Minggu, 07 Oktober 2007

Cerebral Palsy

Definition

  • Disorder of movement and posturing

  • Caused by static brain lesion

  • Acquired during the stage of rapid brain development

  • Manifestations may change with growth and development

Epidemiology

Occurs in 1-5 in 1 000 live births. More common in advanced countries. Advanced perinatal care increases survival of brain-damaged children. Care only slightly reduces incidence of cerebral palsy . More common in socioeconomically disadvantaged.

Aetiology Aetiology

  • Prenatal (30%)

    • Maternal infection - Toxoplasmosis . Rubella . Cytomegalovirus . Herpes . Syphilis

    • Maternal exposure - Alcohol . Drugs

    • Congenital brain malformations

  • Perinatal

    • Birth weight <2500g>(25-40%)

    • Anoxia (10-20%)

  • Postnatal (10%)

    • Meningitis

    • Head injury

    • Immersion


Classification

  • 1. Spastic

    • Most common (60% of cases)

    • Most amenable to surgery

    • Due to upper motor neuron involvement - mild to severe motor impairment

    • Characterized by increased muscle tone and hyperreflexia, with slow, restricted movements (because of co contraction of agonist and antagonists)

    • Spasticity is characterized by increased muscle activity with increasingly rapid stretch (clasp knife & clonus)

    • Contractures

    • hemiplegia (both limbs on one side): arm usually worse than leg - all hemiplegics will walk, regardless of treatment; present with toe walking only

    • diplegia : have more extensive involvement of the lower extremity than the upper extremity; most diplegics will eventually walk; IQ may be normal, strabismus is common; gait is typically characterized by a crouched gait, toe walking, and flexed knees; heel cord lengthening alone may exacerbate crouched gait;

    • paraplegia (both legs): sparing of arms

    • quadriplegia : look for oral, lingual, dys f(x); dysarthria;

  • 2. Athetoid / Dyskinetic

    • Writhing movements. When excited, wriggle as if tickled.

    • 20% of cases

    • Result from basal ganglia involvement

    • Present w/ slow, writhing, involuntary movements

    • may affect the extremities (athetoid), or the proximal parts of limbs and the trunk (dystonic)

    • Hyperextended hips & knees with exaggerated stepping gait. Lean backwards, extending shoulder girdle & trunk.

    • Abrupt, jerky distal movements (Choreiform) also may occur;

    • Movements incr during with emotional tension and disappear during sleep.

    • Dysarthia is present and is often severe.

    • Intelligence normal (often above average)

    • Most difficult to correct with surgery - results are unpredictable & plaster immobilisation hazardous due to friction from constant movements.

  • 3. Ataxic

    • 10% of cases

    • Involvement of the cerebellum or its pathways

    • Weakness, inco-ordination, and intention tremor produce unsteadiness, wide based gait, and difficulty with rapid or fine movements

    • Poorly amenable to surgical correction;

  • 4. Hemiballistic

    • Sudden movements . As if throwing ball.

  • 5. Hypotonic

    • Usually a stage through which an infant passes.

  • 6. Combination


Pathogenesis

1. Weakness

Upper motor neuron lesion causes

  • Loss of voluntary movement

  • Weakness

  • Easy fatigability

2. Spasticity

  • Feature of all lesions of pyramidal system . Cerebral, capsular, pontine, midbrain lesions

  • Related to excessive activity of disinhibited spinal neurones

  • Mediated via stretch reflex . Muscle spindles detect stretch and stimulate muscle to contract . Threshold regulated by descending tracts . Spasticity due to hyperactivity of stretch reflexes

  • Tendon reflexes hypertonic . Clonus may appear

  • Posture characteristic because some neurones more active than others

  • Attempts to change position lead to resistance which quickly yields Clasp-knife phenomenon.

3. Contracture.

  • Nature of muscle contracture is: Shortening of muscle-tendon unit due to failure to keep pace with growth of bones.

  • Muscle adds sarcomeres at musculotendinous junction in response to constant stretch

  • In normal children, walking and movement provide all the stretch needed. When muscles spastic, this mechanism cannot occur.

4. Deformity

  • From unopposed muscle contracture.

  • Hip dislocation. Persistent hip adduction leads to valgus of femoral neck. Persistent hip flexion leads to anteversion of femoral neck. Results in Acetabular dysplasia, Hip subluxation & Hip dislocation

Note:

  • Spasticity - Abnormally increased contraction of a muscle in response to a stretch. Growth of muscles is impaired.

  • Rigidity - Involuntary sustained contraction of a muscle not stretch-dependent. Growth of muscles is not impaired.


Clinical features

1. Spastic quadriplegia. (25%)

  • Initially child floppy and will not feed

  • Choking during feeding from pseudobulbar palsy (difficult swallowing & chewing; dribbling)

  • Fail to thrive

  • Intelligence, vision and hearing affected

  • Only 10-20% will walk

  • Begin to walk up to age 7

  • Usually mentally retarded

  • Develop hip dislocation early and scoliosis.

2. Spastic diplegia.(30%)

  • All developmental milestones delayed

  • Most walk by age 4 .

3. Spastic hemiplegia (40%)

  • Usually noticed at walking age

  • Mean age of walking is 2-3 months later than normal.

  • Limp and one-handedness noted

  • Right-sided form may have speech delay

  • Seizures common.

  • Mild learning problems

  • Hyperactivity

4. Monoplegia (5%)

Associated disorders

  • Most common with total involvement

  • Mental retardation

  • Seizures

  • Learning disorders

  • Emotional and personality derangement

  • Visual defects

  • Hearing impairments

  • Disorders of speech


Assessment

History

  • Abnormal birth history

  • Prematurity

  • Neonatal nursery

  • Normal Developmental milestones (brackets are 95th percentile)

    • Head control -3 mths (6 mths)

    • Sitting independently - 6 mths (9 mths)

    • Crawling - 8 mths (never)

    • Pulling to stand - 9 mths (12 mths)

    • Walking -12 mths (18 mths)

Examination. (Also see CP Examination )

  • Walking- Arm swing . Trunk leans forward. Scissoring (d.t. Hip flexion & adduction). Windswept posture . Knee flexion . Stride length reduced . Narrow walking base. Equinus. Lordosis . Co-ordination in turning. [ Gait Analysis ]

  • Sitting - Legs forward or W . Upright or slouched.

  • Kneeling eliminates contracture effect .

