Musculoskeletal System

Question 1

What is the convex-concave rule?

Answer 1

1. For a convex-on-concave surface movement, the convex member rolls and slides in opposite directions.
2. For a concave-on-convex surface movement, the concave member rolls and slides in similar directions.

Question 2

What is the convex-concave rule or arthrokinematics for glenohumeral flexion?

Answer 2

Spin. The humeral head spins within the glenoid fossa.

• For joint mobilization purposes, the movement at the glenohumeral joint is considered to be convex on concave. During glenohumeral flexion, the convex humeral head of the humerus is thought to roll anteriorly while a posterior glide simultaneously occurs.

Question 3

What is the convex-concave rule or arthrokinematics for glenohumeral extension?

Answer 3

Spin. The humeral head spins within the glenoid fossa.

• For joint mobilization purposes, the movement at the glenohumeral joint is considered to be convex on concave. During glenohumeral extension, the convex humeral head of the humerus is thought to rotate posteriorly while an anterior glide simultaneously occurs.

Question 4

What is the convex-concave rule or arthrokinematics for glenohumeral ABduction (frontal plane)?

Answer 4

Convex on concave. The humeral head rolls superiorly while simultaneously sliding inferiorly.

Question 5

What is the convex-concave rule or arthrokinematics for glenohumeral ADduction (frontal plane)?

Answer 5

Convex on concave. The humeral head rolls inferiorly while simultaneously sliding superiorly.

Question 6

What is the convex-concave rule or arthrokinematics for glenohumeral joint horizontal ABduction (horizontal extension - transverse plane)?

Answer 6

Convex on concave. From a starting position of 90° of glenohumeral ABduction, the humeral head rolls posteriorly while simultaneously sliding anteriorly.

Question 7

What is the convex-concave rule or arthrokinematics for glenohumeral joint horizontal ADduction (horizontal flexion - transverse plane)?

Answer 7

Convex on concave. From a starting position of 90° of glenohumeral ABduction, the humeral head rolls anteriorly while simultaneously sliding posteriorly.

Question 8

What is the convex-concave rule or arthrokinematics for glenohumeral joint internal (medial) rotation?

Answer 8

Convex on concave. The humeral head rolls anteriorly while simultaneously sliding posteriorly.

Question 9

What is the convex-concave rule or arthrokinematics for glenohumeral joint external (lateral) rotation?

Answer 9

Convex on concave. The humeral head rolls posteriorly while simultaneously sliding anteriorly.

Question 10

What is the convex-concave rule or arthrokinematics for humeroradial & humeroulnar flexion?

Answer 10

Concave on convex. The concave surfaces (i.e., trochlear notch of the ulna and fovea of the radial head) roll and slide anteriorly.

Question 11

What is the convex-concave rule or arthrokinematics for humeroradial & humeroulnar extension?

Answer 11

Concave on convex. The concave surfaces (i.e., trochlear notch of the ulna and fovea of the radial head) roll and slide posteriorly.

Question 12

What is the convex-concave rule or arthrokinematics for proximal & distal radioulnar supination?

Answer 12

Proximal radioulnar: Spin. The convex radial head of the radius spins within the fibro-osseous ring formed by the annular ligament and radial notch of the ulna.

• For joint mobilization purposes, the movement at the proximal radioulnar joint is considered to be convex on concave. During forearm supination, the convex radial head of the radius rolls posteriorly (i.e., toward the dorsal aspect of the forearm) while an anterior glide (i.e., volar glide) is thought to simultaneously occur.

Distal radioulnar: Concave on convex. The concave ulnar notch of the radius rolls and slides posteriorly (i.e., toward the dorsal surface of the forearm).

Question 13

What is the convex-concave rule or arthrokinematics for proximal & distal radioulnar pronation?​

Answer 13

Proximal radioulnar: Spin. The radial head of the radius spins within the fibro-osseous ring formed by the annular ligament and radial notch of the ulna.

• For joint mobilization purposes, the movement at the proximal radioulnar joint is considered to be convex on concave. During forearm pronation, the convex radial head of the radius rolls anteriorly (i.e., toward the volar aspect of the forearm) while a posterior glide (i.e., dorsal glide) is thought to simultaneously occur.

Distal radioulnar: Concave on convex. The concave ulnar notch of the radius rolls and slides anteriorly (i.e., toward the volar surface of the forearm).

Question 14

What is the convex-concave rule or arthrokinematics for radiocarpal and midcarpal flexion?​

Answer 14

Convex on concave.

• At the radiocarpal joint, the convex surface of the lunate rolls in the volar direction while simultaneously sliding dorsally.
• At the midcarpal joint, the convex surface of the head of the capitate rolls in the volar direction while simultaneously sliding dorsally.

Question 15

What is the convex-concave rule or arthrokinematics for radiocarpal and midcarpal extension?​

Answer 15

Convex on concave.

• At the radiocarpal joint, the convex surface of the lunate rolls dorsally while simultaneously sliding in the volar direction.
• At the midcarpal joint, the convex surface of the head of the capitate rolls dorsally while simultaneously sliding in a volar direction.

Question 16

What is the convex-concave rule or arthrokinematics for radiocarpal and midcarpal radial deviation?​

Answer 16

Convex on concave.

• At the radiocarpal joint, the convex surfaces of the scaphoid, lunate, and triquetrum roll radially while simultaneously sliding in the ulnar direction.
• At the midcarpal joint, the convex surface of the head of the capitate rolls radially while simultaneously sliding in the ulnar direction.

Question 17

What is the convex-concave rule or arthrokinematics for radiocarpal and midcarpal ulnar deviation?​

Answer 17

Convex on concave.

• At the radiocarpal joint, the convex surfaces of the scaphoid, lunate, and triquetrum roll in an ulnar direction while simultaneously sliding radially.
• At the midcarpal joint, the convex surface of the head of the capitate rolls in an ulnar direction while simultaneously sliding radially.

Question 18

What is the convex-concave rule or arthrokinematics for 1st CMC (thumb) flexion?

Answer 18

Concave on convex. The concave surface of the proximal aspect of the 1st metacarpal rolls and slides in an ulnar direction.

Question 19

What is the convex-concave rule or arthrokinematics for 1st CMC (thumb) extension?

Answer 19

Concave on convex. The concave surface of the proximal aspect of the 1st metacarpal rolls and slides in a radial direction.

Question 20

What is the convex-concave rule or arthrokinematics for 1st CMC (thumb) ABduction?

Answer 20

Convex on concave. The convex surface of the proximal aspect of the 1st metacarpal rolls in a palmar direction while simultaneously sliding dorsally.

Question 21

What is the convex-concave rule or arthrokinematics for 1st CMC (thumb) ADduction?

Answer 21

Convex on concave. The convex surface of the proximal aspect of the 1st metacarpal rolls dorsally while simultaneously sliding in a palmar direction.

Question 22

What is the convex-concave rule or arthrokinematics for 1st MCP (thumb) flexion?

Answer 22

Concave on convex. The concave surface of the base of the proximal phalanx rolls and glides in the palmar direction.

Question 23

What is the convex-concave rule or arthrokinematics for 1st MCP (thumb) extension?

Answer 23

Concave on convex. The concave surface of the base of the proximal phalanx rolls and glides in the dorsal direction.

Question 24

What is the convex-concave rule or arthrokinematics for 1st IP (thumb) flexion?

Answer 24

Concave on convex. The concave surface of the base of the distal phalanx rolls and glides in the palmar direction.

Question 25

What is the convex-concave rule or arthrokinematics for 1st IP (thumb) extension?

Answer 25

Concave on convex. The concave surface of the base of the distal phalanx rolls and glides in the dorsal direction.

Question 26

What is the convex-concave rule or arthrokinematics for 2nd-5th MCP flexion?

Answer 26

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and glide in the palmar direction.

Question 27

What is the convex-concave rule or arthrokinematics for 2nd-5th MCP extension?

Answer 27

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and glide in the dorsal direction.

Question 28

What is the convex-concave rule or arthrokinematics for 2nd MCP ABduction & 3rd MCP radial deviation?

Answer 28

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and slide in the radial direction.

Question 29

What is the convex-concave rule or arthrokinematics for 2nd MCP ADduction & 3rd MCP ulnar deviation​?

Answer 29

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and slide in the ulnar (medial) direction.

Question 30

What is the convex-concave rule or arthrokinematics for 4th & 5th MCP ABduction?

Answer 30

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and slide in the ulnar direction.

Question 31

What is the convex-concave rule or arthrokinematics for 4th and 5th MCP ADduction?

Answer 31

Concave on convex. The concave surfaces of the bases of the proximal phalanges roll and slide in the radial direction.

Question 32

What is the convex-concave rule or arthrokinematics for 2nd-5th PIP and DIP flexion?

Answer 32

Concave on convex. The concave bases of the middle phalanges (for the PIP joints) or the distal phalanges (for the DIP joints) roll and slide in a palmar direction.

Question 33

What is the convex-concave rule or arthrokinematics for 2nd-5th PIP and DIP extension?

Answer 33

Concave on convex. The concave bases of the middle phalanges (for the PIP joints) or the distal phalanges (for the DIP joints) roll and slide in a dorsal direction.

Question 34

What is the convex-concave rule or arthrokinematics for craniocervical flexion?

Answer 34

Atlanto-occipital joint: Convex on concave. The convex occipital condyles roll anteriorly while simultaneously sliding slightly posteriorly.

Atlanto-axial joint complex: The atlas tilts anteriorly.

Intracervical joints (C2-C7): Slide. The inferior articular facets of superior vertebrae slide superiorly and anteriorly, relative to the superior articular facets of the inferior vertebrae.

Question 35

What is the convex-concave rule or arthrokinematics for craniocervical extension?

Answer 35

Atlanto-occipital joint: Convex on concave. The convex occipital condyles roll posteriorly while simultaneously sliding slightly anteriorly.

Atlanto-axial joint complex: The atlas tilts posteriorly.

Intracervical joints (C2-C7): Slide. The inferior articular facets of superior vertebrae slide inferiorly and posteriorly, relative to the superior articular facets of the inferior vertebrae.

Question 36

What is the convex-concave rule or arthrokinematics for craniocervical lateral flexion?

Answer 36

Atlanto-occipital joint: Convex on concave

• Right lateral flexion: The convex occipital condyles roll laterally to the right while simultaneously sliding slightly to the left.
• Left lateral flexion: The convex occipital condyles roll laterally to the left while simultaneously sliding slightly to the right.

Intracervical joints (C2-C7): Slide

• Right lateral flexion: The inferior articular facets of the superior vertebrae slide inferiorly and posteriorly on the right side, and superiorly and anteriorly on the left side.
• Left lateral flexion: The inferior articular facets of the superior vertebrae slide inferiorly and posteriorly on the left side, and superiorly and anteriorly on the right side.

Question 37

What is the convex-concave rule or arthrokinematics for craniocervical axial rotation?

Answer 37

Atlanto-axial joint complex: The ring-shaped atlas and attached transverse ligament “twist” about the dens as the generally flat inferior articular facets of the atlas slide in a curved path across the broad “shoulders” of the superior articular facets of the axis.

Intracervical joints (C2-C7): Slide

• Right rotation: The inferior facets of the superior vertebrae slide posteriorly and inferiorly on the right side, and anteriorly and superiorly on the left side.
• Left rotation: The inferior facets of the superior vertebrae slide posteriorly and inferiorly on the left side, and anteriorly and superiorly on the right side.

Question 38

What is the convex-concave rule or arthrokinematics for thoracolumbar flexion?

Answer 38

Intrathoracic and intralumbar joints: Slide. The inferior articular facets of superior vertebrae slide superiorly and anteriorly, relative to the superior articular facets of the inferior vertebrae

Question 39

What is the convex-concave rule or arthrokinematics for thoracolumbar extension?

Answer 39

Intrathoracic and intralumbar joints: Slide. The inferior articular facets of superior vertebrae slide inferiorly and posteriorly, relative to the superior articular facets of the inferior vertebrae.

Question 40

What is the convex-concave rule or arthrokinematics for thoracolumbar lateral flexion?

Answer 40

Intrathoracic and intralumbar joints

• Right lateral flexion: Slide. The inferior articular facets of the superior vertebrae slide inferiorly and slightly posteriorly on the right side, and slide superiorly and slightly anteriorly on the left side.
• Left lateral flexion: Slide. The inferior articular facets of the superior vertebrae slide inferiorly and slightly posteriorly on the left side, and slide superiorly and slightly anteriorly on the right side.

Question 41

What is the convex-concave rule or arthrokinematics for thoracolumbar axial rotation?

Answer 41

Intrathoracic and intralumbar joints

• Right rotation: Slide. The inferior facets of the superior vertebrae slide posteriorly and slightly inferiorly on the right side, and anteriorly and slightly superiorly on the left side.
• Left rotation: Slide. The inferior facets of the superior vertebrae slide posteriorly and slightly inferiorly on the left side, and anteriorly and superiorly on the right side.

Question 42

What is the convex-concave rule or arthrokinematics for hip flexion?

Answer 42

Spin. The femoral head spins within the acetabulum.

• For joint mobilization purposes, the movement at the hip joint is considered to be convex on concave. During hip flexion, the convex femoral head is thought to roll anteriorly while a posterior glide simultaneously occurs.

