[Orthopedic Neurology] Page | 1

Neuro-Anatomy Neuron:  Is the specialized cell of the nervous system that capable of electrical exciation (action potential) along their axons 2 | 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 1- Spinothalamic (Pain, temp, Stretch reflex crude) arc from ms 2- Indirect pyramid 2- Lemniscal (DC) spindle (proprioception, fine touch) Fibre α Motor (12-20 μm) α Propriocep (12-20 μm) γ fibers B preganglionic B fibres  Touch, vib (5-12 μm) C Postganglionic δ fast pain, temp (2-5μm) C Slow pain, crude (0.2-2µm)  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  GroupToFor   m  fascicles surrounded by perineurium  GroupToFor   m  nerve surrounded by epineurium Muscle:  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  MS CONTRACTION: is the active state of a ms, in which there is response to the neuron action potential either by isometric or iso tonic contraction  ISOMETRIC CONTRACTION: is the contraction in ώ there is  tension ώ out change in the ms length  ISOTONIC CONTRACTION: is the contraction in ώ here is a change in the length of the ms éout change in the tone  MS TONE: is the resting state of tension  MS : is the adaptive structural changes in a ms 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 is impaired  RIGIDITY: Involuntary sustained contraction of a ms not stretch-dependent. Growth of ms is fair [Orthopedic Neurology] Page | 3

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 &  Concentric: ms shortens during contraction length (dynamic) Eccentric: ms lengthens during contraction Isometric Constant ms length (static) Isokinetic Max contraction é constant Concentric velocity over a full ROM Eccentric Aerobic In the presence of O2 Replenishes 34 ATP 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

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Muscle injuries: 1]. Muscle Strain: • Occurs at Musculo-tendinous junction of the ms that cross 2 (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 y sensitivity to acetyl-choline and fibrillation in 2wk Tendons • COMPOSED OF: 1]. Collagen I ...... 80% 2]. Fibroblasts synthesis tropocollagens Æ micro-fibrils Æ sub-fibril Æ fibril Æ fascicle 3]. Loose areolar CT ...... Endotenon Æ epitenon Æ paratenon • TYPES OF TENDONS: a. PARATENON covered tendons rich capillary supply = better healing b. Sheathed tendons ...... segmental bl.supply via mesotenon (VINCULA) • MUSCULO-TENDINOUS JUNCTION: 1]. Tendon 2]. Fibro-cartilage 3]. Mineralized fibrocartilage (SHARPEY’S fibers) 4]. Bone • HEALING 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 healing Ligaments • COMPOSED OF: 1]. Collagen I (same ultrasturcture) ...... 70% 2]. Elastin 3]. Fibroblasts + Loose areolar CT • BL SUPPLY 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 • BONY LIGAMENTOUS JUNCTION: 1]. Ligament 2]. Fibro-cartilage 3]. Mineralized fibrocartilage (SHARPEY’S fibers) 4]. Bone • HEALING starts by fibroblasts and macrophages of the epitenon Phase Time Process Strength 1].Hemostasis 10 min platelet plug Æ fibrin clot Weak 2].Inflammatory 10 days macrophages debride granulation tissue Weak 3].Fibrogenesis 30 days UMC Æ fibroblasts Æ strong type I collagen most strength regained 4].Remodeling 6-18 mo Realignment & cross linking of collagen bundles Max strength

• LIGAMENTS GRAFTING: 1]. Autografts: ...... Faster healing, no disease transmission 2]. Allograft: ...... no donor morbidity but may transmit diseases 3].. Synthetic: (Gortex, Leeds Keio) ...... no initial weakness, but cause sterile effusion [Orthopedic Neurology] Page | 5

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

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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

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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) Classification 1- Spastic ...... (60%) o MOST AMENABLE TO SURGERY o UMNL involvement - mild to severe motor impairment o : % 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 o POORLY AMENABLE TO SURGICAL CORRECTION 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 & ext+ stepping gait + Lean backward, shouler & trunk extension. o Intelligence normal (often above average) o MOST DIFFICULT TO CORRECT - results are unpredictable & POP hazardous ð friction o Types: 1- TENSION ATHETOSIS: . Child is hypertonic but not hyperreflexive (no clonus or Spasticity) . Deafness and absence of an upward gaze. 2- DYSTONIC ATHETOSIS: . Continuous, tortuous, slow, twisting type of motion. . All extremities, as well as the neck and trunk, tend to be involved. 3- CHOREIFORM ATHETOSIS. . More common than dystonic athetosis . Continual movement of the patient's wrist, fingers, ankles, toes, and tongue. 4- DRAMATIC BALLISMUS ATHETOSIS. . Continuous dramatic movement of the trunk and proximal extremities . These patients can injure themselves or their caregivers by this 5- RIGID ATHETOSIS . The most hypertonic & stiff of all CP (Yet no spasticity or clonus) 8 | Page [Orthopedic Neurology]

