Physio Charlie - ist

New website!!

noreply@blogspirit.com (PhysioCharlie) — Mon, 09 Mar 2009 19:22:00 +0100

I have a new website!!

http://physiocharlie.vpweb.co.uk

Chronic Non Specific LBP

noreply@blogspirit.com (PhysioCharlie) — Wed, 21 Jan 2009 11:24:00 +0100

I did this IST a while ago:

CNSLBP

Recent systematic reviews = small, short-term benefits when compared to no treatment or sham treatment:
• Acupuncture
• Exercise
• Psychological
• Manual therapy
• Electrical stimulation

No treatment seems to be superior to any other intervention, including usual GP care & none of the cited interventions can be truly said to offer a solution to the problem of CNSLBP. (Wand et al, 2008)

Why Is Current Rx Ineffective in CNSLBP?

Recent evidence suggests changes in the brain:

Brain degeneration.
Cortical reorganisation - maladaptive plasticity
Brain biochemistry change
Wand and O’Connell, 2008

There is growing evidence that the brains of patients with CNSLBP are different to those of normal subjects, Apkarian et al (2004)

Patients with CBP showed 5–11% less neocortical gray matter volume than control subjects

Thalamic atrophy in CBP is important, because it is a major source of nociceptive inputs to the cortex

Brain Function

Flor et al 1997, evoked magnetic fields in the brain in response to electrical stimulation of the back.

NSCLBP subjects showed activity in the primary somatosensory cortex (S1) was shifted more medially and the S1 representation of the back was expanded

Chronic pain = cortical reorganization or “Maladaptive” plasticity ie; Phantom limb pain, tinitus….can be beneficial in the blind or CVA

Brain Biochemistry.

MR spectroscopy to discriminate subjects with persistent low back pain from control subjects with accuracies of 97%–100% based on regional brain biochemistry. (Siddall et al 2006)
Major step toward having an objective diagnostic technique in the assessment of persistent pain.

Mx Plan

Training the brain = Influence cortical function

Sensory discrimination
Visual feedback - Mirrors - Graded motor imagery
Sensory motor feedback
Proprioception
Exercise needs to be challenging

References

See Lx Anatomy IST for refs

Assessment of the Knee Joint

noreply@blogspirit.com (PhysioCharlie) — Wed, 21 Jan 2009 10:46:27 +0100

This is a copy of the juniors IST on 15/1/09:

Assessment of the Knee Joint

Anterior Cruciate Ligament

Anterior Drawer

With the patient in supine, apply a posteroanterior force to the tibia with the knee flexed to 90o.

As well as testing the ACL it also tests the posterior oblique ligament, the arcuate-popliteus complex, posteromedial, posterolateral joint capsules, medial collateral ligament and the iliotibial band.

The normal amount of movement is around 6mm; excessive movement indicates injury to one or more of the structures above.

Anterior Cruciate Ligament

Lachmans Test

This is a modified draw test, carried out with the patient in supine and with the knee flexed (0-30o). This position is close to the functional position of the knee, in which the ACL plays a major role.

Stabilise the femur and apply a posteroanterior force to the tibia.

As well as testing the ACL it also tests the posterior oblique ligament and the arcuate-popliteus complex.

A positive test is indicated by a soft end feel and excessive motion and indicates injury to one or more of the structures above.

Anterior Cruciate Ligament

Lateral Pivot Shift Manoeuvre

This is the primary test used to assess anterolateral rotary instability of the knee and is an excellent test for ruptures (third-degree sprains) of the ACL.

You are looking for abnormal (excessive) anterior rotation of the tibia on the lateral side relative to the femur. During the test, the tibia moves away from the femur on the lateral side (but rotates medially) and moves anterioly in relation to the femur.

The patient lies supine with the hip both flexed and abducted 30o and relaxed in slight medial rotation (20o).

Hold the patient’s foot with one hand while the other hand is placed at the knee, holding the leg in slight medial rotation. This is done by placing the heel of the hand behind the fibula and over the lateral head of the gastrocnemius muscle with the tibia medially rotated, causing the tibia to sublux anteriorly as the knee is taken into extension.

Anterior Cruciate Ligament

Lateral Pivot Shift Manoeuvre continued

Apply a valgus stress to the knee while maintaining a medial rotation torque on the tibia at the ankle

The leg is then flexed, and at approximately 30o to 40o the tibia reduces or ‘jogs’ backward.

A positive test is indicated by the patient saying that is what the giving way feels like.

If the test is positive the following structures have probably been injured to some degree: ACL, posterolateral capsule, arcuate-popliteus complex, lateral collateral ligament, iliotibial band.

A disadvantage of this test is that in the apprehensive patient, because of the forces applied during the test, protective muscle contraction may lead to a false negative test.

Anterior Cruciate Ligament

Active Pivot Shift Test

The patient sits with the foot on the floor in neutral rotation and the knee flexed 80o to 90o.

Ask the patient to isometrically contract the quadriceps while you stabilise the foot.

A positive test is indicated by anterolateral subluxation of the lateral tibial plateau and is indicative of anterolateral instability.

Studies looking at ACL testing

Benjamise et al (2006) 28 studies

Lachman: most valid, sensitivity 85%, specificity 94%

Pivot shift: specific 98% but sensitivity 25%

Anterior draw: sensitivity 92%, specificity 91%

Kostogiannas (2008)

Pivot shift and Lachmans, 25 patients

Positive pivot shift test 3/12 after injury strong predictor of a need for ACL reconstruction

Negative pivot shift 3/12 after injury low risk of surgery

Pins (2006)

Lachmans test is most sensitive

Pivot Shift most specific

Posterior Cruciate Ligament

Posterior Draw

With the patients knee flexed to 90o, apply an anteroposterior force to the tibia.

As well as testing the PCL it also tests the arcuate-popliteus complex, posterior oblique ligament and anterior cruciate ligament.

Excessive movement indicates injury one or more of the structures above.

Posterior Cruciate Ligament

Reverse Lachmans

The patient lies prone with the knee flexed to 30o, grasp the tibia with one hand and fix the femur with the other hand.

Ensure the hamstrings are relaxed and then pull the tibia up (posteriorly), noting the amount of movement and the quality of the end feel.

Be wary of a false-positive test if the ACL has been torn, because gravity may cause an anterior shift.

This test is not as accurate for the PCL as the posterior draw test, because when the PCL is torn, the greatest displacement is at 90o.

Posterior Cruciate Ligament

Godfrey (gravity) Test

The patient lies supine

Hold both legs with the hips and the knees flexed to 90o

If there is posterior instability, a posterior sag of the tibia is seen.

If manual posterior pressure is applied to the tibia, posterior displacement may increase.

Medial Collateral Ligament

Valgus (abduction) Stress Test

Assessment for one-plane (straight) medial instability, which means that the tibia moves away from the femur on the medial side.

Apply a valgus stress (push the knee medially) at the knee while the ankle is stabilised in slight lateral rotation either with the hand or with the leg held between the examiner’s arm and trunk.

The test should be carried out with the knee first in full extension and then slightly flexed (20o to 30o) so that it is unlocked.

It has been advocated that resting the test thigh on the examining table enables the patient to relax more and is easier for the examiner. The knee rests on the edge of the table; the lower leg is controlled by the examiner stabilising the thigh on the table, and the lower leg is is abducted, applying a valgus stress to the knee.

Lateral Collateral Ligament

Varus (adduction) Stress Test

An assessment for one-plane lateral instability (i.e., the tibia moves away from the femur an excessive amount on the lateral aspect of the leg).

Apply a varus stress ( push the knee laterally) at the knee while the ankle is stabilised.

The test is first done with the knee in full extension and then with the knee in 20o to 30o of flexion.

If the tibia is laterally rotated in full extension before the test, the cruciate ligaments will be uncoiled, and maximum stress will be placed on the collateral ligaments.

Meniscal Testing

Loss of extension

Loss of flexion

Locked knee

Joint line tenderness

Persistent joint effusion

McMurrays test

Medial Meniscus

McMurray’s Test

Palpate the medial joint line and passively flex and then laterally rotate the knee so that the posterior part of the medial meniscus is rotated with the tibia

A snap of the joint will occur if the meniscus is torn

The joint is then moved from this fully flexed position to 90o flexion so that the whole of the posterior part of the meniscus is tested.

A positive test occurs if the clinician feels a click, which may be heard, indicating a tear of the medial meniscus.

Lateral Meniscus

McMurray’s Test

Palpate the lateral joint line and passively flex and then medially rotate the knee so that the posterior part of the lateral meniscus is rotated with the tibia, a snap occurs if the meniscus is torn.

The joint is than moved from a fully flexed position to 90o flexion, so that the whole of the posterior part of the meniscus is tested.

A positive test occurs if the clinician feels a click, which may also be heard, indicating a tear of the lateral meniscus.

Study looking at Meniscal Testing

Mohan et al (2007)

150 patients

94 trauma, 53 sports related

Joint line tenderness and McMurray test

Medial meniscus: 88% accurate, 98% sensitive and 65% specific

Lateral meniscus: 92% accurate, 92% sensitive and 93% specific

Posterior Lateral Corner

Dial Test

The test is designed to show loss of the posterolateral support structures of the knee.

The patient may be placed in supine or prone, flex the knee to 30o, extend the foot over the side of the plinth and stabilise the femur on the plinth.

Laterally rotate the tibia on the femur and compare the amount of rotation to the good side.

If the test is done in supine you can observe the amount of tibial tubercle movement and compare.

The test is repeated with the knee flexed to 90o and the thigh still on the plinth.

If the tibia rotates less at 90o than at 30o, in isolated posterior lateral (popliteus corner) injury is more likely. If the knee rotates more at 90o, injury to both the popliteus corner and PCL injury are more likely.

Observation (QUIZ)

Femoral rotation -internal rot is associated with tight ……………band and poor functioning of posterior……………………..

muscle it is commonly found in patient with patella femoral pain. Enlarged tibial tuberosity is associated with o……………- s……………..

Genu valgum is accociated with lateral tibia torsion and genu varum is associated with …………. ……………………..

Valgus knee are more prone to PF problems and ……………………..compartment problems. Excessive foot ………………….is a contributing

factor of knee pain. Enlarged fat pad usually associated with hyper-…………………… knees and poor …………………… control, particularly

eccentric inner range (0-20 degrees of flexion). Hyper-extended knee (can be associated with ……………………… pelvic tilt and can impinge

the suprapatella bursa

Weight bearing Status

Dynamic posture – gait, squatting,

Observation of Muscle form – strength, length, control

Observation of soft tissue-quality & colour of the skin, swelling, joint effusion, scarring.

Observation of balance – standing on one leg with eyes open/closed (unbalance: proprioceptive dysfunction.

