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Complex Injuries

Back Clinic Complex Injuries Chiropractic Team. Complex injuries happen when people experience severe or catastrophic injuries, or whose cases are more complex due to multiple trauma, psychological effects, and pre-existing medical histories. Complex injuries can be serial injuries of the upper extremity, severe soft tissue trauma, and concomitant (naturally accompanying or associated), injuries to vessels or nerves. These injuries go beyond the common sprain and strain and require a deeper level of assessment that may not be easily apparent.

El Paso, TX’s Injury specialist, chiropractor, Dr. Alexander Jimenez discusses treatment options, as well as rehabilitation, muscle/strength training, nutrition, and getting back to normal body functions. Our programs are natural and use the body’s ability to achieve specific measured goals, rather than introducing harmful chemicals, controversial hormone replacement, unwanted surgeries, or addictive drugs. We want you to live a functional life that is fulfilled with more energy, a positive attitude, better sleep, and less pain. Our goal is to ultimately empower our patients to maintain the healthiest way of living.


The Knee

The Knee

The Knee | MRI may be requested for:

  • Ligament injuries
  • Meniscal tears and degeneration
  • Rheumatoid arthritis
  • Osteochondral fractures
  • Tendon disruptions

Bones & Cartilage Of The Knee

The knee joint is the largest, most complicated, and most vulnerable joint in the body, as it does not have a stable bony configuration. It consists of the tibiofemoral and patellofemoral articulations, which include the femur, tibia, and patella. The knee is a synovial joint that is enclosed by a ligament capsule. The capsule contains synovial fluid that keeps the joint lubricated (Figure 82). The knee provides flexible movement, but must also bear large weight and pressure loads. During walking, the knees support 1.5 times your body weight. When climbing stairs, they support 3-4 times your body weight. When squatting, your knees support 8 times your body weight.

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Figure 82. Anatomy of the knee.

The tibiofemoral articulation is a modified hinge joint that allows bending and straightening, but also allows for slight rotation. This articulation consists of the lateral and medial condyles of the femur resting on the lateral and medial aspects of the tibial plateau. The femoral condyles make up the distal portion of the femur, which is expanded in order to assist with weight distribution at the knee joint. The medial femoral condyle is typically larger and rounder. The condyles are united anteriorly to provide the articular surface for the patella, but they are separated posteriorly by the intercondylar notch. This notch, or fossa, is the attachment site for the cruciate ligaments, the ligaments of Humphrey and Wrisberg, and the frenulum of the patellar fat pad. A large part of the posterior distal femur is called the popliteal surface. This area is covered by fat, which separates it from the popliteal artery. The medial and lateral edges of the popliteal surface are attachment sites for muscles. Superior to the femoral condyles are the epicondyles, which are the attachment sites for muscles, tendons, and capsular ligaments. The medial epicondyle is the attachment site for the medial (or tibial) collateral ligament (Figure 83). The lateral femoral epicondyle is the attachment site for the lateral (or fibular) collateral ligament, as well as the tendon of the popliteus muscle, fibers of the iliotibial tract, and the lateral capsular ligament. Superior and posterior to the epicondyles is the most distal extent of the linea aspera, the bony ridge of the femur.

The tibia is the distal portion of the tibiofemoral articulation at the knee. The tibia is the second longest bone in the body, ranked just behind the femur. Its proximal end is flattened and expanded to provide a larger surface for the body weight that is transmitted through the femur. Like the femur, the proximal tibia has medial and lateral condyles. The medial condyle is larger, and somewhat flattened where it contacts the medial meniscus. The lateral condyle has a circular look to its femoral articular surface. The lateral tibial condyle articulates with the head of the fibula posteriorly, which is as close as the fibula comes to any involvement in the knee joint. Both the medial and lateral condyles rise in the center of the superior aspect of the tibia to form the intercondylar eminence. Posterior to this eminence are the attachments sites for the posterior horns of the medial and lateral menisci, which will be discussed with the ligaments of the knee. The medial and lateral tibial condyles, and the area of the intercondylar eminence are often grouped together and referred to as the tibial plateau (Figure 84). This is a critical weight-bearing area, and greatly affects the stability of the knee joint. The tibial tuberosity (or tubercle) is located on the anterior surface of the proximal tibial shaft. It has a smooth upper portion, and a roughened lower portion, which is the insertion site for the patellar tendon. The lateral side of the tibial tuberosity has a ridge for the attachment of fibers from the iliotibial tract. This is the strongest direct attachment site for the iliotibial tract. The IT tract, or band, helps in limiting lateral movement of the knee.

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Figure 84. Tibial plateau.

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Figure 83. Tibiofemoral anatomy.

 

 

 

 

 

 

 

 

 

 

The patella is the third bone involved in the knee joint, specifically in the patellofemoral articulation. Patella means �little plate� in Latin, which describes the look and function of this sesamoid bone. The patella develops in the tendon of the quadriceps femoris muscle (Figure 85). It moves when the leg moves, and protects the knee joint by relieving friction between the bones and muscles when the knee is bent or straightened. The patellofemoral joint is a saddle-type synovial joint, allowing the patella to glide along the bottom front surface of the femur between the femoral condyles in the patellofemoral groove. Ossification of the patella is typically completed in females by age 10, and in males between the ages of 13-16. If the patella has more than one ossification center, and the additional center does not fuse, it is termed a bipartite patella (Figure 86).

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Figure 86. Bipartite patella.

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Figure 85. Patella location.

 

 

 

 

 

 

 

 

 

 

 

Articular, or hyaline, cartilage covers the ends of the bones involved in any joint. In the knee joint, this includes the distal end of the femur, the proximal end of the tibia, and the posterior aspect of the patella (Figure 87). In larger joints, this cartilage is approximately �� thick. Articular cartilage is white, shiny, rubbery, and slippery, enabling surfaces to slide against one another without damage. Articular cartilage is very flexible, due in part to its high water content, which also makes it highly visible on MRI. In contrast to the bones that it covers, articular cartilage has almost no blood vessels, so it is not good at repairing itself. Bones, on the other hand, have numerous blood vessels, and are good at self-repair.

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Figure 87. Articular cartilage.

Another type of cartilage is found between the femur and tibia- the fibrous cartilage that makes up the medial and lateral menisci. The menisci, also referred to as �articular disks�, wrap around the round ends of the femur to fill the space between the femur and tibia (Figure 88). Since the menisci are more fibrous in composition, they have tensile strength and can resist pressure. They can help spread the force from our body weight over a larger area. By helping with weight distribution, the menisci protect the articular cartilage on the ends of the bones from excessive forces. The menisci are fashioned to be thicker on their outsides, creating a shallow socket on the tibial surface. They act like a wedge on the rounded distal portion of the femur, improving the overall stability of the knee joint by preventing any �rolling� of the femur. Despite how strong they sound, the menisci can crack or tear when the knee is forcefully rotated or bent. The medial meniscus is fused with the medial collateral ligament, so it is less mobile than the lateral meniscus. It is often injured when the anterior or posterior cruciate ligaments are injured. The inner 2/3 of the medial meniscus receives a limited blood supply, so the entire meniscus is usually slow to heal. The lateral meniscus suffers from fewer injuries than the medial meniscus. Meniscal tears are one of the most common causes of knee pain, with suspected meniscal tears the most common indication for an MRI of the knee joint.

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Figure 88. Superior view of menisci of right knee.

Symptoms that might indicate a problem with the bones of the knee joint include locking of the joint, the knee giving way, crackling or grinding felt in the joint, and pain and swelling. Locking of the joint can be indicative of a �loose body� (bone, cartilage, or foreign object) in the joint space, which can often be removed through arthroscopy (Figure 89). A knee that gives way can indicate that the patella is out of the patellofemoral groove, which leaves the knee unstable. Crackling and grinding at the joint can result from degenerative arthritis or osteoarthritis, as well as from a dislocating patella. An increase in pain with activity can occur due to a stress fracture or bone fracture. One of the pathologic conditions that can affect the bones of the knee joint is osteochondritis dissecans, which can affect the distal femur, and was discussed previously with the femur anatomy. Various types of arthritis manifest in the bones of the knee joint, including osteoarthritis, infectious arthritis, and rheumatoid arthritis. Chondromalacia patella, also known as patellofemoral syndrome or �runner�s knee� results from an irritation of the undersurface of the patella (Figure 91). If the patella is not tracking correctly in the patellofemoral groove, the articular cartilage may rub against the knee joint (Figure 90). The cartilage degenerates, and becomes irritated and painful. This condition is most common amongst young, healthy athletes, especially females and runners that are flat-footed. Treatment is typically rest and physical therapy to stretch and strengthen the quads and hamstrings. If surgery is required, it may be to perform a �lateral release�, as the abnormal tracking of the patella can cause a tightening of the lateral tissues of the knee. The lateral release procedure cuts the tight tissues, so the patella can return to its normal position and tracking. Osgood-Schlatter disease involves the anteriorly located tibial tuberosity, and the patellar tendon that inserts on that tuberosity (Figures 92, 93). This condition affects children during their growth spurts, and is typically found more in boys. During growth spurts, contractions of the quad muscle put additional stress on the patellar tendon at its attachment site on the tibial tuberosity. This can result in multiple subacute avulsion fractures and inflammation of the tendon. Excess bone growth occurs on the tuberosity, and a lump on the tuberosity can be seen and felt. This lump can become irritated and swollen, causing knee and leg pain. This condition is typically worsened with running, jumping, and climbing stairs. Osgood-Schlatter usually resolves with rest, ice, compression and elevation, as well as maturity of the youngster�s skeleton.

Figure 89. Intraarticular loose body.

 

Figure 90. Patellofemoral groove.

Figure 91. Patellofemoral syndrome or �runner�s knee�.

 

 

 

 

 

 

 

 

Figure 92. Xray displaying Osgood-Schlatter disease.

 

Figure 93. MRI displaying Osgood- Schlatter disease.

