infection before diagnosing the patient with systemic JRA. One of the most important findings is that the fever goes away for a least part of the day. Usually the fever is high once or twice each day. At those times the child appears systemically ill; when the fever falls the child appears and feels better. This form of JRA is very unpredictable: at times, the child will have only one episode and will recover completely; other times the fevers and rash disappear, but the arthritis progresses over time and may become very severe. This form of systemic JRA can involve the internal organs, and rarely may result in life threatening disease. In addition to this systemic disease these children have an increased likelihood in iatrogenic reactions to many medications and should be monitored very carefully.

There are several other forms of arthritis which can affect children and adolescents which are often lumped together with JRA, but have different outcomes and should be considered separately. These conditions will be reviewed in the following articles in this series on joint pain in children.

One further topic I'd like to just touch on is the growing evidence that rheumatoid arthritis may be caused by an infectious agent. It is clear that autoimmunity plays a major role in the progression of RA. Most rheumatology investigators believe that an infectious agent causes RA. There is, however, little agreement as to the responsible organism. Investigators have proposed the following infectious agents: human T-cell lymphotropic virus type I; rubella virus; cytomegalovirus; herpes virus; and mycoplasma. I will not review the theories on each of this causative agents, since this is far beyond my expertise. We should be aware that patients with RA often respond very favorably to antibiotic therapy.³ It appears that investigations are very close to discovering the true cause of at least some of the arthritides.

References 

1. Lehman T. Arthritis in childhood? Isn't that only an old person's disease? Cornell University Medical Center, public service information, 1997.
2. Nelson A. Joint pain in children, when is it serious? Interstate Postgraduate Medical Assembly, Postgraduate Medicine, 1989.
3. Mercola J. Protocol for using antibiotics in the treatment of rheumatic disease. Presentation at the 31st annual meeting of the American Academy of Environmental Medicine, Boston, Mass., October, 1996.

Fibromyalgia Syndrome

By David BenEliyahu

Fibromyalgia syndrome (FS) is a diagnosis given to patients who present with chronic pain and stiffness. It is a complex syndrome, and although controversial, it is widely recognized by rheumatologists as a distinct diagnostic entity. 
It affects about six million people, four million of which are female. It is often accompanied by fatigue, sleep disturbances, morning stiffness, anxiety and decreased pain thresholds. Widespread pain and tenderness at many tender spots on the body are the hallmark findings. In 1990, the American College of Rheumatology (ACR) developed specific criteria for classifying FS:

I. History of widespread pain: pain present on the right and left side of the body, and both below and above the waist.

Axial skeletal pain must be present in one of these area: cervical spine, dorsal spine, anterior chest and lumbar spine.

II. Pain in at least 11 of 18 tender points:

right/left suboccipital area	second rib
cervical spine C5-C7	lateral epicondyle
trapezius	gluteals
supraspinatus	knee

greater trochanter

FS has been divided into two types. Primary FS occurs in a spontaneous idiopathic form; its cause is unknown. Secondary FS is found in association with a primary associated disorder such as trauma, rheumatoid arthritis, postsurgical, spinal disorders, etc.

FS predominantly affects women. The etiology of FS is poorly understood at this time, however, some studies have implicated neurohormonal, CNS, metabolic and/or biochemical dysfunction. In a study of middle-aged women with FS, SPECT studies were obtained to evaluate cerebral blood flow in the thalamus and caudate nucleus, as well as measuring pain thresholds with psychological assessments. As expected, all three were abnormal in the FS group. Other studies have shown that FS patients have elevated levels of substance P, low levels of serotonin and tryptophan and 5-hydroxytryptamine. As a result, deficient 5-hydroxytryptamine activity can cause altered sleep, substance P metabolism and allodynia. An interesting study on the role of glycolysis and FS revealed increased pyruvate and lactate production in FS patients and hypothyroid patients and decreased ATP and LDH in FS patients, suggesting glycolytic impairment.

Some studies have suggested an association between thyroid dysfunction and FS (myofascitis, also). In a study by Carette et al., symptomatic improvement was noted in 10 of 19 FS patients. In a paper by Lowe et al., it was theorized that there is failed transcription regulation by the thyroid hormone that leads to serotonin deficiency in FS patients. They tend to be euthyroid with normal thyroid blood test findings, due to low affinity thyroid hormone receptors coded by a mutated C-eba beta-1 gene, yielding resistance to thyroid hormone. This causes alpha-adrenergic dominance and an increase in cyclic ADP and inhibitory GI proteins.