  • Hips - Clinical signs of dislocation:

    1. Limited abduction, esp. with rapid stretch (grab test)

    2. Asymmetric knee height with pelvis level & knees flexed ( Galeazzi test )

    3. Windswept posture - one hip adducted & other side abducted

    4. Asymmetric leg length

    5. Hip flexion contractures

  • Muscles:

    • Psoas

      • FFD of hip demonstrated by Thomas test

      • Increased lumbar lordosis and prominent bottom when standing

      • Decreased sacrofemoral angle on standing lateral x-ray

      • Reduced SLR because of flexed pelvis from FFD.

    • Hamstrings

      • Reduced SLR

      • Hip extension contracture

      • FFD at knee

      • Lumbar kyphosis and small bottom when standing

      • Knee flexed at beginning of stance phase

      • False equinus (flexed knee lifts heel from ground)

      • Internal femoral torsion (sitting in W position)

      • Inability to touch toes

      • Reduced popliteal angle (hip at 90o)

      • High patella (flexed knee and spastic quadriceps)

    • Adductors

      • Scissored gait if bilateral

      • Apparent leg length discrepancy if unilateral

      • Trendelenberg limp

      • Decreased hip abduction

      • Eventual hip dislocation

    • Quadriceps

      • Stiff-legged gait (knees never flex)

      • Inability to flex knee when hip extended means rectus is responsible

      • Ely test (child prone, flex knee, if hip flexes = rectus femoris tight).

    • Triceps surae

      • Ankle equinus

      • Tiptoe gait

      • Recurvatum at knee when heel goes down

      • Silverskold's Test - equinus improves with knee flexion = soleus tighter than gastrocnemius

  • Neurology

    • Gross. Weakness

    • Clasp-knife phenomenon

    • Primitive reflexes

      • Moro reflex - Hold child at 45 o . Allow head to drop back . Arms and legs stick out in extension . Normally disappears by 4 mths.

      • Labyrinthine reflex - Tone reduced and arms and legs flex when child prone . Tone increased and arms and legs extend when child supine . Normally disappears by 6 mths.

      • Parachute reflex - When child held head down, both hands put out protectively . Appears at 5 mths.

  • Upper limbs

    • General.

    • Look at resting position.

    • Look for contractures.

    • Assess joint stability

    • Hand placement. Ask patient to place hand on knee and then head.

    • Control.

      • Ask patient to pretend to play piano . Look for independent movement.

      • Ask patient to throw object. Look for grasp and release.

      • Stereognosis. Test ability to recognise shape in palm

  • Predictors of Walking (from 1 year of age):

    1. Asymmetrical tonic neck reflex

    2. Symmetrical tonic neck reflex

    3. Neck righting reflex

    4. Moro reflex

    5. A pattern of extensor thrust & abduction of the legs when supported upright

    6. Parachute reflex

    7. Stepping reflex

    • If any 2 of these 7 responses are inappropriate by 1 year of age it is highly unlikely that the child will walk independently

Birth Injuries

OBSTETRIC BRACHIAL PLEXUS PALSIES (OBPP)

from: McGuinness & Kay. Current Orthopaedics. 13:20-26. 1999.

  • Incidence is approx 2/1,000 births

  • Risk Factors:

    • Child

      • weight > 4000g / large for gestational age

    • Maternal

      • multiparity

      • diabetes

      • sibling with shoulder dystocia or OBPP

    • At Birth

      • shoulder dystocia

      • breech

      • long labour

      • forceps delivery.

  • Investigations:

    • EMG - doesn't correlate with prognosis & can be misleading.

    • MRI - fast spin echo MRI may demonstrate root avulsions.

  • Classification Table:

TYPE (Adler & Patterson)

TYPE (Narakas)

ROOTS

DEFICIT

PROGNOSIS

Erb-Duchenne

Group 1

C5,6

Deltoid, cuff, elbow flexors, wrist & hand dorsiflexors - 'waiters tip'

Best


Group 2

C5-7

Above except with sightly flexed elbow

Poor

Klumpke


C8-T1

Wrist flexors, intrinsics, Horners

Poor

Total Plexus

Group 3

C5-T1

Sensory & motor, flaccid arm

Worse

(Total Plexus + Horners)

Group 4

C5-T1

Sensory & motor, flaccid arm, Horner

Worst

  • Natural History:

    • C8-T1 injury with a Horners syndrome has the worst prognosis.

    • Isolated lower root lesions have a poor prognosis, since they are usually avulsion injuries.

    • The rate of recovery and the time of beginning of recovery affect the outcome.

    • Toronto scoring system (Clarke) assesses the child at 3 months of age

    • No biceps function at 3m indicates a poor prognosis.

    • Patients who show evidence of biceps function before 6 months of age have near-normal to excellent function.

    • In borderline cases exploration of the Brachial Plexus is performed.

    • Early repair has the best prognosis.

    • Recovery continues until 1 year old, then little further recovery thereafter.

  • Management:

    • Early Referral to a specialist unit.

    • Physiotherapy - passive range of motion exercises.

    • Splinting - not popular.

    • Surgery

  • Indications for Surgery:

    • C8-T1 injury with a Horners syndrome

    • C5/6 lesions with no muscle activity & breech baby.

    • Toronto score <>

    • Failure to progress adequately between 12-24 weeks

    • EMG criteria of Smith where doubt exists.

  • Surgical Technique:

    • Transverse incision

    • Neurolysis

    • Nerve grafting (Sural nerve)

    • Nerve transfers (accesory to suprascapular, intercostal to musculocutaneous)

  • Late Deformities:

    • Internal rotation & adduction contraction of the shoulder

      • modified L'Episcopo procedure - involves lengthening of pectoralis major & subscapularis tendons with transfer of teres major & insertions into posterior surface of the humerus to act as external rotators

      • osteotomy - for older children with fixed bony adaptive changes, proximal humeral external rotation osteotomy can be considered; - these patients will most often complain of internal rotation contracture

    • Posterior glenohumeral subluxation: - limitation of external rotation; - in late cases, with a deficient posterior glenoid consider humeral derotational osteotomy.


