A major league pitcher walks into spring training with a simple complaint:

“I’m not in pain. I’m just weaker. After two or three innings my arm is dead.”

His range of motion is full. His cuff tests don’t light him up. His labrum looks “OK for a thrower.” For years, that guy would have been labelled with “rotator cuff tendinitis” or “dead arm,” thrown into generic rehab, and maybe booked for a scope if things dragged on.

Day 1 of this course blew that approach up.

Again and again, the faculty showed versions of the same core idea:

In elite throwers, the problem is almost never just “a sore tendon.” It’s the entire system — nerves, blood supply, decelerators, scapula, trunk — and if you miss the real driver and jump to the wrong surgery, you often don’t get a second chance.

What followed was a full tour through that system: suprascapular nerve neuropathy, musculocutaneous injuries, advanced nerve imaging, vascular catastrophes, latissimus and teres major tears, throwing biomechanics, and a brutally honest shoulder exam.

This is the story – and the playbook – from Day 1.

Why “Doing the Right Thing the First Time” Matters More Than Ever

The day opened with a reminder that many big-league hitters who show up in surgical datasets already carry scars. Labral repairs. Rotator cuff debridements. Biceps tenodeses. Multiple “clean-ups” that didn’t really clean much up.

The point wasn’t to shame those decisions. It was to show their limits.

Take the biceps tenodesis. Moving the long head of the biceps off the superior labrum and fixing it lower down can be helpful in very specific cases – a painful, degenerative biceps tendon, or as part of a salvage plan when a prior slap repair has failed and the joint is still irritable. But that same operation won’t fix:

- Internal impingement in the back of the shoulder

- A hidden suprascapular neuropathy

- A poorly functioning scapula

- A latissimus that can’t decelerate the arm

One of the senior surgeons put it simply:

You want to do the right thing the first time. The “salvage” procedures are useful when the joint is sensitised and you need to quiet it down. They are not magic erasers for complex, multi-factor problems in an MLB shoulder.

Day 1’s agenda was basically a warning label: before you cut, make sure you understand what system is actually failing.

What Is Suprascapular Nerve Entrapment in Baseball Pitchers?

The first deep dive was the suprascapular nerve – a small branch off the C5–C6 roots that quietly runs the supraspinatus and infraspinatus muscles and carries some of the joint’s pain signals. In throwers, its classic pattern is almost eerie:

- Very little pain, especially once the acute episode passes

- Gradual onset of weakness in elevation and external rotation

- Visible atrophy in the infraspinatus, sometimes supraspinatus too

- Normal skin sensation, because it’s mainly a motor nerve

On MRI, you might see “neurogenic” signal in those muscles and early fatty change. On CT you might see a narrow suprascapular notch or a stout spinoglenoid ligament that can trap the nerve. On EMG, the diagnosis becomes clearer: a lesion at the notch or spinoglenoid notch.

What makes this important in baseball is how these injuries happen. It’s rarely a giant cyst or a tumour. In fact, the majority of cases have no mass lesion. Instead, the nerve is irritated by a mix of traction and compression:

- The scapula rotates massively during cocking and follow-through.

- The nerve has to glide through tight bony tunnels and ligamentous roofs.

- Repeated extremes of motion stretch and rub that nerve over time.

The big clinical question is: do you wait or decompress?

Some athletes with mild, non-compressive lesions respond to nonoperative care: full shoulder motion, scapular work, neuromuscular stimulation, time. Others – especially those with clear compression from a cyst or a tight ligament in the spinoglenoid notch – are better served with early decompression.

The surgical playbook is precise: an open decompression at the spinoglenoid notch, an arthroscopic decompression at the suprascapular notch, both done in one sitting. Minimal rehab burden. Often early strength gains. High return-to-sport rates.

The key Day 1 message: painless weakness in a thrower is a nerve problem until proven otherwise, and suprascapular neuropathy must be on that list.

How Does Advanced Nerve Imaging Change Return-to-Play Decisions?

If suprascapular neuropathy is the first clue that nerves matter, musculocutaneous neuropathy is the test case that shows how much imaging can change our choices. Three baseball players, three versions of the same story:

- A sudden “electric” sensation or ache

- Delayed weakness in elbow flexion

- Biceps atrophy

- EMG confirming musculocutaneous involvement

In the past, this often led to a shrug and a long wait. Maybe surgery, maybe not, based mostly on time and guesswork.

Now? MR neurography and high-resolution ultrasound give you a map.

In one player, MR neurography showed a normal musculocutaneous nerve – no swelling, no constriction, no entrapment at the coracobrachialis. With a normal-appearing nerve and a history consistent with neuritis, the team could confidently not operate. The athlete recovered fully with time.

In another, imaging revealed something much stranger: a single bright fascicle within the nerve – like one glowing cable among many – consistent with Parsonage-Turner syndrome (an autoimmune brachial neuritis) rather than mechanical entrapment. Surgery there wouldn’t have helped; immunologic processes and time would.

In the third, MR neurography and ultrasound both showed a crushed, flattened musculocutaneous nerve at the coracobrachialis. No mystery. No waiting. That player went to surgery, had the nerve decompressed, and regained elbow flexion in time to salvage his season.