Special Questions

Giving way: indicates instability of the knee, meniscus pathology, chonromalacia, patellar subluxation

Locking: loose bodies, meniscus pathology

Clicking – muscle tendon over bone,

Clunking – instability

Grinding – bone on bone/degeneration

Patella increases leverage of the knee joint it improves the efficiency of ext during the last 30deg of ext

Base of the patella normally lie +/-5mm from the medial and lateral femoral epicondyles when the knee is flexed 20 degrees.

Glide of the patella on quadriceps contraction:

Palpate left and right base of patella and

vastus medialis and lateralis. Ask the

patient extend the knee (contract the quads). If there is a Lateral patella

Glide it indicates a dynamic problem (VMO can be felt to contract after vastus lateralis/weakness)

Patella tilt is calculated be measuring the distance of the medial and lateral borders of the patella from the femur.

Lateral tilt: The distance is decreased on the lateral aspect and increased on the medial aspect, such that the patella faces laterally. (associated with a tight lateral retinaculum, (deep and superficial fibres) and iliotibial band).

Patellar loading with activity

Walking:

Climbing stairs:

Descending stairs:

Squatting:

0.3 times the body weight

2.5 times the body weight

3.5 times the body weight

7 times the body weight

Strength

Oxford Scale (revision)

0 - No contraction

1 – Flicker of contraction

2 – Full ROM with gravity counterbalanced

3 – Movement against gravity

4 – Movement against gravity with added resistance

5 – muscle functions normally

Hamstrings

Isolating Bicep Fermoris

leg laterally rotated

(pointing outwards)

resistance applied down and

inwards

Isolating semi-tend and

semi-mem, leg medially

rotated (point toe inwards),

Resistance applied down &

Out.

Length

Pop Angle

Knee extension should be

within 20 degree of full

Extension

If hamstrings are tight, the

end feel will be a muscle

stretch

Quads

Resist knee flexion

through range

Resist knee extension

through range

Thomas test

Patient lies supine, one knee flexed to

the chest to stabilise the pelvis and flatten

the lumbar spine

Leg lifts of the table =

Tight hip flexors

The angle of the knee should remain at 90

degrees if it extends slightly =

Tight rectus femoris

If the leg abducts as the other is flexed to

the chest it is indicative of a tight =

Illiotibial band

Gastro

Length: 0-15 degrees

Normal

Strength: Resist

plantar flexion, calf

raise.

Single leg balance

Timed

- Eyes opened

- eyes closed

Poor Balance = proprioceptive dysfunction.

Single knee bend

Long axis of the femur and the 2nd MT in

neutral lime (+/- 10 degrees)

Reduced control = weak glut med

Knee anatomy

noreply@blogspirit.com (PhysioCharlie) — Mon, 19 Jan 2009 17:44:26 +0100

Anatomy of The Knee, Junior IST

Joints

The knee joint is a synovial bicondylar hinge joint between the condyles of the femur and those of the tibia with the patella sitting anteriorly.

The knee joint satisfies the requirements of a weight-bearing joint by allowing free movement in one plane only combined with considerable stability, particularly in extension

The knee allows flexion and extension in the sagittal plane, it also permits a small amount of rotation of the leg, particularly when the knee is flexed and the foot is off the ground

There are three articulations: two femorotibial and one femoropatellar

The lateral tibial condyle is flatter, shorter from anterior to posterior and more oval than the medial

Proximal Tibiofibular Joint

Plane synovial joint between the circular or oval facet on the head of the fibula and a similar facet on the posterolateral aspect of the undersurface of the lateral tibial condyle

The fibular articular facet faces anteriorly, superiorly and medially, while that on the tibia faces posteriorly, inferiorly and laterally

A fibrous capsule attaches at the margins of the facets on both tibia and fibula, and is strengthened by accessory ligaments anteriorly and posteriorly

The joint surfaces are inclined at an angle greater than 20o, generally the greater the angle, the smaller the surface area of the joint

Rotation at this joint occurs during dorsiflexion of the ankle, especially in horizontal joints

In knee flexion, the fibula moves anteriorly, and in extension, posteriorly

Cruciate Ligaments

Anterior Cruciate Ligament

Attached to the tibia immediately anterolateral to the anterior tibial spine

Passes beneath the transverse ligament, blending somewhat with the anterior horn of the lateral meniscus, and runs posteriorly, laterally and proximally to attach to the posterior part of the medial surface of the lateral femoral condyle

Prevents the femur from sliding posteriorly on the tibia, prevents hyperextension of the knee and limits medial rotation of the femur when the foot is on the ground i.e when the leg is fixed

The posterolateral bulk of the ligament is taut in extension, with the anteromedial band lax (and vice versa in flexion)

Posterior Cruciate Ligament

Attaches to the depression in the posterior intercondylar area of the tibia

Runs anteriorly, medially and proximally, passing on the medial side of the ACL to attach to the anterior part of the lateral surface of the medial femoral condyle

The PCL is shorter and less oblique in its course, as well as being almost twice as strong in tension, than the ACL

Closely aligned to the centre of rotation of the knee joint and therefore may be its principal stabilizer

Prevents the femur from sliding anteriorly on the tibia, particularly when the knee is flexed

Cruciate Ligaments

The ACL provides approx 86% of the restraint to anterior displacement, and the PCL about 94% of the restraint to posterior displacement of the tibia on the femur

Rupture of the ACL results in very little increase in the anterior draw, while rupture of the PCL results in a posterior draw of up to 25mm

The latter is probably due to lack of collateral resistance to posterior displacement and a lax capsule posteriorly

The cruciate ligaments also provide some mediolateral stability

Medial (tibial) collateral ligament

Strong flat band, 8-9cm long

Attaches to the medial epicondyle of the femur, is almost aligned with the tendon of the adductor magnus muscle, bridges superficial to the insertion of the semimembranosus muscle, crosses the medial inferior genicular artery and is crossed by three tendons, sartorius, gracillis and semitendinosus

Passes downwards and slightly forwards to attach to the medial condyle of the tibia and the medial side of the shaft

The most superficial fibres descend below the level of the tibial tuberosity, deeper fibres have a shorter course from femur to tibia, with the deepest fibres spreading triangularly to attach to the medial meniscus

Lateral (fibular) collateral ligament

Rounded cord, 5cm long

Attached to the lateral epicondyle of the femur above and behind the groove for popliteus, and passes down to attach to the lateral surface of the head of the fibula in front of the apex, splitting the tendon of biceps femoris as it does so

Cord-like ligament is separated from the lateral meniscus by the width of the popliteus tendon

Menisci

The menisci are cartilaginous and tough where compressed between the femur and tibia, but ligamentous and pliable at their attachments

The menisci conform to the shapes of the surfaces on which they rest

Medial Meniscus

Firmly attached, larger than the lateral meniscus

Semicircular in shape, with its posterior part broader than then anterior. The anterior horn is attached to the anterior part of the intercondylar area on the tibia immediately in front of the ACL

The posterior horn attaches to the posterior intercondylar area between the PCL posteriorly and the posterior horn of the lateral meniscus anteriorly.

Its entire periphery attaches to the joint capsule

Movements on the concave condyle are restricted as the horns are attached further apart

Attaches with the medial collateral ligament

More easily damaged then the lateral meniscus

Lateral meniscus

Loosely attached

Forms about four-fifths of a circle and is uniform breadth throughout

The anterior horn attaches in front of the intercondylar eminence posterolateral to the ACL with which it partially blends. In this region it is twisted upwards and backwards as it rests on the slopping bone of the tibial condyle

The posterior horn attaches behind the intercondylar eminence anterior to the posterior horn of the medial meniscus. Posterolaterally the lateral meniscus if grooved by the tendon of popliteus, from which it receives a few fibres

Can slide anteriorly and posteriorly on the condyle because the horns are attached close together and the coronary ligament is slack

Not often damaged

More important then the medial meniscus plays an important role in the stability of the knee

Removal Results in early onset of OA

Bursa

There are many bursa around the knee joint (12 or more) because most tendons run parallel to the bones and pull lengthwise across the joint during knee movements

Suprapatellar Bursa

Extends approximately 6cm above the patella between the femoral shaft and quadriceps femoris. Initially it develops as a separate bursa, but soon communicates freely with the joint space

Bundles of muscle fibres, articularis genus, from the deep surface of vastas intermedialus, attach to the upper part of the bursa. They serve to maintain the bursa during knee extension

An infection to this bursa may spread to the knee cavity.

Subcutaneous Prepatellar Bursa

Lies between the skin and the lower part of the patella

Subcutaneous Infrapatellar Bursa

Overlies the patella tendon, lies between the skin and tibial tuberosity

Bursa

Deep Infrapatella Bursa

Lies between patellar ligament and anterior surface of tibia.

Popliteus Bursa

Between tendon of popliteus and lateral condyle of tibia

Anserine Bursa

Separates tendons of sartorius, gracillis, and semitendinosus from tibia and tibial collateral ligament

Gastrocnemius Bursa

Lies deep to proximal attachment of tendon of medial head of gastrocnemius

Semimembranosus Bursa

Located between medial head of gastrocnemius and semimembranosus tendon

Movements of the knee

Flexion 135 degrees

Bicep Femoris, Semi-membranosus, semi

tendinosus, sartorius, popliteus,

Gastrocnemius

Extension 0 degrees, -5 hyperextension

Rectus Femoris, vastus intermedius,

vastus medialis & lateralis

Medial rotators of the Tibia

Semi-membranosus, semi-tendinosus,

sartorius, popliteus

Lateral rotators of the Tibia

Bicep Femoris

Rectus Femoris

Origin

Long Head-AIIS

Short Head – Ilium above acetabulum

Insertion

Quadriceps tendon of the patella

Action

Extends the knee and flexes the hip

Innervation

femoral nerve L2-L4

Arterial Supply

Lateral circumflex femoral artery

Vastus Intermedius

Origin

Anterio-lateral surface of proximal

2/3 femur

Insertion

Quadriceps tendon

Action

Extends the knee

Innervation

Femoral nerve L2-L4

Arterial Supply

Lateral circumflex femoral artery

Vastus Lateralis

Origin

Interochanteric line, inferior greater

trochanter, gluteal tuberosity

lateral lip of linea aspera,

Insertion

Lateral margin of the patella

Action

Extends the knee

Innervation

Femoral nerve L2-L4

Arterial Supply

Lateral circumflex femoral artery

Vastus Medialis

Origin

Intertrochanteric line,

linea aspera, medial

supracondyler line

Insertion

Medial border of Patella

Innervation

Femoral nerve L2-L3

Arterial supply

circumflex femoral artery

Sartorius

Orgin

ASIS

Insertions

Upper medial surface

of the tibia

Action Flexes and laterally rotates

the hip joint.