TORTICOLLIS

  • from fibrosis of sternal head of sternocleidomastoid

  • can result from unilateral shortening of sternocleidomastoid, commonly associated with fibrosis of the muscle; (may also involve the platysma and scalene muscles)

  • Aetiology & Natural History

    • birth trauma, occlusion of venous flow, or haematoma results in fibrosis of muscle & palpable mass noted within first 4 weeks of life

    • mass usually resolves within the first year of life (90% resolve)

    • non-tender enlargement may be palpated in body of sternocleidomastoid

  • Grisel's Syndrome:

    • Atlantoaxial Rotary Subluxation in association with pharyngeal infection, occurs predominantly in children

    • it results in severe torticollis, resistant to manual therapy

    • > 5 mm of anterior displacement of arch of C-1 (Fielding type III) indicates disruption of both facet capsules as well as transverse ligament

    • reduction w/ skeletal traction, followed by atlantoaxial fusion, is recommended


  • Rigid Torticollis:

    • may also present as rigid deformity, & sternocleidomastoid is not contracted or in spasm

    • torticollis most often follows an injury to the C1-C2 articulation; - frx of the odontoid in young child may not be apparent on initial x-rays

  • Associated Anomalies:

    • congenital atlanto-occipital abnormalities

    • bony anomalies of the Cervical Spine, esp involving C1 & C2

    • congenital webs of skin along the side of the neck, pteygium colli

    • DDH: (20%

    • plagiocephaly: - w/ persistent contracture of sternocleidomastoid, deformities of face and skull result and are apparent within first year of life; - flattening of face is noted on side of contracted sternocleidomastoid and is probably caused by child's sleeping position

    • metatarsus adductus

    • opthalmic disorders causing the child to tilt the head.

  • Non Operative Treatment:

    • 90% will respond to passive stretching within the first year of life

    • in first yr of life, rx consists of stretching sternocleidomastoid muscle by trying to rotate the head to opposite position. - stretching exercises should include not only lateral rotation, but also side bending to the opposite shoulder

  • Indications for Surgery:

    • failure of non operative treatment after 12 to 24 months of age, surgical intervention is needed to prevent further facial deformity

  • Operative Treatment:

    • involves resection of portion of distal sternocleidomastoid muscle from its sternal and clavicular attachments through transverse incision in the normal skin fold of the neck

    • skin incisions immediately adjacent to clavicle may result in unsightly hypertrophic scars. - transverse skin incisions in skin folds 1.5 cm proximal to clavicle result in imperceptible scars

    • uncommonly, distal resection is insufficient and proximal release of sternocleidomastoid is needed;

Bibliography, Links & Recommended Reading

The following Websites & Books were used in compiling the Orthoteer Summaries: ( Bold = Essential)

Books:

Review of Orthopaedics - Mark Miller

Campbells Operative Orthopedics - Terry Canale

Principles of Orthopaedic Practice - Dee & Hurst
Apley

Orthopaedic Knowledge Updates

Websites:

South Australian Orthopaedic Registrars' Notebook

Entrez-PubMed

University of Washington Radiology Webserver

Journals:

Current Orthopaedics

The Journal of Bone and Joint Surgery

BASIC SCIENCE

The Developing Human - Moore & Persuad

duPont PedOrtho Education Modules
Resident Education Home Page, ALFRED I. DUPONT INSTITUTE
British Society for Children's Orthopaedic Surgery

McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.

Barton. The Upper Limb & Hand. 1999.
Electronic Textbook of Hand Surgery
eRadius - International Distal Radius Fracture Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.

Orthopaedic Knowledge Updates

Websites:

South Australian Orthopaedic Registrars' Notebook

Entrez-PubMed

University of Washington Radiology Webserver

Journals:

Current Orthopaedics

The Journal of Bone and Joint Surgery

BASIC SCIENCE

The Developing Human - Moore & Persuad

duPont PedOrtho Education Modules
Resident Education Home Page, ALFRED I. DUPONT INSTITUTE
British Society for Children's Orthopaedic Surgery

McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.

Barton. The Upper Limb & Hand. 1999.
Electronic Textbook of Hand Surgery
eRadius - International Distal Radius Fracture Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.

Orthopaedic Knowledge Updates

Websites:

South Australian Orthopaedic Registrars' Notebook

Entrez-PubMed

University of Washington Radiology Webserver

Journals:

Current Orthopaedics

The Journal of Bone and Joint Surgery

BASIC SCIENCE

The Developing Human - Moore & Persuad

duPont PedOrtho Education Modules
Resident Education Home Page, ALFRED I. DUPONT INSTITUTE
British Society for Children's Orthopaedic Surgery

McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.

Barton. The Upper Limb & Hand. 1999.
Electronic Textbook of Hand Surgery
eRadius - International Distal Radius Fracture Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.
Apley

Orthopaedic Knowledge Updates

Websites:

South Australian Orthopaedic Registrars' Notebook

Entrez-PubMed

University of Washington Radiology Webserver

Journals:

Current Orthopaedics

The Journal of Bone and Joint Surgery

BASIC SCIENCE

The Developing Human - Moore & Persuad

duPont PedOrtho Education Modules
Resident Education Home Page, ALFRED I. DUPONT INSTITUTE
British Society for Children's Orthopaedic Surgery

McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.

Barton. The Upper Limb & Hand. 1999.
Electronic Textbook of Hand Surgery
eRadius - International Distal Radius Fracture Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.

Arthritis in Children

JUVENILE CHRONIC ARTHRITIS (JCA)

Approximately 1:1000 children will develop swelling of one or more joints persisting for more than 3 months with no specific cause found. 50% of these will progress to JCA.

Aetiology - unknown

Diagnostic Criteria

  • Age under 16 at onset
  • Persistent arthritis in one or more joints for 6 weeks (minimum) to 3 months after other aetiologies have been ruled out. E.g. infection, malignancy, blood dyscrasias, Reiter's, hypogammaglobulinaemia

Classification by onset (Schaller)

1. Systemic onset (Still's disease)

  • Age: usually under 5years but can be any age
  • Sex: <5yr female =" male;">5yr female > male
  • Fever (high with spikes up to 40oC daily) plus one of the following
  1. Maculopapular rash
  2. Iridocyclitis
  3. RhF +ve
  4. Cervical spine involvement
  5. Pericarditis
  • Generalised lymphadenopathy
  • Hepatomegaly
  • Splenomegaly
  • Sites: knees, wrists, ankle, feet

2. Polyarticular onset

  • Age: any, even before age 1year!
  • Sex: female > male
  • 5 or more joints involved in the first 3 months
  • Seronegative (RhFactor -ve)
  • Seronegative (RhFactor -ve)

Sites: knees (60%), wrists, hands

  • RhFactor +ve

Older children (9-10 years) with persistent activity and rapid joint destruction affecting mainly the hands and feet.

