ADVANCED CERVICAL SPINE II
Copyright The Manual Therapy Institute PLLC 1998-2016
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CONTENT
Thoracic outlet syndrome 3
Muscle energy techniques 6
Cervicothoracic 10
First rib 14
Headaches 16
Soft tissue mobilizations, ANTT, FMP 20
Exercises 25
Gait 28
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Thoracic outlet syndrome
Thoracic outlet syndrome (TOS) is a collection of signs and symptoms caused by compression and/or irritation of the brachial plexus and subclavian vessels.
Functional anatomy
Although patients with TOS present with a variety of signs and symptoms caused by compression/irritation of neurovascular structures, less than 5% of the cases are reported with true ischemia or atrophy. Knowledge of the functional anatomy of these neurovascular structures is an important factor in understanding this syndrome.
The upper and middle trunks of the brachial plexus slant downward from the neck. The lower trunk follows a different direction. The C8 nerve root, after it exits from the intervertebral foramen, runs almost horizontally before it is joined by the T1 nerve root to form the lower trunk of the plexus. The T1 nerve root runs cranial and somewhat anterior upon exiting the intervertebral foramen. The brachial plexus and the subclavian artery pass posterior to the anterior scalenus and anterior to the medial scalenus. The lower trunk of the plexus then crosses the first rib to enter the supraclavicular fossa, in close contact with the subclavian artery and vein, which pass under the subclavius muscle. The subclavian artery runs anterior/inferior to the lower trunk of the plexus. Cadaver dissections demonstrate that this lower trunk, while crossing the first rib, is frequently under considerable tension. The neurovascular bundle then passes below the pectoralis minor, near the insertion on the coracoid process. The C8-T1 nerve roots are most often involved in TOS.
TOS often occurs together with other nerve root compression syndromes. When single axons are compressed in one region (resulting in impaired neural function), they become especially susceptible to damage at another site. It is suggested that proximal compression of a nerve lessens its ability to withstand distal compression. This is also described as “double crush phenomenon”. Compression of a peripheral nerve decreases its intra neural circulation.The internal fluid of the nerve is called axoplasm. The axoplasm is rather viscous, five times more viscid than water. The axoplasmic flow is the transport system that maintains a chemical connection between cell body, axon, nerve terminals and target cells. Axoplasm is thixotropic. This means that movement is necessary to keep viscosity low and prevent gelling. Axoplasmic flow varies. At times it can be up to 400 mm per day. At times it is slow, no more than 30 mm per day and is easily altered by compression or blood depletion. Flow alteration is dependent on duration and magnitude of compression. Once the flow is diminished for 8 hours or so, the nerve becomes “sick” and a chain response of problems begins to occur rather like a domino effect. Decrease of axoplasmic flow at one site predisposes the nerve at the other sites to injury; hence the phenomenon of double and multiple crush syndromes.
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Patient profile Female, late teens to 4th decade Sedentary job with static use of UE’s, repetitive use of the hands Deconditioned
Cause of TOS Trauma fracture of first rib, clavicle Congenital cervical rib
abnormal first rib large C7 transverse process
Posture problems forward headdepressed/downwardly rotated scapulaeprotracted shoulders
Structures that can cause thoracic outlet syndrome Scalenus anterior and medius Cervical rib Elevated first rib Costoclavicular space Pectoralis minor Anterior capsule laxity of the glenohumeral joint
SymptomsUsually vague, ill defined and defy categorization. Documentation in the literature of objective signs is rare. Symptoms may include upper quadrant pain, paresthesiae, numbness, weakness, coldness, swelling, discoloration, migraines, memory loss and ear pain. Most complaints of paresthesiae occur in the ulnar nerve distribution.
Vascular symptoms: whole arm numbness, weakness (heavy), cold, blanching, ischemic pain, and decreased radial pulse.
Neurological symptoms: segmental numbness, myotomal weakness, pins/needles (release phenomena), and pain.