The pattern:

- Normal nerve → reassure, protect, let biology recover

- “Hot” fascicle without tight tunnel → inflammatory neuritis, not a target for decompression

- Squashed, hourglass, or constricted nerve → structural problem that will not fix itself

The imaging doesn’t replace clinical judgment or electrodiagnostics. It upgrades them. It converts “let’s see” into “this is safe to wait” or “we must intervene now.”

Why High-Resolution Ultrasound Is Becoming the Thrower’s Stethoscope

If MR neurography is the satellite image, ultrasound is the handheld camera – immediate, dynamic, and surprisingly revealing.

On Day 1, ultrasound kept popping up:

- Visualising a swollen radial nerve compressed at the arcade of Frohse in a pitcher whose velocity and control had mysteriously dipped.

Watching an ulnar nerve literally snap over the medial epicondyle in real time during elbow flexion.

- Seeing classic “hourglass” constrictions in fibular and other peripheral nerves – tight waists between normal segments.

- Comparing normal, dark, healthy muscle next to pale, fibrotic, denervated muscle to localise a nerve lesion.

Just as important, ultrasound guided treatment, not just diagnosis:

- Hydrodissection to physically separate a nerve from tight fascial planes and give it room.

- Precise diagnostic blocks to decide whether pain is articular or neuropathic.

- Simple but powerful injections, like a lidocaine shot around a tight pectoralis minor that instantly relieved neurogenic arm symptoms in an overhead athlete.

By the time the morning was over, one idea was hard to ignore:

- For complex throwing shoulders, a high-frequency ultrasound probe is as essential as a reflex hammer. It’s how you see the moving parts that don’t show up on a standard X-ray or even a routine MRI.

Vascular Problems in Throwers: From “Dead Hand” to Life-Threatening

Most baseball people know about labrums and UCL tears. Fewer think about strokes and threatened hands. But Day 1 didn’t let anyone look away from the vascular side.

Two big buckets matter in throwers: arterial thoracic outlet problems and axillary/posterior circumflex humeral artery issues.

In the first, congenital or acquired bony anomalies – cervical ribs, fused first and second ribs, elongated C7 transverse processes – narrow the space where the subclavian artery passes. Over time, repetitive arm elevation and throwing compress that artery, damaging the intima, leading to stenosis, aneurysm, or thrombosis. Sometimes this presents as a dramatic acute event: a cold, pulseless arm. Other times it’s insidious:

- Fatigue and heaviness with use

- Raynaud-like colour changes in the fingers

- Painful, non-healing calluses at the fingertips from micro-embolisation

In the second bucket, repeated traction and subluxation at the shoulder stretch the axillary system, especially the posterior circumflex humeral artery. Small aneurysms can form in that vessel, then shower tiny clots into the hand every time a pitcher lets a fastball go. Over months, this chews away at blood flow to the digits. Day 1 showed vivid cases:

- Ultrasound of a thickened subclavian with mural thrombus.

- Angiograms with absent radial and ulnar flow, and barely visible collaterals.

- Young pitchers who needed vein or graft bypasses from axillary to brachial arteries to save the limb and their career.

- On the venous side, effort thrombosis (Paget–Schrötter syndrome) of the subclavian-axillary vein also appeared. Here, catheter-directed thrombolysis and suction thrombectomy, followed by rib resection and angioplasty, have largely replaced long, open reconstructions.

The takeaway is simple and brutal:

- If a player complains of hand colour change, fingertip pain, or “dead arm” with true loss of pulse, that’s not “just thoracic outlet.” That’s a vascular emergency dressed in baseball clothes.

Latissimus and Teres Major Tears: The Hidden Decelerator Crisis

If you only remember one muscle from Day 1, it should be the latissimus dorsi. To a back surgeon it’s a spine muscle. To a shoulder surgeon it’s a humeral internal rotator. To a strength coach it’s “the big back muscle.”

But to a throwing coach or performance physio, the lat is core and decelerator. It ties the pelvis and trunk to the arm and helps slam the brakes on after ball release.

That’s why, when a big-league pitcher tears his lat, the pitch usually still reaches the catcher. The injury happens at the very end of the throwing motion. The ball leaves on time. Then the athlete bolts upright in pain as the tendon rips off the humerus. Day 1 walked through:

- How MRI often shows fluid and disruption right at the tendon, not just at a vague muscle–tendon junction.

- How teres major frequently joins the party, showing its own strain signal next to the lat.

- How classification systems (partial vs complete, amount of retraction) help guide treatment.

- The data are clear on one point:

- Type 1–2, partial tears → usually managed nonoperatively. They may take 90–120 days to get back, but many do well, especially position players or lower-level pitchers.

- Type 3–4, complete avulsions from the humerus in high-level pitchers → strongly considered for surgical repair if the athlete wants to return to prior level.

- Nonoperative care can work even in big tears, but there is a cost: recurrent lat symptoms, secondary shoulder problems, and a decelerator that may never quite trust itself again.

And surgery? It’s no small thing.