3. Pauciarticular (most common)

  • 4 or less joints involved in the first 3 months
  • Type I
  • Type I

Younger onset <6yr,>

  • Type II

Older onset 9yr+, with males mainly affected. Association with HLA-B27.


Lab tests


HB

WCC

ESR

RhF

ANA

Systemic

-

++

++

+ve

+ve

Polyarticular

+

+

+

-/+ve

30%+ve (in those with RhF+ve)

Pauciarticular

-

-

+ or -

-ve

-ve (M) +ve (F)


Radiological changes

  • Early features limited to periarticular osteopenia
  • Late features occur after 6 months and include growth disturbance, chondrolysis, joint destruction and erosions. These features are more common in the RhF +ve patients.

Prognosis

  • 80% will eventually be able to lead normal functional lives.
  • Death can occasionally occur in the systemic onset group because of infection or the development of amyloidosis.
  • 60% if seen within 1 year of onset will have normal function at 5 years compared with 25% of those seen after 1 year.
  • Functional outcome is related to joint contractures and destruction.

Poor prognostic factors

  • Onset <>
  • IgM (RhF) +ve
  • Eye involvement
  • Hip involvement leads to a greater functional deficit

Medical Management

  • Aim: to suppress activity and therefore prevent joint deformity
  • Multidisciplinary approach with rheumatologist, PT, OT, child psychologist etc
  • PT to help prevent joint contractures and keep healthy muscles working. Hydrotherapy affective.
  • OT for splints and orthoses

Drug treatment

  • NSAID's
    • Ibuprofen, voltarol, naproxen etc.
    • Aspirin used to be the drug of choice but dangerous with children under the age of 5 years because of the risk of Reye's syndrome.
  • Disease modifying drugs
    • Methotrexate: shown to be effective in polyarticular disease
    • Gold, penicillamine, azathioprine etc.
  • Corticosteroids
    • Systemic: the use of steroids does not affect the ultimate prognosis and there are many complications related to their use, in particular growth disturbance, adrenal suppression etc.
    • Intra-articular/tendon sheath: can be effective in controlling flare ups

Surgical treatment

  • Hip
    • Soft tissue releases for contractures
    • Total joint replacement
  • Knee
    • Soft tissue releases for contractures
    • Synovectomy
    • Epiphyseal stapling
    • Supra-condylar osteotomy
    • Total joint replacement (rarely needed)
  • Foot and ankle
    • Orthoses
    • Triple fusion

Summary

Type

%

Joints

Features

Progression (%)

Systemic (Still's)

25

many

Fever, rash, organomegaly

25

Polyarticular: RhF -ve

15

many

Mild fever

30

Polyarticular: RhF+ve

15

many

Severe joint destruction

25

Pauciarticular I (F)

30

large

Iridocyclitis

15

Pauciarticular II (M)

15

large

Spondylitis, HLA-B27

15


Other arthritides

  • Juvenile psoriatic arthropathy
  • Ankylosing spondylitis
  • Reiter's disease
  • Acute rheumatic fever

Wrist Examination

LOOK

Dorsum, side, palmar- palmar flex wrist to exacerbate dorsal swellings

Deformity e.g. radial deviation after colles, prominent ulna

Swellings e.g. ganglion

Scars, muscle wasting

FEEL

Start radial side & move in a circle around wrist;

Palpate for tenderness of :

- APL, EPL- de Quervain's

- Anatomical snuffbox- scaphoid

- Distal Radioulnar joint

- lunate- locate by dorsiflexing wrist

- ulnar styloid

- Hook of hamate

- Pisiform- pisiform triquetral degen

- Guyons canal

- Over median nerve

MOVE

Dorsiflexion- palms together, lift up elbows. Normal 75 degrees

Palmar flexion- Dorsum of hands in contact, drop elbows. Normal 75 degrees

Radial deviation- in neutral pron-sup. Normal 20 degrees

Ulnar deviation- Normal 35 degrees

Pronation-supination-elbows by sides ask patient to hold pen, measure angle between vertical and pen

-pronation 75 degrees

-supination 80 degrees

SPECIAL TESTS

Pseudostability test-

Hold patients hand in right hand and forearm with left, normal wrist clunks on palmar displacement of hand on forearm. Nonspecific test

DRUJ

1. Piano key sign- for instability = balottment of ulnar head, (prominence of ulna)

2. squeeze and turn test- the examiner stabilises the patient's forearm with one hand while with the other hand, he grasps the patient's hand as if for a vigorous handshake. When the patient resists forced passive rotation, or when there is active rotation against resistance, pain usually is elicited. If the pain is caused by compressing the ulna against the radius, it is mostly suggestive of chondromalacia.

Ulnar impingement test

For TFCC - shake hands with patient; ulnar deviate wrist whilst rotating the forearm. Pain = positive.

CARPAL INSTABILITY TESTS

Matrise Orthopaedics - Physical Examination of Wrist Instabilities

A. Scapholunate instability

1.scapholunate ballotment - using both index fingers and both thumbs, stabilise the lunate between thumb and index finger of one hand and the scaphoid between the thumb and index finger of the other; the scaphoid pushed in a volar to dorsal direction; discomfort in this area suggests the possibility of injury to the Scapholunate Ligament (SLL).

Scapholunate Ballotment Test

2.Kirk Watson's scaphoid shift test- examiner opposite patient, both elbows on table as if arm wrestling ipsilateral arms. Examiners thumb on scaphoid tubercle, index finger on scapholunate ligament to palpate clunk. SLL initiates scaphoid flexion on radial deviation of wrist. Completion of flexion of scaphoid caused by pressure from surrounding bones.

Normal- can feel scaphoid flexing in radial deviation, thumb pushed away

SLL injury- pressure of examiner's thumb prevents initiation of flexion of scaphoid , then Clunk occurs on sudden pressure from bones. Patient may withdraw hand with pain 'apprehension test'

Must compare to opposite wrist.

N.B. 20 % of normal people have positive test

[Watson HK, Ashmead D4, Makhlouf MV : Examination of the scaphoid. J Hand Surg Am. 1988; 13: 657-660.]

