Orthopedic Neurology Page | Neuro-Anatomy

[Orthopedic Neurology] Page | 11

Neuro-Anatomy NNeeuurroonn::

Is the specialized cell of the nervous system that capable of electrical exciation (action potential) along their axons

22 | Page [Orthopedic Neurology]

Peripheral nerve has a mixture of neurons: 1]. Motor 2]. Sensory 3]. Reflex 4]. Sympathetic 5]. Parasympathetic

Types of fibers: A (α , , γ, δ), B, C Motor Sensory Ms reflex sympathetic Parasymp Neuron AHC Dorsal root ganglia AHC IHC relay at organ Root Anterior Dorsal root Ant Ant Ant Tract 1- Direct pyramidal

2- Indirect pyramid

1- Spinothalamic (Pain, temp, crude)

2- Lemniscal (DC) (proprioception, fine touch)

Stretch reflex arc from ms spindle

Fibre α Motor (12-20 μm) α Propriocep (12-20 μm) Touch, vib (5-12 μm) δ fast pain, temp (2-5μm) C Slow pain, crude (0.2-2µm)

γ fibers B preganglionic C Postganglionic

B fibres

A fibers are most affected by pressure C fibers are most affected by anesthesia and are the principle fibers in the dorsal root Neurons are surrounded by endoneurium mGroupToFor fascicles surrounded by

perineurium mGroupToFor nerve surrounded by epineurium MMuussccllee::

Motor unit is the unit responsible for motion and formed of the group of ms fibers and neuromuscular junction and feeding neuron

Ms fibers types: 1- Smooth ms fibers 2- Cardiac ms fibers 3- Skeletal ms fibers:

Type I: slow twitching, slow fatiguability, posture TypeII: fast twitiching, fast fatigue

MMSS CCOONNTTRRAACCTTIIOONN: is the active state of a ms, in which there is response to the neuron action potential either by isometric or iso tonic contraction

IISSOOMMEETTRRIICC CCOONNTTRRAACCTTIIOONN: is the contraction in ώ there is tension ώ out change in the ms length

IISSOOTTOONNIICC CCOONNTTRRAACCTTIIOONN: is the contraction in ώ here is a change in the length of the ms éout change in the tone

MMSS TTOONNEE: is the resting state of tension MMSS CCOONNTTRRAACCTTUURREE: is the adaptive structural changes in a

ms ð prolonged immobilization in a shortened position, in the form of shortening and fibrosis

MMSS WWAASSTTIINNGG: is the adaptive structural changes in a ms ð prolonged disuse of denervation, in the form of hypoplasias and hypotrophy, and eventually shortening and fibrosis

SSPPAASSTTIICCIITTYY:: Abnormal contraction of a ms in response to stretch. Growth of ms is impaired

RRIIGGIIDDIITTYY:: Involuntary sustained contraction of a ms not stretch-dependent. Growth of ms is fair


Sarcomere A band...................................... Actin + myocin (= H + overlap zone) H band .................................... Myocin M line ....................................... Myocin Interconnect I band........................................ Actin Z line ........................................ Actin Anchors

Contraction Definition Phases Isotonic Constant ms tension &

length (dynamic) Concentric: ms shortens during contraction Eccentric: ms lengthens during contraction

Isometric Constant ms length (static) Isokinetic Max contraction é constant

velocity over a full ROM Concentric Eccentric

Aerobic In the presence of O2 Replenishes 34 A TP via Kreb ’s Anerobic In the absence of O2 Glycolysis into lactic and 2 ATP ATP hydrolysis éout O2 ATP hydrolysis to produce direct, fast energy

Dermatome: o Is the area of skin supplied by a specific nerve root

Myotome o Is the group of muscles supplied by a specific nerve root

Sclerotome o Is the area of bone and fascia supplied by a specific nerve root

Sprain: o Tearing or injury of a non contractile motion unit, e.g. Ligament

Strain o Tearing or injury of a contractile motion unit, e.g. Muscle


Muscle injuries: 1]. Muscle Strain:

• Occurs at Musculo-tendinous junction of the ms that cross 2 joint (e.g. gastroc, hamstring)

• First there is inflammation then ends by fibrosis 2]. Muscle tears:

• Occurs at the Musculo-tendinous junction • During the higher eccentric contractions & Heal by dense scarring

3]. Muscle soreness: During the higher eccentric contractions 4]. Muscle denervation: Causes atrophy and sensitivity to acetyl-choline and fibrillation in

2wk TTeennddoonnss

• CCOOMMPPOOSSEEDD OOFF:: 1]. Collagen I ......................................... 80% 2]. Fibroblasts synthesis tropocollagens micro-fibrils sub-fibril fibril fascicle 3]. Loose areolar CT .......................... Endotenon epitenon paratenon

• TTYYPPEESS OOFF TTEENNDDOONNSS:: a. PPAARRAATTEENNOONN covered tendons rich capillary supply = better healing b. Sheathed tendons ....................... segmental bl.supply via mesotenon (VVIINNCCUULLAA)

• MMUUSSCCUULLOO--TTEENNDDIINNOOUUSS JJUUNNCCTTIIOONN:: 1]. Tendon 2]. Fibro-cartilage 3]. Mineralized fibrocartilage (SSHHAARRPPEEYY’’SS fibers) 4]. Bone

• HHEEAALLIINNGG SSTTAARRTTSS by fibroblasts and macrophages of the epitenon in 3 phases: 1]. ................................................................ Initial fibroblastic phase: 10 days (weak) 2]. ................................................................ Intermediate Collagen phase 30 days (most of

the strength is regained) 3]. ................................................................ Late remodeling phase 6 month (maximal

strength is regained) • Collagen tends to arrange along stress lines; so immobilization causes weak healing

LLiiggaammeennttss • CCOOMMPPOOSSEEDD OOFF::

1]. Collagen I (same ultrasturcture) ........ 70% 2]. Elastin 3]. Fibroblasts + Loose areolar CT

• BBLL SSUUPPPPLLYY is uniformly arranged via the ligament insertion at bone • Types of ligamentous insertions:

1]. Indirect: ............................................. superficial fr insert to periosteum @ acute angle 2]. Direct ................................................. Deep fr insert to bone @ 90º

• BBOONNYY LLIIGGAAMMEENNTTOOUUSS JJUUNNCCTTIIOONN:: 1]. Ligament 2]. Fibro-cartilage 3]. Mineralized fibrocartilage (SSHHAARRPPEEYY’’SS fibers) 4]. Bone

• HHEEAALLIINNGG starts by fibroblasts and macrophages of the epitenon Phase Time Process Strength 1].Hemostasis 10 min platelet plug fibrin clot Weak 2].Inflammatory 10 days macrophages debride granulation tissue Weak 3].Fibrogenesis 30 days UMC fibroblasts strong type I collagen most strength regained 4].Remodeling 6-18 mo Realignment & cross linking of collagen bundles Max strength

• LLIIGGAAMMEENNTTSS GGRRAAFFTTIINNGG:: 11]].. Autografts: ..................................................... Faster healing, no disease transmission 22]].. Allograft: ......................................................... no donor morbidity but may transmit diseases 33]].. Synthetic: (Gortex, Leeds Keio) ................ no initial weakness, but cause sterile effusion


Tendon Transfers Definition

A tendon transfer is a procedure in which the tendon of insertion or of origin of the functioning muscle is mobilized, detached or divided and reinserted into a bony part or onto another tendon, to supplement or substitute for the action of the recipient tendon, in order to correct muscle imbalance and keep the corrected position rather than to correct a deformity

Indications 1]. Irreparable nerve damage 2]. Loss of function of a musculotendinous unit due to trauma or disease 3]. In some nonprogressive or slowly progressive neurological disorders

Contraindications 1]. Unstable joint 2]. Stiff joint 3]. Fixed deformity 4]. Advanced arthritis 5]. If affection of all muscles at the same degree 6]. If no suitable tendon or muscle is available for transfer

Principles Preoperative

1]. Age: It is better to delay operations >5y so you can get cooperation in physiotherapy:

o If the patient is skeletally immature do tendon transfers (TT) o If the patient is skeletally mature do fusion + removal of appropriate wege ± TT o If the patient is has talipes valgus add stabilizing bony op. e.g. Grice Green or Evans

2]. Timing: Early tendon transfers – within 12 weeks of injury: If no chance of functional recovery, transfers

should be performed ASAP Late tendon transfers -- If reasonable return of function not present for 3m after the expected Following nerve injury repair, the date of expected recovery can be calculated by measuring the

distance between the injury to the most proximal muscle supplied, assuming a rate of regeneration of 1mm/day

3]. Planning Make a list of deficient functions Make a list of available donor muscles Availability of tendon for transfer:

o If many tendons are available do tendon transfers for all deficient muscles o If 2 tendons are available do TT for the most crucial functional muscle o If one agonist tendon is available do TT to the middle line e.g. Tohen transfer o If one antagonist tendon do split TT & suture under equal tension

Operative

Joint: 1]. Should be stable 2]. Should be a freely mobile joint (free ROM) 3]. Should not have fixed deformity 4]. Should not have advanced arthritis


Muscles: 1]. Adequate donor muscle Strength (G IV, V) 2]. Adequate recipient muscle Excursion:

o Wrist flexors ......................................... 33cm o Finger extensor ................................... 50cm o Finger flexor ......................................... 70cm

3]. Adequate neurologic & blood supply 4]. Agonists better than antagonists 5]. Synergestic better than non synergestic 6]. Start Proximal then distal

Tendon 1]. Should be of an adequate Length 2]. Should pass in a Straight line 3]. Should pass through a Gliding Medium (the best is fat or superficial fascia) 4]. Should be sutured under Moderate Tension 5]. Should be Covered 6]. Better to suture tendon To Bone (pull-out technique)

