1. Thoracic outlet syndrome and the overhead ATHLETE
LISA PIROPATO, PT, DPT, ATC
NORTHEAST INDIANA SPORTS MEDICINE SYMPOSIUM
MARCH 25, 2017

2. Learning objectives
Explain the etiologies of thoracic outlet syndrome.
Differentiate between the types of vascular and neurologic thoracic outlet syndrome.
Identify effective treatment and management strategies incorporating muscle strengthening and neuromuscular control of the upper extremity for patients presenting with thoracic outlet symptoms.
Recommend a return to activity program for overhead athletes following conservative or non-conservative treatment

3. WHAT IS THORACIC OUTLET SYNDROME (TOS)?
Term outlines the location without defining what comprises the problem
Compression of the neurovascular structures in the interscalene triangle
Subcategorized as arterial or venous and neurogenic
NTOS subcategorized into true or disputed
True: condition with objective diagnostic findings
Disputed: condition without objective findings
90% of all cases are NTOS, <1% arterial, 3-5% venous
Combined TOS: vascular and neurological structures involvement

4. pathoanatomy
3 confined spaces from cervical spine to lower pec minor muscles
Interscalene triangle
Costoclavicular space
Thoraco-coraco-pectoral (retropectoralis minor) space
Interscalene triangle:
Borders: anterior scalene anteriorly, middle scalene posteriorly, median surface of 1st rib inferiorly
trunks of brachial plexus and subclavian artery pass through
Costoclavicular space:
Borders: middle 1/3 clavicle anteriorly, 1st rib posteromedially, upper border of scapula posterolaterally
Thoraco-coraco-pectoral space
Borders: coracoid process superiorly, pec minor anteriorly, ribs 2-4 posteriorly

5. Bony causes Cervical ribs <1% of general population
Abnormal 1st rib or clavicle
Exotosis, tumor, callus, fracture
Clavicle fracture – malunion, fragmentation, retrosternal dislocation
Normal movement is essential – ACJ & SCJ
Important for structural and functional integrity of both ACJ and SCJ to allow movement of clavicle in all 3 planes

6. Soft tissue causes
Abnormalities may create compression or tension of the neurovascular structures
Congenital abnormalities with anatomic variation of scalene muscles

7. Arterial Venous True Neurogenic Disputed Neurogenic
Young adults
Hx of vigorous arm activity or spontaneous
Younger men
Preceded by excessive activity in the arm or spontaneous
History of neck trauma
MVA or repetitive stress at work
Pain in hand
Seldom in shld/neck
Edema of the arm
Pain, paresthesia, numbness &/or weakness in hand/arm/shld (C8-T1)
Pallor
Claudication
Coldness and cold intolerance
Cyanosis
Feeling of heaviness
Occipital HA’s
Cold intolerance – Raynaud phenomenon
Parasthesias
Sxs spontaneously stem from aa emboli
Parasthesias in fingers and hand (secondary to edema)
Paresthesias, numbness during the day and at night
“compressors”= sxs day > noc
Loss of dexterity
“releasers”= sxs noc > day
Diagnosis by history
Diagnosis by history and cluster of 2 provocation tests (+) and almost always (+) elevated arm stress test
Objectified weakness &/or sensory = “true”
Subjective weakness &/or sensory = “true”
Diagnosis confirmed through doppler US and angiography in seated position
Diagnosis confirmed through venous US, venous scintillation scans, venography and plethysmography
Diagnosis confirmed through (+) neurophysiological testing
No confirmation through objective testing neurophysiological testing are normal

8. Clinical examination
Neurogenic tos

9. symptoms Radicular vs. non radicular Paresthesia in upper limb
Neck pain
Trapezius pain
Shoulder and/or arm pain
Supraclavicular pain
Chest pain
Occipital headache
Paresthesias of all 5 fingers or 4/5 only or 1-3 only
Classic symptoms:  pain/paresthesia/weakness in hand/arm/shoulder,neck pain, occpital HAs
Can have coldness and color changes in UE due to an overactive sympathetic nervous system