And flexes the knee

Innervation Femoral nerve (L2,

L3, L4)

Arterial Supply femoral artery

Gracilis

Origin

Inferior ramus of pubis

Insertions

Upper aspect of

medial shaft of tibia

Action

Adducts the hip and flexes

the knee

Innervation

Obtutator nerve L3, L4

Artery Supply Obturator artery, medial

Circumflex femoral artery,& muscular

branches of profunda femoris

artery

Biceps Femoris

Origin

Long head-ischial

Tuberosity

Short head – Linea

aspera & lateral

supracondylar ridge

Insertion

Head of fibular, lateral

tibial condyle

Action

Flexes & laterally rotates the knee,

long head extends the hip

Sciatic nerve L5, S1-S3

Semimembranosus

Origin

Ischial tuberosity

Insertions

Posterior aspect of he

medial tibial condyle

Action

Extends the hip, flexes & medially rotates the knee

Sciatic nerve, L5, S1, S2

Semitendinosus

Origin

Ishial tuberosity

Insertions

Medial surface of the

proximal tibia

Action

Extends hip

Flexes & medial rotates

the knee

Sciatic nerve L5, S1, S2

Popliteus

Origin

Lateral condyle femur

Insertion

Proximal aspect of the medial posterior tibia

Action

Knee flexion. Unlocks the extended

knee by medially rotating the tibia

on the femur

Tibial nerve L4, L5, S1

Gastrocnemius

Origin

Lat head – posterior aspect of lateral

fem condyle

Med head – posterior aspect of

medial femoral condyle

Insertion

Posterior surface of calcaneum

Action

Knee flexion and foot plantar

flexion

Tibial nerve, S1, S2

Plantaris

Origin

Lateral supra condylar line

above lateral head of gastro

Insertion

Medial border of tendo achilles

& posterior surface of the

calcaneum

Action

Plantar flexer of ankle and

flexes knee

Tibial nerve S1,S2

Popliteal Fossa

Borders

Lateral

Biceps femoris

Lateral head of gastro/plantaris

Medial

Semi-mem, Semi-tend, medial head

of gastronemius

Contents

popliteal artery, which is a continuation of the femoral artery

popliteal vein

tibial nerve

common peroneal nerve

Six or seven

popliteal lymph nodes are embedded in the fat

Pes Anserinous (the goose’s foot)

The insertion of the conjoined tendons of 3 muscles

- Sartorius

- Gracilis

- Semi-tendinosus

Underneath lies a bursa,

which is a major cause of

chronic knee pain

Shoulder Anatomy, Ax and Impingement

noreply@blogspirit.com (PhysioCharlie) — Fri, 12 Dec 2008 11:48:00 +0100

I did this IST yesterday:

Shoulder Anatomy, Ax and Impingement, Charlie Cotterill, Senior II Physiotherapist, Dec 2008

Shoulder pain is a common problem with a reported prevalence of 6.9 to 34% in the general population and 21% in those over 70 years of age. It accounts for 1.2% of all general practice encounters, being third only to back and neck complaints as musculoskeletal reasons for primary care consultation

ANATOMY

Jarjavay (1867)

Neer (1972)

Subacromial space 10-15mm (Flatlow 1994)

Force couple to counteract downward pull of deltoid (Thompson et al 1996)

Function = scap: humeral rhythm, varies from 1:2 to 1: 4.5 (McQuade et al 1998)

Subacromial impingement syndrome was first recognised by Jarjavay in 1867.

Neer (1972) described it as the “Encroachment of the coracoacromial arch on the underlying mechanism of the rotator cuff”.

Force couple to counteract downward pull of deltoid Thompson et al (1996).

According to Neer, the entrapment syndrome is the result of anatomical variations in build, strain, and repetitive microtrauma. The terms 'impingement' and 'entrapment' refer to the presumed trapping of anatomical structures between the broad greater tuberosity of the humeral head and the acromion during abduction. This would cause a process of degeneration of the rotator cuff, coupled with oedema, bleeding, fibrosis, and calcification. Ultimately this could cause ruptures, osteophyte formation, and spur formation. The 'typical' clinical picture would be characterized by a painful arc during abduction, while other movements of the upper arm painless.

Differential Diagnosis?

Glenohumeral instability, Labrum tear; Bankart, Kim, SLAP lesion,

Avulsion of glenohumeral ligament (superior, middle, inferior), Posterior glenoid spur (a Bennett lesion), Cervical radiculopathy, Tx hypomobility, #, Humeral subluxation/ dislocation, Glenohumeral arthritis, Long thoracic nerve injury, Tumor/Malignancy, Post CVA, Ganglion cyst, Suprascapular nerve entrapment, Quadrilateral space syndrome, Scapulothoracic dysfunction, Impingement of R/C, R/C tear, glenoid erosion, glenoid retroversion, humeral head defects, capsular insufficiency, voluntary instability, hypermobility, RA, Bursitis, Polymyalgia Rheumatica, Biceps tendon rupture/tendinopathy, Calcific tendinitis, Adhesive capsulitis, AC arthritis, Glenohumeral arthritis, Septic arthritis, Gout, Lyme disease, Lupus erythematosus, AVN, Thoracic outlet syndrome, Brachial plexus neuropathy, Trigger points,

Visceral: PE, pleuritis, pericarditis, angina, MI, cholecystitis, pancreatitis, adnexitis.

Approx 57 differential diagnoses!!

Bankart = labrum avulsion from anterior glenoid rim

KIM = Incomplete and concealed avulsion of the postinferior aspect of capsule

SLAP = superior labral anterior-posterior

Aetiology of SIS

Primary/Secondary/ Primary Inflammation Degeneration

Intrinsic/Extrinsic

(Wilson 1999)

Primary – anatomical narrowing of the subacromial space, ie hooked acromion, tendon thickening

Secondary – functional narrowing of the subacromial space, ie muscle imbalance, posture, instability – physio can change

Primary Inflammation Degeneration – Tendon compression/tear, ageing, avascularity – Physio cannot change

Bigliani Classification (1991) Type III poor response to rehab, for surgery

Many causes have been proposed for subacromial impingement syndrome (Aoki M et al. 1986, Bigliani et al. 1986, Codman 1990, Bigliani et al. 1991, Edelson & Taitz 1992, Burns & Whipple 1993, Hutchinson & Veenstra 1993, Davidson et al. 1995). These factors can be broadly classified as intrinsic or intratendinous factors, which are related to the intrinsic theory on the origin of impingement, and extrinsic or extratendinous factors, which are related to the mechanical theory. They can be further characterised as primary or secondary. A primary aetiology — either intrinsic or extrinsic — causes the impingement process by decreasing the subacromial space or by causing a degenerative process of the rotator cuff tendons (Duke & Wallace 1997). A secondary aetiology is the result of another process, such as instability, neurological injury, tight posterior capsule of the glenohumeral joint and muscle dysfunction (Bigliani & Levine 1997, Duke & Wallace 1997). The net effect of secondary causes is usually an anterosuperior translation of the humeral head, which causes impingement of the cuff against the coracoacromial arch (Duke & Wallace 1997).

Aetiology

Aetiology of SIS is multifactoral (Lewis et al 2001).

Mechanical/Anatomical

Primary mechanical impingement (Neer 1972, 1983)

Acromial bone spurs (Neer 1972)

Os acromiale (Neer 1972, 1983)

Corocoacromial ligament (soslosky et al 1994)

Postereosuperior glenoid impingement (Jobe 1997, Riand et al 1998)

Rotator cuff

Overuse (Wickiewicz 1994) proximal migration of HH with fatigue

Weakness (Thompson 1996) loss of infra or subscap = > 400% increase in deltoid power. 1 in 10 cuff tear by 40

Instability/hypermobility

Secondary tensile disease (Meister and Andrews 1993)

Secondary compressive impingement (Warner et al 1990)

Aetiology of SIS is multifactoral, challenges Neer, Lewis et al (2001).

It has been suggested that an intrinsic contractile tension overload on the muscle rather than primary impingement is the major factor in the aetiology of rotator cuff tendinitis (Nirschl 1989). When the arm is in the overhead position, eccentric contraction of the supraspinatus decelerates internal rotation and adduction of the arm, causing an overload (Bigliani & Levine 1997). This phenomenon is most dramatic in persons who go in for overhead sports, and it may also occur in manual labourers who use overhead motions in their work (Bigliani & Levine 1997). The proximal migration of the humeral head has also been associated with muscle fatigue, injury and degenerative changes in the rotator cuff tendons (Jerosch et al. 1989, Leroux et al. 1994).

Decrease in proprioceptive sense with muscle fatigue may play a role in decreasing athletic performance and in fatigue-related shoulder dysfunction (Carpenter et al. 1998). Some functional analysis of rotator cuff muscles has shown disturbances in strength in different pathological conditions, including impingement syndrome (Nirschl 1989, Warner et al. 1990, Leroux et al. 1994). Imbalance of the rotator cuff muscles in athletes, who have developed it as a result of training or sport activities, has generally been found to be a predisposing factor or a consequence of impingement syndrome (McMaster et al. 1991, Burnham et al. 1993, Ticker et al. 1995).

The diagnosis of overuse syndrome can be made after possible extrinsic factors related to the coracoacromial arch that may contribute to the process has been ruled out (Bigliani & Levine 1997). This syndrome also occurs commonly in young competitive athletes and manual labourers who use overhead motions in their work (Bigliani & Levine 1997). Inflammation resulting from repetitive microtrauma increases the area occupied by soft tissues in the subacromial space and leads to friction and wear against the coracoacromial arch (Uhthoff et al. 1988, Jobe et al. 1989, Ark et al. 1992, McCann & Bigliani 1994). However, inflammation of the subacromial bursa may also result from a systemic disease, such as rheumatoid arthritis (Steinfeld et al. 1994, Reveille 1997). The findings of Soslowsky et al (Soslowsky et al. 2000) described in animal tendons changes that result from overuse activity, and they are believed to occur in rotator cuff tendons, too.

Aetiology

Restrictive processes

Restricted glenohumeral capsule (Harryman et al 1990, Matsen and Arntz 1990), restriction of post capsule = increased ant HH translation

Posture

Ayub 1991, Bowling et al 1986, Calliet 1991, Solem-Bertoft et al 1993, Greenfield 1995, Kibler 1998.

Functional scapular instability

Kibler 1991, 1998, 2002, 2003, Warner et al 1992, Lukasiewicz 1999, Ludewig and Cook 2000, Wandsworth, Bullock Saxton 1997)

Lateral Kibler slide test

Posture – Greenfield (1995) impingement had fwd head posture but no difference in Tx Kyphosis. Kibler found increased Tx kyphosis gave protraction and reduced subacromial space.

