Sacrum & Coccyx

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Sacrum & Coccyx

Sacroiliac joint pain

Elicited with patient lying on the affected side without support (Gaenslen's test), directcompression or FABER test (flexion abduction and external rotation)

Local anaesthetic injection can be diagnostic and therapeutic

Fusion only indicated when an infection is present

Ideopathic coccydynia

Frequently associated with psychological conditions

Four types of coccyx:

Type of coccyx Coccyx morphology Coccydynia

1 Slight forward curve, apex dorsal Rare11 Marked curve, apex ventral Common111 Sharp angulation between coccyx

segmentsCommon

1V Ventral subluxation of segments Common

Conservative treatment, donut pillow, NSAIDS, local steroid injection

Complete or partial coccygectomy, in type 111 or 1V may help but hgh risk ofcomplications with wound

Sacral Insufficiency fracture

Occurs in older patients with osteopenia and no history of trauma

Treat conservatively with rest analgesia

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Spinal Injuries - Principles

General Principles Initial Management Definitive Management

Neurological Assessment Incomplete Cord Injuries Long Term Management

GENERAL PRINCIPLES [Back To Top]

Complications of spinal injury

Neurological damage

Damage to vertebral column causing deformity and pain

Stable injuries

Vertebral components won't be displaced by normal movement.

An undamaged spinal cord is not in danger

There is no development of incapacitating deformity or pain

Unstable injuries

Further displacement of the injury may occur

Loss of 50% of vertebral height

Angulation of thoracolumbar junction of > 20 degrees

Failure of at least 2 of Denis's 3 columns

Compression # of three sequential vertebrae can lead to posttraumatic kyphosis

Anatomical considerations

The upper thoracic spine (T1-T10) is protected by the ribs, sternum and the facet joint orientation

At the thoracolumbar junction there is a fulcrum of increased motion, so there is increased risk of injury

The middle thoracic spine is a vascular 'watershed', vascular insult can cause cord ischaemia (Artery ofAdamkiewitz)

Cauda equina begins at L1-L2. Lesions below L1 have a better prognosis as nerve roots, not cord areaffected

Mechanisms of injury


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Hyperextension -common in the neck. Anterior ligaments and disc may be damaged.1.

Flexion- If posterior ligaments intact, wedging of vertebral body occurs. If posterior ligaments torn, maycause subluxation

2.

Axial compression- Causes burst #s. Bony fragments may be pushed into spinal canal3.

Flexion, with posterior distraction- May disrupt middle and posterior columns.4.

Flexion with rotation- Causes dislocation with or without #.5.

Shear.6.

SPINAL SHOCK

Diaphragmatic breathing1.

Flaccid limbs2.

warm periphery3.

decr. pain sensation4.

reduced reflexes5.

erection6.

Urinary retention7.

decr. BP + decr. pulse rate = Neurogenic8.

decr. body temp.9.

Return of bulbocavernosus reflex at 24hrs= end of Spinal Shock10.

INITIAL MANAGEMENT OF SPINAL INJURY PATIENTS [Back To Top]

ABC, Spinal board, hard collar

History

Strongly suspect spinal injury if any major accident, unconscious patient, fall from a height, sudden jerkof neck after rear end car collision, facial injuries or head injury

Ask about neck or back pain, numbness, tingling, weakness, ability to pass urine

Examination

Logroll- look for bruising, palpate for a step, tenderness

Repeated neurological examination to determine neurological damage and its progression/resolution

Thorough overall examination for fractures etc as patient may not feel pain

Imaging

Xrays-Cervical spine AP, Lateral including C7/T1, open mouth view of odontoid. Swimmers view or pullarms down. AP and lateral view of other tender areas of spine

CT scan shows bony injury

MR scan shows soft tissue involvement

If neurological damage

Catheterise

Note reduced BP and bradycardia due to neurogenic shock (temporary generalised sympathectomy).Rule out hypotension due to haemorrhage elsewhere. May need treatment with vasopressors, not fluid


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resuscitation.

Invasive monitoring required

Give methylprednisolone IV 30mg/kg over 15 mins then 5.4mg/kg/hr for next 23 hours. Needs to begiven within 8 hrs. Discuss with the spinal team.

Attend to skin by turning

Cochrane Database Syst Rev 2000;(2):CD001046

Pharmacological interventions for acute spinal cord injury.

Bracken MB; Department of Epidemiology and Public Health, Yale School of Medicine, 60 College street,Box 20834, New Haven, Connecticut 06520-8034, USA. [email protected]

BACKGROUND: Acute spinal cord injury is a devastating condition typically affecting young people with a

preponderance of males. Pharmacological treatment in the early hours of the injury is aimed at reducing theextent of permanent paralysis during the rest of the patient's life.

OBJECTIVES: To review randomized trials of pharmacological therapies for acute spinal cord injury.

SEARCH STRATEGY: The review draws on the search strategy developed by the Cochrane Injuries Group.In addition, files of the National Acute Spinal Cord Injury Study have been reviewed.

SELECTION CRITERIA: All published or unpublished randomized controlled trials of pharmacologicaltreatment for acute spinal cord injury in any language.