It is important for the chiropractic clinician to recognize FS, because it is not uncommonly seen after trauma. In a study of 67 patients with FS that met the ACR criteria, 60% noted onset subsequent to MVA; 12% after a work injury; 7% after surgery; and 5% after sports injury. Posttraumatic FS patients have shown higher degrees of pain disability and life interference, and are more difficult to manage. Fifty-six of the 67 patients had pain in 11 or more of the tender points (averaging 13.5). Patients received medication, biofeedback, manipulation, massage therapy, physical therapy and injections.

There was a dramatic reduction in use of all the therapies after a two year follow-up, although 86% still had symptoms and had signs of FS. This implies that a significant percentage of patients coming to our office may have FS and can benefit from a trial of chiropractic care. It should be noted that the patient would benefit most from a holistic package of chiropractic care, including not only manipulative therapy/adjustments, but with physiotherapy, massage, nutritional supplementation and exercise.

In a study comparing relaxation technique and exercise, aerobic exercise, flexibility and strength training were shown to have a beneficial effect on FS patients, without any adverse effect. In a Norwegian study, FS patients who exercised reported less symptoms than sedentary patients. Similar findings were observed in a Scandinavian study. EMG biofeedback and electroacupuncture have also been demonstrated to help lower pain and EMG activity in FS patients. In a study in the BMJ, was shown to decrease use of analgesics, pain scores, sleep disturbance and morning stiffness. In a study of 90 patients with FS, the usage of complementary therapies/alternative medicine was evaluated. Seventy-one percent of the patients utilized complementary therapies; the most popular was nutritional oral supplementation.

A similar study by Pioro et al. found 91% of the FS patients used alternative therapies. Two thirds of FS patients used multiple interventions.

All of these studies show that FS patients want and need a viable alternative therapy in addition to their standard medical care. Chiropractic doctors who offer advice on nutrition, exercise, and behavioral modification, in addition to chiropractic care, provide these patients with a valuable service. It is imperative to make the patient an active participant in their care and to establish a good home exercise program with stretching, strengthening and aerobic exercise. This will empower the patient to return to a functional lifestyle. Nutritional supplements can include vitamins, mineral and herbal medicine.

It is important to emphasize that FS is not myofascial pain syndrome (MPS), and the tender points are not trigger points. A muscle study showed that there are no histological changes at the tender points. In a review article in JMPT, Schneider pointed out that FS and MPS are two distinct entities that require different treatment approaches. FS is a systemic problem that involves neuroendocrine dysfunction and requires multidisciplinary treatment. MPS is due to muscle dysfunction caused by trigger points which responds well to manual treatment, like myofascial release, ischemic compression, spray-stretch, etc. MPS and FS can be seen in the same patient and coexist, especially subsequent to trauma (MVA or whiplash injuries), so treatment must be individualized to the two different problems.

The doctor of chiropractic should be able to recognize fibromyalgia syndrome and participate in the care of this patient in conjunction with a rheumatologist and or psychotherapist. Kelli et al. in the July/August 1997 issue of JMPT documented the efficacy of chiropractic care in a random clinical trial on fibromyalgia patients. Twenty one rheumatoid patients with FS participated in the study. Four weeks of spinal manipulation, soft tissue therapy, and stretching were compared to control patients taking medication only. Chiropractic care resulted in increased cervical and lumbar ROM, straight leg raise, visual analog pain scores, Oswestry and neck pain disability index scores. The Kelli et al. pilot study suggests that DCs can help FS patients, albeit larger clinical trials are necessary to confirm their findings.

Magnesium, Part II

By G. Douglas Andersen, DC, DACBSP, CCN

How important is magnesium? Last month we reviewed 46 conditions which a magnesium deficiency may cause or exacerbate. Without magnesium, life on this planet would be quite different, if it existed at all. 
The magnesium present in chlorophyll (the substance that gives plants their green color) enables plants to synthesize glucose and oxygen from sunlight and water, and carbon dioxide from photosynthesis.¹

RDA Tables²

Category	Age	Magnesium (in milligrams)
Infants	0-6 months	40
	6-12 months	60
Children	1-3 years	80
	4-6 years	120
	7-10 years	170
Males	11-14 years	270
	15-18 years	400
	19+ years	350
Females	11-14 years	280
	15-18 years	300
	19+ years	280
Pregnant Women		320
Lactating Women	1st 6 months	355
	2nd 6 months	340
Top Food Sources1	Magnesium (mg per 3 1/2 ounce serving)
Wheat bran	597
Wheat germ	364
Sesame seeds	347
Poppy seeds	320
Brazil nuts	318
Soybean flour	310
Almonds	293
Cashews	267
Molasses	258
Peanuts	175
Whole wheat flour	150
Oat flour	110
Beet greens	106
Spinach	104

Formulations

There are many formulations of magnesium available in the marketplace. The most common form is magnesium oxide. It is insoluble in water and, therefore, may not be absorbed in persons with gastrointestinal disorders, including hypoacidity. Magnesium acetate, aspartate, citrate, gluconate, and glycinate are all well absorbed.³ There are not many studies comparing different forms of magnesium head to head. If a patient is displaying signs and symptoms of a magnesium problem and does not respond to supplementation after six weeks, try a different brand and a different form of magnesium for another month before you decide your suspicion of a magnesium problem was incorrect.