Kibler 1998 has described that a scapula positioned in excessive downward rotation due to poor muscular control would reduce acromial elevation which may lead to impingement. Weak lower traps or pec minor or levator scapula short.

Ludewig and Cook 2000 carried out an EMG study and found that the impingement group had more anterior tipping, less upward rotation and greater upper and lower traps activity than non impingement group. 9% reduction in serratus function.

Wandsworth, Bullock Saxton 1997 studied impingement in swimmers and found delayed serratus activity in impingement group. Upper traps and serratus activated prior to movement (similar to TA)

Lukasiewicz 1999, studied 3D movement with impingement and normals. Impingement 8-9% increase in anterior tipping of the scapula.

Lateral Kibler slide test – dist between the inferior point of the scapula and the corresponding spinal vertebrae in 3 different positions; neutral, hands on hips and 90 degrees of GHjt abduction. Hands on hips best reliability (McKenna 2004).

New Theories

Pathology not always = pain

Glutamate

Oxidative stress

Neovascularisation

Calcitonin gene related protein

Matrix substances

Substance P

Nitric Oxide

Bradykinin

1 in 10 cuff tear by 40 and no symptoms

Sher et al – subjects with large tears can have full function as long as rotator cable is intact (band of tissue that fibroses

Glutamate

Oxidative stress = tenocyte death

Neovascularisation = spiders web blood vessels

Calcitonin gene related protein

Matrix substances

Substance P = neurotransmitters increased in tendonopathy tissue

Nitric Oxide = decreased in tendonopathy tissue, vasodilator, found in GTN patches

Bradykinin

Muscle patterning

Inappropriate activation of torque producing muscles

Destabilising shear force across the joint.

Muscle patterning

Inappropriate activation of torque producing muscles ie; lat dorsi, pec major, ant post deltoid. Abnormal muscle patterning creates a destabilising shear force across the joint.

Malone (2004) in patients with anterior instability 58% had a primary problem with Pec major, posterior instability patients showed 74% had inappropriate activation of Lat dorsi or ant deltoid.

Patients can move around the triangle.

What causes muscle patterning? It has been suggested that shoulder dislocation leads to instability, proprioceptive deficits and mechanoreceptor damage Lephart et al (1994). Smith and Brunolli (1989) used a passive mechanical shoulder stimulation device and asked subjects when they detected movement. They found that patients with recurrent traumatic anterior instability demonstrated proprioceptive deficits. Rehab of instability should include re education of the kinaesthetic based neuromuscular control. Has been a specific concept in lower limb rehab but not in upper limb. Kibler (1998) abnormal biomechanics occuring after sports injury are result of alterations in the function of the scapula control muscles. Most efficient way to reorganise normal firing patterns for the scapula is with closed kinetic chain exercises (CKC).

Motor learning is key to establishing or restoring movement patterns.

Kibler (1998) describes the force development of a tennis serve, 54% comes from the legs and trunk. Injury to a distal segment can alter normal motor programmes. Kinetic chain rather than focus on the shoulder girdle.

Kinetic chain; For example sway back posture, increased flexion pattern in activation of GH jt muscles. Ie protraction through pectoralis activation. Links in with the myofascial sling, Myers (2001).

In presence of gluteal inhibition then lat dorsi works hard to compensate. Fixing to the affected side will take place, obs gait and arm swing.

Rx – Evidence - CSP Guidelines

7-21/7 of NSAIDs (A)

St Injections short term benefit (A)

Mobilisation Maitland (A)

HEP; ROM, strength, stability, scap/humeral rhythm (A)

U/S daily for 6/52 for calcification (A)

Isometric strength M & L rotation (B)

Correction of forward head position (B)

Capsular stretching at an early stage (B)

Closed Kinetic chain work (C)

Scapula stability (C)

Cold packs post exercise 10-30 mins(C)

Eccentric loading gives tenocyte repair (Khan & Cook 2004)

U/S daily for 6/52 for calcification (Philadelphia panel 2001)

Education, ?injection

Pain inhibition, rest, sleep, mobs

Scapula stability - serratus

Movement pattern correction

Kinetic chain

Proprioception/neuromuscular control

Humeral head control

Cuff function

Capsular tightness

Posture

Tx, Cx

Change in activity, "live in window"

Workplace modifications

Pain inhibition – selected rest, sleeping position (dressing gown cord and towel under arm) or (supine pillow under elbow), analgesia/NSAIDS, mobilisation, neural mobility, tape, injection (as long as no r/cuff tear), education

Scapula stability – scap setting in prone, weight in hand, elevation control with theraband, then lat rot whilst elevation, use pulleyabove head with theraband whilst work on scap, swiss ball up wall into elev whilst assist scap, elevate using hand first. Use Trp’s in pec minor, lev scap, mobilise, repetition. Kinetic chain, biofeedback, dynamic control of scap. facilitate serratus – press up on wall, forward punch, push up plus, dynamic hug

Humeral head control - Dynamic hug – all r/cuff muscles, subscap setting – slow scapation with med rot, push up plus, middle row, infraspin – T bar eccentric with theraband in supine, press ups, supraspin - T bar

Cuff function

Capsular tightness

Proprioception

Posture

Change in activity and workplace modifications

Scapula Rehab

Kibler2003

Rehabilitation should start at the base of the kinetic chain, which usually means correcting any strength or flexibility deficits in the low back and thoracic levels before starting on the scapular component. This phase includes exercises for flexibility, strengthening the trunk, and correction of postural abnormalities. Intermediate-stage scapular "clock" exercises (arrows indicate direction of scapular motion). A and B, Elevation and depression (12- and 6-o’clock positions, respectively). C and D, Retraction and protraction (9- and 3-o’clock positions).

"Wall washes" for scapular rehabilitation. The hand slides on a smooth-surfaced wall. Trunk extension and rotation and scapular motion are emphasized. Rotator cuff punches with weights. The weight should create a load but allow the arm to be extended. The exercise should start with hip and trunk extension and scapular retraction (B) and then proceed to arm punches at different levels of arm elevation

“Living within a window”

In addition to physical therapy and medications, activity and workplace modifications must be discussed. Patients should attempt to discontinue overhead activities until symptoms diminish. It may be helpful to discuss “living within a window” in which they consciously attempt to keep their hands within an area in front of their body during activity. The “window” should be from chest to waist and 2 to 3 feet wide, allowing the patient to avoid reaching overhead, away from the body, or behind the back, all of which will exacerbate their symptoms

Objective Ax

Posture

Bony Alignment

AROM/ PROM

Muscle Tests

Accessory Mvts

Palpation

Special Tests

Muscle length

Ax of functional movement

Posture – Increased Tx Kyphosis, chin poke posture increased risk of impingement, affected sh will be depressed?

Bony Alignment – no evidence to support ideal scapular position but acromion should be higher than spine of scapular, H of H should be 1/3rd ant 2/3rd posterior, if ant = tight post capsule/ subscapularis or weak infraspinatus

AROM/ PROM – watch Tx in elev. Elev needs 30 lat rot, upper traps is TA of shoulder, needs to fire before mvt in elev and protract. Good inferior translation of HH in abd

Muscle Tests – gerber’s, ext rot, abd

Accessory Mvts; GHjt, Acjt, SCjt

Test Tx and Cx, beighton’s score

Palpation

Special Tests

Muscle length

Ax of functional movement

CONCLUSION

Primary – anatomical narrowing of the subacromial space, ie hooked acromion, tendon thickening

Secondary – functional narrowing of the subacromial space, ie muscle imbalance, posture, instability – physio can change

REFERENCES

Neer CS. Impingement lesions. Clin Orthop Rel Res. 1983;173:70 –77.

Neer, C. S. II. Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J. Bone Joint Surg. 54A:41–50, 1972; 22.

Neer, C. S. II and R. P. Welsh. The shoulder in sports. Orthop. Clin. North Am. 8:583–591, 1977.

Hawkins RJ, Brock RM, Abrams JS, Hobeika P. Acromioplasty for impingement with an intact Rotator cuff. J Bone Joint Surg Br. 1988; 70:795–797.

Michael C. Koester, MD, Michael S. George, MD, John E. Kuhn, MD Shoulder impingement syndromeThe American Journal of Medicine (2005) 118, 452–455

Brox JI et al Arthroscopic surgery compared with supervised exercises in patients with rotator cuff disease (stage II impingement syndrome) BMJ 1993 Oct 9; 307:899-903.

Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD, Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996 Nov;78(11):1685-9.

Downing DS, Weinstein A. Ultrasound therapy of subacromial bursitis. A double blind trial. Phys Ther1986;66:194–9.

Nykanen M. Pulsed ultrasound treatment of the shoulder. A randomised, double blind, placebo controlled trial. Scand J Rehabil Med1995;27:105–8.

Hasson S, Mundorf R, Barnes W, Williams J, Fujii M. Effect of pulsed ultrasound versus placebo on muscle soreness perception and muscular performance. Scand J Rehabil Med1990;22:199–205.

Green S, Buchbinder R, Glazier R, Forbes A. Systematic review of randomised controlled trials of interventions for painful shoulder: selection criteria, outcome assessment and efficacy. Br Med J1998;316:354–60.

Kibler, W. Ben MD a; Uhl, Tim L. PhD, ATC, PT b; Maddux, Jackson W. Q. MD c; Brooks, Paul V. MD a; Zeller, Brian MS, ATC d; McMullen, John MS, ATC 2002. a Qualitative clinical evaluation of scapular dysfunction: A reliability study. Journal of Shoulder & Elbow Surgery. 11(6):550-556,

W. Ben Kibler, MD and John McMullen, ATC , 2003 Scapular Dyskinesis and Its Relation to Shoulder Pain, J Am Acad Orthop Surg, Vol 11, No 2,, 142-151.

Lewis. J, Green. A, Dekel. S, The Aetiology of subacromial impingement syndrome, Physiotherapy Sept 2001, vol 87, No 9, pg 453-468.

McKenna et al (2004) Inter-tester reliability of scapular pposition in junior elite swimmers, Physical therapy in sport 5, 146-155.

Van der Heijden GJMG, van der Windt DAWM, de Winter AF. Physiotherapy for patients with shoulder disorders: a systematic review of randomised controlled clinical trials. Br Med J1997;315:25–30.

C. A. Speed, Rheumatology 2001; 40: 1331-1336, Therapeutic ultrasound in soft tissue lesions

P Frost and JH Andersen, shoulder impingement syndrome in relation to Shoulder intensive workOccup. Environ. Med. 1999;56;494-498

Cools et al (2008) Screening the athlete’s shoulder for impingement symptoms: a clinical reasoning algorithm for early detection of shoulder pathology,BMJ, 2008;42;628-635;

Takwale, Calvert, and Rattue (2000) Involuntary positional instability of the shoulder in adolescents and young adults: IS THERE ANY BENEFIT FROM TREATMENT? J Bone Joint Surg Br, 82-B: 719 - 723.

