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Janda Syndromes

Janda’s Crossed Syndromes
Over time, these imbalances will spread throughout the muscular system in a predictable manner. Janda has classified these patterns as “Upper Crossed Syndrome” (UCS), “Lower Crossed Syndrome” (LCS), and “Layer Syndrome” (LS) (Janda, 1987, 1988). [UCS is also known as “cervical crossed syndrome”; LCS is also known as “pelvic crossed syndrome; and LS is also known as “stratification syndrome.”] Crossed syndromes are characterized by alternating sides of inhibition and facilitation in the upper quarter and lower quarter. Layer syndrome, essentially a combination of UCS and LCS is characterized by alternating patterns of tightness and weakness, indicating long-standing muscle imbalance pathology. Janda’s syndromes are summarized in Figure 1.

Upper crossed syndrome is characterized by facilitation of the upper trapezius, levator, sternocleidomastoid, and pectoralis muscles, as well as inhibition of the deep cervical flexors, lower trapezius, and serratus anterior. Lower crossed syndrome is characterized by facilitation of the thoraco-lumbar extensors, rectus femoris, and iliopsoas, as well as inhibition of the abdominals (particularly transversus abdominus) and the gluteal muscles.
By using Janda’s classification, clinicians can begin to predict patterns of tightness and weakness in the sensorimotor system’s attempt to reach homeostasis. Janda noted that these changes in muscular tone create a muscle imbalance, which leads to movement dysfunction. Muscles prone to tightness generally have a “lowered irritability threshold” and are readily activated with any movement, thus creating abnormal movement patterns. These imbalances and movement dysfunctions may have direct effect on joint surfaces, thus potentially leading to joint degeneration. In some cases, joint degeneration may be a direct source of pain, but the actual cause of pain is often secondary to muscle imbalance. Therefore, clinicians should find and treat the cause of the pain rather than focus on the source of the pain.

Janda Evaluation

Systematic evaluation of muscular imbalance begins with static postural assessment, observing muscles for characteristic signs of hypertonicity or hypotonicity. This is followed by observation of single leg stance and gait. Static posture, gait and balance often give the best indication of the status of the sensorimotor system. Computerized force plate posturography is often valuable in quantifying sensory and motor deficits. Next, characteristic movement patterns are assessed, and specific muscles are tested for tightness or shortness. Surface electromyography is useful in quantifying muscle activation patterns. All the above information collected provides the clinician a system to determine or rule out the presence of muscle imbalance syndromes. Furthermore, identification of specific patterns and syndromes of imbalance also provides the clinician to choose appropriate interventions to address the cause of the dysfunction.