Interactions

Diets high in the following substances may inhibit the absorption and/or increase the excretion of magnesium: alcohol, caffeine, fat, phosphorus, and sugar. Excessive calcium consumption may also exacerbate a magnesium deficiency. Make sure that your patients who are taking high levels of calcium for disorders (such as osteoporosis) are ingesting or supplementing with adequate levels of magnesium. There are many drugs which can interact with magnesium: the most commonly used are antibiotics, diuretics, insulin; they may affect magnesium levels. The following will stimulate magnesium absorption: meals, vitamin D, vitamin B6.⁴

Objective Testing

We definitely lack a gold standard in determining magnesium levels with laboratory testing. This was most evident in a recent study last year on magnesium levels in males with angina. The authors who performed the study used five tests (erythrocyte, mononuclear, 24-hour, serum, and urine) to determine magnesium levels.⁵

Magnesium Challenge Test

• may not be accurate if magnesium deficiency is due to urinary losses;
• requires a four-hour IV drip.

Twenty-four Hour Urinary Excretion of Magnesium

• there's a wide variance in normal populations;
• urinary magnesium doesn't necessarily correlate with serum magnesium concentrations. Erythrocyte Magnesium
• may be normal when plasma levels of magnesium are low;
• doesn't correlate with magnesium levels in other cell types.

Mononuclear Blood Cell Magnesium

• can be normal when plasma magnesium levels are low.

Serum Magnesium

• may not correlate to tissue magnesium levels.

Hair Magnesium

• higher if magnesium is lost from bones;
• lower when gray hair is tested.

Ionized Magnesium

• determined by a nonmagnetic resonance ion-selective electrode specific for magnesium;
• May solve laboratory diagnostic problems, but requires more studies to confirm.

Dosing

The average dietary intake of magnesium by healthy adults in the United States ranges from 143- 266mg per day,⁶ which is easily below the RDA. To dose magnesium, a vitamin supplement with RDA levels is generally appropriate. A more exact supplementation can be based on body weight: healthy patients receiving 3 mg of magnesium per pound of body weight; and patients who are being treated for magnesium-related disorders at a level of 6mg per pound of body weight.⁶

References 

1. Ensminger & Konlande. Foods and Nutrition Encyclopedia. Pegus Press, Clovis, CA. 1983.
2. Recommended Dietary Allowances. National Academy of Sciences. National Academy Press, Washington, DC. 1989.
3. Werbach M. Foundations of Nutritional Medicine. Third Line Press, Tarzana, CA. 1997.
4. Werbach M. Nutritional Influences on Illness. Third Line Press, Tarzana, CA. 1988.
5. Satake, et al. Relation between severity of magnesium deficiency and frequency of anginal attacks in men with variant angina. Journal of the American College of Cardiology 1996;28:897-902.
6. Murray MT. American Journal of Natural Medicine December 1996;3(10):8-19.

Joint Pain in Children, Part IV: Lyme Disease

By Deborah Pate, DC, DACBR

Lyme disease is becoming more widely recognized as a cause of joint symptoms in children. The diagnosis is established from a typical history and physical findings, along with a positive serologic test for Lyme disease.

Lyme disease is transmitted by the deer tick Ixodes dammini, which carries the spirochete Borrelia burgdorferi. The white-tailed deer is usually the host to this tick; the white-footed mouse sometimes carries them. Patients of all ages and sex can be affected. Most cases occur in summer and early fall. The incubation period is 3-32 days.

Symptoms can be divided into early and late stages, but any of the findings can occur any time, alone or with other symptoms. The initial manifestation is a skin lesion, erythema chronicum migrans, which originates at the site of the tick bite and spreads in an expanding circle, often with central clearing. The lesion is accompanied by such constitutional symptoms as malaise, fatigue, arthralgia, headache, and stiff neck. From this early stage, the disease may progress to a second stage in which symptoms and signs of meningitis, neuritis, or cardiac occur weeks to months after the tick bite, and are characterized by chronic neurologic symptoms and most commonly by pauciarticular arthritis. Infection during pregnancy can cause infection of the fetus, and can causing some birth defects, but no pattern has thus far been established. Early treatment is advised after diagnosis.

