I have a new website!!

http://physiocharlie.vpweb.co.uk

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

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

Assessment of the Knee Joint

Anterior Cruciate Ligament

Anterior Cruciate Ligament

Anterior Cruciate Ligament

Anterior Cruciate Ligament

Anterior Cruciate Ligament

Studies looking at ACL testing

Posterior Cruciate Ligament

Posterior Cruciate Ligament

Posterior Cruciate Ligament

Medial Collateral Ligament

Lateral Collateral Ligament

Meniscal Testing

Medial Meniscus

Lateral Meniscus

Study looking at Meniscal Testing

Posterior Lateral Corner

Observation (QUIZ)

Special Questions

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

Patellar loading with activity

Strength

Hamstrings

Length

Quads

Thomas test

Gastro

Anatomy of The Knee, Junior IST

Joints

Proximal Tibiofibular Joint

Cruciate Ligaments

Anterior Cruciate Ligament

Posterior Cruciate Ligament

Cruciate Ligaments

Medial (tibial) collateral ligament

Lateral (fibular) collateral ligament

Menisci

Medial Meniscus

Lateral meniscus

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

Bursa

Movements of the knee

Rectus Femoris

Vastus Intermedius

Vastus Lateralis

Vastus Medialis

Sartorius

Gracilis

Biceps Femoris

Semimembranosus

Semitendinosus

Popliteus

Gastrocnemius

Plantaris

Popliteal Fossa

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)

Differential Diagnosis?

Aetiology of SIS

Aetiology

Aetiology

New Theories

Muscle patterning

Rx – Evidence - CSP Guidelines

Scapula Rehab

Objective Ax

CONCLUSION

REFERENCES

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

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:

1. Muscle atrophy
2. Consistency of muscle fibre i.e.: internal structure.
3. 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

• 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

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.

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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

1. Relative contribution of pre-accident health and psychosocial factors, collision factors, and psych response to the collision.
2. 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:

2.  
   • 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:

2.  
   • 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

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.