PostureRounded shoulders, forward head, accessory breathing
ROMCervical ROM can be mildly limited, most problems occur with rotation/sidebending away. There will be upper thoracic and cervicothoracic restrictions.
Tension signs
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Positive adverse neural tissue tension in UE.
NeurologicalMotor and sensation C4-T2 intact. Symmetrical UE DTR’sMuscle lengthShort pectoralis minor
Special testingAdson’s testPatient rotates head to side of symptoms, tuck chin and extend head slightly, externally rotate and extend arm. Take radial pulse. Patient inhales and holds breath for 10 seconds. Positive test: reproduction of symptoms and radial pulse disappears. Implicates scalenes.
Costoclavicular assessmentExternally rotate and extend the arm, draw the patient’s arm down and back. Palpate radial pulse. Patient inhales and holds breath for 10 seconds. Positive test: reproduction of symptoms and radial pulse disappears. This test is particularly effective in patients who complain of symptoms while wearing a backpack or a heavy coat.
Pectoralis minorRetract patient’s shoulder. Take radial pulse. Have patient exhale and hold for 10 seconds. Positive test: reproduction of symptoms and radial pulse disappears.
Anterior capsuleFlex arm to 90 degrees, then horizontally abduct the arm so that the glenohumeral head glides anterior. Take radial pulse, hold 15 seconds.
Roos testPatient put arms in “stick up” position and slowly flex/extend the fingers for 3 minutes. Positive test: arm feels “heavy”, patient complains of ischemic pain, paresthesiae or reproduction of other symptoms. Minor fatigue and distress are considered to be a negative response.
Evaluation of every structure from which symptoms arise is important. Often there are multiple sites of entrapment. The diagnosis is really a garbage can term. Treat what you find.
Treatment First rib mobilization Address cervical and thoracic joint dysfunctions STM, stretching to scalenes, pectoralis minor Treat ANTT Address postural dysfunction
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Muscle Energy Techniques
O-A side gliding techniqueTo correct ESR lesion.Patient supine. Sideglide patient’s head to the right, up to barrier. Use indirect action, so resist left sidegliding. Hold 6 seconds, 2-3 times. Retest.
Combined movement technique O-ATo correct ESR lesion.Patient supine. Therapist at head of table. Hold occiput with left hand. Right hand controls the chin. Forearm against right side of the head. Flex head at O-A, sidebend left. If chin remains in midline, right rotation is automatic and can be neglected. Resist extension. Hold 6 seconds, then relocalize by flexing, sidebending left. Repeat 2-3 times. Retest.
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C1-2For right rotation restriction.Patient supine. Sidebend head to the left, rotate right into restriction. Resist left rotation of the head (indirect action). Hold 6 seconds, and then pick up slack in right rotation. Repeat 2-3 times. Do not lose left sidebending. Retest.
C1-2-3For left rotation restriction.Patient supine. Fully flex the head and rotate left into restriction. Resist right rotation (indirect action). Hold 6 seconds, then pick up slack in left rotation. Repeat 2-3 times. Retest.
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Mid cervical sidegliding techniqueFor restriction in right side gliding.Side glide segment up to barrier. Have patient push head to the right, hold 6 seconds. Upon relaxation, pick up slack to reach barrier in right sidegliding. Repeat 2-3 times. Retest.
Combined movement techniqueFor restriction of flexion, left rotation and left sidebending (ERSR)Patient sitting. Flex, sidebend left, rotate left up to barrier. Resist right sidebending or extension, hold 6 seconds. Upon relaxation, pick up slack to new barrier in flexion, sidebending and rotation. Repeat 2-3 times. Retest.
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Cervicothoracic (C7-T3)For restriction in extension, left sidebend, left rotation (FRSR).In this technique the upper and mid cervical segments should not be extended. This can be achieved by having the patient tucking the chin. Another option is to use the therapists forearm to protect the neck. Patient seated. Therapist behind patient. Left hand is placed over upper trap with thumb on the TP of affected segment. Right hand and forearm control the head. Extend to barrier. It helps to add some forward pressure with the thumb. By pushing with the left thumb in the direction of the opposite hip, you introduce sidegliding right to give sidebending left, up to barrier. Rotate left. Resist right sidebend or flexion, hold for 6 seconds. Pick up slack in all 3 directions to new barrier. Repeat 3 times. Retest.