 

Ligaments Of The Knee

Ligaments are the tough bands of tissue that connect bones. They are considered to be �viscoelastic�, meaning they can gradually lengthen under tension, but return to their original shape when the tension is removed. However, if they are stretched for a prolonged period of time, or past a certain point, the ligaments cannot retain their original shape, and may eventually tear or snap. This is one of the reasons that a dislocated joint should be re-located as quickly as possible. If the ligaments lengthen, they leave the joint weakened and prone to future dislocations. Controlled stretching exercises to lengthen ligaments, and make the joints more supple, are part of the daily routines of athletes, gymnasts, dancers, etc. Damaged ligaments can lead to unstable joints, wearing of the cartilage, and eventually osteoarthritis. The numerous ligaments of the knee joint are the most important structures in controlling stability of the knee. Many of these ligaments were mentioned in the femur anatomy section, as they have attachments on the distal femur. The more important ligaments will be reviewed here in greater detail, in regards to their functions in the knee joint. The main intracapsular ligaments are the anterior and posterior cruciates (Figures 94, 95). Intracapsular ligaments are not very common in synovial joints. They provide stability, but permit a larger range of motion as compared to capsular or extracapsular ligaments. The anterior cruciate ligament (ACL) stretches from the lateral femoral condyle to the anterior intercondylar area of the tibia, preventing the tibia from being pushed too far anterior relative to the femur. It is the more commonly injured of the cruciate ligaments, and can be torn during twisting and bending of the knee. Women are at higher risk for ACL ruptures due to the facts that the maximum diameter of the intercondylar fossa is in its posterior aspect (the ACL attaches anteriorly), and the overall width of the intercondylar fossa is smaller in females. The posterior cruciate ligament (PCL) stretches from the medial femoral condyle to the posterior intercondylar area of the tibia, preventing posterior displacement of the tibia relative to the femur. It is the stronger of the two cruciate ligaments, and is injured less frequently; however, it can be injured from direct force or trauma. The menisci are also considered to be intracapsular structures, with connections to ligaments inside and outside the joint capsule. Two of their intracapsular ligaments are the anterior and posterior transverse meniscomeniscal ligaments. They attach the medial and lateral menisci to each other at their anterior and posterior aspects. Posterior transverse meniscal ligaments are very rare- only 1-4% of knees will have them. Two additional intermeniscal ligaments are the medial and lateral oblique meniscomeniscal ligaments (Figure 96). Their names describe their anterior horn attachment sites; they attach on the posterior horn of the opposite meniscus (i.e. medial oblique meniscomeniscal attaches to the anterior horn of the medial meniscus and posterior horn of the lateral meniscus). The oblique meniscomeniscal ligaments both traverse the intercondylar notch, and pass between the anterior and posterior cruciate ligaments (Figure 97).

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Figure 94. Cruciate ligaments and menisci.

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Figure 95. Posterior view of cruciate ligaments of left knee.

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Figure 96. Axial fatsat T2 FSE image with arrow indicating
oblique meniscal ligament coursing from anterior horn of
medial meniscus to posterior horn of lateral meniscus.

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Figure 97. Sagittal dual-echo T2 through the intercondylar notch at the level of the posterior cruciate ligament (curved arrow); thin linear structure of low signal intensity inferior to PCL represents the oblique meniscomeniscal ligament (straight arrow); sometimes misinterpreted as displaced meniscal fragment.

 

The medial (or tibial) collateral ligament is considered a capsular ligament, as it is part of the articular capsule surrounding the synovial knee joint. It acts as mechanical reinforcement for the joint, protecting the knee from valgus force, or being bent open medially due to stress on the lateral side of the knee. The medial collateral ligament (MCL) is one of the most commonly injured of all knee ligaments, occurring in all sports, in all ages, and often times with medial meniscal tears (Figures 98-101). It has both superficial and deep components. Fibers from the superficial portion of the MCL attach to the medial epicondyle of the femur and the medial tibial condyle. Fibers from the deep medial collateral ligament attach to the medial meniscus. Proximal to the attachment point, this ligament is referred to as the meniscofemoral ligament, as it attaches the medial meniscus to the medial aspect of the femur. Distal to the meniscal attachment, the ligament is referred to as the meniscotibial (or coronary) ligament, as it attaches the medial meniscus to the medial aspect of the tibia. The meniscofemoral and meniscotibial are also referred to as the meniscocapsular or medial capsular ligaments, as they play an important role in anchoring peripheral parts of the medial meniscus in the medial side of the knee. The meniscotibial ligament is typically injured more often than the meniscofemoral ligament. The meniscotibial ligament attaches to the tibia several millimeters inferior to the articular cartilage. Its job is to stabilize and maintain the meniscus in its proper position on the tibial plateau. Disruption of the meniscotibial ligament can result in a floating meniscus or meniscal avulsion, while the meniscofemoral ligament may not be affected. The deep medial collateral ligament is short, and tightens quickly with rotation motions. It is often damaged, along with the ACL, when the mechanism of injury involves tibial rotation. Diagnosis and surgical repair of the deep medial collateral ligament can be challenging.

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Figure 98. Normal MCL is linear,
has low signal intensity.

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Figure 99. Grade 1 sprain shows adjacent edema, no change in signal intensity of MCL.

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Figure 100. Grade 2 sprain or partial tear shows increased edema,
abnormal signal intensity,
thickening or thinning of ligament.

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Figure 101. Grade 3 involves complete disruption of ligaments or attachments.

 

In addition to fibers of the medial collateral ligament, the deep portion of the capsular compartment of the medial knee is the location of the medial knee�s posterior support. The posterior oblique ligament is attached proximally to the medially located adductor tubercle of the femur, and distally to the tibia and the posterior aspect of the knee joint capsule. If the posterior oblique is injured, it is usually torn from its femoral origin. The posterior oblique ligament provides static resistance to valgus loads as the knee moves into full extension, as well as dynamic stabilization to valgus forces (stress from lateral side) as the knee moves into flexion. It acts as an important restraint to posterior tibial translation in cases of posterior cruciate ligament injury. The posterior oblique ligament has three �arms�. Its superior capsular �arm� becomes continuous with the posterior knee capsule, and the proximal portion of the oblique popliteal ligament. The oblique popliteal ligament is also an important posterior stabilizing structure for the knee joint Figure 102). It extends from the posteromedial aspect of the tibia, running obliquely and laterally upward to insert near the lateral epicondyle of the femur.

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Figure 102. Oblique popliteal ligament in posterior view of knee.

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Figure 103. Medial (tibial) and lateral (fibular) collateral ligaments.

 

The lateral (or fibular) collateral ligament is considered an extracapsular ligament. It helps to provide joint stability and protects the lateral side of the knee from varus forces, or inside bending forces that are directed at the medial side of the knee. Injuries to the lateral collateral ligament are less common than injuries to the medial collateral, as the opposite leg can guard against medial forces that can lead to lateral collateral injuries. Injuries can occur in sports such as soccer and rugby, where the knee is extended and unprotected during running. The lateral, or fibular, collateral ligament stretches obliquely downward and backward, from the lateral epicondyle of the femur to the head of the fibula (Figure 103). It is not fused with the capsular ligament or with the lateral meniscus, so it has increased flexibility and decreased incidence of injury when compared to the medial collateral ligament. Similar to the medial meniscus, the lateral meniscus has a meniscotibial, or coronary, ligament. It connects the inferior edges of the lateral meniscus to the periphery of the tibial plateau. The lateral meniscus also has a meniscofemoral ligament that extends from the posterior horn of the lateral meniscus to the lateral aspect of the medial femoral condyle. It is given two distinct names, based on its location in relation to the posterior cruciate ligament (PCL). The ligament of Humphrey passes in front of the posterior cruciate ligament. It is less than 1/3 the diameter of the posterior cruciate ligament, but may be confused for the posterior cruciate during arthroscopy. The ligament of Wrisberg passes behind the posterior cruciate ligament, and is about � of the posterior cruciate�s diameter (Figure 104). Its femoral origin often merges with the posterior cruciate ligament. Both ligaments are present in only about 6% of knees. Approximately 70% of people have one or the other of these ligaments, with the majority possessing the more posterior ligament of Wrisberg (Figure 105). MRI is the preferred imaging modality for medial collateral or lateral collateral ligament injuries, as it can detect any associated internal knee derangements, cruciate-collateral ligament injuries, or cartilage deficiencies.

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Figure 104. Rendering of posterior knee, arrow indicates Ligament of Wrisberg; courses obliquely from lateral aspect of medial femoral condyle to posterior horn of lateral meniscus,
remains posterior to PCL.

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Figure 105. Arrow indicates �Wrisberg pseudo-tear�; intermediate signal
intensity line at junction of
Ligament of Wrisberg and normal posterior horn of lateral meniscus; often mistaken for a meniscal tear.

The patellar ligament is the connection between the patella and the tibia, extending from the apex (inferior aspect) of the patella to the tibial tuberosity. Technically, it is connecting two bones, so it is a ligament. However, it is most often referred to as the patellar tendon, because the superficial fibers that cover the front of the patella and extend to the tibia are continuous with the central portion of the common tendon of the quadriceps femoris muscle. The posterior surface of the patellar ligament is separated from the synovial membrane of the knee joint by a large infrapatellar pad of fat. Injuries to the patellar ligament can occur from overuse, such as sports that involve jumping and quick directional changes, as well as running-related sports. This is the ligament that is injured in jumper�s knee (or patellar tendonitis), which begins with inflammation, and can lead to degeneration or rupture of the patellar ligament and the tissue around it (Figure 106). Patients with patellar ligament injuries typically complain of pain in the area below the kneecap, which will increase with walking, running, squatting, etc. They can often be treated in the same manner as other soft tissue injuries- with rest, ice, compression and elevation. The patellar ligament attachment at the tibial tuberosity is the site of Osgood-Schlatter disease, which was discussed previously.

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Figure 106. Patellar tendonitis (jumper�s knee).

Along the sides of the patella and the patellar ligament are the medial and lateral patellar retinacula (Figure 107). They are fibrous tissue stabilizers for the patella that form from the medial and lateral portions of the quad tendons as they pass down to insert on either side of the tibial tuberosity. The lateral retinaculum is the thicker of the two, but both have superficial and deep layers. Within the deep layers are various ligaments (whose names indicate the structures they connect) that help support the patella in its position, relative to the femur below it. The deep layer of the lateral patellar retinaculum is the location where the lateral patellofemoral ligament meets the iliopatellar band, which is a tract of fibers from the iliotibial (IT) band that connects to the patella. The deep layer of the medial patellar retinaculum has three focal capsular thickenings, referred to as the medial patellofemoral, medial patellomeniscal, and medial patellotibial ligaments. The medial patellofemoral ligament is strong enough to influence patellar tracking, and acts as a major medial restraint. Imbalances in the forces that control patellar tracking during flexion and extension of the knee can lead to patellofemoral pain syndrome (runner�s knee), one of the most common causes of knee pain. This can result from overuse, trauma, muscle dysfunction, patellar hypermobility, and poor quadriceps flexibility. Typical symptoms include pain behind or around the patella that is increased with running, and activities that involve knee flexion. MRI is typically not necessary for this diagnosis. Physical therapy has been found to be effective for the treatment of patellofemoral pain syndrome.

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Figure 107. Lateral and medial retinaculum.

Muscles & Tendons Of The Knee

The flexor and extensor muscles of the knee have been discussed previously, as the majority of them are the anterior and posterior muscles of the thigh. We will review the thigh muscles involved in knee movement, and add two muscles of the lower leg that also affect the knee. The quadriceps femoris muscles of the anterior thigh are the main knee extensors (Figure 108). As these muscles contract, the knee joint straightens. The tendons of the vastus medialis, vastus intermedius, vastus lateralis, and rectus femoris join at the superior aspect (base) of the patella to form the patellar tendon. This tendon continues over the patella and attaches it to the tibial tuberosity (since it is connecting bone to bone, it is sometimes called the patellar ligament). The quadriceps, along with the gluteal muscles, are responsible for the thrusting forces necessary for walking, running, and jumping. The quads also help control movement of the patella, as they are attached to it by the quadriceps tendons (Figure 109). The patella increases the force exerted by the quadriceps muscles as the knee is straightened.

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Figure 108. Anterior thigh muscles – knee extensors.

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Figure 109. Quadriceps controlling the patella.