DATA COLLECTION AND ANALYSIS: Data have been abstracted from original trial reports. For theNASCIS, Japanese and French trials, additional data (e.g. SDs) have been obtained from the originalauthors.

MAIN RESULTS: There are few trials in this area of medical care. Only one therapy has been extensivelystudied, methylprednisolone sodium succinate, which has been shown to improve neurologic outcome up toone year post injury if administered within 8 hours of injury and in a dose regimen of: bolus 30mg/kgadministered over 15 minutes with a maintenance infusion of 5.4 mg/kg per hour infused for 23 hours. Theinitial North American trial was replicated in a Japanese trial but not in the one from France. Data has beenobtained from the latter study to permit appropriate meta-analysis of all three trials. This analysis indicatessignificant recovery in motor function after methylprednisolone therapy. A more recent trial indicates that ifmethylprednisolone therapy is given for an additional 24 hours (for a total of 48 hours), additionalimprovement in motor neurologic function and functional status is observed. This is particularly observed if

treatment cannot be started until between 3 to 8 hours after injury. The same methylprednisolone therapyhas been found effective in whiplash injuries and a modified regimen found to improve recovery after surgery

for lumbar disc disease.

REVIEWER'S CONCLUSIONS: High dose methylprednisolone steroid therapy is the only pharmacologicaltherapy shown to have efficacy in a Phase Three randomized trial when it can be administered within 8 hours

of injury. High dose methylprednisolone has been accepted as standard therapy in many countries. A recenttrial indicates additional benefit by extending the maintenance dose from 24 to 48 hours if start of treatmentmust be delayed to between 3 and 8 hours after injury. There is an urgent need for more randomized trials of

pharmacological therapy for acute spinal cord injury.)

DEFINITIVE MANAGEMENT [Back To Top]

Objectives

Preserve neurological function1.

Relieve reversible nerve or cord compression2.

Stabilise the spine3.

Rehabilitate patient4.

With no neurological deficit

If stable spinal injury- pain relief, collar or brace. Exception can be a burst #, ? operatively stabilise

If unstable injury, reduce and hold secure until bone / ligts heal with ORIF or traction in tongs, halo vest


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With complete sensory and motor loss

Usually an unstable injury

Only consider conservative management for high thoracic injuries

Early operative stabilisation- to help with nursing, prevent spinal deformity and pain. Speeds up rehab

With Incomplete neurological loss

Stable injury- conservative bed rest, brace. Exception can be burst # ?operatively stabilise

Unstable injury- early reduction and stabilisation

Site for Pedicle Screw Insertion:

NEUROLOGICAL ASSESSMENT IN SPINAL INJURIES [Back To Top]

Aims

To determine the level of the lesion- counted as the lowest level at which neurological function is intactbilaterally

To determine whether damage is complete/ incomplete

To determine prognosis

May be difficult until period of spinal shock (flaccidity, areflexia) is over (24-48 hrs after injury)

1. Tone

2. Power

Diaphragm C3-4-5Shrugging shoulders C4Flex elbows C5,6Extend elbows C7

Abduct fingers C8Active chest expansion T1-T12Hip flexion L2Knee extension L3-4

Ankle dorsiflexion L5-S1Ankle plantar flexion S1-S2Eversion of foot L5Inversion of foot L4


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MRC Power Grading

0 No active contraction1 Visible contraction without movement2 Movement with gravity eliminated3 Movement against gravity4 Movement against resistance but weak5 Normal power

3. Reflexes

Biceps C5-6Triceps C6-7Supinator C5-6Knee jerk L3-4

Ankle jerk L5-S1Plantar response If upgoing = UMN lesion

Abdo cutaneous reflexes If lost = UMN lesionBulbo cavernosis reflex Pull penis, causes anal sphincter tightening

If returned, period of spinal shock is over

4. Sensation

5. PR

Always perform this to assess S2, 3, 4

INCOMPLETE CORD INJURIES [Back To Top]


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Syndrome injury/pathology Features Prognosis

BrownSequard

Penetrating trauma Loss of ipsilateral motor function and vibration and positionsense, contralateral loss of pain and temp

Best

Anterior cord Flexion compression Motor loss , dorsal columns spared PoorCentral cord Age>50 extension

injuriesAffects upper limbs more than lower limbs, motor andsensory loss

Fair

LONG TERM CARE OF NEUROLOGICALLY INJURED SPINAL PATIENTS [Back To Top]

Frankel grade- Useful in monitoring functional improvement from spinal cord injury

Frankel grade FunctionA Complete paralysisB Sensory function only below injury levelC Incomplete motor function below injury level (1or 2/5)D Fair to good motor function (3-4/5) below injury levelE Normal function below injury level

Highest mortality in the first 2 weeks

Most common causes of morbidity and mortality:

Respiratory insufficiency - atelectasis and pneumonia. Any deficit proximal to T10 causes increasedreliance on the diaphragm. Treat with IPPV, physio, tracheostomy and suction, repeatedbronchoscopy

1.

Paralytic ileus - Keep NBM initially for 24 hours, IV fluids2.