Question 43

What is the convex-concave rule or arthrokinematics for hip extension?

Answer 43

Spin. The femoral head spins within the acetabulum.

• For joint mobilization purposes, the movement at the hip joint is considered to be convex on concave. During hip extension, the convex femoral head is thought to roll posteriorly while an anterior glide simultaneously occurs.

Question 44

What is the convex-concave rule or arthrokinematics for hip ABduction (frontal plane)?

Answer 44

Convex on concave. The femoral head rolls superiorly while simultaneously sliding inferiorly.

Question 45

What is the convex-concave rule or arthrokinematics for ​hip ADduction (frontal plane)?

Answer 45

Convex on concave. The femoral head rolls inferiorly while simultaneously sliding superiorly.

Question 46

What is the convex-concave rule or arthrokinematics for hip internal (medial) rotation?

Answer 46

Convex on concave. The femoral head rolls anteriorly while simultaneously sliding posteriorly.

Question 47

What is the convex-concave rule or arthrokinematics for hip external (lateral) rotation?

Answer 47

Convex on concave. The femoral head rolls posteriorly while simultaneously sliding anteriorly.

Question 48

What is the convex-concave rule or arthrokinematics for tibofemoral flexion? Differentiate between femoral-on-tibial and tibial-on-femoral movements.

Answer 48

Femoral-on-tibial flexion (e.g., lowering into a deep squat from standing): Convex on concave. The convex femoral condyles roll posteriorly while simultaneously sliding anteriorly.

Tibial-on-femoral flexion (e.g., sitting knee flexion): Concave on convex. The concave tibial plateau rolls and slides posteriorly.

*Note: For a knee that is fully extended to be unlocked to complete knee flexion, the tibia must first internally rotate slightly to undo the screw-home mechanism.

Question 49

What is the convex-concave rule or arthrokinematics for​ tibiofemoral extension? Differentiate between femoral-on-tibial and tibial-on-femoral movements.​

Answer 49

Femoral-on-tibial extension (e.g., standing up from a deep squat): Convex on concave. The convex femoral condyles roll anteriorly while simultaneously sliding posteriorly.

Tibial-on-femoral extension (e.g., sitting knee extension): Concave on convex. The concave tibial plateau rolls and slides anteriorly.

*Note: During knee extension, the tibia externally rotates in order to lock the knee in full extension (screw-home mechanism).

Question 50

What is the convex-concave rule or arthrokinematics for tibiofemoral internal (medial) rotation and external (lateral) rotation?

Answer 50

Spin. With the knee flexed (i.e., unlocked), a spin occurs between the menisci and the articular surfaces of the tibia and femur.

Question 51

What is the convex-concave rule or arthrokinematics for talocrural dorsiflexion?

Answer 51

Convex on concave. In an unloaded foot, the convex trochlea of the talus rolls anteriorly while simultaneously sliding posteriorly.

Question 52

What is the convex-concave rule or arthrokinematics for talocrural plantarflexion?

Answer 52

Convex on concave. In an unloaded foot, the convex trochlea of the talus rolls posteriorly while simultaneously sliding anteriorly.

Question 53

What is the convex-concave rule or arthrokinematics for subtalar inversion?

Answer 53

Convex on concave. In an unloaded foot, the convex calcaneal component rolls medially while simultaneously sliding laterally.

Question 54

What is the convex-concave rule or arthrokinematics for subtalar eversion?

Answer 54

Convex on concave. In an unloaded foot, the convex calcaneal component rolls laterally while simultaneously sliding medially.

Question 55

What is the convex-concave rule or arthrokinematics for subtalar ABduction and ADduction?

Answer 55

Spin. In an unloaded foot, the convex calcaneal component spins laterally (for ABduction) or medially (for ADduction) within the concave talus component.

Question 56

What is the convex-concave rule or arthrokinematics for the transverse tarsal joint (aka, midtarsal joint)?

Answer 56

Spin. In an unloaded foot at the talonavicular joint, the concave proximal surface of the navicular bone spins around the convex head of the talus. The calcaneocuboid joint remains relatively rigid during the movement.

*Note: The arthrokinematics of the transverse tarsal joint contributes to all movements at the ankle and foot: plantarflexion, dorsiflexion, inversion, eversion, ABduction, and ADduction.

Question 57

What joint motions at the ankle and foot are included in pronation of the foot?

Answer 57

Eversion, ABduction, and dorsiflexion

Question 58

What joint motions at the ankle and foot are included in supination of the foot?​

Answer 58

Inversion, ADduction, and plantarflexion

Question 59

Fill in the blanks: In general, the joint motions at the foot follow a _____-on-_____ movement.

• Flexion of the MTP and IP joints produces (roll/glide) in the _____ direction.
• Extension of the MTP and IP joints produces (roll/glide) in the _____ direction.
• ABduction of the 1st MTP joint (great toe) produces (roll/glide) in the _____ direction.
• ADduction of the 1st MTP joint (great toe) produces (roll/glide) in the _____ direction.
• ABduction of the 3rd-5th MTP joints produces (roll/glide) in the _____ direction.
• ADduction of the 3rd-5th MTP joints produces (roll/glide) in the _____ direction.

Answer 59

Fill in the blanks: In general, the joint motions at the foot follow a concave-on-convex movement.

• Flexion of the MTP and IP joints produces roll and glide in the plantar direction
• Extension produces roll and glide in the dorsal direction.
• ABduction of the 1st MTP joint (great toe) produces roll and glide in the medial direction.
• ADduction of the 1st MTP joint (great toe) produces roll and glide in the lateral direction.
• ABduction of the 3rd-5th MTP joints produces roll and glide in the lateral direction.
• ADduction of the 3rd-5th MTP joints produces roll and glide in the medial direction.

Question 60

What are the descriptions of each oscillatory grade of joint mobilization?

Answer 60

Grade I: Small-amplitude rhythmic oscillations performed at the beginning of the resistance-free range of joint play; usually are rapid oscillations, like manual vibrations

Grade II: Large-amplitude rhythmic oscillations performed within the resistance-free range of joint play up to but not past tissue resistance (R1)

Grade III: Large-amplitude rhythmic oscillations performed past tissue resistance (R1) and up to the anatomical limit of the available motion (R2)

Grade IV: Small-amplitude rhythmic oscillations performed at the anatomical limit of the available motion (R2); usually are rapid oscillations, like manual vibrations

Question 61

What are the descriptions of each sustained grade of joint mobilization?

Answer 61

Grade I (loosen): Small-amplitude distraction within the beginning of the resistance-free range of joint play

• Equalizes cohesive forces, muscle tension, and atmospheric pressure acting on the joint

Grade II (tighten or “taking up the slack”): Moderate-amplitude distraction up to but not past tissue resistance (R1)

• Tightens the tissues around the joint

Grade III (stretch): Large-amplitude distraction or glide is applied past tissue resistance (R1) and up to the anatomical limit of the available motion (R2)

• Places a stretch on the joint capsule and surrounding periarticular structures

Question 62

Which oscillatory and sustained grades are used to address pain vs. joint restrictions or stiffness?

Answer 62

Pain is greater than stiffness:

• Oscillatory grades I and II
• Sustained grades I and II

Stiffness is greater than pain:

• Oscillatory grades III and IV
• Sustained grade III

Pain is equal to stiffness: Treat pain first, and then see what effect the treatment has on stiffness.

Question 63

What is a capsular pattern?

Why are capsular patterns important?

What are examples of causes of these patterns?

Answer 63

1. What: A capsular pattern refers to a “characteristic pattern of restriction in passive range of motion when a joint impairment affects the entire joint.” It has been proposed that each joint demonstrates a specific pattern of restriction, in which the proportional limitation in one motion is greater than one or more other motions.
2. Why: Determining the presence of capsular patterns is helpful in diagnosing articular lesions because the presence of a capsular pattern would indicate that the diagnosis is one in which the entire joint capsule is involved, suggesting that mobilization/manipulation interventions in all directions would be indicated.
3. Examples of causes: Osteoarthritis and conditions involving trauma to the entire joint capsule

Question 64

What is the capsular pattern for the temporomandibular joint (TMJ)?

Answer 64

Limitation in mouth opening

Question 65

What is the capsular pattern at the shoulder joint?

Answer 65

Shoulder capsular pattern: Lateral rotation is more limited than ABduction, which is more limited than medial (internal) rotation

Question 66

What are the capsular patterns at the elbow joints?

Answer 66

Humeroulnar and humeroradial joints: Flexion is more limited than extension.

Proximal and distal radioulnar joints: Pain at the end of the range of motion for pronation or supination or both

Question 67

What is the capsular pattern at the wrist joints?

Answer 67

Radiocarpal and midcarpal joints: Flexion and extension are equally limited.

Question 68

What are the capsular patterns at the hand joints?

Answer 68

1st CMC joint (thumb): Limitation in ABduction and extension, and no limitation in flexion

MCP and IP joints: Flexion is more limited than extension.

Question 69

What is the capsular pattern for the cervical spine?

Answer 69

Lateral flexion and rotation are equally limited; extension is more limited than flexion

Question 70

What is the capsular pattern at the hip joint?

Answer 70

Flexion, ABduction, and medial (internal) rotation are grossly limited; extension is slightly limited

Question 71

What is the capsular pattern at the knee joint?

Answer 71

Gross limitations in flexion accompanied by slight limitations in extension

Question 72

What are the capsular patterns for the ankle and foot joints?

Answer 72

Talocrural joint: If the calf muscles are not short or stiff (i.e., “tight”), plantarflexion is more limited than dorsiflexion, whereas if the calf muscles are short or stiff, the capsular pattern is simply limitation into plantarflexion.

Subtalar joint (aka, talocalcaneal joint): Limitations in inversion

Transverse tarsal joint (aka, midtarsal joint): Limitations in dorsiflexion, plantarflexion, ADduction, and inversion

Metatarsophalangeal (MTP) joints

• 1^st MTP joint (great toe): Marked limitation in extension and slight limitation in flexion
• 2^nd-5^th MTP joints: Variable, but flexion is generally more limited than extension

*No capsular pattern described for the interphalangeal (IP) joints of the foot

Question 73

What muscles are included in the rotator cuff (SITS) muscle group?

Answer 73

Supraspinatus

Infraspinatus

Teres Minor

Subscapularis

Question 74

What are the origins, insertions, actions, and innervations of the supraspinatus?

Answer 74

Origin: Medial 2/3 of supraspinous fossa of the scapula

Insertions:

• Superior facet of greater tubercule of the humerus
• Glenohumeral joint capsule

Innervations:

• Peripheral: Suprascapular nerve
• Segmental: C4, C5, and C6 spinal nerve roots

Actions:

• Shoulder ABduction
• Stabilizes head of the humerus in glenoid cavity during movements
• May assist with shoulder lateral (external) rotation from neutral to full lateral rotation

Question 75

What are the origins, insertions, actions, and innervations of the infraspinatus?

Answer 75

Origin: Medial 2/3 of infraspinous fossa of scapula

Insertions:

• Middle facet of greater tubercle of the humerus
• Glenohumeral joint capsule

Innervations:

• Peripheral: Suprascapular nerve
• Segmental: C4, C5, and C6 spinal nerve roots

Actions:

• Shoulder lateral (external) rotation
• Stabilizes head of the humerus in glenoid cavity during movements
• Scapular internal rotation

Question 76

What are the origins, insertions, actions, and innervations of the teres minor?

Answer 76

Origins: Upper 2/3 and dorsal surface of lateral border of scapula

Insertions:

• Inferior facet of greater tubercle of the humerus
• Glenohumeral joint capsule

Innervations:

• Peripheral: Axillary nerve
• Segmental: C5 and C6 spinal nerve roots

Actions:

• Shoulder lateral (external) rotation
• Stabilizes head of the humerus in glenoid cavity during movements
• Scapular internal rotation

Question 77

What are the origins, insertions, actions, and innervations of the subscapularis?

Answer 77

Origin: Subscapular fossa of scapula

Insertions:

• Lesser tubercle of the humerus
• Glenohumeral joint capsule

Innervations:

• Peripheral: Upper and lower subscapular nerves
• Segmental: C5, C6, and C7 spinal nerve roots

Actions:

• Shoulder internal (medial) rotation
• Stabilizes head of the humerus in glenoid cavity during movements.
• Prevents anterior glide of the humeral head

Question 78

What are the origins, insertions, actions, and innervations of the biceps brachii (short and long heads)?

Answer 78

Origins:

• Short head: Apex of coracoid process of scapula
• Long head: Supraglenoid tubercle of scapula

Insertions:

• Radial tuberosity
• Aponeurosis of biceps brachii

Innervations:

• Peripheral: Musculocutaneous nerve
• Segmental: C5 and C6 spinal nerve roots

Actions:

• Shoulder flexion
• With origin fixed:
  
  • Elbow flexion, moving the forearm toward the humerus
  • Forearm supination
• With insertion fixed:
  
  • Elbow flexion, moving the humerus toward the forearm
  • May contribute to scapular anterior tilt

Question 79

What is adhesive capsulitis?

Answer 79

Adhesive capsulitis (aka, idiopathic frozen shoulder, periarthritis) refers to inflammation and fibrosis of the glenohumeral joint capsule that causes severe pain and a progressive loss of shoulder mobility.