Serologic findings may be negative in the early stage of Lyme disease but become positive as the disease progresses. Incomplete clinical presentations are common, so Lyme disease should be considered in all children with pauciarticular arthritis who have been in an area in which the tick is endemic. A significant elevation in antibody titers is a prerequisite to a definitive diagnosis of Lyme disease.

Length and route of treatment is decided based on the patient's condition. An oral antibiotic such as penicillin, ampicillin, erythromycin or tetracycline is usually the preferred treatment. Treatment is usually given for 10-20 days. Arthritis may be treated with oral antibiotics but sometimes needs intravenous antibiotics.

Prevention

Try to avoid the tick's habitats, mainly high brush areas and grasslands. If you are in the tick's habitat, wear protective clothing and use an insect repellant. Always check for and remove any ticks on you or your family/friends and pets (your pets can also get Lyme disease). Remember that the tick is very small, about 1/2 the size of the dog tick, which does not carry the spirochete.

It is important to remove the tick promptly, but carefully. The best way to remove the tick is with its head intact. Use tweezers or any similar instrument that will allow you to grasp it where its mouth parts enter the skin. Do not squeeze the tick's body. Tug gently at the area where the mouth is attached to the skin until it releases its hold by withdrawing its barbed mouth. It may take some time.

It is good to save the tick in a covered jar or alcohol, with the date and location of the bite and the place where you may have picked up the tick. Wipe the bite area with antiseptic or wash with soap and water. Animal studies suggest that the tick must be attached for at least 24 hours to transmit the spirochete. Call your local or state board of health if you want to have the tick identified.

For further information and a useful brochure for your patients, visit the web site www.ziplink.net/jcwheel/lyme.html. The following is also a brief fact sheet¹ produced by the epidemiology and disease control program of the state of Maryland.

Lyme Disease Fact Sheet

Lyme disease is caused by a bacterium.

You can't catch Lyme disease from another person.

It is transmitted by the bite of a certain type of tick called Ixodes scapularis (formerly I. dammini). Ticks must usually be attached to the body for several hours before they can transmit the Lyme disease bacteria (Borrelia burgdorferi). Very few tick bites will result in Lyme disease.

Symptoms appear 3-32 days after tick bite.

Most people with Lyme disease will get a characteristic rash called erythema migrans (EM) where they were bitten. The rash starts as a small red area which expands in a circular manner to two or more inches. The center of the rash may clear giving a "bulls eye" appearance. Other symptoms such as fever, headaches, tiredness, stiff neck, joint pain and swollen lymph nodes may also appear. If untreated, the heart, nervous system, or joints may be affected weeks to months later.

Anyone can get Lyme disease.

People who spend time outdoors in tick-infested areas (wooded, bushy or grassy places) are at an increased risk of exposure. A person can get Lyme disease more than once.

Blood tests are available.

Blood tests taken in the early stage of illness when treatment should begin may be negative. During this stage, diagnosis is usually made on signs and symptoms and history of tick bite. The tests may remain negative in persons successfully treated with antibiotics. Blood tests are usually positive after 30 days.

Lyme disease can be treated; see your doctor if you think you have Lyme disease.

Treatment for Lyme disease is based on early signs and symptoms and a history of a tick bite or tick exposure. Early treatment will prevent later complications.

You can prevent Lyme disease: 

• Inspect your body (including the hair on your head) for ticks after being outdoors.
• Use tick repellent -- follow directions on the package label.
• Minimize bite by walking in the middle of the paths and staying clear of tick-infested areas.
• Wear light colored clothes to help spot ticks.
• Wear long pants and long sleeved shirts.
• Tuck pant legs into socks, and tuck shirt into pants when hiking.
• Remove attached tick by grasping the tick as close to the skin surface as possible and pulling back with a steady force. Use forceps or tweezers and protect bare hand by using gloves, cloth or tissue. Do not squeeze the tick's body. Clean the bite after removing a tick as you would any minor wound.

Magnesium, Part I

By G. Douglas Andersen, DC, DACBSP, CCN

One evening last summer I was flipping through Dr. Melvyn R. Werbach's latest textbook, Foundations of Nutritional Medicine (Dr. Werbach is the author of Nutritional Influences on Illness, a source book of clinical research and an absolute must for anyone who practices clinical nutrition). 
The first chapter, "Disorders Due to Abnormal Nutriture," summarizes how nutrient deficiencies and excesses affect various disorders.¹

In chiropractic school we learned the importance of the mineral magnesium, and that it is required for literally hundreds of biochemical reactions in the body. If you forgot or didn't realize how critical adequate amounts of magnesium are, take a look at the following list of conditions where magnesium deficiency may exacerbate and/or contribute to the problem (this is not to say abnormal magnesium is the only cause or only cure for these disorders):