Techniques 1]. Multiple short transverse incisions rather than long longitudinal incisions 2]. Careful tendon handling 3]. Joining the tendons

o End to end anastomoses o End to side anastomoses o Side to side anastomoses o Tendon weave procedures can all be used

4]. Achieving proper tension - No general rule, but reasonable to place limb in the position of maximal function of the tendon transfer and suture without tension

Postoperative: 1]. Protect the transferred tendon to avoid stretching 2]. Physiotherapy & training

Famous Transfers Pronator teres to ECR FCU to EDL Palmaris longus to EPL (or split FCU) ECRL to sublimis or profundus Tibialis anterior & Peroneus brevis are preferred in the transfer as Tibialis posterior & Peroneus

longus are important for foot arch Skeletally immature with Varus (alone or with other deformities)

In Drop foot (NO deformity) + skeletally immature Tibialis posterior is the ONLY tendon available for transfer


Cerebral Palsy Definition

Disorder of movement and posturing Caused by static non progressive brain UMNL lesion Acquired during the stage of rapid brain development (perinatal)

Classification 1- Spastic ............................................................................. (60%)

oo MMOOSSTT AAMMEENNAABBLLEE TTOO SSUURRGGEERRYY o UMNL involvement - mild to severe motor impairment o Contractures:

% Walking limb № UL:LL Associated problems 1- Hemiplegia 40 3mo later than N 2 UL>LL Mild learning

Seizures 2- Diplegia 30 4y 4 LL>UL Delayed develop milestones

Strabismus 3- Quadriplagia 25 25% at 7y 4 UL=LL Floppy baby

pseudobulbar palsy fail to thrive IQ, hearing, vision

4- Monoplagia 4 as hemi 1 5- Double hemi <1 4 UL>LL As hemi 6- Total body <1 4 Severe trunk, neck, limb affection 7- Triplagia ? 3

2- Hypotonic Usually a stage through which an infant passes. 3- Hemiballistic Sudden movements . As if throwing ball. 4- Ataxic ...................................................................................................... 10 %

o Involvement of the cerebellum or its pathways o Weakness, incoordination, and intention tremor unsteadiness, wide based gait oo PPOOOORRLLYY AAMMEENNAABBLLEE TTOO SSUURRGGIICCAALL CCOORRRREECCTTIIOONN

5- Combination 6- Athetoid / Dyskinetic .................................................................... 20%

o Writhing involuntary movements: é excited, wriggle as if tickled. é sleep o ð basal ganglia involvement (deposition of bilirubin or erythroblastosis fetalis) o Hips & knees ext+ stepping gait + Lean backward, shouler & trunk extension. o Intelligence normal (often above average) o MMOOSSTT DDIIFFFFIICCUULLTT TTOO CCOORRRREECCTT - results are unpredictable & POP hazardous ð friction o Types:

1- TTEENNSSIIOONN AATTHHEETTOOSSIISS:: Child is hypertonic but not hyperreflexive (no clonus or Spasticity) Deafness and absence of an upward gaze.

2- DDYYSSTTOONNIICC AATTHHEETTOOSSIISS:: Continuous, tortuous, slow, twisting type of motion. All extremities, as well as the neck and trunk, tend to be involved.

3- CCHHOORREEIIFFOORRMM AATTHHEETTOOSSIISS. More common than dystonic athetosis Continual movement of the patient's wrist, fingers, ankles, toes, and

tongue. 4- DDRRAAMMAATTIICC BBAALLLLIISSMMUUSS AATTHHEETTOOSSIISS.

Continuous dramatic movement of the trunk and proximal extremities These patients can injure themselves or their caregivers by this

5- RRIIGGIIDD AATTHHEETTOOSSIISS The most hypertonic & stiff of all CP (Yet no spasticity or clonus)


Epidemiology 1-5 in 1000 live births. More common in advanced countries (ð Advanced perinatal care)

Aetiology 1- Prenatal ............................................................ (30%)

o Maternal infection - Toxoplasmosis . Rubella . Cytomegalovirus . Herpes . Syphilis o Maternal exposure - Alcohol . Drugs o Congenital brain malformations

2- Perinatal o Difficult prolonged labour ð Birth wt >2.5kg (25-40%) o Anoxia .................................................... (10-20%)

3- Postnatal ........................................................... (10%) o Encephalitis o Head injury o Carbon Mono Oxide poisoning

Pathogenesis 1- Brain Damage: according to the site of involvement:

Area 6 precentral gyrus: ................... SSPPAASSTTIICC UUMMNNLL Area 4 precentral gyrus: ............... FFLLAACCCCIIDD UUMMNNLL Combined: .................................... RRIIGGIIDDIITTYY Basal ganglia: ................................ AASSTTHHEETTOOSSIISS Cerebellum: ................................... AATTAAXXIIAA Mid brain: .............................................. TTRREEMMOORRSS

2- Weakness Loss of voluntary movement & Weakness (ð co contraction of agonist & antagonist)

3- Spasticity Feature of all lesions of pyramidal system: Cerebral, capsular, pontine, midbrain lesions Related to DDIISSIINNHHIIBBIITTEEDD SSTTRREETTCCHH RREEFFLLEEXX ώ is regulated by descending tracts SSPPAASSTTIICCIITTYY, HHYYPPEERR--RREEFFLLEEXXIIAA, CCLLOONNUUSS may appear CCLLAASSPP--KKNNIIFFEE PPHHEENNOOMMEENNOONN:: Attempt to change position initial resistance + quickly yield

4- Contracture. Normally ms adds sarcomeres at musculotendinous junction in response to constant

stretch When muscles spastic, this mechanism cannot occur relative shortening of ms in

contrast to bone prolonged shortening and contracture

5- Deformity ð unopposed muscle contracture. Hip Adduction Flexion Flexion + IR Dislocation Knee Flexion Recurvatum Genu valgum Patella alta Ankle Eqinovarus Equinovalgus calcaneus Claw & metatarsus UL shoulder add IR Elbow flex Wrist & finger flex Thumb in palm

1. Hip dislocation: (usually correct 1ry 1st)

1ry: ð paralyzed abductors & extensors (antigravity ms) + good antagonists 2ry: ð adaptive changes:

o Coxa valga: ð absent gluteal pull o Shallow acetabulum o Lax capsule

2. Knee Flexion deformity 1ry: ð tight hamstring Or tight Gracilis 2ry: compensation to hip flexion deformity or equinus Prolonged flexion deformity lengthening of patellar tendon & tight lateral retinaculum


Clinical Feature History Abnormal birth history & Prematurity Neonatal nursery Delayed Developmental milestones (brackets are 95th percentile)

o Head control ................................. 3 mo ........................ (6 mo) o Sitting independently ................ 6 mo ........................ (9 mo) o Crawling ......................................... 8 mo ........................ (never) o Pulling to stand ............................ 9 mo ........................ (12 mo) o Walking ........................................... 12 mo ....................... (18 mo)

Examination General:

1. Mentality 3- Speech 2. hearing 4- Vision

Gait: 1- Trunk leans forward,, SSCCIISSSSOORRIINNGG,, SSTTIIFFFF--LLEEGGGGEEDD,, TTIIPP--TTOOEE GGAAIITT,, CCRROOUUCCHHEEDD 2- Stride length, Narrow walking base 3- Lordosis . Co-ordination in turning.

Hip deformities: 1- Adduction: ..................................... ð adductor spasm ((GGRRAABB TTEESSTT ++VVEE Hip Abduction)) 2- Flexion: ........................................... ð rectus spasm .............. ((EELLYY && TTHHOOMMAASS && SSTTAAHHEELLII ++VVEE)) 3- Flexion internal rotation: ........... ð psoas spasm (tru e scisso rin g ≠ p seu d o scissorin g ð

flexion + anteversion ++VVEE WW SSIIGGNN) 4- Hip dislocation ............................... ð 1ry & 2ry .............. ((GGAALLEEAAZZZZII TTEESSTT ++VVEE))

WWIINNDDSSWWEEPPTT PPOOSSTTUURREE - one hip adducted & other side abducted SSCCIISSSSOORREEDD GGAAIITT if bilateral Apparent LLD if unilateral SSTTAAHHEELLII TTEESSTT is better than Thomas as it is not affected by the other side lumbar lordosis + prominent bottom é standing / sacrofemoral angle SLR because of flexed pelvis from FFD.