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Cervicothoracic junction
HistoryTypically this is not an area the patient points to for pain and/or dysfunction. However this is a key area for cervical mechanics. Usually the CT junction tends to be hypomobile, which contributes to cervical hypermobility.
InspectionLook for increased CT kyphosis (“dowagers hump”).
ROMLook for quality of motion. Frequently the CT junction gets skipped . With hypomobility of the CT junction, cervical flexion will be limited. In extension there will be a hinge point in the lower cervical spine. Rotation and sidebending of the cervical spine are relatively unaffected.
Diagnostic inspectionExtension C7-T1: Tuck chin to lock out mid/upper C spine, then tilt head back.Extension T1-3; Rotate head fully, then glide head posterior (chin tuck)
PalpationUsual STM assessment. Include superior/inferior, medial/lateral skin rolling and cleaning the gutter. If the CTJ is involved there will be significant soft tissue restrictions. The spinous processes may be exquisitely tender on palpation.
Mobilizations
Distraction - pronePatient prone with arms resting on table. Therapist at head of table. Place pisiforms on the TP’s of lower vertebra of involved segment. Mobilize anterior and somewhat inferior.
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Distraction - supinePatient supine. Therapist hooks index fingers under SP, distract in cranial direction.
Flexion - sittingPatient sitting, straddling training bench (or chair). Pillow between chest and bench. To prevent excessive cervical flexion, patient makes cervical collar. Therapist places hand on SP of lower vertebra of involved segment. Can also use cross hand technique. Mobilize CT in flexion. Do not flex patient’s head.
Flexion - pronePatient prone on elbows. Therapist uses pincher grip, contact inferior border of SP of involved segment. Mobilize in anterior/ cranial direction.
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Extension bilateral - sittingPatient sitting. Makes cervical collar. Therapist stands on patient’s side, thigh behind patient’s back. Use pincher grip (or heel of hand) on SP of lower vertebra of involved segment. Other hand under patient’s elbows, lift up to mobilize CTJ in extension.
Extension bilateral - sitting, alternate techniquePatient sitting with arms clasped behind neck. Patient’s elbows on therapist’s thigh. Pincher grip on SP of segment involved. Mobilize in extension.
Rotation - sittingPatient sitting in chair, lean to opposite side of restriction, with arm over therapists knee. Therapist’s thumb stabilizes SP of inferior vertebra of involved segment on side of restriction. Other arm makes a ”turban” around the neck, pinky wraps around superior vertebra of involved segment. Side bend towards restriction, rotate away. Add compression and distraction. Mobilize with thumb in direction of opposite hip, with hand on superior vertebra in rotation.
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Rotation - supinePatient supine, stabilize shoulder, other hand pronates and wraps around SP. Mobilize.
Unilateral down/backPatient sitting. Therapist stands behind patient. Sidebend to restricted side, rotate opposite. Place thumb on side of SP of involved segment. Heel of other hand under occiput of opposite side. Mobilize down and back (towards the opposite hip).
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First rib
Clinical presentationFirst rib problems are unrecognized and under diagnosed. They occur more frequently in young adults. Complaints of pain are located over the upper trapezius. Shoulder movement on the involved side may be painful at endrange. Objective neurological signs are negative. Active or passive depression of the scapula may reproduce some of the symptoms. Unilateral P-A pressure or caudal pressure on the first rib may reproduce some or all of the symptoms. The head may be slightly sidebend to the involved side. The lesion is usually unilateral. Soft tissue restrictions of the upper trapezius and scalenes are common. Paresthesia in C8-T1 nerve root distribution may be present. RSD signs and symptoms (hand-/forearm discoloration, sweating, swelling, weakness, clumsiness) have been reported.