PA Dowdy and SW O'Driscoll (1993) Shoulder instability. An analysis of family history, J Bone Joint Surg Br, Sep 1993; 75-B: 782 - 784.

Gerber and Ganz (1984) Clinical assessment of instability of the shoulder. With special reference to anterior and posterior drawer tests, J Bone Joint Surg Br, Aug 1984; 66-B: 551 - 556.

Robinson M and Aderinto J (2005) Recurrent Posterior Shoulder Instability, Journal of Bone Joint Surg Am.

87:883-892.

Matsen FA 3rd, Titelman RM, Lippitt SB, Rockwood CA Jr, Wirth MA. (2004) Glenohumeral instability. In: Rockwood CA Jr, Matsen FA 3rd, Wirth MA, Lippitt SB, editors. The shoulder. Volume 2. 3rd ed. Philadelphia: Saunders;. p 655-794.

Falla D, Hess S and Richardson C (2003) Glenohumeral Joint Instability Strength In Baseball Players With Physical Signs Of Evaluation Of Shoulder Internal Rotator Muscle, Br. J. Sports Med.;37;430-432

Malone A, Jaggi A et al (2004) Muscle Patterning Instability – Classification and Prevalence in a Tertiary Referral Shoulder Service. Proceedings of the International Congress of Shoulder Surgery. Washington DC.

Lephart et al (1994) Proprioception of the shoulder joint in healthy, unstable and surgically repaired shoulders. Journal of Shoulder and Elbow Surgery, 3 (6), 371-380

Kibler B, Maddux J, Brooks P, Zeller B, McMullen J (2002). A Qualitative clinical evaluation of scapular dysfunction: A reliability study. Journal of Shoulder & Elbow Surgery. 11(6):550-556,

Kibler B, and McMullen J ( 2003) Scapular Dyskinesis and Its Relation to Shoulder Pain, J Am Acad Orthop Surg, Vol 11, No 2,, 142-151.

Kibler B (1998) The role of the Scapula in Athletic shoulder function. The American Journal of Sports Medicine, 26 (2), 325-337

Emery and Mullji (1991) Glenohumeral joint instability in normal adolescents, Journal of Bone Joint Surg, 73 (3) 406-408

Naughton et al (2005) Upper-body wobbleboard training effects on the post-dislocation shoulder, Physical Therapy in Sport, 6, 31-34

Kinetic Control Course Feedback

noreply@blogspirit.com (PhysioCharlie) — Fri, 28 Nov 2008 14:02:27 +0100

This was the IST by my colleague Ruth:

Kinetic Control Course Feedback

20/11/08

TOPIC: The Integrated Local Cylinder

The muscles constituting the Integrated Local Cylinder are:

1. Respiratory Diaphragm
2. Pelvic Floor
3. Posterior fasciculus of Psoas
4. Segmental Multifidus
5. Transverse Abdominis

The function of the Integrated local Cylinder is to control translation in the lumbar spine – flexion, extension and rotation.

The rationale behind testing the low threshold voluntary recruitment of these muscles is to find the ones that need to be reactivated/ rehabilitated.

When testing these muscles the following principles should be remembered:
1. Test in the neutral training position
2. VAK ( visual, auditory and kinaesthetic feedback is vital)
3. Low load, slow speed, consistent holding time

Finding the Neutral Training Region:

Gandevia et al (1992) state that proprioception relates to 3 key sensations: sensation of position and movement of joints; sensation of force, effort and heaviness of workload; and sensation of the perceived timing of muscle contraction. There are few reliable studies examining proprioceptive deficits associated with low back pain ( more so of shoulder and cervical spine): Gill and Callaghan(1998), Taimela et al (1999) and Brumagne et al (1999) report a significant decrease in repositioning ability in patients with low back pain.

Bear the above in mind when finding the neutral training region. Lots of VAK! The neutral training region is a relative region within the patient’s joint mid – range where there is minimal support or restraint of motion from the passive restraints.

Practical ( make personal notes if need to)

Respiratory Diaphragm:

Ideal recruitment
Fully elevate ribs with inspiration and maintain basal rib elevation and prevent rib depression during1/2 expiration.

Check if able to do in sitting, maintaining neutral, no substitutions. The benchmark is 15 secs x 2, feels easy, no VAK.

Substitutions to watch for – Tx flexion during expiration (using rectus abdominis); spinal extension during expiration (inefficient rib elevation); ribcage depression (external oblique dominance); breath holding (global co contraction rigidity).

Pelvic Floor:

Some prelimary studies indicate that some muscles of the pelvic floor complex may have an anticipatory recruitment pattern suggesting a stability role.

There should be sensory discrimination between high and low threshold pelvic floor recruitment strategies.

Examples of high threshold recruitment is: stopping the flow of urine midstream, the “lift”, maintaining a closed sphincter when bracing or bearing down. These high threshold strategies may be useful to train in conjunction with low threshold strategies and is sometimes the only option.

Low threshold facilitation strategies ( NB for motor control of translation of pelvic joints and continence)

1. Front to back

2. Side to side

3. 4 Points to the middle

4. Pelvic Zipper

5. Perineal lift
Ideal function:
In crook lying the patient should have a definite sensation of low force contraction of the pelvic floor. In patients with no SIjt or pelvic floor dysfunction there is usually a good sensory discrimination between being lower or higher, more anterior or posterior, consistency of the contraction, symmetry.

Posterior Fasciculus of Psoas

The Psoas has segmental attachments posteriorly to all lumbar transverse processes. Anteriorly at all lumbar vertebral bodies and to all lumbar discs except L5/S1. The posterior fasciculii fibres are approx 3 – 5cm in length.

“ It has a primary stability role at the lumbar spine for axial compression and it has minimal movement function on the lumbar spine. (Bogduk 1997)”

“It demonstrates a significant decrease in cross sectional area at a segmental level in patients with sciatica. (Dangaria and Naesh 1998)”

“ Psoas is clinically deficient in that it fails to segmentally resist displacement at the level of pain in patients who have segmental lumbar dysfunction.”

“Specific segmental psoas facilitation improves lumbar segmental control of induced displacement. (Cromerford and Emerson 1998).”

Action to facilitate:
The local stability role of the psoas is to longitudinally pull the head of the femue into the acetabulum with the spine fixed and supported in neutral alignment to produce axial compression along its line of pull.

Asess and rate voluntary low threshold recruitment: (palpation of segmental loss of translation stiffness)
VAK –describe where muscle is and its function, holding stack of books which you compress to turn on its side, sucking into socket …
Correct activation, sustained contraction, control of neutral position, benchmark 15 secs x 2, no added feedback, good symmetry.

Substitutions to watch for: pelvic hitching (QL and iliocostalis); pelvic rotation (internal and external obliques); hip MR (TFL and gracilis); PPT/Lx F (ant part of Psoas); APT/LxE (iliocostalis); knee F (hamstrings); knee hyperE (quads); co contraction rigidity.

Facilitation strategies:

No cluers – use movement and load facilitators
1. Side Lying rotation to neutral (can use “waggling” as well)

2. Hand Knee Diagonal Push (multifidus reactivation as well)

3. Sitting Manual Trunk Distraction

Some Idea – specific unloaded facilitation
1. Side Lying

2. Supine

3. Standing on step

Transversus Abdominis

“Activates prior to movement of limbs or trunk in anticipation of load to increase stiffness and stability of the spine.”

“A motor control deficit is present in all subjects with back pain.”

“The normal anticipatory activation of TA is significantly delayed in low back pain subjects.”

Action to facilitate: - hollowing of lower abdominal wall without excessive overflow to the upper abdominal wall.

Assess and rate voluntary low threshold recruitment efficiency:

Crook lying. Cough, laugh, forced expiration can demonstrate that muscles are under voluntary control, but these are phasic contractions. Describe where muscle is and its function. Corset. Moving ASIS together. Maintain control of neutral. Benchmark 15secs x 2. Good symmetry.

Substitutions to avoid – no palpable contraction (more effort); abdominal wall bulge ( internal obliques or intra abdominal pressure); spinal movement (global substitution); pelvic tilt (global muscles); ribcage depression (external obliques); bracing ( co contraction rigidity, intra abdominal pressure); breath holding (global rigidity); inspiration( passive hollowing)

No Idea at All! – sensory mechanical pre load
1. Lattisimus Dorsi Facilitation

Clues? – movement and load facilitators (these load thoraco lumbar fascia)
1. Four point kneeling
2. Prone on elbows ( not for patients with extension related pain)

Some Idea – specific unloaded facilitation
1. Tactile feedback
2. Low abdominal sling
3. Counting

Multifidus

noreply@blogspirit.com (PhysioCharlie) — Fri, 21 Nov 2008 15:16:47 +0100

This is my colleague Cath's IST this week:

Ms/Mnth:Multifidus

Anatomy:

Multifidus lies deep to semispinalis and erector spinae in the groove between the transverse and spinous processes of the sacrum to C2; it consists of a series of fleshy and tendinous fascicles.

Proximal Attachment

• It arises inferiorly from the dorsal surface of the sacrum as low as the fourth sacral foramen (deep to the tendon of erector spinae), the aponeurosis of erector spinae, the posterior superior iliac spine and posterior sacro-iliac ligament. In the lumbar region it arises from the mamillary processes of L1 to L5, in the thoracic region from the transverse processes of T1 to T12 and in the cervical region from the articular processes of C4 to C7.

Distal Attachment

• The fascicles pass obliquely supero-medially to attach to the whole length of the spinous processes of C2 to L5. The muscle is arranged in three layers: the deepest layer attaches to adjacent vertebrae, the intermediate layer to the second or third vertebra above and the superficial layer to the third or fourth vertebra above.

Actions:

• The precise actions of multifidus as well as those of the other short muscles in the back are not fully understood. It is thought that its main role is as a stabilizer of the vertebral column, which is probably of greater functional significance than its role in producing movement. Bogduk (1997) believes that in the lumbar spine; the obliquely orientated fibres of the deepest portion of multifidus; do not play a role in the production of spinal rotation as the lumbar spine has minimal range of rotation. He states the primary role of these deepest fibres is to resist the rotation generated by the obliques, therefore providing segmental stability. Globally the muscles are thought to play a role in extension, lateral flexion and rotation the vertebral column, acting as a series of extensible ligaments, adjusting their length to stabilize adjacent vertebrae (interactive spine).

