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

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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...

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.