PERIPHERAL NERVE (incl CRPS; ) Flashcards Preview

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Patient factors:

  • Age
  • Comorbidities: DM, alcoholism (vit def), malnutrition (vit def), Gout (colchicine inhibit tubulin)
  • Cellular and humoral immune mechanisms
  • Compliance w/ rehab

Nerve factors:

  • Mixed motor and sensory worse than isolated/pure motor or sensory
  • Proximal vs. distal nerve injury
  • Nerve gap
  • Neurotropic and neurotrophic factors
    • neurotropism: factors produced by target to promote distal growth to target
    • neurotrophism: influences that promote ‘maturation and nutrition’ of regenerating axons, includes growth factors, extracellular matrix components and hormones (neuronal growth factor (NGF), IGF, FGF, IL-1

Injury factors:

  • Time since injury
  • Mechanism: crush/avulsion/stretch/contusion vs. clean laceration
  • Open vs. closed; contamination
  • Multi-level injury
  • Associated skeletal, vascular, soft tissue injury overlying/adjacent to nerve injury; devascularization

Repair factors:

  • Delayed repair
  • Tension on repair
  • Nerve gap and graft required



  • Mircrosurgical technique including Careful handling of tissues & dissection
  • Limited devascularization of nerve
  • Resection of neuroma & glioma (*can be difficult to ascertain in crush mechanism – can use frozen sections)
  • Primary repair when possible
  • Tension free repair / avoidance of nerve gaps
  • Use of interpositional nerve graft (or alternative) if tension free primary repair not possible
  • Epineural repair (not better than perineurial repair; use perineurial if grouped motor/sensory fascicles are known)
  • Avoid postural movement to diminish tension
  • Timing – earlier = better (<3/12 for sensory, no motor recovery >1 year)



Direct primary repair – best results within 3 wks

o  Ends:

§ End-to-end (preferred)

§ End-to-side (push, recipient is in continuity, babysitter principle) - to preserve motor end-plates while await more proximal regeneration (ex: AIN to ulnar nerve after direct repair of proximal ulnar nerve injury)

§ end to side (pull, donor is in continuity) - neurotization for sensory re-innervation (ex: corneal neurotization with supraorbital n end-to-side with sural nerve graft directly onto cornea)

o  Epineural repair equivalent to grouped fasicular repair – align fascicles anatomically if possible, based on topographic vascular anatomy on nerve surface

o  Fascicular (perineural) –technically challenging – no proven benefit; if nerve topography known then may be advisable

o  Fibrin glue

o  Laser

Delayed primary repair – excise neuroma/glioma formed w/I 3 wks; then direct repair

Graft across gap

Nerve Transfer

Neurotization (placement directly on muscle fibres; least desirable)



·   Anatomic landmarks – fascicle size, position, epineural vessels

·   Knowledge of internal topography

·   Electrical stimulation – sensory for proximal and motor for distal stump (< 3 days post injury)

·   Histochemical staining – stain for acetylcholinesterase, choline transferase (motor) and carbonic anhydrase (sensory) – <9d



·   mobilization - affords 1-2cm

·   transposition - ie ulnar nerve anterior transposition

·   bone shortening





  • at / above elbow: sensory bundle is fairly discrete from motor and generally more lateral, although should be nerve tested (exclude from repair to direct regenerating axons to motor end-plates)

Median - more complex because more fascicles

  • forearm: AIN radial / posterior
  • Distal: RMB radial and sensory are ulnar; ** in carpal tunnel the most superficial fascicle is sensory branch to long


  • at mid-distal 1/3 becomes clear
    • ulnar dorsal sensory fasicle bundle - branches from main nerve ~ 8-10cm proximal to wrist
    • radial volar sesnory fasicle group
    • ulnar volar motor fasicle group
  • at Guyon's canal
    • Motor group passes dorsally and radially
    • Sensory group becomes superficial and ulnar



·   Plasmatic imbibition (diffusion) for 3 days

·   Inosculation (vascular reconnection) from proximal and distal stumps begins at 3 days

·   Revascularization from surrounding tissue begins by 6 days

·   Blood flow exceeds normal nerves after 6 days



·   Trunk (historical) - cross-section of a whole nerve segment interposed btwn the two ends (central fibrosis impairs growth)

·   Cable – Multiple strands of nerve graft, interposed under minimal tensions, to repair a single larger nerve

·   Interfascicular graft – fascicles dissected proximal and distal, neuroma excised, grafts placed btwn fascicles (use <6cm)

·   Free vascularized ‘graft’ – Controversial, possible improved # axons vs non-vacularized