Kirk-Watson Test

Original Description by Watson:

'The patient is approached by the examiner as if to engage in arm wrestling, face to face across a table with diagonally opposed hands raised (right to right or left to left) and elbows resting on the surface in between. With the patient's forearm slightly pronated, the examiner grasps the wrist from the radial side, placing his thumb on the scaphoid tuberosity (as if pushing a button to open a car door) and wrapping his fingers around the distal radius. The examiner's other hand grasps at the metacarpal level, controlling the wrist position. Starting in ulnar deviation and slight extension, the wrist is moved radially and slightly flexed with constant thumb pressure on the scaphoid. This radial deviation causes the scaphoid to flex. The examiners thumb pressure opposes this normal rotation, causing the scaphoid to shift in relation to the other bones of the carpus. This scaphoid shift may be subtle or dramatic. A truly positive test requires both pain on the back of the wrist (not just where you are pressing on the scaphoid tuberosity), and comparison with the opposite wrist is essential.'

B. Lunotriquetral instability [Back To Top]

1. Reagan test (Lunotriquetral ballotment test) - stabilise the lunate between thumb and index finger of one hand and the triquetrum between the thumb and index finger of the other;the pisiform and triquetrum are pushed in a volar to dorsal direction; discomfort in this area suggests the possibility of injury to lunotriquetral interosseous ligament

[Reagan D.S., Linscheid R.L., Dobyns J.H. Lunotriquetral sprains: J Hand Surg Am 1984; 9:502-514.]

Reagan Test

2. Kleinman shear test (shuck test)- Examiner opposite patient, contralateral thumb over dorsum of lunate, index finger over pisiform. Attempt to squeeze thumb and index finger together. Pushing the pisiform dorsal arouses pain in the lunotriquetral joint.

Kleinman Shear Test

(Examiner's thumbs used in this illustration instead of index finger & thumb)

3. Linscheid's test (ulnar snuff box compression test) - This test may be the least specific according to Kleinman (Figure 25). The thumb placed on the ulnar side of the triquetrum exerts an axial pressure directed toward the lunate, which arouses pain.

[Linscheid RL : Scapholunate ligamentous instabilities. Annales de Chirurgie de la Main. 1984; 3: 323-330]

Tests to distinguish causes of radial pain (to be done early if tenderness on radial side of wrist)

De Quervain's tenosynovitis- Finkelstein's test- ulnar deviation,thumb in palm

Thumb CMC joint- Press over CMC joint and circumduct thumb with axial pressure

STT joint- Resisted pronation causes pain

Wartenburg's (superficial radial nerve irritation) Tinel's test

Phalen's, Tinel tests and Median nerve compression test

Spine Examination

Added by Feroz Dinah , May 2004

Suitably undressed, usually down to underwear. Start with the patient standing, then lying prone and finally lying supine.

1. STANDING

Look

  • Scars: previous surgery
  • Lumps: abscess, tumour (e.g. sacral lipoma), prominent paravertebral muscle spasm
  • Sinuses: deep infection
  • Cafe au lait spots / nodules: Neurofibromatosis
  • Hairy patch (spinal dysraphism)
  • Mongolian blue spot (more common in Asians: no clinical significance)
  • Low hairline due to short neck: Klippel-Feil syndeome: fusion or absence of cervical vertebrae; may be associated with Sprengel shoulder (undescended scapula)
  • Down / Morquio syndromes: Atlanto-axial instability
  • Asymmetry of shoulder height / trunk balance / loin crease: scoliosis (lateral curvature with rotational deformity of vertebral bodies)
  • Leg length discrepancy (check level of iliac crests)
  • If patient consistently stands with one knee bent in spite of equal leg lengths, this may indicate nerve root tension, as knee flexion relieves the pull on the nerve root(s)
  • Lateral deviation of spine (known as 'list' or 'tilt'): may be a sign of prolapsed intervertebral disc causing nerve root ompression
  • Associated anomalies of hands/feet, e.g. syndactyly, pes cavus: may be part of a syndrome
  • Kyphosis and lordosis (best assessed from side): may be exaggerated or reduced
  • Round backing / hunched shoulders: Schuermanns disease/kyphosis
  • Gibbus (aka kyphos): acute angular deformity with bony prominence, e.g. tuberculous vertebral collapse
  • Observe gait

Feel

  • Tenderness: may be bony, intervertebral or paravertebral
  • Bony prominence or steps

Move

  • Flexion: Ensure spinal rather than hip flexion, by marking two spots about 10cm apart on the patient lumbar spine: these should separate by a further 5cm on flexion.
  • Forward bend test: Flexion should accentuate any scoliosis by causing a rib prominence (aka rib hump) on the convexity of the curve and a loin crease on its concavity.
  • If the scoliosis disappears on forward bending, it is postural.o If the scoliosis disappears on sitting, it may be due to leg shortening.
  • Scoliosis may be secondary to nerve root compression and will therefore disappear after resolution (spontaneous or surgical), i.e. sciatic scoliosis
  • Extension: Ask patient to arch backwards, but beware of cheating by trick movement of bending knees.
  • The wall test will unmask even small fixed flexion deformities: Ask patient to stand with his/her back against a wall. Observe if heels, buttocks, shoulders and occiput all touch the wall.
  • Lateral flexion: Ask patient to run hand down ipsilateral thigh on one side, and then the other. Asymmetry in range of movement is clinically more significant than actual range of movement
  • Rotation: Again, of little clinical significance, but as most rotation occurs in the thoracic spine, this should not be reduced in lumbo-sacral disease. Stabilise the patients pelvis with both hands, and ask the patient to twist/turn to either side, looking for asymmetry of range of movement.
  • Rib cage excursion: This should be about 7cm between full inspiration and full expiration.

CERVICAL SPINE
The books are full of normal ranges of neck movements in degrees, but you have to ask the patient to put something in his/her mouth to act as a goniometer. It may be more useful to use (less precise) anatomical landmarks to gauge range of movement. Also, CHANGES in ranges of movement are often more useful.

  • Flexion: Most people can get their chin on their suprasternal notch.
  • Extension: should allow nose or forehead to be parallel to ceiling.
  • Rotation: cheek parallel to shoulder.
  • Lateral flexion: very variable, and first movement to be restricted in arthritis.

NOTES
1. Rotation occurs throughout C-spine, but mainly at atlantoaxial joint (C1/C2).
2. Flexion / extension occurs throughout the C-spine (C0 to C7).
3. No flexion in thoracic spine, because splinted by ribcage.
4. No rotation in lumbar spine, because facet joints are vertical.

LYING PRONE

Look

  • Watch the patient climb on the examination couch.