Janda Treatment

Janda’s Approach to Treatment
1. Normalize the periphery. The Janda approach to treatment of musculoskeletal pain follows several steps. Treatment of muscle imbalance and movement impairment begins with normalizing afferent information entering the sensorimotor system. This includes providing an optimal environment for healing (by reducing effusion and protection of healing tissues, restoring proper postural alignment (through postural and ergonomic education), and correcting the biomechanics of a peripheral joint (through manual therapy techniques).
2. Restore Muscle Balance. Once peripheral structures are normalized, muscle balance is restored. Normal muscle tone surrounding joints must be restored. Sherrington’s law of reciprocal inhibition (Sherrington, 1907) states that a hypertonic antagonist muscle may be reflexively inhibiting their agonist. Therefore, in the presence of tight and/or short antagonistic muscles, restoring normal muscle tone and/or length must first be addressed before attempting to strengthen a weakened or inhibited muscle. Techniques to decrease tone must be specific to the cause of the hypertonicity. These include post-isometric relaxation (PIR) (Lewit, 1994) and post-facilitation stretch (PFS) (Janda, 1988).
Muscles that have been reflexively inhibited by tight antagonists often recover spontaneously after addressing the tightness. In the Janda approach, the coordinated firing patterns of muscle are more important than the absolute strength of muscles. The strongest muscle is not functional if it cannot contract quickly and in coordination with other muscles; therefore, isolated muscle strengthening is not emphasized in the Janda approach. Instead, muscles are facilitated to contract at the proper time during coordinated movement patterns to provide reflexive joint stabilization.
3. Increase afferent input to facilitate reflexive stabilization. Once muscle balance has been addressed, Janda stresses increasing proprioceptive input into the CNS with a specific exercise program, “Sensorimotor Training” (SMT) (Janda & Vavrova, 1996). This program increases afferent information entering the subcortical pathways (including spinocerebellar, spinothalamic, and vestibulocerebellar pathways) to facilitate automatic coordinated movements. SMT involves progressive stimulation through specific exercises with increasing level of challenge to the sensorimotor system. SMT has been proven to improve proprioception, strength, and postural stability in ankle instability (Freeman et al. 1965), knee instability (Ihara & Nakayam, 1996), and after ACL reconstruction (Pavlu & Novosadova, 2001).
4. Increase endurance in coordinated movement patterns. Finally, endurance is increased through repetitive, coordinated movement patterns. Since fatigue is a predisposing factor to compensated movement patterns, endurance is also more important than absolute strength. Exercises are performed at low intensities and high volumes to simulate activities of daily living.
The Janda approach is valuable in today’s managed care environment. Once these patterns and syndromes are identified, specific treatment can be implemented without expensive equipment. Early detection of these causes of chronic pain allows the clinician to treat the patient with fewer visits and less expensive equipment compared to traditional interventions that emphasize modalities and passive treatments. The key to the Janda approach is in the home exercise program. Inexpensive home exercise equipment such as wobble boards, elastic bands, and foam pads are used with a specific progression of exercises as the patient improves in function.
Summary
In summary, the Janda approach emphasizes the importance of the CNS in the sensorimotor system, and its role in the pathogenesis in musculoskeletal pain. In particular: the neurological pre-disposition of muscles to exhibit predictable changes in tone, and the importance of proprioception and afferent information in the regulation of muscle tone and movement. Therefore, assessment and treatment focus on the sensorimotor system, rather than the musculoskeletal system itself. Using a functional, rather than a structural approach, the cause of musculoskeletal pain can be quickly identified and addressed. The Janda approach can be a valuable tool for the clinician in the evaluation and treatment of chronic musculoskeletal pain.

Janda Philosophy

Janda’s approach to the evaluation and management of chronic musculoskeletal pain focuses on the importance of the central nervous system in mediating chronic pain through neuromuscular imbalance.
Structure vs. Function