Question 80

What are the characteristics of the demographic population that is at risk for developing adhesive capsulitis (e.g., gender, age, past medical history)?

Answer 80

• Gender: Female
• Age: 40-65 years old
• Past medical history:
  
  • Diabetes mellitus
    
    • Hyperglycemia is linked to pathological joint inflammation.
  • Thyroid disease (i.e., hyperthyroidism, hypothyroidism)
    
    • Autoimmune disruptions that characterize thyroid disease is linked to pathological inflammation throughout the body.
  • Previous episode of adhesive capsulitis in the contralateral arm
  • Chronic inflammation in the glenohumeral joint capsule or in the tendons of the rotator cuff muscles or biceps brachii (long head)

Question 81

What causes adhesive capsulitis?

Answer 81

Mechanism of injury:

• Usually insidious onset with no known cause (primary frozen shoulder)
• If a cause is known (secondary frozen shoulder), the cause is usually trauma, immobilization, or certain joint diseases such as rheumatoid arthritis or osteoarthritis.

Question 82

How does adhesive capsulitis develop as it progresses?

Answer 82

Stage 1: Characterized by a gradual onset of pain that increases with movement and is present at night. Loss of external rotation motion with intact rotator cuff strength is common. The duration of this stage is usually less than 3 months.

Stage 2 (“Freezing” Stage): Characterized by persistent and more intense pain even at rest. Motion is limited in all directions and cannot be fully restored with an intra-articular injection. This stage is typically between 3 and 9 months after onset.

Stage 3 (“Frozen” Stage): Characterized by pain only with movement, significant adhesions, and limited glenohumeral joint motions. Excessive scapulothoracic movement is a typical compensation. Atrophy of the deltoid, rotator cuff, biceps brachii, and triceps brachii muscles may be noted. This stage occurs between 9 and 15 months after onset.

Stage 4 (“Thawing” Stage): Characterized by minimal pain and no synovitis but significant capsular restrictions from adhesions. Motion may gradually improve during this stage. This stage lasts from 15 to 24 months after onset, although some patients never regain normal ROM.

Question 83

What are the hallmark signs and symptoms of adhesive capsulitis?

Answer 83

• Progressive loss of both active and passive range of motion (loss of AROM = loss of PROM)
• In the beginning stages, will present with intact rotator cuff muscle strength (fair+ [3+] to good [4]). As the disease progresses, there may appear to be muscle weakness, but the presented muscle weakness is due to an increase in pain.
• Observation of a shoulder capsular pattern: Shoulder lateral rotation will be more limited than ABduction, which will be more limited than medial rotation (*see image)
• The glenohumeral joint play of patients with adhesive capsulitis is often be limited in all directions.
• In the later stages, pain gradually improves, but shoulder ROM remains limited.

Question 84

What are the standards by which you determine how likely the adhesive capsulitis is to improve?

Answer 84

On average, spontaneous recovery can occur 2 years from onset. However, there is the possibility that there will be long-term limitations without spontaneous recovery.

Question 85

What is a special test or cluster of tests to rule in or rule out adhesive capsulitis?

Answer 85

None. There is no special test specifically for adhesive capsulitis.

Question 86

What physical therapy interventions are utilized to treat adhesive capsulitis?

Answer 86

• In combination with shoulder mobility and stretching exercises, corticosteroid (i.e., glucocorticoid) injections to dampen the inflammatory response, reduce pain, and improve shoulder range of motion (ROM)
• Patient education that (1) describes the natural course of the disease; (2) promotes activity modification to encourage functional, pain-free ROM; and (3) matches the intensity of stretching to the patient’s current level of irritability (i.e., encourage completing exercises without significant pain)
• Therapeutic modalities (e.g., short-wave diathermy, ultrasound, or electrical stimulation) to alleviate pain associated with adhesive capsulitis
• Joint mobilizations to reduce pain and improve shoulder ROM

Question 87

What are the major indications, contraindications, guidelines, or protocols for treating adhesive capsulitis?​

Answer 87

Treatment management should follow a progression from acute (i.e., maximum protection and focus on pain management during stages 1 and 2), subacute (controlled motion during stage 3), and chronic (return to function during stage 4).

Question 88

How can you distinguish adhesive capsulitis from a commonly associated diagnose (i.e., common misdiagnose) like rotator cuff pathology?

Answer 88

• Rotator cuff pathology
  
  • Resisted muscle tests result in weakness or pain, especially with shoulder ABduction and lateral rotation
  • Special tests: Positive for drop-arm test and empty-can test
  • Pain at night (especially indicative of full-thickness tears)

Question 89

What are open (loose) and close-packed joint positions?

Answer 89

The open-packed joint position (aka, resting position, loose-packed or maximum loose-packed joint position) is the joint position in which there is minimal congruency between the articular surfaces and the joint capsule, with the ligaments being in the position of greatest laxity, and passive separation of the joint surfaces being at the greatest.

• The open-packed joint position allows for the arthrokinematic movements of spin, slide, and roll to occur. Therefore, the open-packed joint position is the most common position used for treatment using joint play mobilizations.

The close-packed position is the joint position in which two joint surfaces fit together precisely—that is, they are fully congruent. The joint surfaces are tightly compressed; the ligaments and capsule of the joint are maximally taut; and the joint surfaces cannot be separated by distractive forces.

• The close-packed position is the position of maximum joint stability. In the close packed position, there is minimal to no accessory movement. Thus, this position is commonly used during treatment to stabilize the joint if an adjacent joint is being treated.

Question 90

What are the open (loose) and close-packed positions for the temporomandibular joint (TMJ)?

Answer 90

Open-packed position: Mouth slightly open

Close-packed position: Mouth closed

Question 91

What are the open (loose) and close-packed positions for the glenohumeral joint?

Answer 91

Open-packed position: 40° to 55° ABduction, 30° horizontal ADduction (scapular plane), slight lateral rotation

Close-packed position: Full elevation (i.e., full ABduction and lateral rotation)

Question 92

What are the open (loose) and close-packed positions for the joints at the elbow?

Answer 92

Humeroulnar joint

• Open-packed position: 70° flexion, 10° supination
• Close-packed position: Full extension and supination

Humeroradial joint

• Open-packed position: Full extension and supination
• Close-packed position: 90° flexion, 5° supination

Proximal radioulnar joint

• Open-packed position: 70° flexion, 35° supination
• Close-packed position: Full supination or full pronation

Distal radioulnar joint

• Open-packed position: 10° supination
• Close-packed position: Full supination or full pronation

Question 93

What are the open (loose) and close-packed positions for the joints at the wrist?

Answer 93

Radiocarpal and midcarpal joints

• Open-packed position: Slight flexion and ulnar deviation
• Close-packed position: Full extension

Question 94

What are the open (loose) and close-packed positions for the joints at the hand?

Answer 94

1st carpometacarpal (CMC) joint (thumb)

• Open-packed position: Midway between ABduction-ADduction and flexion-extension
• Close-packed position: Full opposition

Metacarpophalangeal (MCP) joint

• Open-packed positions
  
  • 1st MCP joint (thumb): Slight flexion
  • 2nd-5th MCP joints: Slight flexion and slight ulnar deviation
• Close-packed positions
  
  • 1st MCP joint (thumb): Full extension
  • 2nd-5th MCP joints: Full flexion

Interphalangeal (IP) joints

• Open-packed position: Slight flexion
• Close-packed position: Full extension

Question 95

What is the open (loose) and close-packed positions for the hip joint?

Answer 95

Open-packed position: 30° flexion, 30° ABduction, and slight external (lateral) rotation

Close-packed position: Full extension, ABduction, and internal (medial) rotation

Question 96

What is the open (loose) and close-packed positions for the knee joint?

Answer 96

Open-packed position: 25° to 40° of flexion

Close-packed position: Full extension

Question 97

What is the open (loose) and close-packed positions of the ankle and foot joints?

Answer 97

Talocrural joint

• Open-packed position: 10° plantar flexion and midway between inversion and eversion
• Close-packed position: Full dorsiflexion

Subtalar joint (aka, talocalcaneal joint)

• Open-packed position: 10° plantar flexion and midway between inversion and eversion
• Close-packed position: Full inversion (supination)

Transverse tarsal joint (aka, midtarsal joint)

• Open-packed position: 10° plantar flexion and midway between inversion and eversion
• Close-packed position: Full inversion (supination)

Metatarsophalangeal (MTP) joints

• Open-packed position: 10° extension
• Close-packed position
  
  • 1st MTP joint (great toe): Full extension
  • 2nd-5th MTP joints: Full flexion

Interphalangeal (IP) joints

• Open-packed position: Slight flexion
• Close-packed position: Full extension

Question 98

What is the position of function of the wrist and hand that is used to create orthoses?

Answer 98

Wrist—20-30° of extension with slight ulnar deviation

Fingers—35-45° of metacarpophalangeal (MCP) joint flexion; 15-30° of proximal interphalangeal (PIP) and distal interphalangeal (DIP) joint flexion

Thumb—35- 45° of carpometacarpal (CMC) joint ABduction

*Note: The individual alignments of the finger and thumb joints in the position of function are based on the open (loose) packed positions of these joints. The exception to this is the alignment of the wrist joint. The wrist is positioned in wrist extension in order to maintain optimal length of the finger flexor muscles and preserve the tenodesis action of the finger flexors.

Question 99

What is subtalar joint neutral?

Answer 99

• Expression is used clinically to establish a baseline or reference position for casting a foot orthotic.
• Defined as the position in which the calcaneus inverts twice as many degrees as it everts (i.e., the subtalar joint is in a position in which it is one-third the distance from full eversion and two-thirds the distance from full inversion)
• Subtalar joint neutral can be found by placing the subject’s calcaneus in a position that allows both the lateral and medial sides of the trochlea (dome) of the talus to be equally exposed for palpation within the mortise formed by the distal ends of the tibia and fibula.

Question 100

What is osteoarthritis (OA)?

Answer 100

Osteoarthritis (OA) (aka, degenerative joint disease) is a slowly evolving articular disorder that affects the entire synovial joint organ and involves inflammation of the articular cartilage and underlying bone (i.e., subchondral bone).

Question 101

What are the characteristics of the demographic population that is at risk for developing osteoarthritis (e.g., gender, age, past medical history)?

Answer 101

• Gender: Most common in men before age 45 years; more common in women after age 45 years
• Age: Usually begins at age 40 years; affects a majority of adults older than age 65 years
  
  • Older age is a risk factor because the incidence of OA increases with age.
• Past medical history:
  
  • Family history of OA (i.e., genetic predisposition)
  • Tobacco smoking
    
    • Tobacco potentially contributes to cartilage degeneration.
  • Obesity
  • Synovial joint injury (e.g., anterior cruciate ligament injury, femoroacetabular impingement, labral tears) or surgery (e.g., meniscectomy)
  • Participation in sports (e.g., football, soccer, hockey, baseball pitchers) that involve high-intensity, acute, direct joint impact from contact with other players, especially when repetitive joint impact and twisting are combined
  • Occupational activities such as kneeling, squatting, heavy lifting, and repetitive use of heavy machinery
  • Generalized ligamentous laxity of joints (e.g., hypermobility joint syndrome, which is characterized by loose and unstable joints)
    
    • Postmenopausal women are at an increased risk for developing hypermobility joint syndrome and OA. This may be related to the presence of estrogen receptors on ligaments and chondrocytes.
  • Muscle weakness (especially of the quadriceps femoris muscle group) secondary to prolonged immobilization, multiple sclerosis, or any of the myopathies (e.g., polymyositis)
    
    • Muscles are normally the major shock-absorbing mechanism of joints (especially the knee) through eccentric muscle contraction.
    • Because of its lack of vascular supply, articular cartilage depends on repetitive mechanical loading and unloading of the synovial joints for diffusion of nutrients and cellular waste products.

Question 102

What causes osteoarthritis?

Answer 102

Mechanism of injury:

• Primary OA: Insidious onset with no known cause (idiopathic)
• Secondary OA: Cause is known (e.g., trauma, infection, hemarthrosis, osteonecrosis, etc.)

Question 103

How does osteoarthritis develop as it progresses?

Answer 103

• Progressive loss of articular cartilage and narrowing of the joint space results in an increase in friction between the articular surfaces of the bones and subsequently inflammation of the articular cartilage and underlying bone. In addition, progressive loss of articular cartilage results in an increase in mechanical loading through the synovial joint.
• In response to the excessive mechanical load, sclerosis of the subchondral bone occurs as new bone is formed (bone remodeling). The formation of new bone contributes to the creation of osteophytes at the margins of the joints. Fissuring and eburnation of the cartilage (i.e., thinning and loss of the articular cartilage resulting in exposure of the subchondral bone, which becomes denser with the surface becoming worn and polished) also occur.
• As OA progresses, other degenerative processes occur at the joint, including inflammation of the synovial membrane (i.e., synovitis) due to the accumulation of fragments of cartilage in the synovial fluid, and degenerative changes in periarticular structures such as menisci, ligaments, and tendons (e.g., ligamentous laxity, progressive muscle weakness and atrophy).
• Osteoarthritis ultimately results in chronic joint pain, joint deformities and malalignment, and loss of joint function.

Question 104

What are the hallmark signs and symptoms of osteoarthritis?