Agitation
Anorexia
Anxiety
Apathy
Arrhythmias
Ataxia
Behavioral Disturbances
Cognitive Impairment
Cold Sensitivity
Coma
Delirium
Depression
Diplopia
Dry Mouth
Dysphagia
Edema
Epilepsy
Fatigue
Growth Impairment
Hemolytic Anemia
Hyperactivity
Hypertension
Hypotension
Insomnia
Irritability
Kidney Stones
Lethargy
Muscle Fasciculations
Muscle Spasms
Muscle Tremors
Muscle Twitches
Muscle Wasting
Myalgia
Myopathy
Nausea
Nervousness
Neuromuscular Excitability
Nystagmus
Peripheral Neuropathy
Psychosis
Sonophobia
Tachycardia
Tetany
Vertigo
Vomiting
Weakness

In the December 1996 issue of the American Journal of Natural Medicine, Dr. Michael T. Murray did an extensive review of the literature on magnesium supplementation.² In addition to Dr. Werbach's findings above, Dr. Murray also documented that magnesium may help in the following:

Acute Myocardial Infarction
Angina
Asthma
Cardiomyopathy
Cardiovascular Disease
Chronic Obstructive Pulmonary Disease
Congestive Heart Failure
Diabetes
Dysmenorrhea
Eosinophilia Myalgia Syndrome
Fatigue
Fibromyalgia
Glaucoma
Hearing Loss
Intermittent Claudication
Low HDL Cholesterol
Mitral Valve Prolapse
Osteoporosis
Pregnancy
Premenstrual Syndrome
Stroke

Although the vast majority of magnesium problems are due to insufficiency, too much magnesium can cause, contribute, or exacerbate the following: diarrhea, hypotension, nausea, vomiting, dry mouth, cognitive impairment, depression, fatigue, flushing, respiratory insufficiency, and polydypsia.

Next month in part II, we will look at dietary sources and supplemental types of magnesium, along with a review of laboratory tests used to measure magnesium.

References 

1. Werbach M. Foundations of Nutritional Medicine. Third Line Press, Tarzana, California, 1997.
2. Murray MT. American Journal of Natural Medicine December 1996, 3(10):8-19.

Why Friction Massage Heals Tendinitis

Latest Information on Why Friction Massage Heals Tendinitis

By Warren Hammer, MS, DC, DABCO

In manual therapy, clinical results usually precede the scientific validation. Most techniques are used because "it works." Usually the author of the method hypothesizes why it works, but the reasoning although appearing logical may have nothing to do with the result. 
According to Frank and Hart¹: "Mechanical loading influences cell behavior in all soft tissues, but how it does so is not fully understood." The latest research on the effect of loading or deep pressure has been directed to the cellular level. In 1979, Meikle et al.² found that continuous stress to newborn rabbit cranial sutures led to an increase in collagen synthesis. Fibroblasts are responsible for increased collagen synthesis. Slack et al.,³ using a model of cyclic tensile loading of isolated embryonic chick tendons in vitro, showed increased synthesis of proteins, glycosaminoglycans and DNA by the fibroblasts.

Healing of tendons occurs in three stages. In the inflammatory stage, platelets and fibrin fill the wound and fibroblasts and phagocytic cells migrate to the injured area. Fibroblasts produce fibronectin, which acts as an adhesive molecule to bind collagen. As healing proceeds the fibroblastic production of fibronectin decreases. In the proliferative stage, the fibroblasts increase in number and synthesize collagen. Finally, in the third stage of remodeling or the maturation stage. there is a realignment of collagen fibers, and the collagen production shifts from the immature Type III to the mature Type I collagen.

Davidson et al.⁴ recently (1997) created a tendinitis in the rat tendon by injecting the enzyme collagenase. This method has also been used to trigger an inflammatory response in horses and ponies. While the collagenase did not cause the typical inflammatory response with the appearance of numerous mononuclear blood cells and lymphocytes at the injured site, the hallmark of tendon injury which is collagen fiber disruption and misalignment was exhibited in the rat tendons. They used augmented soft tissue mobilization (ASTM), which is an aluminum instrument used to apply "considerable pressure" to a tendon without breaking the overlying skin. The tendon was massaged longitudinally moving distal to proximal and proximal to distal along the length of the Achilles tendons of the rats.

There were four groups of rats: a) control; b) collagenase induced tendinitis; c) collagenase induced tendinitis plus ASTM; and d) ASTM alone to a normal tendon. After injecting the collagenase, the tendons were allowed to heal for three weeks. After the three weeks, ASTM was performed on group C and D for three minutes on postoperative days 21, 25, 29 and 33, i.e., four treatments. One week after the last treatment, the tendons were harvested and evaluated under light and electron microscopy and immunostaining for type I and type III collagen and fibronectin.