GI bleeds from haemorrhagic gastritis -? Due to unopposed parasympathetic activity. Give H2antagonists

3.

Urological complications- UMN lesion of bladder, catheterise intermittently to stop urinary stasis andinfection. LMN, may manage with suprapubic pressure to relieve bladder

4.

Pressure sores - Turn every 2 hrs, teach to relieve pressure later5.

Joint contractures - Passive movements +/- splintage 2x per day6.

Psychological withdrawal- multi disciplinary approach.7.


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Spinal Stenosis

Anatomy Aetiology Pathophysiology Clinical

Investigations Natural History Treatment References

Lumbar spinal stenosis is one manifestation of the general process of spinal degeneration that occurs with aging,and often becomes symptomatic in the seventh and eighth decades of life.

Stenosis = narrowing of a hollow tubular structure.

Anatomy [Back To Top]

The central canal of the spinal column conveys the spinal cord in the cervical, thoracic and upper lumbarlevels.In most individuals, the spinal cord ends by the L1 level; below this level the remaining lumbar and sacralnerve roots travel as the cauda equina.The nerve roots are more tolerant of chronic pressure than the spinal cord, which is why an individual maytolerate a higher degree of stenosis in the lower lumbar spine than in the cervical or thoracic region.The boundaries of the central canal vary with the level of the vertebral body:

At the level of a vertebral body, the canal is bordered by the body itself anteriorly, the pedicleslaterally, and the laminae posteriorly. This is the site that is affected in cases of congenitalstenosis , where the pedicles are typically shortened.

At the level of the intervertebral disc, the anterior border is formed by the annulus, the posterolateralborders by the facet joints and capsules, and the posterior border by the ligamentum flavum. Theseare the structures that are most affected by degenerativeprocesses .

The dimensions of the spinal canal and foramen are influenced by dynamic and postural factorswhen a person rises from recumbency to standing, the resulting axial load on the intervertebral disccauses further bulging of the annulus, which in turn further compromises the central canal and theforamen.

The foramina decrease in size while the nerve roots increase in diameter as you move down the

spine . Thus the lumbar spine is most commonly affected.

Aetiology [Back To Top]

Classification -Arnoldi (1976) [Picture ]

CongenitalDevelopmental1.

Achondroplasia2.

1.

AcquiredDegenerative1.

2.


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Spondylolistheticworseifimposedonadevelopmentalnarrowing

DiscHerniation

2.

Degenerative& DiscHerniation

3.

Degenerative&congenital

4.

Others:Paget's1.Spinal tumour2.Infection (TB)3.Post-surgery4.Trauma5.

3.

The L4-L5 segment is the most commonly affected, followed by the L3-L4.Men are more commonly affected than women, because their spinal canals are narrower at the L3-L5levels.

Pathophysiology [Back To Top]

Narrowing of the central canal and/or intervertebral foramina is due to:

annular bulging1.bone spur formation2.facet joint enlargement3.ligamentous hypertrophy4.

Classification by site:

A. Central stenosis

Compression of the thecal sac & cauda equinacaused by: arthritic facets with medial encroachment; congenitally narrow canal ('trefoil' shape);spondylolisthesis; Central disc herniation; Posttraumatic; Post-surgical

B. Lateral stenosi s [ Picture]

compression of the nerve rootsuperior articular facet enlargement; lateral disc herniation; ligamentum flavum hypertrophy; uncinatespurring

lateral recess stenos is - affects the traversing (lower) nerve root1.


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foraminal stenosis - affects the exiting (upper) nerve root2.extra-forami nal (far-out)3.

Mechanism: (Howe et al. Pain , 1977)

when standing or walking the lumbar lordosis increases the stenosissubarachnoid obstruction occursdiffusion of fluid from the endoneurium into the subarachnoid space is impairedincreased endoneurial pressure-> 'Compartment Syndrome' in the nerve roots-> conduction disturbancesa nerve which has been repetitively injured becomes more easily irritated by dynamic factors


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Clinical [Back To Top]

Virtually all individuals in their seventies have at least some degree of spinal stenosis on imaging studies, but only afraction manifest the true symptoms of central and/or foramenal stenosis.

Central stenosis:

neurogenic claudication. (from compression on the cauda equina)increased unsteadiness or loss of balancefeeling better if they walk stooped forwardRarely - urinary incontinence & cauda equina syndrome

Foramenal stenosis:

Radicular signs from narrowing of the lateral recess or the neural foramen.

Physical examination can be unimpressive in patients with central stenosis.

ambulate with a forward-leaning posture and a moderately broad-based gait.check distal pulses to screen for vascular causes of claudication.Stress Test = walk until symptoms occur

Difference to Vascular claudication:

Activity Vascular Claudication Neurogenic Claudication

Walking Distal-proximal pain; calf pain Proximal-distal thigh pain

Uphill Walking Symptoms develop sooner Symptoms develop later

Rest relief with standing relief with sitting or bending

Bicycling Symptoms develop No symptoms


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Lying Flat Relief May increase symptoms

Investigations [Back To Top]

X-rays:

bone spurs, decreased disc height and facet hypertrophy in older patients.