 

 

 

 

 

 

 

 

 

 

 

 

 

The posterior thigh muscles, also known as the hamstrings, are the main knee flexors, with assistance from the sartorius, gracilis, gastrocnemius, and popliteus muscles. The knee bends when the hamstrings contract. The hamstring muscles give the knee joint the strength needed for propulsion in running and jumping. They also help to stabilize the knee by protecting the collateral and cruciate ligaments, especially when the knee twists. The three hamstring muscles have varying attachment sites around the knee joint (Figure 110). The biceps femoris attaches to the head of the fibula and the superolateral aspect of the tibia. The semitendinosus attaches on the anterior aspect of the tibia, medial to the tibial tuberosity, crossing over the medial collateral ligament. The tendon of the semitendinosus muscle is sometimes used for cruciate ligament reconstruction. The semimembranosus attaches at the posteriomedial aspect of the medial tibial condyle. The sartorius muscle is also a knee flexor, although it is an anterior thigh muscle. It inserts on the anterior medical aspect of the tibia. The gracilis muscle of the medial thigh is one of the hip adductors, but also plays a part in knee flexion. Like the semitendinosus tendon, the tendon of the gracilis is sometimes used for cruciate ligament reconstructions. The gracilis attaches to the medial aspect of the proximal tibia.

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Figure 110. Posterior knee
muscles – knee flexors.

Additional flexors of the knee joint include some of the posterior muscles of the lower leg. The large superficial gastrocnemius muscle has a medial and a lateral head, which originate from the medial and lateral femoral condyles, respectively. It runs the length of the posterior lower leg, attaching to the calcaneus by the Achilles tendon. The gastrocnemius gives us the ability to flex our knee while our foot is flexed, as it connects to both joints. It is involved in standing, walking, running, and jumping. The popliteus is a deep posterior lower leg muscle that helps with knee flexion, and also rotates the tibia medially, which aids in knee stability. The popliteus originates from the outer margin of the lateral meniscus of the knee joint. It extends posteriorly and inserts on the medial aspect of the tibia, inferior to the medial tibial epicondyle.

The important tendons of the knee include the quadriceps, patellar, and hamstring tendons, and the iliotibial band (Figure 111). Tendons attach muscles to bones. These major knee tendons have all been discussed with either the bones or the muscles that they attach. The quadriceps tendon was mentioned with the quadriceps muscle as the muscle�s attachment to the patella. The quad tendon continues over the patella, then attaches the apex of the patella to the tibial tuberosity. It is then called the patellar tendon (or ligament). Hamstring tendons were discussed with the hamstring muscles, the posterior muscles that are flexors of the knee. Hamstring tendons are sometimes used for cruciate ligament reconstructions. Tendonitis, which is the inflammation of a tendon, is a common knee injury amongst athletes in a variety of sports. The iliotibial band (or IT tract) functions like a tendon, as it attaches the knee to the tensor fasciae latte muscle. The band is actually a fibrous reinforcement of the fascia lata, or deep tissue of the thigh. It runs from the ilium to the tibia. Proximally, it acts as a hip abductor, while distally it acts as lateral stabilization for the knee, and aids with medial rotation of the tibia. The IT band is in constant use during walking and running, which can lead to irritation at the point where it passes over the lateral femoral epicondyle. A �tight� IT band can cause inflammation and/or irritation at the femoral epicondyle, or at the point of insertion on the lateral tibial condyle. This condition is called IT band friction syndrome. It is common amongst runners, hikers, and cycling enthusiasts.

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Figure 111. Tendons of the knee.

Nerves Of The Knee

The main nerves to the knee that come from the sacral plexus of nerves are the tibial nerve and the common peroneal nerve (Figure 112). Both are branches of the sciatic nerve, and begin posteriorly, slightly above the actual knee joint. Both of these nerves, or their branches, continue through the lower leg and foot, providing sensation and muscle control. The tibial and common peroneal nerves are also both involved in cutaneous innervation, which is the supply of nerves to the skin of the knee. The tibial nerve remains posterior and more medial, branching at the medial ankle to innervate the foot. The common peroneal nerve begins posterolaterally, moving anteriorly near the neck of the fibula. It then branches into the superficial and deep peroneal nerves, which continue their anterior descent to the foot. The tibial and common peroneal nerves are the most commonly injured nerves when a knee is dislocated. Nerves can grow back, but they do so at a rate of approximately � inch per month.

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Figure 112. Sacral plexus nerves of knee.

Nerves from the lumbar plexus that affect the knee include the lateral femoral cutaneous, and the saphenous, which is a branch of the femoral nerve (Figure 113). The saphenous nerve travels more medially and gives off infrapatellar branches around the knee joint. Below the knee, the saphenous nerve sends branches to the skin of the anterior and medial lower leg. The lateral femoral cutaneous nerve sends an anterior branch to the skin of the anterior and lateral thigh, down to the area of the knee. Terminal filaments of this nerve communicate with the infrapatellar branch of the saphenous nerve, forming the peripatellar plexus.

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Figure 113. Lumbar plexus nerves of knee.

Arteries & Veins Of The Knee

The popliteal artery, a branch of the superficial femoral artery, is the main arterial supply to the knee joint. It runs along the posterior aspect of the distal femur, behind the knee joint. At the supracondylar ridge, the popliteal artery gives off the blood supply to the knee, which consists of various genicular arteries (Figure 114). Inferior to the knee joint, the popliteal branches into the anterior and posterior tibial arteries, which supply the lower leg. The popliteal artery is a common site for both atherosclerosis and aneurysms, and is listed as the most common site for peripheral arterial aneurysms. Approximately 50% of these aneurysms are bilateral. Although they rarely rupture, popliteal aneurysms may serve as a focus for abrupt thrombotic occlusion of the involved popliteal artery, which can affect the foot on the same side. A thrombus within an aneurysm can also lead to a distal embolism. The genicular arteries are sources of continued blood flow to the knee and lower limb, in case of an obstructed popliteal artery. The descending genicular, also called the highest or supreme genicular, branches from the femoral artery, just superior to the popliteal branch. It supplies the adductor magnus and hamstring muscles, then joins with the network of genicular arteries around the knee joint. The middle genicular pierces the oblique popliteal ligament, and supplies the ligaments and synovial membrane inside the knee articulation (including the ACL and PCL). The sural artery joins the anastomoses of the genicular arteries, and also supplies muscles of the lower leg, including the large gastrocnemius muscle. The anastomotic pattern around the knee joint is supplied by the popliteal artery posteriorly, the descending genicular artery medially, and the descending branch of the lateral circumflex femoral artery laterally. The genicular arteries involved in the anastomosis are labeled as the medial and lateral superior geniculars, and the medial and lateral inferior geniculars.

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Figure 114. Arteries of knee.

The major deep veins around the knee joint are the popliteal vein, and the anterior and posterior tibial veins (Figure 115). The popliteal vein begins at the junction of the tibial veins in the posterior aspect of the lower leg, just inferior to the knee joint. It ascends posteriorly, continuing as the femoral vein about halfway up the thigh. As deep veins typically follow the arteries, the genicular veins accompany the genicular arteries around the knee joint, then drain into the popliteal vein. The important superficial veins around the knee joint are the small and great saphenous veins. Superficial veins typically do not follow arteries, but rather travel with cutaneous nerves. The small saphenous ascends the lower leg posteriorly, angling from lateral to medial. It merges with the popliteal vein at a position slightly superior to the knee joint. The great saphenous vein, the longest vein in the body, has a medial and anterior course in the lower leg. It moves to a posterior position, but stays medial along the knee joint, moving alongside the medial epicondyle of the femur. The great saphenous then moves anteriorly again through the thigh.

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Figure 115. Veins of knee.

Varicose and �spider� veins are often seen in the leg in the posterior aspect of the knee joint. As mentioned previously, in the femoral vein discussion, veins have valves to ensure the �one-way� uphill flow of blood back to the heart (Figure 116). Communicating vessels, also called perforating veins, exist between the deep and superficial veins to help compensate for valves that may be incompetent, and are allowing blood reflux. If venous walls are weakened or dilated, the cusps of the valves can no longer close properly, and the valves can become incompetent. This leads to an increase in the weight of the column of blood for the veins that are �downstream� from the bad valve. Blood can pool in these veins, causing them to become varicose, where the veins swell, become tortuous, and even bulge through the skin surface. Reticular veins, which are smaller varicose veins that do not bulge through the skin, as well as very small �spider� veins are both typically less severe conditions, but both still involve the backwards flow of blood. Removal of severe varicose veins will actually help blood flow, as the blood will no longer be stagnant in the pooled areas.

the knee

Figure 116. Varicose veins around knee.

Bursae Of The Knee

The synovial knee joint is home to a large number of bursae (Figure 117). These are fluid sacs and synovial pockets that surround and sometimes communicate with the joint cavity. They facilitate friction-free movement between the bones and moving structures (tendon, muscle). Fluid or debris can collect in the bursa, or fluid can extend into the bursa from the adjacent joint in situations such as excessive friction, infection or direct trauma. This type of pathological enlargement of the bursa is referred to as bursitis, which can mimic several peripheral joint and muscle abnormalities. Radiologists must be able to accurately identify bursal pathology, especially amongst the numerous knee bursae (14 reported in some literature). We will identify a few of the more common bursa, beginning with the suprapatellar bursa. This bursa lies between a quadriceps tendon and the femur, superior to the patella (Figure 118). Fluid is commonly found here when patients have a joint effusion. Bursitis of the prepatellar bursa is also known as �housemaid�s knee�. It occurs from repetitive trauma from kneeling, as seen with housemaids, wrestlers, and carpet-layers. This bursa is found between the patella and the skin (Figure 119). Inflammation of the superficial infrapatellar bursa may be called �Clergyman�s knee�, another bursitis that can occur from excessive kneeling. This bursa is located between the distal third of the patellar tendon and the overlying skin (Figure 120).

the knee

Figure 117. Bursae in the knee.

the knee

Figure 118. T2 gradient
displaying suprapatellar
bursa.

the knee

Figure 119. T2
fatsat displaying
prepatellar bursa.

the knee

Figure 120. T2 fatsat
displaying infrapatellar
bursa.

 

The synovial sac of the knee joint sometimes forms a posterior bulge, known as a Baker�s cyst or popliteal cyst (Figure 121). It typically forms between the tendons of the medial head of the gastrocnemius muscle and the semimembranosus muscle, posterior to the medial femoral condyle. Baker�s cysts are not true cysts, as they typically maintain open communication with the synovial sac. However, they can pinch off, and they can rupture. They are usually asymptomatic, but can be indicative of another problem of the knee, such as arthritis or a meniscal tear. Aspiration of the synovial fluid can be performed if the cyst becomes problematic. Treatment is usually necessary if a Baker�s cyst ruptures, as it can cause acute pain behind the knee, and swelling of the calf muscles. A ruptured cyst can also mimic a DVT or thrombophlebitis. Ultrasound and MRI can both be used for confirmation of a Baker�s cyst (Figure 122).

the knee

Figure 121. Lateral view of Baker�s cyst.

the knee

Figure 122. Sagittal image of Baker�s cyst on MRI.