Feel

  • Focal spinal tenderness
  • [Assess sensation on back of whole leg; if worried about cauda equina syndrome, perianal sensation may also be assessed here.]
  • Check popliteal and posterior tibial pulses

Move

  • Femoral nerve stretch: Either acutely flex the knee with the thigh resting on the couch, or extend the hip with the knee in moderate flexion. If pain is elicited, there is a positive nerve stretch test.
  • [Assess hip rotation and ankle reflexes with the knee at 90o of flexion.]

LYING SUPINE

Look

  • Watch the patient turn over onto his/her back.


Feel

  • Sensation can be tested here [or at the end, in the neurological examination]


Move

  • Assess hip/knee mobility if you haven't already.
  • Straight leg raise (SLR): keep the knee extended and passively flex the hip by lifting the heel off the examination couch and estimate the angle of elevation (normally 80 - 90o). If restricted by pain radiating from back to BELOW the knee (i.e. back, buttock, thigh and calf), there is evidence of sciatic nerve root irritation. Tension on the sciatic nerve can be increased by dorsiflexion of the ankle, causing increase in pain.
  • Lasegue's test: Tension is then removed by flexing the knee, often allowing the hip to be fully flexed. If when the knee is extended from this flexed hip/knee position, the pain is reproduced, Lasegue's test is positive.
  • Bowstringing's test: With hip flexed to 90o, extend the knee as far as the patient tolerates. Pressure applied to the hamstrings (possibly pulling on the peroneal nerve) with the thumb will immediately cause pain if there is nerve root irritation.

NOTE: If the pain on SLR is felt in the contralateral limb (cross-leg pain or cross-sciatic tension), there may be a central disc prolapse, with risk of cauda equina syndrome.
Signs of nerve root compression
Standard full neurological examination of both lower limbs, i.e. tone, power (MRC grading), sensation (light touch, pinprick and proprioception if indicated) and reflexes. Usually deficit(s) will follow an anatomical distribution, i.e. dermatome(s) or myotome(s). Whole limb pain, weakness, or anaesthesia suggest supratentorial overlay.

Non-organic signs (Waddell G. et al. Non-organic physical signs in low back pain. Spine 1980; 5: 117)

1. Superficial / non-anatomical tenderness: Lightly pinch the skin on a wide area of lumbar skin (pinch test). If this causes pain, test is positive.
2. Axial loading: Using the flat of his/her hands, the examiner vertically loads the patient's skull. If this causes pain, the test is positive. Similarly, simultaneous ipsilateral rotation of shoulders and pelvis (i.e. log-roll) in the same plane should NOT cause pain.
3. Distraction: If the examiner elicits severe pain on SLR, but the patient is able to comfortably sit forward with legs extended on examination couch, the test is positive. (aka 'flip' test in USA)
4. Regional disturbances: Test is positive in presence of non-anatomical motor or sensory deficits (e.g. normal heel-toe walk, but cog-wheel foot weakness).
5. Over-reaction: Test is positive if muscle spasm, tremor or collapse occur during examination

Shoulder Instability Tests

From University of Washington

Laxity Tests

  • These tests examine the amount of translation allowed by the shoulder starting from positions where the ligaments are normally loose.

  • These are tests of laxity, not tests for instability : Many normally stable shoulders, such as those of gymnasts, will demonstrate substantial translation on these laxity tests even though they are asymptomatic.

  • The amount of translation on laxity testing is determined by the length of the capsule and ligaments as well as by the starting position (i.e. more anterior laxity will be noted if the arm is examined in internal rotation - which relaxes the anterior structures, than if it is examined in external rotation - which tightens the anterior structures).

  • Use the contralateral shoulder as an example of what is 'normal' for the patient.

1. Drawer Test

The patient is seated with the forearm resting on the lap and the shoulder relaxed. The examiner stands behind the patient. One of the examiner's hands stabilizes the shoulder girdle (scapula and clavicle) while the other grasps the proximal humerus. These tests are performed with (1) a minimal compressive load (just enough to center the head in the glenoid) and (2) with a substantial compressive load (to gain a feeling for the effectiveness of the glenoid concavity). Starting from the centered position with a minimal compressive load, the humerus is first pushed forward to determine the amount of anterior displacement relative to the scapula. The anterior translation of a normal shoulder reaches a firm end-point with no clunking, no pain and no apprehension. A clunk or snap on anterior subluxation or reduction may suggest a labral tear or Bankart lesion. The test is then repeated with a substantial compressive load applied before translation is attempted to gain an appreciation of the competency of the anterior glenoid lip. The humerus is returned to the neutral position and the posterior drawer test is performed, with light and again with substantial compressive loads to judge the amount of translation and the effectiveness of the posterior glenoid lip, respectively.(Silliman and Hawkins, 1993)

2. Sulcus Test

The patient sits with the arm relaxed at the side. The examiner centers the head with a mild compressive load and then pulls the arm downward. Inferior laxity is demonstrated if a sulcus or hollow appears inferior to the acromion. Competency of the inferior glenoid lip is demonstrated by pressing the humeral head into the glenoid while inferior traction is applied.

3. Push-Pull Test

The patient lies supine with the shoulder off the edge of the table. The arm is in 90 degrees of abduction and 30 degrees of flexion. Standing next to the patient's hip, the examiner pulls up on the wrist with one hand while pushing down on the proximal humerus with the other. The shoulders of normal, relaxed patients often will allow 50 per cent posterior translation on this test.

Stability Tests

  • These tests examine the ability of the shoulder to resist challenges to stability in positions where the ligaments are normally under tension.

1. Fulcrum Test

The patient lies supine at the edge of the examination table with the arm abducted to 90 degrees. The examiner places one hand on the table under the glenohumeral joint to act as a fulcrum. The arm is gently and progressively extended and externally rotated over this fulcrum. Maintaining gentle passive external rotation for a minute fatigues the subscapularis, challenging the capsular contribution to the anterior stability of the shoulder. The patient with anterior instability will usually become apprehensive as this maneuver is carried out (watch the eyebrows for a clue that the shoulder is getting ready to dislocate). In this test, normally no translation occurs because it is performed in a position where the anterior ligaments are placed under tension.

2. Crank or Apprehension Test

The patient sits with the back toward the examiner. The arm is held in 90 degrees of abduction and external rotation. The examiner pulls back on the patient's wrist with one hand while stabilizing the back of the shoulder with the other. The patient with anterior instability usually will become apprehensive with this maneuver. As for the fulcrum test, no translation is expected in the normal shoulder because this test is performed in a position where the anterior ligaments are placed under tension.