Light microscopy showed increased activated fibroblast proliferation in the tendons of group C and D. ASTM proved to initiate fibroblast activation which eventually leads to collagen synthesis. Group C also showed more fibronectin antibodies than group A. There was little fibronectin in Group B, but an increased amount in Group D. Gait analysis was also performed, and a significant improvement in stride length and stride frequency only occurred for Group C between post surgery day 21 and the final observation day.

ASTM promoted healing and earlier recovery of limb function following collagenase injury by the increased fibroblastic proliferation. The earlier recovery allowed increased limb function which also helped in the promotion of fiber realignment.

Of course, more studies are necessary especially to determine the effect of friction on chronic long-term scar tissue. It definitely appears that applying friction massage with increased pressure creates fibroblastic proliferation.

References 

1. Frank CB, Hart DA. Cellular response to loading. In: Leadbetter WB, Buckwalter JA, Gordon SL. Sports-Induced Inflammation, Amer Acad of Orthop Surgeons, Park Ridge, IL, 1989:555-563.
2. Meikle MC, Reynolds JJ, Sellers A, et al. Rabbit cranial sutures in vitro: A new experimental model for studying the response of fibrous joints to mechanical stress. Calcif Tissue Int 1979;28:137-144.
3. Slack C, Flint MH, Thompson BM. The effect of tensional load on isolated embryonic chick tendons in organ culture. Connect Tissue Res 1984;12:229-247.
4. Davidson CJ, Ganion LR, Gehlsen GM et al. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Medicine & Science in Sports & Exercise. American College of Sports Md, 1997:313-319.

Obesity, Part IV: Weight Loss Tips

By G. Douglas Andersen, DC, DACBSP, CCN

Anyone can lose weight and keep it off, if they want to. The reason why so many people fail at either losing weight, or keeping weight off after they have lost weight, is in this author's opinion 95 percent mental.

Accept responsibility. We live in a time where a significant percentage of people do not accept responsibility for their actions. Do not fall into this trap. If you are overweight, it is your fault. You must admit that you have lacked the discipline to eat the right foods and the self-control to eat the right amounts.

You will be hungry. It's no fun being hungry, but you must get used to it. Being hungry does not mean going so long without food that when you finally do eat you are unable to control yourself. Remember, whenever you are hungry your body is burning fat.

Be patient. It takes a long time to get out of shape and it takes a long time to get into shape. Don't expect that a few weeks of healthy habits will undo years of bad habits.

Get help. You don't need a fancy program, but you should tell your family, friends, and co-workers exactly how much you weigh and ask them to help you lose weight. By making your weight loss a public issue, you will have peer pressure to help you during times of weakness. Encourage those around you to tease you if you overeat and nag you about exercise. (If this doesn't sound fun, it isn't, but if you really want to lose weight, psychosocial factors can be strong motivators.)

Exercise regularly. You wouldn't dream of going weeks or months without bathing or brushing your teeth. Exercise in some form should be done six days per week. There are hundreds of ways to exercise. You can keep it fresh by performing a different activity every day. Not having the time is not an excuse. You must take 15-30 minutes every day to do something that causes you to breathe hard and break a sweat.

Eating Tips: 

1. Set reasonable goals. Depending on how large you are, 1-2 pounds per week is a reasonable goal.


2. Get out of the kitchen. Idle time in the kitchen invariably leads to "grazing."


3. Never go to the market hungry. Hungry shoppers buy more food and the market is designed to tempt you to purchase that which you do not need. Always shop from a list.


4. Do not eat while you prepare meals. This is an easy way to cut out hundreds of calories per week.


5. Put leftovers away immediately.


6. Do not eat a full meal before bed. This is the easiest way for your body to store fat. However, bedtime snacks such as a cup of nonfat yogurt will not get you in trouble.


7. Use smaller dishes. Big dishes equate to big servings.


8. Never get seconds.


9. Eat slower. When we eat too fast, our bodies are unable to inform us we are full until it is too late.


10. Eat breakfast. People who do not eat breakfast will make up those calories later in the day and have less time to burn them off.


11. Snack on fresh fruit. Apples and oranges are healthy, filling, and go anywhere. Eat three pieces a day.


12. Eat at home whenever you can. Restaurant food is high in calories and the portions are large.


13. Drink three quarts of water a day.


14. Eat a high fiber diet. It is good for your intestines, it fills you up, and it reduces the amount of fat your body absorbs.


15. Order sauce and dressing on the side.


16. Read labels carefully. One serving may be low calorie, but if you eat six servings at one time, it no longer is.


17. One bad day is no reason to quit. We're all human and every now and then a slip-up is inevitable.


18. Do not watch TV commercials, since so many of them push the wrong types of food.


19. Every bite counts. Write down everything you eat for a few days. This will help you realize how many extra calories (bites) sneak into your system.