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: ...... SPASTIC UMNL  Area 4 precentral gyrus: ...... FLACCID UMNL  Combined: ...... RIGIDITY  Basal ganglia: ...... ASTHETOSIS  Cerebellum: ...... ATAXIA  Mid brain: ...... TREMORS 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 DISINHIBITED STRETCH REFLEX ώis regulated by descending tracts  SPASTICITY, HYPER-REFLEXIA, CLONUS may appear  CLASP-KNIFE PHENOMENON: 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. Adduction Flexion Flexion + IR Dislocation Flexion Recurvatum Genu valgum Patella alta Ankle Eqinovarus Equinovalgus calcaneus Claw & metatarsus UL add IR 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 : 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 [Orthopedic Neurology] Page | 9

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, SCISSORING, STIFF-LEGGED, TIP-TOE GAIT, CROUCHED 2-  Stride length, Narrow walking base 3- Lordosis . Co-ordination in turning.  Hip deformities: 1- Adduction: ...... ð adductor spasm (GRAB TEST +VE  Hip Abduction) 2- Flexion: ...... ð rectus spasm ...... (ELY & THOMAS & STAHELI +VE) 3- Flexion internal rotation: ...... ð psoas spasm (true scisso ring ≠ pseu d o scisso ring ð flexion + anteversion  +VE W SIGN) 4- Hip dislocation ...... ð 1ry & 2ry ...... (GALEAZZI TEST +VE) . WINDSWEPT POSTURE - one hip adducted & other side abducted . SCISSORED GAIT 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): ...... +VE TRIPOD SIGN & TOE TOUCH 2- Knee recurvatum ...... REVERSED POPLITEAL ANGLE 3- Genu valgum 4- Patella alta (BLUEMANSAAT, INSALL-SALVATI RATIO<1) ð flexed knee & quad spasm . Flexion deformity angle is best assessed by the popliteal angle . Flexion contracture lead to CROUCHED GAIT (also ð hip flexion & calcaneus) . Tight rectus femoris  stiff legged gait (prolonged stance & diff. foot clearance) . Sitting - Legs forward Ankle deformities: 1- Ankle EQUINUS (NB, False equinus = flexed knee lifts heel from ground) 2- CALCANEUS 3- VARUS 4- VALGUS 5- CLAW TOES 6- METATARSUS ADDUCTUS . TIPTOE GAIT . SILFVERSKIÖLD TEST: equinus  é knee flexion = gastroc tight > soleus . Equinus  knee recurvatum in stance phase . Calcaneus  crouch gait Kneeling eliminates contracture effect 10 | Page [Orthopedic Neurology]

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

Neurology o CLASP-KNIFE phenomenon o Primitive reflexes:

A, ASYMMETRICAL TONIC NECK: as head is turned to one side, contralateral arm and knee flex. o B, MORO REFLEX: Hold child at 45 . Allow head to drop back, UL extend away from body and then come together in embracing pattern. C, EXTENSOR THRUST: as child is held upright by armpits, lower extremities stiffen out straight. D, NECK-RIGHTING REFLEX: as head is turned, , trunk, pelvis, and lower limbs follow turned head. E, PARACHUTE REACTION: as child is suspended at waist and suddenly lowered forward toward table, arms and hands extend to table in protective manner. F, SYMMETRICAL TONIC NECK: as neck is flexed, arms flex and legs extend. Opposite occurs as neck is extended. G, FOOT PLACEMENT REACTION: when top of foot is stroked by underside of flat surface, child places foot on surface.

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Potential for walking

Assess (midbrain & perinatal)

If mid brain reflexes appear Perinatal reflexes persist >1y (early balance reaction) (normally disappear at 4-6m) Parachutte reflex Moro Tonic neck (symmetric & asymm) Stepping Neck righting (body follow head turn) Extensor thrust on vertical susp

Can walk Will not walk

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

Radiography: Hip:  WIBERG CE angle  MP of REIMER (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

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Treatment of CP Aphorisms. Priorities Patient priorities are  A little equinus better than calcaneus. 1]. Communication  A little valgus better than varus. 2]. Activities of daily living  A little varus better than a lot of valgus. 3]. Mobility & Walking  A little knee flexion better than recurvatum. Objectives 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.