Answer 104

• Usually begins in the synovial joints on one side of the body
• Primarily affects the weight-bearing synovial joints: hip, knee, shoulder, cervical and lumbar spine, hands (i.e., 1st CMC & MCP joints, 2nd-5th PIP & DIP joints), and feet (i.e., 1st metatarsophalangeal [MTP] joint [great toe])
• Brief morning stiffness (i.e., lasting 5-10 minutes after awakening) that decreases with movement and physical activity
• Limited range of motion at affected synovial joints
• Pain is often described as a deep ache that is worse with activity and better after rest
• Crepitus (i.e., audible crackling or grating sensation produced when roughened articular or extraarticular surfaces rub together during movement)
• Joint deformities such as enlarged joint surfaces due to osteophyte (bone spur) formation (e.g., Heberden nodes at the DIP joints of the hand, Bouchard nodes at the PIP joints of the hand)

Question 105

What are the standards by which you determine how likely the osteoarthritis is to improve?

Answer 105

• Poor correlation between radiographic evidence of OA (e.g., joint space narrowing, osteophyte formation) and the presence of symptoms
• Physical therapists should rely primarily on the clinical examination findings for direction regarding the development of prognosis (including plan of care) and intervention.

Question 106

What is a special test or cluster of tests to rule in or rule out osteoarthritis?

Answer 106

None. There are no special tests for osteoarthritis.

Question 107

What physical therapy interventions are utilized to treat osteoarthritis?

Answer 107

Flexibility (stretching), strengthening, and endurance exercises to improve general mobility as well as improve the ability of muscles to absorb mechanical stress through the synovial joints

• Muscle strength and endurance exercises: Low-intensity and controlled movements that are within the tolerance of the affected joints
• Aerobic conditioning: Activities that have low impact on joints (e.g., walking, biking, swimming). Avoid activities that cause repetitive and intensive loading of the joints (e.g., jogging, jumping). Aerobic exercises can also help to reduce pain.
• Aquatic therapy for flexibility, strengthening, and endurance: Decrease in mechanical stress through joints due to buoyancy of water

Manual therapy to provide short-term pain relief and improve identified restrictions in joint mobility

• Soft-tissue mobilizations of areas with soft-tissue restrictions
• Joint mobilizations and manipulations
  
  • Avoid manipulations and forceful (end-range) mobilizations in the presence of inflammation. Instead, provide gentle oscillating or distraction motions with a focus on addressing pain associated with inflammation.

Therapeutic modalities (e.g., hot packs, ultrasound) for management of short-term pain and activity limitation

Patient education in combination with exercise or manual therapy

• HEP for muscle strength, endurance, and ROM
• Joint unloading strategies (e.g., movement and activity modifications, assistive devices or orthoses)
• Disease progression and symptom management
• Supporting weight reduction when patient is overweight

Impairment-based functional, gait, and balance training

• Due to impaired joint proprioception
• Aquatic therapy for gait and balance training: Decrease in mechanical stress through joints due to buoyancy of water

Question 108

What are the major indications, contraindications, guidelines, or protocols for treating osteoarthritis?

Answer 108

Outcome measures for determining outcomes following arthroplasties to treat OA:

• Western Ontario and McMaster University Osteoarthritis Index (WOMAC)
• Knee Injury and Osteoarthritis Outcome Score (KOOS)
• Lequesne (“Luh-ken”) Index

Clinical practice guidelines to diagnose hip OA:

• Moderate anterior or lateral hip pain during weight-bearing activities
• Morning stiffness less than 1 hour in duration after awakening
• Decrease in hip internal (medial) rotation, flexion
• Increased hip pain with passive hip internal (medial) rotation

Question 109

How can you distinguish osteoarthritis from a commonly associated diagnose (i.e., common misdiagnose)?

Answer 109

Adult rheumatoid arthritis

• Can develop as early as age 25 years
• Insidious onset with intermittent periods of exacerbation (active joint inflammation) and remission (absence of joint inflammation)
• Affects women 3 times as often as compared with men
• Occurs in synovial joints on both sides of the body at the same time
• Can affect any synovial joint in the body but often affects the synovial joints in the upper extremities (especially the joints at the wrist and fingers)
• Characterized by synovial joint swelling (i.e., synovitis) that is red, warm, and painful
• Prolonged morning stiffness lasting 1 hour or more
• Systemic signs and symptoms (e.g., fatigue, malaise, weight loss, fever)
• Presence of elevated levels of rheumatoid factor and C-reactive protein

Question 110

What muscles make up the quadriceps muscle group?

Answer 110

Rectus femoris

Vastus medialis

Vastus lateralis

Vastus intermedius

Question 111

What are the origins, insertions, actions, and innervations of the rectus femoris?

Answer 111

Origins

• Straight head: Anterior inferior iliac spine (AIIS)
• Reflected head: Groove above the rim of the acetabulum of the inominate bone

Insertions

• Proximal border of the patella
• Tibial tuberosity through the patellar ligament

Innervations

• Peripheral: Femoral nerve
• Segmental: L2, L3, and L4 spinal nerve roots

Actions

• Knee extension
• Assists the iliopsoas with hip flexion

*For review of bony landmarks on the femur, see Netter Plate 476.

Question 112

What are the origins, insertions, actions, and innervations of the vastus medialis?

Answer 112

Origins

• Anterior and proximal surface of the femur: Distal half of the intertrochanteric line
• Posterior and proximal surface of the femur: Medial lip of the linea aspera
• Posterior and distal surface of the femur: Proximal part of the medial supracondylar line
• Tendons of the ADductor longus and ADductor magnus
• Medial intermuscular septum

Insertions

• Proximal border of the patella
• Tibial tuberosity throught the patellar ligament

Innervations

• Peripheral: Femoral nerve
• Segmental: L2, L3, and L4 spinal nerve roots

Action

• Knee extension
• *For review of bony landmarks on the femur, see Netter Plate 476.*

Question 113

What are the origins, insertions, actions, and innervations of the vastus lateralis?

Answer 113

Origins

• Anterior and proximal surface of the femur:
  
  • Proximal part of the intertrochanteric line
  • Anterior and inferior borders of the greater trochanter
• Posterior and proximal surface of the femur:
  
  • Proximal half of the lateral lip of the linea aspera
  • Lateral lip of the gluteal tuberosity
• Lateral intermuscular septum

Insertions

• Proximal border of the patella
• Tibial tuberosity throught the patellar ligament

Innervations

• Peripheral: Femoral nerve
• Segmental: L2, L3, and L4 spinal nerve roots

Action

• Knee extension
• *For review of bony landmarks on the femur, see Netter Plate 476.*

Question 114

What are the origins, insertions, actions, and innervations of the vastus intermedius?

Answer 114

Origins

• Anterior surface of the femur: Proximal 2/3 of the anterior and lateral surfaces of the body of the femur
• Posterior surface of the femur: Distal half of the linea aspera
• Lateral intermuscular septum

Insertions

• Proximal border of the patella
• Tibial tuberosity throught the patellar ligament

Innervations

• Peripheral: Femoral nerve
• Segmental: L2, L3, and L4 spinal nerve roots

Action

• Knee extension
• *For review of bony landmarks on the femur, see Netter Plate 476.*

Question 115

Describe what an end feel is, and explain the types of phyiologic (normal) and pathological (abnormal) end feels.

Answer 115

End feel refers to the sensation that the examiner “feels” in the joint as it reaches the end of the ROM during assessment of passive range of motion (PROM) at a joint.

Physiologic (normal) end feels:

• Hard (aka, bone-to-bone): A hard, unyielding sensation as during knee extension
• Soft (aka, soft tissue approximation): A yielding compression (i.e., mushy feel) that stops further movement as during knee flexion
• Firm (i.e., stretch of the muscles, capsules, or ligaments): A feeling of springy or elastic resistance with a slight give as during ankle dorisflexion when the Achilles (calcaneal) tendon is stretched

Pathological (abnormal) end feels:

• Muscle spasm (aka, rubbery): A sudden and hard sensation (“vibrant twang”) as passive movement is abruptly ended
• Hard (aka, bony block): A hard, unyielding sensation before the end of ROM would normally occur or where a bone-to-bone end feel would not be expected (e.g., due to osteophyte formation)
• Soft (aka, mushy): A yielding compression (i.e., mushy feel) when the primary restraints to movement are impaired (e.g., ligament or capsule injury) and other structures are stopping the movement
• Firm (aka, springy block): A rebound sensation with a thick stretching feel (e.g., as with a torn meniscus at the knee when the knee is locked or unable to go into full extension)
• Hard capsular: A springy sensation with a thicker feel to it in the presence of restricted range of motion (e.g., due to capsular patterns as with adhesive capsulitis)
• Soft capsular (aka, boggy): A springy sensation in the presence of restricted range of motion (e.g., due to synovitis, soft-tissue edema, hemarthrosis)
• Empty: No real mechanical resistance is felt due to premature termination of passive movement as a result of pain (e.g., due to acute subacromial bursitits, tumor)

References: Magee (6th ed.), pp.35-36; see also Table 1-17

Question 116

What are the Ottawa knee rules?

Answer 116

The Ottawa knee rules are a set of clincial decision guidelines to help determine the need for diagnostic imaging of acute knee injuries.

According to the Ottawa knee rules, radiographs (aka, X-rays) are only required for patients with acute knee injuries who meet one or more of these criteria:

• 55 years of age or older
• Patellar tenderness
• Fibular head tenderness
• Inability to flex knee to 90°
• Inability to bear weight and walk four steps when examined at time of injury

References:

• Magee (6th ed.), p. 859
• The Ottawa Knee Rule, http://www.theottawarules.ca/knee_rules

Question 117

What is scapulothoracic protraction and retraction?

Answer 117

Scapulothoracic protraction = scapulothoracic ABduction

Scapulothoracic retraction = scapulothoracic ADduction

Question 118

What is scapulohumeral rhythm?

Answer 118

After about 30° of shoulder ABduction, the scapulohumeral rhythm occurs at a ratio of 2:1, meaning that for every 3° of shoulder abduction, 2° occurs by glenohumeral joint ABduction and 1° occurs by scapulothoracic joint upward rotation. Based on a generalized 2:1 scapulohumeral rhythm, a full arc of nearly 180° of shoulder abduction is the result of a simultaneous 120° of glenohumeral joint abduction and 60° of scapulothoracic upward rotation.

Question 119

What is rotator cuff pathology?

Answer 119

Rotator cuff pathology (aka, rotator cuff disease) refers to a continuum of conditions related to the rotator cuff (SITS) muscle group. These conditions include:

• Tendinitis (inflammation of one or more tendons of the rotator cuff muscle group)
• Bursitis (inflammation of the subacromial bursa adjacent to the tendons of the rotator cuff muscle group)
• Partial-thickness tears of one or more rotator cuff tendons (*see image below)
  
  • Partial-thickness tears are incomplete disruptions of the tendon that do NOT extend all the way through the tendon.
• Full-thickness tears in one or more of the rotator cuff tendons (*see image below)
  
  • A full-thickness tear is characterized by a complete disruption or rupture of the tendon that extends ALL the way through the tendon.

*Note: The tendon that is generally involved in rotator cuff pathology is the supraspinatus tendon. Tendinitis or tears usually occur at the insertion of the supraspinatus tendon (i.e., the greater tubercle of the humerus; glenohumeral capsule), and because of the relatively poor blood supply at the insertion site, injury at this location is unlikely to heal well (*adapted from Kisner and Colby [7th ed.], “Insidious [Atraumatic] Onset,” p.569).

References:

• Medscape: Rotator Cuff Pathology–Pathophysiology (https://emedicine.medscape.com/article/1262849-overview#a3)
• Coach K’s Lecture Materials –> Rotator Cuff Tears
• Johns Hopkins Medicine: Partial Rotator Cuff Tear (https://www.hopkinsmedicine.org/health/conditions-and-diseases/partial-rotator-cuff-tear)
• Kisner and Colby (7th ed.), pp.566-569

Question 120

What are the characteristics of the demographic population that is at risk for developing rotator cuff pathology (e.g., gender, age, past medical history)?

Answer 120

• Age: 30-50 years
  
  • Rotator cuff tears are observed more often among individuals older than 40 years of age (*adapted from Kisner and Colby [7th ed], “Intrinsic Impingement: Rotator Cuff Disease,” p.568).
• Past medical history: Pain and weakness after eccentric load (e.g., attempting to control the descent of a falling beer keg)

References:

• Magee (6th ed.), pp.257-258, Table BLE 5-2
• Coach K’s Lecture Materials –> Rotator Cuff Tears

Question 121

What causes rotator cuff pathology?

Answer 121

• Overuse injuries from repeated contact of the rotator cuff muscle tendons and subacromial bursa with the undersurface of the acromion process of the scapula (i.e., subacromial impingement) during overhead activities such as repetitive lifting, pushing, pulling, or throwing
• Traumatic tear of the tendon after a fall, accident, or chronic subacromial impingement
  
  • It has been observed that most cases of rotator cuff tears are preceded by chronic subacromial impingement (*adapted from Kisner and Colby [7th ed.], “Insidious [Atraumatic] Onset,” p.569).
• Degeneration of the tendon over time (e.g., osteophyte or bone spur formation around the acromion process that contributes to degeneration of the supraspinatus tendon)

References:

• Medscape: Rotator Cuff Pathology–Pathophysiology (https://emedicine.medscape.com/article/1262849-overview#a3)
• Coach K’s Lecture Materials –> Rotator Cuff Tears

Question 122

What are the hallmark signs and symptoms of rotator cuff pathology?

