Orthopedic Neurology

8/19/2019 Orthopedic Neurology

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Date

Dr Mohamed Sobhy

Ain Shams University

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بسم لرحمن لرحيم


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[Orthopedic Neurology ] Page | 439

Neuro-AnatomyNeuron:

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


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440

| Page [Orthopedic Neurology ]

• Peripheral nerve has a mixture of neurons:1]. Motor2]. Sensory3]. Reflex4]. Sympathetic5]. Parasympathetic

• Types of fibers: A (α, β, γ, δ), B, C

Motor

Sensory

Ms reflex

sympathetic

Parasymp

Neuron AHC Dorsal root ganglia AHC IHC relay at organRoot Anterior Dorsal root Ant Ant AntTract 1-

Direct pyramidal

2-

Indirect pyramid

1-

Spinothalamic (Pain, temp,crude)

2-

Lemniscal (DC)(proprioception, fine touch)

Stretch reflexarc from msspindle

Fibre

α Motor (12-20 μm) α Propriocep (12-20 μm)

β Touch, vib (5-12 μm)δ fast pain, temp (2-5μm)C Slow pain, crude (0.2-2μm)

γ fibers B preganglionicC 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 epineuriumMuscle:

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

•

Ms fibers types:1-

Smooth ms fibers2-

Cardiac ms fibers3-

Skeletal ms fibers:

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

• MS CONTRACTION

: is the active state of a ms, in whichthere is response to the neuron action potential eitherby isometric or iso tonic contraction

• ISOMETRIC CONTRACTION

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

• I

SOTONIC CONTRACTION

: is the contraction in ώ here is achange in the length of the ms éout change in the tone

•

MS TONE

: is the resting state of tension

•

M

S CONTRACTURE: is the adaptive structural changes in ams ð prolonged immobilization in a shortened position,in the form of shortening and fibrosis

•

MS WASTING

: 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

• SPASTICITY:

Abnormal contraction of a ms in response to stretch. Growth of ms isimpaired

• R

IGIDITY

:

Involuntary sustained contraction of a ms not stretch-dependent. Growth of ms isfair


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442


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 fibrosis2]. Muscle tears:

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

3]. Muscle soreness: During the higher eccentric contractions4]. Muscle denervation: Causes atrophy and sensitivity to acetyl-choline and fibrillation in

2wkTendons

• COMPOSED OF:

1]. Collagen I ......................................... 80%2]. Fibroblasts synthesis tropocollagens micro-fibrils sub-fibril fibril fascicle3]. Loose areolar CT .......................... Endotenon epitenon paratenon

• TYPES OF TENDONS:

a. P

ARATENON

covered tendons rich capillary supply = better healing

b.

Sheathed tendons ....................... segmental bl.supply via mesotenon (V

INCULA

)•

MUSCULO-TENDINOUS JUNCTION:

1]. Tendon2]. Fibro-cartilage3]. Mineralized fibrocartilage (

S

HARPEY

’

S

fibers)4]. Bone

• H

EALING

STARTS

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 healingLigaments

• COMPOSED OF:

1]. Collagen I (same ultrasturcture) ........ 70%2]. Elastin3]. Fibroblasts + Loose areolar CT

• B

L

S

UPPLY

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

1]. Indirect: ............................................. superficial fr insert to periosteum @ acute angle2]. Direct ................................................. Deep fr insert to bone @ 90º

•

B

ONY

L

IGAMENTOUS

J

UNCTION

:1]. Ligament2]. Fibro-cartilage3]. Mineralized fibrocartilage (

S

HARPEY

’

S

fibers)4]. Bone

• H

EALING

starts by fibroblasts and macrophages of the epitenon

Phase Time Process Strength

1].Hemostasis 10 min platelet plug fibrin clot Weak2].Inflammatory 10 days macrophages debride granulation tissue Weak3].Fibrogenesis 30 days UMC fibroblasts strong type I collagen most strength regained4].Remodeling 6-18 mo Realignment & cross linking of collagen bundles Max strength

•

L

IGAMENTS

G

RAFTING

:

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


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Tendon Transfers

Definition

• A tendon transfer is a procedure in which the tendon of insertion or of origin of the functioningmuscle 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 muscleimbalance and keep the corrected position rather than to correct a deformity

Indications

1]. Irreparable nerve damage2]. Loss of function of a musculotendinous unit due to trauma or disease3]. In some nonprogressive or slowly progressive neurological disorders

Contraindications

1]. Unstable joint2]. Stiff joint3].

Fixed deformity4]. Advanced arthritis5]. If affection of all muscles at the same degree6]. If no suitable tendon or muscle is available for transfer

Principles

Preoperative1]. 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 ± TTo

If the patient is has talipes valgus add stabilizing bony op. e.g. Grice Green or Evans2]. 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 ofregeneration 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 muscleso If 2 tendons are available do TT for the most crucial functional muscleo If one agonist tendon is available do TT to the middle line e.g. Tohen transfero If one antagonist tendon do split TT & suture under equal tension

Operative

Joint:1]. Should be stable2]. Should be a freely mobile joint (free ROM)3]. Should not have fixed deformity4]. Should not have advanced arthritis


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

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

3]. Adequate neurologic & blood supply

4].