Knee deformities: 1- Knee flexion contracture (tight hamstring): ....... ++VVEE TTRRIIPPOODD SSIIGGNN && TTOOEE TTOOUUCCHH 2- Knee recurvatum .................... ................................... RREEVVEERRSSEEDD PPOOPPLLIITTEEAALL AANNGGLLEE 3- Genu valgum 4- Patella alta (BBLLUUEEMMAANNSSAAAATT, IINNSSAALLLL--SSAALLVVAATTII RRAATTIIOO<1) ð flexed knee & quad spasm

Flexion deformity angle is best assessed by the popliteal angle Flexion contracture lead to CCRROOUUCCHHEEDD GGAAIITT (also ð hip flexion & calcaneus) Tight rectus femoris stiff legged gait (prolonged stance & diff. foot clearance) Sitting - Legs forward

Ankle deformities: 1- Ankle EEQQUUIINNUUSS (NB, False equinus = flexed knee lifts heel from ground) 22-- CCAALLCCAANNEEUUSS 33-- VVAARRUUSS 44-- VVAALLGGUUSS 55-- CCLLAAWW TTOOEESS 66-- MMEETTAATTAARRSSUUSS AADDDDUUCCTTUUSS

TTIIPPTTOOEE GGAAIITT SSIILLFFVVEERRSSKKIIÖÖLLDD TTEESSTT:: equinus é knee flexion = gastroc tight > soleus Equinus knee recurvatum in stance phase Calcaneus crouch gait

Kneeling eliminates contracture effect


Upper limbs 1- Shoulder adduction internal rotation 2- Elbow flexion 3- Forearm pronation 4- Wrist & finger flexion 5- Thumb in palm o Hand placement. Ask patient to place hand on knee and then head. o Stereognosis. Test ability to recognise shape in palm Spine o Scoliosis usually present at age 5. Reaches 50º. by age 15 o Treated initially with chair that fits the curve. o Braces of little benefit. Only 15% respond. o If curve reaches 60º segmental fusion indicated. o Indications for Surgery = curves > 50º. or progression > 10º. o Scoliosis curves are divided into Group 1 (ambulators) or 2 (non-ambulators):

Group 1 double small curves- thoracic & lumbar Posterior fusion Luque rods & sublaminar wires Group 2 large thoracolumbar or lumbar curve

pelvic obliquity Ant + Post Fusion Luque rods & sublaminar wires &

Galveston pelvic fixation

Neurology o CCLLAASSPP--KKNNIIFFEE phenomenon o Primitive reflexes:

A, AASSYYMMMMEETTRRIICCAALL TTOONNIICC NNEECCKK: as head is turned to one side, contralateral arm and knee flex. B, MMOORROO RREEFFLLEEXX: Hold child at 45o. Allow head to drop back, UL extend away from body and then come together in embracing pattern. C, EEXXTTEENNSSOORR TTHHRRUUSSTT: as child is held upright by armpits, lower extremities stiffen out straight. D, NNEECCKK--RRIIGGHHTTIINNGG RREEFFLLEEXX: as head is turned, shoulders, trunk, pelvis, and lower limbs follow turned head. E, PPAARRAACCHHUUTTEE RREEAACCTTIIOONN: as child is suspended at waist and suddenly lowered forward toward table, arms and hands extend to table in protective manner. F, SSYYMMMMEETTRRIICCAALL TTOONNIICC NNEECCKK: as neck is flexed, arms flex and legs extend. Opposite occurs as neck is extended. G, FFOOOOTT PPLLAACCEEMMEENNTT RREEAACCTTIIOONN: when top of foot is stroked by underside of flat surface, child places foot on surface.


If any 2 of 7 are inappropriate by 1y it is highly unlikely to walk independently

Radiography: Hip: WWIIBBEERRGG CE angle MP of RREEIIMMEERR (migration percentage = head coverage %) Sacrofemoral angle: between top of sacrum and femoral shaft (N 40-60º) in FFD Acetabular dysplasia Dislocation

Knee: Flexion Deformity Recurvatum Insall-Salvati Ratio <1 Blumansaat Line Below The Patella Alta

Principle Diagnostic Features:

UMNL Delayed milestones Persistent Primitive reflexes Abnormal posture & movement

Potential for walking

Assess (midbrain & perinatal)

If mid brain reflexes appear(early balance reaction)

Parachutte reflexStepping

Can walk

Perinatal reflexes persist >1y(normally disappear at 4-6m)

MoroTonic neck (symmetric & asymm)Neck righting (body follow head turn)Extensor thrust on vertical susp

Will not walk


AApphhoorriissmmss.. A little equinus better than calcaneus. A little valgus better than varus. A little varus better than a lot of valgus. A little knee flexion better than recurvatum.

Treatment of CP PPrriioorriittiieess Patient priorities are

1]. Communication 2]. Activities of daily living 3]. Mobility & Walking

OObbjjeeccttiivveess 1]. Maintain straight spine and level pelvis 2]. Maintain located, mobile, painless hips 3]. Maintain mobile knees for sitting and bracing for transfer 4]. Maintain plantigrade feet 5]. Provide maximal functional positions for sitting, feeding, and hygiene 6]. Provide appropriate adaptive equipment, incl. Wheelchairs 7]. Avoid hip dislocation.

o Painful o Make nursing difficult o pelvic obliquity & scoliosis difficult wheelchair ambulation o quality of life.

8]. Strategy o 0-3 y ................................... physiotherapy o 4-6 y ................................... surgery o 7-18 y ................................. schooling and psychosocial development o 18 yrs + ............................... work, residence and marriage.

LLOOWWEERR LLIIMMBBSS

1- PPHHYYSSIIOOTTHHEERRAAPPYY - physiotherapy approaches contractures or development, ROM: o Neurodevelopmental approach ( exaggerated reflexes by certain positions) o Sensorimotor approach ( exaggerated reflexes by sensory ) o Proprioceptive approach (proprioception used to improve posture) o Neuromuscular reflex approach (graduated pattern of movement learning)

2- CCAASSTT CCOORRRREECCTTIIOONN - Inhibitive casting. Stimulation of sole can cause muscles to contract was basis of inhibitive casting. Not used much now.

3- CCOORRRREECCTTIIVVEE CCAASSTTIINNGG - for mild fixed equinus. Well-padded POP é max dorsiflexion 4- BBRRAACCIINNGG - Useless for treating fixed deformity AFO's useful for Dynamic equinus 5- NNEEUURROOSSUURRGGEERRYY - Selective posterior RRHHIIZZOOTTOOMMYY of rootlets used. Via laminectomy. 30-70%

of posterior rootlets cut. Decreases feedback from stretch receptors. Can rootlets to find which mediate spinal reflex. If only these cut, sensation unchanged. Results promising.

6- CCHHEEMMOONNEEUURREECCTTOOMMYY: selective neurectomy is done using certain chemical substances: aa.. AALLCCOOHHOOLL 45% gives improvement for 6 wks bb.. PPHHEENNOOLL 5% 2ml gives permanent effect cc.. BBOOTTUULLIINNUUMM TTOOXXIINN gives 6m improvement ( acetyle choline) dd.. BBAACCLLOOFFEENN intrathecal implanted pump (GABA agonist excitatory

transmitters)


AADDDDUUCCTTEEDD SSUUBBLLUUXXEEDD HHIIPP Assess RMP

<50% >50%

Bony operations

Soft tissue operations

>50% MP Hip Dysplasia Dislocated >45° flexion Subluxed <30°Abd

VDO Total Add tenotomy ±

Psoas

Adductor Brevis

lengthen

Ant. Obturator nurectomy

Acetabulo-plasty

OR+VDO+ Chiari

<5y <50% MP No dislocation

7- Orthopaedic operations

IInnddiiccaattiioonnss:: 1]. Postural contractures 2]. Correction of fixed deformities 3]. Stabilizing unstable joints 4]. Spastic CP: Quadri hip release at 3y / hemi TAL at 4y / Diplegics 5y hip release 5]. Rigidity signify marked brain damage so only correct severe deformities 6]. Tendon transfers: remove the dynamic force and serve as motorized tenodesis (unlike

polio and nerve injury where it act as coordinated functional solution): 1- Impaired & slow voluntary control 2- Spasticity &sensory problems 3- Dysphasic contractions i.e. antagonistic activity unrelated to the action 4- Skilled coordinated learning of movement after transfer is difficult

7]. Athetosis will not benefit from transfer as this shift the problem to another region not ttt AA.. HHiipp PPrroocceedduurreess:: 1. Hip at risk :

<50% RREEIIMMEERR’’SS MMIIGGRRAATTIIOONN PPEERRCCEENNTTAAGGEE Abduction < 25º Broken Shenton Treated by psoas, adductor and hamstring LLEENNGGTTHHEENNIINNGG.

2. Subluxed hip é RMP > 50%. VVAARRUUSS DDEERROOTTAATTIIOONN OOSSTTEEOOTTOOMMYY

3. Adducted hip: CCOOMMPPLLEETTEE AADDDDUUCCTTOORR TTEENNOOTTOOMMYY ± obturator neurectomy All the Add longus, brevis, most of magnus, & gracilis Still the patient can adduct with pectineus

4. Adducted subluxed hip:


5. Flextion deformity (<20º may correct by traction) 1]. SSOOUUTTTTEERR’’SS sartorius, rectus, & tensor fascia lata (flexor release) via Smith Peterson 2]. MMUUSSTTAARRDD:: iliopsoas tendon transfer to GT 3]. SSHHAARRRRAARRDD: iliopsoas transfer + iliacus insertion transfer

from anterior to posterior iliac wing, the latter can compensate for Glut maximus

4]. All followed by hip spica in neutral rotation and sagittal 5]. Other alternative: OOBBEERR’’SS operation (sacrospinalis

transfer to act as hip extensor

6. Flexion + internal rotation

7. Dislocation:

8. Pelvic obliquity

Flexion

Flexion Pure

Sou tter’s Then do Thomas test

Still there is FFD

Mustard Sharrard

No FFD

Neutral spica

Flexion + IR

Flexible

Sou tter’s + ER spica

Iliopsoas recession to ant capsule

Lateralization of hamstring origin

Fixed

Soft + Derotation osteotomy

Dislocation

Painless Reducible

Correct Muscle

Sharrard or

Mustard

Correct valgus

VDO

Correct dysplasia

Salter Chiari

Painless Irreducible

Adductor release ±

neurectomy + traction

When head at acetab do

OR & proceed as

painless reducible

Painful Irreducible

Open reduction +

Fusion Schanz pelvic

support osteotomy

Fixed obliquity Dynamic obliquity PSF Abd release of opposite side

Address ipsilateral knee deformity & lig before hip fusion


BB.. KKnneeee PPrroocceedduurreess I. Flexion deformity:

Due to: AA.. 1ry hamstring Spasticity BB.. 2ry to hip FFD or equinus

Treatment:

1. EEGGGGEERR’’SS Hamstring transfer: Transfer the hamstring from the back of the tibia to the back of the femur Some advocated the lengthening of membranosus to prevent recurvatum Followed by a long leg cast for 6 wk Disadvantages:

A]. Genu recurvatum: contraindicated in equinus B]. lumbar lordosis CC]].. weak knee flexion