Scan Setups

The following are HMSA suggestions for knee imaging. Knee protocols should be designed to yield diagnostic images of the menisci, bones, articular cartilage, and all ligamentous structures of the knee. While many radiologists may require additional imaging of the ACL, protocols that are designed for optimal imaging of the cartilage and menisci should also produce adequate images of the ACL. Always check with your radiologist for his/her imaging preferences.

Axial Scans

When positioning axial slices for the knee, sagittal and coronal images can be used to insure inclusion of all pertinent anatomy. The slices should extend superiorly to include the entire patella, and inferiorly to include the tibial tuberosity and patellar tendon insertion. A presat can be placed over the unaffected lower extremity to reduce the possibility of wrap-around artifact, as seen in the coronal image in Figure 139.

the knee

Figure 139. Axial slice setup using sagittal and coronal images.

Coronal Scans

Coronal slices of the knee should include the anatomy from the posterior femoral condyles to the anterior portion of the patella. Visualize a line connecting the lateral and medial condyles of the femur. Typically, the coronal slices are angled so that they are parallel to that line, as seen in the axial image in Figure 140.

the knee

Figure 140. Coronal slice setup using axial and sagittal images.

Sagittal Scans

Sagittal slices should include the anatomy from the medial condyle to the lateral condyle. The slice group may be angled per your radiologist�s preference, but should remain perpendicular to the coronal slices. Typically, the slice group is angled so that it is parallel to the medial border of the femoral condyle, as seen in the axial image in Figure 141.

the knee

Figure 141. Sagittal slice setup using axial and coronal images.

In addition to routine oblique sagittal images, some radiologists prefer an additional sagittal scan of the ACL with thin slices and high spatial resolution. Axial and coronal images can be used for slice setup. Referenced literature recommends that the angle of the slice group should not exceed 10� from a line drawn perpendicular to the bicondylar line (line that connects the posterior femoral condyles), as seen in Figure 142.

the knee

Figure 142. Sagittal ACL slice setup using axial and coronal images.

 

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Figures 150, 151- www.gla.ac.uk/ibls/US/fab/tutorial/anatomy/jiet.html

Figure 153- www.athletictapeinfo.com/?s=tennis+leg

Figure 154- radsource.us/clinic/0608

Figure 155- www.eorthopod.com/content/achilles-tendon-problems

Figure 156- achillesblog.com/assumptiondenied/not-a-rupture/

Figure 181- www.orthopaedicclinic.com.sg/ankle/a-patients-guide-to-ankle-anatomy/

Figure 182- www.activemotionphysio.ca/article.php?aid=47

Figure 183- www.ajronline.org/content/193/3/687.full

Figures 184, 186- www.eorthopod.com/content/ankle-anatomy

Figure 185- www.crossfitsouthbay.com/physical-therapy/learn-yourself-a-quick-anatomy-reference/ankle/

Figures 187, 227- www.activemotionphysio.ca/Injuries-Conditions/Foot/Foot-Anatomy/a~251/article.html

Figure 188- inmotiontherapy.com/article.php?aid=124

Figures 189, 190- home.comcast.net/~wnor/ankle.htm

Figure 191- skillbuilders.patientsites.com/Injuries-Conditions/Ankle/Ankle-Anatomy/a~47/article.html

Figure 192- metrosportsmed.patientsites.com/Injuries-Conditions/Foot/Foot-Anatomy/a~251/article.html

Figure 193- musc.edu/intrad/AtlasofVascularAnatomy/images/CHAP22FIG30.jpg

Figure 194- musc.edu/intrad/AtlasofVascularAnatomy/images/CHAP22FIG31B.jpg

Figure 195- veinclinics.com/physicians/appearance-of-vein-disease/

Figure 196- mdigradiology.com/services/interventional-services/varicose-veins.php

Figure 216- kidport.com/RefLib/Science/HumanBody/SkeletalSystem/Foot.htm

Figure 217- www.joint-pain-expert.net/foot-anatomy.html

Figure 218- www.thetoedoctor.com/turf-toe-symptoms-and-treatment/

Figures 219, 220- radsource.us/clinic/0303

Figure 221- www.ajronline.org/content/184/5/1481.full

Figure 222- www.answers.com/topic/arches

Figure 223- www.mayoclinic.com/health/medical/IM00939

Figure 224- radsource.us/clinic/0904

Figure 225- www.ortho-worldwide.com/anfobi.html

Figure 226- www.coringroup.com/lars_ligaments/patientscaregivers/your_anatomy/foot_and_ankle_anatomy/

Figure 228- www.stepbystepfootcare.ca/anatomy.html

Figure 229- iupucbio2.iupui.edu/anatomy/images/Chapt11/FG11_18aL.jpg

Figure 230- www.ajronline.org/content/184/5/1481.full.pdf

Figure 231- metrosportsmed.patientsites.com/Injuries-Conditions/Foot/Foot-Anatomy/a~251/article.html

Figure 232- www.painfreefeet.com/nerve-entrapments-of-the-leg-and-foot.html

Figures 233, 234- emedicine.medscape.com/article/401417-overview

Figure 235- web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v03/030676r00.HTM

Figure 236- www.nysora.com/peripheral_nerve_blocks/classic_block_tecniques/3035-ankle_block.html

Figure 237- ultrasoundvillage.net/imagelibrary/cases/?id=122&media=464&testyourself=0

Figure 238- www.joint-pain-expert.net/foot-anatomy.html

Figure 239- jap.physiology.org/content/109/4/1045.full

Figure 240- microsurgeon.org/secondtoe

Figure 241- elu.sgul.ac.uk/rehash/guest/scorm/406/package/content/common_iliac_veins.htm

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Sports Injury Treatment | Turf Toe | Video

Sports Injury Treatment | Turf Toe | Video

Sports Injury Treatment: PUSH-as-Rx ��: 915-203-8122 | Dr. Alex Jimenez � Chiropractor: 915-850-0900 PUSH-as-Rx ���is leading the field with laser focus supporting our youth sport programs.� The�PUSH-as-Rx ���System is a sport specific athletic program designed by a strength-agility coach and physiology doctor with a combined 40 years of experience working with extreme athletes. At its core, the program is the multidisciplinary study of reactive agility, body mechanics and extreme motion dynamics. Through continuous and detailed assessments of the athletes in motion and while under direct supervised stress loads, a clear quantitative picture of body dynamics emerges. Exposure to the biomechanical vulnerabilities are presented to our team. �Immediately,�we adjust our methods for our athletes in order to optimize performance.� This highly adaptive system with continual�dynamic adjustments has helped many of our athletes come back faster, stronger, and ready post injury while safely minimizing recovery times. Results demonstrate clear improved agility, speed, decreased reaction time with greatly improved postural-torque mechanics.��PUSH-as-Rx ���offers specialized extreme performance enhancements to our athletes no matter the age.

Sports Injury Treatment

sports injury treatment

Vincent Garcia, an athlete training in mixed martial arts, or MMA, suffered a knee injury and developed turf toe, but that hasn’t stopped him from participating in his regular training regimen. In order to return to as well as improve his original physical performance, Vincent Garcia found treatment with Dr. Alex Jimenez, doctor of chiropractic. Now recovering from his sports injuries, Vincent Garcia looks forward to regaining his strength, flexibility and mobility to return to sport.

Dr. Alex Jimenez D.C. – Treats Vince Garcia MMA Fighter for Sports Injuries, including knee pain and turf toe. Dr. Jimenez D.C can be reached at (915) 850-0900 or visit our website at www.DrAlexJimenez.com

Please Recommend Us: If you have enjoyed this video and/or we have helped you in any way please feel free to recommend us. Thank You.

Chiropractic Relieves Sacroiliac Joint Pain

Chiropractic Relieves Sacroiliac Joint Pain

Chiropractic Relieves: How can a body part you have probably never heard of hurt so BAD? This is a common question we hear from individuals suffering from sacroiliac joint pain.

The sacroiliac�joint is formed by the sacrum and the ilium where they meet on either side of the lower back, with the purpose of connecting the spine to the pelvis. This small joint is one of the most durable parts of the human body, and it is responsible for a big job.

chiropractic relieves

The unassuming little sacroiliac joint withstands the pressure of the upper body’s weight pushing down on it, as well as pressure from the pelvis. It’s basically the cushion between the torso and the legs. As such, it handles force from pretty much every angle.

While immensely strong and durable, this joint is not indestructible. Sacroiliac joint pain usually crops up as lower back pain, or pain in the legs or buttocks.

Weakness in these areas may also be present. The typical culprits in causing the sacroiliac joint to exhibit pain are traumatic injuries to the lower back, but more frequently develops over a longer period of time.

Sacroiliac joint pain is often misdiagnosed as soft tissue issues instead of the joint itself. Doctors may rule out other medical conditions before settling on a diagnosis that includes a sacroiliac joint problem.

If you have suffered an injury, a degenerative disease, or otherwise damaged the sacroiliac joint, there are treatments available to help manage pain, promote healing, and lessen the chances of recurrence. Here are a four helpful guidelines to assist in effectively handling sacroiliac joint pain.

chiropractic relieves

Chiropractic Relieves:

First, rest and ice the area. Avoid exaggerated movements of your lower back in order to relieve some of the body’s pressure on the sacroiliac joint. Also apply ice wrapped in a towel periodically to soothe the area and minimize the pain.

A second way to handle sacroiliac pain is with therapeutic massage. Tightness around the joint is a common cause of discomfort and pain. Professional massage serves to loosen and relax the lower back, buttocks, and leg areas, offering relief from pain.

Third, consider chiropractic and seeing a chiropractor. Chiropractic relieves pain, treatment known as adjustments, not only provides great options for pain relief but also helps promote the healing process of this joint.

A chiropractor is specifically trained to guide you through several phases of care. They don�t focus just on pain relief but are primarily interested in helping you fix the problem.

They�re also very well trained in rehabilitation of the spine. This approach will help loosen the muscles surrounding the joint as well as strengthen them. This will decrease the risk of pain returning down the road.

Finally, in very rare cases, doctors will choose to apply an injection to the area to alleviate pain and inflamed tissue. Obviously, the injection won�t fix the problem but may give the patient relief temporarily. Surgery is rarely a viable option.

If you show symptoms of sacroiliac pain, it’s important to see a Doctor of Chiropractic so he or she can perform tests to correctly diagnose your condition. It could very well be another type of lower back problem. Remember chiropractic relieves, so quit suffering and give us a call!

Pregnancy & Chiropractic Care

Ankle Injuries: Chiropractic Care Rehab

Ankle Injuries: Chiropractic Care Rehab

An ankle can be injured as glamorously as falling off a $400 platform stiletto heel, stepping off a Parisian curb, or as mundanely as tripping over a toy truck, or falling over a rock on your way to the mailbox. No matter the cause, ankle injuries are painful and problematic, and cause recurring problems if left untreated.

The poor ankle sure has it rough. It supports a person’s entire body weight, twists and turns many times a day, and maintains proper balance. This heavy responsibility takes its toll. Emergency rooms treat approximately one million patients ever year for ankle injuries.