LOWER LIMBS

1- PHYSIOTHERAPY - 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- CAST CORRECTION - Inhibitive casting. Stimulation of sole can cause muscles to contract was basis of inhibitive casting. Not used much now. 3- CORRECTIVE CASTING - for mild fixed equinus. Well-padded POP é max dorsiflexion 4- BRACING - Useless for treating fixed deformity AFO's useful for Dynamic equinus 5- NEUROSURGERY - Selective posterior RHIZOTOMY 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- CHEMONEURECTOMY: selective neurectomy is done using certain chemical substances: a. ALCOHOL 45% gives improvement for 6 wks b. PHENOL 5% 2ml gives permanent effect c. BOTULINUM TOXIN gives 6m improvement (  acetyle choline) d. BACLOFEN intrathecal implanted pump (GABA agonist  excitatory transmitters) [Orthopedic Neurology] Page | 13

7- Orthopaedic operations Indications: 1]. Postural contractures 2]. Correction of fixed deformities 3]. Stabilizing unstable 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 A. Hip Procedures: 1. Hip at risk : . <50% REIMER’S MIGRATION PERCENTAGE . Abduction < 25º . Broken Shenton . Treated by psoas, adductor and hamstring LENGTHENING. 2. Subluxed hip é RMP > 50%. . VARUS DEROTATION OSTEOTOMY 3. Adducted hip: . COMPLETE ADDUCTOR TENOTOMY ± obturator neurectomy . All the Add longus, brevis, most of magnus, & gracilis . Still the patient can adduct with pectineus 4. Adducted subluxed hip:

ADDUCTED SUBLUXED HIP Assess RMP

<50% >50%

<5y <50% MP No dislocation Soft tissue Bony operations operations

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

VDO OR+VDO+ Total Add Adductor Ant. Chiari tenotomy ± Brevis Obturator Psoas lengthen nurectomy Acetabulo-plasty 14 | Page [Orthopedic Neurology]

5. Flextion deformity (<20º may correct by traction) 1]. SOUTTER’S sartorius, rectus, & tensor fascia lata (flexor release) via Smith Peterson 2]. MUSTARD: iliopsoas tendon transfer to GT 3]. SHARRARD: 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: OBER’S operation (sacrospinalis transfer to act as hip extensor

6. Flexion + internal rotation Flexion

Flexion Pure Flexion + IR

So u tter’s Flexible Fixed Then do Thomas test

So u tter’s + ER Soft + Derotation Still there is FFD No FFD spica osteotomy

Iliopsoas recession Mustard Sharrard Neutral spica to ant capsule

Lateralization of hamstring origin

7. Dislocation:

Dislocation

Painless Painless Painful Reducible Irreducible Irreducible

Correct Correct Correct Adductor Open Schanz pelvic Muscle valgus dysplasia release ± reduction + neurectomy Fusion support + traction osteotomy Sharrard VDO Salter Chiari or Mustard When head at acetab do OR & proceed as painless reducible Address ipsilateral knee deformity & lig 8. Pelvic obliquity before hip fusion  Fixed obliquity Dynamic obliquity   PSF Abd release of opposite side

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B. Knee Procedures I. Flexion deformity:  Due to: A. 1ry hamstring Spasticity B. 2ry to hip FFD or equinus  Treatment:

Knee Flexion

Prolonged Correctable Fixed = Patellar malalignment

+ Hip adduction Check Hip & E g g er’s Test abd in E g g er’s + E g g er’s + ankle for + IR Pure Flexion + deformity flexion & Insall lat ret Hauser extension release Patellar plication

Same  in flexion E g g er’s E g g er’s Release = Gracilis = Hamstring + Gage

Adductor tenotomy ± E g g er’s release neurectomy

1. EGGER’S 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]. : contraindicated in equinus B]. lumbar lordosis C]. weak knee flexion 2. TACHDJIAN Fractional Lengthening of Hamstring Tendons:  Z-plasty of gracilis and semitendinosus ± biceps + recession of semimembranosus 3. SUTHERLAND TRANSFER  Lateral Transfer of Medial Hamstrings for Internal Rotational Deformity of Hip 4. GAGE DISTAL RECTUS TRANSFER + hamstring release  Gives an advantage of enhancing the knee flexion in the swing phase 5. Ischeal tuberosity transfer to back of femur 6. EVAN’S lengthening plasty 7. Selective neurectomy of hamstring 8. all may be added ITB division ± Extension osteotomy (better in polio)