2. TTAACCHHDDJJIIAANN Fractional Lengthening of Hamstring Tendons: Z-plasty of gracilis and semitendinosus ± biceps + recession of semimembranosus

3. SSUUTTHHEERRLLAANNDD TTRRAANNSSFFEERR Lateral Transfer of Medial Hamstrings for Internal Rotational Deformity of Hip

4. GGAAGGEE DDIISSTTAALL RREECCTTUUSS TTRRAANNSSFFEERR + hamstring release Gives an advantage of enhancing the knee flexion in the swing phase

5. Ischeal tuberosity transfer to back of femur 6. EEVVAANN’’SS lengthening plasty 7. Selective neurectomy of hamstring 8. all may be added ITB division ± Extension osteotomy (better in polio)

Knee Flexion

Correctable

Check Hip & ankle for deformity

Fixed

+ Hip adductionTest abd in flexion & extension

Same= Gracilis

Adductor tenotomy ±neurectomy

in flexion= Hamstring

Eg g er’s release

+ IR

Eg g er’s + Gage

Pure Flexion

Eg g er’s R elease

Prolonged= Patellar

malalignment

Eg g er’s +Insall lat ret

release

Eg g er’s+

Patellar plication

Eg g er’s + Hauser


II. Knee Recurvatum: Recurvatum may be:

1]. 1ry: quadriceps spasticity or quadriceps spasticity > hamstrings & gastroc spasticity 2]. 2ry to Egger’s or Equinus (to detect equinus causation apply POP in dorsiflexion

and see if the recurvatum is corrected or not) Treatment:

1- Sage proximal rectus femoris Z plasty lengthening 2- Equinus TAL 3- Neurectomy of femoral nerve 4- Irwin femoral flexion osteotomy

III. Genu valgum: Usually ð:

1- hip adduction and coupled é Flexion IR 2- Tight ITB

Treatment: 1- Correct the hip via Adductor and iliopsoas release 2- Yount ITB resection 3- Supracondylar varus osteotomy

IV. Patella alta: ð quad spasm or long knee FFD ttt as in prolonged knee FFD

V. Patellar subluxation and dislocation: 1]. In valgus knee 2]. Flexion adduction and IR of the hip Q angle

Treatment: ttt the cause + Insall release of Fulkerson osteotomy


CC.. AAnnkkllee ddeeffoorrmmiittiieess::

Any calcaneus must have cavus as the pt can not walk on the heal only Calcaneocavus = calcaneus started 1st. Pes cavus means that the cavus started 1st. In skeletally immature; stabilizing operations are done only in valgus. In varus soft tissue op. When tendon transfer is considered if there is only one tendon then transfer it to the mid foot.

If many tendons then transfer one to the affected side. I. Equinus:

Pathology (5types according to Triceps surae vs Dorsiflexors): 1- Spastic vs spastic 2- Spastic vs normal 3- Spastic vs flaccid 4- Normal vs flaccid 5- Flaccid vs flaccid

The exact offending ms (gastroc or soleus) can be done by SSiillffvveerrsskkiiöölldd TTeesstt The muscle nature must be determined - spastic or contractured - by procain injection

Non Operative Ttt in the form of manual stretching, bracing, casting Operative Ttt: if failed non operative ttt:

1- Neurectomy: for spastic equinus (not contractures) & for clonus é WB cut it from origin or at insertion

2- Triceps surae release: a. SSiillffvveerrsskkiiöölldd Gastroc recession (spasm): distal recession of gastroc origin b. Gastroc slide (contracture): lengthening of gastroc tendon c. TAL (this is for gastroc and soleus after Silfverskiöld testing):

Strayer transverse release Vulpius V-shaped release Baker tongue shaped release Semi open (lateral distal release if equinovalgus) Percutaneus (medial distal release if equinovarus)

3- MMUURRPPHHYY Heel cord advancement: In spastic vs spastic dorsiflexors replacing TA more ant in front of FHL

II. Varus: Due to:

TP spasm TA or Tendoachillis tightness & evertor

weakness may assist

Treatment (according to rule no bony operation):

SSKKEELLEETTAALLLLYY IIMMMMAATTUURREE:: 1- TP Lengthening ((MMAAJJEESSTTRROO)) 2- TP Rerouting in front of med malleolus ((BBAAKKEERR)) 3- TP transfer via Interosseous membrane to dorsum of Foot ((BBIISSLLAA)) 4- TP split transfer to the proneus Brevis ((KKAAUUFFEERR)) 5- TA split transfer to the cuboid ((HHOOFFFFEERR)) 6- FDL & FHL transfer to Dorsum ((OONNOO)) 7- TA & EHL transfer to the mid dorsum or lateral Dorsum ((TTOOHHEENN))

SSKKEELLEETTAALLLLYY MMAATTUURREE:: Triple fusion + Laterally based wedge ((DDWWYYEERR)) + tendon transfer


Talipes EquinoValgus

Immature

TAL + post capsulotomy

P.Brevis to cunieform

Grice Green or Dillwyn Evan

Mature

Triple fusion Remove Med Wedge

Other soft tissue

III. Valgus: more common than varus o Pathology:

Usually it is associated with equinus More ð tight triceps surae (less ð evertor invertor imbalance) Dorsiflexion occur at the mid tarsal + eversion of the calcaneus + MT abduction Sustentaculum tali is shifted lat & downward talar head sublux medially

o Treatment:

GGRRIICCEE GGRREEEENN extra-articular lateral subtalar arthrodesis DDEENNNNYYSSOONN AANNDD FFUULLFFOORRDD MMOODDIIFFIICCAATTIIOONN uses screw between talus and calcaneus.

Iliac crest graft in sinus tarsi. Walking cast for 12 weeks. DDIILLLLWWYYNN--EEVVAANN’’SS transverse calcaneal osteotomy + fibular BG (lateral lengthening) Medial sliding calcaneal osteotomy may be done instead of medial closing

wedge IV. Calcaneocavus:

o Due to: 2ry to excessive TAL 1ry to spastic dorsiflexors (EDL & TA) in relation to weak Triceps surae

SSKKEELLEETTAALLLLYY IIMMMMAATTUURREE:: 2ry ................. Talectomy but painful pseudoarthrosis, LLD, deforming, one way 1ry ................. ▪ Partial EDL denervation

TA shortening & transfer to Tendo Achilles Cavus Steindler ± Samilson calcaneal crescent osteotomy Valgus Grice or Dillwyn

SSKKEELLEETTAALLLLYY MMAATTUURREE:: 1- There is tendon to transfer:

(1) EELLMMSSLLII 2 stage operation: Stage 1 Stage 2 Osteotomy Dorsal Wedge Posterior Wedge Fusion TNJ subtalar Cut Steindler TA + PL transfer to tendo-achilles POP Full dorsi-flexion to correct cavus In plantar flexion to aid healing

(2) Triple fusion + Tendon transfer 2- No tendon for transfer:

Pantalar fusion


V. Claw toes: o Neurectomy of the motor br of the lateral pantar nerve o Release of the insertion of the FDB

VI. Metatarsus adductus o Resection of the abductor hallucis & its tendon

Four Stages of Winter: Treatment Stage I Weak TA No tightness of triceps surae . AFO. Stage II Above + tight triceps surae + TP TA lengthening + split TP transfer. Stage III Above + quad & hams spasticity. + hams lengthening + rectus transfer Stage IV Above + hip flexor & add spasticity + psoas + adductor release.

DD.. UUppppeerr LLiimmbb ddeeffoorrmmiittyy::

I. Shoulder adduction internal rotation 1- SSEEVVEERR’’SS release: subscap, pec major, coracobrachialis, short head biceps, coraco-

humeral lig. 2- LL’’EEPPIISSCCOOPPOO ZZAACCHHAARRYY: Sever’s + Teres & latissimus transfer to post-lat aspect of prox

humerus 3- RROOTTAATTIIOONNAALL HHUUMMEERRAALL OOSSTTEEOOTTOOMMYY

II. Elbow flexion 1. Flexor tenotomy 2. Biceps transfer to triceps

III. Forearm pronation 1. Pronator tenotomy 2. FCU to ECR

Gershwind & Tonkin Classification TREATMENT Group 1 Active supination beyond neutral No surgery Group 2 Active supination to neutral or less Pron quad release ± flexor aponeurotic release Group 3 No active sup, loose passive sup Pronator teres transfer Group 4 No active sup, tight passive sup Pron quad release ± flexor aponeurotic release

IV. Wrist & finger flexion 1. Arthrodesis wrist 2. Release common flexor origin 3. FDP high cut & FDS low cut; then suture the tendons together

V. Thumb in palm 1. Cut pollicis (adductor, flexor, opponense) & 1st interossei 2. Tendon transfer to restore the thumb abduction: Pronator teres transfer

ZZAANNCCOOLLLLII CCLLAASSSSIIFFIICCAATTIIOONN TREATMENT 1 finger ext é wrist <20º flex Flexor Aponeurotic Release (FAR) ± FCU tenotomy 2A Finger ext é wrist > 20º flexion + active ext FAR + FCU tenotomy 2B same + No active wrist extensor FAR + FCU to ECRB 3 No Finger extension FCU to EDL or Prox row carpectomy or Wrist Fusion

or FDS to FDP.