In musculoskeletal medicine, there are two main schools of thought, that is, a structural or functional approach. In the structural approach, the pathology of specific static structures is emphasized; this is the typical orthopaedic approach that emphasizes diagnosis based on localized evaluation and special tests (X-Ray, MRI, CT Scan, etc). On the other hand, the functional approach recognizes the function of all processes and systems within the body, rather than focusing on a single site of pathology. While the structural approach is necessary and valuable for acute injury or exacerbation, the functional approach is preferable when addressing chronic musculoskeletal pain.
The Sensorimotor System
In chronic pain, special diagnostic tests of localized areas (for example, low back radiographs) are often normal, although the patient complains of pain. The site of pain is often not the cause of the pain. Recent evidence by supports the fact that chronic pain is centrally-mediated (Staud et al. 2001). Similarly, research on the efficacy of different modes of exercise management of chronic pain has shown a central effect of exercise in decreasing chronic low back pain (Mannion et al. 1999). This research supports the basis of Janda’s approach: the interdependence of the musculoskeletal and central nervous system. Janda states that these two anatomical systems cannot be separated functionally. Therefore, the term “sensorimotor” system is used to define the functional system of human movement. In addition, changes within one part of the system will be reflected by compensations or adaptations elsewhere within the system because of the body’s attempt at homeostasis (Panjabi, 1992).
The muscular system often reflects the status of the sensorimotor system, as it receives information from both the musculoskeletal and central nervous systems. Changes in tone within the muscle are the first responses to nociception by the sensorimotor system. This has been supported by various studies demonstrating the effect of joint pathology on muscle tone. For example, the presence of knee effusion causes reflex inhibition of the vastus medialis (Stokes & Young, 1984). The multifidus has been shown to atrophy in patients with chronic low back pain (Hides et al. 1994), and muscles demonstrate increased latency after ankle sprains (Konradsen & Raven, 1990) and ACL tears (Ihara & Nakayama, 1986). The global effect of joint pathology on the sensorimotor system was demonstrated by Bullock-Saxton (1994). She noted a delay in firing patterns of the hip muscles and decreased vibratory sensation in patients with ankle sprains.
Because of the involvement of the CNS in muscle imbalance and pain, Janda emphasizes the importance of the afferent proprioceptive system. A reflex loop from the joint capsular mechanoreceptors and the muscles surrounding the joint is responsible for reflexive joint stabilization (Guanche et al. 1995; Tsuda et al. 2001). In chronic instability, deafferentation (the loss of proper afferent information from a joint) is often responsible for poor joint stabilization (Freeman et al. 1965).
Tonic and Phasic Muscle Systems
Janda identified two groups of muscles based on their phylogenetic development (Janda, 1987). Functionally, muscles can be classified as “tonic” or “phasic”. The tonic system consists of the “flexors”, and is phylogenetically older and dominant. These muscles are involved in repetitive or rhythmic activity (Umphred, 2001), and are activated in flexor synergies. The phasic system consists of the “extensors”, and emerges shortly after birth. These muscles work eccentrically against the force of gravity and emerge in extensor synergies (Umphred, 2001).
Janda noted that the tonic system muscles are prone to tightness or shortness, and the phasic system muscles are prone to weakness or inhibition (Table 1). Based on his clinical observations of orthopedic and neurological patients, Janda found that this response is based on the neurological response of nociception in the muscular system. For example, following structural lesions in the central nervous systems (such cerebral palsy or cerebrovascular accident), the tonic flexor muscles tend to be spastic and the phasic extensor muscles tend to be flaccid. Therefore, patterns of muscle imbalance may be due to CNS influence, rather than structural changes within the muscle itself.
It’s important to note that this classification is not rigid, in that some muscles may exhibit both tonic and phasic characteristics. It should also be noted that in addition to neurological predisposition to tightness or weakness, structural changes within the muscle also contribute to muscle imbalance. However, in chronic pain that is centralized within the CNS, patterns of muscle imbalance are often a result of neurological influence rather than structural changes.

Tonic Muscles Prone to Tightness or Shortness	Phasic MusclesProne to Weakness or Inhibition
Gastroc-SoleusTibialis Posterior Hip Adductors Hamstrings Rectus Femoris Iliopsoas Tensor Fascia Lata Piriformis Thoraco-lumbar extensors Quadratus Lumborum Pectoralis Major Upper Trapezius Levator Scapulae Scalenes Sternocleidomastoid Upper limb flexors	Peroneus Longus, BrevisTibialis Anterior Vastus Medialis, Lateralis Gluteus Maximus, Medius, Minimus Rectus Abdominus Serratus Anterior Rhomboids Lower Trapezius Deep neck flexors Upper limb extensors

Table 1: Tonic & Phasic Muscles

About Dr. Janda

Excerpted from Assessment and Treatment of Muscle Imbalance: The Janda Approach
Vladimir Janda was born in 1928. At the age of 15, he contracted polio. He was paralyzed as a quadriplegic and unable to walk for 2 years. He eventually recovered walking function, but developed post-polio syndrome and was forced to use a walker until the end of his life in 2002.
As a physician, he focused on post-polio patients early on. One of his early influences was Sister Kinney in 1947, who introduced the treatment of polio in Czechoslovakia. He served as an interpreter for Sister Kinney as a first year medical student, and decided to pursue an interest in physiotherapy after medical school. He received the “Kinney Physiotherapist” certificate after graduation from medical school. He was one of the first physicians to combine therapy and medicine in a ‘hands-on’ approach, becoming one of the earliest to practice physical medicine and rehabilitation.
He became more interested in pain syndromes of the locomotor system. His first book in 1949 at the age of 21 was on muscle testing and function, which was the first of its kind in Czech. He continued as a prolific researcher and writer; before his death, he published over 16 books and over 200 papers on muscle function.
At the age of 24, he was working in a rehabilitation center for post-polio patients. He was interested in evaluating the claims from muscle testing textbooks at the time. Using EMG, he began studying the muscle activity of the hip joint in physiotherapist students. He found muscles that weren’t supposed to be activated actually were, noting the accessory role of muscles outside of their primary movements. Specifically, he found subjects without activity in the gluteus maximus during hip extension movements used an increased pelvic tilt to accomplish the extension. This led to his lifelong passion to study movements, rather than individual muscles as was common at the time of the polio era. He recognized the importance of testing muscle function rather than strength. This was the beginning of thinking globally rather than locally in terms of muscle function.
In the 1960s, Freeman and Wyke published several papers on the importance of afferent input and mechanoreceptors. They described the use of wobble boards in the treatment of chronic ankle instability. Janda noted a connection between chronic ankle instability and chronic low back pain: proprioception. This led to Janda’s development of “Sensorimotor Training”, a progressive exercise program using simple exercises and unstable surfaces. He rarely recommended strengthening exercises, instead focusing on balance and function. This was in contrast to the traditional rehabilitation approach in the 60’s and 70’s emphasizing strength training.
Janda completed his thesis in 1964 on patients with sacroiliac dysfunction, finding weakness and inhibition of the gluteus maximus, even in the absence of pain. He recognized that certain other muscles were prone to weakness. Janda subsequently defined movement patterns to estimate the quality of movement. He discovered that muscle imbalance was systematic, predictable, and involved the entire body.
In 1979, he defined his “crossed syndromes”: Upper crossed, lower crossed, and layer syndrome. He subsequently noted that his crossed syndromes were his only ‘discovery’; he always gave credit to others influencing his approach. Janda had a wide range of influences that provided him a comprehensive viewpoint:

• Berta Botath, a physiotherapist and her husband Karel Bobath, a neurophysiologist from London, who were leaders in neurodevelopmental principles and treatment in physiotherapy
• Austrian physician Hans Kraus, who first described “hypokinetic disease” in low back pain before the second world war, which as noted as a “lack of movement.”
• His colleague and lifelong friend, Karel Lewit MD, who practiced with Janda in Prague for many years and shared his expertise on manual therapy and the locomotor system.
• Vaclav Vojta MD, a Czech physician who described the influence of developmental kinesiology in human movement and pathology.
• Alois Brugger MD, A Swiss neurologist who described the neurologic basis muscle imbalance.
• Florence Kendall PT, who first influenced Janda on the concept of muscle imbalances.
• John Basmajian MD, a Canadian expert in EMG analysis who lead Janda’s postdoctoral studies
• David Simons MD, an expert in trigger points and muscle pain

Janda was an avid reader and collector of books and papers on muscles. His ability to fluently speak as many as 5 different languages gave him the ability to read and learn more from all over the world.  His international influence continued to spread as a consultant to the World Health Organization in the 1960s and 70s.
Janda founded the Department of Rehabilitation Medicine and directed the physiotherapy school at the Charles University Third School of Medicine, where he continued to practice until his death on November 25, 2002.  The authors of this text had the opportunity to be with him three months prior on his last visit to North America. The “Father of Czech Rehabilitation” will continue to be missed by many. For an excellent review of Janda’s life and contributions, read the paper by Morris and colleagues, Vladimir Janda, MD, DSc: tribute to a master of rehabilitation. (Spine. 2006 Apr 20;31(9):1060-4.)

Know your food!

Food Groups: Base of the food balance

You are what you eat. Everything that you eat and drink has an effect on your body. Nutrition is the basic prerequisite to sustain a healthy life. All the food that we eat provides us with a range of nutrients, each with its own role to play. Eating a balanced, varied diet everyday ensures that you have everything you need for a good health. Our diet must provide all the essential nutrients in the right amounts. To perform various functions normally you need a complete range of nutrients from various food groups. Broadly there are 7 food groups which have been grouped together as they share similar nutritional properties. These food groups are:

1. Cereals:Cereals form the staple diet in India, e.g., rice, wheat, maize. Cereals are the main source of energy, contributing 60-70% of daily energy needs. Cereals are a source of protein, calcium, iron and B-complex vitamins. Whole-grains (grains with the intact outer layer like in brown rice, corn) are a good source of fibre and B-complex vitamins and should be included in daily diet.
2. Pulses (legumes):Pulses are a rich source of proteins (up to 22%) and meet the protein requirement of the vegetarians. They are also rich in B complex vitamins. Germination (sprouting) of pulses increases the vitamin C and B group vitamins and also improves the digestibility.
3. Milk and Milk Products:
   This category includes liquid and powdered milk, paneer, curd, buttermilk etc. They are not only a good source of quality protein but also calcium and riboflavin. These should be a part of everyday’s diet and especially essential for children as they support healthy growth.
4. Fruits and Vegetables: these include
   1. Roots and Tubers: these are rich in carbohydrates and are good sources of energy and calcium. Root vegetables like carrots are a good source of vitamin A.
   2. Vegetables and Green Leafy Vegetables (GLV’s): vegetables add both color and variety to the diet. They provide minerals, vitamins and fiber (which add bulk to the diet). GLV’s are a rich source of calcium iron, vitamin A (β-carotene), vitamin C, folic acid.
   3. Fruits: these provide vitamins and fiber. Green, Yellow and Orange fruits are a rich source of beta carotene. Citrus fruits, amla, and guava are rich in vitamin C. dried fruits like dates supply iron. Seasonal fruits should be encouraged. Fruits also contain pectins which provide bulk to the diet and helps bowel movement.
5. Animal Foods:This category includes eggs, chicken, meat, fish etc. They are a good source of high quality protein and other important nutrients. Fish is rich in omega-3 PUFA which is protective against cardiovascular diseases and calcium as well. A special feature in flesh foods is the presence of vitamin B12, which is absent in plant foods.
6. Fats, Nuts and Oils:
   These are calorie-rich foods, and are useful for increasing the energy density of foods. Fats can be the visible fats (ghee, butter, oil) or the invisible fats (present inherently in each food). They are required in moderate quantities in the daily diet as they provide essential fatty acids and promote absorption of fat soluble vitamins along with improving the palatability of the food. However, the total calories from fat should not exceed 10-15%.
7. Sugars:
   This group includes table sugar, jaggery, honey, syrups etc which are energy concentrates. They are the sweetening agents which should be consumed in moderation as they provide calories but not much in the way of nutrition. Also excessive sugar consumption has been linked to weight gain.

Ignacio Ponseti 

 

Ignacio Ponseti (3 June 1914 – 18 October 2009) was a physician, specializing in orthopedics. A native of Spain, he fled the Spanish Civil War and became a faculty member and practicing physician at the University of Iowa.
He developed in the 1950s the Ponseti Method (also known as the Ponseti Technique), a non-surgical technique that uses a series of casts, followed by a brace, to correct congenital clubfoot. The condition causes a baby's feet to turn inward and downward; if not corrected, a child is unable to walk or move properly.

Biography

Known for the method for the clubfoot treatment that bears his name, Ignacio Ponseti was Professor Emeritus in the Department of Orthopaedic Surgery at University of Iowa Hospitals and Clinics.
Born 3 June 1914 in Menorca, part of the Balearic Islands, Spain, Ponseti was the son of a watchmaker and helped repair watches. The skill was said to eventually contribute to his abilities as an orthopedist.^[1]
Ponseti studied medicine at Barcelona University. Not long after he graduated, fighting broke out between the Nationalists and the Republicans - the start of the Spanish Civil War. Ponseti served as a medical officer with the Loyalists as a lieutenant, then captain, in the Orthopaedic and Fracture Service. His duties included setting fractures, which put him on a career in orthopaedics. Without ambulances, Ponseti used the help of local smugglers to take the injured into France.^[1] He soon escaped to France himself and went to Mexico, where for two years he practiced family medicine. A physician there helped Ponseti get to Iowa in 1941 to study orthopaedics under Arthur Steindler, M.D. Ponseti completed a residency at Iowa in 1944 and became a member of the orthopaedic faculty at University of Iowa Hospitals and Clinics.
Early in his career at Iowa, Ponseti saw that the outcomes of clubfoot surgical treatments were not very good—patients had limited movement. He set out to develop a treatment that made the most of babies' flexible ligaments.^[2] The method was met with some opposition but over the past 50 years it has been adopted by many doctors and other health care providers worldwide, including in Britain ^[3] and Turkey ^[4]
Well into his nineties, Ponseti continued to see patients and trained visiting doctors from around the world. He also developed new prosthetic devices with John Mitchell of MD Orthotics [1] and produced training and information DVD's on the method.
Ponseti's other research focused on congenital and developmental bone and joint disorders, skeletal growth disorders in children, and the biochemistry of cartilage. He gained insight in the early 1950s on the effect of amino nitriles on collagen cross linking, defined the curvature patterns of idiopathic scoliosis, and demonstrated that curves progressed after skeletal maturity. He also conducted many studies evaluating the long-range results of treatments for congenital dislocation of the hip, clubfoot and scoliosis.