·   Nerve conduit – gaps up to 3cm



·   Non-vascularized

  • Leg: sural n., medial or lateral n. of thigh,
  • Arm: MABC, LABC, PIN (good for digital nerve graft),
  • Neck: cervical plexus
  • Other: cutaneous portion of a nerve that has been injured proximally

·   Vascularized (radial nerve-artery, sural nerve-artery, ulnar nerve + superior ulnar collateral artery, deep peroneal nerve-dorsalis pedis artery)




Nerve graft (autologous) - best results overall and for gaps > 5cm

  • non-vascularized, vascularized

Nerve graft (alloplastic)

  • gaps < 30-50mm
  • scaffold for nerve regeneration
  • processed (requires immunosuppression until renervation across coaptation) vs. decellularized

Autogenous conduit: Vein graft

  • gaps < 30-50mm

Synthetic conduit 

  • gaps < 30mm
  • polyglycolic, collagen, caprolactone


how do you classify nerve injury?

·   Anatomic location: supraclavicular (roots, trunks); retroclavicular (divisions); infraclavicular (cords, branches)

o  Supraclavicular can be grouped as: pre-ganglionic (avulsed roots, complete motor & sensory deficit, preclude spontaneous recovery; tend to be lower roots) vs. post-ganglionic (may retain cell body within ventral horn, rupture, tend to be upper roots)

·   Mechanism: open (penetrating, gunshot, missile, avulsion) vs. closed (blunt, traction, crush)

·   Degree of nerve injury: Seddon/Sunderland classification


what features are UNCOMMON in neurapraxia/conduction block?

§ Complete nerve palsy

§ Wound over course of nerve

§ Vasomotor or sudomotor paralysis in territory

§ Tinel sign

§ Neuropathic pain


Describe what happens to cell body, proximal stump, distal stump, motor endplate, nerve ending after nerve injury

Cell Body

  • Nucleus and cell body swells as the cell undergoes metabolic changes to help rebuild the damaged axon
  • Neurotransmitter synthesis diminishes

Proximal Stump = chromatolysis

  • Limited Wallerian degeneration, variable distance (unmyelinated) or to adjacent node of Ranvier (myelinated)

Distal Stump = Wallerian degeneration

  • Increased cytoplasmic Ca++ --> Myelin phagocytosed --> End result is a hollow endoneurial sheath --> scaffold of schwann cells & macrophages for new neuronal growth (band-like appearance under EM, called Bands of Bunger)
  • Endoneurial sheath shrinks approx. 1 month after injury if no axon grows into it

Motor End-Plate

  • muscle fibre atrophy within weeks of injury —> eventually fibrosis; irreversible fibrosis at 12-18mos
  • initially increased ACh receptors along the cell membrane (not just NMJ) leading to denervation super sensitivity with stimulation (fibrillations)

Nerve End-Organ

  • Pacinian corpuscle and Merkel cells degenerate but regain function with re-innervation
  • Meissner corpuscle degeneration permanent > 6 months
  • Re-innervation of receptors may not correlate with functional recovery, regeneration up to 20yrs
  • 2PD lost after 6-12mo delay in re-innervation; but protective sensation is possible even after years



  • Quiescent period
  • Elongate as growth-cone (regenerating unit) with single axon sprouting multiple daughter axons (filopodia, rich in actin) 5 - 24 hours after injury
  • Growth cone preferentially target appropriate end-organ receptors from distal stump via contact guidance and neurotrophic factors (neurotrophins)
  • Functional synapse is made and remaining daughter sprouts degenerate / are pruned back (neuroma = poor pruning)
  • Rate limiting step of neuroregeneration is axonal transport of actin, tubulin and neurofilaments (
  • Regeneration rate: initial lag phase of ~ 30 days (to cross coaptation and clear cellular debris) then ~ 1mm/d


Describe axonal regeneration to distal target

  • Axonal regeneration to distal target end-plate promoted via neurotropism and neurotrophism
  • Neurotropism: regenerating fibres demonstrate tissue and end-organ specificity (factors produced by distal target that promote regenerating fibres get to the distal target)
  • Neurotrophism - enhanced elongation and maturation of regenerating nerve fibres to correct distal stump via autocrine / paracrine secretion of neurotrophic / nutritional factors (food for nerves)
    • Neurotrophic factors expressed by Schwann cells, fibroblasts, myocytes, injured axons
    • Ex: nerve growth factor, glial growth factor, epidermal growth facto, insulin-like growth factor I/II



o  Neurotropism: regenerating fibres demonstrate tissue and end-organ specificity (factors produced by distal target that promote regenerating fibres get to the distal target)



o  Neurotrophism - enhanced elongation and maturation of regenerating nerve fibres to correct distal stump via autocrine / paracrine secretion of neurotrophic / nutritional factors (food for nerves)