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II. Knee Recurvatum:  Recurvatum may be: 1]. 1ry: quadriceps spasticity or quadriceps spasticity > hamstrings & gastroc spasticity 2]. 2ry to Eg g er’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

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C. Ankle deformities:  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 Silfverskiöld Test  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. Silfverskiöld 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- MURPHY 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): SKELETALLY IMMATURE: 1- TP Lengthening (MAJESTRO) 2- TP Rerouting in front of med malleolus (BAKER) 3- TP transfer via Interosseous membrane to dorsum of Foot (BISLA) 4- TP split transfer to the proneus Brevis (KAUFER) 5- TA split transfer to the cuboid (HOFFER) 6- FDL & FHL transfer to Dorsum (ONO) 7- TA & EHL transfer to the mid dorsum or lateral Dorsum (TOHEN) SKELETALLY MATURE:  Triple fusion + Laterally based wedge (DWYER) + tendon transfer 18 | Page [Orthopedic Neurology]

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: Talipes EquinoValgus

Immature Mature

TAL + post P.Brevis to Grice Green or Remove Med Other soft capsulotomy cunieform Dillwyn Evan Triple fusion Wedge tissue

. GRICE GREEN extra-articular lateral subtalar arthrodesis . DENNYSON AND FULFORD MODIFICATION uses screw between talus and calcaneus. Iliac crest graft in sinus tarsi. Walking cast for 12 weeks. . DILLWYN-EVAN’S 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 SKELETALLY IMMATURE: . 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 SKELETALLY MATURE: 1- There is tendon to transfer: (1) ELMSLI 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 [Orthopedic Neurology] Page | 19

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.

D. deformity: 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 humerus 3- ROTATIONAL HUMERAL OSTEOTOMY 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 ZANCOLLI CLASSIFICATION 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.

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

20 | Page [Orthopedic Neurology]

  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 (SABIN live attenuated vaccine oral drops, SALK IM killed vaccine) Ætiology:  Organism: o Polio virus: small RNA virus (3 types; BRÜNHILDE, LANSING, LEON)  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

[Orthopedic Neurology] Page | 21

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 op assess 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 of humerus 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]. ZANCOLLI ...... biceps rerouting around radial neck 4- Wrist: 1]. Extensor paralysis ...... Pronator to ECR 2]. Flex paralysis (wrist & hand) ...... ECRL to sublimis 3]. : ...... 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 ...... (BRAND) 3] Sublimis ...... (ROYLE THOMPSON) o Loss of opposition (as in median) ...... 1] Ring sublimis ...... (RIORDAN) (= Abd & rotation at CMCJ + flex IP) 2] EIP ...... (BURKHALTER) 3] Riordan + FCU 7- Intrinsic Minus hand o Claw hand as low ulnar & median ...... 1] ECRL ...... (BRAND) 2] Sublimis ...... (BUNELL) 3] EIP ...... (RIORDAN) 8- Index: o Loss of abduction (Ulnar): ...... EIP or Abd Pollicis ...... (NAVIASER) 22 | Page [Orthopedic Neurology]