CT:

more accurate and detailed picture of the bony anatomyless accurate than MRI in estimating the degree of compromise of the soft tissue elements.thus can underestimate the degree of stenosisspinal canal < 10mm AP diameter = Absolute Stenosis

MRI: (without gadolinium)

currently represents the "gold standard" in the evaluation of central stenosis.It allows the visualization of the disc, neural elements, ligamentum flavum & thecal sac

Epiradicular Nerve root block:

improvement of radicular symptoms after injection of anaesthetic is suggestive of lateral (foraminal)stenosis.

Myelography: is no longer routinely necessary, although it can be useful in selected cases

Natural History [Back To Top]

2 studies following 49 patients (Hayashi) and 32 patients (Johnsson) for 5 years (with non-operative treatment):

Symptoms unchanged in 60-70%Worse in 15-20%Improved in 15-20%

Treatment [Back To Top]

Non-Operative:

NSAIDs1.

Muscle relaxants2. Antidepressants for chronic radicular pain3.Epidural & nerve root block steroid injections - good long-term relief in patients with foramenal or lateralrecess stenosis

4.

Physiotherapy (with massage, ultrasound, TENS, braces or supports, acupuncture, biofeedback, hot orcold packs, traction, or manipulation) can offer symptomatic relief of radicular or low back pain, but not forclaudicant symptoms.

5.

Flexion brace (Williams brace) - prevents lordosis. Not well tolerated.6.Calcitonin7.

Operative

Indications:

Severe neurological symptoms1.

failed conservative treatment + impaired ADL (activities of daily living)2.

Decompression Procedures

Central Stenosis

Partial Laminectomy - for patients without segmental instability (eg. spondylolisthesis)Total Laminectomy - should be avoided

Lateral Recess Stenos is

Medial Facetectomy - the medial margin of the superior facet, facing the spinal canal, is resectedonly

Foraminal & extra-foraminal Stenosis

extra-spinal approach to dorsal root ganglion (in the intervertebral foramen)resect the lower lamina laterally & caudally until the dural sac is seen; pediculotomy may be required


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Spinal Fusion

preoperative instabilty (spondylolisthesis)instability expected from resection of the facet jointsagittal inclination of the facet jointhigh demand post-op activities

Operative Results

Variable due to:

not all stenotic sites necessarily cause symptoms, therefore selecting decompression levels can be difficult1.insufficient decompression2.incorrect levels3.post-operative instability4.regrowth of resected tissue & scarring5.

Multi-level involvement does not do well due to post-op instability (should consider fusion, but very invasive)

Careful attention to patient selection and meticulous operative planning are important in optimizing surgicaloutcome.

Refereneces: [Back To Top]

Current Orthopaedics. Mini-Symposium: 13(3). July 1999.ApleyMiller

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Spine Embryology

Vertebral Growth

Vertebral formation at 3-5 weeks with segmentation occurring at 6-8 weeks

Each vertebrae forms from 2 adjacent sclerotomes and so becomes an inter segment structure

Notochord degenerates but between vertebrae it persists to form the nucleus pulposusDuring the 6th week chondrification occursTwo centres in each centrum fuse at the end of the embryonic period resulting in one centre evident in the centrum after thisperiod (defects here -> hemi vertebrae)2 Centres in the neural arches fuse with each other and the centrumThe two 1/2's of the neural arch usually fuse in the first year and these to the centrum in ~ the 3rd to 6th year

At about puberty five secondary centres appear (upper and lower body, and one in the tip of the TPs and spinous process)

Ossification begins in the embryonic period and ends at about 25 years.Longitudinal growth is via superior and inferior apophysis.

Horizontal growth is by periosteal apposition

Spinal canal enlarges by growth of the pedicles and posterior elements, enlarging rapidly from birth to five years and more slowlyfrom 5-10 years.

The spinal canal reaches its final dimensions relatively early compared with the continual growth of the rest of the vertebralstructuresThe final height of vertebral column is reachedgirls by 11 - 13 yearsboys by 14 - 16 yearsBoys grow ~ 3.5cm and girls 1.5cm after Risser IV


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The Developing Human - Moore & Persuad

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Spondylolysis & Spondylolisthesis

SPONDYLOLYSIS

caused by a defect in the pars interarticularis

usually a fatigue fracture from repetitive hyperextension stresses (gymnasts)

most common cause of LBP in adolescents

Radiology

plain x-rays demonstrate 80% of lesions

oblique views - additional 15% picked up - 'Scottie dog' sign (Lachapelle)

CT - may miss fracture

Bone Scan - incr. uptake indicates an acute lesion which will probably heal

Non-union is common

SPONDYLOLISTHESIS

"spondy" refers to the vertebrae and "listhesis" means "to slip"

usually L4/5 and L5/S1

Normally laminae & facets constitute a locking mechanism preventing forward slippage [see Video ]

Classification: (Newman, Wiltse, McNab)

Congenital/Dysplastic (20%)superior articular facets are congenitally defectiveassociated with spina bifida occulta

Isthmic (50%)

caused by spondylosis (L5/S1)

a. Lytic-fatigue fracture of the pars interarticularisb. Elongated but intact pars interarticularisc. Acute fracture of the pars interarticularis

Degenerative (25%) degenerate facet joints (L4/L5)

Post-traumatic

from an acute fracture in some other portion of the vertebra that allows a slip to occur.An isolated pars fract ure is not seen with this lesion.