It is a neuromuscular disorder 2ry to viral infection é subsequent development of deformities

Epidemiology It is considered to be eradicated from all the developed countries Our county is declared to be eradicated from endemic polio especially after free vaccination

programs (SSAABBIINN live attenuated vaccine oral drops, SSAALLKK IM killed vaccine) Ætiology::

Organism: o Polio virus: small RNA virus (3 types; BBRRÜÜNNHHIILLDDEE, LLAANNSSIINNGG, LLEEOONN)

Route of infection: o The virus enters the body via feco-oral route o 10 Incubation period during which the virus reaches the peripheral circulation o Viraemia then occurs till the virus reaches the CNS

Pathogenesis:: Subclinical infection: no manifestation even of viraemia (local immunity) Minor illness Abortive infection: no paralysis Major illness

Pathology:: CNS: (AHC, Dorsal root ganglia, Internuclear cells) Affect the AHC:

1- Irritative: temporary paralysis 2- Reversible toxic changes: cloudy swelling and chromatolysis reversible paralysis

éin 2y 3- Irreversible damage

Motor cranial nerve nuclei (bulbar palsy) Brain stem and cerebellar nuclei may lead to sympathetic and extrapyramidal manif Meningitis Dorsal root ganglia & internuclear cells pain & spasm of ms continuous contraction that

may end with a contracture as well Peripheral nerves: Axonal degeneration and replacement by fibrofatty tissue Muscle

1]. Fibrofatty degeneration and atrophy 2]. Fibrosis and shortening

Bone: 1]. Disuse atrophy ð ms stresses 2]. Short limbs

Joints: Unbalanced and instability


Polio In The Upper Limb

1- Shoulder: Deltoid, subscapularis, supraspinatus, infraspinatus, and serratus paralysis Skeletally immature ((SSAAHHAA TTEENNDDOONN TTRRAANNSSFFEERRSS))

1]. Deltoid .....................................................................trapezius to humerus transfer 2]. Subscapularis .........................................................superior 2 digits of serratus to subscap transfer 3]. Suraspinatus .........................................................levator scapulae or sterno-mastoid transfer 4]. Infraspinatus .........................................................latissimus or teres transfer 5]. Serratus ...................................................................pec minor transfer

Skeletally mature: 1]. Shoulder fusion ...................................................45º abd, 30º IR, 15º flexion (hand to face)

2- Elbow: Flexor paralysis: ((MMUUSSTT HHAAVVEE GGOOOODD HHAANNDD FFUUNNCCTTIIOONN))

1]. BBRROOOOKKSS--SSEEDDDDOONN ...............................................all pec major to biceps 2]. CCLLAARRKK’’SS ...................................................................sternal pec major to biceps 3]. HHOOVVNNAANN ................................................................Latissimus origin to biceps 4]. Pec mior to biceps 5]. Sterno-mastoid to biceps (fascial graft to give more length webbing of neck) 6]. Triceps to biceps 7]. SSTTEEIINNDDLLEERR FFLLEEXXOORRPPLLAASSTTYY ...............................advancement of the common flexor origin to lower humerus; before op

assess flexors, doing elbow flexion 90º hand clench test, if he can not do, cancel the operation 8]. BBUUNNNNEELL modification .........................................augment the transfer by fascia and attach it to the lat border of

humerus for better pronation 9]. MMAAYYEERR--GGRREEEENN .....................................................flexor palsty to the anterior aspect of humerus (better pronation)

Extensor paralysis: 1]. Latissimus transfer 2]. Brachio-radialis transfer

3- Forearm 1]. Pronation deformity (supinator weak): 2]. Pronator teres + FCR...........................................around ulna to radius 3]. Supination deformity (pronation paralysis) 4]. ZZAANNCCOOLLLLII ................................................................biceps rerouting around radial neck

4- Wrist: 1]. Extensor paralysis ...............................................Pronator to ECR 2]. Flex paralysis (wrist & hand) ............................ECRL to sublimis 3]. Wrist Drop: ............................................................wrist fusion

5- Fingers: 1]. Flexor paralysis ......................................................ECRL to sublimis or profundus 2]. Extensor paralysis ...............................................FCU to EDL + palmaris longus to EPL (or split FCU)

6- Thumb: Loss of pinch: o Loss of adduction (as in Ulnar) ......................1] Brachioradialis ........................... (BBOOYYEESS)

2] ECRL .............................................. (BBRRAANNDD) 3] Sublimis ........................................ (RROOYYLLEE TTHHOOMMPPSSOONN)

o Loss of opposition (as in median) .................1] Ring sublimis ............................... (RRIIOORRDDAANN) (= Abd & rotation at CMCJ + flex IP) 2] EIP .................................................. (BBUURRKKHHAALLTTEERR)

3] Riordan + FCU 7- Intrinsic Minus hand

o Claw hand as low ulnar & median ............ 1] ECRL .............................................. (BBRRAANNDD) 2] Sublimis ........................................ (BBUUNNEELLLL) 3] EIP ................................................... (RRIIOORRDDAANN)

8- Index: o Loss of abduction (Ulnar): ............................... EIP or Abd Pollicis .......................... (NNAAVVIIAASSEERR)


TTHHUUMMBB AADDDDUUCCTTIIOONN TTHHUUMMBB OOPPPPOOSSIITTIIOONN CCLLAAWW HHAANNDD


Polio in Lower Limb 1- Hip

1]. FFLLEEXXIIOONN DDEEFFOORRMMIITTYY .........................................As CP 2]. PPAARRAALLYYTTIICC DDIISSLLOOCCAATTIIOONN .................................As CP 3]. FFLLAAIILL HHIIPP : (according to the condition of spine, epsilateral knee, contralateral hip)

a. Free ...............................................................Fusion b. Abnormal ...................................................Orthosis

44]].. FFLLEEXXIIOONN AABBDDUUCCTTIIOONN c. Mild ................................................................YYOOUUNNTT’’SS ITB & lateral IM septum release d. Severe ..........................................................CCAAMMPPBBEELLLL Iliac crest transfer above the acetabulum e. Alternative ..................................................IIRRWWIINN CCOOMMBBIINNAATTIIOONNSS::

i. Mild ...................................................Yount’s + Soutter’s ii. Severe ..............................................Yount’s + C am pbell

2- Knee: 1]. FFLLEEXXIIOONN DDEEFFOORRMMIITTYY::

a. Mild ...............................................................POP wedging b. Moderate (30-40º) ...................................Supracondylar extension osteotomy ((RREEVVEERRSSEEDD IIRRWWIINN)) c. Severe (90º) ..................................................... Post capsulotomy + hamstring lengthen/transfer to patella

2]. RREECCUURRVVAATTUUMM : a. Type I ...............................................................(Quad =0 / Hamstring =5)

i. IIRRWWIINN Supracondylar flexion osteotomy ii. Biceps to patella

b. Type II ..............................................................(Quad = 5 / Hamstring = 0) iii. Long Leg Brace iv. Soft operation:

HHEEYYMMAANN .........................Collateral ligaments reconstruction PPEERRRRYY ..............................Triple tenodesis (ITB, ST, Biceps)

v. Bony operations: MMÜÜLLLLEERR ..........................Tibilaization of patella Fusion

3]. GGEENNUU VVAALLGGUUMM:: ...................................................MMOODDIIFFIIEEDD MMCCEEWWIINN’’SS osteotomy (¾ osteotomy/ ¼ clasis) 4]. FFLLAAIILL KKNNEEEE:: ...........................................................Long Leg Brace or Fusion

3- Foot & Ankle Deformity Immature Mature

Wedge Fusion Tendon transfer No Tendon 1].Varus Mild ............ Hoffer, Kaufer, Tohen

Severe ........ Drennan TA Post transfer Lateral (Dwyer) TF Same TF + Dwyer

2].Valgus P. Brevis to cuneiform + GGGG or EEVV GG or EV TF P.B to C TF + GG or EV 3].Equinus TAL + Bisla ± Ankle fusion Lambrinudi TF TAL + Bisla Ankle Fusion 4].TEV TAL + Bisla ± Steindler AnteroLateral TF TAL + Bisla Ankle or Pantalar 5].TE valgus TAL + PB to Cuneiform + GG or EV Anteromedial TF TAL + PB to C Ankle or Pantalar 6].TC Valgus Banta + PL & PB relocation + GG or EV Posteromedial TF Banta Pantalar 7].Cavus (Plantaris) Steindler + Jones or Hibbus Japas Dorsal V-shaped osteotomy of the tarsus 8].Calcaneo Cavus Steindler + Banta + Samilson Elmsli or TF Banta Pantalar 9].Pes cavovarus Steindler + BBIISSLLAA + Tohen Dwyer or lateral calcaneal displacement osteotomy

10].Claw Toes Big ............... Jones Toes ............ Hibbus Or ................ Taylor FDL to EDL

Same + IP fusion + MP capsulotomy

If there is OA DuVries MP excision arthroplasty or Fusion

11].Hammer Toe FDL tenotomy DuVries PIP Excision arthroplasty or Fusion 12].Mallet Toe FDL tenotomy DuVries DIP Excision arthroplasty or Fusion 13].Dorsal Bunnion Lapidus (TA to Nav + FHL to P.Phx base + Nav-Cuneiform fusion + Cuno-MT fusion + plantar IP capsulotomy)

GG= Grice Green (Tibial graft) / EV= Evans (Fibular Graft) / PB= Proneus Brevis / PL= Proneus Longus / C = Cuneiform Proneus Translocation must be done before age of 1 year:

1]. Eliminates the calcaneus and valgus force early before 2ry bone changes 2]. No orthosis can control the calcaneus deformity at the walking age


IInnttrroodduuccttiioonn It is not a commonly encountered though grave injury

BBrraacchhiiaall pplleexxuuss aannaattoommyy 5 roots: C5,6,7,8,T1 3 Trunks: Upper, Middle, Lower 6 divisions: 3 anterior, 3 posteior 3 cords: lateral, medial, posterior Nerves from the roots: Long thoracic (C5,6, 7), Phrenic (C5), Dorsal scapular (C5) Nerves from the trunks: Suprascapular nerve, n to subclavius (form upper) Nerves from cords: Lateral cord: LL Musculocutaneous Medial cord: MMMM Ulnar Posterior cord: ULNAR