AnatomyThe first rib is acutely curved, short, broad and flat. It slopes obliquely down and forwards. The head is small and round and has an almost circular facet, articulating with the first thoracic vertebral body. The tubercle is wide and prominent; medially an oval facet articulates with T1 transverse process.
The first rib is considered a-typical: It only attaches to the vertebral body of T1, not to the disc and lower vertebral body,
like ribs 2-10 It articulates with T1 via a small round head, whereas typical ribs articulate via 2
demi facets. There is lack of ligamentous support at the CT joint.The first rib functions as the insertion for the scalenus anterior and medius.
BiomechanicsUncertainty exists about the exact movements taking place at the first rib during inhalation/exhalation.
DysfunctionPrimary first rib dysfunction: caused by a sudden powerful contraction of the scalenes, or extrinsic trauma
Secondary first rib dysfunction: following cervical dysfunction, thoracic dysfunction, or dysfunctional UE movement pattern
Evaluation Positional fault: 4-6mm higher on involved side. If difference is more than ¾ inch,
suspect a cervical rib. The superior/posterior surface is palpated through upper trapezius. The anterior/superior surface is palpated in the supraclavicular fossa. Use caution when palpating the anterior/superior surface, as the long thoracic nerve can be injured. Palpate the sternal articulation just below the clavicle.
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Movement assessment: check first rib during inhalation/exhalation (exhalation restriction most common). Place index finger in first intercostal space, contacting the inferior portion of the first rib next to the manubrium. Ask patient to inhale/exhale deeply.
Spring testing: stiffness noted on involved side. Palpation: displacement of the head of the first rib, at the anterior/superior
surface or at it’s sternal end. There may be swelling, hyperesthesia or tenderness at the head, at the costosternal joint or in the supraclavicular fossa.
Differential diagnosis Cervical rib. This is the costal element of C7. It may be a mere epiphysis on its
transverse process but more often has a head, neck and tubercle, with or without a shaft which, varying in length, extends anterolaterally into the posterior triangle of the neck. There it may end freely or join the first rib or costal cartilage, or even the sternum. The lower trunk of the brachial plexus and subclavian vessels are superior and apt to suffer compression in a narrow angle between the first rib and scalenus anterior.
Cervical disc Pancoast tumor Osteophytes
TreatmentMET
Joint mobilization
Therapeutic exercises
Manipulation
Self mobilization
Often the scalenes, subclavius, upper trapezius and SCM are short and hypertone. Stretching of these muscles is indicated to prevent recurrence. Correction of forward head posture is essential because of its effect on the dimensions of the thoracic outlet.
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Headaches
A headache is experienced in some form by 80% of the population at some stage in their lives. No age group is immune. The most common types of frequent intermittent headaches are:
Tension type headaches (37%) Migraine (27%) Cervicogenic (18%) Indefinable (18%)
Symptomatic overlap can confound the diagnosis. Neck pain is associated with 70% of all headaches. 10-20% of chronic recurrent headache are related to cervical musculoskeletal disorders. Evidence shows that manual therapy is beneficial for cervicogenic headaches, but there is no substantial benefit of manual therapy for migraine and tension type headaches.
MigrainesHeadache attacks lasting 4-72 hoursUnilateral (can change sides within or between attacks)Pulsating qualityModerate to severe intensity (limits daily activity)Aggravated by physical activityNausea or vomitingPhotophobia, phonophobiaOther causes of headache ruled outMigraine with aura: aura precedes headache and lasts approximately 60 minutes
Tension headachesHeadache lasting 30 minutes to 7 daysPressing, tightening, non pulsating qualityBilateral, band like headacheMild to moderate intensity (may inhibit, not prohibit activity)Not aggravated by physical activityNo nausea, vomitingPhotophobia,phonophobia is presentOther headache forms ruled out
Cervicogenic headachesSigns and symptoms of neck involvement:
Precipitation of comparable head pain by neck movement/postures and/or by pressure over upper cervical/occipital region
Decreased cervical ROM Decreased upper cervical segmental mobility
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Shoulder-, neck-, or arm painUnilateral cervical pain without shift
Head pain characteristics: Moderate-severe non throbbing and non lancinating pain, usually starting in
the neck Episodes of varying duration Fluctuating continuous pain
Marginal or no effect of NSAIDsFemale to male ratio 4:1Not infrequent history of head or indirect neck trauma, usually of more than medium severity
Do not assume that if neck pain is associated with headaches, that the headache is cervicogenic
There is no evidence that cervical musculoskeletal impairment has a role in migraine and tension type headache:
Despite the presence of any headache Whether as a single headache Whether as one of multiple headache
Tests and Measures Restricted ROM and joint mobility in the cervical spine.