Pathological tumours, Paget's

Post-operative

Severity of Slip:

1. Percentage of slip of the AP diameter of the vertebra below:

Grade I - < 25%

Grade II - 25-50%

Grade III - 50-75%

Grade IV - 75-100%

Grade V - >100% (spondyloptosis)

2. Slip Angle

normal = > 0 degrees

Clinical


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may be discovered only incidentally on x-rays

injury may aggravate any symptoms

usually pain begins insidiously during the second or third decade with walking and standing

Flattening of the back

Spinous process step-off

Claudication may signal the development of lateral stenosis

Radiology

Plain x-rays should be taken standing

grade slip

slip angle

Oblique x-rays

Bone scans - (see above)

MRI

evaluates disc

but can see a pseudodisc herniation due to rotatory element of slip

Treatment

Non-operative:

reduce sports

adolescents - x-rays every 6 months until maturity

Risk factors for Slip progression:

young age at presentation1.

females2.

slip angle > -10 degrees3.

high grade slip4.

dome shaped sacrum5.

inclined sacrum (>30deg. beyond vertical)6.

Operative:

Indications:

slip > 50% or progressing in adolescents

back and/or leg pain unresponsive to non-operative treatment

functionally significant neurological deficit

Grade I & II - in situ fusion (& decompression);

Repair of the pars defect & fixation using a lag screw or wires has been described for low grade slips (


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Waddells Nonorganic Signs

Screening for Psychological Factors in Patients With Low

Back Problems: Waddell's Nonorganic Signs

Adapted from: Scalzitti DA. Screening for psychological factors in patients with low back

problems: Waddell's nonorganic signs. Phys Ther. 1997;77:306-312.

For the majority of patients with low back pain (LBP), the cause of their pain is unknown.1

Psychological factors, which may include behavioral, cognitive, or somatoform components,can be just as important as the diagnosis of pathology affecting the low back in a patient's

recovery from a low back problem.2-5A recent US Agency for Health Care Policy andResearch clinical practice guideline recommends exploration of psychological factors when anindividual with an acute low back problem is having difficulty regaining his or her tolerance to

activity.4

Feuerstein and Beattie5 discussed several biobehavioral instruments that can be used toidentify psychological factors in individuals with LBP. If factors are identified that are potentialcontributors to the low back problem, the physical therapist can then refer the patient to theappropriate professional. Routine application of these instruments, however, may beimpractical during physical therapy examinations because of the time required foradministration and scoring as well as the expertise needed to interpret the results. Thus, thereis a need for a brief screening tool to help identify patients who may require more detailedpsychological testing. A review of the description and diagnosis of psychological disorders thatmay relate to LBP is beyond the scope of this update. For further information on these areas,

the reader is referred elsewhere.5-7

Signs of organic problems are findings from the physical examination that indicate thepresence of pathology or disease. Paresthesia over the lateral border of the foot, for example,is a sign for S-1 nerve root involvement. Signs of nonorganic problems, in contrast, are findings

that deviate from the usual presentation of disease.8 Both organic and nonorganic signs maybe present in a patient with LBP. Therefore, the presence of nonorganic signs should not beequated with malingering or the presence of a psychological problem, but only with the needfor further investigation.

Waddell et al8 described a group of signs that indicate the presence of nonorganic problemsfor patients with LBP. Waddell has also referred to these signs as "behavioral signs" or

"inappropriate signs."2,9 Testing for these signs is performed as part of the physical

examination and takes less than 1 minute.8 Nonorganic signs have been used to describedifferent characteristics of patients with LBP. The purpose of this update is to describe the useof Waddell's nonorganic signs as a screening tool for psychological factors in patients withLBP. Additionally, the relationship between the nonorganic signs and physical impairments,disability, and treatment outcomes will be discussed.

Waddell's Nonorganic Signs

In the early 1900s, nonorganic signs were frequently used to detect malingering in patients with

LBP.10,11As medical and psychological knowledge progressed, it became clear that thediagnosis of malingering may have been based on overly simplistic assumptions, and the useof these nonorganic signs fell out of favor. The modern use of nonorganic signs for patients

with low back problems increased greatly after 1980, when Waddell et al8 grouped eight signsinto five types. These five types, or categories of signs, are tenderness, simulation, distraction,regional disturbances, and overreaction (Table). Waddell and colleagues investigated 16 othersigns, including grip strength, lumbar sensory changes, and pretibial tenderness, but did notinclude them in their final battery because of poor intertester and intratester reliability, overlapwith other signs, and difficulty for the examiner to learn.