20. Be careful during social activities. Chips, dips, and cocktails can cost you hundreds and even thousands of calories without noticing.

Exercise and Pregnancy

By Kim Christensen, DC, DACRB, CCSP, CSCS

Both exercise and pregnancy exert stresses on the body, and the cumulative effects must be considered when recommending a rehabilitative exercise program to pregnant women.¹Credible human research about the topic is sparse, and animal studies provide conflicting findings.

Chronic disorders such as diabetes, hypertension, and heart disease are clear reasons to discourage persons at risk from intense rehabilitative exercising while pregnant. Also, small or underweight women probably should be cautioned, since these women bear more premature and low birth weight infants than larger, normal-weight women.

Getting in Shape

Weight loss endeavors during pregnancy should be discouraged regardless of whether a decreased caloric intake or exercise is used, because neuropsychological abnormalities in infants have been associated with pregnancy. Adolescents are particularly prone to exercise during pregnancy, but a "get-in-shape" program should be deferred until after delivery if it is not undertaken before pregnancy. The existing level of aerobic fitness is an important factor in determining the eligibility of a pregnant woman for a rehabilitative exercise program. The effects of aerobic training are rapidly lost when activity ceases.

Walking is an excellent activity for the pregnant woman. Jogging should be discouraged, at least in the later stages of pregnancy, because of progressive lordosis and possible strain on the pelvic ligaments. A conservative approach to exercise seems wise because of its effects on the fetal heart rate and breathing movements. The maternal heart rate should not exceed 140 to 150 beats per minute for about 15 minutes, three to five times a week. Exercise at this level elicits an aerobic training effect in most women of childbearing age, while producing minimal fetal responses.

Gentle stretching and a warmup period before each exercise period are important measures. A cool down period of 10 to 15 minutes is also recommended. And because increased weight shifts anteriorly over the course of a pregnancy, it is also recommended that pregnant patients be fitted for custom made flexible orthotics. The ideal orthotic would be one which absorbs heel-strike shock, provides firm arch support and combats the high stress levels which commonly affect the lumbar spine of the mother-to-be.

Sedentary women should not begin vigorous rehabilitative exercise or try to get into shape during pregnancy. The time to get into good physical condition is before or after pregnancy. Once pregnant, a sedentary woman can begin a walking program or something similar. However, a woman who has been exercising can pursue a rehabilitative exercise program during pregnancy by adjusting the intensity of the program, according to how she feels, and keeping her heart rate in the 140 to 150 beats per minute range.

Fetal Heart Rates

Doppler monitoring of fetal heart rates, showing fetal bradycardia during vigorous maternal exercise, has given rise to concern for fetal safety. Because Doppler measurement of fetal heart rate during maternal exertion is difficult, two-dimensional ultrasonic imaging was used by Carpenter et al.² to record the fetal heart rate and determine the effect of submaximal and maximal maternal exertion and the incidence of fetal bradycardia.

Forty-five women with a mean gestation of 25 weeks performed exercise twice on separate days using a cycle ergometer. Resting measurements were taken with the women seated on the ergometer for 10 minutes. They underwent 85 submaximal and 79 maximal cycle ergometer tests.

Fetal cardiac activity was monitored continuously and videotaped during exercise and rest periods using a linear array two-dimensional ultrasound system. The average fetal heart rate did not change during maternal exertion, but 15 of 16 post-exercise episodes of bradycardia occurred within three minutes after maximal maternal exertion. There were 18 episodes of fetal bradycardia; one occurred during exercise.

Brief submaximal exercise up to 70% of maximal aerobic power seems to have no effect on fetal heart rate. Maximal exertion, on the other hand, is commonly followed by fetal bradycardia. The significance of this bradycardia is as yet unknown, but it seems prudent to recommend that pregnant women limit vigorous exercise to activities of no more than 150 beats per minute and conclude their exertion with a cool-down period.

Supine Exercise

Several investigators have monitored fetal hart rate (FHR) as a way to assess fetal hypoxia or distress in response to maternal exercise. An early study reported little effect on FHR, whereas later studies yielded conflicting results when using the FHR response to exercise as a screening test for uteroplacental insufficiency. Recent studies have reported a transient increase in baseline FHR. The effect of brief periods of mild, supine exercise on FHR in the late second trimester and mid-third trimester was studied by Nesler et al.³

Twenty-five healthy, regularly-exercising women were studied: 12 in the late second trimester, and 13 in mid third trimester. Although significant increases in maternal mean arterial pressure and pulse occurred, the exercise intensity was mild, with the average percent maximal pulse being 46 +/- 5% in the second trimester group and 49 +/- 5% in the third trimester group. Small increases in FHR were observed in both groups, which were insignificant statistically and physiologically. No patient experienced significant FHR abnormalities as a consequence of the exercise sequence.