Answer 122

• General:
  
  • Pain at night
    
    • Due to laying on affected shoulder
    • Night pain is especially indicative of full-thickness tears.
  • If supraspinatus tendon is involved, pain referral pattern that radiates into the lateral elbow
  • Protective shoulder hike may be observed in conjunction with shoulder stiffness due to muscle guarding and reduced use of the affected arm.
  • Tender to palpation over the rotator cuff muscles or tendons
• Subacromial impingement and partial-thickness tears
  
  • PROM of the affected shoulder can be painful if impingement of the tendon occurs (e.g., during shoulder ABduction [frontal plane]) or when the shoulder is moved into a position that stretches the partially torn tendon and muscle (e.g., into shoulder ADduction [frontal plane])
  • Reduced shoulder ABduction (frontal plane) or rotation AROM that is painful
    
    • Painful arc sign may be present if subacromial impingement is the primary issue.
  • Resisted isometric movements result in pain and weakness (i.e., MMT grade of fair or 3), especially during shoulder ABduction (frontal plane) and lateral (external) rotation
    
    • Usually occurs when partial-thickness tear is the primary issue
• Full-thickness tears
  
  • PROM is painless and full
  • Reduced AROM that is painless
  • Resisted isometric movements is painless but severely weak, especially during shoulder ABduction (frontal plane) and lateral (external) rotation

References:

• Coach K’s Lecture Materials –> Rotator Cuff Tears
• Magee (6th ed.): Table BLE 5-2, pp.257, 258; Table BLE 5-3, p.258

Question 123

What is a special test or cluster of tests to rule in or rule out rotator cuff pathology?

Answer 123

The following special tests can be positive in the presence of rotator cuff pathology:

• Painful Arc
• Supraspinatus (“Empty-Can” or Jobe’s) Test
• Drop-Arm Test

References:

• Coach K’s Lecture Materials –> Rotator Cuff Tears
• Magee (6th ed.), pp.257-258, Table BLE 5-2
• File Explorer –> JYOUNG Passport –> WUSTL DPT’19 –> Classroom Files –> Year 2 –> Fall 2017 –> DMMC II –> Lecture Materials –> Shoulder Unit –> Intro to Shldr Exam & Special Tests –> “Special Tests for Source of Shlder Sxs” Word doc

Question 124

What are physical therapy interventions utilized to treat rotator cuff pathology?

Answer 124

Acute: Protection and pain management

• Therapeutic modalities (e.g., ultrasound, e-stim, cold pack) for pain management and *facilitation of tissue healing (*see rationale below)
• Low-intensity cross-friction massage to promote tissue healing by increasing blood flow to the injured tissues (i.e., inducing local inflammation to promote repair and regeneration of the tissues)
• Arm sling to support and rest the affected arm
• Isometric (aka, muscle-setting) exercises to stimulate the stabilizing function and maintain the muscle performance of the rotator cuff and scapulothoracic muscles
  
  • Avoid the impingement positions (e.g., midrange of ABduction with internal rotation; end-range position when the involved muscle is on a stretch such as putting the hand behind the back).
  • Scapulothoracic muscles to focus on strengthening include the serratus anterior, middle and lower trapezius, and rhomboids (*from Kisner and Colby [7th ed.], p.572).
• Pendulum exercises without weights to maintain glenohumeral joint mobility and reduce pain through grade II joint distraction and oscillation motions

Subacute: Controlled motion

• Joint mobilizations (e.g., inferior glides for shoulder ABduction) to improve glenohumeral joint mobility and faciliate normal motion at the shoulder
• Muscle stretching of the pectoralis minor, levator scapulae, and the shoulder internal (medial) rotators (i.e., pectoralis major, latissimus dorsi, teres major, and subscapularis).
  
  • Common postural dysfunctions associated with rotator cuff pathology include increased thoracic kyphosis, forward head (i.e., excessive cervical extension), and ABducted and anteriorly-tilted scapulae. As a result, the pectoralis minor, levator scapulae, and shoulder internal rotators may become short and stiff (*adapted from Kisner and Colby (7th ed.), p.569).
• Progressive strengthening of the rotator cuff and scapulothoracic muscles

Chronic: Return to function

• Functional mobility training

References:

• Kisner and Colby (7th ed.), pp.571-573

Question 125

What are the major indications, contraindications, guidelines, or protocols for treating rotator cuff pathology?

Answer 125

If the supraspinatus tendon is torn, magnetic resonsance imaging (MRI) of the affected shoulder will show a superior displacement of the humeral head.

Reference:

• For MRIs of rotator cuff tears–Magee (6th ed.), pp. 371-372, Figs. 5-200 & 5-202

Question 126

How can you distinguish rotator cuff pathology from a commonly associated diagnose (i.e., common misdiagnose)?

Answer 126

Adhesive capsulitis:

• Progressive loss of both active and passive range of motion (loss of AROM = loss of PROM)
• In the beginning stages, will present with intact rotator cuff muscle strength (fair+ [3+] to good [4]). As the disease progresses, there may appear to be muscle weakness, but the presented muscle weakness is due to an increase in pain.
• Observation of a shoulder capsular pattern: Shoulder lateral rotation will be more limited than ABduction, which will be more limited than medial rotation
• Special tests for rotator cuff pathology may be negative or inconclusive. If the patient is in stage 2-4 of adhesive capsulitis, patient may not be able to position affected shoulder into the test positions due to pain or limited shoulder mobility.

Question 127

What is the supraspinatus (“empty-can” or Jobe’s) test? What is its purpose? What is a positive result, and what does a positive result indicate?

Answer 127

Test procedure:

• Examiner places the patient’s arm in 90° of shoulder ABduction with neutral (no) rotation, and examiner provides manual resistance against shoulder ABduction.
• The shoulder is then medially rotated and angled forward 30° (“empty-can” position) so that the patient’s thumbs point toward the floor in the plane of the scapula. Resistance against shoulder ABduction is again given.

Positive result: Weakness or pain in the “empty-can” position

Interpretation of positive result: Tear of the supraspinatus tendon or muscle, or neuropathy of the suprascapular nerve

Reference:

• Magee (6th ed.), p.341 (*see also Figure 5-143)

Question 128

What is the drop-arm (Codman’s) test? What is its purpose? What is a positive result, and what does a positive result indicate?

Answer 128

Test procedure: Examiner places the patient’s shoulder in 90° of ABduction and then asks the patient to slowly lower the arm to the side in the same arc of movement

Positive result: Patient is unable to return the arm to the side slowly or has severe pain when attempting to do so.

Interpretation of positive result: Tear of the rotator cuff tendon

Reference:

• Magee (6th ed.), Figure 5-127, p.334; p.332

Question 129

What is painful arc sign? What is a positive result, and what does a positive result indicate?

Answer 129

Test procedure: Examiner instructs the patient to perform active shoulder ABduction in the patient’s preferred manner.

Positive result: Shoulder ABduction is painful throughout a range of 60-120°. Pain may be present during the raising motion into shoulder ABduction or the lowering motion into shoulder ADduction.

Interpretation of positive result: Mechanical impingement of structures underneath the acromion process (aka, subacromial impingement). Involved structures include the subacromial bursa or the rotator cuff tendon insertions (especially the supraspinatus).

References:

• Magee (6th ed.), pp.272-274 (*see also Figure 5-29)
• TherapyEd Review Study Guide, p.29

Question 130

What muscles are included in the hamstrings muscle group?

Answer 130

Biceps femoris–long head

Biceps femoris–short head

Semitendinosis

Semimembranosis

Question 131

What are the origins, insertions, actions, and innervations of the semimembranosus?

Answer 131

Origin:

• Ischial tuberosity (proximal and lateral to the origins of the semitendinosus and biceps femoris [long head])

Insertion:

• Posteromedial aspect of the medial condyle of the tibia

Innervations

• Peripheral: Tibial nerve
• Segmental: L4, L5, S1, and S2 spinal nerve roots

Actions:

• Knee flexion
• Knee internal (medial) rotation
• Hip extension
• Assists with hip internal (medial) rotation

Question 132

What are the origins, insertions, actions, and innervations of the semitendinosus?

Answer 132

Origin:

• Ischial tuberosity via the tendon common with the biceps femoris (long head)

Insertions

• Proximal part of the anteromedial surface of the body of the tibia
• Deep fascia of the lower leg

Innervations

• Peripheral: Tibial nerve
• Segmental: L4, L5, S1, and S2 spinal nerve roots

Actions:

• Knee flexion
• Knee internal (medial) rotation
• Hip extension
• Assists with hip internal (medial) rotation

Question 133

What are the origins, insertions, actions, and innervations of the biceps femoris (long head)?

Answer 133

Origins:

• Posterior part of the ischial tuberosity
• Distal part of the sacrotuberous ligament

Insertions:

• Lateral side of the head of the fibula
• Lateral condyle of the tibia
• Deep fascia of the lateral side of the lower leg

Innervations

• Peripheral: Tibial nerve
• Segmental: L5, S1, S2, and S3 spinal nerve roots

Actions:

• Knee flexion
• Knee lateral (external) rotation
• Hip extension
• Assists with hip lateral (external) rotation

Question 134

What are the origins, insertions, actions, and innervations of the biceps femoris (short head)?

Answer 134

Origin:

• Lateral lip of the linea aspera
• Proximal 2/3 of the lateral supracondylar line
• Lateral intermuscular septum

Insertions:

• Lateral side of the head of the fibula
• Lateral condyle of the tibia
• Deep fascia of the lateral side of the lower leg

Innervations

• Peripheral: Common fibular nerve
• Segmental: L5, S1, and S2 spinal nerve roots

Actions:

• Knee flexion
• Knee lateral (external) rotation

*For review of bony landmarks on the femur, see Netter Plate 476.

Question 135

What is rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA)?

Answer 135

Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disorder that is characterized by inflammation and destruction of the synovial joint capsule (i.e., articular manifestations) (especially the synovium) and elsewhere throughout the body (i.e., extraarticular manifestations–e.g., eye lesions, osteoporosis, cardiopulmonary impairments).

Juvenile idiopathic arthritis is included under rheumatoid arthritis. Juvenile idiopathic arthritis (JIA) (aka, juvenile rheumatoid arthritis, or JRA) is an umbrella term for a heterogeneous group of disorders among children that develop and present similarly to RA. Juvenile idiopathic arthritis usually begins before 16 years of age and is characterized by complete remission in 75% of children.

References:

• Goodman & Fuller (4th ed.), pp.192 (“Rheumatoid Arthritis”), 1317-1318 (“Overview;” “Pathogenesis”), 1328 (“Overview and Incidence”)
• TherapyEd Review Study Guide, p. 53

Question 136

What are the characteristics of the demographic population that is at risk for developing rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) (e.g., gender, age, past medical history)​?

Answer 136

Age

• RA: Initial onset of 25-50 years, peak onset of 30-60 years
• JIA: Children younger than 16 years

Gender

• RA: Affects women 3 times as often compared with men
• JIA: Affects girls more often than boys

Reference:

• Goodman and Fuller (4th ed), p.1317 (“Incidence and Risk Factors”), p.1330 (“Etiologic and Risk Factors and Pathogenesis”)

Question 137

What causes rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA)?

Answer 137

The cause of RA and JIA is unknown and poorly understood, but it is most likely from a combination of genetic and environmental factors.

Reference:

• Goodman and Fuller (4th ed.), p.1317 (“Incidence and Risk Factors”), p.1330 (“Etiologic and Risk Factors and Pathogenesis”)

Question 138

What are the hallmark signs and symptoms of rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA)?

Answer 138

• Insidious onset with intermittent periods of exacerbation (active joint inflammation) and remission (absence of joint inflammation)
• Occurs in synovial joints on both sides of the body at the same time
• Can affect any synovial joint in the body but often affects the synovial joints in the upper extremities (especially the joints at the wrist and fingers)
• Characterized by synovial joint swelling (i.e., synovitis) that is red, warm, and painful
• Prolonged morning stiffness lasting 1 hour or more
• Systemic signs and symptoms (e.g., fatigue, malaise, weight loss, fever)
• Presence of elevated rheumatoid factor and C-reactive protein

References:

• Goodman & Fuller (4th ed.), p.1317 (Table 27-2), p.1318 (“Pathogenesis”), p.1319 (Box 27-8), pp.1318-1321 (“Clinical Manifestations”), 1326 (“Remission”)

Question 139

What physical therapy interventions are utilized to treat rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA)? Compare and contrast the active and remission periods.

Answer 139

Active inflammatory period

• Gentle joint mobilizations to reduce pain (e.g., grade I and II distraction and oscillation techniques)
• PROM or AAROM to maintain available joint motion
• Isometric (aka, muscle-setting) exercises to minimize muscle atrophy and maintain the ability of muscles to absorb mechanical stress through the synovial joints (*see OA flashcards)

Remission period

• Aquatic therapy for flexibility, strengthening, and endurance
  
  • Decrease in mechanical stress through joints due to buoyancy of water

References:

• Kisner & Colby (7th ed.), pp.337-341
• Goodman & Fuller (4th ed.), p.1328 (“Aquatic Therapy”)

Question 140

What physical therapy interventions are contraindicated for patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA)?