Agonists better than antagonists5]. Synergestic better than non synergestic6]. Start Proximal then distal

Tendon1]. Should be of an adequate Length 2]. Should pass in a Straight line3]. Should pass through a Gliding Medium (the best is fat or superficial fascia)4]. Should be sutured under Moderate Tension 5]. Should be Covered6]. Better to suture tendon To Bone (pull-out technique)

Techniques1]. Multiple short transverse incisions rather than long longitudinal incisions2]. Careful tendon handling3]. Joining the tendons

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

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

Postoperative:1]. Protect the transferred tendon to avoid stretching2]. 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 & Peroneuslongus are important for foot arch Skeletally immature with Varus (alone or with otherdeformities)

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


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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)

Classification1-

Spastic ............................................................................. (60 ) oo MOST AMENABLE TO SURGERY

o UMNL involvement - mild to severe motor impairmento Contractures:

Walking limb№ UL:LL Associated problems

1-

Hemiplegia

40 3mo later than N 2 UL>LL •

Mild learning•

Seizures2-

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 15-

Double hemi

LL • As hemi6-

Total body


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446

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Clinical FeatureHistory• 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,

SCISSORING, STIFF-LEGGED, TIP-TOE GAIT, CROUCHED

2-

Stride length, Narrow walking base3-

Lordosis . Co-ordination in turning.

•

Hip deformities:1-

Adduction: ..................................... ð adductor spasmG

RAB

T

EST

+V

E

Hip Abduction)

2-

Flexion: ............................................ ð rectus spasm

.......

ELY & THOMAS & STAHELI +VE

)

3-

Flexion internal rotation: ........... ð psoas spasm (true scissoring ≠ pseudo scissoring ðflexion + anteversion

+V

E

W

S

IGN

)4-

Hip dislocation ............................... ð 1ry & 2ry ...............

GALEAZZI TEST +VE

)

WINDSWEPT POSTURE

- one hip adducted & other side abducted

S

CISSORED

G

AIT

if bilateral Apparent LLD if unilateral

STAHELI TEST

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): ........+V

E

T

RIPOD

S

IGN

&

T

OE

T

OUCH

2-

Knee recurvatum .................... ....................................R

EVERSED

P

OPLITEAL

A

NGLE

3-

Genu valgum4-

Patella alta (BLUEMANSAAT

,INSALL-SALVATI RATIO

soleus Equinus knee recurvatum in stance phase Calcaneus crouch gait

Kneeling eliminates contracture effect


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448


• Upper limbs1-

Shoulder adduction internal rotation2-

Elbow flexion3-

Forearm pronation4-

Wrist & finger flexion5-

Thumb in palmo Hand placement. Ask patient to place hand on knee and then head.o Stereognosis. Test ability to recognise shape in palm

•

Spineo Scoliosis usually present at age 5. Reaches 50º. by age 15o 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 wiresGroup 2

large thoracolumbar or lumbar curve pelvic

obliquity

Ant + Post Fusion Luque rods & sublaminar wires &

Galveston pelvic fixation

• Neurologyo

CLASP-KNIFE

phenomenon o Primitive reflexes:

A, A

SYMMETRICAL TONIC NECK

: as headis turned to one side, contralateralarm and knee flex.B,

M

ORO

R

EFLEX

: Hold child at 45o. Allow head to drop back, UL extendaway from body and then come

together in embracing pattern.C,

E

XTENSOR

T

HRUST

: as child is heldupright by armpits, lower extremitiesstiffen out straight.D,

N

ECK

-R

IGHTING

R

EFLEX

: as head isturned, shoulders, trunk, pelvis, andlower limbs follow turned head.E,

P

ARACHUTE

R

EACTION

: as child issuspended at waist and suddenlylowered forward toward table, armsand hands extend to table inprotective manner.F,

S

YMMETRICAL

T

ONIC

N

ECK

: as neck isflexed, arms flex and legs extend.Opposite occurs as neck is extended.G,

F

OOT

P

LACEMENT

R

EACTION

: whentop of foot is stroked by underside offlat surface, child places foot onsurface.


12/42

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Page |449


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450


Aphorisms.

• 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

Priorities

Patient priorities are1]. Communication2]. Activities of daily living3]. Mobility & Walking

Objectives

1].

Maintain straight spine and level pelvis2]. Maintain located, mobile, painless hips3]. Maintain mobile knees for sitting and bracing for transfer4]. Maintain plantigrade feet5]. Provide maximal functional positions for sitting, feeding, and hygiene6]. Provide appropriate adaptive equipment, incl. Wheelchairs7]. Avoid hip dislocation.

o Painfulo Make nursing difficulto pelvic obliquity & scoliosis difficult wheelchair ambulationo quality of life.

8]. Strategyo 0-3 y .................................... physiotherapyo 4-6 y .................................... surgeryo 7-18 y .................................. schooling and psychosocial developmento 18 yrs + ............................... work, residence and marriage.

g g g g g g b i i i i i i i

LOW ER LIMBS

1-

P

HYSIOTHERAPY

- physiotherapy approaches contractures or development, ROM:o

Neurodevelopmental approach (Θ exaggerated reflexes by certain positions)o Sensorimotor approach (Θ exaggerated reflexes by sensory ⊕)o Proprioceptive approach (proprioception used to improve posture)o Neuromuscular reflex approach (graduated pattern of movement learning)

2-

CAST CORRECTION

- Inhibitive casting. Stimulation of sole can cause muscles to contractwas basis of inhibitive casting. Not used much now.