- The posterior axillary approach sits right next to the neurovascular bundle. The tendon has to be found, mobilised, and anchored back to the humerus, often with cortical buttons that, in rare cases, can create stress risers and even humeral fractures when a pitcher returns to 98 mph.

- Yet the return-to-play numbers after well-done repairs are compelling: most elite throwers get back, usually around 12–15 months, and many report that by about a year they’ve stopped thinking about their lat entirely.

The bigger lesson is psychological:

- You don’t have to panic. If a complete lat tear is missed acutely, it can still be fixed a year or more later. The muscle is large, the tendon robust.

- This is not like a chronic distal biceps where the window closes quickly. That knowledge alone changes how you counsel players and teams under pressure.

What Actually Causes Throwing Shoulder Injuries? (It’s Not Just “Too Many Pitches”)

By the afternoon, Day 1 zoomed out from structures to systems – especially how trunk and shoulder motion shape injury risk. A few themes surfaced:

- First, trunk and hip rotation. Studies on youth and pro players show that limited rotation between pelvis and trunk – poor “hip–shoulder separation” – increases the odds of shoulder and elbow pain as pitch counts climb. If the pelvis doesn’t rotate well, the arm has to make up that lost velocity upstream.

- Second, external rotation and internal impingement. Advanced imaging in abducted, externally rotated positions shows that:

Dominant shoulders in throwers have more internal impingement contact area than non-dominant shoulders.

- More external rotation in that position increases the contact area further.

So at first pass, you’d think “more layback = more impingement = worse.” But epidemiology keeps complicating that story. Several large studies have found that:

- Players with less external rotation and a reduced total rotational arc are more likely to end up with shoulder surgery.

- Bony adaptation (increased humeral retroversion) that allows more layback appears to be protective, up to a point.

So we’re left with a paradox:

- More ER can mean more internal impingement, but less ER may equal more catastrophic breakdown.

Day 1’s practical answer was nuanced:

- Chase a balanced total arc of motion between sides, rather than obsessing over a few degrees of internal rotation loss.

- Respect that some ER in the throwing shoulder is a normal adaptation, not a disease to be stretched away.

- Put serious effort into trunk and hip rotation, where gains can reduce arm stress without sacrificing mechanics.

In other words, stop trying to make a 20-year-old professional pitcher’s shoulder look like a 14-year-old non-thrower’s. The goal is a functional, not “normal,” shoulder.

How Do You Actually Examine a Baseball Shoulder?

The final live session of Day 1 anchor everything in the clinic: a complete throwing shoulder exam, start to finish. A few highlights stood out. The exam started behind the athlete, not in front. From there you can:

- Inspect scapular position and look for atrophy in supra- and infraspinatus.

- Palpate the cervical spine, AC joint, and periscapular muscles.

- Watch for scapular winging during wall push-ups, which hints at serratus or long thoracic problems.

- Cervical motion and Spurling’s test came next, because not every arm symptom is a shoulder problem.

Then, shoulder-specific work:

- Sulcus sign in neutral and external rotation to gauge inferior laxity and superior capsular integrity.

- Apprehension testing in abduction–external rotation (for anterior instability), with relief when a posteriorly directed force is applied.

Posterior load-and-shift, jerk, and Kim-type manoeuvres for posterior instability – often more painful than obviously unstable.

- A battery of labral tests (O’Brien, dynamic labral shear, crank, biceps load I and II, resisted supination–external rotation) used in combination rather than as magical single answers.

Overlaying all of this were condition-specific checks:

- Latissimus: palpate deep in the posterior axilla, then resist adduction and internal rotation, watching for pain or loss of power.

- Obliques: rotational trunk movements with overpressure and then resisted, reproducing those “it hurts when I turn and throw” rib pains.

And then, a simple but blunt principle:

- One of the best tests is whether the athlete can do the thing they’re paid to do.

- Can your shortstop swing without pain? Can your pitcher get to late cocking without apprehension? Can they decelerate without guarding? Video and live “functional tests” are part of the exam, not an optional extra.

The Real Lesson of Day 1

On paper, Day 1 looked like a random walk: biceps tenodesis, suprascapular nerve, musculocutaneous neuritis, MR neurography, ultrasound, vascular catastrophes, lat tears, thrower’s biomechanics, shoulder exam. In reality, it was a single argument, repeated from different angles:

- Elite throwing shoulders are complex systems. If you treat them like simple tissue problems, you’ll do the wrong surgery, at the wrong time, for the wrong reason.

The antidote isn’t more MRI scans or fancier anchors. It’s a mindset shift:

- From “What structure is torn?”

- To “Which system – nerve, vessel, decelerator, scapula, trunk – is failing, and why?”

For clinicians like you, that means slowing down before you speed up. Using nerve imaging and ultrasound to decide if surgery is needed, not just which one. Respecting the strange, adaptive nature of a thrower’s ROM instead of trying to normalise it. Learning to see the lat, teres, and obliques as part of shoulder health, not just performance.

Day 1 didn’t offer a single magic technique. It offered something better: a way to think that makes bad decisions harder and good outcomes more likely.