


Introduction to Physical Therapy and Patient Skills?

CHAPTER 4: Foundations of Movement



CHAPTER OBJECTIVES
At the completion of this chapter, the reader will be able to:
1. Discuss the various periods of normal prenatal development
2. Describe the normal sequence in which nervous tissue, connective tissue, and skeletal muscle develop
3. Describe how the motor unit works
4. List the different kinds of feedback receptors
5. Describe the various physiologic processes by which the body produces energy
6. Discuss the external and internal forces of the body that are either generated or resisted during the course of daily activities
7. Describe the various types of levers and give real life examples of each
8. Describe the various components of the stresses and strains that occur with connective tissues
9. List the various planes and axes of the body
10. Explain the concept of degrees of freedom and give examples of each
11. Explain the difference between osteokinematic motion and arthrokinematic motion
12. Discuss the difference between open and closed kinetic chains
13. Describe the various theories of motor development, motor control, and motor learning
14. List the different kinds of motor tasks and describe the differences
15. Describe how early motion develops in terms of stability and mobility
16. Discuss the various methods of skill acquisition
17. Describe the factors that affect normal development and the impact that physical therapy can have
OVERVIEW
Normal movement, which is an amalgamation of strength, endurance, speed, and accuracy, is essential to normal functioning. In turn, normal functioning is dependent on normal development. A physical therapist can be viewed as an expert on movement, both normal and abnormal, through an acquired knowledge of neuromusculoskeletal development. This working knowledge is applied to make a number of decisions about the overall clinical program of a patient (see Chapter 7).
HUMAN DEVELOPMENT
 Human development is a continuum, starting with fertilization, prenatal development, birth, and ending with growth up to adulthood. Embryology is	



the study of prenatal development. Prenatal development, or fetal development, is the term given to the process of gestation (pregnancy) that an embryo undergoes. Human gestation lasts an average of 266 days (38 weeks) from conception (fertilization) to parturition (childbirth).

From a clinical perspective, the course of pregnancy is divided into three month intervals called trimesters:  First trimester (first 12 weeks)
 Second trimester (weeks 13 to 24)  Third trimester (week 25 to birth)
From a biological perspective, human development occurs in three main stages. The first two weeks (approximately 16 days) after conception are known as the pre embryonic period; day 17 through the eighth week are known as the embryonic period; and the time from the beginning of the ninth week until birth is known as the fetal period.
The internal physiologic changes that occur in all body systems throughout these developmental periods provide a substrate for movement. In particular, maturation of the nervous system occurs in the presence of a continually changing musculoskeletal system. Movement itself influences the quality of muscle contractions, shapes the body's joints, and prepares body parts for stabilizing or mobilizing functions.
Pre embryonic Period
The early embryonic events, such as body axis formation, gastrulation, and neurulation, are crucial for normal embryogenesis and greatly influence both the formation of the basic body plan. This two week period involves three main processes:
 Cleavage (cell division) (Figure 4 1)
 Implantation, in which the egg becomes embedded in the mucosal lining of the uterus (see Figure 4 1)
 Embryogenesis, in which the embryonic cells migrate and differentiate into three tissue layers called the ectoderm, mesoderm, and endoderm

FIGURE 4 1


Migration of the oocyte and subsequent cleavage




The human ovary usually releases one egg (oocyte) per month around day 14 of a typical 28 day ovarian cycle. In order for normal fertilization to occur, a number of conditions need to be met:
 An egg must be present in the uterine (fallopian) tube. The egg is swept into the fallopian tube by the beating of cilia on the tube's epithelial cells. The egg is surrounded by a thin layer of protein and polysaccharides, called the zona pellucida (see Figure 4 1), and a layer of granulocytic cells, called the corona radiata, both of which provide a protective shield around the egg as it enters the uterine tube during its three day journey. If the egg is not fertilized, it dies within 24 hours and gets no more than one third of the way to the uterus.1
 Large numbers of spermatozoa must be ejaculated. Only about 100 of the spermatozoa survive to encounter the ovum in the uterine tube. The anterior tip of the sperm contains a specialized lysosome called an acrosome, a packet of enzymes used to penetrate the egg and certain barriers around it.
The main function of fertilization is to combine the haploid sets of chromosomes from two individuals into a single diploid complement of chromosomes the zygote (fertilized ovum).
After fertilization, the embryogenesis starts. Within 30 hours following fertilization, the zygote undergoes a mitotic division called cleavage, progressing through 2 cell, 4 cell, 8 cell, and 16 cell stages (morula) (see Figure 4 1). The morula floats within the uterine cavity for approximately three days, as it gradually fills with fluid and forms two distinct groups of cells. At this time, the structure becomes known as a blastocyst (see Figure 4  1), and its fluid filled sac is called a blastocyst cavity (Figure 4 2). The outer layer of cells of the blastocyst is referred to as the trophoblast, whereas the inner layer is called the embryoblast. The trophoblast cells eventually contribute to fetal membrane systems; the inner cell mass plays a large role in the formation of the embryo and fetus. The developmental characteristics of the embryo and fetus according to gestational age are outlined in Table 4 1. The termination of the cleavage stage of development terminates with the formation of the blastocyst. The process of implantation occurs as the blastocyst embeds itself into the endometrium of the uterine wall and prevents itself from being aborted by secreting a hormone that indirectly prevents menstruation.

FIGURE 4 2



Implantation

TABLE 4 1
Developmental Characteristics of the Embryo and Fetus According to Gestational Age



Gestational Age 

Developmental Characteristics


2.5 weeks
Neural plate formation; shape and length begin to be determined.


Three weeks
Cell differentiation occurs formation of ectoderm (nervous system, sensory systems and many other tissues), mesoderm (muscles, skeleton, and other tissues), endoderm (respiratory system, digestive system, and other tissues). Early in the third week, a thick linear band called the primitive streak appears along the posterior midline of the embryonic disk. Derived from mesodermal cells, the primitive streak establishes a structural foundation for embryonic morphogenesis along a longitudinal axis. As the primitive streak elongates, a prominent thickening called the primitive node appears at its cranial end, which later gives rise to the mesodermal structures of the head and to a rod of mesodermal cells called the notochord. It is the notochord that forms a midline axis that is the basis for the embryonic skeleton.


Four weeks
The embryo increases about 4 mm (0.16 inches), reaching a length of 0.75 to 1 cm and weighing 400 mg. A connecting stalk, which is later involved in the formation of the umbilical cord, is established from the body of the embryo to the developing placenta. By this time, a rudimentary heart is already pumping blood with a regular rhythm to all parts of the embryo, the head and jaw are apparent, and the primordial tissue that will form the eyes, brain, spinal cord, lungs, and digestive organs has developed.
Lateral wings bend forward, meeting at the center, and will eventually form the body. Head tilts forward and makes up about one third of the entire structure.
The superior and inferior limb buds have the appearance of small swellings on the lateral body walls.


Fifth week
The head enlarges, and the developing eyes, ears, and nasal pit become obvious. The embryo reaches a length of 2.5 cm (1 in) and weighs 20 g.
The heart has a definite septum and valves.
The appendages have formed from the limb buds, and paddle shaped hand and foot plates develop. External genitalia are evident, but gender is not obvious.


Sixth week
The embryo reaches a length of 16 24 mm (0.64 0.96 inches).






The head is larger than the trunk, and the brain has undergone marked differentiation. The limbs lengthen and are slightly flexed.
Considered as the most critical time for the development for many organs.


Seventh and eighth weeks
The embryo reaches a length of 28 40 mm (1.12 1.6 inches).
The body organs are formed, and the nervous system starts to coordinate body activity.
The body systems are developed by the end of the eighth week, and from this time on the embryo is called a fetus.


9 to 12 weeks
By the beginning of the ninth week, the head of the fetus is as large as the rest of the body. Head growth slows during the next three weeks, while lengthening of the body accelerates. Ossification centers appear in most bones during the ninth week.
By the end of the 12th week the fetus is 87 mm (3.5 inches) long and weighs about 45 g (1.6 ounces).
The nervous system and muscle coordination are developed so that the fetus will withdraw its leg if tickled. Some movement is occurring, but it is usually too faint for the mother to feel.
The fetal heart can be heard with an electronic device called a Doppler.


13 to 16 weeks
The facial features of the fetus are well formed.
Epidermal structure such as eyelashes, eyebrows, hair on the head, fingernails, and nipples begin to develop. Liver and pancreatic secretions are present.
Fetus starts to make sucking motions with the mouth. The fetal heartbeat can be detected using a stethoscope.
By the end of the 16th week, the fetus reaches a length of 140 mm (5.5 inches) and weighs 200 g (7 ounces).


17 to 20 weeks
The mother starts to feel fetal movement (quickening).
Development of the fetal position, with the head flexed down and in contact with the flexed knees. A 20 week old fetus is about 119 mm (7.5 inches) long and weighs about 460 g (16 ounces).


21 to 25 weeks
The fetus increases weight substantially to about 900 g (32 ounces). Pupils are reactive to light.
Surfactant, a phospholipid substance essential to lung function, is formed and excreted by cells in the alveoli.


26 to 29 weeks
Toward the end of this stage, the fetus reaches a length of 275 mm (11 inches) and weighs approximately 1300 g (46 ounces). Fetus could possibly be viable if born now and cared for in a neonatal intensive care unit, but the mortality rate is high.
Testes begin descent into the scrotal sac from the lower abdominal cavity if the fetus is male. The brain is rapidly developing.
Eyelids, which fused in the 12th week, start to open.
The fetus rotates to a vertical position in which the head is directed toward the cervix.


30 to 38 weeks
At the end of 38 weeks, the fetus is considered full term.
The fetus reaches a length of 360 mm (14 inches) and weighs about 3400 g (7.5 pounds). Fetus hears sounds and responds with movement.
Soles of the feet have only one or two creases.
The central nervous system has greater control over body functions. Iron stores begin to develop.



Data from Van de Graaff KM, Fox SI: Developmental anatomy and inheritance, in Van de Graaff KM, Fox SI (eds): Concepts of Human Anatomy and Physiology. New York, WCB/McGraw Hill, 1999, pp 954 984.
During the second week of development, the embryoblast becomes completely embedded within the endometrium surface and undergoes marked differentiation, with the appearance of a slit like space called the amniotic cavity between the embryoblast and the invading trophoblast. The



embryoblast flattens into the embryonic disk, which consists of two germ layers: an upper ectoderm, which is closer to the amniotic cavity, and a lower endoderm, which borders the blastocyst cavity (Figure 4 3). A short time later, a third layer called the mesoderm forms between the endoderm and ectoderm. These three primary germ layers give rise to all of the specific tissues and organs in the developing embryo:
 Ectoderm: gives rise to the outer layer of the skin (epidermis) including hair, nails, skin glands, and portions of the sensory organs, as well as the neural crest, and other tissues that eventually form the nervous system. Neurulation, the formation of a neural plate, a thickening of the ectoderm, occurs around week 3. An invagination of the neural plate produces a longitudinal neural grooves, and closure of this groove results in the formation of a neural tube and neural crest:
 Neural tube: gives rise to the brain and spinal cord (central nervous system). By approximately the fourth week, the cranial end of the neural tube expand into three primary brain vesicles (prosencephalon, mesencephalon, and rhombencephalon), which in turn subdivide to form five secondary brain vesicles (telencephalon, diencephalon, mesencephalon, metencephalon, and myelencephalon) (Table 4 2).
 Neural crest: this is sometimes referred to as the fourth germ layer because of its importance. It gives rise to the neurons and glial cells of the sensory, sympathetic, and parasympathetic nervous systems (peripheral nervous system).
 Mesoderm, which eventually forms the skeleton, muscles, blood, reproductive organs, dermis of the skin, and connective tissue. Formation of the notochord from mesoderm during gastrulation results in delineation of the primitive axis of the embryo. The mesoderm on either side of the notochord subdivides into paraxial, intermediate, and lateral columns.
 Paraxial. Further subdivision of the paraxial mesoderm gives rise to somites, from which are formed the bones of the appendicular skeleton as well as the muscles, bones, and connective tissue of the axial skeleton (excluding the skull). Typical somites further differentiate into three components: a superficial posterolateral mass, the dermatome; a deeper posterolateral mass, the myotome; and an anteromedial mass, the sclerotome.2 The dermatomes extend the nisi overlying ectoderm and are destined to become the dermis and hypodermis. Striated, voluntary, skeletal muscle originates from several sources. The axial muscles (the muscles that attach to the head, neck, vertebral column, thorax, abdomen, and pelvis) develop from myotomal mesoderm of the somites. The appendicular muscles (the muscles of the upper and lower extremities) develop from mesenchyme of the limb buds. The mesenchymal cells differentiate into myoblasts, which further develop into muscle fibers and myofilaments.
 Intermediate. This is located between the paraxial mesoderm and the lateral plate and develops into the part of the urogenital system (kidneys and gonads), as well as the reproductive system.
 The lateral plate. This separates into posterior (somatic) and anterior (visceral) layers. Cells from the lateral plate mesoderm and the myotome migrate to the limb field and proliferate to create the limb bud.
 Endoderm, which gives rise to the epithelium lining of the digestive system, the respiratory system, the urinary bladder and urethra, and organs associated with the digestive system, including the liver and pancreas.

FIGURE 4 3


Formation of the primary germ layers (gastrulation)





TABLE 4 2
Derivation and Functions of the Major Brain Structures




Region 
Structure 
Description/Function


Prosencephalon (forebrain)
Telencephalon
Cerebrum
Consists of six paired lobes within two convoluted hemispheres. The outer part of the cerebral hemispheres is called the cerebral cortex. The elevated folds of the convolutions (crests) are called the cerebral gyri, and the depressed grooves (fissures) are the cerebral sulci.




Limbic system
Phylogenetically, the oldest part of the brain. Controls most sensory and motor activities; reasoning, memory, intelligence, etc. Instinctual and limbic functions include basic emotional behavior, such as anger, fear, sex, and hunger.



Diencephalon
Thalamus
The principal function of the thalamus is to act as a relay center for all sensory impulses, except smell, to the cerebral cortex and subcortical regions. Also performs initial autonomic response to pain and crude awareness.




Hypothalamus
Regulation of food and water intake, body temperature, heartbeat, etc.; control of secretory activity in the anterior pituitary; instinctual and limbic functions.




Epithalamus
Production of cerebrospinal fluid by the choroid plexus.





Influence of the circadian rhythm through the release of hormones from the pineal gland.





Integration of olfactory, visceral, and somatic afferent pathways via the habenular nuclei.













Pituitary gland
Regulation of various endocrine functions.


Mesencephalon (midbrain)
Mesencephalon
Corpora quadrigemina
Consists of the superior colliculi (visual reflexes, hand eye coordination) and the inferior colliculi (auditory reflexes).




Cerebral peduncles
Cylindrical structures composed of ascending and descending projection fiber tracts that support and connect the cerebrum to other regions of the brain to allow reflex coordination.




The mesencephalic aqueduct (Sylvius)
Connects the third and fourth ventricle.




Red nucleus
Functions in reflexes concerned with motor coordination and maintenance of posture.




Substantia nigra
Functions to inhibit involuntary movements. It is a major element of the basal ganglia. Degeneration of pigmented neurons in the substantia nigra region is the principal pathology that underlies Parkinson's disease.


Rhombencephalon (hindbrain)
Metencephalon
Pons
Balance and motor coordination
The nuclei of the pons serve a number of important functions:
Some of the nuclei function with nuclei of the medulla oblongata to regulate the rate and depth of breathing.
Several nuclei (tegmentum) within the pons are associated with specific cranial nerves (trigeminal [V], abducens [VI], facial [VII], and vestibulocochlear [VIII]).
The surface fibers extend transversely to connect with the cerebellum through the middle cerebellar peduncles.
Raphe nuclei are involved with pain modulation and the control of arousal.




Cerebellum
The principal functions of the cerebellum include:
Coordination of skeletal muscle contractions by recruiting precise motor units within the muscles, such as accurate force, direction, and extent of movement, and sequencing of movements (neocerebellum).
Equilibrium, and regulation of muscle tone via the flocculonodular lobe and proprioceptive input.
Modification of muscle tone and synergistic actions of muscles.



Myelencephalon
Medulla oblongata
Relay center that connects the spinal cord with the pons; contains many nuclei; visceral autonomic center (e.g., respiration, heart rate, vasoconstriction).
Composed of vital nuclei and white matter that form all of the descending and ascending tracks communicating between the spinal cord and various parts of the brain. Most of the fibers within these tracks cross over (decussate) to the opposite side through the pyramidal region of the medulla oblongata permitting one side of the brain to receive information from, and send information to, the opposite side of the body.



Data from Van de Graaff KM, Fox SI: Central nervous system, in Van de Graaff KM, Fox SI (eds): Concepts of Human Anatomy and Physiology. New York, WCB/McGraw  Hill, 1999, pp 407 446.




FIGURE 4 4


The pharyngeal pouches

Embryonic Period
During this stage of development, which begins around day 16 and extends to the end of week 8, the placenta and other accessory structures develop, and all of the organ systems begin to develop from the three germ layers. The formation of organs and organ systems during this time, which is called organogenesis, requires a precise integration of many developmental processes that involve the coordination of complex genetic and developmental networks, including the provision of:
Nutrients and oxygen through the formation of a vascular connection between the uterus of the mother and the embryo (the placenta and umbilical cord). The blood vessel that will become the heart starts to pulse.
Internal and external structural support for the embryo. In weeks 3 to 4, the embryo grows rapidly and folds around the yolk sac, converting the flat embryonic disk into a somewhat cylindrical form. As the superior and inferior ends curve around the ends of the yolk sac, the embryo becomes T shaped, with the head and tail almost touching (Figure 4 5). Around the fourth week, the head begins to form, quickly followed by the eyes, nose, ears, and mouth.
A protective environment around the embryo (the amniotic sac).



 A structural foundation along a longitudinal axis to allow for morphogenesis the embryo begins to fold on itself in both the sagittal and transverse planes, producing a posterior convexity and an anterior concavity. By about the fifth week, the limb buds begin to direct themselves anteriorly; in addition, the upper limbs externally rotate 90  and the lower limbs internally rotate 90  so that the elbows are directed posteriorly and the knees are projected anteriorly.2

FIGURE 4 5


Embryonic folding

At approximately the 10th week of development, the embryo has all of the basic organs and parts except those of the sex organs.
Fetal Period
Once cell differentiation is mostly complete, the embryo becomes known as a fetus. The primary changes in the fetal period are that the organ systems become functional and the fetus rapidly gains weight and becomes more human looking.1 The early body systems and structures established in the embryonic stage continue to develop, with the limbs growing more rapidly than the trunk. The neural tube develops into the brain and spinal cord, and neurons form. Sex organs begin to appear during the third month of gestation. The heart, which has been beating since the fourth week, now circulates blood and grows stronger. Fingernails, hair, eyelashes, and toenails form.

NORMAL DEVELOPMENT OF MOVEMENT COMPONENTS



Throughout the human body, there are four major types of tissues:
 Epithelial. Covers all internal and external body surfaces and include structures such as the skin and the inner lining of the blood vessels.
 Connective. Connective tissue (CT) is the most abundant, widely distributed, and histologically variable of the primary tissues,3 and one of its variants, fibrous connective tissue, includes bone, cartilage, tendons, ligaments, and blood tissue. CT provides protection, movement, and structural and metabolic support for other tissues and organs of the body.
 Nervous. Nervous tissue provides communication between the central nervous system (the brain and spinal cord), the peripheral nervous system, muscles, organs, and various other systems.
 Muscle. Muscles are classified functionally as either voluntary or involuntary, and structurally as either smooth, striated (skeletal). or cardiac. There are approximately 430 skeletal muscles in the body, each of which can be considered anatomically as a separate organ. Of these 430 muscles, about 75 pairs provide the majority of body movements and postures.4
Neuromusculoskeletal structures, which interact together to produce movement, include the nervous, connective, and skeletal muscle tissues.
Connective Tissue
Connective tissue (CT) is divided into subtypes according to the matrix that binds the cells. CT proper has a loose flexible matrix, called ground substance. The most common cell within CT proper is the fibroblast. Three types of protein fibers are found in fibrous connective tissue: collagenous, reticular, and elastic fibers.
 Collagenous fibers. Collagen is the body's most abundant protein.3 The collagens are a family of extracellular matrix (ECM) proteins that play a dominant role in maintaining the structural integrity of various tissues and in providing tensile strength to tissues.
 Reticular fibers. These fibers form a spongelike framework for such organs as the spleen and lymph nodes.3
 Elastic fibers. Elastic fibers are composed of a protein called elastin. As its name suggests, elastin provides elastic properties to the tissues in which it is situated.5 Elastin fibers can stretch, but they normally return to their original shape when the tension is released. Thus, elastic fibers of elastin determine the patterns of distention and recoil in most structures.
Fibrous connective tissue is divided into two broad categories according to the relative abundance of fiber: loose and dense CT. The various anatomic and functional characteristics of loose and dense collagen are summarized in Table 4 3. Collagenous and elastic fibers are sparse and irregularly arranged in loose CT but are tightly packed in dense CT.6 Bundles of collagen and elastin combine to form a matrix of CT fascicles. This matrix is organized within the primary collagen bundles as well as between the bundles that surround them.7



TABLE 4 3
Loose and Dense Collagen 

Joint Type 
Anatomic Location
Fibers 
Mechanical Specialization
Dense irregular connective tissue (CT)
Composes the external fibrous layer of the joint capsule; forms ligaments, bone, aponeuroses, and tendons
Parallel, tightly aligned fibers
Ligament: binds bones together and restrains unwanted movement at the joints; resists tension in several directions
Tendon: attaches muscle to bone
Loose irregular connective tissue
Found in capsules, muscles, nerves, fascia, and skin
Random fiber orientation
Provides structural support


The various types of fibrous CT as relates to the musculoskeletal system are described as follows.
Fascia 

Fascia is viewed as a loose CT that provides support and protection to the joint, and acts as an interconnection between tendons, aponeuroses, ligaments, capsules, nerves, and the intrinsic components of muscle.8,9
Tendons