3-

C

ORRECTIVE

C

ASTING

- for mild fixed equinus. Well-padded POP é max dorsiflexion

4-

BRACING

- Useless for treating fixed deformity AFO's useful for Dynamic equinus

5-

N

EUROSURGERY

- Selective posterior R

HIZOTOMY

of rootlets used. Via laminectomy. 30-70%of posterior rootlets cut. Decreases feedback from stretch receptors. Can ⊕ rootlets to findwhich mediate spinal reflex. If only these cut, sensation unchanged. Results promising.

6-

CHEMONEURECTOMY

: selective neurectomy is done using certain chemical substances: aa.. ALCOHOL 45% gives improvement for 6 wks bb.. PHENOL 5% 2ml gives permanent effect

cc.. BOTULINUM TOXIN gives 6m improvement (Θ acetyle choline) dd.. BACLOFEN intrathecal implanted pump (GABA agonist Θ excitatory

transmitters)


14/42


A

DDUCTED SUBLUXED

H

IP

Assess RMP

50%

Bony

operations

Soft tissue

operations

>50% MP Hip Dysplasia Dislocated>45° flexion Subluxed


15/42

452

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16/42

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17/42

454


Knee Recurvatum:

• Recurvatum may be:1]. 1ry: quadriceps spasticity or quadriceps spasticity > hamstrings & gastroc spasticity2]. 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 lengthening2-

Equinus TAL3-

Neurectomy of femoral nerve4-

Irwin femoral flexion osteotomy

Genu valgum:

• Usually ð:1-

hip adduction and coupled é Flexion IR2-

Tight ITB• Treatment:

1-

Correct the hip via Adductor and iliopsoas release2-

Yount ITB resection3-

Supracondylar varus osteotomy

V Patella alta:

• ð quad spasm or long knee FFD• ttt as in prolonged knee FFD

V Patellar subluxation and dislocation:

1]. In valgus knee2]. Flexion adduction and IR of the hip Q angle

• Treatment: ttt the cause + Insall release of Fulkerson osteotomy


18/42


CC.. A Annkkllee ddeef f oorrmmiittiieess:: • 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.Equinus:

Pathology (5types according to Triceps surae vs Dorsiflexors):

1-

Spastic vs spastic2-

Spastic vs normal3-

Spastic vs flaccid4-

Normal vs flaccid5-

Flaccid vs flaccidThe exact offending ms (gastroc or soleus) can be done by

Silfverskiöld Test

The muscle nature must be determined - spastic or contractured - by procain injectionNon 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 insertion2-

Triceps surae release:a

Silfverskiöld

Gastroc recession (spasm): distal recession of gastroc originb

Gastroc slide (contracture): lengthening of gastroc tendonc 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-

M

URPHY

Heel cord advancement:

•

In spastic vs spastic dorsiflexors replacing TA more ant in front of FHL

Varus:

Due to: TP spasm TA or Tendoachillis tightness & evertor

weakness may assist

Treatment (according to rule no bonyoperation):S

KELETALLY

I

MMATURE

:

1-

TP Lengthening (MAJESTRO)

2-

TP Rerouting in front of med malleolus (B

AKER

)

3-

TP transfer via Interosseous membrane to dorsum of Foot (BISLA)

4-

TP split transfer to the proneus Brevis(K

AUFER

)

5-

TA split transfer to the cuboid (HOFFER)

6-

FDL & FHL transfer to Dorsum(O

NO

)

7-

TA & EHL transfer to the mid dorsum or lateral Dorsum (TOHEN)

SSKKEELLEET T A ALLLL Y Y MM A AT T UURREE::

• Triple fusion + Laterally based wedge (D

WYER

)

+ tendon transfer


19/42

456

6

| Page

III Valgus

o

o

IV Calcan

o

TAL + postcapsulotomy

s: more coPathology:

Us Mo Do Sus

Treatment:

GRI

DEN

Ilia

D

ILL

Mewe

neocavus:

Due to: 2ry 1ry

SKELETALLY

2ry

1ry

SKELETALLY

1-

Th

2-

No

Imm

P.Brecunie

mon tha ally it is assre ð tight tsiflexion otentaculu

CE GREEN

eNNYSON AN

crest graf LWYN

-E

VA N

dial slidindge

to excessi to spastic

Y IMMATURE :

.................. T

..................▪

Y MATURE:

re is tend(1)

ELMSLI

Osteotom

Fusion

Cut

POP

(2)

Tripletendon fo Pantal

[Ortho

ture

is toform

G

varus

ociated wiiceps suracur at thetali is shift

xtra-articulND FULFORD

in sinus taN

’