ÆÆttiioollooggyy::

1- Open Plexus injury: sharp knif & glass (usually associated é vascular and visceral injuries) 2- Closed Brachial plexus injury:

1- Obstetric birth plasy: High birth wt > 4 kg Shoulder dystocia Breach

2- Traumatic: Traction injury: mostly due to motor cycle accidents & sport injury ð sudden fall on tip of

the shoulder sudden traction injury Compression by:

(1) Direct blunt trauma to the side of the neck (2) Fractures: transverse process, rib, clavicale, scapula (3) Dislocations: shoulder, AC, Sternoclavicular

3- Inflammatory: Radiation plexopathy: pain after radiation DXT 4- Tumors:

Neural: neurolemmoma, plexiform neurofibromatosis Non neural: Pancoast tumor

5- Compression neuropathy: Thoracic outlet syndrom e: thoracic rib,…

6- Vascular ischemia 7- Iatrogenic: ð mal position of a patient on the operative table (usually neuropraxia)

Pathology:

1]. Preganglionic injury: o Avulsions form the spinal cord herniation of the dura o Injury proximal to the DRG i.e. intact axons the DRG cells does not degenerate but there is

loss of sensation o Back muscles are denervated o Usually + phrenic + long thoracic + dorsal thoracic + Horner o All nerves that emerges from the roots are injured

2]. Postganglionic: o Ruptures distal to the DRG they degenerate + loss of sensation o Back muscles only are intact o No herniation of dura

3]. Trunks o Intact nerves: long thoracic and pectoral nerves o Suprascapular nerve is affected o Upper trunk (deltoid & biceps) o Middle trunk (radial n) o Lower trunk (ulnar + median)

4]. Cords o All the 3 nerves are intact o Medial (UMMMM) o Lateral (LLM) o Posterior (ULNAR)


MMiiccrroossccooppiiccaallllyy:: SSEEDDDDOONN’’SS CCLLAASSSSIIFFIICCAATTIIOONN:

1]. Neuroparaxia (conduction block that recover = 1 Sunderland) 2]. Axonotemesis (cutting of axons but intact peri and epineurium = 2.3) 3]. Neurotemesis (all are cut = 4,5)

SSUUNNDDEERRLLAANNDD CCLLAASSSSIIFFIICCAATTIIOONN 1]. Type 1 : neuraparaxia 2]. Type 2 : axonotemesis with intact endoneurium 3]. Type 3 : severe axontemesis with only intact peri & epineurium 4]. Type 4 : neurotemesis é only intact epineurium 5]. Type 5 : neurotemesis is complete with fibrosis

11--NNEEUURRAAPPAARRAAXXIIAA:: 1]. Physiological Conduction block 2]. No degeneration reaction occur 3]. Due to myelin disintegration 4]. Regeneration of myelin occur with schwann cells with regain of the full function

22-- WWAALLLLEERRIIAANN DDEEGGEENNEERRAATTIIOONN FFOORR AAXXOONNOO && NNEEUURROOTTEEMMEESSIISS • Proximal to axonotemesis or neurotemesis

1]. Perikaryon: swell then retract, nucleus becomes more peripheral, chromatolysis (Niessers granules desintigrate)

2]. Adjacent cells show similar changes 3]. Retrograde degeneration of the axon till the next NNOODDEE OOFF RRAANNVVIIEERR

• Distal to the cut:

1]. Axon maintain activity for 4 days then degeneration starts 2]. Axonal Degenration and disintegration down till the end of the nerve fiber 3]. Myelin disintegrate 4]. Schwann cells and macrophages clean the debris 5]. Schwann cells multiply and form Bunger tubes for future axon sprouts to come in 6]. Muscle atrophy, fasciculations, polyphasia

• Regeneration:

1]. 30-40 days latency occurs till the beginning of the regeneration 2]. Axon sprouts starts to bridge the gap till it finds the way in the distal end 3]. Axons travel 1mm/d till reach the distal organ 4]. MMUUSSCCLLEE: № of motor end plate, sensitivity, then starts to respond & fasciculation 55]].. SSEENNSSOORRYY IISS BBEETTTTEERR TTHHAANN MMOOTTOORR: and can wait for longer periods till start to regenerate


CClliinniiccaallllyy:: 1- Motor: Flaccid paralysis or weakness (LMNL):

1- EERRBB’’SS DDUUCCHHEENNNNEE:: Upper roots C5,6 (30%) + C7 (50%) : Arm adducted, elbow flexed, forearm pronated, fingers flexed (C7) Winging of scapula + lost protraction = preganglionic injury

2- DDEEJJEERRIINNEE KKLLUUMMPPKKEE PPAALLSSYY:: Lower roots (C8,T1) avulsion + upper roots rupture (20%) Complete flail paralysis Phrenic

3- CCOOMMPPLLEETTEE + Horner marble skin

2- Sensory: o Diminished spinothalamic sensations:

Pain, Temp, Crude touch o Diminished Lemniscal sensation:

Fine touch (tactile discrimination, 2 point discrimination, moving discrimination, depth discrimination, streognosis)

Proprioception: sense of position, sense of movement Sense of vibration

3- Autonomic: Vasomotor: VD followed by VC Sodomotor: anhydorsis (in complete) hypohydrosis (in incomplete) using the

Guttman quinizarine test + coffee and aspirin powder turns purple Atrophy

4- Reflexes: Lost deep and superficial reflexes 5- Causalgia: pain due to injury of a sensory nerve (e.g. median)


EElleeccttooddiiaaggnnoossiiss:: 1- Reaction of degenration:

lost response to faradic current (sustained contraction) Slow response to galvanic current Polar reversal: anodal closing current > cathodal closing current

2- CCHHRROONNAAXXIIEE (time needed for DDOOUUBBLLEE RRHHEEOOBBAASSEE = the minimal current can cause a contraction) 3- SD (strength duration) curve:

Normally: 100 msec voltage threshold is < double 10 msec threshold Denervation: the curve is steep and the 100 msec voltage threshold is > 2x 10 msec

threshold ώ is slower than normal 4- EMG:

1- Normal pattern Insertional potential; normally immediate and brief Resting potential: normally no fibrillation nor fasciculation Motor unit firing: bizarre, giant, dublette, polyphasia are abnormal Recruitment pattern (normally complete interference pattern = disapp of baseline)

2- Can detect the level 3- Can detect the acute and chronic 4- Can detect the regeneration pattern: polyphasia, and giant waves 5- Severity

But purely motor, does not evaluate the motor root function, does not measure pain 5- Nerve conduction:

1- Nerve conduction velocity: by of a nerve at a point & record the stimulus at another point in the course of the same nerve then measure the velocity of conduction

a. If slow conduction .... Myelin problems & compression b. If motor is absent + intact sensory ..................... preganglionic injury c. If both are intact despite the injury ................... neurapraxia d. If both are absent ...... .............................................. neurotemesis

2- Root assessment by delayed responses: HH--RREEFFLLEEXX (electric ankle jerk) by submaximal nerve γ fibers dorsal root

monosynaptic of AHC ms contraction FF RREESSPPOONNSSEE: (antidromic motor nerve conduction) stimulation of a motor nerve

produce normal orthodromic propagation of action potential to the muscle and in the same time there is an antidromic volley that travel to the perikaryon Renshaw cells till the cell itself another response F response

Still both are motor, not for muscles that are innervated by multiple roots or you can not differentiate, and can not differentiate bet acute and chronic

6- Bulbocavernosus reflex perineal contraction 7- SEP: Stimulation of nerve electrodes at spine & cortex

1- Can purely measure the root function 2- Can measure the conduction velosity 3- Does not depend on motor function 4- Can detect delays due to CNS delays e.g. MS 5- Can detect th e root avulsions in Erb’s plasy

PPXXRR Detect phrenic paralysis Detect fractures of 1st rib or tumors Cervical myelography diverticulosis of the preganglionic injury


TTrreeaattmmeenntt::

Non operative: Literature indicates that the spontaneous recovery is the rule in 80% Usually if closed injury é early biceps twitches Physiotherapy is mandatory to maintain normal ROM Ms is important to keep active ms Operative:

11-- IINNDDIICCAATTIIOONNSS AANNDD TTIIMMIINNGG:: 1]. If the point of 3mo passed without evidence of biceps regeneration 2]. Reconstructive surgery for late sequelae

22-- FFIINNDDIINNGGSS:: 1]. Root avulsion 2]. Continuous root and trunk (traction injury) 3]. Neuroma formation

33-- TTEECCHHNNIIQQUUEE:: 1]. Neurolysis if the lesion is in continuity

2]. Direct repair (not in root avulsions; but in peripheral nerves):

o Timing: Acute repair if clean cut and every thing is ready 2 weaks: is the rule for the oedema to subside & the soma is fully active Delayed if (6wk) if contaminated or é vascular and tendon injury to avoid fibrosis

o Methods: a. Perineural b. Fascicular c. Group Fascicular d. Perineural and fascicular

o Avoid: Gaps Infection Tension:

(1) <5cm: transposition, limb position, neurolysis, cut of unnecessary branche (2) >5 cm: nerve grafting:

o Fibrin & plasma glue: may be used to operative time and the use of suture fibrosis o Postoperative:

Immobilization: 2-6 wk Physiotherapy

3]. Nerve Grafting o Nerves to be used: sural, medial cut n of fore arm, superficial radial o Technique:

a. Interfascicular b. Inlay: in neuroma c. Cable grafting d. Pedical rotational intergrafting (bet ulnar and median)

4]. Homografts are immunogenic


5]. Neurotization: two types: 1]. Internal Plexo-Plexus:

C7 to upper trunk C3,4 to upper trunk

2]. External: (to upper trunk, musculocutaneous, axillary, suprascapular, radial, median) Pectoral nerves Intercostal n Spinal accessory Long thoracic, thoraco-dorsal, subscapular