The function of a tendon is to attach a muscle to a bone at each end of the muscle, and, when stretched, store elastic energy that contribute to movement.10 In addition, tendons enable the muscle belly to be an optimal distance from the joint on which it is acting. Tendons are primarily composed of collagen, proteoglycans, cells, and water.10 The collagen fibers of tendons are arranged in a quarter stagger arrangement, which gives the tendon a characteristic banding pattern and provides high strength and stability.11 A loose CT matrix surrounds the bundles of collagen fibrils. The thickness of each tendon varies and is proportional to the size of the muscle from which it originates. Tendons display viscoelastic mechanical properties that confer time  and rate dependent effects on the tissue. Specifically, tendons are more elastic at lower strain rates and stiffer at higher rates of tensile loading. Tendons deform less than ligaments under an applied load and are able to transmit the load from muscle to bone.7 As with all CT, tendons have a positive adaptive response to repeated physiologic mechanical loading, which results in biologic and mechanical changes.
Although tendons withstand strong tensile forces well, they resist shear forces less well and provide little resistance to compression force.7 A tendon can be divided into three main sections10:
 The bone tendon junction. At most bone tendon interfaces, the collagen fibers insert directly into the bone, in a gradual transition of material
composition. The physical junction of tendon and bone is referred to as an enthesis12 and is an interface that is vulnerable to acute and chronic injury.13 One role of the enthesis is to absorb and distribute the stress concentration that occurs at the junction over a broader area.
 The tendon midsubstance. Overuse tendon injuries can occur in the midsubstance of the tendon, but not as frequently as at the enthesis.
 The musculotendinous junction (MTJ). The MTJ is the site where the muscle and tendon meet. The MTJ comprises numerous interdigitations between muscle cells and tendon tissue, resembling interlocked fingers. Despite its viscoelastic mechanical characteristics, the MTJ is very vulnerable to tensile failure.14,15





Ligaments

Skeletal ligaments are fibrous bands of dense CT that connect bones across joints. Ligaments can be named for the bones into which they insert (coracohumeral), their shape (deltoid), or their relationships to each other (cruciate).20 The gross structure of a ligament varies according to location (e.g., intra articular or extra articular, or capsular) and function.21 The collagen in ligaments has a less unidirectional organization than it does in tendons, but its structural framework still provides stiffness (resistance to deformation).22 Small amounts of elastin are present in ligaments, with the exception of the ligamentum flavum and the nuchal ligament of the spine, which contain more. The cellular organization of ligaments makes them ideal for sustaining tensile load, with many containing functional subunits that are capable of tightening or loosening in different joint positions.23 At the microscopic level, closely spaced collagen fibers (fascicles) are aligned along the long axis of the ligament and are arranged into a series of bundles.20 Ligaments contribute to the stability of joint function by preventing excessive motion,24 acting as guides or checkreins to direct motion, and providing proprioceptive information for joint function through sensory nerve endings and the attachments of the ligament to the joint capsule.25, 26 and 27 Many ligaments share functions. For example, although the anterior cruciate ligament of the knee is considered the primary restraint to anterior translation of the tibia relative to the femur, the medial and lateral collateral ligaments together with the posterior capsule of the knee also help in this function.20 The vascular and nerve distribution to ligaments is not homogenous. For example, the middle of the ligament is typically avascular, whereas the proximal and distal ends enjoy a rich blood supply. Similarly, the insertional ends of the ligaments are more highly innervated than the midsubstance.
Cartilage 

Cartilage is a relatively stiff CT with a semisolid, flexible. Cartilage tissue exists in three forms: hyaline, elastic, and fibrocartilage.
 Hyaline cartilage, also referred to as articular cartilage, covers the ends of long bones and permits almost frictionless motion to occur between the articular surfaces of a synovial joint.28 The various types of joints, and their classifications, are outlined in Table 4 4. Articular cartilage is a highly organized viscoelastic material composed of cartilage cells called chondrocytes, water, and an ECM. Articular cartilage, the most abundant cartilage within the body, is devoid of any blood vessels, lymphatics, and nerves.29,30 Most of the bones of the body form first as hyaline cartilage, and later become proper bone in a process called endochondral ossification (see Bone). The normal thickness of articular cartilage is determined by the contact pressures across the joint the higher the peak pressures, the thicker the cartilage.21 Articular cartilage functions to distribute the joint forces over a large contact area, dissipating the forces associated with the load. This distribution of forces allows the articular cartilage to remain healthy and fully functional throughout decades of life. The patella has the thickest articular cartilage in the body.
Articular cartilage may be grossly subdivided into four distinct zones with differing cellular morphology, biomechanical composition, collagen orientations, and structural properties, as follows:
The superficial zone. The superficial zone, which lies adjacent to the joint cavity, comprises approximately 10 to 20% of the articular cartilage thickness and functions to protect deeper layers from shear stresses. The collagen fibers within this zone are packed tightly and aligned parallel to the articular surface. This zone is in contact with synovial fluid and is responsible for most of the tensile properties of cartilage.
The middle (transitional) zone. In the middle zone, which provides an anatomic and functional bridge between the superficial and deep zones, the collagen fibril orientation is obliquely organized. This zone comprises 50% of the total cartilage volume. Functionally, the middle zone is the first line of resistance to compressive forces.



 The deep or radial layer. The deep layer comprises 30% of the matrix volume. It is characterized by radially aligned collagen fibers that are perpendicular to the surface of the joint and which have a high proteoglycan content. Functionally, the deep zone is responsible for providing the greatest resistance to compressive forces.
 The tidemark. The tidemark distinguishes the deep zone from the calcified cartilage, the area that prevents the diffusion of nutrients from the bone tissue into the cartilage.
Elastic cartilage is a very specialized CT, primarily found in locations such as the outer ear and portions of the larynx.
Fibrocartilage functions as a shock absorber in both weight bearing and non weight bearing joints. Its large fiber content, reinforced with numerous collagen fibers, makes it ideal for bearing large stresses in all directions. Fibrocartilage is an avascular, alymphatic, and aneural tissue and derives its nutrition by a double diffusion system.33 Examples of fibrocartilage include the symphysis pubis, the intervertebral disks, and the menisci of the knee.




TABLE 4 4
The Classification of Joints

Major Type of Joint 
Other Name(s)

Description

Example 
Bony
Synostosis
An immobile joint formed when the gap between two bones ossifies and they become, in effect, a single bone. A bony joint can form by ossification of either fibrous or cartilaginous joints.
The attachment of the first rib to the sternum, and the epiphysis and diaphysis of long bones with maturation
Fibrous
Synarthrosis
A point at which adjacent bones are bound by collagen fibers that emerge from the matrix of one bone, cross the space between them, and penetrate into the matrix of the other. Three types are recognized: sutures, gomphosis, and syndesmosis.
Suture: bind the bones of the skull to each other
Gomphosis: a tooth socket Syndesmosis: the interosseous membrane between the radius and ulna
Cartilaginous
Amphiarthrosis
Occur when two bones are linked by either hyaline cartilage (synchondroses) or fibrocartilage (symphyses).
Synchondroses: the epiphyseal plate of a long bone in a child Symphysis: the pubic symphysis
Synovial
Diarthrosis
The facing surfaces of two bones are covered with articular cartilage and are lubricated by synovial fluid. Synovial joints can be classified as ball and socket, condylar, saddle, plane, hinge, or pivot.
Ball and socket: shoulder, hip Condylar: radiocarpal
Saddle: trapeziometacarpal joint Plane: carpal bones of the wrist Hinge: elbow, knee, and interphalangeal joints
Pivot: Atlantoaxial joint


Data from Saladin, KS: Joints, in Human Anatomy. New York, McGraw Hill, 2012, pp 204 234.


Bone 

The function of bone is to provide support, enhance leverage, protect vital structures, provide attachments for both tendons and ligaments, and store minerals, particularly calcium. Bones also may serve as useful landmarks during the palpation phase of the examination. Bone is a highly vascular form of CT, composed of collagen, calcium phosphate, water, amorphous proteins, and cells. It is the most rigid of the CTs because of its calcified matrix.
Despite its rigidity, bone is a dynamic tissue that undergoes constant metabolism and remodeling. Normal, healthy bone will deform under moderate load, returning to the original position once the loads have been removed. It is the different physical characteristics of bone, as well as variables related to the type of imposed loads, that determine a bone's exact response to loading. The collagen of bone is produced in the same manner as that of ligament and tendon, but by a different cell, the osteoblast.6 At the gross anatomic level, each bone has a distinct morphology comprising both cortical bone and cancellous bone.
 Cortical bone is found in the outer shell.
 Cancellous bone is found within the epiphyseal and metaphyseal regions of long bones as well as throughout the interior of short bones.14 The development of bone occurs in one of two ways:



 Intramembranous ossification. Mesenchymal stem cells within mesenchyme or the medullary cavity of a bone initiate the process of intramembranous ossification. This type of ossification occurs in the flat bones of the cranium and facial bones and, in part, in the ribs, clavicle, and mandible.
 Endochondral ossification. The first site of ossification occurs in the primary center of ossification, which is in the middle of the diaphysis (shaft). About the time of birth, a secondary ossification center appears in each epiphysis (end) of long bones. Between the bone formed by the primary and secondary ossification centers, cartilage persists as the epiphyseal (growth) plate between the diaphysis and the epiphysis of a long bone.
This type of ossification occurs in the long and short bones of the appendicular and axial bones.
The periosteum is formed when the perichondrium that surrounds the cartilage develops into the periosteum. Chondrocytes in the primary center of ossification begin to grow (hypertrophy) and begin secreting alkaline phosphatase, an enzyme essential for mineral deposition. Calcification of the matrix follows, and apoptosis of the hypertrophic chondrocytes occurs. This creates cavities within the bone. The exact mechanism of chondrocyte hypertrophy and apoptosis is currently unknown. The hypertrophic chondrocytes (before apoptosis) also secrete a substance called vascular endothelial cell growth factor that induces the sprouting of blood vessels from the perichondrium. Blood vessels forming the periosteal bud invade the cavity left by the chondrocytes and branch in opposite directions along the length of the shaft. The blood vessels carry osteoprogenitor cells and hematopoietic cells inside the cavity, the latter of which later form the bone marrow. Osteoblasts, differentiated from the osteoprogenitor cells that enter the cavity via the periosteal bud, use the calcified matrix as a scaffold and begin to secrete osteoid, which forms the bone trabecula. Osteoclasts, formed from macrophages, break down the spongy bone to form the medullary cavity (bone marrow). The strength of a bone is related directly to its density. Of importance to the clinician, is the difference between maturing bone and mature bone. The epiphyseal plate or growth plate of a maturing bone can be divided into four distinct zones34:
 Reserve zone: produces and stores matrix.
 Proliferative zone: produces matrix and is the site for longitudinal bone cell growth.
 Hypertrophic zone: subdivided into the maturation zone, degenerative zone, and zone of provisional calcification. It is within the hypertrophic zone that the matrix is prepared for calcification, and is here that the matrix is ultimately calcified. The hypertrophic zone is the most susceptible of the zones to injury because of the low volume of bone matrix and the high amounts of developing immature cells in this region.35
 Bone metaphysis: the part of the bone that grows during childhood.
Nervous Tissue
The development and maturation of the nervous system have the most significant impact on the development of movement. The greatest rate of growth of the brain occurs at birth, and rapid growth occurs during the first six months of life. In utero movements begin as stereotypical movements involving simple flexion extension motions, which then become goal directed during the first 6 to 10 months of life. When movements become goal directed, it is critical that a normal sensorimotor system be in place so that these movements can become refined.
The nerve cell, or neuron, which serves to store and process information, is the functional unit of the nervous system. The other cellular constituent is the neuroglial cell, or glia, which function to provide structural and metabolic support for the neurons.36
Although neurons come in a variety of sizes and shapes, there are four functional parts to each nerve fiber (Figure 4 6):
 Dendrite. Dendrites serve a receptive function and receive information from other nerve cells or the environment.
 Axon. The axon cylinder, in which there is a bi directional flow of axoplasm, conducts information and nutrition to other nerve cells and the tissues that the nerve innervates. Many axons are covered by myelin, a lipid rich membrane. In myelinated fibers, there is a direct proportional relationship between fiber diameter and conduction velocity.37 This membrane is divided into segments about 1 mm long by small gaps, called nodes of Ranvier, where the myelin is absent.38 Myelin has a high electrical resistance and low capacitance and serves to increase the nerve conduction velocity of neural transmissions through a process called salutatory conduction.
 Cell body. The cell body contains the nucleus of the cell and has important integrative functions.



 Axon terminal. The axon terminal is the transmission site for action potentials, the messengers of the nerve cell.

FIGURE 4 6


Schematic drawing of a neuron

The communication of information from one nerve cell to another occurs at junctions called synapses, where a chemical is released in the form of a neurotransmitter. A difference in concentration of potassium, sodium, and chloride ions exists across the cell membrane. These ions can selectively permeate ion channels in the membrane so that an unequal distribution of net charge occurs. The resting membrane potential results from an internal negativity resulting from the active transport of sodium from inside to outside the cell, and potassium from outside to inside the cell.37
The central nervous system (CNS) consists of the brain and an elongated spinal cord. The spinal cord participates directly in the control of body movements, the processing and transmission of sensory information from the trunk and limbs, and the regulation of visceral functions.39 The spinal cord also provides a conduit for the two way transmission of messages between the brain and the body. These messages travel along pathways, or tracts, that are fiber bundles of similar groups of neurons. Tracts may descend or ascend.
The spinal cord has an external segmental organization. Each of the 31 pairs of spinal nerves that arise from the spinal cord has an anterior (ventral) root and a posterior (dorsal) root, with each root made up of one to eight rootlets and consisting of bundles of nerve fibers.38 In the posterior (dorsal) root of a typical spinal nerve lies a spinal (sensory) ganglion (posterior [dorsal] root ganglion), a swelling that contains nerve cell bodies.
Three membranes, or meninges, envelop the structures of the CNS: dura mater, arachnoid, and pia mater. The meninges and related spaces are important to both the nutrition and the protection of the spinal cord. The cerebrospinal fluid that flows through the meningeal spaces, and within the ventricles of the brain, provides a cushion for the spinal cord. The meninges also form barriers that resist the entrance of a variety of noxious organisms.



The peripheral nervous system consists of the cranial nerves (with the exception of cranial nerve II the optic nerve) and the spinal nerves. Cranial nerves (CNs), of which there are traditionally 12 pairs, emerge directly from the brain, whereas spinal nerves emerge from segments of the spinal cord. As a simplistic description, cranial nerves bring information from the sense organs to the brain, control some muscles, or help control the function of glands or internal organs such as the heart and lungs. The term spinal nerve generally refers to a mixed spinal nerve, which carries motor, sensory, and autonomic signals between the spinal cord and the body. Each spinal nerve is formed by the combination of nerve fibers from the anterior and posterior roots of the spinal cord. The anterior roots carry efferent motor axons, whereas the posterior roots carry afferent sensory axons.
Feedback Receptors

All synovial joints of the body are provided with an array of receptor endings (nociceptors, thermoreceptors, and mechanoreceptors) embedded in articular, muscular, and cutaneous structures with varying characteristic behaviors and distributions (Table 4 5). These receptors provide information for the somatosensory system, which mediates signals related to multiple sensory modalities (pain, temperature, and proprioception). The nociceptors provide information with regard to pain, whereas the thermoreceptors provide feedback related to temperature. The mechanoreceptors, which are stimulated by mechanical forces (soft tissue elongation, relaxation, compression, and fluid tension), are usually classified into three groups based on receptor type: joint, muscle, or cutaneous. There are four primary types of joint receptors that include Pacinian corpuscles, Ruffini endings, Golgi tendon organ (GTO) like endings, and bare nerve endings.40, 41 and 42
TABLE 4 5
Classification of Afferent, Cutaneous, and Efferents

Type 
Conduction Velocity (m/s)
Function 
Afferents 
I
70 120
Provide input from muscle and tendon receptors
II
36 72
Afferents from muscle spindles
III
27 68
Pressure/nociceptive afferents from joints and aponeuroses
IV
1 4
Pain
Cutaneous 
A? , ?
30 70
Tactile receptors
A?
12 30
Cold; fast nociception
C
0.5 1.0
Warmth; tissue damage nociception
Efferents
a
60 100
Extrafusal muscle fibers
Y
10 30
Intrafusal muscle fibers
B
3 30
Preganglionic autonomic
C
0.5 2.0
Postganglionic autonomic






Box 4 1: Muscle Spindle and Golgi Tendon Organ

Muscle Spindle
Muscle spindles are encapsulated spindle shaped structures lying in parallel with skeletal muscle fibers in the muscle belly. Essentially, the purpose of the muscle spindle is to compare the length of the spindle with the length of the muscle that surrounds the spindle. Spindles have three main components1:
Intrafusal muscle fibers. 2 12 long, slender, and specialized skeletal muscle fibers. The central portion of the intrafusal fiber is devoid of actin or myosin and thus is incapable of contracting. As a result, these fibers are capable of putting tension on the spindle only. These intrafusal fibers are of two types: nuclear bag fibers and nuclear chain fibers. Nuclear bag fibers primarily serve as sensitivity meters for the changing lengths of the muscle.2,3 Nuclear chain fibers each contain a single row or chain of nuclei and are attached at their ends to the bag fibers.
Sensory neuron endings that wrap around the intrafusal fibers. The sensory neurons are afferent structures (groups Ia and II afferents) that send information regarding static muscle length and changes in muscle length to the posterior root ganglia of the spinal cord. The group Ia afferents relay information regarding rates of change, whereas the group II afferents relay information regarding steady state muscle length.
Motor axons. Whereas muscles are innervated by alpha motor neurons, muscle spindles have their own motor supply, namely gamma motor neurons.
The muscle spindle can be stimulated in two different ways:
By stretching the whole muscle, which stretches the mid portion of the spindle and depolarizes the Ia afferents. Ia afferents depolarization can trigger two separate responses1:
1. A monosynaptic or disynaptic spinal reflex
2. A long loop transcortical reflex
By contracting only the end portion of the intrafusal fibers, exciting the receptor (even if muscle length does not change).
If the length of the muscles surrounding the spindle is less than that of the spindle, a decrease in intrafusal fiber afferent activity occurs. For example, a quick stretch applied to a muscle reflexively produces a quick contraction of the agonistic and synergistic muscle (extrafusal) fibers. This has the effect of producing a smooth contraction and relaxation of muscle and eliminating any jerkiness during movement. The firing of the type Ia phasic nerve fibers is influenced by the rate of stretch: the faster and greater the stimulus, the greater the effect of the associated extrafusal fibers.6,4
Golgi Tendon Organs
Golgi tendon organs (GTOs) are small, encapsulated structures spaced in series along the musculotendinous junction that become activated by stretch.1 In contrast to the muscle spindle, GTOs function to protect muscle attachments from strain or avulsion, by using a postsynaptic inhibitory synapse of the muscle in which they are located.5 The signals from the GTO may go both to local areas within the spinal cord and through the



 Ruffini endings. These slow adapting, low threshold stretch receptors are important postural mediators, signaling actual joint position or changes in joint positions.47 They are primarily located on the flexion side (detect the stretch with extension of the joint) of the joint capsule, but are also found in ligaments, primarily near the origin and insertion.48,49 These slowly adapting receptors continue to discharge while the stimulus is present and contribute to reflex regulation of postural tone, to coordination of muscle activity, and to a perceptional awareness of joint position. An increase in joint capsule tension by active or passive motion, posture, mobilization, or manipulation causes these receptors to discharge at a higher frequency.42,50
 Pacinian corpuscles. These rapidly adapting, low threshold receptors function primarily in sensing joint compression and increased hydrostatic pressure in the joint.51 They are primarily located in the subcapsular fibroadipose tissue, the cruciate ligaments, the annulus fibrosis, and the fibrous capsule. These receptors are entirely inactive in immobile joints but become active for brief periods at the onset of movement and during rapid changes in tension. They also fire during active or passive motion of a joint, or with the application of traction. This behavior suggests their role as a control mechanism to regulate motor unit activity of the prime movers of the joint.
 Golgi tendon organ like receptors. These receptors, also referred to as Golgi ligament organs (Box 4 1), are found in the joint capsule, ligaments, and menisci.52 These slow adapting and high threshold receptors function to detect large amounts of tension. They only become active in the extremes of motion such as when strong manual techniques are applied to the joint. Their function is protective to prevent further motion that would over displace the joint (a joint protective reflex) and their firing is inhibitory to those muscles that would contribute to excessive forces.
 Bare nerve endings. These high threshold, nonadapting, free nerve ending receptors are inactive in normal circumstances but become active with marked mechanical deformation or tension.53,54 They may also become active in response to direct mechanical or chemical irritation, and their sensitivity usually increases when joints are inflamed or swollen.55
Structurally, the CNS is organized in a hierarchical and parallel fashion, with the most complex processing located in the cortical centers of the brain and the most basic processing located in the spinal cord.48 At the upper end of the hierarchy, the motor cortex has a motor program, defined as an abstract plan of movement that, when initiated, results in the production of a coordinated movement sequence.56,57 At the lower end of the hierarchy, specific motor units must contract to accomplish the movement. Rapid motor responses to somatosensory feedback mediated in the spinal cord are referred to as spinal reflexes.48 These reflex actions include preparatory postural adjustments58 and reaction movements. Although the hierarchy is well established, research suggests that these components also work in parallel so that any of the components may predominate in controlling some aspects of movement; the system is built for efficiency and redundancy (see normal Development of Motor Control and Motor Learning).56
Skeletal Muscle
The microstructure and composition of skeletal muscle have been studied extensively. The class of tissue labeled skeletal muscle consists of individual muscle cells or fibers that work together to produce the movement of bony levers. A single muscle cell is called a muscle fiber or myofiber. Individual muscle fibers are wrapped in a CT envelope called endomysium. Bundles of myofibers, which form a whole muscle (fasciculus), are encased in the
 perimysium. The perimysium is continuous with the deep fascia. Groups of fasciculi are surrounded by a connective sheath called the epimysium.	