S transver calcane

e TALorsiflexors

:

lectomy b

Partial EDL

TA Ca Val

n to transf 2 stage op

Stage 1

my

Dorsal W

TNJ

Steindler

Full dorsi-

usion + Te transfer:r fusion

pedic Neur

Ta

Equin

rice Green orillwyn Evan

th equinus(less ð ev

mid tarsaled lat & do

r lateral sD

MODIFICAT

si. Walkin

e calcanel osteoto

(EDL & TA

ut painf

denervati

shorteninus Steindlgus

er:eration:

dge

lexion to cor

don trans

ology ]

alipes

noValgus

Triple fu

rtor invert eversion

wnward

btalar arthTION

uses s

cast for 1

l osteoto y may b

) in relatio

l pseudoa

n

& transferer ± Samils Grice or D

rect cavus

fer

ionRe

r imbalanf the calc talar hea

rodesis crew bet

weeks.

y + fibulare done in

to weak T

rthrosis, LL

to Tendon calcaneillwyn

Stage 2

Posterior W

subtalar

TA + PL tra

In plantar fl

Mature

ove MedWedge

e)neus + MTsublux m

een talus

BG (lateralstead of

riceps sura

D, deformi

chillesal crescent

edge

sfer to tendo

xion to aid h

Other sof tissue

abductiondially

and calca

lengtheniedial clo

e

g, one w

osteotomy

-achilles

ealing

eus.

g)sing

y


20/42


V

Claw toes:

o Neurectomy of the motor br of the lateral pantar nerveo Release of the insertion of the FDB

V 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 transferStage IV Above + hip flexor & add spasticity + psoas + adductor release.

DD.. UUppppeerr LLiimmbb ddeef f oorrmmiitt y y ::

I. Shoulder adduction internal rotation

1-

SEVER’S

release: subscap, pec major, coracobrachialis, short head biceps, coraco-humeral lig.

2-

L’EPISCOPO ZACHARY

: Sever’s + Teres & latissimus transfer to post-lat aspect of prox

humerus3-

ROTATIONAL HUMERAL OSTEOTOMY

II.

Elbow flexion

1.

Flexor tenotomy2.

Biceps transfer to triceps

III.

Forearm pronation

1.

Pronator tenotomy2.

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 releaseGroup 3 No active sup, loose passive sup Pronator teres transferGroup 4 No active sup, tight passive sup Pron quad release ± flexor aponeurotic release

IV.

Wrist & finger flexion

1.

Arthrodesis wrist2.

Release common flexor origin3.

FDP high cut & FDS low cut; then suture the tendons together

V.

Thumb in palm

1.

Cut pollicis (adductor, flexor, opponense) & 1st interossei2.

Tendon transfer to restore the thumb abduction: Pronator teres transfer

Z

ANCOLLI

C

LASSIFICATION

TREATMENT

1 finger ext é wrist 20º flexion + active ext FAR + FCU tenotomy2B same + No active wrist extensor FAR + FCU to ECRB3 No Finger extension FCU to EDL or Prox row carpectomy or Wrist Fusion

or FDS to FDP.


21/42

458


Poliomyelitis• 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 (S

ABIN live attenuated vaccine oral drops,S

ALK IM killed vaccine) Ætiology :

• Organism:o Polio virus: small RNA virus (3 types;

B

RÜNHILDE

,L

ANSING

,L

EON

)• Route of infection:

o The virus enters the body via feco-oral routeo 10 Incubation period during which the virus reaches the peripheral circulationo 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 paralysis2-

Reversible toxic changes: cloudy swelling and chromatolysis reversible paralysiséin 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 atrophy2]. Fibrosis and shortening

• Bone:1]. Disuse atrophy ð ms stresses2]. Short limbs

• Joints: Unbalanced and instability


22/42


Polio In The Upper Limb

1- Shoulder: Deltoid, subscapularis, supraspinatus, infraspinatus, and serratus paralysis • Skeletally immature

(SAHA TENDON TRANSFERS)

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:MUST HAVE GOOD HAND FUNCTION)

1]. BROOKS-SEDDON

................................................ all pec major to biceps 2].

CLARK’S

.................................................................... sternal pec major to biceps 3].

HOVNAN

................................................................. 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].

STEINDLER FLEXORPLASTY

................................ advancement of the common flexor origin to lower humerus; before opassess flexors, doing elbow flexion 90º hand clench test, if he can not do, cancel the operation

8]. BUNNEL

modification ......................................... augment the transfer by fascia and attach it to the lat border ofhumerus for better pronation

9]. MAYER-GREEN

...................................................... 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].

Z

ANCOLLI ................................................................. 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 ............................. (

BOYES

)

2] ECRL ............................................... (B

RAND)3] Sublimis ......................................... (

ROYLE THOMPSON

)

o Loss of opposition (as in median) ................. 1] Ring sublimis ................................ (R

IORDAN

)(= Abd & rotation at CMCJ + flex IP) 2] EIP .................................................... (

B

URKHALTER

)3] Riordan + FCU

7- Intrinsic Minus hand

o Claw hand as low ulnar & median ............ 1] ECRL ................................................ (BRAND

)2] Sublimis .......................................... (

BUNELL

)3] EIP ..................................................... (

R

IORDAN

)8-

Index

: o Loss of abduction (Ulnar): ............................... EIP or Abd Pollicis ........................... (

NAVIASER

)


23/42

460


THUMB ADDUCTION

THUMB OPPOSITION

C

LAW

H

AND

G

ENU

R

ECURVATUM


24/42

Pol1-

2-

3-

De

1].

2].

3].

4].5].

6].7].8].9].

10].

11].

12].

13].

