6.1 Shoulder Complex Assessment

Practice Analysis, 8th Edition (PA8) Domain II, task 0202, asks the athletic trainer to perform a physical examination using appropriate diagnostic techniques. At the shoulder that means naming the joint you are stressing, clustering tests instead of hanging a diagnosis on one maneuver, and knowing when a positive finding is a syndrome—not a torn structure.

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Four Joints, One Shoulder

The shoulder complex is four articulations sharing one kinetic chain:

• Glenohumeral (GH) joint: a shallow ball-and-socket. The labrum deepens the socket; the rotator cuff centers the humeral head.
• Acromioclavicular (AC) joint: distal clavicle to acromion, restrained by AC and coracoclavicular (conoid + trapezoid) ligaments.
• Sternoclavicular (SC) joint: the only true bony attachment of the upper limb to the axial skeleton.
• Scapulothoracic (ST) articulation: not a synovial joint. Scapular upward rotation, posterior tilt, and external rotation set the glenoid.

Scapulohumeral rhythm is classically about 2:1 GH-to-ST motion after the first ~30° of elevation (roughly 120° GH and 60° ST to reach 180°). Loss of scapular upward rotation or posterior tilt narrows the subacromial space and mimics cuff pain. Watch the scapula; do not treat the GH joint as an isolated hinge.

Observation before you touch

Compare both sides from front, side, and back, arms at rest and then elevated.

• Step-off: a high distal clavicle after AC sprain (type III or higher), or a squared-off lateral deltoid after GH dislocation. Posterior dislocation can look almost normal from the front—loss of external rotation is the giveaway.
• Scapular winging: medial winging on a wall push-up points to long thoracic nerve / serratus anterior. Lateral (trapezius) winging with abduction points to spinal accessory nerve. Subtle medial-border prominence in late cocking is common in throwers and is a finding, not a stand-alone diagnosis.
• Atrophy in the infraspinatus fossa (suprascapular nerve or chronic cuff tear), an AC bump, and a proximal Popeye biceps contour belong on the same 10-second scan.

Range of motion and GIRD

Measure active then passive GH rotation at 90° abduction with the scapula stabilized. Overhead athletes typically gain external rotation (ER) and lose internal rotation (IR) on the throwing side. That total-arc shift can be adaptive.

Glenohumeral internal rotation deficit (GIRD) is IR loss versus the non-throwing shoulder. Isolated IR loss with preserved total rotational motion (TROM) (IR + ER) is often anatomic. Pathologic GIRD is the combination that matters: IR loss commonly described as greater than about 18–20° plus a TROM deficit (Wilk and colleagues linked a >5° side-to-side TROM deficit to higher injury rates). If you do not stabilize the scapula, you will measure scapulothoracic IR and falsely 'find' GIRD.

Posterior capsule/cuff tightness with pathologic GIRD drives the humeral head posterosuperior in abduction–external rotation (ABER). That is the mechanical setup for internal impingement (articular-sided posterior cuff against the posterosuperior glenoid/labrum) and the peel-back SLAP mechanism—not a primary acromial hook.

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Rotator Cuff: Pain Provocation Versus Lag

Pain on a cuff test is not the same as a full-thickness tear. Lag signs (the athlete cannot hold the position you placed) imply weakness of that tendon.

A painful empty can plus a negative drop-arm and full ER/IR strength is tendinopathy or bursal pain, not an automatic surgical cuff tear. Pair these tests with a cervical screen (C5–C6 can mimic lateral shoulder pain) and scapular observation.

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'Impingement' Is a Syndrome, Not a Structure

Neer's sign: scapula stabilized, passive flexion with IR, jamming the greater tuberosity under the coracoacromial arch. Hawkins-Kennedy: 90° flexion, 90° elbow flexion, then IR, driving the greater tuberosity against the coracoacromial ligament.

Both tests squeeze everything in the subacromial space (bursa, cuff, CA ligament) and can also provoke AC pain. Hegedus and colleagues (2008) pooled Neer sensitivity 79% and specificity 53%—useful as a screen, useless as a tissue name. Hawkins-Kennedy shows a similar pattern: moderate sensitivity, poor specificity across studies. A positive test means subacromial pain was reproduced. It does not mean the acromion is the disease, that the bursal side of the cuff is torn, or that the athlete needs a decompression.