According to Waddell et al,8 a nonorganic sign (an indication of a nonorganic contribution to apatient's low back problem) observed during the physical examination is scored as positive. If asign is positive, then that type of nonorganic sign is present. One nonorganic sign in isolationmay be present with some organic conditions and should therefore be discounted. A sensory


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regional disturbance, for example, may be present in persons with spinal stenosis with multiplenerve root involvement.

Waddell et al8 found that the presence of three or more types of nonorganic signs correlatedwith the results of psychological tests indicating problems. According to Waddell et al, thepresence of a single sign is not associated with an indication of psychological problems. Thepresence of three or more types of nonorganic signs has been the most consistently usedcriterion for the finding of a positive Waddell's nonorganic signs test, although other methods

have been proposed.12,13 Unless otherwise specified in this update, therefore, a positive testfor nonorganic signs refers to finding the presence of three or more types of nonorganic signs.

A negative nonorganic signs test is the finding of only one or two types of signs, although apatient may have more than three nonorganic signs because of multiple signs within a specifictype.

Reliability

Agreement was high (86%) for two examiners in detecting the presence of nonorganic signs in

a group of 50 patients with chronic LBP.8Agreement between examinations in the samepatients was 85%. (The mean length of time between examinations was 23 days.) McCombe

et al14 reported poor intertester reliability between two orthopedic surgeons and between asurgeon and a physical therapist in detecting individual nonorganic signs. Confidence intervalsof Kappa coefficients included zero for the nonorganic signs of tenderness and regionaldisturbances, suggesting that agreement was not better than chance. McCombe et al,however, did not examine the reliability of the examiners in determining the presence of three or

more nonorganic signs. This finding should caution clinicians regarding the use of positivenonorganic signs in isolation.

The nonorganic sign of overreaction requires the clinician to make judgments based onobservations of the patient's behavior. The other signs are from tests conducted during routineexaminations. The presence of overreaction, therefore, may be more difficult to identify thanother nonorganic signs. Several methods and instruments can be used to quantify observation

of a patient's behavior during the physical examination.15 Keefe and Block16 described amethod for observing overt pain behaviors to provide a means of identifying the presence ofguarding, bracing, rubbing, grimacing, and sighing during a physical examination. Waddell and

Richardson9 obtained a Pearson product-moment correlation coefficient of .65 whenexamining the relationship between the nonorganic signs test and overt pain behaviors in 120patients who had LBP for at least 3 months. Measurements obtained with the UAB PainBehavior Rating Scale, which is one instrument for measuring pain behavior, were also highly

correlated (r=.73) with the results of the nonorganic signs test in 103 patients with LBP.17

Nonorganic Signs and Psychological Findings

In their original study of nonorganic signs, Waddell et al8 reported a correlation between thepresence of nonorganic signs and scores on the hypochondriasis, depression, and hysteriascales of the Minnesota Multiphasic Personality Inventory. These scales of the MinnesotaMultiphasic Personality Inventory traditionally represent a measure of psychological distress inpatients with LBP. In addition, correlations have been found between the presence ofnonorganic signs and other psychological instruments, including the disease affirmation and

hypochondrial disturbance scales of the Illness Behavior Questionnaire (IBQ),18 the Distress

and Risk Assessment Method (DRAM),19 and pain drawings.8,20 Waddell et al8 caution,however, that nonorganic signs should not be overinterpreted and used as substitutes forcomprehensive psychological assessment. Instead, they should be used as part of an

examination to identify patients who require more detailed testing.

The sensitivity and the specificity of eight psychometric instruments, including Waddell'snonorganic signs test, for detecting psychological disturbances in patients with LBP were

determined in a group of 264 persons.12 Results from each instrument were compared with a"gold standard" of psychological disturbance, which was defined as a positive response tothree or more of the eight psychometric tests. Specificity of the nonorganic signs for correctlyidentifying patients who were nonpsychologically disturbed was 86% in men and 84% inwomen. Sensitivity of the nonorganic signs for correctly identifying patients who werepsychologically disturbed was 44% in men and 48% in women. This study was limited,however, by the lack of a universal "gold standard" of psychological disturbances with which tocompare the different instruments. In the study, measurements with each instrument werecompared with a compilation of measurements obtained with the other instruments.Correlations among the eight instruments may not have been found if the instruments were


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measuring different aspects of psychological disturbances.

Nonorganic Signs and Demographics

Age, gender, occupation, or compensation status do not appear to influence the results of the

nonorganic signs test.8 Hayes et al,21 however, found nonorganic signs more frequently inpatients with LBP who were anticipating or receiving financial compensation as compared withthose who were not anticipating or receiving compensation. In this study, however, otherfactors differed between the two groups of patients. Thus, the role of the nonorganic signs isdifficult to assess.

The length of time that a patient has had LBP appears to increase the likelihood of finding a

positive nonorganic signs test. Waddell et al8 reported that 12% of patients with LBP who wereseeing an orthopedist for the first time showed three or more nonorganic signs. The authorsreported three or more nonorganic signs in 33% of two different samples of patients withchronic LBP and in 50% of a third sample of patients with chronic LBP. The three samples ofpatients had all been off from work for many months with a high incidence of previously failedtreatments. No positive tests were detected among subjects without LBP. Factors responsiblefor the increased occurrence of nonorganic findings in patients with chronic LBP have notbeen identified. The likelihood of finding three or more nonorganic signs may increase with theduration of the problem or because of the failed treatments.