Ankles are technically “the joint where the foot joins the leg.”� In reality, there are more moving parts involved than that simplified definition allows. Multiple bones and two separate joints actually converge in the ankle area, which increases the chance of an ankle injury.

Ankle Injuries:

ankle injuries

Sprains:

When you roll your ankle outward, the movement damages the ligaments on the outside of the ankle. This is a common sports injury and, unfortunately, once you have sprained your ankle it’s more likely to recur. Up to half of the people who suffer from a sprained ankle will sprain it again.

Strains:

There are two tendons in the ankle that are commonly strained, usually over stretching from overuse or trauma.

Fractures:

This injury happens when one or more of the three bones in the ankle is injured. While less common than a sprain or strain, a fractured ankle may also involve damaged ligaments and require surgery.

Many instances of ankle injuries are avoidable. Be sure to wear proper shoes when exercising or participating in sports, avoid uneven walking surfaces, and keep stairways and floors in your home clear of clutter

And, ladies, avoid the really high heels. We know, we know, they are just so cute! 🙂

Even with ankle-protecting precautions, you still may end up on your rump in the grass nursing your swollen ankle. What should you do if you injure your ankle? There are several forms of treatment for an ankle injury depending on its severity.

Rest and ice: For mild injuries, stay off your ankle and use ice packs to reduce the swelling. Rest allows the injured area to heal faster.

Visit a doctor: If you experience severe pain, swelling, and are unable to put weight on your ankle, see a doctor, as some ankle injuries grow worse without treatment. Injuries may require a brace, cast, or even surgery.

See a chiropractor: Patients frequently see strongly positive results in ankle injuries from a series of chiropractic treatments. Chiropractors understand the way the ankle is built, and use chiropractic adjustments to reduce pain and inflammation and promote faster healing.

Exercise rehab: Once you are healed, it’s vital to build up the ankle’s strength to avoid re-injury. Your chiropractor can lay out an exercise routine that you can employ into your regular workouts that will improve your balance and increase mobility. Performing these moves helps dramatically decrease dealing with this again down the road.

Ankle injuries are common and, whether or not you maintain an active lifestyle, you may end up suffering from one. By visiting a chiropractor on the front end, you can better plan a course of treatment that will heal your ankle quickly, reduce the pain effectively, and minimize the chance of a recurrence.

Golf & Chiropractic Care

Defeat Chronic Pain

Defeat Chronic Pain

Defeat Chronic Pain: If you are one of the estimated 50 to 100 million Americans who struggles with Chronic Pain, you are aware of just how miserable and life-altering it can be. There is not a single area of you life that remains unaffected. You no longer sleep well. Your SEX LIFE is non-existent. Everyday activities have become your own personal �Mount Everest �. You cannot concentrate because the pain IS ALWAYS ON YOUR MIND. It is wearing you out, physically, mentally, and emotionally. It’s sapping your ability to think clearly or make decisions. In short we’re here to defeat chronic pain.

People can see the pain on your face and in your eyes. Chronic Pain and the inability to do the things you love, is making you feel DEPRESSED (not the other way around like your doctor may have suggested). Recent studies have even shown that brains of people suffering with Chronic Pain, show patterns of atrophy that are virtually indistinguishable from what is seen in patients with dementia or ALZHEIMER’S. In fact, a recent study from a prominent Canadian University showed that Chronic Pain causes the brain to degenerate at almost 10 times the rate of someone without pain!

Although Chronic Pain may seem hopeless, there are some things that you can do to help yourself � even though your doctor undoubtedly failed to educate you in this regard. Some of the most basic of these include eating only healthy foods (I recommend a PALEO DIET), taking only WHOLE FOOD SUPPLEMENTS, drinking more WATER, giving up the CIGARETTES, and EXERCISING to the degree that you can (difficult when suffering with Chronic Pain or FIBROMYALGIA).

Although DOING THESE SIMPLE THINGS will certainly help a large percentage who suffer and be able to defeat chronic pain; there is a significant percentage of you whose pain is not greatly diminished by these measures. It is for you that I created this website. But before we move on to treatment of Chronic Pain, you must first understand what Chronic Pain is and how it really works.

Defeat Chronic Pain: It Works Like This

For years, neuro-scientists have known that Chronic Pain can cause brain atrophy (shrinkage) that is indistinguishable from Alzheimer�s or Dementia. More recently, the prestigious Journal of Neuroscience reported research from McGill University showing that, “The longer the individual has had Fibromyalgia, the greater the gray matter loss, with each year of Fibromyalgia being equivalent to 9.5 times the loss in normal aging”. Think about this statement for a moment. Every single year you live with some sort of CHRONIC PAIN SYNDROME (or syndromes as the case may be) is the equivalent of nearly 10 times the brain loss seen in the normal aging process. Re-read this paragraph until the urgency of your situation sinks in!

Although there are several types of pain (the study of Chronic Pain can get extremely complex), we are going to try and keep this as simple as possible. For our purposes, there are two types of Chronic Pain. It has to do with where the pain comes from. Chronic Pain originates in one of the two following areas.

  • The Central Nervous System
  • The Body

As we will discuss shortly, Chronic Pain that arises in the CNS is frequently ‘learned’ pain. Let me explain. In order to learn how to SHOOT FREE THROWS, use chop sticks, PLAY THE PIANO, speak Swahili, you have to practice. Everyone remembers the old adage; Practice makes Perfect. If you stimulate pain pathways in the Brain & Nervous System long enough, or are exposed to enough stressors in your life (CHEMICAL, AUTOIMMUNE, EMOTIONAL, DIETARY, FOOD SENSITIVITIES, PHYSICAL, BACTERIAL, VIRAL, PARASITIC, FUNGAL, MOLD, ELECTROMAGNETIC, etc), you can alter the way your Brain and Central Nervous System function.

Hopefully your pain, even though severe, is still Type II (THE THREE TYPES OF PAIN). As people start losing control of numerous areas of physiology (DIGESTION, HORMONAL, IMMUNITY, BLOOD SUGAR REGULATION, HYPERSENSITIVITY, DYSBIOSIS, etc), the problems ramp up. Over time this pain can (will) become locked into the brain. Although pathological Pain Syndromes arising from a malfunctioning CNS are not the most common causes of Chronic Pain, if this is where you are at, you are going to have to find a way to deal with these underlying issues (FUNCTIONAL NEUROLOGY can be a fantastic starting point). Although I provide information that helps many people help themselves with the severe metabolic and neurological problems, this website is chiefly devoted to defeat chronic Pain that is not locked into the Brain, but is instead originating from the body (Type II Pain).

Defeat Chronic Pain: Nociception

“Simple Nociception” is the most basic type of pain. If someone steps on your toe, it hurts. This is normal, and means that your nervous system is functioning properly. Get the person off your toe, and the pain goes away — almost immediately. Simple. There are several different types of Nociceptive Pain, but the one that we are most concerned about on this website is the one that has to do with ‘deep’ musculoskeletal pain, otherwise known as Deep Somatic Pain (Greek �Soma� = body). Deep Somatic Pain is pain that originates in tissues that are considered to be ‘deep’ in the body. Although we do not always think of many of these tissue types as being deep, this category includes things like LIGAMENTS, TENDONS, MUSCLES, FASCIA, blood vessels, and bones. There are two main types of Nociceptors, chemical and mechanical.

I. Chemical Nociception

The Chemical Nociceptors are stimulated by noxious chemicals. The chief of these are the chemicals we collectively refer to as INFLAMMATION (bear in mind that once Inflammation is involved, we begin moving away from Type I pain and into Type II pain — Nociception is still involved, but so is the Inflammatory Cascade). Inflammation is actually made up of a large group of chemicals manufactured within your body as part of the normal Immune System response. They have names like prostaglandins, leukotrienes, histamines, cytokines, kinins, etc, etc, etc. When these chemicals are out of increased beyond what’s needed for normal tissue repair, the result will be a whole host of health problems —- and Chronic Pain.

Although “SYSTEMIC INFLAMMATION” is at the root of the vast majority of America’s health problems (DIABETES, CANCER, FIBROMYALGIA, THYROID PROBLEMS, ARTHRITIS, HEART DISEASE, and numerous others), you will soon see that even though Inflammation is always involved with the tissues of the “Deep Soma,” it sometimes gets more credit than it deserves. However, you also have to be aware that exposing MICROSCOPIC SCAR TISSUE to chronic inflammation can potentially hyper-sensitize nerves. This hypersensitization makes the nerves within Scar Tissue as much as 1,000 times more pain sensitive than normal (the work of the famous neurologist, DR. CHAN GUNN).

INCREASED TISSUE ACIDITY (usually caused by hypoxia — diminished tissue oxygen levels) is another common form of Chemical Nociception. This frequently occurs as the result of a JUNKY DIET, but is also caused by relentless Mechanical / Neurological / Immune System Dysfunction. It is a big reason that my Decompression Protocols utilize OXYGEN THERAPY extensively.

II. Mechanical Nociception

As you can imagine, Mechanical Dysfunction stimulates the Mechanical Nociceptors. This group of nociceptors (pain receptors) is stimulated by constant mechanical stress in the tissues of the Deep Soma — particularly ligaments, tendons, and fascia. Mechanical tension, mechanical deformation, mechanical pressure, etc are the things that cause Mechanical Nociception, which can in turn, cause pain — chronic, unrelenting, pain. Remove the offending mechanical stressor, and you can oftentimes remove the pain. Sounds simple, doesn�t it? Unfortunately, nothing is ever quite as simple as it initially appears.

Be aware that Nociceptive Pain can actually become Brain-Based over time. This is called ‘Supersensitivity’ and is caused by alterations in the Brain and Central Nervous System that perpetuate the pain cycle (many in the medical community are calling it CENTRALIZATION OR CENTRAL SENSITIZATION. In Mechanical Nociception, even though the injured tissue has, according to all of the medical tests, HEALED, it has healed improperly; i.e. microscopic scar tissue and tissue adhesion — particularly in the FASCIA. I probably do not need to tell you that this can be really really bad news — particularly because it is a significant feature of what I call “CHRONIC PAIN’S PERFECT STORM“.

As nerve function and PROPRIOCEPTION become increasingly fouled up, degenerative arthritis and joint deterioration begin to set in (HERE). Because of involvement in the Brain or Central Nervous System, this kind of pain is often referred to as Neuropathic Pain or Neruogenic Pain. Sometimes people end up with HYPERALGIA (Extreme sensitivity to pain. Stimulus that should cause a little pain, causes extraordinary amounts of pain). Or they end up with ALLODYNIA (Stimulus which do not normally elicit any pain at all, now causes pain). Sometimes these two overlap. Stay with me and you will begin to understand why.

Defeat Chronic Pain: Hypersensitized Nerves Relationship To Injured Or Damaged Fascia

Think of nerve endings as the twigs at the very end of a tree limb. Nerves (just like a tree) begin with a large trunk, which splits / divides into smaller and smaller branches until eventually you arrive at the end � the tiny twig (or nerve ending) at the end of the very smallest branches.