10. INCREASES TENSION LOADING OF THE BRACHIAL PLEXUS
presentation
Rounded shoulders
Forward head
Increased thoracic kyphosis
Anterior tilt/downward rotn/depression scapulae
Clinical examination needs to include mobility of first rib, clavicle, thoracic spine, and GH end range to stress clavicle and brachial plexus
INCREASES TENSION LOADING OF THE BRACHIAL PLEXUS

11. Clinical testing Roos/elevated arm stress
Supraclavicular pressure test
Adson’s test
Costoclavicular maneuver/ Military Brace
Wright’s test/ hyperabduction test
Cyriax release test
Upper limb neural tension test**
Roos: arms above 90 degrees in ABD and full ER; patient opens and closes fists for 3 minutes. Positive is pain/ paresthesias and relief of symptoms with discontinuation
Supraclavicular pressure test: thumb over anterior scalene, fingers over upper trap then squeeze for 30 seconds – positive is reproduction of paresthesias
Adson’s test: Palpate the radial pulse with the elbow fully extended. Patient rotates towards side being tested and extends the neck. Next, abduct, extend, and laterally rotate the shoulder. From this position, have the patient take a deep breath and hold. Assess the pulse response. A positive test is a decrease in pulse vigor from the starting position to the final position. 
Costoclavicular maneuver: palpate radial pulse with elbow extended. Ask the patient patient to perform an exaggerated military position (have them pull their shoulder blades down and back). A positive test is a decrease in pulse vigor. 
Wright’s test: Palpate the patient's radial pulse. Have them abduct their shoulder to >90 degrees with extension. Ask the patient to take a deep breath and hold. A positive test is a decrease in radial pulse vigor.
Cyriax Release test: Patient is seated or standing. Examiner stands behind patient and grasps under the forearms, holding the elbows at 80 degrees of flexion with the forearms and wrists in neutral. Examiner leans the patient’s trunk posteriorly and passively elevates the shoulder girdle. This position is held for up to 3 minutes. Positive test: Paresthesia and/or numbness (release phenomenon) or symptom reproduction.
Upper limb neural tension test: sensitive for irritation of neural tissue; high sensitivity for TOS; not specific but can guide treatment to address neural mobilization.  Can also perform in sitting with patient reproducing this position
Most tests are looking for a change in pulse vigor and can yield a fairly high percentage of false positives. We should use these positions of the tests for symptom provocation rather than radial pulse change.
These tests combined with history and other clinical findings are more important than the clinical tests alone.

12. Diagnostic testing Venous TOS Arterial TOS True NTOS Venous US
Venous scintillation scans
Venography
Plethysmography
Arterial TOS
Doppler US
Angiography
True NTOS
Nerve conduction velocities
Electromyography
Diagnostic tests are negative for disputed NTOS so we must rely on a thorough history and cluster of clinical findings

13. management
surgical

14. Arterial tos
Goal: decompression of structures compression subclavian artery, repair artery, and restore distal blood flow
Thrombolytic therapy or thrombolectomy for acute ischemia
Distal bypass grafting or formal arterial reconstruction for chronic symptoms

15. Venous tos
Thrombolytic therapy is 1st line to dissolve acute thrombosis
Angioplasty to decompress venous stenosis
If unsuccessful
Vein patch angioplasty or venous bypass in order to restore normal circulation

16. Ntos: Surgical decompression
Goal: relieve mechanical load on neurovascular structures
Resection of 1st rib, cervical ribs
Anterior and middle scalenectomies
Performed for those with true neurological symptoms
Weakness
Wasting of hand intrinsic muscles
NCV less than 60m/sec (norm: 85m/sec)
Fail conservative therapy

17. management
Nonsurgical/conservative

18. DISCLAIMER: we can make these patients worse if not managed correctly!!!!!!

19. conservative
Poor outcomes associated with obesity, worker’s compensation, and double crush pathology (cubital or carpal tunnel)
Focus of treatment: SYMPTOM REDUCTION
NSAIDs – reduce pain and inflammation
Botox injection – anterior and middle scalenes