Nonorganic Signs and Tests of Musculoskeletal Performance

Nonorganic contributions to a patient's LBP may coexist with organic contributions. Organicfindings may be influenced by nonorganic factors, and in some patients, nonorganic findings

may be influenced by organic factors. Waddell et al22 evaluated the relationship between thepresence of the nonorganic signs and 27 tests of musculoskeletal impairments in 120 patientswith chronic LBP. Reproduction of the patient's pain during hip and knee movements andlimitations in passive knee flexion, hip flexion force, hip abduction force, and prone isometrictrunk extension were positive more frequently in the patients who had two or more nonorganicsigns (29%) than in the patients who had only one or no nonorganic signs (71%). The onlyimpairments not correlated with a nonorganic component were those related to spinal postureand lumbar flexion. Based on these findings, the authors concluded that the physical tests ofmusculoskeletal impairments that they investigated were better indicators of illness behaviorthan of physical impairment.

Groups of patients with LBP with three or more nonorganic signs performed poorer on tests offorce production, range of motion, and motor skills than did groups of patients with LBP

without nonorganic signs.23-26 These tests included tests of lumbar range of motion andisometric force on an Isostation B-200 lumbar dynamometer,23,24 and tests of lifting,

gripping, and physical dexterity on an ERGOS Work Simulator,25 Menard et al26 found thatpatients with LBP with nonorganic signs produced lower torques for isometric elbow flexionand isometric knee extension than did patients without nonorganic signs. The authorscontended that musculoskeletal performance as measured by dynamometers does notnecessarily reflect maximum physical capacity. Low values on any of these tests, however,could not be used to identify individuals with nonorganic problems, because some individualswith a positive nonorganic signs test scored as well as some individuals without nonorganicsigns.

Cooke et al24 measured force and range of motion in patients with chronic LBP, using alumbar dynamometer. The same test was repeated after 4 weeks of an active reconditioningexercise program. Patients with a positive nonorganic signs test demonstrated improvements in

force that were greater than improvements that might be expected as a result of physiologicchanges or a learning effect of the test procedure. The authors suggested that the improvedforce generation might have been due to alterations in illness behavior rather than to animprovement in physical capacity.

Findings that nonorganic components may contribute to measures of musculoskeletalimpairments suggest that these measures, which are frequently used by physical therapists forpatients with LBP, may also reflect a psychological component of disability. In addition, thesedata suggest that physical therapists may want to continue measuring musculoskeletalimpairments but need to consider the influence of other factors, such as illness behavior, onthese tests. Likewise, benefits from treatment focused on physical reconditioning may result inreducing disability by improving an individual's psychological status, and thus his or hertolerance to activity, rather than just improvements in the measurement of musculoskeletalimpairments, such as peak torque of the lumbar extensors.


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Relationship Between Nonorganic Signs and Treatment Outcomes

Nonorganic phenomena can interact with expected treatment outcomes in patients with LBP.

Several investigators27-29 have described poorer results from lumbar surgery in patients with

nonorganic signs. McCulloch27 found that 97 of 109 patients with a nonorganic componentwho underwent chemonucleolysis continued to have back or leg pain that prevented theirreturn to full activity. One hundred eighty-six of 327 patients without nonorganic signs, incontrast, were free of pain or had minimal limitations in activity following the chymopapain

injection. Dzioba and Doxey28 found that only 49% of patients with two or more nonorganicsigns were approved to return to work by a physician 12 months after various forms of lumbarsurgery, as compared with 78% of patients who had only one or no nonorganic signs followingsurgery.

In a prospective study by Waddell et al,29 psychological factors, including the presence of apositive test for nonorganic signs, correlated with a poor surgical outcome, as assessed by aphysician, the patient, and the patient's work status. A poor surgical outcome in this study wasdefined as postsurgical episodes of disabling back or leg pain, chronic use of narcoticmedications, further surgery, or inability to return to work. Relief from pain and reduceddisability depended on the presence of an accurate diagnosis of a surgically treatablepathological condition without the presence of nonorganic signs.

Outcomes of nonsurgical treatments of patients with LBP have also been influenced by the

presence of nonorganic signs. Lehmann et al30 found that electroacupuncture treatment of

patients with chronic LBP who had three or more nonorganic signs was no more effective forpain reduction than a sham treatment. In contrast, the authors found that treatment of patientswith electroacupuncture, in the absence of nonorganic signs, resulted in a greater decrease inpain than did the sham treatments.

Patients with illness behavior as measured by the presence of nonorganic signs, nonorganicsymptoms, and a pain drawing received more treatments than did patients who did not exhibit

illness behavior in a study by Waddell et al.31 These treatments included medication use,lumbar injections, orthopedic supports, physical therapy, spinal manipulation, and bed rest.Based on this finding, a clinician should seriously consider whether there is overutilization oftreatments when patients who test positive for nonorganic signs show no progress. For thesepatients, treatment might be directed toward addressing the illness behavior.