GG•

io in LoHip

1]. FLEXION

]. PARALY

]. F

LAIL

H

a. Fb. A

4]].. FLEXION

c.

Md. Se. Al

Knee:

1]. F

LEXION

a. Mb. Mc. S

]. R

ECURV

a.

Typ

b.

Typ

]. G

ENU

V

]. FLAIL K

Foot Ank

eformity

Varus

Valgus

Equinus

TEV

TE valgus

TC Valgus

Cavus (Plant

Calcaneo Ca

Pes cavovaru

Claw Toes

Hamm er Toe

Mallet Toe

Dorsal Bunni

Grice Greeroneus Tr1]. Elimina

]. No orth

er Limb

N DEFORMIT

YTIC D ISLOCA

H

IP

: (accordee ..................bnormal ......N ABDUCTIO

ild ....................vere ..............lternative .....

i.

Mild .....ii. Severe .

N

D

EFORMIT

ild ..................oderate (30vere (90º) ..

VATUM

: e I ...................

i.

I

RWIN ii.

Biceps te II ..................

i. Long Le

ii.

PERRY, O

iii.

Bony bl

iv .

Fusion ..V

ALGUM :

......KNEE :

..............kle

Mild .....Severe .

P. Brevi

TAL + B

TAL + BTAL + P

Banta ris) Steindle

avus Steindle

us Steindle

Big

.......Toes .....Or .........

e FDL ten

FDL ten

on Lapidus

(Tibial graft)nslocationes the calcaosis can co

TY

.....................ATION

............

ing to the c..................................................

ON

..................................................

.........................

.........................

.........................

TY :

......................... -40º) ...........................................

.........................

upratuberco patella

.........................g Brace ........

O’BRIEN, HOD

Posterior

caGracilis & SITB to Segastroc oriock operatiH

EYMAN

.....M

AYER

........

H

ONG

-X

UE

.........................

.........................

.........................

Immatu

.......Hoffer, K

.......Drennan

to cuneifor

Bisla ± Ankle

Bisla ± SteindB to Cuneifo

PL & PB reloer + Jones oer + Banta er

+

B

ISLA

+

T

.......Jones

.......Hibbus

.......Taylor F

notomy

notomy

s (TA to Nav +

EV= Evansmust be dneus and v trol the cal

[Orth

......................

......................

ondition of...................... F......................

...................... Y......................C

......................I

R

...................... Y

...................... Y

...................... P

...................... S........................ P

...................... (

lar open w

...................... (

..................... if

DGSON

....... ifpsular adva posteior cimembran

in (in a dians ............... if

...................... T

...................... IliE ..................... I...................... f ......................

M

...................... L

ure

Kaufer, Tohe

n TA Post tran

+GG

orEV

fusion

dler rm + GG or

ation + GG o

r Hibbus Samilson

Tohen

DL to EDL

FHL to P.Phx

(Fibular Graf one beforelgus force eaneus defo

opedic N

s CP s CP

pine, epsilausion rthosis

Y

OUNT

’

S ITBC

AMPBELL

IliRWIN

C

OM B

I

ount’s + Soount’s + Ca

OP wedginpracondylst capsuloto

uad =0 /

edge tibial

uad = 5 /30º (triplencement.eckrein.osus & Bional fashio

severe degibilaizationac crest intr

verted patils due to b

M

ODIFIED

M

C

ong Leg Br

We

en fer

Lateral

V

GG or

Lambri

AnteroV Antero

EV PosteroJapas

Elmsli o

Dwyer

Same+ IP fusi+ MP ca

DuVrie

DuVrie

base + Nav-C

) / PB= Pro age of 1 y arly beforemity at the

urology ]

eral knee, c

& lateral IMc crest tranINATIONS

:

tter’s

pbell

r extensionmy + hamstri

amstring =

steotomy.

amstring =

tenodesis).

eps to M).

ee.

f patella.

a-articular p

lla to tibia (d muscle a

C

E

W IN

’

S

ostce or Fusio

edge F

Dwyer) T

V T

nudi

T

ateral T edial T

medial T orsal V-sha

or T or lateral cal

nsulotomy

es PIP Excisio

es DIP Excisio

neiform fusio

eus Brevis /ear:ry bone chalking ag

ontralateral

eptum relefer above t

osteotomyg lengthen/

) with bon

0).

dial

tella to tibi

fter patelled other joi

eotomy (¾

Matu

usion Tendo

F Same

F P.B to

F TAL +

F TAL +F TAL +

F Bantaed osteotoF Bantacaneal displ

If theDuVr

or Fu

arthroplast

n arthroplas

n + Cuno-MT

PL= Proneus

anges

hip)

ase e acetabul

(R

EVERSED

I

transfer to pa

changes.

BG.

tomy). ts conditiosteotomy/

ure

on transfer

T

C T

Bisla

BislaPB to C

P y of the tars Pcement oste

re is OA ries MP excission

or Fusion

y or Fusion

usion + plant

Longus / C

Page |

m

I

RWIN

)

tella

.