If you have ever seen a �topped� tree, you can understand what happens to nerve endings that are found in microscopic scar tissue. Professional Tree Trimmers cut (or �top�) the largest branches just above where the trunk splits into two or three limbs. What happens to these stubs? Instead of having limbs that continue to branch out and divide into ever-smaller limbs in a normal fashion, you get a stub or stump, that in a short matter of time, swells up and has hundreds of tiny twig-like limbs growing from it. �Topping� stimulates the growth of twigs from the stump. The injured nerves found in microscopic scar tissue act in much the same way.

As the larger nerves that are found in soft tissues are injured, you end up with an inordinate number of immature nerve endings (twigs) growing out of an inflamed nerve �stump�. As you might imagine, extra pain receptors are never a good thing! And because there in Inflammation present, this often leads to Microscopic Scar Tissue, which, even though it is up to 1,000 times more pain-sensitive than normal tissue, cannot be seen with even the most technologically advance imaging techniques such as CT / MRI (HERE). This is a commonly seen phenomenon in Facial Adhesions, and is why even though the people living this nightmare believe that because their pain is so severe that it should make their MRI “Glow Red”, it shows nothing. This tends to lead to deer-in-the-headlight looks when you ask your doctor what might be causing your pain, not to mention accusations of malingering, drug seeking, or attempting to get on Disability.

Defeat Chronic Pain: Nerves Are Like Tree Branches

Uninjured Nerves

defeat chronic pain

Photo by Stephen McCulloch

Injured Nerves

defeat chronic pain

Photo by Linda Bailey

 

Defeat Chronic Pain: Fascial Adhesions

Microscopic Scar Tissue & Chronic Pain

One of the biggest revelations for many people suffering with Chronic Pain is the absurd numbers of CHRONIC PAIN SYNDROMES brought on by microscopic scarring of the FASCIA. It gets even worse once you realize that this Fascia is the most pain-sensitive tissue in the body —- yet it does not show up on even the most technologically advanced imaging techniques, including MRI. Simply read our “Fascia” page to see why microscopic scarring of this specific “Connective Tissue” is at the root of all sorts of Chronic Pain Cases — not to mention ILL HEALTH.

Destroy Chronic Pain / Doctor Russell Schierling

Medical Inc Teaser

Tendinitis vs Tendinosis | Chronic Pain

Tendinitis vs Tendinosis | Chronic Pain

My doctor told me I have tendinosis, I’ve heard of tendinitis, what is the difference?

Dr. Jimenez considers this dilemma of similar words that cause confusion to patients. Below is an explanation of clinical presentations and anatomical disorders that shed light on the similarities and differences between tendinosis and tendinitis.

Tendons are the tough, white, cords that connect muscles to bones, and are the least elastic of the collagen-based soft tissues (LIGAMENTS, MUSCLES & FASCIA) I work with on a day-to-day basis. How common are tendon problems? Government statistics tell us that overuse injuries of tendons are a leading reason for doctor visits. And although most of these tendon problems are referred to generically as tendinitis, in the vast majority of cases, tendinitis is actually an incorrect and outdated term.

Over the past decade, medical research has conclusively shown that the major cause of tendinopathies is not inflammation (aka “itis”), which even a decade ago was nothing new. For decades, the scientific community has been concluding that wile the immune system mediators we collectively refer to as “INFLAMMATION” are probably present in tendinopathies; inflammation itself is rarely the cause. So, if inflammation is not the primary cause of most tendon problems, what is? Follow along as I show you from peer-review, that since the early 1980’s, research has shown the primary culprit in most tendinopathies is something called “osis”. Thus the name, “tendon � osis” (tendinosis). But what the heck is osis?

The suffix “osis” indicates that there is a derangement and subsequent deterioration of the collagen fibers that make up the tendon. The truth is, even though doctors still use the term “tendinitis” with their patients, their AMA-mandated Diagnosis Codes almost always indicates the problem is “tendinosis” or “tendinopathy” (HERE). Is this differentiation between tendinitis and tendinosis really that important, or am I splitting hairs and making a big deal out of nothing — making a mountain out of a molehill, semantically speaking? Instead of answering that question myself, I will let two of the world�s preeminent tendon researchers — renowned orthopedic surgeons — answer it for me.

“Tendinosis, sometimes called tendinitis, or tendinopathy, is damage to a tendon at a cellular level (the suffix �osis� implies a pathology of chronic degeneration without inflammation). It is thought to be caused by micro-tears in the connective tissue in and around the tendon, leading to an increased number of tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of repetitive injury or even tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community.” Tendon researcher and orthopedic surgeon, Dr. GA Murrell from a piece called, �Understanding Tendinopathies� in the December 2002 issue of The British Journal of Sports Medicine.

“Tendinitis such as that of the Achilles, lateral elbow, and rotator cuff tendons is a common presentation to family practitioners and various medical specialists.1 Most currently practicing general practitioners were taught, and many still believe, that patients who present with overuse tendinitis have a largely inflammatory condition and will benefit from anti-inflammatory medication. Unfortunately this dogma is deeply entrenched. Ten of 11 readily available sports medicine texts specifically recommend non-steroidal anti-inflammatory drugs for treating painful conditions like Achilles and patellar tendinitis despite the lack of a biological rationale or clinical evidence for this approach. Instead of adhering to the myths above, physicians should acknowledge that painful overuse tendon conditions have a non-inflammatory pathology.” Karim Khan, MD, PhD, FACSP, FACSM, and his group of researchers at the Department of Family Medicine & School of Human Kinetics at the University of British Columbia, from the March 2002 edition of the BMJ (British Medical Journal).

The information in the preceding paragraphs (which was not new when they were published over a decade and a half ago) is so important as to be considered revolutionary for those of you who have spent time on the MEDICAL MERRY-GO-ROUND with tendon problems. Why? Because, as stated by Dr. Murrell above, most medical professionals have, “a limited understanding of tendinopathies”. Why is this? Why do more doctors not grasp what is going on with the majority of Tendinopathies? Why does such a big portion of the medical community continue to ignore their own profession�s scientific conclusions, while continuing to treat tendinopathies with drugs and surgery? Of course there’s always the issue of money. There is also the fact that if you have tendon problems, you are probably being treated using a model that is at least 25-30 years behind the times as far as the medical research is concerned (HERE). If you think I’m being harsh, read what Dr. Warren Hammer, a board certified Chiropractic Orthopedist in practice since the late 1950?s, had to say about Tendinosis in a 1992 issue of Dynamic Chiropractic.

“The American Academy of Orthopedic Surgeons has provided a new classification of tendon injuries�. In the microtraumatic tendon injury the main histologic features represent a degenerative tendinopathy thought to be due to an hypoxic [diminished oxygen] degenerative process. The similarity to the histology [study of the cells] of an acute wound repair with inflammatory cell infiltration as in macrotrauma seems to be absent. A new classification of tendon injury called �tendinosis� is now accepted. �Tendinosis� is a term referring to tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise). Histologically there is a non-inflammatory tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise), as well as a non-inflammatory intratendinous collagen degeneration with fiber disorientation, hypocelluarity, scattered vascular ingrowth, and occasional local necrosis or calcification.”

If your doctor is still treating you for tendinitis and not tendinosis, they are caught in a time warp. According to what the American Academy of Orthopedic Surgeons said over two and a half decades ago, tendinosis is not an inflammatory condition (itis)! It is a degenerative condition (osis)! Not only is there some debate over whether or not tendinitis actually exists at all, but as you will see in a moment, the anti-inflammation medications and corticosteroid injections that your doctor has been prescribing you are actually creating more degeneration. Track & Field athletes make it a point to keep up with the cutting edge diagnosis and treatment of tendinous SPORTS INJURIES. See what their official medical team has to say on the subject of Tendinosis and Tendinopathy……..

“The relatively new term ‘Tendinopathy’ has been adopted as a general clinical descriptor of tendon injuries in sports. In overuse clinical conditions in and around tendons, frank inflammation is infrequent and if seen, is associated mostly with tendon ruptures. Tendinosis implies tendon degeneration without clinical or histological signs of intratendinous inflammation, and is not necessarily symptomatic. The term ‘Tendonitis’ is used in a clinical context and does not refer to a specific histological entity. [The term] Tendonitis is commonly used for conditions that are truly Tendinosis, however, and leads athletes and coaches to underestimate that proven chronicity of this condition……. Most articles describing the surgical management of partial tears of a given tendon in reality deal with degenerative tendinopathies [Tendinosis].” From an official document found on the website of the International Association of Athletics Federations (IAAF) — the official governing body of professional Track and Field

The Science:

“Tendinosis is a medical term used to describe the tearing and progressive degradation of a tendon. Tendons are structural components of the human body that ensure muscles remain bound to the correct bone during normal daily activities. Tendinosis differs from tendonitis in that the affected tendon is not inflamed.” Rachel Amhed from a July 2010 article for Lance Armstrong’s ‘Livestrong Website’ called Tendinosis Symptoms.

“Based on the information of various lines of investigation of tendinopathy, we can summarize some major points which must be considered in the formulation of a unified theory of pathogenesis in our model of tendinopathy….. The primary results of pathology are the progressive collagenolytic [Collagen-Destroying] injuries co-existing with a failed healing response, thus both degenerative changes and active healing are observed in the pathological tissues….. These pathological tissues may aggravate the nociceptive responses [PAIN] by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis [NSAIDS & Cortcosteroids]; otherwise the insidious mechanical deterioration without pain may render increased risk of tendon rupture.

For example, overuse is a major etiological factor but there are tendinopathy patients without obvious history of repetitive injuries. It is possible that non-overuse tendon injuries may also be exposed to risk factors for failed healing. Overuse induces collagenolytic [DEGENERATIVE] tendon injuries and it also imposes repetitive mechanical strain which may be unfavorable for normal healing. Stress-deprivation also induces MMP expression [Matrix Metallo Proteinase — an enzyme which breaks down Connective Tissues], and whether over- or under-stimulation is still an active debate. It is possible that tenocytes [tendon cells] are responsive to both over- and under-stimulation, both tensile and compressive loading….. By proposing a process of failed healing to translate tendon injuries into tendinopathy, other extrinsic and intrinsic factors would probably enter the play at this stage, such as genetic predisposition, age, xenobiotics (NSAIDs and corticosteroids) and mechanical loading on the tendons….. Classical characteristics of “tendinosis” include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer “tendinitis”.” Cherry-picked quotes from a comprehensive collaboration by teams from the Department of Orthopaedics & Traumatology at Prince of Wales Hospital, The Chinese University of Hong Kong, and the Department of Orthopaedic Surgery at Huddinge University Hospital in Stockholm. The study was published in a 2010 issue of Sports Medicine Arthroscopy & Rehabilitation Therapy Technology.

“Rotator Cuff Tendinosis is a degenerative (genetic, age or activity related) change that occurs in our rotator cuff tendons over time. Rotator cuff tendinosis is exceptionally common. Many, many people have tendinosis of the rotator cuff and do not even know it. Why rotator cuff tendinosis bothers some people and doesn�t bothers others is currently a question the orthopedic surgery community can not answer. Rotator cuff tendinosis is just as likely to be found in a professional body builder as it is likely to be found in a true couch potato.” From an August 2011 online article / newsletter by Dr. Howard Luks, an Orthopedic Surgeon and Associate Professor of Orthopedic Surgery at New York Medical College as well as being Chief of Sports Medicine and Arthroscopy at Westchester Medical Center.