Under an electron microscope, it can be seen that each of the myofibers consists of thousands of myofibrils, which extend throughout its length. Myofibrils are composed of sarcomeres arranged in series.59 All skeletal muscles exhibit four characteristics60:
1. Excitability, the ability to respond to stimulation from the nervous system
2. Elasticity, the ability to change in length or stretch
3. Extensibility, the ability to shorten and return to normal length
4. Contractility, the ability to shorten and contract in response to some neural command. The tension developed in skeletal muscle can occur passively (stretch) or actively (contraction). When an activated muscle develops tension, the amount of tension present is constant throughout the length of the muscle, in the tendons, and at the sites of the musculotendinous attachments to bone.1 The tensile force produced by the muscle pulls on the attached bones and creates torque at the joints crossed by the muscle. The magnitude of the tensile force is dependent on a number of factors.
One of the most important roles of fibrous CT is to mechanically transmit the forces generated by the skeletal muscle cells to provide movement. Each of the myofibrils contains many fibers called myofilaments, which run parallel to the myofibril axis. The myofilaments are made up of two different proteins: actin (thin myofilaments) and myosin (thick myofilaments), which give skeletal muscle fibers their striated (striped) appearance.59

The striations are produced by alternating dark (A) and light (I) bands that appear to span the width of the muscle fiber. The A bands are composed of myosin filaments, whereas the I bands are composed of actin filaments. The actin filaments of the I band overlap into the A band, giving the edges of the A band a darker appearance than the central region (H band), which contains only myosin. At the center of each I band is a thin, dark Z line. A sarcomere represents the distance between each Z line. Each muscle fiber is limited by a cell membrane called a sarcolemma. The protein dystrophin plays an essential role in the mechanical strength and stability of the sarcolemma.61 Dystrophin is lacking in patients with Duchenne muscular dystrophy.

Structures called cross bridges serve to connect the actin and myosin filaments. The myosin filaments contain two flexible, hinge like regions, which allow the cross bridges to attach and detach from the actin filament. During contraction, the cross bridges attach and undergo power strokes, which provide the contractile force. During relaxation, the cross bridges detach. This attaching and detaching is asynchronous, so that some are attaching while others are detaching. Thus, at each moment, some of the cross bridges are pulling, while others are releasing.
The regulation of cross bridge attachment and detachment is a function of two proteins found in the actin filaments: tropomyosin and troponin (Figure 4 7). Tropomyosin attaches directly to the actin filament, whereas troponin is attached to the tropomyosin rather than directly to the actin filament.

FIGURE 4 7



Troponin and tropomyosin



The Motor Unit

Each muscle fiber is innervated by a somatic motor neuron. One neuron and the muscle fibers it innervates constitute a motor unit, or functional unit of the muscle. Each motor neuron branches as it enters the muscle to innervate a number of muscle fibers.

The release of a chemical called acetylcholine from the axon terminals at the neuromuscular junction (NMJ) causes electrical activation of the skeletal muscle fibers. When an action potential propagates into the transverse tubule system (narrow membranous tunnels formed from and continuous with the sarcolemma), the voltage sensors on the transverse tubule membrane signal the release of Ca2+ from the terminal cisternae portion of the sarcoplasmic reticulum (SR; a series of interconnected sacs and tubes that surround each myofibril).62 The released Ca2+ then diffuses into the sarcomeres and binds to troponin, displacing the tropomyosin, and allowing the actin to bind with the myosin cross bridges (see Figure 4 7).
Whenever a somatic motor neuron is activated, all of the muscle fibers that it innervates are stimulated and contract with all or none twitches.
Although the muscle fibers produce all or none contractions, muscles are capable of a wide variety of responses, ranging from activities requiring a high level of precision, to activities requiring high tension.




At the end of the contraction (the neural activity and action potentials cease), the SR actively accumulates Ca2+ and muscle relaxation occurs. The return of Ca2+ to the SR involves active transport, requiring the degradation of adenosine triphosphate (ATP) to adenosine diphosphate. (ADP*).62 Because SR function is closely associated with both contraction and relaxation, changes in its ability to release or sequester Ca2+ markedly affect both the time course and magnitude of force output by the muscle fiber.63

*The most readily available energy for skeletal muscle cells is stored in the form of ATP and phosphocreatine (PCr). Through the activity of the enzyme ATPase, ATP promptly releases energy when required by the cell to perform any type of work, whether it is electrical, chemical, or mechanical.
Muscle Fibers

On the basis of their contractile properties, two major types of muscle fiber have been recognized within skeletal muscle: type I (slow twitch fibers), and type II (fast twitch fibers) (Table 4 6).64 Slow twitch fibers are richly endowed with mitochondria and have a high capacity for oxygen uptake. They are, therefore, suitable for activities of long duration or endurance, including the maintenance of posture. In contrast, fast twitch fibers are suited to quick, explosive actions, including such activities as sprinting. A number of muscle subtypes have been recognized based on their qualities and aerobic to anaerobic capabilities.
TABLE 4 6
Comparison of Muscle Fiber Types

Characteristics
Type I
Type IIA 
Type IIAB 
Type IIB 
Size (diameter)
Small
Intermediate
Large
Very large
Resistance to fatigue
High
Fairly high
Intermediate
Low
Glycogen content
Low
Intermediate
High
High
Twitch rate
Slow
Fast
Fast
Fast
Myosin ATPase content
Low
High
High
High
Major storage fuel
Triglycerides
Creatine phosphate Glycogen
Creatine phosphate Glycogen
Creatine phosphate Glycogen


ATP, Adenosine triphosphate.
Type A: possess good aerobic and anaerobic characteristics



 Type B: possess fair aerobic and poor anaerobic characteristics
 Type AB: possess aerobic and anaerobic characteristics somewhere between types A and B
Based on the above, four fiber types can be distinguished: I, IIA, IIB, and IIAB.65 The type II (fast twitch) fibers are separated based on mitochondria content into those that have a high complement of mitochondria (type IIA) and those that are mitochondria poor (type IIB). Type IIAB fibers exhibit structural features of both red and white fibers and thus have fast contraction times and good fatigue resistance. Within this list, there appears to be a consistent order of recruitment based on fiber size: type I fibers first, followed by IIA, IIAB, and, finally, IIB fibers.65 The smaller type I fibers are the easiest to stimulate as they have the smaller motor units.

Theory dictates that a muscle with a large percentage of the total cross sectional area occupied by slow twitch type I fibers should be more fatigue resistant than one in which the fast twitch type II fibers predominate.
Different activities place differing demands on a muscle (Table 4 7).66 For example, movement activities involve a predominance of fast twitch fiber recruitment, whereas postural activities and those activities requiring stabilization entail more involvement of the slow twitch fibers. In humans, most limb muscles contain a relatively equal distribution of each muscle fiber type, whereas the back and trunk demonstrate a predominance of slow twitch fibers. Although it would seem possible that physical training may cause fibers to convert from slow twitch to fast twitch or the reverse, this has not been shown to be the case.67 However, fiber conversion from type IIB to type IIAB and IIA, and vice versa, has been found to occur with training.68



TABLE 4 7
Functional Division of Muscle Groups

Movement Group 
Stabilization Group
Primarily type IIA
Primarily type I
Prone to develop tightness
Prone to develop weakness
Prone to develop hypertonicity
Prone to muscle inhibition
Dominate in fatigue and new movement situations
Fatigue easily
Generally cross two joints
Primarily cross one joint
Examples 
Examples 
Gastrocnemius/Soleus
Peronei
Tibialis posterior
Tibialis anterior
Short hip adductors
Vastus medialis and lateralis
Hamstrings
Gluteus maximus, medius, and minimus
Rectus femoris
Serratus anterior
Tensor fascia lata
Rhomboids
Erector spinae
Lower portion of trapezius
Quadratus lumborum
Short/deep cervical flexors
Pectoralis major
Upper limb extensors
Upper portion of trapezius
Rectus abdominis
Levator scapulae

Sternocleidomastoid

Scalenes

Upper limb flexors



Data from Jull GA, Janda V: Muscle and motor control in low back pain, in Twomey LT, Taylor JR (eds), Physical Therapy of the Low Back: Clinics in Physical Therapy. New York, Churchill Livingstone, 1987, p 258.
The effectiveness of a muscle in producing movement depends on a number of factors. These include the location and orientation of the muscle attachment relative to the joint, the tightness or laxity present in the musculotendinous unit, the type of contraction, the point of application, and the actions of other muscles that cross the joint.4

Types of Muscle Contractions



As previously mentioned, depending on the type of muscular contraction, the length of a muscle can remain the same (isometric), shorten (concentric), or lengthen (eccentric). The rate of muscle shortening or lengthening substantially affects the force that a muscle can develop during contraction.
 Shortening contractions. As the speed of a muscle shortening increases, the force it is capable of producing decreases.72,73 The slower rate of shortening is thought to produce greater forces than can be produced by increasing the number of cross bridges formed. This relationship can be viewed as a continuum, with the optimum velocity for the muscle somewhere between the slowest and fastest rates. At very slow speeds, the force that a muscle can resist or overcome rises rapidly up to 50% greater than the maximum isometric contraction.72,73
 Lengthening contractions. The following changes in force production occur during an eccentric contraction:
 Rapid lengthening contractions generate more force than do slow ones (slower lengthening contractions).

The force and speed of a muscle contraction are based on the requirements of an activity and are dependent on the ability of the central nervous system to control the recruitment of motor units.4 The motor units of slow twitch fibers generally have lower thresholds and are relatively easier to activate than those of the fast twitch motor units. Consequently, the slow twitch fibers are the first to be recruited, even when the resulting limb movement is rapid.79
As the force requirement, speed requirement, or duration of an activity increases, motor units with higher thresholds are recruited. Type IIA units are recruited before type IIB.80


Force Production

Although each muscle contains the contractile machinery to produce the forces for movement, it is the tendon that transmits these forces to the bones



in order to achieve movement or stability of the body in space.7 The angle of insertion the tendon makes with a bone determines the line of pull, whereas the tension generated by a muscle is a function of its angle of insertion. A muscle generates the greatest amount of torque when its line of pull is oriented at a 90 degree angle to the bone, and it is attached anatomically as far from the joint center as possible.4
Just as there are optimal speeds of length change, and optimal muscle lengths, there are optimal insertion angles for each of the muscles. The angle of insertion of a muscle, and therefore its line of pull, can change during dynamic movements.78 The angle of pennation is the angle created between the fiber direction and the line of pull. When the fibers of a muscle lie parallel to the long axis of the muscle, there is no angle of pennation. The number of fibers within a fixed volume of muscle increases with the angle of pennation.78 Although maximum tension can be improved with pennation, the range of shortening of the muscle is reduced. Muscle fibers can contract to about 60% of their resting length. Because the muscle fibers in pennate muscles are shorter than the nonpennate equivalent, the amount of contraction is similarly reduced. Muscles that need to have large changes in length without the need for very high tension, such as the sartorius, do not have pennate muscle fibers.78 In contrast, pennate muscle fibers are found in those muscles in which the emphasis is on a high capacity for tension generation rather than range of motion (e.g., gluteus maximus).

Cardiovascular System
The heart is a hollow, muscular organ that functions to pump blood around the body through the blood vessels using repeated, rhythmic contractions. The human heart (Latin cor) is derived embryologically from mesoderm that forms the heart tube. The muscle tissue of the heart is composed of muscle fibers called myocardium.

Cardiac muscle fibers have numerous mitochondria, exhibit rhythmicity of contraction, and can work continuously without fatigue.

The heart consists of four chambers, the two upper atria (singular: atrium) and the two lower ventricles. Blood is pumped through the heart chambers aided by four heart valves.




Right Atrium

The right atrium (RA) receives blood from the systemic circulation via the superior vena cava, which drains the upper part of the body, and the inferior vena cava, which drains the lower part of the body. The coronary sinus is an additional venous return into the right atrium, receiving blood from the heart itself. Blood passes from the right atrium into the right ventricle via the right atrioventricular (AV) valve (also known as the tricuspid valve, because it is formed of three triangular leaflets or cusps).

Right Ventricle

The right ventricle (RV) receives blood from the RA. The ventricular contraction causes the right AV valve to close and the oxygen depleted blood to leave the RV via the pulmonary trunk to the lungs. The blood then enters the capillaries of the right and left pulmonary arteries, where gaseous exchange takes place and the blood releases carbon dioxide into the lung cavity and picks up oxygen. The oxygenated blood then flows through pulmonary veins to the left atrium.

Left Atrium

The left atrium (LA) receives the oxygenated blood from the lungs via four pulmonary veins (two left and two right pulmonary veins). From the LA the blood passes through the mitral (bicuspid) valve to enter the left ventricle.

Left Ventricle

The left ventricle (LV), which forms most of the diaphragmatic side of the heart, receives blood from the LA. The left ventricle is longer and more conical in shape than the right.




The LV is much more muscular (1.3 to 1.5 cm thick) than the RV (0.3 to 0.5 cm thick) because it has to pump blood around the entire body, which involves exerting a considerable force to overcome the vascular pressure (because the RV only needs to pump blood to the lungs, it requires less muscle). The aortic valve allows blood to flow from the LV into the aorta, and then closes to prevent blood from leaking back into the LV.

A septum (also known as the fiber skeleton of the heart) divides the right atrium and ventricle from the left atrium and ventricle, preventing blood from passing between them. Even though the ventricles lie below the atria, the two vessels through which the blood exits the heart (the pulmonary artery and the aorta) leave the heart at its top side.

The function of the right side of the heart is to collect deoxygenated blood from the body and pump it into the lungs so that carbon dioxide can be dropped off and oxygen picked up. This happens through a process called diffusion. The left side collects oxygenated blood from the lungs and pumps it out to the body.
Respiratory System
The pulmonary or respiratory system is contained within the sternum, 12 pairs of ribs, the clavicle, and the vertebrae of the thoracic spine, which together form the thoracic cage.
The primary function of the respiratory system is to exchange gases (oxygen and carbon dioxide) between tissue, the blood, and the environment so that arterial blood oxygen, carbon dioxide, and pH levels remain within specific limits throughout many different physiologic limits.86 The pulmonary system also plays a number of other roles, including contributing to temperature homeostasis via evaporative heat loss from the lungs, and filtering, humidifying, and warming or cooling the air to body temperature.86 These processes protect the remainder of the respiratory system from damage caused by dry gases or harmful debris.86




The respiratory system is arranged basically as an upside down tree, which can be divided into two main portions:86
 The conducting portion includes the upper airways, the lower airway (trachea, bronchi, and bronchioles). Within this portion, air moves by bulk flow under the pressure gradients created by the respiratory muscles and the elastic recoil of the lungs. The left main bronchus branches at a more acute angle and is longer than the right main bronchus, which is more directly in line with the trachea.86 This relationship predisposes to aspiration of material into the right rather than the left lung.86 Two body defense mechanisms are located within the walls of the trachea and bronchi:
 Cilia and goblet cells. These function to eliminate inhaled minute particulate matter.
 Irritant receptors. These receptors, which are located in the larynx, trachea, bronchi, pleura, and diaphragm, are responsible for the cough reflex.
 The respiratory portion includes the terminal portion of the bronchial tree and alveoli, the site of gas exchange.87 The total cross sectional area rapidly increases at the respiratory zone. Forward velocity of air flow therefore decreases, and the gases readily move by diffusion through the alveoli into the pulmonary capillaries.


The diaphragm, innervated by the phrenic nerve, is the primary muscle of inspiration, contributing two thirds of the airflow in the sitting or standing position, and three quarters of the airflow in the supine position. The diaphragm, which forms a partition between the thoracic and the abdominal cavities, is made up of two hemidiaphragms, each with a central tendon. When the diaphragm is at rest, the hemidiaphragms are arched high into the thorax. When the diaphragm contracts, it descends over the abdominal contents, flattening the dome, which causes the lower ribs, which serve as levers, to move outward, resulting in protrusion of the abdominal wall. In addition, the contracting diaphragm causes a decrease in intrathoracic pressure, which pulls air into the lungs.88 The other muscles of respiration include the external intercostal muscles, which are active on inspiration, and the internal intercostals, which are active during forced expiration. A number of accessory inspiratory muscles are recognized and include the scalenus and sternocleidomastoid. The abdominal muscles can be used for forceful exhalation.
Respiratory muscle activity involves multiple components of the neural, mechanical, and chemical control and is closely integrated with the



The central chemoreceptors monitor the carbon dioxide levels of both the arterial blood and cerebrospinal fluid.86 A second group of chemoreceptors, the peripheral chemoreceptors, are located in the carotid and aortic bodies86:
 The carotid chemoreceptors are stimulated by low arterial oxygen tensions, high arterial carbon dioxide tensions, and acidosis (arterial pH below 7.35).
 The aortic chemoreceptors are not involved in ventilation, but produce reflex cardiovascular responses (i.e., stimulation increases the heart rate and raises the blood pressure). In addition to responding to the same stimuli as the carotid chemoreceptors, they are also stimulated by a low oxygen content of the arterial blood.

The Energy for Movement
Movement requires muscular and neural activity. The energy required to power muscular activity is derived from the hydrolysis of ATP to ADP and inorganic phosphate (Pi). Despite the large fluctuations in energy demand just mentioned, muscle ATP remains practically constant and demonstrates
a remarkable precision of the system in adjusting the rate of the ATP generating processes to the demand.90 There are three energy systems that contribute to the resynthesis of ATP via ADP rephosphorylation. These energy systems are as follows:
 Phosphagen system. The phosphagen system is an anaerobic process it can proceed without oxygen (O2). Within the skeletal muscle cell at the
onset of muscular contraction, phosphocreatine (PCr) represents the most immediate reserve for the rephosphorylation of ATP. The phosphagen system provides ATP primarily for short term, high intensity activities (i.e., sprinting) and is active at the start of all exercises regardless of intensity.91 One disadvantage of the phosphagen system is that because of its significant contribution to the energy yield at the onset of near  maximal exercise, the concentration of PCr can be reduced to less than 40% of resting levels within 10 seconds of the start of intense exercise.92
Glycolysis system. The glycolysis system is an anaerobic process that involves the breakdown of carbohydrates either glycogen stored in the muscle or glucose delivered in the blood into pyruvate to produce ATP. Pyruvate is then transformed into lactic acid. Because this system relies on a series of nine different chemical reactions, it is slower to become fully active. However, glycogenolysis has a greater capacity to provide energy than does PCr, and therefore it supplements PCr during maximal exercise and continues to rephosphorylate ADP during maximal exercise after PCr reserves have become essentially depleted.91 The process of glycolysis can go one of two ways, termed fast glycolysis and slow glycolysis, depending on the energy demands within the cell. If energy must be supplied at a high rate, fast glycolysis is used primarily. If the energy demand is not as high, slow glycolysis is activated. The main disadvantage of the fast glycolysis system is that during very high intensity exercise, hydrogen ions dissociate from the glycogenolytic end product of lactic acid.90 The accumulation of lactic acid in the contracting muscle is recognized in sports and resistance training circles. An increase in hydrogen ion concentration is believed to inhibit glycotic reactions and directly interfere with muscle excitation contraction and coupling, which can potentially impair contractile force during exercise.91 This inhibition occurs once the



muscle pH drops below a certain level, prompting the appearance of phosphofructokinase (PFK), resulting in local energy production ceasing until replenished by oxygen stores.
Oxidative system. As its name suggests, the oxidative system requires O2 and is consequently termed the "aerobic" system. The oxidative system is
the primary source of ATP at rest and during low intensity activities. It is worth noting that at no time during either rest or exercise does any single energy system provide the complete supply of energy. Although it is unable to produce ATP at an equivalent rate to that produced by PCr breakdown and glycogenolysis, the oxidative system is capable of sustaining low intensity exercise for several hours.91 However, because of its greater complexity, the time between the onset of exercise and when this system is operating at its full potential is around 45 seconds.93 A phenomenon, called steady state, occurs after some 5 to 6 minutes of exercise at a constant intensity level.94 During steady state, the rate of mitochondrial ATP production is closely matched to the rate of ATP hydrolysis and demonstrates the existence of efficient cellular mechanisms to control mitochondrial ATP synthesis in a wide dynamic range.95

The relative contribution of these energy systems to ATP resynthesis has been shown to depend on the intensity and duration of exercise, with the primary system used being based on the duration of the event96:
 0 10 seconds: ATP PCr
 10 30 seconds: ATP PCr plus anaerobic glycolysis  30 seconds 2 minutes: anaerobic glycolysis
 2 3 minutes: anaerobic glycolysis plus oxidative system  >3 minutes and rest: oxidative system
Recovery

The performance of any activity requires a certain rate of oxygen consumption, so that an individual's ability to perform an activity is limited by the maximal amount of oxygen the person is capable of delivering into the lungs.97 Fatigue and recovery from fatigue are complex processes that depend on physiologic and psychological factors. The physiologic factors include the adequacy of the blood supply to the working muscle and the maintenance of a viable chemical environment, whereas the psychological factors include motivation and incentive.98 After an intense exercise session, anaerobic energy sources must be replenished before they can be called on again to provide energy for muscular contraction. The anaerobic energy sources of ATP PCr and lactic acid are ultimately replenished by the oxidative energy system. The extra oxygen that is taken in to replenish the anaerobic energy sources after cessation of the exercise effort was previously referred to as the oxygen debt, but is now more accurately referred to as excess postexercise oxygen consumption (EPOC).
Muscle Performance
Movement of the body, or any of its parts, involves considerable muscular activity from those muscles directly responsible for the movement. Muscle is the only biological tissue capable of actively generating tension. This characteristic enables human skeletal muscle to perform important functions including the maintenance of an upright body posture, the movement of body parts, and the absorption of the various forces that act on the body. The ability of a muscle to carry out its various roles is a measure of muscle performance. Muscle performance can be measured using a number of parameters. These include strength, endurance, and power.
 Strength. Strength may be defined as the amount of force that may be exerted by an individual in a single maximum muscular contraction against
	a specific resistance, or the ability to produce torque at a joint. Three types of contraction are commonly recognized: isometric, concentric, and	



eccentric.99
 Isometric contraction. Isometric contractions do not produce any appreciable change in muscle length.
 Concentric contraction. A concentric contraction produces a shortening of the muscle length. When a muscle contracts concentrically, the distance between the Z lines decreases, the I band and H bands disappear, but the width of the A band remains unchanged.62 This shortening of the sarcomeres is not produced by a shortening of the actin and myosin filaments, but by a sliding of actin filaments over the myosin filaments, which pulls the Z lines together (sliding filament theory).
 Eccentric contraction. An eccentric contraction produces a "lengthening" of the muscle length. In reality, the muscle does not actually lengthen, it merely returns from its shortened position to its normal resting length.
 Endurance. Muscular endurance is the ability of a muscle, or group of muscles, to continue to perform without fatigue. The nature of muscular endurance encourages the body to work aerobically steady state. Endurance exercise training produces an increase in mitochondrial volume density in all three muscle fiber types100 and thus muscle aerobic power. With a higher mitochondrial density in trained muscle, the rate of substrate flux per individual mitochondrion will be less at any given rate of ATP hydrolysis.95 Therefore, the required activation of mitochondrial respiration by adenosine diphosphate (ADP) to achieve a given rate of ATP formation will be less, resulting in increased ADP sensitivity of muscle oxidative phosphorylation.95
 Power. Mechanical power is the product of force and velocity. Muscular power, the maximum amount of work an individual can perform in a given unit of time, is the product of muscular force and velocity of muscle shortening. Muscular power is an important contributor to activities requiring both strength and speed. Maximum power occurs at approximately one third of maximum velocity.101 Muscles with a predominance of fast twitch fibers generate more power at a given load than those with a high composition of slow twitch fibers.102 The ratio for mean peak power production by type IIB, type IIA, and type I fibers in skeletal tissue is 10:5:1.67
These three components of muscle performance are important in functional activities as they can allow a patient to interact with the environment in a more efficient and pain free way through increased movement control and capacity.