¼ clasis)

No Tendon

F + Dwyer

F + GG or E

nkle Fusion

nkle or Pantnkle or Pant

antalars

antalarotomy

ion arthropl

r IP capsuloto

Cuneiform

461

n

alaralar

sty

my)


25/42

462

Intr

Bra

2

| Page

roduction

• It is no

achial plex

• 5 roots:• 3 Trunk• 6 divisi• 3 cords:• Nerves• Nerves• Nerves•

Lateral• Medial• Posteri

a commo

xus anatom

C5,6,7,8,T1: Upper,ns: 3 anter lateral, merom the rrom the trrom cords:

ord: LL Mord: MMMr cord: UL

raly encoun

my

iddle, Low ior, 3 postedial, posteots: Long tnks: Supr

sculocutaM Ulnar AR

[Ortho

hialtered thou

erioriorhoracic (Cscapular n

eous

pedic Neur

lexgh grave i

,6, 7), Phrerve, n to s

ology ]

us jury

nic (C5), Dubclavius (

njurie

orsal scaporm uppe

lar (C5))


26/42


Ætiology:

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, Sternoclavicular3-

Inflammatory: Radiation plexopathy: pain after radiation DXT4-

Tumors: Neural: neurolemmoma, plexiform neurofibromatosis Non neural: Pancoast tumor

5-

Compression neuropathy: Thoracic outlet syndrome: thoracic rib,…

6-

Vascular ischemia7-

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 durao Injury proximal to the DRG i.e. intact axons the DRG cells does not degenerate but there is

loss of sensationo Back muscles are denervatedo Usually + phrenic + long thoracic + dorsal thoracic + Hornero All nerves that emerges from the roots are injured

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

3]. Trunkso Intact nerves: long thoracic and pectoral nerveso Suprascapular nerve is affectedo

Upper trunk (deltoid & biceps)o Middle trunk (radial n)o Lower trunk (ulnar + median)

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


27/42

464


Microscopically:

SEDDON’S CLASSIFICATION

: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)

S

UNDERLAND

C

LASSIFICATION

1]. Type 1 : neuraparaxia2]. Type 2 : axonotemesis with intact endoneurium3]. Type 3 : severe axontemesis with only intact peri & epineurium4]. Type 4 : neurotemesis é only intact epineurium5]. Type 5 : neurotemesis is complete with fibrosis

1-N

EURAPARAXIA

:

1]. Physiological Conduction block2]. No degeneration reaction occur3]. Due to myelin disintegration

4].

Regeneration of myelin occur with schwann cells with regain of the full function

2-

W

ALLERIAN

D

EGENERATION FOR

A

XONO

&

N

EUROTEMESIS

• Proximal to axonotemesis or neurotemesis1]. Perikaryon: swell then retract, nucleus becomes more peripheral, chromatolysis (Niessers

granules desintigrate)2]. Adjacent cells show similar changes3]. Retrograde degeneration of the axon till the next

N

ODE

O

F

R

ANVIER

• 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 fiber3]. Myelin disintegrate4]. Schwann cells and macrophages clean the debris5]. Schwann cells multiply and form Bunger tubes for future axon sprouts to come in6]. Muscle atrophy, fasciculations, polyphasia

• Regeneration:1]. 30-40 days latency occurs till the beginning of the regeneration2]. Axon sprouts starts to bridge the gap till it finds the way in the distal end3]. Axons travel 1mm/d till reach the distal organ

4]. MUSCLE

: № of motor end plate, sensitivity, then starts to respond & fasciculation

55]]..

S

ENSORY IS BETTER THAN

M

OTOR: and can wait for longer periods till start to regenerate


28/42


Clinically:

1-

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

ERB’S DUCHENNE:

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

2-

DEJERINE KLUMPKE PALSY:

Lower roots (C8,T1) avulsion + upper roots rupture (20%) Complete flail paralysis Phrenic

3-

C

OMPLETE + Horner marble skin

2-

Sensory:o Diminished spinothalamic sensations:

Pain, Temp, Crude toucho 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 reflexes5-

Causalgia: pain due to injury of a sensory nerve (e.g. median)


29/42

466

Ele

1-

2-

3-

4-

5-

6-

7-

PXR

•

•

•

6

| Page

ctodiagno

Reaction

CHRONA

SD (streng

EMG:1-

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ty: by ⊕ofnerve the .... Myelin

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Treatment

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 msOperative:

1-

I

NDICATIONS

A

ND

T

IMING

:

1]. If the point of 3mo passed without evidence of biceps regeneration2]. Reconstructive surgery for late sequelae

2-

F

INDINGS

:

1]. Root avulsion2]. Continuous root and trunk (traction injury)3]. Neuroma formation

3-

T

ECHNIQUE

:

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. Perineuralb. Fascicularc. Group Fasciculard. Perineural and fascicular

o Avoid: Gaps

Infection Tension:

(1)

5 cm: nerve grafting:o Fibrin & plasma glue: may be used to operative time and the use of suture fibrosiso 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 neuromac. Cable graftingd. Pedical rotational intergrafting (bet ulnar and median)

4]. Homografts are immunogenic


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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].

FAIRBANK

release of the subscapularis + pec major + ant capsule2].

S

EVER

’

S

release of the subscapularis + Pec major lengthening3].

L’EPISCOPO

: transfer of Latissimus & teres major to the back of the humerus ER (ZACHARY

,T

ACHIDJIAN

modifications)4].

H

OFFER

transfer of latissimus and teres into the rotator cuff ER + abduction5].