C1-2 is the joint primarily involved. Ogince (2007) checked C1-2 rotation with the cervical flexion-rotation test. He showed a significant difference in C1-2 ROM when comparing the control group with the cervicogenic headache group (39 degrees vs 20 degrees). A positive test is <32 degrees of rotation. Reliability: kappa: 0.81
Poor deep neck flexor enduranceTest: Patient supine, bloodpressure cuff under neck. Have patient flex the C spine by tucking the chin. Avoid retraction or activation of SCM. Normal test: patient should be able to generate 26-28mm Hg pressure for 10 seconds without compensation.
Alternate testPatient supine in hooklying with occiput on table. Ask patient to tuck chin and hold head up. While maintaining flexion, raise the head off the table 2.5 cm. Time stops when pt can no longer hold the head up or cannot maintain chin tuck. Normal: >38 seconds
Soft tissue restrictions
Greater occipital nerve ANT
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A diagnostic cluster for cervicogenic headaches was developed by Jull (2007):Sensitivity: 100%, Specificity: 94%
Decreased AROM in cervical extension Palpably painful OA-C3-4 joint dysfunctions Deep cervical flexor strength impairments
Those conditions are NOT present in migraine or tension type headaches.
ReferenceJull G et al. A randomized controlled trial of exercise and manipulative therapy for cervicogenic headaches. Spine 2002;17
Subjects: 200 patients with cervicogenic headaches. They were randomized to one of four groups: manipulation, exercise, combined, control. They were treated for 6 weeks (8-12 visits). Follow up was done at 7 weeks, 3,6 and 12 months.
TreatmentTherapeutic exercise: deep neck flexor strengthening with cuff, strengthening serratus and lower trap. HEP BIDPostural education: sitting with neutral spine, elongation of cervical spine with longus colli activation, retraction and adduction of scapulae. Throughout day. Manual therapy: joint mobilizations and manipulations to patient specific cervical spine mobility restrictionsManual therapy and therapeutic exercise: 30 minutes of combined treatmentControl: no interventions
Primary outcome: change in headache frequency, duration and intensity. Success was defined apriori as 50% decrease in headache frequency.
At 1-year assessment, both manipulation and exercise groups had significantly reduced headache frequency and intensity, and the effects were maintained.
76% were at least 50% better in headache frequency, 35% had complete relief.
The combined therapy was not significantly superior to either therapy alone, but more patients (10%) gained relief with the combination
Medication use was reduced in all groups compared to the control group. In the combined group, medication use had decreased by 93%
Deep cervical flexor strength had not improved in the manual therapy group at 12 months. Both exercise groups had improved.
A multimodal program of education, manual therapy and specific research based exercises is efficacious in the management of cervicogenic headaches:
Fix the joint dysfunction Tissue specific exercises for impairment in flexor and extensor mm. General
strengthening ex are not all that effective
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References
1. Jull, G. The diagnosis and management of headache. AAOMPT annual conference 2005.
2. Jull, G. Niere, K.R. The cervical spine and headache. In: Boyling, Jull eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Churchill Livingstone 2004
3. Hall T et al. Efficacy of a C1-2 self sustained natural apophyseal glide (SNAG) in the management of cervicogenic headaches. JOSPT 2007;37:100-107
4. Jull G et al. A randomized controlled trial of exercise and manipulaticve therapy for cervicogenic headaches. Spine 2002;17
5. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophysial joint pain syndromes. Med J Aust 1988;148:233-6.