To assess muscle performance, strength values using manual muscle testing (MMT) (see Chapter 12) have traditionally been used between similar muscle groups on opposite extremities, or antagonistic ratios. Strength measures the ability with which musculotendinous units act across a bone  joint lever arm system to actively generate motion, or passively resist movement against gravity and variable resistance.103
Range of Motion and Flexibility

The terms range of motion and flexibility are often used synonymously by clinicians, yet they are not the same.
 Range of motion refers to the distance and direction a joint can move. Each specific joint has a normal range of motion that is expressed in degrees. Within the field of physical therapy, goniometry is commonly used to measure the total amount of available motion at a specific joint (see Chapter 11). Range of motion of a joint may be limited by the shape of the articulating surfaces and by capsular and ligamentous structures surrounding that joint.
 Flexibility refers to the ability to move a joint or series of joints through a full, nonrestricted, injury  and pain free range of motion. Flexibility is dependent on a combination of joint range of motion, muscle flexibility, and neuromuscular control. When injury occurs, there is almost always



some associated loss of the ability to move normally due to the pain, swelling, muscle guarding or spasm. The subsequent inactivity results in a shortening of connective tissue and muscle, loss of neuromuscular control, or a combination of these factors.104
When referring to range of motion, three major movements are recognized104:
 Passive range of motion (PROM). PROM, refers to the degree to which a joint can be passively moved to the endpoint in the range of motion. PROM is indicated when the patient's own muscle force is inadequate to produce sufficient motion at a joint, when active contraction of the muscle would be harmful, or as a means of educating a patient about a particular movement. PROM does not prevent muscle atrophy, increase strength or endurance, or assist circulation to the same extent that active, voluntary muscle contraction does. PROM is contraindicated during stages of tissue healing in which motion could prevent or inhibit tissue repair, in the presence of muscle guarding, or in the presence of increasing pain.
 Active range of motion (AROM). AROM refers to the degree to which a joint can be moved by a single muscle contraction, usually through the mid  range of movement. AROM is indicated when the patient is able to perform a movement safely, effectively, and with minimum pain. AROM does not maintain or increase strength, or develop skill or coordination except in the movement patterns used. AROM is contraindicated in the acute stage of healing (12 48 hours after the trauma) or in the presence of any adverse response to the motion (pain that persists more than two hours after the activity, an undesired cardiopulmonary response, or an increase in effusion/inflammation).
 Active assisted range of motion (AAROM). AAROM is active range of motion where the effect of gravity has been removed or when manual assistance is necessary to complete the motion. For example, performing shoulder abduction while lying supine removes the effect of gravity.

When referring to flexibility, two types are recognized, static and dynamic.
 Static flexibility. Static flexibility is defined as the passive range of motion available to a joint or series of joints.105,106 Increased static flexibility should not be confused with joint hypermobility, or laxity, which is a function of the joint capsule and ligaments. Decreased static flexibility indicates a loss of motion. The end feel encountered may help the clinician differentiate the cause among adaptive shortening of the muscle (muscle stretch), a tight joint capsule (capsular), and an arthritic joint (hard). Static flexibility can be measured by a goniometer or by a number of tests, such as the toe touch and the sit and reach, all of which have been found to be valid and reliable.107,108
 Dynamic flexibility. Dynamic flexibility refers to the ease of movement within the obtainable range of motion. Dynamic flexibility is measured actively. The important measurement in dynamic flexibility is stiffness, a mechanical term defined as the resistance of a structure to deformation.109,110 An increase in range of motion around a joint does not necessarily equate to a decrease in the passive stiffness of a muscle.111, 112 and 113 However, strength training, immobilization, and aging have been shown to increase stiffness.114, 115, 116 and 117 The converse of stiffness is pliability. When a soft tissue demonstrates a decrease in pliability, it has usually undergone an adaptive shortening, or an increase in tone, termed hypertonus. There is a growing research to suggest that the limiting factors to preventing increases in range of motion are not only the connective tissues but are also the result of neurophysiologic phenomena controlled by the higher centers of the CNS.118
NORMAL DEVELOPMENT OF FUNCTIONAL MOVEMENT
In addition to the normal development of the neuromusculoskeletal structures as previously described, the normal development of functional movement depends on many fundamental factors, including an efficient production of energy and the ability to produce and overcome forces. The physical therapist needs an appreciation of these underlying factors as well as a working knowledge of the biomechanics of movement.



 Kinesiology is the study of movement.
 Kinetics is the term applied to the forces acting on an individual segment (e.g., hand) or combined segment (e.g., upper extremity) of the body.
 Kinematics is the branch of classical mechanics that describes the motion of points, objects, and groups of objects without consideration of the causes of the motion.
Although a deeper study of biomechanics will be provided to the reader as part of the physical therapy curriculum, this section provides a basic outline to form a foundation for an understanding of the fundamental principles. A working knowledge of the mechanics behind each movement enables the clinician to both diagnose and treat a movement dysfunction. This knowledge also helps the clinician in decision making during such activities as dependent patient transfers and mobility tasks.
Kinetics

Posture and movement are both governed by the control of forces. The same forces that move and stabilize the body also have the potential to deform and injure the body.119 Broadly speaking, force can be defined as a push or pull that can produce, halt, or modify movement. A combination of push and pull forces produce rotations. Forces can be further differentiated as external or internal. A wide range of external and internal forces are either generated or resisted by the human body during the course of daily activities (Table 4 8). Examples of these external forces include ground reaction force, gravity, and applied force through contact. Examples of internal forces include muscle contraction, joint contact, and joint shear forces (Figure 4 8). Whether the body is able to respond to these stresses depends on the extent of the stress and the health of the tissues sustaining the stress. It is important to remember that too little stress, such as occurs with immobilization or decreased activity levels, can be as detrimental as too much stress. The former can result in muscle atrophy, bone loss, and weakening of ligaments and tendons, whereas the latter can lead to tissue damage.
TABLE 4 8
Potential Forces That Can Be Applied to the Body

Type of Force 

Definition
Tension
A force that pulls on each end of a surface or attempts to stretch or lengthen a tissue.
Distraction
A pulling force that tries to separate two surfaces from each other.
Compression
A force that pushes two surfaces together. Axial compression is a compressive force that is directed along the long axis of a structure.
Pressure
The amount of force across a given area. A force over a small area increases pressure, whereas applying the same amount of force over a large area decreases pressure.
Shear
Two forces acting in opposite directions that are parallel to the contact surface.
Bending
A combination of tension and compression that bends a structure around a pivot point.
Torsion
A twisting force that occurs about a structure's long axis.



FIGURE 4 8


Internal forces acting on the body




A number of forces can act on the body. These include compression, tension, shear, and torsion (see Figure 4 8).
 Compression. Compression can be viewed as a squeezing force that pushes two surfaces together. Pressure is defined as the amount of force acting over a given area.
 Axial compression. Axial compression occurs when a compressive force is directed along the long axis of a structure. Axial compression occurs throughout the spine in weight bearing, whether in standing or sitting.
 Tension. Tensile force is the opposite of a compressive force and can be viewed as a pulling or stretching force.
 Distraction. A distraction force is one that attempts to separate two surfaces from each other.



Shear. Shear forces tend to cause one portion of an object to slide or displace with respect to another portion of the object. Whereas compressive and tensile forces act along the longitudinal axis of a structure to which they are applied, shear forces act parallel or tangent to a surface. For example, when bending forward at the waist, shear forces are produced between the lumbar vertebral bodies and their respective intervertebral disks.
Torsion. Torsional forces (torque) occur when a structure is made to twist about its longitudinal axis, typically when one end of the structure is fixed. For example, torsional forces occur in the lower extremity if a directional change is attempted while the sole of the foot is planted firmly on the ground.

One of these responses to resist internal and/or external forces is the maintenance of balance as the body's center of mass (COM) shifts as the segments of the body change position, or if weight is added to or removed from the body. For example, if a weight is added to a body segment, the COM moves toward the added weight, whereas if a weight is removed, the COM moves away from the removed weight.
Newton's laws of motion help to explain the relationship between forces and their impact on body segments, as well as on total body motion (Table 4  9).



TABLE 4 9
Newton's Laws of Motion


Definition
Description
Real life Example
Clinical Example
First law (inertia)
An object continues to move in a state of constant velocity unless acted on by an external net force or resultant force.
Directly connects inertia with the concept of relative velocities.
Describes the reluctance of an object that is in a state of equilibrium to change its movement pattern. The larger the mass or inertia of an object, the more difficult it is to alter its motion.
While traveling in a moving vehicle at a constant velocity, a person can throw a ball straight up in the air and catch it without worrying about applying a force in the direction the vehicle is moving.
It is easier to start and stop an empty wheelchair than it is to start or stop a wheelchair in which a patient is seated.
Second law (force = mass   acceleration)
Motion is inversely related to mass. An unbalanced force acting on an object will result in the object's momentum changing over time. The relationship between an object's mass m, its acceleration a, and the applied force F is F = ma.
Can be used to determine how velocities change when forces are applied a measurement of the strength of forces. More force is required to change the speed of a heavy object than a lighter one.
Landing from a jump with the knees extended is much harder than bending the hips and knees when landing.
The patient who is having difficulty overcoming inertia in order to come from a sitting position to a standing position will often roll forward and backward to gain momentum.
Third law (action  reaction)
For every action there is an equal and opposite reaction.
All forces are interactions
between different bodies.
During gait, when the foot strikes the ground, the ground applies a force in the opposite direction (ground reaction force) depending on the firmness of the surface.
Using the hands to push up from a stable surface during a sit to stand transfer.



Levers

Biomechanical levers can be defined as rotations of a rigid surface about a pivot point or axis. The majority of body movements involve the use of levers. For simplicity's sake, biomechanical levers are usually described using a straight bar, which is the lever, and the fulcrum, which is the point on which the bar is resting. Two sources of effort are required: a load and an effort. A load is typically an external force placed on an object or structure (see Table 4 8). The effort forces attempt to cause movement of the load. That part of the lever between the fulcrum and the load is the load arm. There are three types of levers (Figure 4 9):

FIGURE 4 9



Class of levers

 First class: occurs when two forces are applied on either side of an axis and the fulcrum lies between the effort and the load (see Figure 4 9), like a seesaw. Examples in the human body include the contraction of the triceps at the elbow joint, or tipping of the head forward and backward.
 Second class: occurs when the load (resistance) is applied between the fulcrum and the point where the effort is exerted (see Figure 4 9). This has the advantage of magnifying the effects of the effort so that it takes less force to move the resistance. Examples of second class levers in everyday life include the nutcracker, and the wheelbarrow with the wheel acting as the fulcrum. Examples of second class levers in the human body include weight bearing plantarflexion (rising up on the toes) (see Figure 4 9). Another would be an isolated contraction of the brachioradialis to flex the elbow, which could not occur without the other elbow flexors being paralyzed.
 Third class: occurs when the load is located at the end of the lever (see Figure 4 9) and the effort lies between the fulcrum and the load (resistance), like a drawbridge or a crane. The effort is exerted between the load and the fulcrum. The effort expended is greater than the load, but the load is moved a greater distance. Most movable joints in the human body function as third class levers an example is flexion at the elbow.
Moments

A moment (sometimes erroneously referred to as torque) is a mathematical value defined as the product of the force and the moment arm, with the moment arm defined as the distance from the linear force to the axis the perpendicular distance from the point of rotation. In practice, the terms torque and moment are not interchangeable:
 Torque: the rate of change of angular momentum of an object such that one or both of the angular velocity or the moment of inertia of an object are changing. Inertia is the property of any physical object to resist a change in its state of motion or rest, or the inclination of an object to resist any change in its motion.
 Moment: the tendency of one or more applied forces to rotate an object about an axis, but not necessarily to change the angular momentum of the object.
Although muscles produce linear forces, motions at joints are all rotary. The rotary force is the product of the linear force and the moment arm (mechanical advantage) of the muscle about the joint's center of rotation.

To understand the concept of a moment arm, an understanding of the anatomy and movement (kinematics) of the joint of interest is necessary. For example, some joints can be considered to rotate about a fixed point. A good example of such a joint is the elbow. At the elbow joint, where the



humerus and ulna articulate, the resulting rotation occurs primarily about a fixed point, referred to as the center of rotation (COR). In the case of the elbow joint, this COR is relatively constant throughout the joint range of motion. However, in other joints (for example, the knee) the COR moves in space as the knee joint rotates because the articulating surfaces are not perfect circles. In the case of the knee, it is not appropriate to discuss a single COR rather, we must speak of a COR corresponding to a particular joint angle, or, using the terminology of joint kinematics, we must speak of the instant center of rotation (ICR), that is, the COR at any "instant" in time or space. Thus, the moment arm is defined as the perpendicular distance from the line of force application to the axis of rotation.
Force Couples

A special case of moments is a force couple. A force couple consists of two parallel forces that are equal in magnitude, opposite in direction, and do not share a line of action. A force couple does not produce any translation, only rotation about a pivot point. For example, a force couple is involved when two hands work together to turn a steering wheel. A number of force couples exist throughout the body, particularly at the shoulder, where various muscles work together to help the scapula rotate during arm elevation. Force couples can also be used in a number of functional movements. For example, scooting forward in a chair rotates the pelvis around a pivot point.
Mechanical Advantage

When a machine puts out more force than is put in, the machine is said to have mechanical advantage (MA). Moments and moment arms can be internal or external. The MA of the musculoskeletal lever is defined as the ratio of the internal moment arm to the external moment arm. Depending on the location of the axis of rotation, the first class lever can have an MA equal to, less than, or greater than 1.119 Second class levers always have an MA greater than 1. Third class levers always have an MA less than 1. The majority of muscles throughout the musculoskeletal system function with an MA of much less than 1. Therefore, the muscles and underlying joints must "pay the price" by generating and dispersing relative large forces, respectively, even for seemingly low load activities.119
Stress and Strain

During activities of daily living, the body is subject to a number of forces, including gravity. The terms stress and strain, which are commonly used to describe some of these forces, have specific mechanical meanings.
 Stress. Stress or load is given in units of force per area and is used to describe the type of force applied. Stress is independent of the amount of a material, but is directly related to the magnitude of force and inversely related to the unit area.120
 Strain. Strain is defined as the change in length of a material due to an imposed load divided by the original length.120 The two basic types of strain are linear strain, which causes a change in the length of a structure, and shear strain, which causes a change in the angular relationships within a structure. It is the concentration of proteoglycans in solution that is responsible for influencing the mechanical properties of the tissue, including compressive stiffness, shear stiffness, osmotic pressure, and regulation of hydration.121
The inherent ability of a tissue to tolerate stress or strain can be observed experimentally in graphic form.
Linear forces (line of action) are depicted as straight arrows in which the arrowhead points in the direction of the force being exerted. When a force is acting at an angle to a surface, the components of the force can be divided into those forces acting perpendicular to the surface and those forces acting in parallel to the surface.
Gravity is represented as a vertical force pointing downward.
When any stress is plotted on a graph against the resulting strain for a given material, the shape of the resulting load deformation curve depends on the kind of material involved. The load deformation curve, or stress strain curve, of a structure (Figure 4 10) depicts the relationship between the amount of force applied to a structure and the structure's response in terms of deformation or acceleration. The horizontal axis (deformation or strain) represents the ratio of the tissue's deformed length to its original length. The vertical axis of the graph (load or stress) denotes the internal resistance generated as a tissue resists its deformation, divided by its cross sectional area. The load deformation curve can be divided into four regions, each region representing a biomechanical property of the tissue (see Figure 4 10):



FIGURE  4 10


The stress strain curve

 Toe region. Collagen fibers have a wavy, or folded, appearance at rest. When a force that lengthens the collagen fibers is initially applied to connective tissue, these folds are affected first. As the fibers unfold, the slack is taken up (see Crimp later). The toe region is an artifact caused by this take up of slack, alignment, and/or seating of the test specimen. The length of the toe region depends on the type of material and the waviness of the collagen pattern.
 Elastic deformation region. Within the elastic deformation region the structure imitates a spring the geometric deformation in the structure increases linearly with increasing load, and after the load is released, the structure returns to its original shape. The slope of the elastic region of the load deformation curve from one point in the curve to another is called the modulus of elasticity, or Young's modulus, and represents the extrinsic stiffness or rigidity of the structure the stiffer the tissue, the steeper the slope. Young's modulus is a numerical description of the relationship between the amount of stress a tissue undergoes and the deformation that results. The ratio of stress to strain in an elastic material is a measure of its stiffness. Mathematically, the value for stiffness is found by dividing the load by the deformation at any point in the selected range. All normal tissues within the musculoskeletal system exhibit some degree of stiffness. Young's modulus is independent of specimen size and is therefore a measure of the intrinsic stiffness of the material. The greater the Young's modulus for a material, the better it can withstand greater forces. Larger structures will have greater rigidity than smaller structures of similar composition.
 Plastic deformation region. The end of the elastic range and the beginning of the plastic range represents the point where an increasing level of stress on the tissue results in progressive failure and microscopic tearing of the collagen fibers. Further increases in strain result in microscopic damage and in permanent deformation. The permanent change results from the breaking of bonds and their subsequent inability to contribute to the recovery of the tissue. Unlike the elastic region, removal of the load in this region will not result in a return of the tissue to its original length.
 Failure region. Deformations exceeding the ultimate failure point (see Figure 4 10) produce mechanical failure of the structure, which in the human body may be represented by the fracturing of bone or the rupturing of soft tissues.




Biological tissues are anisotropic, which means they can demonstrate differing mechanical behavior as a function of test direction. The properties of extensibility and elasticity are common to many biologic tissues. Extensibility is the ability to be stretched, and elasticity is the ability to return to normal length after extension or contraction.122
A number of protective mechanisms exist in connective tissue to help respond to stress and strain, including crimp, viscoelasticity, creep and stress relaxation, plastic deformation, and stress response.


Crimp 

The crimp of collagen is one of the major factors behind the viscoelastic properties of connective tissue. Crimp, a collagen tissue's first line of response to stress, is different for each type of connective tissue, providing each with different viscoelastic properties. Collagen fibers are wavy in appearance and are oriented obliquely when relaxed. However, when a load is applied, the fibers line up in the direction of the applied force as they uncrimp.
Crimping is seen primarily in ligaments, tendons, and joint capsules and occurs in the toe phase of the stress strain curve (see Figure 4 10).


Viscoelasticity

Viscoelasticity is the time dependent mechanical property of a material to stretch or shorten over time and to return to its original shape when a force is removed. The mechanical qualities of a tissue can be separated into categories based on whether the tissue acts primarily like a solid, a fluid, or a mixture of the two. Solids are described according to their elasticity, strength, hardness, and stiffness. Bone, ligaments, tendons, and skeletal muscle are all examples of elastic solids. Biological tissues that demonstrate attributes of both solids and fluids are viscoelastic. The viscoelastic properties of a structure determine its response to loading. For example, a ligament demonstrates more viscous behavior at lower loads, whereas at higher loads, elastic behaviors dominate.20
Creep and Stress Relaxation

Creep and stress relaxation are two characteristics of viscoelastic materials that are used to document their behavior quantitatively.122
Creep is the gradual rearrangement or deformation of collagen fibers, proteoglycans, and water that occurs because of a constantly applied force after the initial lengthening caused by crimp has ceased. Creep is a time dependent and transient biomechanical phenomenon. Short duration stresses
 (less than 15 minutes) do not have sufficient time to produce this displacement; however, longer times can produce it. Once creep occurs, the tissue	



has difficulty returning to its initial length (see later discussion).
Stress relaxation is a phenomenon in which stress or force in a deformed structure decreases with time, while the deformation is held constant.122 Unlike creep, stress relaxation responds with a high initial stress that decreases over time until equilibrium is reached and the stress equals zero; hence the label relaxation. As a result, no change in length is produced.
Thus, stress to connective tissues can result in no change, a semipermanent change, or a permanent change to the microstructure of the collagenous tissue. The semipermanent or permanent changes may result in either microfailure or macrofailure.
Plastic Deformation

Plastic deformation of connective tissue occurs when a tissue remains deformed and does not recover its pre stress length. Once all of the possible realignment has occurred, any further loading breaks the restraining bonds, resulting in microfailure. On average, collagen fibers are able to sustain a 3% increase in elongation (strain) before microscopic damage occurs.123 Following a brief stretch, providing the chemical bonds remain intact, the collagen and proteoglycans gradually recover their original alignment. The recovery process occurs at a slower rate and often to a lesser extent. The loss of energy that occurs between the lengthening force and the recovery activity is referred to as hysteresis. The more chemical bonds that are broken with applied stress, the greater the hysteresis. If the stretch is of sufficient force and duration and a sufficient number of chemical bonds are broken, the tissue is unable to return to its original length until the bonds are re formed. Instead, it returns to a new length and to a new level of strain resistance. Increased tissue excursion is now needed before tension develops in the structure. In essence, this has the effect of decreasing the stabilizing capabilities of the connective tissue.
Stress Response

Exercises may be used to change the physical properties of both tendons and ligaments, as both have demonstrated adaptability to external loads with an increase in strength: weight ratios.124, 125 and 126 The improved strength results from an increase in the proteoglycan content and collagen cross  links.124, 125 and 126


Movements of the Body Segments

When describing movements, it is necessary to have a starting position as the reference position. This starting position is referred to as the anatomic reference position. The anatomic reference position for the human body is described as the erect standing position with the feet just slightly separated and the arms hanging by the side, the elbows straight, and the palms of the hand facing forward (Figure 4 11).