O

BER

long head triceps + short head biceps transfer to acromion6].

GILBERT & MAYER

trapezius transfer to humerus7].

S

AHA

acromion with the attached trapezius advancement to humerus as distal as possible

8].

Humerus derotation osteotomy9]. Arthrodesis is the last resort

Lesion procedure as recommended by AAOS

Adduction + IR Subscapularis ReleaseSupra or infraspinatus Dysfunction Latissimus to greater tuberosityDeltoid Dysfunction Saha or HofferIR or ER + incongruent shoulder joint Humeral derotation osteotomySevere dysfunction of shoulder Glenohumeral arthrodesis

7]. Elbow reconstruction:

Flexor paralysis:(M

UST

H

AVE

G

OOD

H

AND

F

UNCTION

)

B

ROOKS

-S

EDDON

.................... all pec major to biceps

C

LARK

’

S

...................................... sternal pec major to biceps

H

OVNAN

.................................... Latissimus origin to biceps Pec mior to biceps Sternomastoid to biceps ..... using a fascia to give more length webbing of neck Triceps to biceps

S

TEINDLER

F

LEXORPLASTY

...... advancement of common flexor origin to lower humerus;assess 1st flexors condition by doing elbow flexion 90º hand clench test

B

UNNEL

modification ............ augment by fascia &fix to lat humerus (better pronation)

M

AYER

-G

REEN

.......................... 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 ...........

Z

ANCOLLI

biceps rerouting around the radial neck

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


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R

ECENT

T

RENDS

I

N

N

ERVE

R

EPAIR

1. Phamacoloical agents

1-

Gangliosides2-

Polyamines

2. Immune system modulators

1-

Azathioprine2-

Corticosteroids3-

Cyclosporin A4-

Cvclophosphamides3. Enhancing factors

1-

Nerve growth factor2-

Fibronectin3-

Insulin-like growth factor4-

Ciliarv neurotrophic factor

4 Entubulation chambers

1-

Autogenous vein2-

Silicone Polvglycolic acid G3-

Gore-tex

Prognosis

A]. Preoperative:1]. Level of injury: the distal the better2]. Delay of injury: the more acute the better3]. Type of injury: the apraxia the better4]. Type of nerve: the pure the better & the small the better5]. Type of pt: the younger the better

B]. Operative:6].

Huge gaps

7]. Huge tension8]. Huge suture (we use 8-0 or 9-0)

C]. Postoperative9]. Hematoma

10]. Infection11]. Inadequate physiotherapy


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THUMB ADDUCTION

THUMB OPPOSITION

CLAW HAND


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Carpal Tunnel SyndromeCommonest middle aged F:M = 3-5:1Anatomy Of Carpal Tunnel

• 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 NerveFlexor tendons run deep to nerve

Causes (ICRAMPS)

• Idiopathic• Colles, Cushings• Rheumatoid• Acromegaly, amyloid

•

M yxoedeoma, mass, (diabetes) mellitus• Pregnancy, Persistent median a.• Sarcoidosis, SLE

Symptoms

not always classical

1-

Aching and parasthesia in thumb , index middle and 1/2 of ring finger2-

worse at night3-

forearm pain4-

dropping things

Signs

1].

Hand normal looking2]. If severe, thenar wasting, trophic ulcers3]. weakness of thumb abduction4]. Semmes Weinstein monofilament test & Vibration test are more sensitive than 2 point

discrimination test in assessment of the slowly progressive sensory compression change5]. 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 distributionof the median nerve

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

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

Differential diagnoses

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


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InvestigationsNerve 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 supplied2]. Latency = time between stimulus and MAP3]. Conduction velocity, normal = 40-60 m/s4]. compression causes CV in a segment5]. If very severe MAP also reduced

• Sensory 1]. SNAP recorded in proximal nerve after distal stimulation2]. 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

ManagementConservative -

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

1]. open /endoscopic decompression1]. Need to bear in mind anatomical variations2]. Beware palmar cutaneous branch of median nerve, and motor branch3]. Apply volar splint to hold the wrist in extension bowstring & RDS

Complications of surgery 1]. Complex Regional Pain Syndrome

2].

Tender hypertrophic scar pillar pain3]. neuroma in palmar branch4]. tenosynovitis / tendon adhesions5]. bowstringing of tendons

Endoscopic release Okutso&Agee1]. one or two incisions2]. less scarring3]. less pillar pain4]. quicker return of strength and to work5]. but:6]. Anecdotal reports of disasters

7].

Big learning curve8]. Time consuming, expensive


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Pronator Teres SyndromeCompression at

• Lacertus Fibrosus = biceps aponeurosis • pronator teres muscle• fibrous arcade of FDS•

Ligamentum Struthers (present in 1.5 % of people)Causes

1]. Repeated minor trauma/ repetitive use of elbow2]. fracture / fracture dislocation of elbow3]. Tight/scarred lacertus fibrosus4]. Tendinous bands in pronator teres5]. Tight fibrous arch at prox FDS

Symptoms

1]. Aching / fatigue of forearm after heavy use 2]. Clumsiness3]. Vague, intermittent parasthesia, but rarely numbness

Signs 1]. local tenderness to deep pressure and reproduction of symptoms22]].. TINELS TEST

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

Investigations

1]. NCS

not much use, intermittent symptoms2].