Answer 140

• Do not perform stretching techniques across swollen joints. When there is effusion, limited motion is the result of excessive fluid in the joint space. Forcing motion on the distended capsule overstretches it, leading to subsequent hypermobility (or subluxation) when the swelling abates. It may also increase the irritability of the joint and prolong the joint reaction.
• Avoid exercises that cause excessive stress to bone or joints (e.g., jogging, jumping). Patients with RA or JIA may have osteoporosis and ligamentous laxity due to use of steroidal medications to treat the condition.
• Avoid vigorous stretching or high-velocity thrust manipulative techniques of affected joints. The joint capsule, ligaments, and tendons may be structurally weakened by the rheumatic process or secondary to steroidal use, and forceful (end-range) techniques can result in muscle guarding, pain, and greater tissue damage.

Reference:

• Kisner & Colby (7th ed.), pp.339-341

Question 141

What is fibromyalgia?

Answer 141

Fibromyalgia (aka, fibromyalgia syndrome, or FMS) is a chronic muscle pain syndrome characterized by widespread muscle pain with allodynia or hyperalgesia to pressure pain. In particular, fibromyalgia is a disorder of pain processing (i.e., abnormal pain modulation with hypersensitivity to painful stimuli and reduced pain inhibition).

Reference:

• Goodman & Fuller (4th ed.), p.310 (“Definition and Overview”)

Question 142

What are the hallmark signs and symptoms of fibromyalgia?

Answer 142

• Muscle pain (aka, myalgia) that is described as aching or burning
• Diffuse pain or tender points on both sides of the body
• Fatigue and exhaustion due to sleep distrubances secondary to muscle pain
• Visual problems (e.g., blurring, double vision, bouncing images) possibly due to hypersensitivity to visual stimuli

References:

• Goodman & Fuller (4th ed.), Table 7-6, p.314; p.312 (“Clinical Manifestations”)
• Medscape: Fibromyalgia–Patients Hypersensitive to Nonpain Sensations (https://www.medscape.com/viewarticle/831831)

Question 143

What physical therapy interventions are utilized to treat fibromyalgia?

Answer 143

• Aerobic fitness and strength training to reduce muscle pain and other symptoms
  
  • Example: Aquatic therapy due to reduced joint loading secondary to buoyancy of water (*see OA flashcards)
• Slow and gentle soft-tissue techniques to reduce muscle pain and intensity of tender points
  
  • Avoid cross-friction massage.
• Therapeutic modalities (e.g., ultrasound, interferential current) to reduce muscle pain.

References:

• Goodman & Fuller (4th ed.), p.316 (“Modalities and Fibromyalgia), 316-317 (“Exercise and Firbomyalgia”)
• Kisner & Colby (7th ed.), pp.345-346

Question 144

What is osteoporosis?

Answer 144

Osteoporosis is a chronic, progressive disease characterized by low bone mass, impaired bone quality, decreased bone strength, and enhanced risk of fractures.

Reference:

• Goodman & Fuller (4th ed.), p.1211 (“Definition and Overview”)

Question 145

What physical therapy interventions are utilized to treat osteoporosis?

Answer 145

• Strengthening exercises, weight-bearing exercises (e.g., walking, jogging, climbing stairs, jumping, standing partial squats)
  
  • Muscle contraction (e.g., during strengthening exercises and resistance training) and mechanical loading (i.e., e.g., during weight-bearing activities) deform bone. This deformation stimulates osteoblastic activity and improves bone mineral density.
  • Physical activity has been shown to have a positive effect on bone remodeling. In children and adolescents, this activity may increase the peak bone mass. In adults, it has been shown to maintain or increase bone density; in the elderly, it has been shown to reduce the effects of age-related or disuse-related bone loss.

Reference:

• Kisner and Colby (7th ed.), pp.348-349

Question 146

What physical therapy interventions are contraindicated for patients with osteoporosis?

Answer 146

• Avoid spinal flexion activities and exercise (e.g., supine curl-ups and sit-ups) as well as the use of sitting abdominal machines. Osteoporosis changes the shape of the vertebral bodies (i.e., they become more wedge shaped), leading to kyphosis. Stress into spinal flexion increases the risk of a vertebral compression fracture.
• Avoid combining spinal flexion and rotation to reduce stress on the vertebrae and the intervertebral discs.
• Avoid high-intensity resistance exercises that go beyond the structural capacity of the affected bones.

Reference:

• Kisner and Colby (7th ed.), p.349 (“Precautions and Contraindications”)
• “Reasons for Spinal Compression Fractures” YouTube video (https://www.youtube.com/watch?v=LILgFAEMAbg&feature=emb_title)
• NCBI-StatsPearl BookShelf: “Vertebral Compression Fractures” (https://www.ncbi.nlm.nih.gov/books/NBK448171/)

Question 147

What is scoliosis?

Answer 147

Scoliosis is an abnormal lateral curvature of the spine. Curves are designated as right or left, depending on the convexity (e.g., right thoracic scoliosis describes a curve in the thoracic spine with convexity to the right). In the thoracic spine, rotational deformity on the convex side (i.e., rotation of the vertebral bodies toward the convex side) is observed as a rib hump sometimes seen in the upright position, but always apparent in the forward bend position.

Reference:

• Goodman and Fuller (4th ed.), p.1164 (“Definition”), p.1166 (“Clinical Manifestations”)
• Kisner and Colby (7th ed.), p.432

Question 148

What causes scoliosis? Distinguish between functional and structural scoliosis.

Answer 148

Functional (postural) scoliosis is NOT due to vertebral involvement. Functional scoliosis is therefore also called non-structural scoliosis. The abnormal lateral curves in functional scoliosis disappear when the underlying cause is addressed. Examples of these causes include:

• Leg-length discrepancy
• Poor posture
• Pain or muscle spasm

Structural scoliosis IS due to vertebral involvement–in particular, deformity of the vertebral bodies. Most cases of structural scoliosis are idiopathic.

Reference:

• Goodman and Fuller (4th ed.), p.1165 (“Etiologic Factors”)

Question 149

What is ankylosing spondylitis?

Answer 149

Ankylosing spondylitis (aka, Marie-Strümpell disease) is a chronic systemic and inflammatory disorder that primarily affects the joints of the axial skeleton and the sacroiliac (SI) joint. Ankylosing spondylitis is also characterized by extraarticular complications (e.g., eye, cardiopulmonary) and can be associated with asymmetrical involvement of the large peripheral joints, including the hip, knee, and shoulder.

References:

• Goodman and Fuller (4th ed.), p.1332 (“Overview and Incidence”), 1334
• Kisner and Colby (7th ed.), p.473

Question 150

What are the characteristics of the demographic population that is at risk for developing anklyosing spondylitis (e.g., gender, age, past medical history)​?

Answer 150

Gender: Male

Age: 15-30 years

Past medical history: Genetic predisposition with family history of anklyosing spondylitis

Reference:

• Goodman and Fuller (4th ed.), p.1333 (“Overview and Incidence,” “Eiologic and Risk Factors”)

Question 151

How does anklyosing spondylitis develop as it progresses?

Answer 151

Anklyosing spondylitis is marked by chronic inflammation at the area where the ligaments attach to the vertebrae (an area called the enthesis), initially in the lumbar spine and then in the sacroiliac joint. Disruption of this ligamentous–osseous junction results, and reactive bone formation occurs as part of the repair process. The replacement of inflamed cartilaginous structures by bone contributes to progressive ossification with bony growth between the vertebrae, leading to a fused, rigid, or bamboo spine that is characteristic of end-stage disease (*see image below).

References:

• Goodman and Fuller (4th ed.), p.1333 (“Pathogenesis”)

Question 152

What are the hallmark signs and symptoms of ankylosing spondylitis?

Answer 152

• Insidious onset of low back or buttock pain and stiffness lasting for at least 3 months
• Significant morning stiffness lasting more than 1 hour
• Flexion posture characterized by thoracic kyphosis, hip flexion contractures, and loss of lumbar extension
• Rigid gait due to loss of spinal extension and rotation
• Systemic signs and symptoms (e.g., fever, fatigue, loss of appetite, weight loss)

Reference:

• Goodman and Fuller (4th ed.), pp.1333-1334 (“Clinical Manifestations”)

Question 153

What physical therapy interventions are utilized to treat ankylosing spondylitis?

Answer 153

• Patient education on how to faciliate a functional thoracic kyphotic posture before the entire spine becomes fused (i.e., maintaining exaggerated lumbar extension by sleeping in the prone position; using a towel roll or pillow behind the lumbar spine when sitting)
• Strengthening exercises focused on the muscles at the trunk (e.g., back extensors) and scapulae in order to improve the stability of the spine and facilitate the functional posture position
• Stretching exercises focused on reducing hip flexion contractures
• Aerobic exercise (e.g., aquatic therapy) that are low intensity and emphasize spinal extension and rotational components to maintain joint mobility at the spine
• Gentle joint mobilizations (i.e., grades I and II oscillatory and sustained techniques) for pain mangement at segments unaffected by ankylosing spondylitis

References:

• Kisner and Colby (7th ed.), p.473
• Goodman and Fuller (4th ed.), p.1337 (“Exercise Prescription”)

Question 154

What physical therapy interventions are contraindicated for patients with anklyosing spondylitis?

Answer 154

• Avoid high-impact and flexion exercises due to increased risk for vertebral fractures secondary to the associated thoracic kyphotic posture and the development of the stiff and osteoporotic spinal column

References:

• Goodman and Fuller (4th ed.), p.1334 (“Complications”), 1337 (“Exercise Prescription”)
• “Reasons for Spinal Compression Fractures” YouTube video (https://www.youtube.com/watch?v=LILgFAEMAbg&feature=emb_title)

NCBI-StatsPearl BookShelf: “Vertebral Compression Fractures” (https://www.ncbi.nlm.nih.gov/books/NBK448171/)

Question 155

What is gout?

Answer 155

Gout is a metabolic disorder that is also described as a crystalopathy (aka, crystal-induced arthritis). Gout is characterized by elevated levels of uric acid in the blood and subsequent deposition of monosodium urate crystals in the joints, soft tissues, and kidneys.

Reference:

• Goodman and Fuller (4th ed.), pp.1344-1345 (“Overview,” “Pathogenesis”)

Question 156

What are the characteristics of the demographic population that is at risk for developing gout (e.g., gender, age, past medical history)?

Answer 156

Gender: Male

Age: Older than 30 years of age

• Predominantly associated with middle-aged men around 50 years of age

Past medical history

• Heavy alcohol consumption (especially beer)
• Obesity
• Diet rich in:
  
  • Purines, or nitrogen-containing com-pounds found in foods such as shellfish, trout, sardines, anchovies, meat (especially organ meats), asparagus, beans, peas, spinach
  • Fructose-sweetened foods and beverages

Reference:

• Goodman and Fuller (4th ed.), p.1345 (“Incidence,” “Etiologic and Risk Factors”)

Question 157

How does gout develop as it progresses?

Answer 157

Uric acid is a substance that normally forms when the body breaks down cellular waste products called purines. In healthy people, uric acid dissolves in the blood, passes through the kidneys, and is then excreted through the urine. If the body produces more uric acid than the kidneys can process or if the kidneys are unable to handle normal levels of uric acid, then the acid level in the blood rises. When the uric acid in the blood reaches high levels, it may precipitate out and accumulate in body tissues (e.g., joints and kidneys), forming supersaturated body fluids that develop into monosodium urate crystals. The crystals trigger an inflammatory response, resulting in local tissue necrosis and a proliferation of fibrous tissue secondary to an inflammatory foreign-body reaction.

References:

• Goodman and Fuller (4th ed.), p.1345 (“Pathogenesis”)
• Medscape: Gout and Pseudogout–Pathophysiology (https://emedicine.medscape.com/article/329958-overview#a3)

Question 158

What are the hallmark signs and symptoms of gout?

Answer 158

• Severe joint pain (e.g., at the 1st metatarsophalangeal joint [great toe]) occuring suddenly at night
• Erythema, warmth, extreme tenderness, and hypersensitivity at the affected joints
• Chills, fever, and tachycardia

Question 159

What physical therapy interventions are utilized to treat gout?

Answer 159

Acute: Protection and Pain Management Phase

• Orthosis or bracing to support and protect the affected joint (e.g., orthotic shoe insert and well-constructed shoes for gout of the 1st MTP joint [great toe])
• Gentle joint mobilizations to reduce joint pain (e.g., grade I and II oscillatory and distraction techniques)
• PROM, AAROM, and AROM as tolerated to maintain joint mobility
• Gentle isometric (aka, muscle-setting) exercises to reduce muscle atrophy and maintain muscle performance in the area around the affected joint
• Aquatic therapy for low-impact, buoynacy-assisted exercises to maintain joint mobility and muscle strength

Subacute and Chronic: Controlled Motion and Return to Functional Mobility

• Joint mobilization and stretching exercises to improve joint mobility

Reference:

• Kisner and Colby (7th ed.), pp.856-858

Question 160

What is torticollis?