The Ponseti Method

Clubfoot affects well over 100,000 newborns annually.^[5] Early in his career at the University of Iowa, Ponseti realized that surgical approaches did not fully correct clubfoot and/or created problems later in life, such as severe arthritis or even requiring more surgery.^[2] In working to develop a new approach, he determined it could be nonsurgical. The Ponseti method uses gentle, manual manipulation of the foot, followed by application of toe-to-groin plaster casts. The casts are changed weekly after a clinician manipulates softened foot ligaments to gradually achieve near-normal muscle and bone alignment.
In addition to the improved physical outcomes, compared to surgery, the Ponseti method is less expensive and can be taught to nonphysician health care providers, which is useful in areas with few or no doctors. Nearly 80 percent of children born with clubfoot live in impoverished nations. The Ponseti method is used, for example, in Uganda, where efforts continue to improve the availability of the treatment.^[6]
Information about the use of Ponseti method can be found at these sites: World Health Organisation, American Academy of Orthopedic Surgeons, Pediatric Orthopaedic Society of North America, STEPS Charity UK and STEPS Charity South Africa.
At the 2007 International Clubfoot Symposium attended by 200 doctors from 44 countries, papers were presented regarding an estimated 10,000 children successfully treated with the technique around the world in the past few years.
The Ponseti International Association for the Advancement of Clubfoot Treatment was founded in 2006 to improve the treatment of children born with clubfoot through education, research and improved access to care. PIA has a related Web site devoted to the interests and needs of parents.^[7] Groups that work with Ponseti International include Cure International and A Leg to Stand On (India).


The Ponseti method is a manipulative technique that corrects congenital clubfoot without invasive surgery. It was developed by Dr. Ignacio V. Ponseti of the University of Iowa, USA in the 1950s, and was repopularized in 2000 by Dr. John Herzenberg in the USA and Europe and in Africa by NHS surgeon Steve Mannion. It is a standard^[1] for the treatment of club foot.

Description

Ponseti treatment was introduced in UK in the late 1990s and widely popularized around the country by NHS physiotherapist Steve Wildon. The manipulative treatment of clubfoot deformity is based on the inherent properties of the connective tissue, cartilage, and bone, which respond to the proper mechanical stimuli created by the gradual reduction of the deformity. The ligaments, joint capsules, and tendons are stretched under gentle manipulations. A plaster cast is applied after each manipulation to retain the degree of correction and soften the ligaments. The displaced bones are thus gradually brought into the correct alignment with their joint surfaces progressively remodeled yet maintaining congruency. After two months of manipulation and casting the foot appears slightly over-corrected. After a few weeks in splints however, the foot looks normal.
Proper foot manipulations require a thorough understanding of the anatomy and kinematics of the normal foot and of the deviations of the tarsal bones in the clubfoot. Poorly conducted manipulations will further complicate the clubfoot deformity. The non-operative treatment will succeed better if it is started a few days or weeks after birth and if the podiatrist understands the nature of the deformity and possesses manipulative skill and expertise in plaster-cast applications.^[2]