Assessment:

Looking at:

Muscle atrophy
Consistency of muscle fibre i.e.: internal structure.
Contraction: whether it is a) symmetrical

b) at adjacent levels

c) Fatigue levels: gold standard to hold contraction for 15sec x 2

Ultrasound Imaging:

Changes in consistency of the multifidus can be easily observed using ultrasound imaging. The ultrasound appearance of muscle is usually dark because of its high fluid content (blood). The presence of fatty infiltration, fibrous changes or scar tissue (non-contractile tissue) leads to a change in the appearance as non contractile tissue is white in appearance. These changes can be seen at specific vertebral levels and are not difficult for the clinician to detect using ultrasound imaging.
In contrast, measurement of the multifidus cross-sectional area requires extensive training and practice to become proficient. Care should be taken as measurement error may be greater than the changes measured with rehabilitation; therefore not reflecting the actual changes (Richardson et al, 2004).

Clinical Assessment:

Palpation of the muscle at each segment with the patient relaxed in prone position.

(Page 195 - 196: Richardson et al, 2004)

The muscle is palpated adjacent to the spinous process.
Side-to-side comparison is made at each level.
Comparison is made of the segments above and below.
Feel for any loss in muscle consistency at each segment (spongy feeling).

For stabilization and joint protection, it is the activation of the deep multifidus fascicles that need to be particularly tested. They contract isometrically and segmentally. Therefore for assessment an isometric and segmental contraction must be used.

Procedure

(Page:196 Richardson et al, 2004)

Encourage the patient to visualise multifidus as deep triangles running down from every spinous process. Demonstrate a contraction of a muscle e.g.: swelling of the forearm with making a fist.

(A: deep and B: Superficial fibres Lumbar multifidus)

A variety of hand positions can be used to perform the test. Thumbs, index or middles fingers or your thumb and index finger either side of the segment.
It is important to sink your fingers in firmly before asking the patient to contract (swell) their muscles. But it is also important for the clinician to release the pressure as the patient contracts the muscle, otherwise, the compressive force could inhibit the contraction.
Prompts to the patient: ‘gently swell your muscles under my fingers without moving anything else, and breathe normally’…..
Ideally the muscle will harden as it generates tension. There should be a similar contraction between adjacent segmental levels and there should be symmetrical contraction between left and right sides at the same segmental level.
As a gold standard this contraction should be able to be held for 15 seconds and consistently repeated 2 times.
The inability to segmentally activate a symmetrical contraction indicates a loss of control of the deep segmental fibres of Lumbar multifidus (Richardson et al, 2004).

Phasic facilitators: if the patient is struggling to elicit any contraction.

These manoeuvres can be used to demonstrate the muscles action:

Cough

Laugh

Forced expiration

Lift, push or pull against resistance.

However, this type of contraction employs predominately phasic recruitment and is not appropriate for motor control stability re-training!

Optimal facilitation and re-training requires achieving control at an appropriate low load facilitation and feedback.

The prone position is not necessarily the best position to teach or facilitate the activation of lumbar multifidus if it is dysfunctional. It is unloaded and there is no weight-bearing facilitation and so could be considered a motor challenge. For the majority of patients, upright postures, such as sitting or standing, are the positions where it is easiest to facilitate and teach the correct activation of lumbar multifidus.

During active re-training of lumbar multifidus it is also essential to identify and eliminate various substitution strategies and faults.

Substitutions to be avoided

OBSERVATION	IMPLICATION
No palpable contraction	More effort required
Spinal movement	Global substitution
Pelvic movement	Global substitution
Bracing	Global co-contraction rigidity & excess IAP
Pushing back from hips and legs	Global substitution

Clinically, it seems acceptable to feel a definite contraction of the oblique abdominals, transverse abdominis and a sensation of bracing during segmental multifidus facilitation.

Re-training of Multifidus

Re-training must be facilitated in a pain-free posture or position.
The neutral spine posture is an ideal position for this.
The simple process of achieving a neutral spine posture may significantly activate transverse abdominis and lumbar multifidus in some subjects with low back pain.

Specific unloaded facilitation

Tactile feedback

Sit with the spine in neutral alignment. Place fingers / thumbs on the muscles just to the side of the vertebrae and let them sink firmly into the muscle.
Lean slightly forward from the hips (keeping the spine neutral) and feel the muscle tension.
Then lean slightly back from the hips until the trunk is directly over the centre of gravity and the muscles relax.
In this position with the muscle initially relaxed, instruct the patient to locally (or swell) the muscles into the finger and thumb.
Ideally the muscle will harden as it generates tension. There should be a similar contraction between adjacent segmental levels and there should be symmetrical contraction between left and right sides at the same segmental level.
The contraction should be able to be maintained for 10seconds 10 times.

Movement and load facilitators

Contra-lateral arm lift

Start in sitting and progress to standing.
Palpate the dysfunctional multifidus with one hand and lift the opposite arm forward and away from the body. Repetitively lift and lower the arm from neutral to 90º flexion and back to the side. Do not allow the spine or pelvis to move.
The contra-lateral multifidus activates automatically to counter-balance the spinal movement of the arm loading during concentric lifting and eccentric lowering of the arm.
There are 2 points during the repetitive flexion when multifidus activity diminishes (i.e.: when no load to counter-balance). 1) When the arm is hanging by the side and 2) When the movement changes from lifting to lowering.
The motor challenge and therefore the re-training exercise is to sustain the contraction during the points when multifidus activity decreases. Maintained for 10 seconds of repetitive movements 10 times.
To progress also you can make the arm movements faster.

Clinically, this is useful for low back pain associated with upper quadrant loading e.g.: throwing, swimming and racquet sports.

Walk Stance: Forward weight transfer

Stand with one foot in front of the other as in normal gait and with full weight on the rear foot. Palpate the dysfunctional multifidus on the rear foot side and move the body weight forward onto the front foot.
The muscle will activate during forward and lateral weight transfer away from the rear foot because it is load facilitated in preparation to support that side of the pelvis and control pelvic rotation during the swing phase of gait.
Multifidus should activate just after heel lift. If it does not activate until the weight is fully on the front foot the timing is late. Timing may be delayed for several reasons:

1) Pelvic sway

Pelvic sway is a powerful inhibitor of lumbar multifidus and if pelvic sway leads the weight shift multifidus activates late, if at all. Correction is achieved by leading weight transfer with the sternum.

2) Over rotation of the pelvis

Bogduk (1997) suggests the role of the segmental or oblique fibres of multifidus are to counter-act the rotation moment of the oblique abdominals. If, during weight transfer, the pelvis over-rotates away from the front foot then the oblique abdominals are not activating efficiently to control pelvic rotation. Consequently, multifidus also is not activated efficiently. Correction is achieved by controlling pelvic rotation and ensuring that the pelvis faces the direction of weight transfer.

3) Rear foot gluteal inefficiency

The front leg pulls the weight forward instead of the gluteal muscles on the rear leg pushing the body forward. Correction is achieved by conscious activation of the rear foot gluteals to push the body forward.

The motor control challenge and therefore the re-training exercise is to try to sustain the contraction during the points when multifidus activity decreases. Try to maintain active muscle tension during slow transferral of weight back from the front foot to the rear, just prior to heel touch. Sustain contraction while repeating forward and backward movement for 10seconds 10 times.

Clinically useful for low back pain associated with gait e.g.: walking, running.

References:

Bogduk: 1997. Clinical anatomy of the lumbar spine and sacrum. Edinburgh. Churchill Livingstone: 1-261

Richardson, Hodges and Hides: 2004. Theraputic exercise for lumbar stabilization: A motor control approach for the treatment and prevention of low back pain. Churchill Livingstone.

Interactive spine: http://www.owlnet.rice.edu/~kine351/spine_biomechanics.pdf

Lx Anatomy IST

noreply@blogspirit.com (PhysioCharlie) — Fri, 21 Nov 2008 09:54:01 +0100

I did this IST last week:

Lx Anatomy

l 1. How much of the general population suffer from back pain during their lifetime?

• A) Up to 78%

• B) Above 90%

• C) Most people

• D) Up to 50%

• E) Up to 84%

l 2. How many people with back pain go on to develop chronic, disabling LBP?

• A) 20%

• B) 1%

• C) 10%

• D) 5%

Name the structures of a typical lumbar vertebrae

l Spinous

l Transverse processes

l Joints

• facet (zygopophyseal)

• interbody

l Pedicles

l Body

l Lamina

l 3. How many degrees of rotation are available at the lumbar segment?

• A)2 B)3 C)4 D)5

l 4. Which movements make the Lx more vulnerable to injury?

• A) Flexion

• B) Flexion and side flexion

• C) Flexion and rotation

• D) Extension and side flexion

l 5. Name the Lx ligaments

l 6. The nerve root occupies how much of the space in the intervertebral foramen?

• A) 1/3

• B) 1/4

• C) 2/3

• D) 1/2

l 7. The spinal cord extends in the vertebral canal to the level of the….?

• A) L1 vertebrae

• B) T12/L1 disc space

• C) L1/2 disc space

• D) L2 vertebrae

l 84% of the general population suffer from back pain during their lifetime

l 10% will go on to develop chronic disabling LBP

l Most cases (90%) are best described as non-specific low back pain (NSLBP)

l The cost of healthcare for Chronic LBP has been estimated at £1623 million

Structure of a typical lumbar vertebrae

l Spinous

l Transverse processes

l Joints

• facet (zygopophyseal)

• interbody

l Pedicles

l Body

l Lamina

Structure lumbar vertebrae

l Large discs for weight bearing and shock absorbing

l Large Joints that limit movement - rotation is about 1 degree per level in each direction

l Small range of overall movement

l Vulnerable in flexion and rotation

Intervertebral foramen

l Foramen

• formed between pedicles above & below

• the vertebral body and discs in front

• the joint behind

l Contains

• nerve root and sinuvertebral nerve

• blood vessels

• lymphatic vessels

• fat

Ligaments

l Anterior Longitudinal

l Posterior Longitudinal

l Ligamentum Flava

l Interspinous Ligts

l Supraspinous Ligts

l Intertransverse Ligts

l Transforaminal Ligts

l Iliolumbar Ligts

Intervertebral foramen

l Nerve root occupies…

l … 1/3 of the space in the intervertebral foramen

l Contains the dorsal root ganglion

l Stenosis of the foramen can occur through…?