6]. Late Reconstructive surgery to shoulder: 1]. FFAAIIRRBBAANNKK release of the subscapularis + pec major + ant capsule 2]. SSEEVVEERR’’SS release of the subscapularis + Pec major lengthening 3]. LL’’EEPPIISSCCOOPPOO: transfer of Latissimus & teres major to the back of the humerus ER (ZZAACCHHAARRYY,

TTAACCHHIIDDJJIIAANN modifications) 4]. HHOOFFFFEERR transfer of latissimus and teres into the rotator cuff ER + abduction 5]. OOBBEERR long head triceps + short head biceps transfer to acromion 6]. GGIILLBBEERRTT && MMAAYYEERR trapezius transfer to humerus 7]. SSAAHHAA acromion with the attached trapezius advancement to humerus as distal as possible 8]. Humerus derotation osteotomy 9]. Arthrodesis is the last resort

Lesion procedure as recommended by AAOS Adduction + IR Subscapularis Release Supra or infraspinatus Dysfunction Latissimus to g reater tuberosity Deltoid Dysfunction Saha or Hoffer IR or ER + incongruent sh oulder joint Humeral derotation osteotomy Severe dysfunction of shoulder Glenohumeral arthrodesis

7]. Elbow reconstruction:

Flexor paralysis: ((MMUUSSTT HHAAVVEE GGOOOODD HHAANNDD FFUUNNCCTTIIOONN)) BBRROOOOKKSS--SSEEDDDDOONN .................... all pec major to biceps CCLLAARRKK’’SS ..................................... sternal pec major to biceps HHOOVVNNAANN ................................... Latissimus origin to biceps Pec mior to biceps Sternomastoid to biceps ..... using a fascia to give more length webbing of neck Triceps to biceps SSTTEEIINNDDLLEERR FFLLEEXXOORRPPLLAASSTTYY ...... advancement of common flexor origin to lower humerus;

assess 1st flexors condition by doing elbow flexion 90º hand clench test BBUUNNNNEELL modification ............ augment by fascia &fix to lat humerus (better pronation) MMAAYYEERR--GGRREEEENN ......................... flexor palsty to the anterior humerus (better pronation)

Extensor paralysis: Latissimus transfer Brachio-radialis transfer

8]. Forearm Pronation deformity (supinator weak): Pronator teres + FCR around ulna to radius Supination deformity ........... ZZAANNCCOOLLLLII biceps rerouting around the radial neck

9]. Wrist: Wrist Drop ............................... FCU to ECRB


RREECCEENNTT TTRREENNDDSS IINN NNEERRVVEE RREEPPAAIIRR

11.. PPhhaammaaccoollooiiccaall aaggeennttss 1- Gangliosides 2- Polyamines

22.. IImmmmuunnee ssyysstteemm mmoodduullaattoorrss 1- Azathioprine 2- Corticosteroids 3- Cyclosporin A 4- Cvclophosphamides

33.. EEnnhhaanncciinngg ffaaccttoorrss 1- Nerve growth factor 2- Fibronectin 3- Insulin-like growth factor 4- Ciliarv neurotrophic factor

44 EEnnttuubbuullaattiioonn cchhaammbbeerrss 1- Autogenous vein 2- Silicone Polvglycolic acid G 3- Gore-tex

PPrrooggnnoossiiss A]. Preoperative:

1]. Level of injury: the distal the better 2]. Delay of injury: the more acute the better 3]. Type of injury: the apraxia the better 4]. Type of nerve: the pure the better & the small the better 5]. Type of pt: the younger the better

B]. Operative: 6]. Huge gaps 7]. Huge tension 8]. Huge suture (we use 8-0 or 9-0)

C]. Postoperative 9]. Hematoma

10]. Infection 11]. Inadequate physiotherapy


TTHHUUMMBB AADDDDUUCCTTIIOONN TTHHUUMMBB OOPPPPOOSSIITTIIOONN

CCLLAAWW HHAANNDD


Commonest middle aged F:M = 3-5:1 AAnnaattoommyy OOff CCaarrppaall TTuunnnneell

floor and walls bony carpus roof flexor retinaculum /transverse carpal ligt radial attachment tubercle of scaphoid + ridge of trapezium ulnar attachment hook of hamate + pisiform Contents FPL / FCR (deep to FPL) / FDS - middle & ring lie superficial / FDP

Median Nerve Flexor tendons run deep to nerve

CCaauusseess ((IICCRRAAMMPPSS)) Idiopathic Colles, Cushings Rheumatoid Acromegaly, amyloid Myxoedeoma, mass, (diabetes) mellitus Pregnancy, Persistent median a. Sarcoidosis, SLE

SSyymmppttoommss not always classical

1- Aching and parasthesia in thumb , index middle and 1/2 of ring finger 2- worse at night 3- forearm pain 4- dropping things

SSiiggnnss

1]. Hand normal looking 2]. If severe, thenar wasting, trophic ulcers 3]. weakness of thumb abduction 4]. Semmes Weinstein monofilament test & Vibration test are more sensitive than 2 point

discrimination test in assessment of the slowly progressive sensory compression change 5]. Tinels Sign -74% sensitivity, 91 % specificity: Gentle tapping over median nerve at the wrist

in a neutral position. Positive if this produces paraesthesia or dysaesthesia in the distribution of the median nerve

6]. Phalens Sign –61% sensitivity, 83% specificity: Elbows on the table allowing the wrists to passively flex. If symptoms provoked within 60 secs then positive

7]. Median Compression Test – 86% sensitivity, 95% specificity* : Elbow ext, forearm supination, wrist flex 60º, one thumb pressure over the carpal tunnel. Test positive if parasthesia or numbness within 30 secs

DDiiffffeerreennttiiaall ddiiaaggnnoosseess

Cervical radiculopathy Spinal cord lesions - tumour, MS, syrinx Peripheral neuropathy- toxic, alcoholic, ureamic, diabetic


Investigations Nerve conduction studies :

sensory conduction prolongation ......... >3.5ms (more sensitive) distal motor latency .................................... >4.0 ms accuracy = 85-90% 10-15% false negative

Reminder of how nerve conduction studies are performed: Motor

1]. stimulus to skin over nerve, Motor Action Potential recorded in muscle supplied 2]. Latency = time between stimulus and MAP 3]. Conduction velocity, normal = 40-60 m/s 4]. compression causes CV in a segment 5]. If very severe MAP also reduced

Sensory 1]. SNAP recorded in proximal nerve after distal stimulation 2]. sensation often affected before motor function 3]. SEP (Somato sensory evoked potential) record response in brain or spinal cord, used to

diagnose brachial plexus injuries Management Conservative-

Night splint, injection, NSAIDs, correct any cause (75-81% relief short term) Surgical-

1]. open /endoscopic decompression 1]. Need to bear in mind anatomical variations 2]. Beware palmar cutaneous branch of median nerve, and motor branch 3]. Apply volar splint to hold the wrist in extension bowstring & RDS

Complications of surgery 1]. Complex Regional Pain Syndrome 2]. Tender hypertrophic scar pillar pain 3]. neuroma in palmar branch 4]. tenosynovitis / tendon adhesions 5]. bowstringing of tendons

Endoscopic release Okutso&Agee 1]. one or two incisions 2]. less scarring 3]. less pillar pain 4]. quicker return of strength and to work 5]. but: 6]. Anecdotal reports of disasters 7]. Big learning curve 8]. Time consuming, expensive


CCoommpprreessssiioonn aatt

Lacertus Fibrosus = biceps aponeurosis pronator teres muscle fibrous arcade of FDS Ligamentum Struthers (present in 1.5 % of people)

CCaauusseess 1]. Repeated minor trauma/ repetitive use of elbow 2]. fracture / fracture dislocation of elbow 3]. Tight/scarred lacertus fibrosus 4]. Tendinous bands in pronator teres 5]. Tight fibrous arch at prox FDS

SSyymmppttoommss 1]. Aching / fatigue of forearm after heavy use 2]. Clumsiness 3]. Vague, intermittent parasthesia, but rarely numbness

SSiiggnnss 1]. local tenderness to deep pressure and reproduction of symptoms 22]].. TTIINNEELLSS TTEESSTT 3]. pain on resisted pronation of forearm with elbow extended = Pronator teres 4]. pain on resisted elbow flexion and supination= lacertus fibrosus 5]. pain on resisted flexion of PIP joint middle finger = FDS arch

IInnvveessttiiggaattiioonnss 1]. NNCCSS not much use, intermittent symptoms 2]. EEMMGG innervation of muscles & differentiate from CTS

MMaannaaggeemmeenntt 1]. Conservative-avoidance of repetitive elbow movements, NSAIDS, Splintage with elbow

flexed with pronation 2]. Surgical- Decompress all the structures

Anterior Interosseous Syndrome Compression under humeral part of pronator teres Anterior interosseous nerve motor to FPL, radial side of FDP and pronator quadratus Does not supply skin sensation Afferent sensory fibres from capsular ligament structures of wrist and DRUJ

CClliinniiccaall ddiiaaggnnoossiiss spontaneous vague forearm pain reduced dexterity weakness of pinch unable to make 'OK Sign' due to weakness of FPL & FDP index finger (makes square

instead of circle) weak pronation with elbow in full extension (isolates PQ) direct pressure over nerve can elicit symptoms Tinels sign usually negative

IInnvveessttiiggaattiioonnss EMG + NC unhelpful

MMaannaaggeemmeenntt Conservative- NSAIDS, avoiding aggravating movements Surgical exploration- most common compressing structure deep head of pronator teres