Clubfoot (talipes equinovarus) affects almost 150,000 children annually. Almost 80% of these children live in developing nations. Dr Ponseti's technique is painless, fast, cost-effective and successful in almost 100% of all congenital clubfoot cases. The Ponseti method is endorsed and supported by World Health Organization^[3][4]National Institutes of Health^[5], American Academy of Orthopedic Surgeons^[6], Pediatric Orthopedic Society of North America^[7], European Pediatric Orthopedic Society^[8], CURE^[9], STEPS Charity UK^[10], STEPS Charity South Africa^[11], A Leg to Stand On (India)^[12] and others.
At the 2007 International Clubfoot Symposium attended by 200 doctors from 44 countries, papers were presented for an estimated 10,000 children successfully treated with the technique around the world in the past few years.
The Ponseti International Association for the Advancement of Clubfoot Treatment was founded in 2006 at the University of Iowa. The Ponseti International Association aims to improve the treatment of children born with clubfoot through education, research and improved access to care.
Steps are as follows:
1. The calcaneal internal rotation (adduction) and plantar flexion is the key deformity. The foot is adducted and planter-flexed at the subtalar joint, and the goal is to abduct the foot and dorsiflex it. In order to achieve correction of the clubfoot, the calcaneum should be allowed to rotate freely under the talus, which also is free to rotate in the ankle mortise. The correction takes place through the normal arc of the subtalar joint. This is achieved by placing the index finger of the operator on the medial malleolus to stabilize the leg and levering on the thumb placed on the lateral aspect head of the talus while abducting the forefoot in supination. Forcible attempts at correcting the heel varus by abducting the forefoot while applying counter pressure at the calcaneocuboid joint prevents the calcaneum from abducting and therefore everting.
2. Foot cavus increases when the forefoot is pronated. If cavus is present, the first step in the manipulation process is to supinate the forefoot by gently lifting the dropped first metatarsal to correct the cavus. Once the cavus is corrected, the forefoot can be abducted as outlined in step 1.
3. Pronation of the foot also causes the calcaneum to jam under the talus. The calcaneum cannot rotate and stays in varus. The cavus increases as outlined in step 2. This results in a bean-shaped foot. At the end of step 1, the foot is maximally abducted but never pronated.
4. The manipulation is carried out in the cast room, with the baby having been fed just prior to the treatment or even during the treatment. After the foot is manipulated, a long leg cast is applied to hold the correction. Initially, the short leg component is applied. The cast should be snug with minimal but adequate padding. The authors paint or spray the limb with tincture of benzoin to allow adherence of the padding to the limb. The authors prefer to apply additional padding strips along the medial and lateral borders to facilitate safe removal of the cast with a cast saw. The cast must incorporate the toes right up to the tips but not squeeze the toes or obliterate the transverse arch. The cast is molded to contour around the heel while abducting the forefoot against counter pressure on the lateral aspect of the head of the talus. The knee is flexed to 90° for the long leg component of the cast. The parents can soak these casts for 30–45 minutes prior to removal with a plaster knife. The authors' preferred method is to use the oscillating plaster saw for cast removal. The cast is bivalved and removed. The cast then is reconstituted by coapting the 2 halves. This allows for monitoring of the progress of the forefoot abduction and, in the later stages, the amount of dorsiflexion or equinus correction.
5. Forcible correction of the equinus (and cavus) by dorsiflexion against a tight Achilles tendon results in a spurious correction through a break in the midfoot, resulting in a rockerbottom foot. The cavus should be separately treated as outlined in step 2, and the equinus should be corrected without causing a midfoot break. It generally takes up to 4–7 casts to achieve maximum foot abduction. The casts are changed weekly. The foot abduction (correction) can be considered adequate when the thigh-foot axis is 60°After maximal foot abduction is obtained, most cases require a percutaneous Achilles tenotomy. This is performed in the cast room under aseptic conditions. The local area is anesthetized with a combination of a topical lignocaine preparation (eg, EMLA cream) and minimal local infiltration of lidocaine. The tenotomy is performed through a stab incision with a round tip (#6400) Beaver blade. The wound is closed with a single absorbable suture or with adhesive strips.The final cast is applied with the foot in maximum dorsiflexion, and the foot is held in the cast for 2–3 weeks.
6. Following the manipulation and casting phase, the feet are fitted with open-toed straight-laced shoes attached to a Dennis Brown bar. The affected foot is abducted (externally rotated) to 70° with the unaffected foot set at 45° of abduction. The shoes also have a heel counter bumper to prevent the heel from slipping out of the shoe. The shoes are worn for 23 hours a day for 3 months and are worn at night and during naps for up to 3 years.
7. In 10–30% of cases, a tibialis anterior tendon transfer to the lateral cuneiform is performed when the child is approximately 3 years of age. This gives lasting correction of the forefoot, preventing metatarsus adductus and foot inversion. This procedure is indicated in a child aged 2–2.5 years with dynamic supination of the foot. Prior to surgery, cast the foot in a long leg cast for a few weeks to regain the correction.