“The gross pathology of Angiofibroblastic Tendinosis is [that] there are no inflammatory cells in this tissue. Therefore the term “Tendinosis” is much better [than Tendinitis]. The pathological tissue is instead characterized by very immature tissue and nonfunctional vascular elements.” Loosely quoted from a YouTube video of famed tendon researcher / surgeon Dr. Robert P. Nirschl’s (Nirchl Orthopedics) presentation to the American Academy of Orthopedic Surgeons annual meeting (2012).

“The more commonly used term of tendinitis has since been proven to be a misnomer for several reasons. The first of which is that there is a lack of inflammatory cells in conditions that were typically called a tendonitis…. The other two findings present in tendinosis, increased cellularity and neovascularization has been termed angiofribroblastic hyperplasia by Nirschl…… These are cells that represent a degenerative condition. Neovascularization [the creation of abnormally large numbers of new blood vessels] found in tendinosis has been described as a haphazard arrangement of new blood vessels, and Kraushaar et al. even mention that the vascular structures do not function as blood vessels. Vessels have even been found to form perpendicular to the orientation of the collagen fibers. They then concluded that the increased vascularity present in tendinosis is not associated with increased healing. Take Home Points: Chronic tendon injuries are degenerative in nature and NOT inflammatory. Anti-inflammatory medications (NSAIDs) and/or corticosteroid injections can actually accelerate the degenerative process and make the tendon more susceptible to further injury, longer recovery time and may increase likelihood of rupture.” Quotes cherry-picked from a recent online article called ‘Tendonosis vs. Tendonitis’ by Dr. Murray Heber, DC, BSc(Kin), CSCS, CCSS(C), Head Chiropractor for Canada’s Bobsleigh / Skeleton Team.

“The data clearly indicates that painful, overuse tendon injury is due to tendinosis�the histologic entity of collagen disarray, increased ground substance, neovascularization, and increased prominence of myofibroblasts. [It is] the only clinically relevant chronic tendon lesion, although minor histopathologic variations may exist in different anatomical sites. The finding that the clinical tendon conditions in sportspeople are due to tendinosis is not new. Writing about the tendinopathies in 1986, Perugia et al noted the ‘remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory because the ending ��-itis�� is used) and their histopathologic substratum, which is largely degenerative” Dr. Khan once more showing that tendon problems are not caused by inflammation.

“Overuse tendinopathies are common in primary care. Numerous investigators worldwide have shown that the pathology underlying these conditions is tendinosis or collagen degeneration. This applies equally in the Achilles, patellar, medial and lateral elbow, and rotator cuff tendons. If physicians acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must modify patient management in at least eight areas.” Dr. Karim Kahn M.D / Ph.D and his research team from University of British Columbia’s School of Kinesiology in an article published in the May 2000 issue of The Physician and Sportsmedicine called “Overuse Tendinosis, Not Tendinitis”.

Eight areas? Wow! And that quote is almost two decades old. Now, take a look at something that came from a Medical Textbook that was published over three decades ago in Italy. The medical community knew back then that most overuse tendon problems were not inflammatory (itis), but instead degenerative (osis).

“[There is a] remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory since the ending ‘itis’ is used) and their histopathologic substratum, which is largely degenerative.” From an Italian medical text called, “The Tendons: Biology, Pathology, Clinical Aspects” (1986).

Tendinosis Overview:

The truth is that I could go on and on and on and on with quotes from similar studies. Hopefully you get the point! You should be starting to see that most of what you thought about chronic tendon problems needs to be flushed down the toilet or thrown out with the weekly trash. That’s because there’s a new model in town. Tendinosis is it’s name; and if you want any hope of a solution to your tendon problem, you will have to step outside of the medical “box” and start thinking of your problem in terms of “osis” instead of “itis”. Failure to grasp the new model leaves you vulnerable to treatments which, while possibly bringing some temporary relief, will ultimately make you worse — possibly much worse! By the way, the following points are observations that you yourself will understand if you read the above quotes.

  • Tendinosis is a Degenerative Condition without inflammation. Scratch that. Science has recently shown us that there is inflammation in tendinosis — there should be, at least in the initial phase of healing. However, it’s the SYSTEMIC INFLAMMATION that’s been shown to be the biggest problem. Bottom line, this doesn’t really affect anything I’m telling you in this post, other than to reinforce your need to address systemic inflammation (hint: it can’t be done with drugs).
  • Tendinosis is the proper model for understanding the majority of Tendinopathies. As a model for understanding
  • Tendinopathies, Tendinitis has been retired for at least two and a half decades.
  • Tendinosis is both misunderstood and mismanaged by the majority of the Medical Community.
  • Traditional Therapies / Interventions for Tendinopathies significantly increase one’s chance of Tendon Rupture.
  • Most Coaches and Athletes do not understand the difference between Tendinitis and Tendinosis.
  • If it does exist, Tendinitis (Inflammation of the Tendon) is rare, short lived, and mostly associated with Tendon Tears or Ruptures.
  • Tendinosis is caused by both overuse and under-use.
  • Tendinosis is often times Asymptomatic (no symptoms), until it becomes a painful and potentially debilitating problem.
  • Drugs; particularly NSAIDS & CORTICOSTEROIDS, as well as CERTAIN ANTIBIOTICS actually cause Tendinosis — and Tendon Rupture. They also slow down (or reverse) the healing process.

Best Treatment: Tendinosis & Tendonopathies

Anti-Inflammatory Medication

tendinosis

“I knew then and there I was in the wrong place.” Thoughts running through the mind of a new patient who had recently visited an Orthopedic Specialist’s office for a tendon problem and asked him about the difference between Tendinitis and Tendinosis. The doctor answered, “There is no difference between Tendinitis and Tendinosis. They are one and the same —- two different names for the same problem.”
Even though medical research has conclusively shown us for over three decades that tendinopathies have as their primary cause of pain and dysfunction tissue derangement and degeneration, anti-inflammation drugs continue to be the medical profession�s go-to method of treatment. It�s not difficult to see why this is not working:

Although there is undoubtedly a certain amount of SYSTEMIC INFLAMMATION present with tendinosis, research has conclusively shown that tendon problems are not primarily problems of inflammation, but of degeneration.
Scientific studies have actually shown that non-steroidal anti-inflammatory medications (NSAID�s) such as Aspirin, Tylenol, Nuprin, Ibuprofen, Naproxen, Celebrex, Vioxx (oops � one of the #1 drugs in America for 10 years running was taken off the market because it was found to be a huge cause of chronic illness and death), & numerous others, actually cause injured collagen-based tissues like tendons, ligaments, muscles, fascia, etc, to heal up to 33% weaker, with as much as 40% less tissue elasticity.

Corticosteroid Injections are even worse. Medicine’s dirty little secret of treating connective tissue injuries with steroids is that they actually deteriorate or ‘eat’ the collagen foundation. This is why they deteriorate ever tissue in the joint, including bone. This is bad news considering collagen is the tissue that is deranged — the very tissue that needs to heal the most. This is why corticosteroids are a known cause of DEGENERATIVE ARTHRITIS and OSTEOPOROSIS, not to mention a whole host of easily-verified systemic side effects. The fact that steroid injections are ridiculously degenerative is why doctors ration or limit the number of steroid injections a person can receive � even if they seem to be working. And understand; it’s not that drugs don’t sometimes do what they claim to do. It’s that they never reverse the underlying pathophysiology (HERE). They simply cover symptoms.

Years ago, the Journal of Bone and Joint Surgery reported that corticosteroids are so degenerative that if you have more than one injection in the same joint over the course of your lifetime; your chance of premature degeneration in the injected joint is (gulp) 100%! Ultimately, the problem of corticosteroids (or NSAID�s for that matter) being used to treat tendons or other collagen-based tissues, is that short term relief is being traded for long term (and often permanent) damage. In other words, tomorrow is being traded for today. Kind of reminds you of our government�s short-sighted fiscal policies, doesn�t it? It is also another in a long line of evidences that the gap between medical research and medical practice is growing (HERE).

Collagen is the building block of all connective tissues, including tendons (you probably learned a great deal about collagen on our FASCIAL ADHESION PAGE as well as our COLLAGEN SUPER-PAGE). If one looks at normal collagen fibers from tendons or other connective tissues under a microscope, each individual cell lines up parallel to the surrounding cells. This allows for maximum tissue flexibility (sort of like well-combed hair).

With tendinopathies (whether TRAUMATIC OR REPETITIVE � yes, trauma can cause tendinosis), the tissue uniformity becomes disrupted and unorganized, causing restriction and a severe loss of function. This in turn causes a loss of flexibility, tissue weakness, tissue fraying, increased rigidity, and stiffness (sort of like KNOTTED HAIR OR A HAIRBALL — or gristle in a bite of steak). This leads to a loss of strength and function, which ultimately means that you end up with pain and dysfunction of the affected joint or body part. As I will soon show you, loss of normal function is one of just a few known causes of joint degeneration. This is why anyone who has suffered through Chronic Tendinosis knows how debilitating it can really be.

Normal Tendons Vs Tendinosis

Tendons are one of the Elastic, Collagen-Based Connective Tissues that are Made up of
Three Individual Collagen Fibers Braided Together into Wavy Sheets or Bands

tendinosis

Photo by User Vossman

COLLAGEN is a wavy protein. The waves are what give it the ability to stretch and elast. And although Tendons are said to be the least flexible and stretchy of the Elastic, Collagen-Based Connective Tissues (Muscles, Ligaments, & Fascia are all more elastic), they have to have at least a bit of give. The waves in the individual collagen fibers are what allow for this stretching to take place. Tendinosis occurs most often where the muscle meets the tendon. This is due to an especially dense amount of Collagen at this “Transition Zone”.

Tendinosis Looks Like:

NORMAL TENDON
Uniform, Organized, & Parallel

tendinosis

Normal, healthy Tendons are like these ropes. Not only are the fibers all running uniformly in the same direction, there is little or no fraying. This gives the tendon the ability to stretch and elast. Photo by Procsilas Moscas

FRAYED TENDON (TENDINOSIS)
Unorganized, Tangled, & Random

tendinosis

Tendinosis is characterized by incredible fraying, fragmenting, tangling, and twisting, of the tendon. This causes weakness and inelasticity that can not only painfully debilitating, it can lead to Tendon Rupture. Photo by Martyn Gorman

NOTICE THE FRAYED & TORN APPEARANCE.
THIS IS WHAT CHARACTERIZES TENDINOSIS

tendinosis

Photo by Andrjusgeo

NORMAL HEALTHY TENDON

NOTICE THE COLLAGEN WAVES

tendinosis

Photo by Nephron

SCAR TISSUE & ADHESION
(Note the Complete Lack of Uniformity in the Tissue Fibers)

Scar Tissue / Fibrosis

tendinosis

DRDoubleB

Tendinosis Looks Like Tangled Fishing Line

tendinosis

Photo by Daplaza

Tendinosis is characterized by Collagen Fibers that have disrupted alignment. It also shows fraying of the individual fibers. This is why most tendinopathies are now classified as Tendinosis and considered to be degenerative (osis = degeneration), as opposed to Tendinitis (itis = inflammation). The problem is, most of the medical community does not seem to grasp this yet.