Cauda Equina

l The spinal cord extends in the vertebral canal to the level of…

l … L1/2 disc space

l Below this level the cauda eqiuna is formed

Movements

Flexion

l Movement occurs at the upper lx levels, limited by the joint capsules.

l Range = 40°

Extension

l Limited by impact of spinous processes or inferior articular processes on underlying lamina.

l Range = 30°

Rotation

l Very limited in Lumbar spine

l Tx has approximately 4 ´ the range available in the lx

l 1.5° rotation available in each direction from neutral

l Limited by the joint on the side opposite to that of the direction of rotation

Lateral flexion

l Complex movement that involves rotation as in Cx

l 20 - 30° in each direction

QUIZ Answers

l 1. E) Up to 84%

l 2. C) 10%

l 3. B) 3

l 4. C) Flexion and rotation

l 5. Anterior Longitudinal, Posterior Longitudinal, Ligamentum Flava, Interspinous Ligts, Supraspinous Ligts, Intertransverse Ligts, Transforaminal Ligts, Iliolumbar Ligts

l 6. A) 1/3

l 7. C) L1/2 disc space

The Aim Of The Clinical Ax Is:

l Exclude Red Flags

l Identify any neurological deficit requiring urgent specialist management

l Ax functional limitations caused by the pain

l Ax for Yellow flags – barriers to recovery

l Determine clinical management options

RED FLAGS

• Cauda Equina Syndrome

• History of cancer

• Age of onset < 20 or > 50

• New symptom onset

• Violent trauma, Minor in OP

• Fever (TB, infection – epidural abcess, osteomyelitis etc)

• Recent bacterial infection

• Severe, unremitting night pain

• Thoracic pain (Potts disease-TB, HIV) (Tx aortic anuerysm)

• Systemic steroids

• Drug abuse, HIV

• Systemically unwell

• Weight loss

• Severe restrict. of lumbar flx

• Widespread neurology

• Structural deformity

• Pain worse in supine

Yellow Flags

Yellow Flags indicate psychosocial barriers to recovery:

l Belief that pain and activity are harmful

l ‘Sickness behaviours’ (like extended rest)

l Low or negative moods, social withdrawal

l Treatment that does not fit best practice

l Problems with claim and compensation

l History of back pain, time-off, other claims

l Problems at work, poor job satisfaction

l Heavy work, unsociable hours

l Overprotective family or lack of support

New Zealand Acute LBP guidelines

ACUTE LBP

l Pain that has persisted for 5–11 days

l Explanation, assurance, allay fears, avoid passive therapies. (Koes et al 2001)

l Advice to stay active (Van Tulder et al 2000, Hayden et al 2005).

l Over 70% of patients can expect to become pain-free, with a recurrence rate of less than 25%. (Koes et al 2001)

SUB-ACUTE

l Pain that has persisted for up to 12 weeks

l Evidence of effectiveness of a graded activity exercise program in occupational settings. (Hayden et al 2005).

l An exercise programme led by a physiotherapist in the community and based on cognitive behavioural principles helped patients to cope better with their pain and function better even one year later. (Moffett et al. 1999)

CHRONIC Non Specific LBP (CNSLBP).

l Pain that has persisted for longer than 3 months

l Daily multidisciplinary bio psychosocial rehabilitation ( > 100 hours of therapy) with functional restoration. (Guzman et al. 2001) ? Useful in PC

l Exercise is at least as effective as other conservative treatments. (Hayden et al. 2005)

l A general exercise program reduced disability in short term more than a stabilization exercise approach. (Koumantakis et al. 2005)

l Return to Work programmes, single studies show efficacy (Watson et al., 2004).

CNSLBP

l Recent systematic reviews = small, short-term benefits when compared to no treatment or sham treatment:

• Acupuncture

• Exercise

• Psychological

• Manual therapy

• Electrical stimulation

l No treatment seems to be superior to any other intervention, including usual GP care & none of the cited interventions can be truly said to offer a solution to the problem of CNSLBP. (Wand et al, 2008)

Why Is Current Rx Ineffective in CNSLBP?

Recent evidence suggests changes in the brain:

l Brain degeneration.

l Cortical reorganisation - maladaptive plasticity

l Brain biochemistry change

Wand and O’Connell, 2008

l There is growing evidence that the brains of patients with CNSLBP are different to those of normal subjects, Apkarian et al (2004)

l Patients with CBP showed 5–11% less neocortical gray matter volume than control subjects

l Thalamic atrophy in CBP is important, because it is a major source of nociceptive inputs to the cortex

Brain Function

l Flor et al 1997, evoked magnetic fields in the brain in response to electrical stimulation of the back.

l NSCLBP subjects showed activity in the primary somatosensory cortex (S1) was shifted more medially and the S1 representation of the back was expanded

l Chronic pain = cortical reorganization or “Maladaptive” plasticity ie; Phantom limb pain, tinitus….can be beneficial in the blind or CVA

Brain Biochemistry.

l MR spectroscopy to discriminate subjects with persistent low back pain from control subjects with accuracies of 97%–100% based on regional brain biochemistry. (Siddall et al 2006)

l Major step toward having an objective diagnostic technique in the assessment of persistent pain.

Mx Plan

Training the brain = Influence cortical function

l Sensory discrimination

l Visual feedback - Mirrors - Graded motor imagery

l Sensory motor feedback

l Proprioception

l Exercise needs to be challenging

REFERENCES

Moore et al (2000) A randomized trial of a cognitive-behavioral program for enhancing back pain self care in a primary care setting, Pain 88 (2000) 145±153

Boduck N (2004) Management of chronic low back pain MJA 2004; 180: 79–83

Koes BW, can Tulder M, Ostelo R, et al. (2001) Clinical guidelines for the management of low back pain in primary care: an international comparison. Spine; 26: 2504-2513

Guzman J, Esmail R, Karjalainen K, et al. Multidisciplinary rehabilitation for chronic back pain: systematic review. BMJ 2001; 322: 1511-1516.

Van Tulder MW, Koes BW, Bouter LM. (1995) A costofillness study of back pain in the Netherlands. Pain;62:23340.

Van Tulder M, Malmivaara A, Esmail R, Koes B. Exercise therapy for low back pain: a systematic review within the framework of the cochrane collaboration back review group. Spine. 2000;25:2784-96.

Moffett and McLean, (2006) The role of physiotherapy in the management of non-specific back pain and neck pain Rheumatology.; 45: 371-378

Moffett et al. (1999) Randomised controlled trial of exercise for low back pain: clinical outcomes, costs, and preferences BMJ, 319 (7205): 279.

Hayden, J. A., van Tulder, M. W., Malmivaara, A. V., Koes, B. W. (2005). Meta-Analysis: Exercise Therapy for Nonspecific Low Back Pain. ANN INTERN MED 142: 765-775

Koumantakis, G. A, Watson, P. J, Oldham, J. A (2005). Trunk Muscle Stabilization Training Plus General Exercise Versus General Exercise Only: Randomized Controlled Trial of Patients With Recurrent Low Back Pain. ptjournal 85: 209-225

Kekki P. (1990) Teamwork in primary health care. World Health Organisation.

The Secretary of State for Health. (1997) The New NHS – Modern and

Dependable. Cm. 3807. HMSO. December.

Hacett GI, Hudson MF, Wylie JB et al. (1987) Evaluation of the efficacy and acceptability to patients of a physiotherapist working in a health centre. BMJ 294: 24-6.

Salmon P, Peters S, Stanley IM. (1998) Patients perceptions of medical

explanations for somatisation disorders: qualitative analysis. Br Med J,318:

372–376

Clinical Standards Advisory Group (1994). Back Pain: Report of a Clinical Standards Advisory Group on Back Pain, HMSO.

New Zealand Acute Low Back Pain Guide, Incorporating the Guide to Assessing Psychosocial Yellow Flags in Acute Low Back Pain (2003) http://www.nzgg.org.nz/guidelines/dsp_guideline_popup.cfm?guidelineCatID=9&guidelineID=72

Wand and O’Connell, 2008 Chronic non-specific LBP – sub-groups or a single mechanism? BMC Musculoskeletal Disorders, 9:11

Waddell G: The Back Pain Revolution Edinburgh: Churchill Livingstone; 2004.

Watson P.J., Booker C.K., Moores L., Main C.J. (2004). Returning the chronically unemployed with low back pain to employment. European Journal of Pain 8, 359-369.

Apkarian AV, Sosa Y, Sonty S, Levy RM, Harden RN, Parrish TB, Gitelman DR: Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neurosci 2004, 24:10410-10415.

Flor H, Elbert T, Braun C, Birbaumer N: Extensive cortical reorganization in chronic back pain patients. NeuroImage 1997, 5(4):S216.

Siddall PJ, Stanwell P, Woodhouse A, Somorjai RL, Dolenko B, Nikulin A, Bourne R, Himmelreich U, Lean C, Cousins MJ, Mountford CE: Magnetic resonance spectroscopy detects biochemical changes in the brain associated with chronic low back pain: A preliminary report. Anesthesia Analgesia 2006, 102:1164-1168.

Cervical spine Mx

noreply@blogspirit.com (PhysioCharlie) — Fri, 31 Oct 2008 11:25:00 +0100

We had an IST yesterday lead by my colleague which was very interesting:

Management of acute neck pain in general practice

(Vos et al 2007)

High incidence of neck pain - 66% of people will experience neck pain at some point.

Prevalence rises with age.

Gender differences: women 2x more common than in men.

10% of neck pains become chronic.

Study looked at what did the GP do with new neck pain presentations:

No advice given 2%
Wait and see 23%
Improve posture 22%
Rest 18%
Specific home exs 9%
Sick leave 3%
"Other" 3%
Medication 42%

74% of those referred for physio reported recovery in a year.

79% of those not referred for physio reported recovery in a year.

2 main pathways

"Wait and see" and NSAIDs/analgesics.

Physio plus more restricted analgesia.

"Expectations of GP's role in acute neck pain seem to differ substantially between patient and GP"

Problems with that research:

No results re which method worked best.
No idea of whether the physio group were worse off at the start of treatment or not.
No discussion re whether the baseline was the same.
Non-representative group.

Vos et al, “Management of acute neck pain in general practice”, BJGP;57:23-28

So what's physios role in management of neck pain?

Moffet and McLean (2005) wrote a paper about this very thing!

First contact: usually GPs but now us as well - hence we need to know red flags.
History taking (subjective exam)
Physical (objective) exam
Explanation / education.
Encouragement / motivation

Evidence for “brief intervention”

Less useful with neck pain than with back pain.
More recent research showed good exercises with info as useful as “physiotherapy”.

Neck schools:

Potentially cost effective.
No evidence cited re neck schools.
No evidence to support effectiveness of back schools.

Psychosocial factors:

“psychosocial factors are very important and must be considered for each patient, especially those with chronic pain”.
Hurt ≠ harm.
CBT.
Consistency of message.

Specific exercises

Euro guidelines do not recommend the use of any specific programmes.
Exercise choice comes down to experience and how you were trained.
Stabilization exercises have been shown to be helpful.

General exercises

Multimodal treatment appears to be more effective than single treatment regimes. IE mobes + HEP better than either mobes or HEP on their own.