Answer 160

Torticollis (aka, congenital muscular torticollis [CMT]; wry neck) means “twisted neck” and is characterized by a contracted state of the sternocleidomastoid muscle (SCM), producing head tilt (i.e., cervical lateral flexion) to the affected side with rotation of the chin to the opposite side (*see image below). Torticollis is designated as right or left depending on side the head tilt is directed toward (e.g., right cervical lateral flexion = right torticollis).

Reference:

• Goodman and Fuller (4th ed.), p.1199

Question 161

What are the hallmark signs and symptoms of torticollis?

Answer 161

• Lateral flexion to the affected side with rotation to the opposite side
• Firm, nontender, palpable enlargement of the sternocleidomastoid (SCM) muscle
• Craniofacial asymmetry (i.e., plagiocephaly, or flat head syndrome) characterized by flattening of the infant’s face, ear, and head from resting on the affected side

Question 162

What physical therapy interventions are utilized to treat torticollis?

Answer 162

• Passive stretching exercises for the shortened sternocleidomastoid (SMC) muscle to improve cervical spine movement as well as improve muscle length of the affected SCM
  
  • Be sure to stabilize the proximal attachment of the SCM and trapezius during passive stretching exercises.

References:

• Goodman and Fuller (4th ed.), p.1200 (“Clinical Manifestations–Treatment”)
• TherapyEd Review Study Guide, p.56

Question 163

What are the origins, insertions, actions, and innervations of the sternocleidomastoid (SCM)?

Answer 163

Origins:

• Sternal head: Manubrium of the sternum
• Clavicular head: Medial 1/3 of the clavicle

Insertion:

• Lateral surface of the mastoid process of the temporal bone
• Lateral 1/2 of the superior nuchal line of the occipital bone

Innervations

• Peripheral: Spinal accessory nerve (CN XI)
• Segmental: Anterior primary rami of the C1 and C2 spinal nerve roots

Actions:

• Unilaterally: Cervical rotation to the opposite side, and lateral cervical flexion to same side
• Bilaterally: Flexion of the lower cervical spine (C3 - C7) with anterior translation of the cervical vertebrae and no sagittal rotation; extension of the upper cervical spine (occiput, atlas, axis) (i.e., capital extension, or head-on-neck extension)

Question 164

What is lateral elbow tendinosis?

Answer 164

Lateral elbow tendinosis (aka, “tennis elbow”) is an overuse injury characterized by degeneration and weakening of the superficial extensor muscle tendons (i.e., extensor carpi radialis brevis, extensor digitorum, extensor digiti minimi, and extensor carpi ulnaris) at their shared origin attachment via the common extensor tendon to the lateral epicondyle of the distal humerus. Lateral elbow tendinosis is also called lateral elbow tendinopathy, lateral epicondylitis, lateral epicondylalgia, or lateral epicondylosis.

*Note #1: The primary muscle involved in lateral elbow tendinosis is the extensor carpi radialis brevis muscle. In about 50% of patient cases, the extensor digitorum is involved as well.

*Note #2: The extensor carpi radialis brevis and extensor carpi ulnaris contribute to wrist extension only. The extensor digitorum and extensory digiti minimi contribute to both wrist and finger extension (*see Neumann [3rd ed.], p.235 [“Wrist Extensor Muscles” Box]).

References:

• Kisner and Colby (7th ed.), p.641 (“Overuse Syndromes: Repetitive Trauma Syndromes,” “Related Pathologies–Lateral Elbow Tendinopathy”)
• Moore et al. (8th ed.), p.222, p.235 (“Clinical Box: Forearm–Elbow Tendinitis”)

Question 165

What causes lateral elbow tendinosis?

Answer 165

Repetitive loading of the superficial extensor muscle tendons during:

• Activities requiring repetitive or forceful grasp, such as hammering or playing tennis
  
  • The main function of the wrist extensors is to position and stabilize the wrist during activities involving active flexion of the digits. For example, when making a fist, the wrist extensor muscles counterbalance the significant wrist flexion torque produced by the finger flexor muscles and place the wrist in an extended position, optimizing the length-tension relationship of the extrinsic finger flexors and thereby facilitating maximal grip strength (*adapted from Neumann [3rd ed.], p.236; see also Figure 7.25).
• Prolonged positioning of the wrist in extension, such as when typing on a computer keyboard

References:

• Kisner and Colby (7th ed.), p.641 (“Lateral Elbow Tendinopathy”)
• Neumann (3rd ed.), p.236
• Sahrmann (2011), p.299 (“Symptoms and History”)

Question 166

What are the hallmark signs and symptoms of lateral elbow tendinosis?

Answer 166

• Complaints of lateral elbow pain during gripping activities such as lifting or pouring a gallon of milk
  
  • Pain may radiate distally along the posterior aspect of the forearm
• The following tests for source will be positive.
  
  • Palpation tenderness on or near the lateral epicondyle
  • Pain at the lateral epicondyle during:
    
    • Resisted wrist extension performed with the elbow flexed, forearm pronated, and wrist in slight extension
    • Resisted middle finger extension (aka, Maudsley’s test)
      
      • If pain is instead over the medial border of the extensor carpi radialis brevis, positive for radial nerve compression (aka, radial tunnel syndrome).
    • Pain with passive wrist flexion with the elbow extended and forearm pronated (aka, Mill’s test)
      
      • Due to stretch of the superficial extensor muscles of the forearm

Reference:

• Kisner and Colby (7th ed.), p.641
• Sahrmann (2011), p.288 (“Test for Radial Nerve Compression in the Forearm”), 290 (“Test for Wrist Extension with Forearm Pronation”), 299 (“Symptoms and History”)
• Magee (6th ed.), p.408 (“Mill’s Test,” “Maudsley’s Test”)

Question 167

What is medial elbow tendinosis?

Answer 167

Medial elbow tendinosis (aka, “golfer’s elbow”) is an overuse injury characterized by degeneration and weakening of the superficial pronator and flexor muscle tendons (i.e., pronator teres, flexor carpi radialis, palmaris longus, and flexor carpi ulnaris) at their shared origin attachment via the common flexor tendon to the medial epicondyle of the distal humerus. Medial elbow tendinosis is also called medial elbow tendinopathy, medial epicondylitis, medial epicondylalgia, or medial epicondylosis.

*Note: The flexor carpi radialis, flexor carpi ulnaris, and palmaris longus contribute to wrist flexion only (*see Neumann [3rd ed.], p.239 [“Wrist Flexor Muscles” Box]). The pronator teres contributes to forearm pronation.

References:

• Kisner and Colby (7th ed.), p.641 (“Overuse Syndromes: Repetitive Trauma Syndromes,” “Related Pathologies–Medial Elbow Tendinopathy”)
• Moore et al. (8th ed.), p.217

Question 168

What causes medial elbow tendinosis?

Answer 168

Repetitive loading of the superficial pronator and flexor muscle tendons during:

• Repetitive movements into wrist flexion, such as swinging a golf club or pitching a ball

References:

• Kisner and Colby (7th ed.), p.642 (“Medial Elbow Tendinopathy”)

Question 169

What are the hallmark signs and symptoms of medial elbow tendinosis?

Answer 169

• Complaints of medial elbow pain with wrist flexion
  
  • Pain may radiate distally along the anterior aspect of the forearm.
• The following tests for source will be positive.
  
  • Palpation tenderness on or near the medial epicondyle
  • Pain at the medial epicondyle during:
    
    • Resisted wrist flexion
    • Passive wrist extension performed with the elbow extended and forearm supinated (aka, “golfer’s elbow” test)
      
      • Due to stretch of the superficial pronator and flexor muscles

References:

• Magee (6th ed.), p.408 (“Medial Epicondylitis [Golfer’s Elbow] Test”), 426 (Table 6-5)
• Medscape: Medial Epicondylitis Clinical Presentation (https://emedicine.medscape.com/article/97217-clinical)

Question 170

What is Osgood-Schlatter disease?

Answer 170

Osgood-Schlatter’s disease is a traction phenomenon in which the fibers of the patellar tendon pull small bits of immature bone from the tibial tuberosity. Inflammation of the patellar ligament (i.e., tendinitis) is also associated with Osgood-Schlatter’s disease.

Reference:

• Goodman and Fuller (4th ed.), p.1369 (“Overview”)
• Medscape: Osgood-Schlatter’s Disease (https://emedicine.medscape.com/article/1993268-overview)

Question 171

What are the characteristics of the demographic population that is at risk for developing Osgood-Schlatter’s disease (e.g., gender, age, past medical history)?

Answer 171

Gender: Male

Age: 10-15 years

Personal medical history:

• Actively involved in sports
• Abnormal alignments of the lower extremities such as genu valgum (aka, knock-knees) or pes planus (aka, flat-foot) that create large Q-angles (*see image below)
  
  • Large Q-angles place more tension on the tibial tuberosity.
• High-riding patella (aka, patella alta)

Reference:

• Goodman and Fuller (4th ed.), p.1369 (“Etiologic Factors and Pathogenesis”)

Question 172

What causes Osgood-Schlatter disease?

Answer 172

• Indirect trauma (i.e., a force produced by the sudden, powerful contraction of the quadriceps femoris muscle group during an activity such as running and jumping)
• Repetitive stress (e.g., repeated knee flexion against a short or stiff quadriceps femoris muscle group)
• Longstanding tension on the patella and patellar ligament during rapid growth spurts

Reference:

• Goodman and Fuller (4th ed.), p.1369 (“Etiologic Factors and Pathogenesis”)

Question 173

What are the hallmark signs and symptoms of Osgood-Schlatter disease?

Answer 173

• Complaints of constant and localized aching and pain at the site of the tibial tuberosity
• Swelling over the tibial tuberosity that is warm and tender (*see image below)
• Pain with activities involving forceful contraction of the patellar ligament against the tibial tuberosity (e.g., active knee extension, resisted knee flexion, ascending or descending stairs, running, jumping, biking, hiking, kneeling, squatting)
• Significant shortness and stiffness of the hamstrings muscle group, quadriceps femoris muscle group, iliotibial band, or triceps surae muscle group.
  
  • Shortness and stiffness in these structures can potentially increase the knee flexion internal moment and subsequently the stresses at the tibial tuberosity.

Reference:

• Goodman and Fuller (4th ed.), p.1369 (“Clinical Manifestations”)

Question 174

What is patellofemoral syndrome?

Answer 174

Patellofemoral syndrome (aka, patellofemoral pain syndrome) refers to a collection of signs and symptoms associated with the patellofemoral joint that is characterized by a general description of anterior knee pain.

*Note: The patellofemoral joint refers to the articulation between the articular side of the patella and the trochlear groove of the femur (*from Neumann [3rd ed.], p.556).

References:

• Kisner and Colby (7th ed.), p.792 (“Related Patellofemoral Pathologies and Etiology of Symptoms”)
• Medscape: Patellofemoral Syndrome (https://emedicine.medscape.com/article/308471-overview)

Question 175

What are the characteristics of the demographic population that is at risk for developing patellofemoral syndrome (e.g., gender, age, past medical history)?

Answer 175

Gender: Female

Reference:

• Kisner and Colby (7th ed.), p.793 (“Focus on the Evidence”)

Question 176

What causes patellofemoral syndrome?

Answer 176

Examples of causes include:

• Direct trauma to (i.e., overloading of) the patellofemoral joint
• Overuse of the patellofemoral joint
• Faulty patellar tracking during knee movements
• Patellofemoral joint degeneration
• Soft tissue length and strength imbalances in the hip, knee, or ankle and foot

References:

• Kisner and Colby (7th ed.), p.792 (“Related Patellofemoral Pathologies and Etiology of Symptoms”)
• Medscape: Patellofemoral Syndrome Clinical Presentation–Causes (https://emedicine.medscape.com/article/308471-clinical#b5)

Question 177

What are the hallmark signs and symptoms of patellofemoral syndrome?

Answer 177

• Pain that is located behind the patella (i.e., retropatellar)
• Increased pain during activities that increase patellofemoral joint compressive forces through repetitive knee flexion (e.g., running, biking) or large amounts of knee flexion (e.g., squatting, prolonged sitting with flexed knees, and ascending and descending stairs)
  
  • Pain during prolonged sitting with the knee flexed is called the “theater sign” or “movie-goer’s knee.”
• Altered lower extremity alignment: Increased hip ADduction, internal (medial) rotation, and dynamic genu valgum that occurs during weight-bearing activities (e.g., ascending and descending stairs, squatting, landing after a jump)

References:

• Kisner and Colby (7th ed.), p.792 (“Related Patellofemoral Pathologies and Etiology of Symptoms”), 794 (“Common Impairments”)
• Medscape: Patellofemoral Syndrome–Practice Essentials (https://emedicine.medscape.com/article/308471-overview#a1)
• Medscape: Patellofemoral Syndrome–Presentation History (https://emedicine.medscape.com/article/308471-clinical)
• Physiopedia: Patellofemoral Joint–Kinetics (https://physio-pedia.com/Patellofemoral_Joint?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal)

Question 178

What is Legg-Calvé-Perthes disease?

Answer 178

Legg-Calvé-Perthes disease (aka, coxa plana, or “flat hip;” osteochondritis deformans juvenilis) refers to avascular necrosis of the proximal end of the femur at the femoral head (aka, capital femoral epiphysis of the immature femur) (*see image below).