FIGURE  4 11


The anatomic reference position



In general, there are two types of motions: translation, which occurs in either a straight or curved line, and rotation, which involves a circular motion around a pivot point. Movements of the body segments occur in three dimensions along imaginary planes and around various axes of the body.
Planes of the Body

There are three traditional planes of the body corresponding to the three dimensions of space: sagittal, frontal, and transverse127 (Figure 4 12).
 Sagittal. The sagittal plane, also known as the anterior posterior or median plane, divides the body vertically into left and right halves of equal size.
 Frontal. The frontal plane, also known as the lateral or coronal plane, divides the body equally into front and back halves.
 Transverse. The transverse plane, also known as the horizontal plane, divides the body equally into top and bottom halves.

FIGURE  4 12

Planes of the body



Because each of these planes bisects the body, it follows that each plane must pass through the COM or COG.* If the movement described occurs in a plane that passes through the COM, that movement is deemed to have occurred in a cardinal plane. An arc of motion represents the total number of degrees traced between the two extreme positions of movement in a specific plane of motion.103 If a joint has more than one plane of motion, each type of motion is referred to as a unit of motion. For example, the wrist has two units of motion: flexion extension (anterior posterior plane), and ulnar radial deviation (lateral plane).103
Few movements involved with functional activities occur in the cardinal planes. Instead, most movements occur in an infinite number of vertical and horizontal planes parallel to the cardinal planes (see discussion that follows).
*The center of mass may be defined as the point at which the three planes of the body intersect each other. The line of gravity is defined as the vertical line at which the two vertical planes intersect each other.
Axes of the Body

Three reference axes are used to describe human motion: frontal, sagittal, and longitudinal (Figure 4 13). The axis around which the movement takes place is always perpendicular to the plane in which it occurs.
 Frontal. The frontal axis, also known as the M L axis, is perpendicular to the sagittal plane.
 Sagittal. The sagittal axis, also known as the A P axis, is perpendicular to the frontal plane.



 Longitudinal. The longitudinal axis, also known as the vertical axis, is perpendicular to the transverse plane.

FIGURE  4 13


Axes of the body
A P   Anterior posterior M L   Medial lateral

Most movements occur in planes and around axes that are somewhere in between the traditional planes and axes. However, nominal identification of every plane and axis of movement is impractical. The structure of the joint determines the possible axes of motion that are available. For example, a hinge joint has only one axis. Condyloid (ovoid) joints have two axes. Ball and socket joints have three axes. The axis of rotation remains stationary only if the convex member of a joint is a perfect sphere and articulates with a perfect reciprocally shaped concave member. The planes and axes for the more common planar movements (Figure 4 14) are as follows:
 Flexion, extension, hyperextension, dorsiflexion, and plantarflexion occur in the sagittal plane around a M L axis.
 Abduction and adduction, side flexion of the trunk, elevation and depression of the shoulder girdle, radial and ulnar deviation of the wrist, and eversion and inversion of the foot occur in the frontal plane around a sagittal axis.
 Rotation of the head, neck, and trunk; internal rotation and external rotation of the arm or leg; horizontal adduction and abduction of the arm or thigh; and pronation and supination of the forearm occur in the transverse plane around the vertical axis.



 Arm circling and trunk circling are examples of circumduction. Circumduction involves an orderly sequence of circular movements that occur in the sagittal, frontal, and intermediate oblique planes, so that the segment as a whole incorporates a combination of flexion, extension, abduction, and adduction. Circumduction movements can occur at biaxial and triaxial joints. Examples of these joints include the tibiofemoral, radiohumeral, hip, glenohumeral, and spinal joints.
FIGURE  4 14


Movements of the body

Both the configuration of a joint and the line of pull of the muscle acting at a joint determine the motion that occurs at a joint:  A muscle that has a line of pull that is lateral to the joint is a potential abductor.
 A muscle that has a line of pull that is medial to the joint is a potential adductor.
 A muscle that has a line of pull that is anterior to a joint has the potential to extend or flex the joint. At the knee, an anterior line of pull may cause the knee to extend, whereas at the elbow joint, an anterior line of pull may cause flexion of the elbow.
 A muscle that has a line of pull that is posterior to the joint has the potential to extend or flex a joint (refer to preceding example).
Degrees of Freedom



The number of independent modes of motion at a joint is called the degrees of freedom (DOF). A joint can have up to 3 degrees of angular freedom, corresponding to the three dimensions of space.119 If a joint can swing in one direction or can only spin, it is said to have 1 DOF.128, 129, 130 and 131 The proximal interphalangeal joint is an example of a joint with 1 DOF. If a joint can spin and swing in one way only or it can swing in two completely distinct ways, but not spin, it is said to have 2 DOF.128, 129, 130 and 131 The tibiofemoral joint, temporomandibular joint, proximal and distal radioulnar joints, subtalar joint, and talocalcaneal joint are examples of joints with 2 DOF. If the bone can spin and also swing in two distinct directions, then it is said to have 3 DOF.128, 129, 130 and 131 Ball and socket joints such as the shoulder and hip have 3 DOF.

Because of the arrangement of the articulating surfaces the surrounding ligaments and joint capsules most motions around a joint do not occur in straight planes or along straight lines. Instead, the bones at any joint move through space in curved paths. This can best be illustrated using Codman's paradox.
1. Stand with your arms by your side, palms facing inward, thumb extended. Notice that the thumb is pointing forward (Figure 4 15).
2. Flex one arm to 90 degrees at the shoulder so that the thumb is pointing up (Figure 4 16).
3. From this position, horizontally extend your arm so that the thumb remains pointing up but your arm is in a position of 90 degrees of glenohumeral abduction (Figure 4 17).
4. From this position, without rotating your arm, return the arm to your side and note that your thumb is now pointing away from your thigh (Figure 4 18).

FIGURE  4 15


Codman's paradox: start position




FIGURE  4 16


Codman's paradox: 90  of glenohumeral flexion




FIGURE  4 17

Codman's paradox: 90  of glenohumeral abduction


FIGURE  4 18


Codman's paradox: end position Codman's paradox: end position



Referring to the start position, and using the thumb as the reference, it can be seen that the arm has undergone an external rotation of 90 degrees. But where and when did the rotation take place? Undoubtedly, it occurred during the three separate, straight plane motions or swings that etched a triangle in space. What you have just witnessed is an example of a conjunct rotation a rotation that occurs as a result of joint surface shapes and the effect of inert tissues rather than contractile tissues. Conjunct rotations can only occur in joints that can rotate internally or externally. Although not always apparent, most joints can so rotate. Consider the motions of elbow flexion and extension. While fully flexing and extending your elbow a number of times, watch the pisiform bone and forearm. If you watch carefully you should notice that the pisiform and the forearm move in a direction of supination during flexion and pronation during extension of the elbow. The pronation and supination motions are examples of conjunct rotations.
Most habitual movements, or those movements that occur most frequently at a joint, involve a conjunct rotation. However, the conjunct rotations are not always under volitional control. In fact, the conjunct rotation is only under volitional control in joints with 3 DOF (glenohumeral and hip joints). In joints with fewer than 3 DOF (hinge joints, such as the tibiofemoral and ulnohumeral joints), the conjunct rotation occurs as part of the movement but is not under voluntary control. The implications become important when attempting to restore motion at these joints: the mobilizing techniques must take into consideration both the relative shapes of the articulating surfaces and the conjunct rotation that is associated with a particular motion.
Kinematics

In studying kinematics, two major types of motion are involved: (1) osteokinematic and (2) arthrokinematic.
Osteokinematic Motion

Osteokinematic motion occurs when any object forms the radius of an imaginary circle about a fixed point. The axis of rotation for osteokinematic motions is oriented perpendicular to the plane in which the rotation occurs.127 The distance traveled by the motion may be a small arc or a complete circle and is measured as an angle, in degrees. All human body segment motions involve osteokinematic motions. Examples of osteokinematic motion include abduction or adduction of the arm, flexion of the hip or knee, and side bending of the trunk.
Arthrokinematic Motion

The motions occurring at the joint surfaces are termed arthrokinematic movements (Figure 4 19). At each synovial articulation, the articulating
 surface of each bone moves relative to the shape of the other articulating surface. A normal joint has an available range of active, or physiologic,	



motion, which is limited by a physiologic barrier as tension develops within the surrounding tissues, such as the joint capsule, ligaments, and CT. At the physiologic barrier, there is an additional amount of passive, or accessory, range of motion. The small motion, which is available at the joint surfaces, is referred to as accessory motion, or joint play motion. This motion can only occur when resistance to active motion is applied, or when the patient's muscles are completely relaxed.132

FIGURE  4 19


Arthrokinematics of motion

Beyond the available passive range of motion, the anatomic barrier is found (Figure 4 20). This barrier cannot be exceeded without disruption to the integrity of the joint.

FIGURE  4 20


Various ranges of motion

Both the physiologic (osteokinematic) and accessory (arthrokinematic) motions occur simultaneously during movement and are directly proportional to each other, with a small increment of accessory motion resulting in a larger increment of osteokinematic motion. Normal arthrokinematic motions must occur for full range physiologic motion to take place. Mennell133,134 introduced the concept that full, painless, active range of motion is not possible without these motions and that a restriction of arthrokinematic motion results in a decrease in osteokinematic motion.
Kinematic Chains

When a body moves, it will do so in accordance with its kinematics, which in the human body takes place through arthrokinematic and osteokinematic



movements. The expression kinematic chain is used in rehabilitation to describe the function or activity of an extremity or trunk in terms of a series of linked chains. A kinematic chain refers to a series of articulated segmented links, such as the connected pelvis, thigh, leg, and foot of the lower extremity.119

According to kinematic chain theory, each of the joint segments of the body involved in a particular movement constitutes a link along the kinematic chain. Because each motion of a joint is often a function of other joint motions, the efficiency of an activity can be dependent on how well these chain links work together.135

Two types of kinematic chain systems are recognized: closed kinematic chain (CKC) systems and the open kinematic chain (OKC) system (Table 4  1 0).136
TABLE 4 10
Differential Features of OKC and CKC Exercises

Exercise Mode 

Characteristics

Advantages 

Disadvantages 
Open kinematic chain
1. Single muscle group
2. Single axis and plane
3. Emphasizes concentric contraction
4. Non weight bearing
1. Isolated recruitment
2. Simple movement pattern
3. Isolated recruitment
4. Minimal joint compression
1. Limited function
2. Limited complexity
3. Limited eccentrics
4. Less proprioception and joint stability with increased joint shear forces
Closed kinematic chain
1. Multiple muscle groups
2. Multiple axes and planes
3. Balance of concentric and eccentric contractions
4. Weight bearing exercise
1. Functional recruitment
2. Functional movement patterns
3. Functional contractions
4. Increase proprioception and joint stability
1. Difficult to isolate
2. More complex
3. Loss of control of target joint
4. Compressive forces on articular surfaces


Data from Greenfield BH, Tovin BJ: The application of open and closed kinematic chain exercises in rehabilitation of the lower extremity. J Back Musculoskel Rehabil 2:38 51, 1992.
Examples of closed kinematic chain exercises (CKCEs) involving the lower extremities include the squat and the leg press. The activities of walking,



running, jumping, climbing, and rising from the floor all incorporate closed kinematic chain components. An example of a CKCE for the upper extremities is the push up (Figure 4 21), or when using the arms to rise out of a chair.
FIGURE  4 21


Upper extremity closed kinetic chain exercise


Open kinematic chain exercises (OKCEs) involving the lower extremity include the seated knee extension and prone knee flexion. Example OKCEs of the upper extremity include hitting a ball (Figure 4 22), the biceps curl, and the military press, using very light weights.

FIGURE  4 22


Upper extremity open kinetic chain activity



Once significant resistance is applied to the end of an extremity, there is some debate as to whether the activity or exercise changes from an OKCE to a CKCE. For example, many activities that include a load on the end segment, such as swimming and cycling, have been traditionally viewed as OKC activities even though the end segment is not "fixed" and restricted from movement. This ambiguity of definitions for CKC and OKC activities has allowed some activities to be classified in opposing categories.137 Thus, there has been a growing need for clarification of OKC and CKC terminology, especially when related to functional activities.
Motor Progression
Motor progression refers to the complex processes of change in motor behavior that start in utero and continue over the life span. These changes in human motor behavior are influenced by psychomotor, physiologic, biochemical, biomechanical, psychosocial, and even gender considerations.138,139 The study of motor progression helps with the early detection of problems in individuals who do not develop normally by using references that are developmentally appropriate. Two such references are:
 Age appropriate. This refers to individuals who pass through the predictable sequences of growth and development through which most children pass. An understanding of these sequences provides a basis from which to provide the best rehabilitation approach.
 Individual appropriate. This refers to individuals who do not pass through the sequences in the same manner or within the same period, but is based more on the stage of a specific individual's development.



















There are many theories as to how motor progression occurs. These include:
 Cephalocaudal: progression occurs from the top of the body (head) to the tail (feet).
 Proximodistal: progression occurs from points close to the center of the body to points close to the periphery.
 Differentiation: progression occurs from gross, immature movement to precise, well controlled, intended movement.
 Integration: progression occurs from the integration of the various systems, particularly the neuromuscular system, to produce a well controlled, intended movement.
There are two main schools of thought with regard to how best enhance motor progression:
 Product approach. This is a task oriented approach that measures the development of a skill based on the end results or outcome.
 Process approach. This is a process oriented approach that emphasizes the movement itself with little attention to the outcome.
The Development of Early Movement

A milestone is a significant point in development or a significant functional ability achieved during the developmental process. The various developmental milestones for both sensory and motor development are depicted in Tables 4 11, 4 12, and 4 13. An analysis of the progressions involved in the developmental milestones reveals the following progressive sequence:
 Prone
 Prone on elbows  Rolling, sidelying  Supine
 Sitting
 Quadruped  Kneeling
 Half kneeling
	Standing	



TABLE 4 11
Major Milestones

Milestone 
Approximate Age (in months) Able to Perform 
Roll
3 4
Sit independently
5 6
Belly crawl
7 8
Creep (quadruped)
8 9
Pull to stand
9 10
Cruise
11
Walk
12


Data from van Blankenstein M, Welbergen UR, de Haas JH: Le Developpement du Nourrisson: Sa Premiere Annee en 130 Photographies. Paris, Presses Universitaires de France, 1962.
TABLE 4 12
Gross Motor Checklist 







Month/Year 
Position/Activity
Milestone 


One month
Prone
Lifts head and turns to side


Two months
Vertical
Rights head



Prone
Recurrently lifts head to 45 



Supported sitting
Head erect and bobbing


Three months
Prone
Lifts head to 45  (sustained) Recurrently lifts head to 90  Supports self on forearms Rolls to side


Four months
Prone
List head to 90  (sustained)




Rolls to supine



Supine
Rolls to prone




Assists with head when pulled to sit



Supported sitting
Head steady, set forward












Five months
Prone
Supports self on extended arms






Rolls to supine segmentally





Supine
Lifts head when pulled to sitting.






Rolls to prone segmentally





Supported sitting Standing
Head erect and steady






Takes weight on lower extremities




Six months
Prone
Can lift one arm and weight bear on the other






Pivots in a circle





Sitting
Erect for one minute with hands propped forward






Protective extension sideways




Seven months
Prone
Up on all fours






Progress is forward in any manner





Sitting
Erect without support but unsteady






Protective extension forward




Eight months
Prone
Crawls in any manner





Sitting
Erect without support





Standing
Pulls to stand




Nine months
Prone/supine
Rotates to sitting





Sitting
Goes to prone






Protective extension backwards





Standing
Pulls to standing with rotation and support




10 months
Sitting
Pivots





Locomotion
Cruises




12 months
Locomotion
Stands up without support






Walks with high guard




15 months
Kneeling
Kneels without support











Downloaded 2024 3 16 1:33 P Your IP is 155.33.135.27 CHAPTER 4: Foundations of Movement,
 2024 McGraw Hill. All Rights Reserved. Terms of Use   Privacy Policy   Notice   Accessibility


Page 58 / 88




Locomotion
Walks with medium guard




Can stop, start, and change directions without falling


18 months
Locomotion
Walks with no guard carrying object




Walks fast with feet flat




Squats to play




Goes up/down stairs on all fours


Two years
Locomotion
Walks up/down stairs one at the time holding rail




Walks with heel total gait




Runs forward well


Three years
Locomotion/Skills
Jumps forward on both feet




Alternates feet going upstairs




Walks backward easily




Hops up to six times


Four years
Locomotion/Skills
Walks downstairs with alternating feet, holding rail




Skips on one foot




Throws overhand




Moves backward and forward with equal agility


Five years
Locomotion/Skill
Pedals and steers tricycle well




Able to walk long distances on toes




Gallops




Hops up to nine times on one foot




Smooth reciprocal movements in walking and running


Six years
Skill
Throws a small ball at a target and hits the target




Broad jumps up to three feet



TABLE 4 13
Development Milestones According to Position














































Age 
Prone 
Supine 
Sitting
Standing
Comments 













































Neonate: 0 to 14 days
Physiologic flexor activity in the ankles, knees, hips, and elbows.
Lack of trunk muscular control the back is round and the head flops forward.
Demonstrates the remarkable capabilities of primary standing automatic walking when supported.
Grasp is a reflex in which the hand automatically closes on objects the baby touches because of tactile stimulation of the palm of the hand.
The hands will randomly swing out wide (neonatal reaching).
No organized response to postural perturbations.




Newborn (0 1
month)
Arms and hands tucked in close to the body, rounded shoulders, elbows flexed. Hands are closed loosely and positioned close to mouth.
No control of neck flexion in supine is present, so the baby cannot maintain the head in midline, but keeps it rotated to one side.
Sacral sitting if supported.

Period dominated by physiological flexion.
Poor head control.
Very active when awake.
Random wide ranging movements primarily in supine.
Soft tissue tightness holds the hips in flexion/abduction/external rotation.
The baby touches and feels, and is soon sucking and learning about the hands.
Vision limited to 8 9 feet. Skeletal characteristics include coxa valgus, genu varum, tibial varum and torsion, calcaneal varus, and occasionally, metatarsus adductus.




1 month
Head lifting in prone may appear to be improved.
Increased cervical rotation mobility.
Elbows moving forward, arms away from body.
Head to one side resulting in lateral vision becoming dominant, and eye  hand regard and uncontrolled swiping at toys at the baby's side is frequently observed.
Wider ranges of
movement. Heels hit surface.

Positive support and primary walking reflexes in supported standing.
Decreasing physiologic flexion (less "recoil").
Increasing level of arousal. Neonatal reaching.
Able to visually track a moving object horizontally.




2
months
Able to hold the head steady in all positions and to raise it about 45  because of increased activity of active shoulder abduction. The
Increased asymmetry with more visual interaction.
Head lag occurs with pull to sit. Begins to
May not accept weight on lower extremities (astasia abasia).
No more neonatal
Increasing asymmetry/decreased tone.
Increased head and trunk control
lets the baby use the arms for







arms and hands begin to work to support the actions of the head and trunk.
Hand movements more goal directed.

develop head and trunk control and more attempts at sustained extension.
Head bobs in supported sitting.
stepping.
reaching and playing rather than for support. Holds objects placed in the hand.




3
months
Change occurs in the general position of the arms, from a position where the arms are tucked in close to the body with the elbows near the ribs, to one in which the elbows are almost in line with the shoulders, which allows for forearm weight  bearing.
Legs abducted and externally rotated
Face can be raised 45 90  when prone.
Beginning of symmetry is evident
 the head is in midline with chin tucking and the hands are in midline on the chest/to mouth.
Attempts pull to sit but falls forward.
Minimal weight through extended legs.
Period of controlled symmetry. The grasp becomes more controlled and voluntary, and the hands can adjust to the shape of objects.
Symmetry is very obvious in the lower extremities as they assume their "frog legged" position of hip abduction, external rotation and flexion, and knee flexion. The feet come together and the baby is able to take some weight with toes curled in supported standing.




4
months
Able to prop up on the forearms and look around. The head and chest are lifted and maintained in midline.
Prone pivots.
Can roll from prone to side and from supine to side, although these are usually accidental occurrences.
Able to bring the hands together in the space above the body due to increased shoulder girdle control.
Hands to knees. Active anterior and posterior pelvic tilt.
Assists in pull to sit by flexing elbows. Very minimal head bobbing  stabilized through shoulder elevation.
Tends to sit in a slumped position.
Protective reactions develop, first laterally, then forward, and then backward.
Because of the increased head neck  trunk control, the baby is able to take more of his/her weight when placed in standing and can now be held by the hands instead of at the chest. Legs are extended and the toes are clawed.
Ulnar palmar grasp develops. Able to perform bilateral reaching with the forearm pronated when the trunk is supported.
Side lying.
Starts hand to mouth activities. Emerging righting and equilibrium reactions.
Findings of concern include poor midline orientation (persistent ATNR), imbalance between flexors and extensors, poor visual attention/tracking, persistent wide base of support in standing, and poor antigravity strength.




5
months
Equilibrium reactions begin in prone position.
Can roll from prone to supine. Able to assume and maintain a position of extended arm weight
bearing in prone and can weight
Chin tuck, downward gaze. Feet to mouth. Anterior and posterior pelvic tilt more active.
There is no head lag when the baby is pulled from supine to sit. Assists during
Tends to be able to bear almost all weight.
Finding of concern include: Poor antigravity flexion.
Poor tolerance for prone/inability to bear weight to extended arms/poor
weight shifting.






shift from one forearm to the other end to reach out to with one arm.
Active role to sideline.
Manipulation and transfer of toys.
pull to sit with chin tuck and head lift.
Able to control head in supported sitting, although still leans forward from the hips.




