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

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

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

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

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

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

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

Clinical examination Neurogenic tos

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

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

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.

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

management surgical

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

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

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

management Nonsurgical/conservative

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

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

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

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

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

Application to overhead athlete

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

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

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

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

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

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

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

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): 74-83. 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: 586-595.  Watson LA, et al. Thoracic outlet part 2: conservative management of thoracic outlet. Man Ther. 2010; 15(4): 305-14.  Chandra V, Little C, Lee JT. Thoracic outlet syndrome in high-performance athletes. J Vasc Surg. 2014; 60(4): 1012-7. Richardson AB. Thoracic outlet syndrome in aquatic athletes. Clin Sports Med. 1999; 18(2):361-78. Thompson RW, et al. Performance metrics in professional baseball pitchers before and after surgical treatement for neurogenic thoracic outlet syndrome. Ann Vasc Surg. 2016.