These results indicate that pregnant women may continue submaximal supine exercise of short duration through the 36th week of gestation without harmful effects to the fetus. Thus, moderate exercising by pregnant women does not cause increases in the FHR. However, exercising while in a supine position instead of on a cycle ergometer may be a better choice. However, it appears from comparison of studies that the more vigorous exercise program used by Carpenter et al.² demonstrated no more danger to the fetus than did the more conservative program described by Nesler et al.³

Aerobic Exercise

The health and fitness of pregnant women at the onset of gestation affect the course and outcome of the pregnancy. Whether pregnancy reduces physical fitness as measured by maximal oxygen consumption between the second and third trimesters, and whether maintaining a regular exercise program during the second half of pregnancy influences fitness, were determined in 23 women by South-Paul et al.⁴ at the beginning of the second trimester.

Patients were randomly assigned to either a non-exercising or an exercising group. They completed a maximal progressive exercise test on a cycle ergometer at 20 weeks and 30 weeks, during which time pulmonary parameters or aerobic capacity were assessed.

The exercising women had greater improvement in aerobic capacity than the non-exercising women, manifested by increases in tidal volume and oxygen consumption and a stable ventilatory equivalent for oxygen. Pregnancy did not decrease the maximal oxygen consumption between the second and third trimesters, during which detraining could have been substantial.

This study points out the value of exercising during pregnancy. In fact, none of the women in this study was previously trained and the average baseline oxygen consumption was in the low range for both groups. Yet, when placed in a supervised exercise program, the exercise group improved their fitness, as demonstrated by an increased maximal oxygen consumption per kilogram of body weight.

The effects of exercise on the fetus are important in view of the increasing participation by women in rehabilitative exercise clinics. Dale et al.⁵ undertook a retrospective study of 21 women who had been pregnant in the past five years and who had participated in running during the course of pregnancy. A prospective sample of 12 women who were currently pregnant and running was also done with 11 controls matched with the runners for age, race, and parity. Electronic fetal monitoring was carried out in four subjects, all with favorable obstetric outcomes.

Subjects in the retrospective sample had a mean age of 30 years and had run for an average of four years; the mean prepregnancy weekly distance was 18.7 miles. Mean distances run in the three trimesters were 14.2, 10.9, and 6.6 miles a week, respectively. Eight of the 21 subjects competed in races while pregnant. Mean maternal weight gain was 24.4 pounds. In the prospective study, the only major obstetric complication in a runner was threatened abortion. There were no neonatal complications in the running group except for jaundice in an infant. Electronic fetal monitoring during treadmill running showed transient bradycardia, with a return of fetal heart rate to normal during continued exercise.

The course of pregnancy and complications appear to be similar in women who run during pregnancy and those who do not. Women who run exhibit a trend toward failure to progress during labor, resulting in an increased rate of cesarean section delivery. There is no evidence from Dale et al.⁵ of a compromised neonatal status in cases of women who run during pregnancy. Exercise appears not to seriously compromise uteroplacental function. Whether the fetal bradycardia observed during initial exercise is a response to transient hypoxia, a result of shunting of blood to the leg muscles, or an effect of other stress remains to be determined.

In the Dale⁵ study that evaluates 33 pregnant runners and 11 pregnant nonrunners, there is a more concerned note, perhaps, about potential major obstetrical complications in runners than controls, and the possibility of a higher Cesarean section rate in this group because of failure of progression during labor. More data would be necessary to confirm this, but this would be another argument for caution in prescribing running during pregnancy. There was no significant difference between runners and nonrunners with respect to weight gain, length of labor, and delivery, and the absolute incidence of obstetric complications. Dale5 did note fetal bradycardia, usually transient for a 2 1/2 to 3 1/2 minute interval, with spontaneous recovery during exercise. This is the point of concern. Again, pregnant women should limit exercise to activities requiring heart rates of no more than 150 beats per minute and conclude their exertion with a cool-down period.

References 

1. Snyder DK, Carruth BR. J Adolesc Health Care 1984; 5:34-36.
2. Carpenter MW, Sady SP et al. JAMA 1988; 259:3006-3009.
3. Nesler DL, Hassett SL, Brooke J. Am J Perinatol 1988; 5:159-163.
4. South-Paul JE, Rajagopo KR, Tenholder MF. Obstet Gynecol 1988; 71:175-179.
5. Dale E, Mullinax KM, Bryan DJ. Can J Appl Sports Sci 1982; 7:98-103.