THUMB ADDUCTION

THUMB OPPOSITION

CLAW HAND

[Orthopedic Neurology] Page | 23

Polio in Lower Limb 1- Hip 1]. FLEXION DEFORMITY ...... As CP 2]. PARALYTIC DISLOCATION ...... As CP 3]. FLAIL HIP : (according to the condition of spine, epsilateral knee, contralateral hip) a. Free ...... Fusion b. Abnormal ...... Orthosis 4]. FLEXION ABDUCTION c. Mild ...... YOUNT’S ITB & lateral IM septum release d. Severe ...... CAMPBELL Iliac crest transfer above the acetabulum e. Alternative ...... IRWIN COMBINATIONS: i. Mild ...... Yount’s + Soutter’s ii. Severe ...... Yount’s + Cam pbell 2- Knee: 1]. FLEXION DEFORMITY: a. Mild ...... POP wedging b. Moderate (30-40º) ...... Supracondylar extension osteotomy (REVERSED IRWIN) c. Severe (90º) ...... Post capsulotomy + hamstring lengthen/transfer to patella 2]. RECURVATUM : a. Type I ...... (Quad =0 / Hamstring =5) i. IRWIN Supracondylar flexion osteotomy ii. Biceps to patella b. Type II ...... (Quad = 5 / Hamstring = 0) iii. Long Leg Brace iv. Soft operation: HEYMAN ...... Collateral ligaments reconstruction PERRY ...... Triple tenodesis (ITB, ST, Biceps) v. Bony operations: MÜLLER ...... Tibilaization of patella Fusion 3]. GENU VALGUM: ...... MODIFIED MCEWIN’S osteotomy (¾ osteotomy/ ¼ clasis) 4]. FLAIL KNEE: ...... Long Leg Brace or Fusion 3- Foot & Ankle Deformity Immature Mature Wedge Fusion Tendon transfer No Tendon 1].Varus Mild ...... Hoffer, Kaufer, Tohen Lateral (Dwyer) TF Same TF + Dwyer Severe ...... Drennan TA Post transfer 2].Valgus P. Brevis to cuneiform + GG or EV 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 + BISLA + Tohen Dwyer or lateral calcaneal displacement osteotomy 10].Claw Toes Big ...... Jones Same If there is OA  Toes ...... Hibbus + IP fusion DuVries MP excision arthroplasty Or ...... Taylor FDL to EDL + MP capsulotomy or Fusion 11]. 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 24 | Page [Orthopedic Neurology]

      Introduction  It is not a commonly encountered though grave injury

Brachial plexus anatomy  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 [Orthopedic Neurology] Page | 25

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, Sternoclavicular 3- Inflammatory: Radiation plexopathy: pain after radiation DXT 4- Tumors: . Neural: neurolemmoma, plexiform neurofibromatosis . Non neural: Pancoast tumor 5- Compression neuropathy: . Th oracic ou tlet synd rom 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) 26 | Page [Orthopedic Neurology]

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)

SUNDERLAND CLASSIFICATION 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

1-NEURAPARAXIA: 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

2- WALLERIAN DEGENERATION FOR AXONO & NEUROTEMESIS • 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 NODE OF RANVIER

• 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]. MUSCLE: y № of motor end plate, y sensitivity, then starts to respond &z fasciculation 5]. SENSORY IS BETTER THAN MOTOR: and can wait for longer periods till start to regenerate

[Orthopedic Neurology] Page | 27

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- COMPLETE + 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) 28 | Page [Orthopedic Neurology]

Electodiagnosis: 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-  CHRONAXIE (time needed for DOUBLE RHEOBASE = 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: . H-REFLEX (electric ankle jerk) by submaximal nerve   γ fibers  dorsal root  monosynaptic  of AHC  ms contraction . F RESPONSE: (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 the root avulsions in Erb’s plasy

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

[Orthopedic Neurology] Page | 29

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 ms Operative: 1- INDICATIONS AND TIMING: 1]. If the point of 3mo passed without evidence of biceps regeneration 2]. Reconstructive surgery for late sequelae 2- FINDINGS: 1]. Root avulsion 2]. Continuous root and trunk (traction injury) 3]. Neuroma formation 3- TECHNIQUE: 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 30 | Page [Orthopedic Neurology]

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 capsule 2]. SEVER’S release of the subscapularis + Pec major lengthening 3]. L’EPISCOPO: transfer of Latissimus & teres major to the back of the humerus  ER (ZACHARY, TACHIDJIAN modifications) 4]. HOFFER transfer of latissimus and teres into the rotator cuff  ER + abduction 5]. OBER long head triceps + short head biceps transfer to acromion 6]. GILBERT & MAYER trapezius transfer to humerus 7]. SAHA 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 SubscapularisRelease Supra or infraspinatus Dysfunction g reatLatissimuser tuberos toity Deltoid Dysfunction Saha or Hoffer IR or ER +s incongruenthoulder joint Humeral derotation osteotomy Severe dysfunction of shoulder Glenohumeral arthrodesis