6. Jull G, Stanton W. Predictors of responsiveness to physiotherapy treatment of cervicogenic headache. Cephalalgia 2005;25:101-8.
7. Jull G, Treleaven J, Falla D, Sterling M, O'Leary S. A therapeutic exercise approach for cervical disorders. In: Boyling J, Jull G, editors. Grieves' Modern Manual Therapy of the Vertebral Column. 3rd ed. Edinburgh: Churchill Livingstone, Elsevier, 2004:451-70.
8. Jull G, Trott P, Potter H, Zito G et al. A randomized controlled trial of exercise and manipulative therapy for cervicogenic headaches. Spine. 2002; 17:1835-1843.
9. McDonnell MK, Sahrmann SA, van Dillen L. A specific exercise program and modification of postural alignment for treatment of cervicogenic headache: a case report. J Ortho Sports Phys Ther. 2005: 35:3-15.
10. Nilsson N, Christensen HW, Hartvigsen J. The effect of spinal manipulation in the treatment of cervicogenic headache. J Manip Physiol Ther. 1997; 20:326-330.
11. Nilsson N. The prevalence of cervicogenic headache in a random population sample of 20-59 year olds. Spine 1995;20:1884-8.
12. O’Leary S, Falla D, Jull G, Vicenzino B. Muscle specificity in tests of cervical flexor muscle performance. J Electromyogr Kinesiol 2007;17:35-40.
13. Ogince M, Hall T, Robinson K, Blackmore A. The diagnostic validity of the cervical flexion-rotation test in C1/2-related cervicogenic headache. Man Ther 2007.
14. Petersen S. Articular and muscular impairments in cervicogenic headache: a case report. J Orthop Sports Phys Ther 2003;33:21-30.
15. Sjaastad O, Fredriksen TA, Pfaffenrath V. Cervicogenic headache: diagnostic criteria. The Cervicogenic Headache International Study Group. Headache 1998;38:442-5.
16. Zito G, Jull G, Story I. Clinical tests of musculoskeletal dysfunction in the diagnosis of cervicogenic headache. Man Ther. 2006; 11:118-129.
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Soft tissue mobilizationsFunctional movement patterns
ANTT
STM to scalenes, SCM and sub occipitals in supine; with or without 4-inch ethafoam roll and belt
sidebending rotation
sidebending with roll rotation with roll
FMP to increase cervical rotation. Patient supine. Therapist uses fist to stabilize.
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Suboccipital release. Can use contract relax, using eye movements.
Foraminal opening with UE in tension position
Sidegliding in tension positions
A-P mobilizations (oscillations and sustained) Use head and neck flexion FMP during sustained A-P cervical mobilization.
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Seated cervical STM with FMP: flexion and diagonal flexion.
FMP to improve thoracic extension. Patient is seated with hands clasped behind head. Elbows on therapists neck.
Anterior cervical spine sidegliding and A-P techniques
Sideglide A-P
STM on ethafoam roll; use belt and ULTT signs
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Circumferential contract-relax upper and lower extremities
STM to upper extremity and various triggerpoints with ULTT
Pump massage on triggerpoints or along nerve tracts coupled with ULTT (i.e. tennis elbow)
First rib depression. Use breathing
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Any component of various ULTT tests into or out of tension
Mobilize peripheral joints in tension position (i.e. radial head)
Stretch pectoral musculature with arm in tension position
Use contract-relax with ULTT
FMP - sustained pressure extensor tendons forearm with weight bearing
Mobilize costovertebral joint- manually or with tennis ball
Mobilize thoracic spine- manually, double tennis ball or roll
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Exercises
Active cervical rotation with resisted chin flexion
Supine lat pull downs with elbow extension
Cervical retraction. Pt prone, head of table, retract C spine. Super impose alternate UE flexion
Self mobilization thoracic spine, supine
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Swimmers
Armcircles. Pt in sidelying, roll under thorax. STM quadrangular space
Scapulohumeral stretch
Unilateral pivot prone. STM to pectoralis minor, mobilize shoulder girdle in retraction
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Latissimus stretch. Sidebend, keep low back against wall.