Reference:

• Goodman and Fuller (4th ed.), p.1365 (“Definition and Overview”)
• Palisano et al. (5th ed.), p.319 (“Legg-Calvé-Perthes Disease)

Question 179

What are the characteristics of the demographic population that is at risk for developing Legg-Calvé-Perthes disease (e.g., gender, age, past medical history)?

Answer 179

Gender: Male

Age: 3-12 years

Ethnicity: White

Reference:

• Goodman and Fuller (4th ed.), p.1365 (“Definition and Overview”)

Question 180

What causes Legg-Calvé-Perthes disease?

Answer 180

The cause of the avascular necrosis that is characteristic of Legg-Calvé-Perthes disease is unknown.

Reference:

• Goodman and Fuller (4th ed.), p.1366 (“Etiologic Factors”)

Question 181

What are the hallmark signs and symptoms of Legg-Calvé-Perthes disease?

Answer 181

• Complaints of insidious onset of hip pain that is described as sore or aching
  
  • Pain may also be present in the groin and along the path of the obturator nerve (i.e., the proximal anteromedial surface of the thigh). Pain may also be referred to the knee.
  • Pain is aggravated by activity and fatigue and relieved somewhat by rest.
• Palpation over the hip capsule produces pinpoint tenderness.
• Limping presentation on the involved side
  
  • Pathological gait patterns of compensatory Trendelenberg gait, antalgic gait, or psoatic limp may be present.
• Short stature as a result of epiphyseal dysplasia
• ROM limitations in the directions of hip ABduction and internal (medial) rotation

References:

• Goodman and Fuller (4th ed.), p.1367 (“Clinical Manifestations”)
• Obturator Nerve - Cutaneous Innervation: Moore et al. (8th ed.), p.697 (Figure 7.17); Netter Plate 526

Question 182

What are the standards by which you determine how likely the Legg-Calvé-Perthes disease is to improve?

Answer 182

The process of Legg-Calvé-Perthes disease lasts from 2-5 years and typically ends with resolution of the disease and return to normal functioning of the hip joint. As a result, a non-surgical treatment approach with physical therapy is typically recommended.

References:

• Goodman and Fuller (4th ed.), p.1366 (“Pathogenesis,” Table 27-4), 1368
• Osmosis: “Legg-Calve-Perthes disease” video (https://www.youtube.com/watch?v=ylhiGkrQ8A8–1:59 to 2:23)

Question 183

What physical therapy interventions are utilized to treat Legg-Calvé-Perthes disease?

Answer 183

• Aquatic therapy and gait training to maintain involvement in weight-bearing activities as tolerated so as to facilitate the bone remodeing process (*see “Osteoporosis” flashcards)
  
  • Weight-bearing activities should be completed in hip ABduction in order to contain the capital femoral epiphysis (aka, femoral head) within the depths of the acetabulum.
    
    • Containment prevents deformities of the diseased epiphysis from occuring, equalizes the pressure on the femoral head, and allows the molding action of the acetabulum to occur to ensure a perfectly smooth interface between the femoral head and acetabulum.
  • With aquatic therapy, the buoyancy of the water decreases joint loading and subsequently makes it easier to perform weight-bearing exercises.
• Hip mobility exercises to restore and prevent loss of ROM at the hip joint (especially hip ABduction and internal [medial] rotation)
  
  • The buoyancy of water associated with aquatic therapy also facilitates hip mobility exercises.

References:

• Palisano et al. (5th ed.), p.320 (“ROM is limited in the directions of…”), 321 (“Containment is an important principle of…”)
• Goodman and Fuller (4th ed.), p.1368 (“Special Implications for the Therapist”)

Question 184

What is slipped capital femoral epiphysis (SCFE)?

Answer 184

Slipped capital femoral epiphysis refers to the displacement of the femoral head (aka, capital femoral epiphysis) relative to the femoral neck and shaft. The displacement or “slippage” occurs at the proximal epiphyseal plate (aka, growth plate) (*see image below).

References:

• Palisano et al. (5th ed.), p.323
• Medscape: Slipped Capital Femoral Epiphysis–Funtional Anatomy (https://emedicine.medscape.com/article/91596-overview#a7)

Question 185

What are the characteristics of the demographic population that is at risk for developing slipped capital femoral epiphysis (SCFE) (e.g., gender, age, past medical history)?

Answer 185

Gender: Male

Age: 10-16 years; average of 14 years

Past medical history:

• Metabolic disorders such as obesity
  
  • Obesity creates a higher mechanical load across the proximal epiphyseal plate (aka, growth plate).

Reference:

• Palisano et al. (5th ed.), p.323 (“The presence in boys [13.35 per 100,000] is higher than…;” “The presence of these symptoms when presenting…”)

Question 186

What causes slipped capital femoral epiphysis?

Answer 186

• Abnormally widened and weakened proximal epiphyseal plate (aka, growth plate)
• May or may not be caused by trauma (e.g., fall or twist)
  
  • Due to increased mechanical shear forces through the proximal epiphyseal plate (aka, growth plate) as a result of trauma or an abnormally shaped proximal femur
    
    • Abnormalities at the proximal femur that increase mechanical shear forces across the epiphyseal plate include: (1) Femoral retrotorsion (aka, “femoral retroversion”), (2) a decreased femoral neck-shaft angle (i.e., angle of inclination) called coxa vara, or (3) a deeper acetabulum.
      
      • Rationale: Femoral retrotorsion positions the proximal femur close to the medial-lateral axis through the femoral condyles, and coxa vara positions the epiphyseal plate more vertically (*see image below). A deeper acetabulum is associated with the femoral head being anchored more completely within the acetabulum, making the proxmial epiphyseal plate more vulnerable to mechanical shear forces at the extremes of hip motion.

References:

• Palisano et al. (5th ed.), p.323 (“The eitology of SCFE is multifactorial…”)
• Medscape: Slipped Capital Femoral Epiphysis–Functional Anatomy (https://emedicine.medscape.com/article/91596-overview#a7)
• For more about femoral torsion, version, and angle of inclination: Neumann (3rd ed.), pp.484-485 (“Shape of the Proximal Femur”); KINES II –> Developmental Kinesiology –> Lecture Notes –> Lecture #9b_Developmental Biomechanics (pp.11-14); DMNMC II –> Lecture Materials –> Exam #1 –> Cerebral Palsy (p.4)

Question 187

What are the hallmark signs and symptoms of slipped capital femoral epiphysis?

Answer 187

Acute (i.e., due to trauma; symptoms present for less than 3 weeks)

• Severe, fracture-like pain in the groin, thigh, or knee
• Unable to bear weight on the affected lower extremity
• Position of comfort is hip lateral (external) rotation of the affected hip
• Observable shortening of the affected lower extremity

Chronic (i.e., symptoms present for several months)

• Vague and intermittent pain in the groin and upper or lower thigh
  
  • Increased pain with running or sport activities
  • Tender to palpation over the anterior hip joint
• Hip capsular pattern: Limitations in flexion, ABduction, and internal (medial) rotation
• Limping presentation on the involved side
  
  • Pathological gait patterns of compensatory Trendelenberg gait, antalgic gait, or backward trunk lean (due to gluteus maximus weakness) may be present.
• Affected lower extremity is held in a position of hip lateral (external) rotation
• Muscle atrophy of the affected thigh
• Observable shortening of the affected lower extremity

References:

• Palisano et al. (5th ed), p.323 (“SCFE may be classified by the onset of…”)
• Coach’s K Lecture Materials –> SCFE vs. LCPD (slide 12)

Question 188

What are the standards by which you determine how likely slipped capital femoral epiphysis is to improve?

Answer 188

Older children generally have more severe slips or displacements of the proximal epiphyseal plates. Therefore, they have a poorer prognosis than younger children.

In general, emergent surgery is required to prevent the progression of SCFE.

References:

• Palisano et al. (5th ed.), p.323 (“Also of note is that older children generally…”), 324 (“Options for surgical management include…”)
• Medscape: Slipped Capital Femoral Epiphysis–Treatment & Management (https://emedicine.medscape.com/article/91596-treatment)

Question 189

What are the major indications, contraindications, guidelines, or protocols for treating slipped capital femoral epiphysis?

Answer 189

When a child is suspected to have SCFE, immediate referral with radiology testing is recommended. Once the diagnosis has been confirmed, absolutely no weight bearing is recommended because this can lead to osteonecrosis. The child is then treated with emergent surgery to prevent the progression of SCFE.

References:

• Palisano et al. (5th ed.), p.324
• Medscape: Slipped Capital Femoral Epiphysis–Treatment & Management (https://emedicine.medscape.com/article/91596-treatment)​

Question 190

What is Duchenne muscular dystrophy?

Answer 190

Duchenne muscular dystrophy is a genetic disorder that is characterized by progressive degeneration of skeletal and cardiac muscle fibers and subsequent weakening of the muscles.

References:

• Vander’s (15th ed.), p.283 (“Muscular Dystrophy”)
• Palisano et al. (5th ed.), pp. 242-265​

Question 191

What are the characteristics of the demographic population that is at risk for developing Duchenne muscular dystroophy (e.g., gender, age, past medical history)?

Answer 191

Gender: Male

Past medical history:

• Family history of DMD (genetic predisposition)

Reference:

• Goodman and Fuller (4th ed.), p.1182 (“Incidence and Etiologic Factors”)

Question 192

What causes Duchenne muscular dystrophy (DMD)?

Answer 192

Genetic cause–DMD is a a sex-linked recessive disorder caused by a mutation in a gene on the X chromosome that codes for the protein dystrophin. The defective gene can result in either a nonfunctional or missing dystrophin protein.

*Note: Dystrophin is an extremely large protein that normally forms a link between the contractile filament actin and proteins embedded in the overlying sarcolemma (i.e., plasma membrane of a muscle fiber) (*see also Goodman and Fuller [4th ed.], p.1184, Figure 23-17). Lack of normal dystrophin makes the sarcolemma susceptible to damage during muscle contraction–relaxation cycles. Disruption of the sarcolemma and muscle fiber necrosis are initiated by muscle contraction, especially eccentric contraction.

References:

• Vander’s (15th ed.), p.284 (“Muscular Dystrophy”)
• Goodman and Fuller (4th ed.), p.1185 (“Duchenne and Becker Muscular Dystrophies”)

Question 193

What are the hallmark signs and symptoms of Duchenne muscular dystrophy (DMD)?

Answer 193

• Psudohypertrophy and contracture of the posterior calf muscles due to connective tissue and fat deposits
• Difficulty getting up off the floor (i.e., Gowers sign) due to weakening of the hip and trunk muscles
  
  • In Gowers sign, the patient places the hands on the thighs and walks up the legs with the hands until the weight of the trunk can be placed posterior to the hip joint (*see image below). This sign is characteristic of weakness of the lumbar and gluteal muscles.
• Lumbar lordosis (which may present also as a protuberant or bulging abdomen) that places the line of gravity behind the hip joint to compensate for shoulder girdle, abdominal, and hip extensor weakness
• Pathological gait patterns: Waddling gait due to proximal muscle weakness, compensatory Trendelenberg gait due to hip ABductor weakness, toe walking due to posterior calf muscle contractures and anterior lower leg muscle weakness
• Progressive restrictive respiratory impairment secondary to weakness and contracture of the respiratory muscles
• Frequent falls
• Difficulty climbing stairs

Reference:

• Goodman and Fuller (4th ed.), p.1182 (“Definition and Overview”), 1188-1189 (“Duchenne Muscular Dystrophy”)

Question 194

What are the standards by which you determine how likely Duchenne muscular dystrophy (DMD) is to improve?

Answer 194

Duchenne muscular dystrophy is rapidly progressive, with a loss of walking ability by 9-10 years; death around 20 years.

References:

• Vander’s (15th ed.), p.284 (“Muscular Dystrophy”)
• Goodman and Fuller (4th ed.), p.1184 (Table 23-5)

Question 195

What physical therapy interventions are utilized to treat Duchenne muscular dystrophy (DMD)?

Answer 195

• Aquatic therapy to improve muscle endurance
  
  • Because of the benefit of reduced joint and muscle loading with aquatic therapy, exercise is best done in the pool, where exercise is concentric. Any exercise program should produce only minimal fatigue with no post-exercise soreness, because the amount of damage to the sarcolemma with exercise is related directly to the magnitude of the stress placed on it during contraction.
• Diaphragmatic or deep-breathing exercises or airway clearance techniques to address respiratory impairments
• Splinting and night positioning as well as AROM and PROM exercises to reduce the extent of muscle contractures and maintain joint mobility
• Adaptive equipment training (e.g., grab bars, power wheelchairs) to maintain functional mobility and independence as disease progresses

Reference:

• Goodman and Fuller (4th ed.), pp.1193-1194

Question 196

What are the major indications, contraindications, guidelines, or protocols for treating Duchenne muscular dystrophy (DMD)?

Answer 196

• Avoid low-repetition maximum weightlifting, especially eccentric strengthening.
  
  • Strenuous exercise may facilitate the breakdown of muscle fibers.
• Because of respiratory involvement, careful monitoring of breathing techniques, respiratory movements, and oxygen saturation levels is required.

Reference:

• Goodman and Fuller (4th ed.), pp.1193-1194