7]. Elbow reconstruction: Flexor paralysis: (MUST HAVE GOOD HAND FUNCTION) . BROOKS-SEDDON ...... all pec major to biceps . CLARK’S ...... sternal pec major to biceps . HOVNAN ...... Latissimus origin to biceps . Pec mior to biceps . Sternomastoid to biceps ..... using a fascia to give more length  webbing of neck . Triceps to biceps . STEINDLER FLEXORPLASTY ...... advancement of common flexor origin to lower humerus; assess 1st flexors condition by doing elbow flexion 90º hand clench test . BUNNEL modification ...... augment by fascia &fix to lat humerus (better pronation) . MAYER-GREEN ...... 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 ...... ZANCOLLI biceps rerouting around the radial neck 9]. Wrist: . Wrist Drop ...... FCU to ECRB

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Prognosis 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

RECENT TRENDS IN NERVE REPAIR

1. Phamacoloical agents 1- Gangliosides 2- Polyamines 2. Immune system modulators 1- Azathioprine 2- Corticosteroids 3- Cyclosporin A 4- Cvclophosphamides 3. Enhancing factors 1- Nerve growth factor 2- Fibronectin 3- Insulin-like growth factor 4- Ciliarv neurotrophic factor 4 Entubulation chambers 1- Autogenous vein 2- Silicone Polvglycolic acid G 3- Gore-tex 32 | Page [Orthopedic Neurology]

THUMB ADDUCTION

THUMB OPPOSITION

CLAW HAND

[Orthopedic Neurology] Page | 33

    Commonest middle aged F:M = 3-5:1 Anatomy 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 Nerve Flexor tendons run deep to nerve Causes (ICRAMPS)  Idiopathic  Colles, Cushings  Rheumatoid  Acromegaly, amyloid  Myxoedeoma, 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 finger 2- worse at night 3- forearm pain 4- dropping things

Signs 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: 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

Differential diagnoses  Cervical radiculopathy  Spinal cord lesions - tumour, MS, syrinx  Peripheral neuropathy- toxic, alcoholic, ureamic, diabetic 34 | Page [Orthopedic Neurology]

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

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    Compression 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 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 Symptoms 1]. Aching / fatigue of forearm after heavy use 2]. Clumsiness 3]. Vague, intermittent parasthesia, but rarely numbness Signs 1]. local tenderness to deep pressure and reproduction of symptoms 2]. 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 symptoms 2]. EMG  innervation of muscles & differentiate from CTS Management 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 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 unhelpful Management  Conservative- NSAIDS, avoiding aggravating movements  Surgical exploration- most common compressing structure deep head of pronator teres 36 | Page [Orthopedic Neurology]

Cubital Tunnel Syndrome  Ulnar nerve entrapment about the level of the elbow Aetiology: 1]. At elbow: o ○ Trauma o Bony spurs ○ Tumours 2]. Proximal 8cm by ‘‘Arcade Of Struthers’ ≠ ligam en t o f Struthers’. 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 Symptoms  Vague dull aching forearm, intermittent parasthesia, ulnar side of hand Signs 1]. Hypoesthesia ulnar side of hand + 1½ fingers 2]. Tinels TEST, 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 sition of the ulnar n’ 2]. Transposition: - subcutaneously/ Submuscularly (better) 3]. +/- medial epicondylectomy Results  Sensation improves better than motor function over 3-5 y period Complications 1]. Recurrence ð inadequate decompression or irritation or redislocation or neuoma 2]. CRPS [Orthopedic Neurology] Page | 37

    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

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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

Investigations  NCS -decreased latency across arcade of Frohse  EMG denervation fibrillations of affected muscles Treatment  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 [Orthopedic Neurology] Page | 39

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 Differential diagnosis  Tennis elbow Management  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

NERVE SITE CAUSE SYMPTOM ILIO-INGUINAL Hypertrophied abdominal ms Intense training Pain & parasthesia OBTURATOR Hip adductor Skaters Medial thigh pain FEMORAL LAT. CUT. ASIS Tight belt Lateral thigh pain Meralgia paresthetica 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 Inversion injury Dorsal foot pain & pierce the deep fascia paresthesia SURAL 12 cm distal to Lat Malleolus Jon e’s fr Lat. foot parasthesia DEEP PERONEAL Inf. extensor retinaculum Inversion injury Sole pain & parasthesia (anterior tarsal tunnel $) POSTERIOR TIBIAL Flexor retinaculum FDL accessorius, RA, Sole pain & paresthesia (Tarsal tunnel $) tumors, ganglion 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 Push phase in runners Digital pain, parasthesia, (M orton ’s N eurom a) dead toe

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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 1. A d so n ’sTEST 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 2. R everseAd so n ’sTEST 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