Areas Most Affected By Tendinosis

Sometimes Tendionosis is clinically impossible to distinguish from FASCIAL ADHESIONS and microscopic scar tissue. Often times they are present together. The bottom line is that whether the adhesions are in fascia or whether they are tendon DOESN’T REALLY MATTER — they must both be broken. Sometimes there is a great excess of calcium built up at the point where the tendon anchors to the bone. This must be broken up as well. Because the models for understanding various soft tissues are virtually identical; the models for treating said tissues are likewise very similar. As you might imagine, this is fantastic news for the patient. Bear in mind that I have not included each and every specific area you can develop tendinopathy because it can attack anywhere that you have a tendon. The following list happens to be the areas that I treat most frequently in my clinic.

IMPORTANT: Please note that some muscles only cross one joint. However, many muscles cross two joints. Muscles that act on more than one joint have a greater propensity for problems. It also means that one muscle has the potential to give you problems (including tendinosis) at two different joints. Also note that Tendinosis is usually a bit tougher to deal with than Fascial Adhesions.

  • ROTATOR CUFF TENDINOSIS: The Rotator Cuff is made up of four muscles that surround the shoulder.
  • SUPRASPINATUS TENDINOSIS: The Supraspinatus Tendon is not only the most commonly injured of the Rotator Cuff Muscles, it is the most common to find tendinopathy in as well.
  • TRICEP TENDINOSIS: Tricep Tendinosis is rare. About the only people I ever find it in is carpenters (hammering) and weightlifters. However, here is the webpage.
  • BICEPS TENDINOSIS: Because both heads of the bicep muscle have attachment points in the front of the shoulder, Biceps Tendinosis is frequently mistaken for Bursitis or a Rotator Cuff problem.
  • LATERAL EPICONDYLITIS (Tennis Elbow): Although I have never seen anyone who got this problem playing tennis, it is nonetheless extremely common.
  • MEDIAL EPICONDYLITIS (Golfer�s Elbow): Not quite as common as Tennis Elbow above.
  • WRIST / FOREARM FLEXOR TENDINOSIS: This is tendinopathy on the palm side of the forearm and wrist.
  • WRIST / FOREARM EXTENSOR TENDINOSIS: This is tendinopathy on the backhand side of the forearm and wrist.
  • THUMB TENDINOSIS / DeQUERVAIN’S SYNDROME: This extremely common problem can be debilitating. You will frequently hear Thumb Tendinosis referred to as DeQuervain�s Syndrome.
  • GROIN (Hip Adductor) TENDINOSIS: I have included Tendinosis of the Groin under �Hip Flexor Tendinosis� below.
  • HIP FLEXOR TENDINOSIS: Hip Flexor Tendinosis will manifest in the upper front thigh or groin area. This is incredibly common in athletes — particularly soccer players.
  • PIRIFORMIS TENDINOSIS: This problem is related to PIRIFORMIS SYNDROME, and causes pain in the butt (sometimes with sciatica as well).
  • SPINAL TENDINOSIS: Although most people never think of it, the potential for developing Spinal Tendinosis is greater than you ever imagined possible.
  • KNEE TENDINOSIS: This is arguably the single most common reason that people visit a Sports Physician.
  • QUADRICEPS / PATELLAR TENDINOSIS: A form of Knee Tendinosis
  • HAMSTRING TENDINOSIS: Hamstring Tendinosis can cause knee, hip, and buttock problems.
  • ACHILLES TENDINOSIS: Achilles Tendinosis is found in the large tendon in the very back of the lower leg / ankle.
  • ANKLE TENDINOSIS: This common Tendinosis can typically be dealt with by following a few simple procedures.
  • TIBIALIS ANTERIOR TENDINOSIS: This is related to the category above, and is typically found in the front of the ankle.
  • POSTERIOR TIBIAL TENDINOSIS: This is related to the category above, and is typically found near the bony knob on the inside of the ankle.
  • APONEUROSIS / APONEUROTICA TENDINOSIS: Although you have probably never heard the word before, �Aponeurosis� are flattened out tendons. They are almost always referred to as fascia, but technically this is incorrect. They are most often associated with SKULL PAIN.

Effectively Dealing With Tendinosis

Let me begin by saying that I cannot help everyone�s Tendinopathy. And yes, I am very aware that there are thousands of websites out there giving all sorts of free, do-it-yourself advice on how to fix these problems without going to a doctor. Most of this advice concerns common sense treatments that everyone should try before seeking any sort of professional care. These lists frequently include things like STRETCHING / SPECIAL EXERCISES, ICING, resting, EATING AN ANTI-INFLAMMATORY DIET, drinking plenty of water, SPECIAL SUPPLEMENTS FOR CONNECTIVE TISSUES, etc. All of these are great, and highly recommended by me. The truth is, advice like this is going to save a lot of people a lot of time and money by helping the biggest portion of the population get over minor Tendinopathies / Tendinosis on their own, without jumping on the MEDICAL MERRY GO ROUND.

There is a significant portion of the tendinosis-suffering population who have tried all of these things. Every type of pill imaginable, including ANTIBIOTICS (believe it or not, I have seen this used numerous times � some of which, like CIPRO, actually cause tendon weakness and rupture), TENS Units, braces & supports of all kinds, PLATELET INJECTION THERAPY, high powered ultrasound (a form of litho-tripsy called arthro-tripsy), prolotherapy (sugar water injections), all sorts of surgeries, and heaven only knows what else. And this doesn’t even start touching on many of the common drugs, which I’ve already dealt with.

The bottom line is that if your pain is being caused by adhesions, restrictions, and microscopic scarring in the collagen fibers that make up the affected tendon (or the fascial membranes that attach to the tendon), you are going to have a hard time dealing with it using the standard fare found in your average medical clinic. Although their various treatments may cover the symptoms for awhile, you are already becoming painfully aware (no pun intended) that standard medical therapies such as those listed earlier, are not likely to help with Tendinosis over the long haul. And although stretching and specific exercise can be of tremendous benefit, most clinicians tend to put the cart in front of the horse. Those things will not be effective until after the tissue adhesion has been removed (broken), except in minor cases.

Be aware that because of its microscopic nature, the collagen derangement associated with Tendinopathies will rarely if ever show up with even advanced diagnostic imaging (this is true even for MRI, unless your doctor is using a brand new machine with an extra large magnet, or your problem is especially severe). And whether it shows on the MRI or not, will not really change the way that your doctor treats the problem.

Effectively Treat Tendinosis At The Source

If tendinopathies do not show up well with the diagnostic tests that are commonly run by your doctor, how in the world can a chiropractor practicing in tiny town determine whether or not this micro-derangement of a tendon�s collagen fibers is present and potentially causing your pain and dysfunction? I use one of the newer forms of SCAR TISSUE REMODELING. Although this has only been around for three decades in its present form, the Chinese have used something similar for several thousand years. Be aware that breaking these adhesions / restrictions sometimes causes some BRUISING, depending on where it’s at.

Conclusion: Systemic Tendinosis

Not all cases of Tendinosis are rooted in purely biomechanical causes. There are all sorts of things that can create an environment within the body that leads to multiple Tendinopathies. As you might imagine, bilateral Tendinosis, or Tendinosis at multiple sites begins to raise some red flags for me concerning this issue. Not that it is always the case, but when I see people who have several areas of Tendinosis, I began to question whether there might be a deeper problem at work.

If it is not caused by Fluoroquinolone Antibiotics, very frequently, this underlying problem turns out to be some sort of poorly understood or difficult-to-detect AUTOIMMUNE DISEASE. If for whatever reason, your body is making antibodies to attack it’s own tendons or connective tissues, you have a serious problem on your hands — a problem that will not respond to the Scar Tissue Remodeling Treatments that I do, and a problem whose cause likely won’t show up on standard medical tests.

Destroy Chronic Pain / Doctor Russell Schierling

Sherry McAllister, DC, MS (Ed), CCSP Recommends Chiropractic

Shin Splint Sufferers Should Consider Chiropractic

Shin Splint Sufferers Should Consider Chiropractic

Shin Splint: Whether you are an avid exerciser, an exuberant shopper, or a small child chaser, you have probably felt tightening and burning in your shin at one point in your life. Sometimes, the pain stops when the activity ceases, but other times the pain remains. If shin pain continues bothering you, it may be time to face the fact you have shin splints.

The shin is a bone located in the front part of your lower leg. Shin splints commonly occur in athletes who have intensified or changed their training routines. They also show up in regular people who have changed or added activity to their routine.

The shin has a lot of responsibility during exercise, as it absorbs the shock of the steps, raises the toes, and support the arch of the foot.

A few main culprits play a part in shin splints:

  • failing to stretch properly before exercising
  • walking or running on hard surfaces, like pavement
  • wearing the wrong type of shoes during activity
  • over-exerting the body with strenuous activity
  • skipping periods of rest between exercise

Individuals who perform any type of exercise should take appropriate measures to alleviate the above risk factors of shin splints. If you notice pain and soreness in the front part of your lower leg, know how to treat this injury properly.

If rest and ice aren�t doing the job and you’re still suffering pain, it’s time to see a doctor. A thorough exam and possibly an x-ray will diagnose the problem.

Chiropractic care is a powerful choice for treating shin splints and reducing their recurrence.

Chiropractic Treatment Benefits Those Suffering From Shin Splint/s:

shin splint

Reduction In Pain

Chiropractic is proven to relieve the pain associated with bodily injuries and medical conditions, including shin splints. Sometimes one visit is enough to relieve the pain, other times the pain decreases over a series of appointments. Being able to diminish a high degree of pain down to a manageable level is possible for shin splint patients through chiropractic.

Full Body Alignment

The premise behind chiropractic is that it treats the body as a whole, and, in doing so, promotes healing and health to the injured or diseased areas. A chiropractor may work on your neck to help your calf. With shin splints, he or she may align your spine and joints to lessen the impact of activity on your shins. Again, the entire body is treated in order to create the best environment for health restoration.

Healing Through Adjustments

Treating shin splints is a common procedure for chiropractors. Common practice is to adjust the calf, ankle, and foot to stretch and increase blood flow to the area.

Drug Free Treatment Option

A primary benefit of chiropractic care is it requires no over-the-counter or prescription drugs. Individuals who suffer from stomach issues, or simply prefer to avoid drugs, find chiropractic visits a productive alternative to manage pain and promote healing.

Strengthening Exercises

Chiropractors don’t just treat the spine. Your Doctor of Chiropractic will set an overall plan of attack for optimal recovery when dealing with shin splints.

It’s routine for chiropractic treatment of shin splints to include a series of stretching and strengthening exercises the individual performs at home between visits. These exercises further expand on the positive effects of the chiropractic therapy.

If you are one of the many people dealing with shin splints, don’t despair! Consider chiropractic care as your main treatment option or in conjunction with other modes of treatment. Within a few visits, you will experience pain reduction, and enjoy a decreased risk of ever dealing with painful shin splints again.

Athletic TIPS