6
months
Completes turning and can roll from prone to supine.
Can lie prone on hands with the elbows extended and is able to weight shift on extended arms from hand to hand and to reach forward because of sufficient shoulder girdle control.
Active hip extension. Transfers toys.
Flexes head independently.
Can sit independently, although initially uses the arms and hands for support.
In standing, is able to bear weight on both legs and bounce and can independently hold onto the support of a person because of sufficient trunk and hip control.
Uses rolling for locomotion. Findings of concern include:
Poor tolerance for prone position.
Paucity of movement patterns.
Inability to sit independently. Inability to roll or rolling with neck hyperextension.


7
months
Trunk and arms free
Able to achieve and maintain the quadruped position, although the prone is usually the preferred position.
Can pivot on belly, often moving body in a circle.
Tends to avoid except for playing.
Protective reactions more consistent.
Able to perform trunk rotation in sitting.
Can assume the sitting position from the quadruped position.
Can often pull to stand from the quadruped position.
Able to actively flex and extend both legs simultaneously while standing and supporting independently.
Very active with large variety of movements and positions available.
May show fear of strangers. Findings of concern include:
Lack of weight shifting in prone.
Reliance on more primitive movement patterns as compensations in order to explore.
Inability to assume or maintain quadruped. Poor weight bearing in supported stance.


8
months
Minimal time spent in prone.

Full equilibrium reactions in sitting, and the beginning of equilibrium reactions in quadruped.
Able to side sit and is also
able to go
Can stand by leaning on supporting surfaces.
Able to pull to stand. Early walking, cruising.
Can reach out for objects and reach across the midline of the body without losing balance. The thumb can wrap around objects now the baby can hold
two small objects, such as cubes, in one hand.
Findings of concern include: Poor sitting ability.
Unable to use hand for play.
Overall reliance on upper







from sitting to quadruped. May also kneel.

extremities.


9
months
Able to creep/crawl in the quadruped
position as the primary means of locomotion.

Large variety of sitting positions and movement. Pivoting/long sitting.
Sitting often used as a transitional position.
Uses arms, hands, and body together while pulling up to standing through half kneel position (nine months).
Immature stepping. The sequence in rising to standing is kneeling, half kneeling, weight shift forward, squat, then upright.
The index finger starts to move separately from the rest of the hand when poking at objects. This leads to the pincer grasp, with the tips of the thumb and index finer meeting in a precise pattern.
The baby's ability to let go of an object smoothly has also improved.
Findings of concern include: Poor standing control. Poor/inadequate sitting. Inability to assume quadruped.


10
months


Arms reach above shoulders. Active site sitting.
Rarely stationary.
Creeping/climbing. Legs very active. "High guard." Cruising with wide base of support.



11
months


Able to play and move hands across midline.
Mostly using legs. Very symmetrical standing with a wide base of support.



12 to 15 months



Many babies are walking unassisted.
Able to self feed.
Can build a tower of two cubes.


Two years



Runs well.
Goes upstairs using reciprocal pattern (reciprocal stair climbing).




Data from van Blankenstein M, Welbergen UR, de Haas JH: Le Developpement du Nourrisson: Sa Premiere Annee en 130 Photographies. Paris, Presses Universitaires de France, 1962. ATNR   Asymmetrical tonic neck reflex




Although this progressive sequence appears to be somewhat arbitrary, it is the same sequence that is used to progress a patient who has undergone a compromise to the neuromotor system with such tasks as bed mobility training and balance retraining. Other components worth mentioning because of their importance in neuromuscular rehabilitation but which may not appear in the foregoing developmental sequence of milestones are bridging, supine on elbows, and hooklying.
 Bridging. This involves the lifting of the hips and lower back while in the supine position (Figure 4 23). To avoid putting too much stress on the cervical spine while achieving trunk extension, the patient can use the upper arms to push down into the bed. In addition, assistance can be provided by stabilizing the patient's feet or by having the patient wear shoes to increase the grip. From a functional perspective, acquisition of this skill allows items such as bedpans to be placed underneath the patient, provides pressure relief, and serves as a precursor to scooting in supine.
 Supine on elbows (Figure 4 24). This position involves the raising of the trunk and head off the bed and both elbows placed on the bed to support the position. From a functional perspective, this position is a precursor for scooting in supine in a variety of directions, which is particularly important for bed mobility training (see Chapter 10).
 Hooklying (Figure 4 25). This position involves flexion of both hips and knees in the supine position. From a functional perspective, it is the precursor for bridging, scooting, and rolling (see Chapter 10).

FIGURE  4 23


Bridging


FIGURE  4 24


Supine on elbows




FIGURE  4 25


Hooklying


NORMAL DEVELOPMENT OF MOTOR CONTROL AND MOTOR LEARNING
The term motor control refers to processes of the brain and spinal cord that govern the mechanisms essential to regulate or direct posture and movement using perception and cognition.138 The hallmarks of cognition are observable: selection, sequence generation, and working memory.
Motor learning is a complex set of internal processes that involve the relatively permanent acquisition and retention of a skill or task through practice or the reacquisition of skills that are difficult to perform or cannot be performed because of injury or disease.140, 141 and 142
The traditional study of motor control and development was characterized by detailed observations of progressive changes of different kinds of motor sequences, including actions such as grasping, rolling, crawling, and walking (see Motor Progression). Until fairly recently, many of the theoretical concepts used in physical therapy evaluation and therapeutic intervention were based on the theoretical constructs developed in the 1930s and 1940s. Specifically much credence was given to the neuromaturational theory of development, in which structure preceded function such that changes in motor development were thought to be the results of maturation of the CNS. With development of the CNS, higher centers inhibited lower centers, thereby eliciting voluntary movements through a process of hierarchical control. Since the late 1980s, the CNS has been hypothesized to be multilevel and multisystem rather than hierarchical.
Motor Control



The field of motor control is directed at understanding the control of those movements already acquired and how the neuromuscular system functions to activate and coordinate the muscles and limbs involved in the performance of a motor skill.143 It is thought that infants attain gross and fine motor control along a predetermined and sequential path. Factors that affect motor control include the task, the environment, and the neuromotor capabilities of the individual. Over the years, many theories concerning motor control have evolved in an attempt to describe how movement is controlled. A description of the various theories of motor control follows.
Reflex Theory

In this theory, a stimulus triggers a combined action of individual reflex circuits that create a complex response, such that the performer is a passive recipient responding to the stimuli present in the environment and with which he or she is confronted. The problem with this theory is that not all movement is spontaneous, or activated by an environmental agent. In addition, there is no room for goal oriented or goal directed behavior within such a theory.
Hierarchical Theory

The hierarchical theory of motor control describes how motor programs begin with a definition of a fixed set of commands that can be structured before movement initiation. These motor patterns emerge in orderly predetermined genetic sequences and are based on a number of parameters that specify how a particular movement pattern is to be expressed in terms of the overall duration of a movement, the overall force needed to accomplish the movement, the temporal phasing of the movement pattern, and the spatial and temporal order in which the components of the movement are to be executed. Hierarchical theorists consider that basic motor skills, such as standing and walking, are not learned by experience but are the result of cerebral maturation. More recently, this theory has been modified to recognize the fact that each level of the nervous system can act on other levels (higher and lower) depending on the task and that reflexes are not considered the sole determinant of motor control, but as one of the many processes important to the generation and control of movement.144


Motor Programming Theory 

Although reflex theories are useful in explaining certain stereotyped patterns of movement, they cannot be used to explain all types of movement. It is currently believed that there are certain motor program generators for movement patterns that are inherent in the CNS, and that these naturally develop during the maturation process of the CNS. For example, gait on a level surface is controlled by a set of neural circuits known as a central pattern generator (CPG). CPGs are neural networks that can endogenously (i.e., without rhythmic sensory or central input) produce rhythmic patterned outputs; these networks underlie the production of most rhythmic motor patterns, such as the gait cycle.57,147, 148 and 149
Once this pattern is formed, the individual no longer has to concentrate on performing the activity, but can do so with very little cortical involvement. The motor program for each of these activities is saved in an engram (a hypothetical means by which a patterned response has been stabilized at the level of unconscious competence) within the cerebral cortex.150, 151 and 152 Thousands of repetitions (practice) are required to begin the engram formation, and millions are needed to perfect it.152 Skilled performance is developed in proportion to the number of repetitions of an engram practiced just below the maximal level of ability to perform.153,154




CLINICAL PEARL 

A motor plan is defined as an idea or plan for purposeful movement that is made up of component motor programs.147
A motor program is defined as an abstract representation that, when initiated, results in the production of a coordinated movement sequence.57 Motor programs are codes within the nervous system that when initiated, produce coordinated movement sequences.57 These programs are usually under central control. Sensory input is used extensively in selecting the appropriate motor program, in monitoring whether or not movement is consistent with expectations, and in reflexively modulating the movement so that it is specific to environmental variables.48,57
Reflexes are evoked responses and depend on a stimulus to be initiated. They are involuntary, stereotyped, and graded responses to sensory input, and they have no threshold except that the stimulus must be great enough to activate the relevant sensory input pathway.
Fixed action patterns (sneezing, orgasm) are involuntary and stereotyped, but typically have a stimulus threshold that must be reached before they are triggered and are less graded and more complex than reflexes.
Directed movements (reaching) are voluntary and complex, but are generally neither stereotyped nor repetitive.
Rhythmic motor patterns (walking, scratching, breathing) are complex (unlike reflexes), stereotyped (unlike directed movements), and, by definition, repetitive (unlike fixed action patterns), but are subject to continuous voluntary control.


Many different mechanisms seem to be involved in controlling the timing of movements, from CPGs, to cerebellar estimators, to cortical mechanisms.155 In much the same way as there is a CPG for locomotion, the nervous system has a number of built in corrections that can occur rapidly and automatically to counteract perturbations and continually adjust its position in space. As the infant learns to move against gravity, a number of reactions occur in response to sensory input. These include righting, protective, and equilibrium reactions.
 Righting. Righting reactions function to keep the correct orientation of the head and the body in relation to the ground.
 Protective. Protective reactions are extremity responses to rapid displacement of the body by horizontal or diagonal forces.
 Equilibrium. Equilibrium reactions occur when the center of gravity is changed either by movement of the supporting surface or of the body. The three most common equilibrium reactions include:
 Trunk rotation away from the weight shift
 Lateral head and trunk righting away from the weight shift  Abduction of the arm and leg away from the weight shift
Anticipatory postural adjustments occur in response to internal perturbations such as voluntary movements of the body by activating muscle synergies in advance of the actual perturbation. Research has shown that anticipatory postural adjustments are highly adaptable and vary according to the task demands.156, 157 and 158 For example, postural muscles in standing humans are activated before (and during) voluntary movement of an upper limb and are specific to this movement. Anticipatory postural adjustments have also been studied during leg movements,159,160 trunk movements,161,162 and arm movements in standing subjects,156,163 and during load release from extended arms.164, 165 and 166
Whereas anticipatory reactions are initiated by the subject, compensatory reactions, which occur later, are initiated by sensory feedback triggering signals. With anticipatory reactions, the CNS tries to predict postural perturbations associated with a planned movement and minimize them with anticipatory corrections in a feedforward manner. Compensatory reactions deal with actual perturbations of balance that occur because of the suboptimal efficacy of the anticipatory components. Another motor program that is particularly important is the one responsible for postural stability
 the ability to maintain stable upright stance against internal and external perturbations. Postural balance results from an integration of three components167:



 The nervous system, which provides sensory processing for perception of body orientation in space provided mainly by the visual, vestibular, and somatosensory systems. The sensory motor integration provides motor strategies for the planning, programming, and execution of balance responses.168
 Musculoskeletal contributions including postural alignment, flexibility, joint integrity, muscle performance, and mechanoreceptor sensation.
 Contextual effects that interact with the nervous and musculoskeletal systems. These effects include whether the environment is closed (predictable) or open (unpredictable), the support surface, the amount of lighting, the effects of gravity and inertial forces on the body, and the characteristics of the task (new versus well learned, predictable versus unpredictable, single versus multiple).
The Equilibrium Point (EP)

The EP theory was first described in the 1960s and 1970s.169 Over the past 50 years, it has been revised and refined to a theory addressing the production of complex movements, such as multijoint movement and locomotion, while uniting the processes underlying movement production and perception. Fundamental to the EP theory is the concept that threshold position control triggers intentional motor actions such that electrochemical influences descending from the brain in the presence of proprioceptive feedback to the motoneurons are transformed into modifications in the threshold muscle lengths or joint angles at which these motoneurons begin to be recruited, thus setting the spatial activation range in reference to the body geometry. This allows control levels of the CNS to specify where, in spatial coordinates, muscles are activated without being concerned about the exact details on when and how they are activated.
Motor Learning
Certain assumptions are made with regard to motor learning170:
 The nervous system has the ability to modify neural connections to perform more efficiently, known as neural plasticity.  Short term, or working, memory is necessary for learning new movements.
 Long term memory, the ability to save and retrieve, is necessary for lasting change.  Motor learning occurs naturally during task performance.
Learning, unlike performance, is not something that can be directly measured. Rather, we measure behavior and infer learning when a set of processes associated with practice or experience results in a change in behavior that seems relatively permanent.171

Learning involves both acquisition and retention of a skill. Two main types of learning are recognized171:
1. Declarative or explicit the learning of factual knowledge that can be consciously recalled and thus requires processes such as awareness, attention, and reflection. Examples include buttoning a shirt and tying a shoelace.
2. Nondeclarative or implicit learning that is dependent on practice, association (associating a particular stimulus with another stimulus, or a certain stimulus with a certain response, or a certain response with a certain result), adaptation (making adjustments based on previous results), habituation (filtering out irrelevant stimuli), and sensitization (integration of relevant stimuli). Procedural learning, another type of nondeclarative



   learning, refers to the learning of a task that can be performed automatically without attention or conscious thought, like a habit.143 The most commonly recognized motor learning theories associated with complex skills are discussed next.
Adams' Closed loop Theory

In a closed loop process, sensory feedback is used for the ongoing production of skilled movement.172 The closed loop theory of motor learning also proposes that two distinct types of memory are important in this process:
 Memory trace: used in the selection and initiation of the movement
 Perceptual trace: built up over a period of practice and becomes the internal reference of correctness
This theory proposes that when learning a new movement skill, movement is selected and initiated by a memory trace, which is modified by a perceptual trace with repeated practice, and that the more an individual practices the specific movement, the stronger the perceptual trace becomes. Theoretically, the more time spent in practicing the movement as accurately as possible, the better the learning. However, Adams' theory has been refuted by studies involving animals and humans that have demonstrated that motor learning can occur without sensory feedback, and studies that have indicated that variability in practice may be superior in promoting motor learning than errorless practice.
Schmidt's Schema Theory

This theory emphasizes open loop control processes and the generalized motor program (GMP) concept a set of general rules that can be applied to a variety of contexts.172,173 The schema is a generalized motor program that consists of four parts:
 Initial situation (start of the movement)
 Response specifications (the parameters used in the execution of the movement, e.g., speed)  Sensory consequence (how the movement feels)
 Response outcome (knowledge of result)
These four parts are stored in the memory following the movement as a GMP. A GMP is created from every past movement, and these GMPs are recalled from memory to influence the motor performance of a new task. As a movement is repeated, the GMP becomes stronger. The GMP is considered to contain the rules for creating the spatial and temporal patterns of muscle activity needed to carry out a given movement. A recall schema initiates the GMP that closely resembles the desired movement, and the recognition schema evaluates the last executed movement attempt based on the initial conditions, past actual outcomes, and past sensory information.174 The recall schema is then modified by the movement experience. For example, with every attempt, the recall schema updates the instruction to the muscles based on the recognition schema (it continually revises the initial conditions, past outcomes, and past sensory consequences), which eventually leads to a more accurate response. A major limitation of the original schema theory is that it did not explain how GMPs are initially formed. However, Schmidt's theory has evolved over time and has provided the important motor learning notions of knowledge of results (KR) and variability of practice (see Chapter 7).173
Ecological Theory

This theory, which clarifies the role of perception in motor learning, is based on the concept of search strategies during practice there is a search for optimal strategies to solve the task, based on the task constraints. The hypothesis behind this theory is that constraints in the sensory system and biases in the motor system may have an important adaptive role in ontogeny.




Critical to the search for optimal strategies is the exploration of the perceptual motor workspace, or environment, which requires exploring all possible perceptual cues to identify those that are most relevant to the performance of a specific task. Actions require perceptual information that is specific to a desired goal directed action performed within a specific environment such that the organization of action is specific to the task and the environment in which the task is being performed.144
Dynamic Systems Theory (DST)

One of the most currently accepted approaches to motor and skill learning appears to be Thelen's176, 177 and 178 dynamical functional perspective.176, 177 and 178 DST places less emphasis on the nervous system by viewing movement as emerging from the interaction of three general systems: the person, the task, and the environment.


In contrast to the hierarchical concept of the nervous system, no subsystem has higher control than another, and development is a nonlinear process. Instead, movement is produced from the interaction of multiple subsystems within the framework of degrees of freedom and within the context of a specific task within the context of self organization. According to the DST, cooperating systems, which include musculoskeletal components, sensory systems, central sensorimotor integrated mechanisms, and arousal and motivation, spontaneously self organize, or come together and interact in a specific way, to produce the most efficient movement solution for each specific task to gradually optimize skilled function.179,180 Thus, movements can emerge as a result of interacting elements that interact with one another to either support or constrain movement without the need for specific commands or motor programs within the nervous system. A small but critical change in one subsystem can cause the whole system to shift, resulting in a new motor behavior.




TABLE 4 14
Cognitive Development 

Age Group 
Cognitive Development 
Preschool (3 6 years)
Can remember basic information and recall that information on demand Can answer simple who and what questions
Tend to learn from trial and error
Have short attention spans (5 15 minutes) and selective attention Can identify the missing parts of familiar objects
Can follow simple rules but need visual cues and frequent reminders
Middle childhood (6 11 years)
See things as here and now, right or wrong, and black or white Engage in magical thinking and may believe they have unique powers
Can understand the intent of instructions given and can follow directions Can apply factual knowledge to familiar situations
Can recognize differences between personal performance and the performance or skill of others


According to this theory, the number of biomechanical degrees of freedom of the motor system is dramatically reduced through the development of coordinative structures or temporary accumulations of muscle complexes.181 Degrees of freedom refer to the gradual increase in smoothness of performance of a skilled movement. DST theory suggests that when a novice or an infant is first learning a new skill, the degrees of freedom available in the body are constrained as they perform the task. Descriptive evidence has highlighted that in some tasks the number of degrees of freedom is initially reduced and subsequently increased.182 Although an individual can reasonably perform the task in the early stages of learning, the movement is not efficient and the individual is not able to adapt to environmental changes. Starting with fewer degrees of freedom has been shown to enable a more efficient exploration of the sensorimotor space, and although this does not necessarily lead to optimal task performance, it guides the coordination of additional degrees of freedom.183 Bernstein182 showed that this release of additional degrees of freedom allows for optimal task performance and more tolerance and adaptation to environmental interaction. Several other studies have reported a freezing of joint segments in the initial stage of learning a motor task, including adults learning to write a signature with the nondominant hand184 and to perform tasks while using a ski simulator.185 Based on these observations, three stages of motor learning have been described185, 186 and 187:
Novice. During this stage, the learner simplifies the movement in order to reduce the number of individual elements (degrees of freedom) that must be controlled he or she freezes the degrees of freedom. Examples of freezing the degrees of freedom include blocking some joints within limbs so that the limb moves as a single unit rather than as a multijoint system.



 Advanced. During the advanced stage, the learner begins to free up movement possibilities so that the previously frozen joints are incorporated into larger and more sophisticated units of action (synergies) over the course of practice.
 Expert. The expert stage is one in which the individual has learned to release all the degrees of freedom necessary to perform the task and has learned to take advantage of the mechanics of the musculoskeletal system and of the environment to optimize the efficiency of the movement. Thus, the learner learns to exploit the internal and external forces to achieve the most energetically efficient movement patterns.
The reduced complexity of the motor system theorized in DST encourages the development of functionally preferred or "attractor" states to support goal directed actions. Within each of these attractor regions, the system dynamics are highly ordered and stable, leading to a consistent movement pattern for a specific task. A highly illustrative example of this arises from a series of studies188,189 focusing on the orientation behaviors of the common house fly. Detailed analysis revealed that, as flies orient toward moving objects as part of their mating behavior, the circuitry underlying this behavior forms a motion detection system fed by luminance changes on the fly's facet eye, which in turn drives the flight motor, generating a sufficient amount of torque that is a function of where the motion was detected on the sensory surface. For example, if the speck of motion is detected on the right, a torque to the right is generated and vice versa. This meaningful behavior emerges as a stable state, an attractor, from the neural circuitry that links the sensory surface to the flight motor which, together with the physics of flight, establishes a dynamical system. The research also found that the fly's simple nervous system was able to compute an expected visual motion from its own motor commands and treat the detected visual motion that matched the predicted motion differently than extraneous motion signals related to movement of an object relative to the fly. So even this very simple control system provides hints that uncovering the dynamics from which behavior emerges requires more than a simple input output analysis.

DST has emerged as a viable framework for rehabilitation. Patterns of movement are flexible, adaptable, and dynamic, yet have "preferred" paths. However, flexible and adaptive motor system behavior results from variations between these multiple attractor regions, which encourage the exploration of performance contexts by an individual. Stable movement patterns are those movement patterns that are difficult to change, whereas unstable movement patterns are those that are relatively easy to change. How people switch intentionally from one pattern of movement to another is constrained by stability.190 Only when states are released from stability does behavioral flexibility arise. This release from stability takes the form of instabilities created when the restoring forces around an attractor become too weak to resist change. It would appear that movement coordination emerges as a stable state from a nonlinear, potentially multistable dynamics, realized by neural networks coupled to the body in a structured environment. Movement plans evolve continuously in time191 and are updated at any time during movement preparation when sensory information changes.192 This paradoxical relationship between the stability inherent in simple tasks and the variability in more complex tasks explains why skilled athletes are capable of persistent changes in motor output during high level sports performance. Eventually, the explored task and environmental constraints become stable motor solutions over time, thereby enhancing the coordination of body segments to optimize energy and momentum transfer.