3. Jerk Test

The patient sits with the arm internally rotated and flexed forward to 90 degrees. The examiner grasps the elbow and axially loads the humerus in a proximal direction. While axial loading of the humerus is maintained, the arm is moved horizontally across the body. A positive test is indicated by a sudden jerk as the humeral head slides off the back of the glenoid. When the arm is returned to the original position of 90-degree abduction, a second jerk may be observed, that of the humeral head returning to the glenoid.

Strength Tests

The strength of abduction and rotation are tested to gauge the power of the muscles contributing to stability through concavity compression. The strength of the scapular protractors and elevators are also tested to determine their ability to position the scapula securely.

Shoulder Examination

Look

From the front, side and above

  • Asymmetry, scars, deltoid wasting, SCJ or ACJ deformity, swelling of the joint

From behind

  • Look and feel for rotator cuff wasting, scapula shape and situation e.g. winging, Sprengel shoulder etc

Feel

  • SCJ to the ACJ and acromion
  • Greater and lesser tuberosity, feel for rotator cuff defects
  • Glenohumeral joint: anterior and posterior aspects
  • Biceps tendon/bicipital groove
  • Spine of scapula

Move

ALWAYS EXAMINE THE CERVICAL SPINE FIRST

  • Move both arms at the same time. Active then passive ROM.
  • Quick screening test: "Arms above the head and behind the back "
  • Flexion : 0-180 o
  • Abduction : 0-180 o check for painful arc and watch the scapulothoracic rhythm
  • If restricted then repeat with the scapula fixed to check for the amount of glenohumeral movement
  • Internal rotation: T4
  • External rotation : 70 o

Feel for crepitation during motion

Special tests

1. Impingement

  • Neer's sign: Hold scapula down, pronate forearm and flexion will cause pain
  • Hawkin's test: Flexion to 90 o internal rotation will cause pain
  • Neer's test: Pain caused by Neer's test eliminated by local anaesthetic injection
  • Scarf test: forced cross body adduction in 90 o flexion, pain at the extreme of motion indicative of ACJ pathology

2. Rotator cuff Integrity

Supraspinatus/anterosuperior cuff:

  • Resisted abduction with arms by side
  • Jobe's test: arm abducted to 20, in the plane of the scapula, thumb pointing down

Infraspinatus+teres minor/posterior cuff:

  • Resisted ER with the arms by side
  • Drop test : with arms fully ER by side (= massive infraspinatus tear)
  • Patte's test: 90 o flexion, flexed elbow and resisted external rotation
  • Hornblower's sign (Emery): similar to Patte's test inability to ER & Abduct from hand in front of mouth (against gravity)
  • Hornblower's sign (JBJS, 1998) / Drop test: with arm in 90 o abduction & ER, elbow 90 o (+ve = massive tear of both infraspinatus and teres minor and operative repair will result in 50% failure)
  • Pointing elbow test: place hand on opposite shoulder and ask pt to hold shoulder flexed to 90 o

Subscapularis/anteroinferior cuff:

  • Gerber's lift off test: push examiner's hand away from 'hand behind back position' (eliminates pectoralis major)
  • Internal rotation lag sign: inability to hold hand away from back
  • Napoleon test: if pt cannot fully internally rotate, push on their belly, elbow will drop backwards if +ve

Biceps

  • Check for long head of biceps rupture
  • Speed's test: supinated arm flexed forwards against resistance pain felt in the bicipital groove indicates biceps tendon pathology
  • Yergason's test: feel for subluxation of the biceps tendon out of the bicipital groove when the arm is gently internally and externally rotated in adduction
  • AERS test: Abduction External Rotation Supination test. Pt feels pain on resisted supination in this position. Test with elbow abducted & ER to 90 o .

Deltoid: resisted abduction at 90 o

Serratus anterior : "Winging" test

3. Instability testing

Patient supine
  • Anterior and posterior draw "Lachmann of the shoulder"(Gerber and Ganz)
Patient seated
  • Inferior draw "sulcus sign"
  • Anterior subluxation test: abduction and external rotation "apprehension test" with thumb posteriorly and fingers anteriorly over humeral head
  • Posterior subluxation test: internal rotation, adduction, flexion and push posteriorly

Imaging

XR: AP, Lateral/axial/trans-scapular/Wallace, sub-acromial view

CT: good for glenoid fractures

MR: Good for labral tears anteriorly-inferiorly-posteriorly. Not superiorly

OK for rotator cuff pathology

USS: Now thought to be superior to MR for rotator cuff pathology but operator dependent

Short Case Examination Tips / Approach

Look at the:

  • Patient

  • Problem

  • Props (aids, testing devices etc.)

Ask:

  • about tender areas

Feel

Move

  • Active

  • Passive

Special Tests


Neurological Problem

  • Test sensation before motor

  • Patient

  • Problem

  • Props (aids, testing devices etc.)

Ask:

  • about tender areas

Feel

Move

  • Active

  • Passive

Special Tests


Neurological Problem

  • Test sensation before motor

RUPTURE OF THE CENTRAL SLIP OF THE EXTENSOR HOOD OF THE FINGER. A TEST FOR EARLY DIAGNOSIS

By Elson, R. A.

JBJS - VOL. 68-B, NO. 2, MARCH 1986, pp. 229-231

From the Northern General Hospital, Sheffield

ABSTRACT: Closed rupture of the middle slip of the extensor hood of a finger is easily missed until the late appearance of a buttonhole deformity. Early diagnosis gives the best chance of satisfactory treatment, but Boyes' test becomes positive only at a late stage. A new test is described in which, from a 90 degrees flexed position over the edge of a table, the patient tries to extend the proximal interphalangeal joint of the involved finger against resistance. The absence of extension force at the proximal joint and fixed extension at the distal joint are immediate signs of complete rupture of the central slip. The theoretical basis and the method of performing the test are discussed. END OF ABSTRACT

Closed rupture of the central slip of the extensor tendon hood of the finger can easily be missed at an initial examination, even when it is suspected. Later, a classic buttonhole deformity will develop, but by then correction is difficult. Early diagnosis is essential for successful treatment. Boyes (1970) described a test for the integrity of the central slip. If the proximal interphalangeal joint is held passively extended, it is then possible for the normal individual to flex the terminal interphalangeal joint in isolation. However, if the central slip has been ruptured, there is increasing difficulty in performing this action. Unfortunately this test only becomes positive when the proximal part of the ruptured central slip has retracted and become adherent to the surrounding tissues. The test which is described below becomes positive immediately after complete rupture of the central slip.