EMG

innervation of muscles & differentiate from CTSManagement

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

flexed with pronation2]. 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

Clinical diagnosis

• 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

Investigations

• EMG + NC unhelpfulManagement

•

Conservative- NSAIDS, avoiding aggravating movements•

Surgical exploration- most common compressing structure deep head of pronator teres


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474


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

Aetiology:1]. At elbow:

o Cubitus Valgus ○ Traumao Bony spurs ○ Tumours

2].

Proximal 8cm by‘ Arcade Of Struthers’ ≠ ligament of Struthers’. It is a

thin aponeurotic band extending From Medial Head Of Triceps To TheMedial Intermuscular Septum; it is 8 cm proximal to the medialepicondyle; it may look like triceps fibers crossing superficial to the ulnar n.& usually it is not site for entrapment under ordinary circumstances, but itdo é anterior transposition of ulnar nerve is performed

3]. Distal by hypertrophied FCU

Symptoms

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

Signs

1].

Hypoesthesia ulnar side of hand + 1½ fingers2]. Tinels

TEST

, behind medial epicondyle3]. Wartenburg’s sign weakness of abduction of little finger4]. Froment’s Sign pinch grip and grasping, both of which are impaired by a low ulnar nerve

palsy due to weakness of adductor pollicis5]. 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 neuropathyInvestigation

1]. NCS reduced nerve conduction velocity2]. EMG evidence of denervation of muscles

ManagementConservative

1]. Avoidance of repetitive bending of elbow; Extension Block night splint.1]. injection contraindicatedSurgical -controversy

1]. Decompression- ‘Cubital Tunnel $ Does Not require transposition of the ulnar n’

2].

Transposition: - subcutaneously/ Submuscularly (better)3]. +/- medial epicondylectomyResults

• Sensation improves better than motor function over 3-5 y period

Complications

1]. Recurrence ð inadequate decompression or irritation or redislocation or neuoma2]. CRPS


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Ulnar Tunnel SyndromeGuyons 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 interosseousManagement

• Conservative

1].

Splinting2]. Avoidance of repetitive trauma• Surgical

1]. Decompression of motor and sensory branches2]. +/- excision of pisiform/ hook of hamate


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476

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Radial Tunnel SyndromePain & No Paresis)

• Mild compression of post interosseous nerve without paresis

Causes

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

DiagnosisSymptoms

• 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 thepain. Due to ECRB inserting into base of 3rd metacarpal.

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

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

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

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

Differential diagnosis

•

Tennis elbowManagement

• 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.


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Nerve Entrapment in Lower Limb

N

ERVE SITE CAUSE SYMPTOM

ILIO-INGUINAL Hypertrophied abdominal ms Intense training Pain & parasthesia

OBTURATOR Hip adductor Skaters Medial thigh pain

F

EMORAL

L

AT

.

C

UT

.

ASISMeralgia paresthetica

Tight belt Lateral thigh pain

SCIATIC Ischial tuberosity, pyriformis ms Pyriformis Sciatica

S

APHENOUS

Hunter’s canal Quad or sartorius Infero-medial knee pain

C

OMMON

P

ERONEAL

Fibular head Direct blow Foot drop

SUPERF PERONEAL 12 cm above Lat.Maleolus, as itpierce the deep fascia

Inversion injury Dorsal foot pain &paresthesia

SURAL 12 cm distal to Lat Malleolus Jone’s fr Lat. foot parasthesia

DEEP PERONEAL Inf. extensor retinaculum(anterior tarsal tunnel $)

Inversion injury Sole pain & parasthesia

P

OSTERIOR

T

IBIAL

Flexor retinaculum(Tarsal tunnel $) FDL accessorius, RA,tumors, ganglion Sole pain & paresthesia

1

ST

L

AT

.P

LANTAR

Bet AHL fascia, quadratus plantae High heels Plantar fasciitis

MEDIAL PLANTAR Henry Knot (cross of FDL & FHL) Orthotics Big toe pain & parasthesia

I

NTERDIGITAL

Bet MT 3-4 plantar to deep MT lig(Morton’s Neuroma)

Push phase in runners Digital pain, parasthesia,dead toe


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T T h h o o r r a a c c i i c c O O u u t t l l e e t t S S y y n n d d r r o o m m e e • 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 TOSo Fibrous bandso Scaleneus anterior constriction

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

3]. Pancoast tumour

Examination:

1]. Tenderness or mass in supra-clavicular fossa2]. Lower trunk C8/T1 manifestation:3]. Sensory changes in the Ring and Little finger4]. Intrinsic weakness5]. Vascular Examination

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

Provocative Tests1.

Adson’s TEST

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

2.

Reverse Adson’s TEST o As above but head turned away from the affected side

3.

Wright’s test (Hyperabduction stress test)o Axillary vessels and plexus bent 90º at the junction of the glenoid and humeral heado Place extremity in full abduction, external rotation and reach back as far possible. Turn

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

4.

Roos overhead exercise testo 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 tumour3-

MR scan to exclude cervical disc disease

Treatment1-

Non-Operative (for At Least 4 Months)o Postural re-educationo Activity modificationo 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

Orthopedic Neurology

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