Task oriented Approach

This approach is based on DST in addition to the newest theories and concepts that are emerging from research in the fields of motor control, motor learning, and rehabilitation science.144 Similar to DST, this theory assumes that normal movement emerges as an interaction among many different systems, each contributing different aspects of control.144 In addition, it is theorized that movement is organized around a behavioral goal that is controlled by the environment, so that the role of sensation in normal movement is not limited to a stimulus/response reflex mode, but is crucial to predictive and adaptive control of movement as well. Under this theory, impairments within one or more of the systems controlling movement will result in abnormal motor control such that abnormal movement occurs because of a combination of the lesion itself and the efforts of the remaining systems to compensate for the loss while still being functional.144
From a rehabilitation standpoint, it is important that the clinician select functional tasks that are contextually suitable for the specific patient, rather than movement patterns for movement's sake alone, so that the patient learns by actively attempting to solve the problems inherent in a functional task rather than repetitively practicing normal patterns of movement.144 Clinical practice strategies must emphasize functional, age appropriate tasks incorporated into naturally occurring activities during the day coupled with maximizing practice time (see Chapter 7).
Skilled Movement: Stability and Mobility
Motor function is the ability to demonstrate the skillful and efficient assumption, maintenance, modification, and control of voluntary postures and movement patterns.195 Multiple variables contribute to the initiation and execution of a functional movement (Table 4 15). The criteria for simple motor patterns are that the movement196,197:
 Is performed exactly in the desired direction  Is smooth and of a constant speed
 Follows the shortest and most efficient path  Is performed in its full range



TABLE 4 15
Motor Control Variables 

Variable
Description
Sensorimotor
Those physiologic mechanisms or processes that reside within the nervous system, e.g., central pattern generators (CPGs). Movement synergies and neural mechanisms that alter or regulate them.
Mechanical
Changes in total body mass and relative distribution of mass during development are accompanied by changes in length and center of mass of the body segment, which in turn alter inertial forces due to gravity and during movement.
The viscoelastic properties of musculoskeletal tissues.
Cognitive
May include variables that are dependent on conscious and subconscious processes such as reasoning, memory, or judgment to optimize performance (arousal, motivation, anticipatory or feedforward strategies, a selective use of feedback, practice, and memory).
Task requirements
May include any variable that can contribute to or in some way alter movement, including biomechanical requirements, meaningfulness, predictability, or any other variable associated with a given movement context.


Data from Bradley NS, Westcott SL: Motor control: Developmental aspects of motor control in skill acquisition, in Campbell SK, Vander Linden DW, Palisano RJ (eds): Physical Therapy for Children (ed 3). St Louis, Saunders, 2006, pp 77 130.
The necessary motor responses for functional movements rely on processing and planning at different levels: spinal cord, the brainstem and cerebellum, and the cerebral cortex. The complexity of the processing affects the speed of motor responses, with spinal reflexes representing the shortest neuronal pathway and consequently the most rapid response to afferent stimuli. The criteria for complex motor patterns are as follows196:
 Synchronization between the primary movers in the distal regions with those more proximal  Smooth propagation of motion from one region of the body to another
 Absence of inefficient movement patterns or muscle recruitment
 Optimal relationship between the speed of motion initiated in one region and the speed of motion in other regions
For purposeful and skilled motions to take place, the muscles producing movement must have a stable base from which to work. Thus, integral to the performance of functional movements is the ability to produce a delicate balance between stability and mobility. Stability, the ability of something to remain in place, can be either static or dynamic. Mobility, which refers to the ease at which something can be moved, can be either controlled or uncontrolled. Both stability and mobility are related to the BOS and the COM.




Static stability: the ability to maintain the COM within the BOS so that the body's orientation in space is controlled without movement. For example, an individual who is able to sit upright while maintaining his or her arms down by the sides demonstrates static stability.
Dynamic stability: the ability to maintain and control the body's orientation in space (the COM within the BOS) during movement. For example, the ability to sit upright while the upper extremities perform reaching activities requires dynamic stability.
Controlled mobility: occurs when the COM can be moved beyond and then back within the BOS. The fall that occurs at the initiation of gait so that an individual must take the first step is controlled by the central nervous system.

















In both the spine and the extremities, certain muscles work as either mobilizers or stabilizers. The peripheral stabilizers rely on stabilization of the two primary dynamic bases or core structures the pelvis and the scapula. The pelvis acts as a base for the whole body, especially for the spine and the lower limbs, whereas the scapula acts as a base for its respective upper limb.81 During peripheral joint movement, the peripheral stabilizer muscles normally contract first to stabilize the core structures from which the mobilizers work.81,198 The mobilizers then contract, resulting in a controlled movement pattern. For example, during upper extremity activity, the scapular stabilizers contract first to stabilize the scapula before the other shoulder muscles move the upper extremity into a functional position. However, with injury, a pathologic process, or other abnormality, an abnormal stabilizer recruitment pattern can develop, resulting in a dominance of the mobilizer muscles and eventual weakening of the local stabilizers.81,198 The clinician must therefore ensure that a stable base is present from which the mobilizers can act. The body has several natural stabilization methods including muscle contraction, muscle spasm, osteophyte formation, scar tissue formation, and adaptive shortening of inert tissue or muscle.81 Although the clinician cannot affect some of these natural stabilization methods such as osteophyte and scar tissue formation, the clinician can use muscle contraction and adaptive shortening to the patient's advantage. Factors that the clinician can control include the COM of an object and the BOS (see Kinetics earlier).

Gravity also has an impact on stability. When the line of gravity intersects the BOS in such a way that it provides for the greatest range of movement within the base, stability is enhanced. To promote stability, the clinician must minimize the distance between the COM and the BOS (crouching, kneeling, or sitting lower the COM and increase stability) and ensure that the force of gravity on the COM is acting at or near the center of the BOS. In contrast, to promote mobility, the clinician should reduce the BOS, allow the force of gravity to act beyond the center of the BOS, and increase the



distance between the COM and the BOS.

The various applications of these principles are described throughout a number of chapters in the second half of this book.
REFERENCES

1. Saladin KS: Human development, in Human Anatomy (ed 3). New York, McGraw Hill, 2011, pp 82 105.

2. Christian EL: Embryology and the evolution of movement and function, in Scully RM, Barnes MR (eds): Physical Therapy (ed 1). Philadelphia, JB Lippincott, 1989, pp 48 62.

3. Saladin KS: Histology The study of tissues, in Human Anatomy (ed 3). New York, McGraw Hill, 2011, pp 52 81.

4. Hall SJ: The biomechanics of human skeletal muscle, in Hall SJ (ed): Basic Biomechanics. New York, McGraw Hill, 1999, pp 146 185.

5. Starcher BC: Lung elastin and matrix. Chest 117(5 Suppl 1):229S 34S, 2000. CrossRef [PubMed: 10843923] 

6. Engles M: Tissue response, in Donatelli R, Wooden MJ (eds): Orthopaedic Physical Therapy (ed 3). Philadelphia, Churchill Livingstone, 2001, pp 1  24.

7. Teitz CC, Garrett WE Jr, Miniaci A et al.: Tendon problems in athletic individuals. J Bone Joint Surg 79A:138 152, 1997.

8. Barnes J: Myofascial Release: A Comprehensive Evaluatory and Treatment Approach. Paoli, PA, MFR Seminars, 1990.

9. Smolders JJ: Myofascial pain and dysfunction syndromes, in Hammer WI (ed): Functional Soft Tissue Examination and Treatment by Manual Methods The Extremities. Gaithersburg, MD, Aspen, 1991, pp 215 234.

10. Curwin SL: Tendon pathology and injuries: Pathophysiology, healing, and treatment considerations, in Magee D, Zachazewski JE, Quillen WS (eds): Scientific foundations and principles of practice in musculoskeletal rehabilitation. St Louis, Mo, WB Saunders, 2007, pp 47 78.

11. Amiel D, Woo SL Y, Harwood FL: The effect of immobilization on collagen turnover in connective tissue: A biochemical biomechanical correlation. Acta Orthop Scand 53:325 332, 1982.
CrossRef [PubMed: 7090757] 

12. Benjamin M, Toumi H, Ralphs JR et al.: Where tendons and ligaments meet bone: attachment sites ("entheses") in relation to exercise and/or mechanical load. J Anat 208:471 490, 2006.




13. Maganaris CN, Narici MV, Almekinders LC et al.: Biomechanics and pathophysiology of overuse tendon injuries: ideas on insertional tendinopathy. Sports Med 34:1005 1017, 2004.
CrossRef [PubMed: 15571430] 

14. Reid DC: Sports Injury Assessment and Rehabilitation. New York, Churchill Livingstone, 1992.

15. Garrett W, Tidball J: Myotendinous junction: Structure, function, and failure, in Woo SL Y, Buckwalter JA (eds): Injury and Repair of the Musculoskeletal Soft Tissues. Rosemont, Ill, AAOS, 1988.

16. Garrett WE Jr: Muscle strain injuries: clinical and basic aspects. Med Sci Sports Exerc 22:436 443, 1990. CrossRef [PubMed: 2205779] 

17. Garrett WE: Muscle strain injuries. Am J Sports Med 24:S2 S8, 1996. CrossRef [PubMed: 8947416] 

18. Safran MR, Seaber AV, Garrett WE: Warm up and muscular injury prevention: An update. Sports Med 8:239 249, 1989. CrossRef [PubMed: 2692118] 

19. Huijbregts PA: Muscle injury, regeneration, and repair. J Man Manip Ther 9:9 16, 2001. CrossRef

20. Hildebrand KA, Hart DA, Rattner JB et al.: Ligament injuries: pathophysiology, healing, and treatment considerations, in Magee D, Zachazewski JE, Quillen WS (eds): Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St Louis, Mo, WB Saunders, 2007, pp 23 46.

21. Vereeke West R, Fu F: Soft tissue physiology and repair, Orthopaedic Knowledge Update 8: Home Study Syllabus. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2005, pp 15 27.

22. Amiel D, Kleiner JB: Biochemistry of tendon and ligament, in Nimni ME (ed): Collagen. Boca Raton, FL, CRC Press, 1988, pp 223 251.

23. Woo SL Y, An K N, Arnoczky SP et al.: Anatomy, biology, and biomechanics of tendon, ligament, and meniscus, in Simon S (ed): Orthopaedic Basic Science. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1994, pp 45 87.

24. Safran MR, Benedetti RS, Bartolozzi AR, III et al.: Lateral ankle sprains: a comprehensive review: part 1: etiology, pathoanatomy, histopathogenesis, and diagnosis. Med Sci Sports Exerc 31:S429 S437, 1999.
CrossRef [PubMed: 10416544] 

25. Smith RL, Brunolli J: Shoulder kinesthesia after anterior glenohumeral dislocation. Phys Ther 69:106 112, 1989. [PubMed: 2913578]


26. McGaw WT: The effect of tension on collagen remodelling by fibroblasts: a stereological ultrastructural study. Connect Tissue Res 14:229, 1986. CrossRef [PubMed: 2938879] 

27. Inman VT: Sprains of the ankle, in Chapman MW (ed): AAOS Instructional Course Lectures, 1975, pp 294 308.

28. Cohen NP, Foster RJ, Mow VC: Composition and dynamics of articular cartilage: structure, function, and maintaining healthy state. J Orthop Sports Phys Ther 28:203 15, 1998.




29. Junqueira LC, Carneciro J, Kelley RO: Basic Histology. Norwalk, Conn, Appleton and Lange, 1995.

30. Lundon K, Bolton K: Structure and function of the lumbar intervertebral disk in health, aging, and pathological conditions. J Orthop Sports Phys Ther 31:291 306, 2001.
CrossRef [PubMed: 11411624] 

31. Mankin HJ, Mow VC, Buckwalter JA et al.: Form and function of articular cartilage, in Simon SR (ed): Orthopaedic Basic Science. Rosemont, IL, American Academy of Orthopaedic Surgeons, 1994, pp 1 44.

32. Muir H: Proteoglycans as organizers of the extracellular matrix. Biochem Soc Trans 11:613 622, 1983. [PubMed: 6667766] 

33. Buchbinder D, Kaplan AS: Biology, in Kaplan AS, Assael LA (eds): Temporomandibular disorders diagnosis and treatment. Philadelphia, WB Saunders, 1991, pp 11 23.

34. Tippett SR: Considerations for the pediatric patient, in Voight ML, Hoogenboom BJ, Prentice WE (eds): Musculoskeletal Interventions: Techniques for Therapeutic Exercise. New York, McGraw Hill, 2007, pp 803 820.

35. Iannotti JP, Goldstein S, Kuhn J et al.: The formation and growth of skeletal tissues, in Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopedic Basic Science. Rosemont, Ill, American Academy of Orthopedic Surgeons, 2000, pp 77 109.

36. Waxman SG: Correlative Neuroanatomy (ed 24). New York, McGraw Hill, 1996.

37. Butler DS, Tomberlin JP: Peripheral nerve: structure, function, and physiology, in Magee D, Zachazewski JE, Quillen WS (eds): Scientific foundations and principles of practice in musculoskeletal rehabilitation. St Louis, Mo, WB Saunders, 2007, pp 175 189.

38. Pratt N: Anatomy of the Cervical Spine. La Crosse, Wisc, Orthopaedic Section, APTA, 1996.

39. Martin J: Introduction to the central nervous system, in Martin J (ed): Neuroanatomy: Text and Atlas (ed 2). New York, McGraw Hill, 1996, pp 1 32.

40. Chusid JG: Correlative Neuroanatomy & Functional Neurology (ed 19). Norwalk, Conn, Appleton Century Crofts, 1985, pp 144 148.

41. Freeman MAR, Wyke BD: An experimental study of articular neurology. J Bone Joint Surg 49B:185, 1967.

42. Wyke BD: The neurology of joints: a review of general principles. Clin Rheum Dis 7:223 239, 1981.

43. Voight ML, Cook G: Impaired neuromuscular control: Reactive neuromuscular training, in Voight ML, Hoogenboom BJ, Prentice WE (eds): Musculoskeletal Interventions: Techniques for Therapeutic Exercise. New York, McGraw Hill, 2007, pp 181 212.

44. Voss H: [Tabulation of the absolute and relative muscular spindle numbers in human skeletal musculature]. Anat Anz 129:562 72, 1971. [PubMed: 4260484] 

45. Peck D, Buxton DF, Nitz A: A comparison of spindle concentrations in large and small muscles acting in parallel combinations. J Morphol 180:243  252, 1984.
CrossRef [PubMed: 6235379] 

46. Nyland J, Lachman N, Kocabey Y et al.: Anatomy, function, and rehabilitation of the popliteus musculotendinous complex. J Orthop Sports Phys Ther 35:165 179, 2005.




47. Grigg P, Hoffmann AH: Properties of Ruffini afferents revealed by stress analysis of isolated sections of cat knee capsule. J Neurophysiol 47:41 54, 1982. [PubMed: 7057224] 

48. Williams GN, Krishnan C: Articular neurophysiology and sensorimotor control, in Magee D, Zachazewski JE, Quillen WS (eds): Scientific foundations and principles of practice in musculoskeletal rehabilitation. St Louis, Mo, WB Saunders, 2007, pp 190 216.

49. Zimny ML: Mechanoreceptors in articular tissues. Am J Anat 182:16 32, 1988. CrossRef [PubMed: 3291597] 

50. Wyke BD: Articular neurology and manipulative therapy, in Glasgow EF, Twomey LT, Scull ER et al. (eds): Aspects of Manipulative Therapy (ed 2). New York, Churchill Livingstone, 1985, pp 72 77.

51. Grigg A, Hoffman AH, Fogarty KE: Properties of Golgi Mazzoni afferents in cat knee joint capsule, as revealed by mechanical studies of isolated joint capsule. J Neurophysiol 47:31 40, 1982. [PubMed: 7057223] 

52. Schutte MJ, Happel RT: Joint innervation in joint injury. Clin Sports Med 9:511 517, 1990. [PubMed: 2183957] 

53. Milne RJ, Foreman RD, Giesler GJ et al.: Convergence of cutaneous and pelvic visceral nociceptive inputs onto primate spinothalamic neurons. Pain 11:163 183, 1981.
CrossRef [PubMed: 7322601] 

54. Vierck CJ, Greenspan JD, Ritz LA: Long term changes in purposive and reflexive responses to nociceptive stimulation following anterior lateral chordotomy. J Neurosci 10:2077 2095, 1990. [PubMed: 2376769] 

55. Schaible HG, Schmidt RF: Discharge characteristics of receptors with fine afferents from normal and inflamed joints: influence of analgesics and prostaglandins. Agents Actions Suppl 19:99 117, 1986. [PubMed: 3463187] 

56. Rose J: Dynamic lower extremity stability, in Hughes C (ed): Movement Disorders and Neuromuscular Interventions for the Trunk and Extremities  Independent Study Course 18.2.5. La Crosse, Wisc, Orthopaedic Section, APTA, Inc, 2008, pp 1 34.

57. Schmidt R, Lee T: Motor control and learning (ed 4). Champaign, Ill, Human Kinetics, 2005.

58. Lee WA: Anticipatory control of postural and task muscles during rapid arm flexion. J Mot Behav 12:185 196, 1980. CrossRef [PubMed: 15178529] 

59. Jones D, Round D: Skeletal muscle in health and disease. Manchester, UK, Manchester University Press, 1990.

60. Loitz Ramage B, Zernicke R: Bone biology and mechanics, in Zachazewski J, Magee D, Quillen W (eds): Athletic Injuries and Rehabilitation. Philadelphia, WB Saunders, 1996.

61. Armstrong RB, Warren GL, Warren JA: Mechanisms of exercise induced muscle fibre injury. Med Sci Sports Exerc 24:436 443, 1990.

62. Van de Graaff KM, Fox SI: Muscle tissue and muscle physiology, in Van de Graaff KM, Fox SI (eds): Concepts of Human Anatomy and Physiology. New York, WCB/McGraw Hill, 1999, pp 280 305.

63. Williams JH, Klug GA: Calcium exchange hypothesis of skeletal muscle fatigue. A brief review. Muscle Nerve 18:421, 1995.




64. Brooke MH, Kaiser KK: The use and abuse of muscle histochemistry. Ann N Y Acad Sci 228:121, 1974. CrossRef [PubMed: 4152235] 

65. Staron RS, Hikida RS: Histochemical, biochemical, and ultrastructural analyses of single human muscle fibers, with special reference to the C fiber population. J Histochem Cytochem 40:563 568, 1992.
CrossRef [PubMed: 1552189] 

66. Jull GA, Janda V: Muscle and motor control in low back pain, in Twomey LT, Taylor JR (eds): Physical Therapy of the Low Back: Clinics in Physical Therapy. New York, Churchill Livingstone, 1987, pp 258 278.

67. Fitts RH, Widrick JJ: Muscle mechanics; adaptations with exercise training. Exerc Sport Sci Rev 24:427 473, 1996. CrossRef [PubMed: 8744258] 

68. Allemeier CA, Fry AC, Johnson P et al.: Effects of spring cycle training on human skeletal muscle. J Appl Physiol 77:2385, 1994. [PubMed: 7868459]


69. Nilsson J, Tesch PA, Thorstensson A: Fatigue and EMG of repeated fast and voluntary contractions in man. Acta Physiol Scand 101:194, 1977. CrossRef [PubMed: 920213] 

70. Sell S, Zacher J, Lack S: Disorders of proprioception of arthrotic knee joint. Z Rheumatol 52:150 155, 1993. [PubMed: 8368019] 

71. Mattacola CG, Lloyd JW: Effects of a 6 week strength and proprioception training program on measures of dynamic balance: a single case design. J Athl Training 32:127 135, 1997.

72. McArdle W, Katch FI, Katch VL: Exercise Physiology: Energy, Nutrition, and Human Performance. Philadelphia, Lea and Febiger, 1991.

73. Astrand PO, Rodahl K: The Muscle and its Contraction: Textbook of Work Physiology. New York, McGraw Hill, 1986.

74. Edman KAP RC: The sarcomere length tension relation determined in short segments of intact muscle fibres of the frog. J Physiol 385:729 732, 1987.
CrossRef

75. Boeckmann RR, Ellenbecker TS: Biomechanics, in Ellenbecker TS (ed): Knee Ligament Rehabilitation. Philadelphia, Churchill Livingstone, 2000, pp 16 23.

76. Brownstein B, Noyes FR, Mangine RE et al.: Anatomy and biomechanics, in Mangine RE (ed): Physical Therapy of the Knee. New York, Churchill Livingstone, 1988, pp 1 30.

77. Deudsinger RH: Biomechanics in clinical practice. Phys Ther 64:1860 1868, 1984. [PubMed: 6505030] 

78. Lakomy HKA: The biomechanics of human movement, in Maughan RJ (ed): Basic and Applied Sciences for Sports Medicine. Woburn, Mass, Butterworth Heinemann, 1999, pp 124 125.

79. Desmendt JE, Godaux E: Fast motor units are not preferentially activated in rapid voluntary contractions in man. Nature 267:717, 1977. CrossRef [PubMed: 876393] 




80. Gans C: Fiber architecture and muscle function. Exerc Sport Sci Rev 10:160, 1982. CrossRef [PubMed: 6749514] 

81. Magee DJ, Zachazewski JE: Principles of stabilization training, in Magee D, Zachazewski JE, Quillen WS (eds): Scientific foundations and principles of practice in musculoskeletal rehabilitation. St Louis, Mo, WB Saunders, 2007, pp 388 413.

82. Lash JM: Regulation of skeletal muscle blood flow during contractions. Proc Soc Exp Biol Med 211:218 235, 1996. CrossRef [PubMed: 8633102] 

83. Rosenbaum D, Henning EM: The influence of stretching and warm up exercises on Achilles tendon reflex activity. J Sports Sci 13:481, 1995. CrossRef [PubMed: 8850574] 

84. Astrand PO, Rodahl K: Physical Training: Textbook of Work Physiology. New York, McGraw Hill, 1986.

85. Grimes K: Heart disease, in O'Sullivan SB, Schmitz TJ (eds): Physical Rehabilitation (ed 5). Philadelphia, FA Davis, 2007, pp 589 641.