Anatomy

The extensor mechanism of the human finger is complex, but its basic pattern is of three relatively uncompliant bands: one central slip and two lateral bands. These arise from the extensor communis tendon (Fig. 1). During flexion of a finger at both interphalangeal joints, the extensor hood mechanism moves distally, but the lateral bands must travel further than the central slip because they cross two joints. In addition, the finger lengthens during flexion because of the shape of the condyles of the middle and proximal phalanges, a point emphasised by Stack (1962). Harris and Rutledge (1972) demonstrated that, during flexion, the lateral bands sublux in a volar direction on either side of the head of the proximal phalanx, a movement facilitated by the conical shape of the bone. They also showed that during extension, the lateral bands recover their position on the dorsum of the finger and that this is not due to any elastic recoil from the triangular ligament. This could be divided; the lateral bands still returned to their dorsal position on extension provided that the central slip was intact (Fig. 2). Few individuals can flex the interphalangeal joints independently; this is because both flexor profundus and flexor superficialis act on the check-rein afforded by the extensor hood with its three uncompliant components. Action by the profundus tendon alone must take up the slack in the extensor hood as a whole and result in simultaneous flexion of both interphalangeal joints. Flexor superficialis acting alone must draw the hood distally, relaxing the lateral bands and allowing weak flexion of the distal joint by the normal tone of the flexor profundus. The well-known manoeuvre first described by Apley in 1956 demonstrates the integrity of flexor superficialis to one finger by neutralising the action of its profundus tendon and thus allowing the proximal interphalangeal joint to move in isolation.

Independent flexion of the distal interphalangeal joint can be achieved by holding the proximal joint in full extension. The action of flexor superficialis is blocked and flexor profundus can act on the distal joint alone (Fig. 3). When it does so, the lateral bands tighten, drag the extensor hood distally, and relax the central slip (which relates to the mechanism of Boyes' test). Some individuals with hypermobile proximal interphalangeal joints, can hyperextend and lock the joint in this position by the action of the central slip. They are then able to contract the profundus tendons to all the fingers and produce the unusual posture shown in Figure 4.

Theoretically, the oblique retinacular ligaments of Landsmeer (1949) should preclude flexion at the distal interphalangeal joint while the proximal joint is fully extended, but in practice, as shown above, this is not the case. Only later may contracture of the retinacular ligaments contribute to holding the lateral bands in subluxation; they play no effective part in the findings in acute injury. This was recognised by Harris and Rutledge (1972) and by Bendz (1985). The retinacular ligaments may therefore be neglected in describing the new test.

When the proximal interphalangeal joint is held at 90 degrees flexion the central slip is drawn distally and the lateral bands therefore become slack unless the distal joint is also flexed; this is easily demonstrated (Fig. 5), and it is in this posture that the new test is effective.

Test for integrity of the central slip.

The finger to be examined is flexed comfortably at a right angle at the proximal interphalangeal joint, over the edge of a table and firmly held in this position by the examiner (Fig. 6). The patient is then asked to attempt gently to extend the proximal interphalangeal joint. Any pressure felt by the examiner through extension of the middle phalanx in the posture described can only be exerted by an intact central slip. Final proof is that the distal interphalangeal joint remains flail during this effort, since the competent central sip prevents the lateral bands from acting distally.

In the presence of complete rupture of the central slip, any extension effort perceived by the examiner will be accompanied by rigidity at the distal interphalangeal joint with a tendency to extension (Figs 7 and 8). This is produced by the extensor action of the lateral bands alone. This test will not demonstrate partial rupture of the central slip, and its performance may be impeded by pain or by lack of co-operation from the patient. Pain can be relieved, if necessary, by proximal infiltration of the dorsal nerves of the finger.

Boyes' test for rupture of the central slip uses a different mechanism. It depends upon retraction of the proximal end of the ruptured central slip and its adhesion to surrounding tissues, and will, therefore, not become positive until these adhesions have developed. Irrespective of the chosen method of treatment, it is clear that early diagnosis of complete rupture of the central slip is essential; this can be achieved by the test which has been described.

Article Figure Legends

FIGURE 1: Diagrams to show the central slip and one of the lateral bands arising from point X. Distal pull on the central slip relaxes the lateral band, while a distal pull on the lateral band relaxes the central slip. These effects can readily be demonstrated in a fresh dissection.

FIGURE 2: Diagram of the distal end of a proximal phalanx, to show the conical shape which facilitates volar displacement of the lateral bands during flexion of the proximal interphalangeal joint. During extension they move in the direction indicated by the arrows provided that the central slip is intact (modified from Harris and Rutledge 1972).

FIGURE 3: If the proximal joint is held extended by an examiner, isolated flexion of a normal distal interphalangeal joint is possible. This is not possible once adhesions have developed after a rupture of the central slip (Boyes' test).

FIGURE 4: In some individuals, hypermobility of the proximal interphalangeal joints allows them to lock into hyper-extension. The flexor profundus can then act in isolation on the distal joints. Locking is maintained by the bowstring tension induced in the lateral bands; in this position the central slip is relaxed because the lateral bands have pulled the extensor hood distally.

FIGURES 5 and 6: Diagram and photograph showing a normal proximal interphalangeal joint flexed passively to 90 degrees. The origin of the lateral bands is drawn distally by the intact central slip, which allows the distal joint to remain flail. Attempted active extension affects the middle phalanx but leaves the distal joint flail.

FIGURES 7 and 8: Diagram and photograph to show the effect of division of the central slip. This allows proximal movement of the origin of the lateral bands; they hold the distal joint in extension.

References

Apley AG. Test for the power of flexor digitorum sublimis. Br Med J 1956;i:25-6.

Bendz P. The functional significance of the oblique retinacular ligament of Landsmeer: a review and new proposals. J Hand Surg 1985;10-B:25-9.

Boyes J, reviser. Bunnell's surgery of the hand. 5th ed. Philadelphia: JP Lippincott, 1970:440-1.

Harris C Jr, Rutledge GL Jr. The functional anatomy of the extensor mechanism of the finger. J Bone Joint Surg [Am] 1972;54-A:713-26.

Landsmeer JMF. The anatomy of the dorsal aponeurosis of the human finger and its functional significance. Anat Rec 1949;104:31-44.

Stack HG. Muscle function in the fingers. J Bone Joint Surg [Br] 1962;44-B:899-909.