Ability of Nonorganic Signs to Predict Return to Work

A common goal in the rehabilitation of workers with LBP is to return them to work. There isconflicting evidence about the ability to use nonorganic signs for predicting return to work.

Bradish et al32 reported that a positive nonorganic signs test at initial assessment in a group ofworkers with a low back injury (N=120) did not correlate with work status between 12 and 18

months after injury. In contrast, hlund et al17 found a relationship (r=.34) betweennonorganic signs and the time needed by a group of automobile workers (N=103) to return towork. In this study, return to work was defined as the return to the same job at least half-time.

Lancourt and Kettelhut,33 in a study of 134 patients with LBP, found that the nonorganic signsof axial loading, simulated rotation, distraction, and a sensory regional disturbance were amongthe factors that were better predictors of return to work than were ankle and knee reflexes,motor loss, and sensory loss in a dermatomal pattern. This relationship was seen for patientswho returned to work within the first 6 months after injury but not for patients who were off

work for greater than 6 months. Recently, Kummel34

described two new nonorganic signs:lumbar pain during isolated cervical movement and lumbar pain limiting active shouldermovement. The presence of these two signs in addition to the presence of three or more ofWaddell's nonorganic signs improved the ability to predict patients who failed to return to workin this retrospective study of 717 patients.

The treatment received by injured workers may influence their return to work. Werneke et al13

evaluated a physical conditioning program designed to meet each patient's job requirement for170 workers with LBP. One hundred fifteen of the patients showed work status improvementwithin 3 months of completing the program. At least one nonorganic sign was present in 47%of the patients whose work status did not improve, as compared with 12% of the patients whodemonstrated improvement. The number of nonorganic signs present at discharge from theprogram was reduced for 82% of the patients whose work status improved. In contrast to thehigh success rate from physical conditioning, when patients with nonorganic findings received


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treatments described as "symptomatic and at the discretion of the physician," less than 40%

returned to work.32

Other factors, besides the presence of nonorganic signs, may influence an injured worker

returning to previous job duties. Waddell et al29 found return to work after lumbar surgery waspredicted by physical, psychological, and occupational factors. Physical therapists shouldconsider the relationship of these factors in the treatment of injured workers. The referral to anappropriate professional or multidisciplinary team should be made for management of anyconfounding factors when a patient's work tolerance fails to improve from physical therapy.

Clinical Implications

A physical problem may coexist with the presence of nonorganic signs. Thus, the presence ofnonorganic signs does not eliminate the need for a complete physical examination. A patientwith a cauda equina syndrome, for example, may be classified as exhibiting nonorganicbehavior based on sensory and motor losses and overreaction to the examination because ofthe intensity of symptoms. Physical examination, however, should identify the structural etiologyof the problem, and appropriate treatment should be directed toward the pathologicalcondition.

According to Waddell et al,8 nonorganic signs by themselves should not be equated withmalingering or the presence of a psychological problem. Rather, the finding of nonorganicsigns should alert the clinician to the need for more comprehensive testing. Labeling a patientas a malingerer does little to help the patient enhance his or her tolerance for activity. Instead,the factors that are limiting the patient from recovering his or her tolerance for activity should be

identified, and interventions should be targeted toward modification of the limiting factors.5

Classification of movement dysfunction in patients with LBP may help clinicians to identifyindividuals who will benefit from specific treatments. Failure to account for the presence ofnonorganic findings may lead to the misclassification of patients, because nonorganic factors

may influence patients' performance on tests used to classify them. Delitto et al35 screen fornonorganic signs in their treatment-based classification scheme and suggest referral to an

appropriate practitioner when screening is positive. Marras et al36 developed a classificationscheme for patients with low back disorders based on the higher derivatives of trunk velocity.Using this method, Marras et al found that patients with nonorganic findings weredistinguishable from patients in nine other low back disorder categories.

The utility of Waddell's nonorganic signs has been described for patients with LBP. To date,nonorganic signs tests for musculoskeletal problems in other regions of the body are not

commonly used. Development of nonorganic signs tests for patients with other musculoskeletalproblems may help to guide management of these patients.

Nonorganic signs are found more frequently in persons with chronic LBP as compared withpersons with acute LBP. Further investigation may reveal how nonorganic behaviors increaseand develop in patients with chronic LBP. Treatment focused on prevention of thedevelopment of nonorganic signs may reduce the occurrence of chronic LBP and back-relateddisability.

Summary

The role of Waddell's nonorganic signs test as a screening tool for psychological factors in theexamination of patients with low back problems has been described. The presence ofnonorganic signs should alert the physical therapist to the need for additional psychologicaltests and should not necessarily be considered an indicator of malingering. Nonorganic signsmay coexist with organic findings. An illness behavior role of the nonorganic signs issuggested, as they have been related with disability in addition to physical impairments.Physical therapy management for these patients should focus on treatment of illness behaviorand on combating disability.

AcknowledgmentsI thank Louise J White, PT, and Pamela J Woodall, PT, for their kind assistance with thepreparation of this update.

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