Cubital Tunnel Syndrome Ulnar nerve entrapment about the level of the elbow

Aetiology: 1]. At elbow:

o Cubitus Valgus ○ Trauma o Bony spurs ○ Tumours

2]. Proximal 8cm by ‘‘Arcade O f Struth ers’ ≠ lig am en t o f Stru th ers’. It is a thin aponeurotic band extending From Medial Head Of Triceps To The Medial Intermuscular Septum; it is 8 cm proximal to the medial epicondyle; it may look like triceps fibers crossing superficial to the ulnar n. & usually it is not site for entrapment under ordinary circumstances, but it do é anterior transposition of ulnar nerve is performed

3]. Distal by hypertrophied FCU

SSyymmppttoommss Vague dull aching forearm, intermittent parasthesia, ulnar side of hand

Signs 1]. Hypoesthesia ulnar side of hand + 1½ fingers 2]. Tinels TTEESSTT, behind medial epicondyle 3]. Wartenburg’s sign weakness of abduction of little finger 4]. Froment’s Sign pinch grip and grasping, both of which are impaired by a low ulnar nerve

palsy due to weakness of adductor pollicis 5]. Ulnar clawing if severe (Note - Ulnar Paradox - no clawing if FDP & intrinsics weak) 6]. Wasting: 1st dorsal Interosseus + hypothenars + ulnar FA (FDP & FCU)

Differential Diagnosis Cervical radiculopathy Thoracic outlet $ Amyotrophic lateral sclerosis (MND) Localized peripheral neuropathy

Investigation 1]. NCS reduced nerve conduction velocity 2]. EMG evidence of denervation of muscles

Management Conservative 1]. Avoidance of repetitive bending of elbow; Extension Block night splint. 1]. injection contraindicated Surgical -controversy 1]. Decompression- ‘Cubital Tunnel $ Does Not req u ire tran sp o sitio n o f th e u ln ar n ’ 2]. Transposition: - subcutaneously/ Submuscularly (better) 3]. +/- medial epicondylectomy Results Sensation improves better than motor function over 3-5 y period

CCoommpplliiccaattiioonnss 1]. Recurrence ð inadequate decompression or irritation or redislocation or neuoma 2]. CRPS

http://www.wheelessonline.com/ortho/triceps_brachii


Guyons Canal

Anatomy Of Guyons Canal Floor transverse carpal ligt to pisiform Ulnar wall pisiform Radial distal wall hook of hamate Roof volar carpal ligt Contains Ulnar nerve + art

Causes Repetitive indirect trauma most common Tumours- ganglion, lipoma Pisiform instability Pisotriquetral arthritis Fractured hook of hamate / pisiform Ulnar artery thrombosis

Symptoms Weakness atrophy para / hypoasthesia ulnar side of hand motor sensory or both Dorsoulnar sensory branch spared

Signs Local tenderness, tinels test, phalens sign, local swelling, negative allens test, severe ulnar

clawing (remember Ulnar Paradox) Investigations

Ncs, show delayed motor latency from wrist to 1st dorsal interosseous Management

Conservative 1]. Splinting 2]. Avoidance of repetitive trauma

Surgical 1]. Decompression of motor and sensory branches 2]. +/- excision of pisiform/ hook of hamate


Posterior Interrosseous Syndrome (Pain And Paresis)

Causes (FREAS & Monteggia) 1]. Fibrous tendinous band at origin of supinator (30% of people) 2]. Radial recurrent vessels (the Leash Of Henry) (less convincing evidence) 3]. Extensor carpi radialis brevis 4]. Arcade of Frohse 5]. Supinator (the distal border). 6]. Monteggia fracture especially types ! & III 7]. R.A of elbow 8]. surgical resection of radial head 9]. mass lesions

Symptoms pain in 50% weakness of extension of wrist and MCP joints

Signs Radial deviation of wrist with dorsiflexion (ECRL supplied by Radial nerve) If partial, pseudo clawed hand Able to extend IP joints due to interrossei no loss of sensation

IInnvveessttiiggaattiioonnss

NCS -decreased latency across arcade of Frohse EMG denervation fibrillations of affected muscles

TTrreeaattmmeenntt Conservative observe for 8-12 wks if no evidence of mass lesion Surgical decompression

Important tests Jeanne's Sign Thumb MP hyperextension 10° -15° é key pinch or gross grip. Froment's Sign Thumb IP hyperflexion é key punch by FPL in ulnar nerve palsies. Wartenberg's Sign Inability to adduct the extended little finger ð ulnar nerve palsy Duchenne's Sign Clawing of the ring and small fingers ð ulnar nerve palsy Pollock's Sign Inability to flex the DIP of the ring and small fingers in high palsies Phalens Sign Elbows on the table allowing the wrists to passively flex. If median

nerve symptoms provoked within 60 secs = positive


Radial Tunnel Syndrome (Pain & No Paresis)

Mild compression of post interosseous nerve without paresis

Causes As for posterior interosseus syndrome but not usually any mass lesions

Diagnosis

Symptoms dull aching in extensor muscle mass worse at end of day

Signs local tenderness 5cm distal to lat epicondyle pain elicited by resisted active supination Middle Finger Test.

o Each finger is tested under resisted extension. Testing the middle finger increases the pain. Due to ECRB inserting into base of 3rd metacarpal.

o Performed with the elbow and middle finger completely extended with the wrist in neutral position.

o Firm pressure is applied by the examiner to the dorsum of the proximal phalanx of the middle finger.

o The test is positive if it produces Pain At The Edge Of The ECRB in the proximal forearm.

Investigation NCS Increased motor latency in active forceful supination Injection of local anaesthetic into radial tunnel

DDiiffffeerreennttiiaall ddiiaaggnnoossiiss Tennis elbow

MMaannaaggeemmeenntt Conservative, anti inflammatories, avoidance of repetitive provoking activities Surgical, decompression. Internervous plane between ECRB and E Digitorum developed.

PIN found just proximal to arcade of Frohse.

Wartenberg Syndrome Described in 1932- isolated neuritis of superficial sensory branch of radial nerve As it winds out from deep fascia beneath brachio-radialis, to be superficial to ECRL Both tendons may act as scissors entrapping the n Pain & parasthesia over the distribution of RSN; with hyperpronation + Tinel’s sign Treatment- local steroid injection, surgical exploration and release.


Nerve Entrapment in Lower Limb

NNEERRVVEE SSIITTEE CCAAUUSSEE SSYYMMPPTTOOMM ILIO-INGUINAL Hypertrophied abdominal ms Intense training Pain & parasthesia OBTURATOR Hip adductor Skaters Medial thigh pain FEMORAL LAT. CUT. ASIS

Meralgia paresthetica Tight belt Lateral thigh pain

SCIATIC Ischial tuberosity, pyriformis ms Pyriformis Sciatica SAPHENOUS H unter’s can al Quad or sartorius Infero-medial knee pain COMMON PERONEAL Fibular head Direct blow Foot drop SUPERF PERONEAL 12 cm above Lat.Maleolus, as it

pierce the deep fascia Inversion injury Dorsal foot pain &

paresthesia SURAL 12 cm distal to Lat Malleolus Jon e’s fr Lat. foot parasthesia DEEP PERONEAL Inf. extensor retinaculum

(anterior tarsal tunnel $) Inversion injury Sole pain & parasthesia

POSTERIOR TIBIAL Flexor retinaculum (Tarsal tunnel $)

FDL accessorius, RA, tumors, ganglion

Sole pain & paresthesia

1ST LAT.PLANTAR Bet AHL fascia, quadratus plantae High heels Plantar fasciitis MEDIAL PLANTAR Henry Knot (cross of FDL & FHL) Orthotics Big toe pain & parasthesia INTERDIGITAL Bet MT3-4 plantar to deep MT lig

(M orton ’s N eurom a) Push phase in runners Digital pain, parasthesia,

dead toe


TThhoorraacciicc OOuuttlleett SSyynnddrroommee Impingement of subclavian v v, and lower trunk (C8 /T1) of

brachial plexus Boundries: scalenus anterior and medius, and the 1st rib Age 18-40 (never before puberty rare after 50yr)

Aetiology: 1]. Neck:

o Cervical Rib ......... 10 % will have TOS o Fibrous bands o Scaleneus anterior constriction

2]. Shouder o G VI Acromio-clavicular dislocations & Clavicular fractures o In some cases, by recurrent anterior shoulder instability, µß Dead Arm $

3]. Pancoast tumour

Examination:: 1]. Tenderness or mass in supra-clavicular fossa 2]. Lower trunk C8/T1 manifestation: 3]. Sensory changes in the Ring and Little finger 4]. Intrinsic weakness 5]. Vascular Examination

o Radial pulse obliteration + Reproduction Of Symptoms is specific (radial alone is not)

Provocative Tests 11.. A dson ’s TTEESSTT

o Arm of the affected side adducted with forearm supinated o Turn head toward the affected side o Extend neck and hold breath o Positive test is obliteration of the radial pulse

22.. R everse A dson ’s TTEESSTT o As above but head turned away from the affected side

3. W righ t’s test (Hyperabduction stress test) o Axillary vessels and plexus bent 90º at the junction of the glenoid and humeral head o Place extremity in full abduction, external rotation and reach back as far possible. Turn

head away and check for decrease or loss of radial pulse o Creation of a bruit in the supraclavicular area is further evidence

4. Roos overhead exercise test o Above head repeated forearm exercise may reproduce symptoms

Investigations: 1- X-ray -Cervical ribs may be seen but more commonly the cause is a fibrous band (not seen) 2- CXR to rule out pancoast tumour 3- MR scan to exclude cervical disc disease

Treatment 1- Non-Operative (for At Least 4 Months)

o Postural re-education o Activity modification o Weight loss

2- Operative (rarely required) o Excision of first rib with fibrous band and anterior scalene muscle via supra-clavicular,

subclavicular or axillary approach

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