Selfmobilization CT junction
Mobilization lower border ribcage
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GAIT
Philosophy
Observing someone’s gait is an excellent evaluation tool. Obviously, ambulation is extremely functional. It many times can directly
relate to goal setting. Use your imagination and knowledge of what is normal to help assess what is
abnormal. Look at athletes with fluid, flowing, and well-synchronized movements as a
model of ideal gait. Look at the body as building blocks, one on top of another. Are there hinges
or areas of breakdown? If you could “freeze frame” their movement what would it look like? Does the person spend less time on one limb vs. another? Are there areas that look stiff, glued, and immobile or simply where it looks
like the person is “moving around.” A great place to train your eye is the mall or airport. Study the gait of
different people and try to figure out areas of hypo or hyper mobility. Then do the same with your patients and trust your eyes. Once you think you have something, assess it. This will help you build a database and confidence.
Common faults:
Decreased great toe extension. Decreased dorsiflexion. Early heel off. Decreased push off. Excessive pronation. Rear wheel drive vs. front wheel drive. Hyperextension of knee. Lack of full extension of knee. Valgus of knee; knee over second toe. IR of femur on tibia. Internal or external rotation of hip. Decreased hip extension. Movement about an immobile SI. Excessive rotation at low lumbar. Excessive hyperextension at low lumbar. Excessive flexion at low lumbar. Poor hip disassociation. Decreased trunk rotation. Decreased thoracic extension; lower border of rib cage expansion. Positive Trendelenburg.
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Decreased arm swing. Decreased acceptance of weight over leg.
Confirmation of Possible Fault; Assessment
AROM, PROM, end feel Great toe. Ankle. Knee. Hip flexion, extension, IR, ER. Trunk. Springing.
Muscle length tests, palpation Calf. Hamstring. Quads-Ely ITB-Ober Gluteals, lateral rotators Iliopsoas-Thomas.
Muscle Imbalance tests SLR Prone knee bend Clam Bent knee fall out Pivot prone Stand one leg Seated leg extension
Lumbar stability tests
SI tests, pendulum
Axial compression
Lumbar protective mechanism
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Treatment
FMP great toe FMP talus Posterior tibialis strengthening-toe curl Mobilizations of the knee Stretch knee extension, (extender board) FMP prone TKE Stand one leg Clam progression Bent knee fall out Prone knee bend; with hip extension FMP to increase hip extension in half kneeling Half kneeling hip flexor/ITB Thomas test position to stretch hip flexors Calf stretch STM lower border rib cage Pivot prone Resisted bridge, bridge with stick All fours with stick Resisted walking manual Sports cord, pulley Unloading Resisted crawling Vigor knee over second toe, stand, squat Lumbar stabilization Use of mirror, video Steamboat, standing TKE Walk over cups PNF hip Stretch supine thoracic over roll Contract/relax stretch quadratus lumborum over roll STM, joint mobilization all stiff, immobile areas with stretch then
neuromuscular re-education.
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During gait, the trunk should sidebend to side of supporting leg during stance phase, and should be symmetrical left and right. The trunk should also rotate during gait, check arm swing. If there’s shoulder girdle dysfunction, this can affect gait pattern.
Varus give in knee during stance phaseTight IT band, fibular head in anterior/superior position, decreased internal rotation of the tibia, increased lateral glide of the tibia, distal fibula is positioned posterior, decreased dorsal/plantar mobility of cuboid.
Valgus give in the knee during stance phaseThis looks like squinting patella or an increased Q angle. The femur is abducted on the knee.The fibular head is inferior/posterior, increased medial glide of the tibia; decreased internal rotation of tibia, decreased posterior glide of talus and distal fibula is anterior.
Most restrictions you see here are neurologically influenced (too much/too little tone), adaptive shortening doesn’t happen a whole lot.
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