86. Shaffer TH, Wolfson MR, Gault JH: Respiratory Physiology, in Irwin S, Tecklin JS (eds): Cardiopulmonary Physical Therapy (ed 2). St Louis, Mosby, 1990, pp 217 244.

87. Van de Graaff KM, Fox SI: Respiratory system, in Van de Graaff KM, Fox SI (eds): Concepts of Human Anatomy and Physiology. New York, WCB/McGraw Hill, 1999, pp 728 777.

88. Collins SM, Cocanour B: Anatomy of the cardiopulmonary system, in DeTurk WE, Cahalin LP (eds): Cardiovascular and Pulmonary Physical Therapy: an Evidence Based Approach. New York, McGraw Hill, 2004, pp 73 94.

89. Schmitz TJ: Vital signs, in O'Sullivan SB, Schmitz TJ (eds): Physical Rehabilitation (ed 5). Philadelphia, FA Davis, 2007, pp 81 120.

90. Sahlin K, Tonkonogi M, Soderlund K: Energy supply and muscle fatigue in humans. Acta Physiol Scand 162:261 266, 1998. CrossRef [PubMed: 9578371] 

91. McMahon S, Jenkins D: Factors affecting the rate of phosphocreatine resynthesis following intense exercise. Sports Med 32:761 784, 2002. CrossRef [PubMed: 12238940] 

92. Walter G, Vandenborne K, McCully KK et al.: Noninvasive measurement of phosphocreatine recovery kinetics in single human muscles. Am J Physiol 272:C525 C534, 1997. [PubMed: 9124295] 

93. Bangsbo J: Muscle oxygen uptake in humans at onset and during intense exercise. Acta Physiol Scand 168:457 464, 2000. CrossRef [PubMed: 10759582] 

94. Hoppeler H, Fluck M: Plasticity of skeletal muscle mitochondria: structure and function. Med Sci Sports Exerc 35:95 104, 2003. CrossRef [PubMed: 12544642] 

95. Tonkonogi M, Sahlin K: Physical exercise and mitochondrial function in human skeletal muscle. Exerc Sport Sci Rev 30:129 137, 2002. CrossRef [PubMed: 12150572] 

96. Sahlin K, Ren JM: Relationship of contraction capacity to metabolic changes during recovery from a fatiguing contraction. J Appl Physiol 67:648  54, 1989. [PubMed: 2793665] 




97. Sells P, Prentice WE: Impaired endurance: Maintaining aerobic capacity and endurance, in Voight ML, Hoogenboom BJ, Prentice WE (eds): Musculoskeletal Interventions: Techniques for Therapeutic Exercise. New York, McGraw Hill, 2007, pp 153 164.

98. Kiser DM: Physiological and biomechanical factors for understanding repetitive motion injuries. Semin Occup Med 2:11 17, 1987.

99. Luttgens K, Hamilton K: The musculoskeletal system: The musculature, in Luttgens K, Hamilton K (eds): Kinesiology: Scientific Basis of Human Motion (ed 9). Dubuque, Iowa, McGraw Hill, 1997, pp 49 75.

100. Howald H, Hoppeler H, Claassen H et al.: Influences of endurance training on the ultrastructural composition of the different muscle fiber types in humans. Pflugers Arch 403:369 376, 1985.
CrossRef [PubMed: 4011389] 

101. Hill AV: The heat and shortening and the dynamic constants of muscle. Proc R Soc Lond B126:136 195, 1938. CrossRef

102. Tihanyi J, Apor P, Fekete GY: Force velocity power characteristics and fiber composition in human knee extensor muscles. Eur J Appl Physiol 48:331 343, 1982.
CrossRef

103. American Medical Association: Guides to the Evaluation of Permanent Impairment (ed 5). Chicago, American Medical Association, 2001.

104. Prentice WE: Impaired mobility: Restoring range of motion and improving flexibility, in Voight ML, Hoogenboom BJ, Prentice WE (eds): Musculoskeletal Interventions: Techniques for Therapeutic Exercise. New York, McGraw Hill, 2007, pp 165 180.

105. The American Orthopaedic Society for Sports Medicine: Flexibility. Chicago, The American Orthopaedic Society for Sports Medicine, 1988.

106. Gleim GW, McHugh MP: Flexibility and its effects on sports injury and performance. Sports Med 24:289 299, 1997. CrossRef [PubMed: 9368275] 

107. Kippers V, Parker AW: Toe touch test: a measure of validity. Phys Ther 67:1680 1684, 1987. [PubMed: 3671506] 

108. Jackson AW, Baker AA: The relationship of the sit and reach test to criterion measures of hamstring and back flexibility in young females. Res Q Exerc Sport 57:183 186, 1986.
CrossRef

109. Litsky AS, Spector M: Biomaterials, in Simon SR (ed): Orthopaedic Basic Science. Chicago, The American Orthopaedic Society for Sports Medicine, 1994, pp 447 486.

110. Johns R, Wright V: Relative importance of various tissues in joint stiffness. J Appl Physiol 17:824 830, 1962.

111. Toft E, Espersen GT, Kalund S et al.: Passive tension of the ankle before and after stretching. Am J Sports Med 17:489 494, 1989. CrossRef [PubMed: 2782533] 

112. Halbertsma JPK, Goeken LNH: Stretching exercises: effect of passive extensibility and stiffness in short hamstrings of healthy subjects. Arch Phys Med Rehab 75:976 981, 1994.

113. Magnusson SP, Simonsen EB, Aagaard P et al.: A mechanism for altered flexibility in human skeletal muscle. J Physiol 497:291 298, 1996. CrossRef [PubMed: 8951730] 

 114. Klinge K, Magnusson SP, Simonsen EB et al.: The effect of strength and flexibility on skeletal muscle EMG activity, stiffness and viscoelastic stress 



relaxation response. Am J Sports Med 25:710 6, 1997. CrossRef [PubMed: 9302482] 

115. Lapier TK, Burton HW, Almon RF: Alterations in intramuscular connective tissue after limb casting affect contraction induced muscle injury. J Appl Physiol 78:1065 1069, 1995. [PubMed: 7775299] 

116. McNair PJ, Wood GA, Marshall RN: Stiffness of the hamstring muscles and its relationship to function in ACL deficient individuals. Clin Biomech 7:131 137, 1992.
CrossRef

117. McHugh MP, Magnusson SP, Gleim GW et al.: A cross sectional study of age related musculoskeletal and physiological changes in soccer players. Med Exerc Nutr Health 2:261 268, 1993.

118. Hutton RS: Neuromuscular basis of stretching exercise, in Komi PV (ed): Strength and Power in Sports. Oxford, Blackwell Science, 1993, pp 29 38.

119. Neumann DA: Getting started, in Neumann DA (ed): Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. St Louis, Mo, Mosby, 2002, pp 3 24.

120. Topoleski LD: Mechanical properties of materials, in Oatis CA (ed): Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Lippincott Williams & Wilkins, 2004, pp 21 35.

121. Woo SL Y, Buckwalter JA: Injury and Repair of the Musculoskeletal Tissue. Park Ridge, IL, American Academy of Orthopaedic Surgeons, 1988.

122. Goel VK, Khandha A, Vadapalli S: Musculoskeletal Biomechanics, Orthopaedic Knowledge Update 8: Home Study Syllabus. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2005, pp 39 56.

123. Noyes FR, Butler DL, Paulos LE et al.: Intra articular cruciate reconstruction. I: Perspectives on graft strength, vascularization and immediate motion after replacement. Clin Orthop 172:71 77, 1983. [PubMed: 6337002] 

124. Laros GS, Tipton CM, Cooper R: Influence of physical activity on ligament insertions in the knees of dogs. J Bone Joint Surg 53B:275 286, 1971.

125. Nimni ME: Collagen: structure function and metabolism in normal and fibrotic tissue. Semin Arthritis Rheum 13:1 86, 1983. CrossRef [PubMed: 6138859] 

126. Noyes FR, Torvik PJ, Hyde WB et al.: Biomechanics of ligament failure: II. An analysis of immobilization, exercise, and reconditioning effects in primates. J Bone Joint Surg 56A:1406 1418, 1974.

127. Hall SJ: Kinematic concepts for analyzing human motion, in Hall SJ (ed): Basic Biomechanics. New York, McGraw Hill, 1999, pp 28 89.

128. Lehmkuhl LD, Smith LK: Brunnstrom's Clinical Kinesiology. Philadelphia, FA Davis, 1983, pp 361 390.

129. MacConnail MA, Basmajian JV: Muscles and Movements: A Basis for Human Kinesiology. New York, Robert Krieger, 1977.

130. Rasch PJ, Burke RK: Kinesiology and Applied Anatomy. Philadelphia, Lea and Febiger, 1971.

131. Steindler A: Kinesiology of the Human Body under Normal and Pathological Conditions. Springfield, Ill, Charles C Thomas, 1955.

132. Williams PL, Warwick R, Dyson M et al.: Gray's Anatomy (ed 37). London, Churchill Livingstone, 1989.

133. Mennell JB: The Science and Art of Joint Manipulation. London, J & A Churchill, 1949.



134. Mennell JM: Back Pain. Diagnosis and Treatment Using Manipulative Techniques. Boston, Mass, Little, Brown, 1960.

135. Marino M: Current concepts of rehabilitation in sports medicine, in Nicholas JA, Herschman EB (eds): The Lower Extremity and Spine in Sports Medicine. St Louis, Mo, Mosby, 1986, pp 117 195.

136. Blackard DO, Jensen RL, Ebben WP: Use of EMG analysis in challenging kinetic chain terminology. Med Sci Sports Exerc 31:443 448, 1999. CrossRef [PubMed: 10188750] 

137. Dillman CJ, Murray TA, Hintermeister RA: Biomechanical differences of open and closed chain exercises with respect to the shoulder. J Sport Rehabil 3:228 238, 1994.

138. Van Sant AF: Concepts of neural organization and movement, in Connolly BH, Montgomery PC (eds): Therapeutic Exercise in Developmental Disabilities (ed 2). Thorofare, NJ, Slack, Inc, 2001, pp 1 12.

139. Lewis C: Physiological response to exercise in the child: considerations for the typically and atypically developing youngster, Proceedings from the American Physical Therapy Association combined sections meeting. San Antonio, Texas, 2001.

140. Winstein CJ, Knecht HG: Movement science and its relevance to physical therapy. Phys Ther 70:759 762, 1990. [PubMed: 2236219] 

141. Winstein CJ: Knowledge of results and motor learning implications for physical therapy. Phys Ther 71:140 149, 1991. [PubMed: 1989009]


142. Winstein CJ: Motor learning considerations in stroke rehabilitation, in Duncan PW, Badke MB (eds): Stroke Rehabilitation: The Recovery of Motor Control. Chicago, Yearbook Medical Publishers, 1987, pp 109 134.

143. Shumway Cook A, Woollacott MH: Motor learning and recovery of function, in Shumway Cook A, Woollacott MH (eds): Motor Control  Translating Research into Clinical Practice. Philadelphia, Lippincott Williams & Wilkins, 2007, pp 21 45.

144. Shumway Cook A, Woollacott MH: Motor control: issues and theories, in Shumway Cook A, Woollacott MH (eds): Motor Control Translating Research into Clinical Practice. Philadelphia, Lippincott Williams & Wilkins, 2007, pp 3 20.

145. Horak FB: Assumptions underlying motor control for neurologic rehabilitation, in Lister MJ (ed): Contemporary Management of Motor Control Problems: Proceedings of the II STEP Conference. Alexandria, VA, Foundation for Physical Therapy, 1991, pp 11 27.

146. Campbell SK: The child's development of functional movement, in Campbell SK, Vander Linden DW, Palisano RJ (eds): Physical Therapy for Children. St Louis, Mo, Saunders, 2006, pp 33 76.

147. O'Sullivan SB: Strategies to improve motor function, in O'Sullivan SB, Schmitz TJ (eds): Physical Rehabilitation (ed 5). Philadelphia, FA Davis, 2007, pp 471 522.

148. Thompson S, Watson WH 3rd: Central pattern generator for swimming in Melibe. J Exp Biol 208:1347 1361, 2005. CrossRef [PubMed: 15781895] 

149. Yamaguchi T: The central pattern generator for forelimb locomotion in the cat. Prog Brain Res 143:115 122, 2004. [PubMed: 14653156]


150. Agnati LF, Franzen O, Ferre S et al.: Possible role of intramembrane receptor receptor interactions in memory and learning via formation of long lived heteromeric complexes: focus on motor learning in the basal ganglia. J Neural Transm Suppl 65:1 28, 2003. [PubMed: 12946046]





151. Agnati LF, Fuxe K, Ferri M et al.: A new hypothesis on memory a possible role of local circuits in the formation of the memory trace. Med Biol 59:224 229, 1981. [PubMed: 7339294] 

152. Morris C, Chaitow L, Janda V: Functional examination for low back syndromes, in Morris C (ed): Low back syndromes: Integrated clinical management. New York, McGraw Hill, 2006, pp 333 416.

153. Kottke FJ: From reflex to skill: the training of coordination. Arch Phys Med Rehabil 61:551 561, 1980. [PubMed: 7458618] 

154. Kottke FJ, Halpern D, Easton JK et al.: The training of coordination. Arch Phys Med Rehabil 59:567 572, 1978. [PubMed: 736762] 

155. Ivry RB, Diedrichsen J, Spencer R et al.: A cognitive neuroscience perspective on bimanual coordination and interference, in Swinnen SP, Duysens J (eds): Neuro Behavioral Determinants of Interlimb Coordination An Interdisciplinary Approach. Dordrecht, The Netherlands, Kluwer Academic, 2004, pp 259 295.

156. Cordo PJ, Nashner LM: Properties of postural adjustments associated with rapid arm movements. J Neurophysiol 47:287 302, 1982. [PubMed: 7062101] 

157. Nashner LM, Forssberg H: Phase dependent organization of postural adjustments associated with arm movements while walking. J Neurophysiol 55:1382 1394, 1986. [PubMed: 3734862] 

158. Krishnamoorthy V, Latash ML: Reversals of anticipatory postural adjustments during voluntary sway in humans. J Physiol 565:675 684, 2005. CrossRef [PubMed: 15790661] 

159. Rogers MW, Pai YC: Dynamic transitions in stance support accompanying leg flexion movements in man. Exp Brain Res 81:398 402, 1990. CrossRef [PubMed: 2397765] 

160. Mouchnino L, Aurenty R, Massion J et al.: Coordination between equilibrium and head trunk orientation during leg movement: a new strategy build up by training. J Neurophysiol 67:1587 1598, 1992. [PubMed: 1629766] 

161. Oddsson L, Thorstensson A: Fast voluntary trunk flexion movements in standing: motor patterns. Acta Physiol Scand 129:93 106, 1987. CrossRef [PubMed: 3565047] 

162. Pedotti A, Crenna P, Deat A et al.: Postural synergies in axial movements: short and long term adaptation. Exp Brain Res 74:3 10, 1989. CrossRef [PubMed: 2924840] 

163. Friedli WG, Hallett M, Simon SR: Postural adjustments associated with rapid voluntary arm movements 1. Electromyographic data. J Neurol Neurosurg Psychiatry 47:611 622, 1984.
CrossRef [PubMed: 6736995] 

164. Aruin AS, Latash ML: The role of motor action in anticipatory postural adjustments studied with self induced and externally triggered perturbations. Exp Brain Res 106:291 300, 1995.
CrossRef [PubMed: 8566194] 

165. De Wolf S, Slijper H, Latash ML: Anticipatory postural adjustments during self paced and reaction time movements. Exp Brain Res 121:7 19, 1998. CrossRef [PubMed: 9698185] 




166. Benvenuti F, Stanhope SJ, Thomas SL et al.: Flexibility of anticipatory postural adjustments revealed by self paced and reaction time arm movements. Brain Res 761:59 70, 1997.
CrossRef [PubMed: 9247066] 

167. Kloos A: Mechanics and control of posture and balance, in Hughes C (ed): Movement Disorders and Neuromuscular Interventions for the Trunk and Extremities Independent Study Course 18.2.2. La Crosse, Wisc, Orthopaedic Section, APTA, Inc, 2008, pp 1 26.

168. Horak FB: Postural orientation and equilibrium: what do we need to know about neural control of balance to prevent falls? Age Ageing 35 Suppl 2:ii7 ii11, 2006.
CrossRef [PubMed: 16926210] 

169. Latash ML, Levin MF, Scholz JP et al.: Motor control theories and their applications. Medicina (Kaunas) 46:382 392, 2010. [PubMed: 20944446]


170. Cole M: Applied theories in occupational therapy: a practical approach. Thorofare, NJ, Slack Inc, 2007.

171. Buford JA: Neuroscience of motor control and learning, in Hughes C (ed): Movement Disorders and Neuromuscular Interventions for the Trunk and Extremities Independent Study Course 18.2.1. La Crosse, Wisc, Orthopaedic Section, APTA, Inc, 2008, pp 1 23.

172. Shumway Cook A, Woollacott MH: Motor learning and recovery of function, in Shumway Cook A, Woollacott MH (eds): Motor Control: Theory and Practical Applications (ed 2). Philadelphia, Lippincott Williams & Wilkins, 2001, pp 26 49.

173. Schmidt RA: Motor schema theory after 27 years: reflections and implications for a new theory. Res Q Exerc Sport 74:366 375, 2003. CrossRef [PubMed: 14768837] 

174. Zwicker JG, Harris SR: A reflection on motor learning theory in pediatric occupational therapy practice. Can J Occup Ther 76:29 37, 2009. CrossRef [PubMed: 19341020] 

175. Newell KM: Constraints on the development of coordination, in Wade MG, Whiting HTA (eds): Motor Development in Children: aspect of Coordination and Control. Boston, Martinus Nijhoff, 1985, pp 341 360.

176. Thelen E: Motor development. A new synthesis. Am Psychol 50:79 95, 1995. CrossRef [PubMed: 7879990] 

177. Thelen E, Corbetta D: Exploration and selection in the early acquisition of skill. Int Rev Neurobiol 37:75 102, 1994. [PubMed: 7883488]


178. Thelen E, Ulrich BD: Hidden skills: a dynamic systems analysis of treadmill stepping during the first year. Monogr Soc Res Child Dev 56:1 98, 1991. CrossRef [PubMed: 1922136] 

179. Palisano RJ, Campbell SK, Harris SR: Evidence based decision making in pediatric physical therapy, in Campbell SK, Vander Linden DW, Palisano RJ (eds): Physical Therapy for Children. St Louis, Mo, Saunders, 2006, pp 3 32.

180. Shumway Cook A, Woollacott MH: The growth of stability: postural control from a development perspective. J Mot Behav 17:131 47, 1985. CrossRef [PubMed: 15140688] 

181. Turvey MT: Coordination. Am Psychol 45:938 953, 1990.
CrossRef [PubMed: 2221565] 



182. Bernstein N: The Coordination and Regulation of Movement. London, Pergamon, 1967.

183. Shemmell J, Riek S, Tresilian JR et al.: The role of the primary motor cortex during skill acquisition on a two degrees of freedom movement task. J Mot Behav 39:29 39, 2007.
CrossRef [PubMed: 17251169] 

184. Newell K, van Emmerik R: The acquisition of coordination: Preliminary analysis of learning to write. Hum Mov Sci 8:17 32, 1989. CrossRef

185. Vereijken B, van Emmerik R, Whiting H et al.: Freezing degrees of freedom in skill acquisition. J Mot Behav 24:133 142, 1992. CrossRef

186. Konczak J, Vander Velden H, Jaeger L: Learning to play the violin: motor control by freezing, not freeing degrees of freedom. J Mot Behav 41:243  252, 2009.
CrossRef [PubMed: 19366657] 

187. Newell KM, Broderick MP, Deutsch KM et al.: Task goals and change in dynamical degrees of freedom with motor learning. J Exp Psychol Hum Percept Perform 29:379 387, 2003.
CrossRef [PubMed: 12760622] 

188. Poggio T, Reichardt W: Visual control of orientation behaviour in the fly. Part II. Towards the underlying neural interactions. Q Rev Biophys 9:377  438, 1976.
CrossRef [PubMed: 790442] 

189. Reichardt W, Poggio T: Visual control of orientation behaviour in the fly. Part I. A quantitative analysis. Q Rev Biophys 9:311 375, 428 38, 1976. CrossRef [PubMed: 790441] 

190. Scholz JP, Kelso JAS, Sch ner G: Dynamics governs switching among patterns of coordination in biological movement. Phys Lett A134:8 12, 1988.

191. Ghez C, Favilla M, Ghilardi MF et al.: Discrete and continuous planning of hand movements and isometric force trajectories. Exp Brain Res 115:217 233, 1997.
CrossRef [PubMed: 9224851] 

192. Goodale MA, Pelisson D, Prablanc C: Large adjustments in visually guided reaching do not depend on vision of the hand or perception of target displacement. Nature 320:748 750, 1986.
CrossRef [PubMed: 3703000] 

193. Mathiowetz V, Bass Haugen J: Assessing abilities and capacities: Motor behavior, in Radomski MV, Trombly Latham CA (eds): Occupational Therapy for Physical Dysfunction (ed 6). Baltimore, Williams & Wilkins, 2008, pp 186 211.

194. Mathiowetz V: Task oriented approach to stroke rehabilitation, in Gillen G (ed): Stroke Rehabilitation: A Function Based Approach (ed 3). St Louis, Mo, Mosby, 2011, pp 80 99.

195. Guide to physical therapist practice. Phys Ther 81:S13 S95, 2001.

196. Vasilyeva LF, Lewit K: Diagnosis of muscular dysfunction by inspection, in Liebenson C (ed): Rehabilitation of the Spine: A Practitioner's Manual. Baltimore, Lippincott Williams & Wilkins, 1996, pp 113 142.



197. Janda V: Muscle Function Testing. London, Butterworths, 1983.

198. Comerford MJ, Mottram SL: Movement and stability dysfunction contemporary developments. Man Ther 6:15 26, 2001. CrossRef [PubMed: 11243905] 

























































































