Exam trap: writing impingement as if it were a ligament you can grade. Call it subacromial pain syndrome, then ask why the space is angry: scapular dyskinesis, GIRD/internal impingement in a thrower, AC arthropathy, a bursal-sided cuff, instability with superior humeral-head migration, or cervical referred pain. Park and colleagues described a more useful cluster for subacromial pain (Hawkins-Kennedy + painful arc + infraspinatus weakness), still a syndrome cluster, not an MRI report.

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Instability, Labrum, and AC

Instability

Labrum (cluster, never one test)

O'Brien (active compression): arm 90° flexion, 10–15° adduction, full IR (thumb down), resist a downward force; repeat in ER (palm up). Positive when pain or click in IR lessens in ER. Deep joint pain suggests SLAP; superficial pain on top of the shoulder suggests AC. Hegedus 2012 meta-analysis: about 67% sensitivity and 37% specificity for SLAP—do not diagnose a SLAP from O'Brien alone. The test is more specific for AC when pain is clearly on top of the joint.

Crank: elevation ~160°, axial load, IR/ER. Click or reproduction of deep pain suggests a labral tear, again not standalone.

Biceps load II: 120° abduction, max ER, elbow 90°, resist elbow flexion. Deep pain suggests a SLAP because the long head peels the superior labrum.

Use these as a cluster with history (dead-arm, click, pain in late cocking) and instability tests. Speed and Yergason load the long head of the biceps; they do not separate biceps tendinopathy from a SLAP because the tendon anchors on the superior labrum. Internal impingement in throwers: ABER reproduces posterior joint-line pain; the articular cuff and posterosuperior labrum are being pinched. That is a different problem than subacromial bursal pain even if Neer is mildly positive.

AC joint

Piano-key: springy inferior pressure on a high distal clavicle (higher-grade AC). Cross-body (horizontal) adduction: AC-localized pain. Pair with O'Brien if the pain is on top of the shoulder and with direct AC palpation. Cross-body also stresses the posterior capsule, so where it hurts matters.

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Neurovascular Tests: TOS with Caution

Thoracic outlet syndrome (TOS) tests (Adson, Wright/hyperabduction, Roos/EAST) look for pulse loss or reproduction of arm symptoms in a compressed scalene–first-rib–pectoralis-minor corridor. Pulse disappearance is common in healthy people. Poor specificity is the BOC point: do not diagnose TOS from a lost radial pulse. Need a history of positional neurovascular symptoms, a cervical/first-rib exam, and referral—not a one-test label. A cervical rib is a congenital bony TOS risk, not something you invent from Adson alone.

Always include a cervical screen (active rotation, Spurling only if the neck is stable—see 6.3) and a distal neurovascular exam (axillary sensation over the lateral deltoid, distal pulses, and C5–T1 myotomes).

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Worked Scenario: Quarterback with Dead-Arm

A collegiate quarterback comes off after a long series. The last throw 'died' at the end of late cocking; he describes a dead-arm (sudden loss of velocity and control) and deep posterior shoulder pain, not lateral bursal pain. No dislocation event today. Observation: mild scapular dyskinesis, no step-off. ROM at 90° abduction, scapula held: throwing-side IR 40° versus 65° opposite (25° IR loss); ER 130° versus 115°; TROM is 10° down on the throwing side (pathologic GIRD pattern, not a pure ER-gain shift). Cuff: 5/5, no ER lag, no drop-arm, belly-press intact. Neer and Hawkins mildly painful but he points deep posterior, not to the acromion. Apprehension at 90/90 with relocation relief. O'Brien: deep pain in IR that eases in ER. Crank and biceps load II both reproduce the click. Posterior ABER compression reproduces the throwing pain. Adson loses a pulse on both sides (ignore that). AC is non-tender.

Interpretation: thrower's spectrum—pathologic GIRD, internal impingement, and a positive labral/anterior-instability cluster. You do not diagnose 'impingement' or book a subacromial decompression because Neer was a little sore. You do not call TOS because Adson is bilaterally noisy. Hold throwing, restore IR/posterior-capsule mobility and scapular control, and refer for imaging if the labral cluster plus dead-arm history persists. First-time dislocation with axillary-nerve deficit (deltoid weakness, numb badge area), a deformity suggesting fracture, or a hot, feverish, immobile joint (septic GH) is a different case: immobilize or withhold, and refer now—do not keep special-testing.

Exam trap: treating a positive Neer/Hawkins as a structure you can grade, or using a single O'Brien to 'confirm' a SLAP. Cluster, name the joint, and refer the red flags.