Manips and mobes:

Manips + “best GP care” is better than just “best GP care”.
Mobes “can be useful”.

Massage:

Usually not recommended in clinical guidelines.
“However, as a preliminary to more active forms of treatment, on pragmatic grounds its use should not be totally discounted”.

Other physical modalities:

TENS/heat/cold/traction/US/laser/IF/collars.
No good evidence.
Might have large placebo effect.
Could encourage dependency/passivity.

Persistent problems

Needs MDT approach.
Pain management.
EPP.

Moffet J and McLean S, “The role of physiotherapy in the management of non-specific back pain and neck pain”, Rheumatology 2006;45:371-378

Assessment part 1 - Subjective

Mechanism of injury
Acute/Sub-acute/chronic
Progression of problem
Pre-existing condition
Investigations
Red flags
- Age <20 or >55
- Trauma
- Constant unremitting pain not related to movement/activity
- T.spine pain
- Hx of Ca
- Steroid use
- Drug abuse or immunosuppression
- systemically unwell
- weight loss
- structural deformity
- fever
D’s
- Dizziness
- Diplopia
- Dysarthria
- Dysphagia
- Drops
N’s
- Nausea
- Nystagmus
- Numbness
Yellow flags
- Belief that pain is harmful and/or disabling.
- Fear/pain avoidance behaviour.
- Reduced activity level.
- Low mood / withdrawal from social interaction.
- Belief that passive treatment will help.
Pattern of pain – where is it?
Aggs and ease factors.

Predictors of persistent neck pain after whiplash

(Atherton et al 2006)

Study to look at

Relative contribution of pre-accident health and psychosocial factors, collision factors, and psych response to the collision.
To identify those at high risk by using info on the factors in A.

Over 25% of WAD patients report persistent pain 1 year after the accident.

Can we predict which 25%?

Results:

Associated with increased risk:

- Age. Increased age = increased risk
- “widespread body pain prior to collision”.
- Self-rated collsion severity “medium or high” increased risk.
- Being in a vehicle that wasn’t a car.
- Psych distress.

Not associated:

- Self-reported general health prior to collision.
- History of neck pain prior to collision.
- Speed.
- Direction of impact.
- Anticipation of impact.
- Position in car.
- Lack of head rest.
- Air bag or not.

Issues:

50% questionnaire return. Would those not suffering bother to fill them in?
Didn’t look at predictors of severity of pain in short term.
Didn’t look at compensation claims, although it is noted that those with significant psych distress were more likely to claim compensation. Another point is that they’re looking at initial presentation (IE directly after the accident in A+E) so the patient may not have known re compensation.
The WAD classification system was not used – “[it’s] only moderately predictive of persistent pain”.
No of participants who were in “other vehicles” was a very small subset so stats may not be reliable.

Atherton et al, “Predictors of persistent neck pain after whiplash injury”, Emergency Medicine 2006;23:195-201

Assessment part 2 - Objective

Posture
Basic ROM ± over-pressure
Neuro
- Reflexes
- Myotomes
- Dermotomes
- Neurodynamics
Signs of instability (thanks Sheena for these)
- Loss of balance with relation to head movements.
- Face/lip parasthesia, reproduced by active or passive c.spine movements.
- Bilateral or quadrilateral limb parasthesia, constant or reproduced by c.spine movement.
- Nystagmus produced by neck movements.
Special tests
- Spurling’s – should recreate radicular pain.
  - Found to be “not sensitive” but “highly specific”.
  - In other words, loads of false negatives but when positive it’s strongly indicative of radicular problem.
- Sharp-Purser – instability.
- Alar and transverse ligament tests.
- VBI
  - When NOT to test?
    - Hypertension (140/90 or higher)
    - Increased cholesterol.
    - DM
    - Family history of cardiac or vascular disease.
    - Smoking.
    - BMI >30
    - C.spine instability signs.
  - Minor risk factors
    - Oestrogen contraceptive.
    - HRT.
    - Infections.
    - Poor diet.
    - Diseases which may have upper c.spine instability involved eg RA, Down’s syndrome.
    - Clotting disorders.
    - Hypermobility.
    - BMI 25-29
Palpation
Assess shoulders?
- Where do other joints refer to on the neck?
  - ACJ
  - SCJ
  - 1st rib
Trigger points?

So how good can we be at C.spine assessment?

We know that certain histories produce likely outcomes. Eg RTA is likely to lead to WAD.

But we need to know what else may happen.

So we have our red flags and yellow flags. Patients are normally pre-screened by GPs as well but this can’t be taken for granted.

Pool et al (2004) studied how much the interrater reliability was for physical examination of c.spine.

Their starting point was “Several studies have drawn different conclusions with regard to the reproducibility of manual assessment techniques.”

They used a standard protocol to assess “general mobility” and “intersegmental mobility”.

All their subjects had neck pain.

2 Physios, experienced and specifically trained in how to use the standard protocol assessed these patients separately.

They tested

General mobility
- Full flexion and extension.
- High cervical flexion (nodding) and extension C0-1.
- Left and right rotation.
- Side flexion.
- Combined rotation, side flexion and extension.
- Combined side flexion with “heterolateral” rotation.
All tested with overpressure.
Segmental mobility
- Passively done in supine (PPIVMs).

Result

“Despite considerable training and the use of a standardized protocol, the results of this study showed that the reproducibility of cervical mobility and pain provoked during mobility assessments was highly variable and unacceptable.”

“[…] it is difficult to achieve reasonable agreement and reliability between 2 examiners.”

Problems/issues with the study

Limited number of patients (32).
No PPAIVMs.

Pool et al, “The interexaminer reproducibility of physical examination of the cervical spine.” J Manipulative Physiol Ther 2004;27:84-90

Out if interest there is a published case of a man “referred for physical therapy for the treatment of neck pain following trauma” (Ross and Cheeks 2008).

It’s a case study of a man post-RTA.

Subjective:

62 years old.
“He drove off a 10m cliff in reverse”.
Head and neck pain immediately.
Xray c.spine = NAD. CT head = NAD. (NB PT had no access to the reports re these)
Prescribed analgesia at A&E and sent home.
Pt returned to A&E 3 days later with no improvement to symptoms to be given reassurance and no further investigation.
GP supplied further analgesia and referred for physio.
Saw physio 8 weeks post accident.

Pain:

Constant dull ache throughout c.spine.
Intermittent sharp pain upper c.spine with rotation.
Unable to turn neck.
Aggravated by rotation mainly.
Eased by heat.
Best 1st thing am, worse through the day.
Slight improvement in pain intensity since accident.
No prior Hx of c.spine pain.
No d’s, no n’s.
Only PMH was hypertension which is controlled.
Borg scale: 1-2/10 at rest, 4-5/10 at worst.

Obj:

All c.spine movements reduced, limited by pain.
Neuro: NAD.
PAs revealed “significant pain C2-3 with muscle guarding.
Shoulders NAD.

Physio went for manual therapy and HEP. But she also referred for xrays again before trying any manual therapy.

Xray showed major “Hangman’s fracture”.

Referred to neurosurgeon.

Final outcome was no pain, improved ROM and function. He had no surgery and no further physio beyond the initial assessment and HEP/advice.

Ross M and Cheeks J, “Undetected Hangman’s fracture in a patient referred for physical therapy for the treatment of neck pain following trauma”, Physical Therapy, 2008;88:98-104

Hamstrings

noreply@blogspirit.com (PhysioCharlie) — Fri, 17 Oct 2008 15:53:00 +0200

Muscle	Origin	Insertion	Nerve
semitendinosus	ischial tuberosity	medial surface of tibia	tibial
semimembranosus	ischial tuberosity	medial tibial condyle	tibial
biceps femoris - long head	ischial tuberosity	lateral side of the head of the fibula	tibial
biceps femoris - short head	linea aspera near the head of the femur	lateral side of the head of the fibula (common tendon with the long head)	common fibular

The hamstrings cross and act upon two joints - the hip and the knee.

Semitendinosus and semimembranosus extend the hip when the trunk is fixed or extend the trunk when the hip is fixed; they also flex the knee and medially (inwardly) rotate the lower leg when the knee is bent.

The long head of the biceps femoris extends the hip as when beginning to walk; both short and long heads flex the knee and laterally (outwardly) rotates the lower leg when the knee is bent.

The hamstrings play a crucial role in many daily activities, such as, walking, running, jumping, and controlling some movement in the trunk. In walking, they are most important as an antagonist to the quadriceps in the deceleration of knee extension

Assessment of the Hamstrings

Palpation

The hamstrings can be felt as a group as they arise from the ischial tuberosity and extend along the lateral posterior aspect of the thigh. The tendons of the hamstrings can be observed and palpated at the borders of the politeal fossa. The biceps femoris tendon is on the lateral side of the fossa. The most lateral tendon on the medial side and the most prominent tendon when the knee is flexed against resistance is the semimembranosus tendon. While sitting on a chair with your knee flexed, press your heel against the leg of the chair and feel your biceps tendon laterally and trace it to the head of fibula. Also feel the semitendinosus tendon medially, which pulls away from the semimembranosus tendon that attaches to the superomedial part of the tibia.

Length

Start position: patient in supine with the lower extremities in the anatomical position

Stabilisation: it is difficult to stabilise the pelvis when performing passive SLR and pelvic rotation is not eliminated from the movement.

To stabilise the pelvis, the contralateral thigh can be held on the plinth by using a strap or by the therapist placing one knee over the anterior surface of the thigh. When interpreting the results, the therapist should consider that changes in passive SLR might also result from changes in the degree of pelvic rotation.

End position: the hip is flexed to the limit of motion whilst maintaining knee extension, so that the biceps femoris, semitendinosus and semimembranosus are put on full stretch. The ankle is relaxed in plantarflexion during the test.

Measurement: a restriction of less than 80o for SLR in normal subjects is generally imposed by lack of extensibility of hamstrings. Normal ROM of hamstring length is about 80o hip flexion.

Alternative position: the hamstrings can also be tested in sitting by extending the knee with the ankle relaxed in plantarflexion. It is important to watch for a trick movement as the patient may lean back to posteriorly tilt the pelvis, extending the hip joint to place the hamstrings on slack therefore allowing increased knee extension.

Strength

The hamstrings are able to develop greater tension and demonstrate greater strength if the patient is tested in a position of hip flexion. This position places the muscle in a stretched position, as opposed to a position of hip extension, which places the muscles in a shortened position.

The strength of the hamstrings can be tested in sitting or in prone lying. The hamstrings are often tested in prone lying. If the knee is flexed to 90o and the heel is turned out the greatest stress is placed on biceps femoris with resisted knee flexion. If the heel is turned in the greatest stress is placed on semimembranosus and semitendinosus.