20. Pt management Restore normal arthrokinematics of surrounding joints
1st rib mobility
SC and AC joints
Correcting related muscle weaknesses and imbalances
Diaphragmatic breathing
Scalene muscles
Pectoralis major and minor
Posture
All therapeutic exercises should focus on muscle endurance rather than strength
Diaphragmatic breathing to reduce activity of scalenes and accessory respiratory muscles to increase costoclavicular space

21. Pt management
Improve nerve mobility to decrease tension on brachial plexus
Neural mobilizations
Emphasize proximally with 1st rib inferior mobilizations
All mobilizations should be pain free
Start at 20 repetitions and increase up to 100 repetitions as tolerated for 1-2x/day
Unloading tape
Sleep adjustments

22. Rehab exercises Multi angle isometrics Prone row Prone extension
Rhythmic stabilization
Weight bearing
Elevation in scapular plane
Thoracic extension and rotation
Neural flossing/mobilizations
Deep cervical flexion
Core activation
Cautious with rhythmic stabilizations in OKC due to neural tension positions

23. Application to overhead athlete

24. “one of the most difficult upper limb conditions to manage”
watson3

25. considerations
TOS: pain, paresthesia, weakness, & discomfort in UE aggravated by elevation of the arms or movement of head/neck
Repeated overuse in the overhead position
GH instability
“Double crush” – proximal compression could cause compression at distal sites along the nerve

26. ROM Progression Scapular position in lower ranges (<30 deg ABD)
Flexion control – use of serratus anterior without pec minor recruitment concentrically and eccentrically
>90 deg ABD

27. Special precautions
Do not OVER retract – may create a relative entrapment of retro pectoralis minor space
Careful with ER since may provoke neurological symptoms
Add once patients have sufficient scapular control
May be too aggressive for some patients

28. Return to sport5 High physical performance demands
Pressure to return to previous level of performance
Timeframes NTOS
11 months out of sport prior to surgery
4.4 months full return following surgery
Successful conservative approach
shorter duration of symptoms prior to beginning PT (3 months vs. 15 months)
Lower quick DASH baseline score
81.5% successfully return to full activity

29. Swimming6
Different complaints from classic swimmer's shoulder (MDI/impingment)
No GH instability
Pain both anterior and posterior to clavicle
Radicular symptoms
Inability to keep fingers together to control hand movement during the pull- through phase

30. Throwing7
Trouble with grabbing, holding, and throwing ball due to loss of intrinsic muscle strength of hand
Career-threatening 
Study showed postop pitching performance largely equivalent to before tx
Gradual recovery is crucial (~1 year postop for MLB pitchers)
Gradual recovery  crucial- neural healing is an extremely slow process and may only begin after decompression
- must also think of compensatory posture and mechanics that need to be corrected to minimize brachial plexus irritation

31. references
Hooper TL, et al. Thoracic outlet syndrome: a controversial clinical condition. Part 1: anatomy, and clinical examination/diagnosis. J Man Manip Ther. 2010; 18(2):
Hooper TL, et al. Thoracic outlet syndrome: a controversial clinical condition. Part 2: non-surgical and surgical management. J Man Manip Ther. 2010; 18(3):132-8. 
Watson LA, et al. Thoracic outlet part 1: clinical manifestations, differentiation and treatment pathways. Man Ther. 2009; 14:  
Watson LA, et al. Thoracic outlet part 2: conservative management of thoracic outlet. Man Ther. 2010; 15(4):  
Chandra V, Little C, Lee JT. Thoracic outlet syndrome in high-performance athletes. J Vasc Surg. 2014; 60(4):
Richardson AB. Thoracic outlet syndrome in aquatic athletes. Clin Sports Med. 1999; 18(2):
Thompson RW, et al. Performance metrics in professional baseball pitchers before and after surgical treatement for neurogenic thoracic outlet syndrome. Ann Vasc Surg