§ Neurotrophic factors expressed by Schwann cells, fibroblasts, myocytes, injured axons

§ Ex: nerve growth factor, glial growth factor, epidermal growth facto, insulin-like growth factor I/II



·   Defined as the process that occurs to the proximal stump of an injured peripheral nerve when regenerating axon sprouts / growth cones do not enter the distal stump and instead grow into the surrounding mesoneurial tissue

o  Schwann cells and fibroblasts produce disorganized collagen, forms encapsulated firm scar;

§ more proximal injury = bigger neuroma




  • Triad of symptoms: discrete area of pain (in scar), altered sensation in peripheral nerve distribution, stagnant tinel
    • Only nerves w/ sensory components are symptomatic (i.e. motor nerves will not form a symptomatic neuroma)
    • Pain relieve by local anaesthetic block is helpful for diagnosis (ie compare w/ saline infiltration)
    • Cause pain by:
  • a) persistent mechanical or chemical irritation of axons or
  • b) persistent spontaneous activation of axons leading to activity in DRG



OT/PT, desensitization, TENS (transcutaneous nerve stimulation), medications (gabapentin, pregabalin, TCA/lyrica)



o  Neuroma in continuity – neuroma in a nerve that has not been completely divided

§ Spindle = connective tissue can constrict nerve = irritation

§ Lateral neuroma – partial transection

§ Neuroma following repair

o  Neuroma in completely severed nerve



o  prevention; excision of neuroma (and glioma) and:

§ direct repair / grafting of nerve (direction for axons to go, even if reinnervation not the goal);

§ transposition into muscle/vein/bone/well - vascularized soft tissue

§ relocation away from mechanical stress/pressure point

§ closure of epineurium w/ glue

§ silicone cap (poor results)

§ not useful: crushing, cauterizing, ligating, multiple sectioning



o  no regeneration in distal stump therefore neuroma does not form

o  glioma is the minor fibroblast and schwann cell response


what is the etiology of brachial plexopathy?




  • Congenital anomaly of the cervical rib
  • Scalene anticus syndrome (Naffziger’s syndrome)

Acquired (vitamin)



  • Aneurysm of subclavian artery


  • ?viral Parsonage-Turner


  • Multiple neuritis, post-radiation

Trauma (most common)

  • Closed (Traction or compression) – MVA, pedestrian, sports, falls, #/dislocation of shoulder, neck, clavicle
  • Open – knife, GSW, glass




  • Allergic plexopathy




  • Plexopathy of unknown origin


  • Open: Intra-op injuries,
  • Closed: positioning (post-anaesthetic), Radiation


  • Post Vaccination


  • Benign – plexiform neuroma, benign schwannomas
  • Malignant – tumours of neck, malignant schwannomas, pancoast tumour


How do you classify BPI?

  • Congenital vs. acquired
  • By level
    • Root/trunk/division/cord/branches
    • Supraclavicular (pre-ganglionic vs. post-ganglionic)
    • Retroclavicular
    • Infraclavicular
  • By mechanism:
    • Open: penetrating (clean, contused), avulsion, gunshot, missile
    • Closed: crush, traction, fall, mvc


List findings that differentiate a pre-ganglionic injury (infer avulsion)

  • On history:
    • Nerve pain / deafferentiation pain
  • On physical:
    • proximal motor weakness (levator, rhomboids, paraspinals)
    • anaesthesia at/above the glenohumeral joint
    • Horner's syndrome (miosis, anhydrosis, ptosis, enophthalmos)
    • No or weak Tinel in supraclavicular neck
  • On investigations:
    • C-spine fracture
    • Elevation hemi-diaphragm (phrenic nerve palsy)
    • CT myelogram shows pseudomeningocele +/- absent ventral root
    • EDS show proximal muscle denervation
    • NCS show present SNAP in anesthetic limb
  • On special tests:
    • negative SSEP intraoperative
    • positive histamine triple response (vasodilation, wheal, flare) in anaesthetic limb


what to know on history for acquired BPI?

  • Rule out life or limb threatening injuries; LOC / altered level of consciousness – head injury
  • ID: age, hand dominance, occupation, hobbies
  • Mechanism of injury: timing, open (penetration, knife edges, gsw, missile, etc) vs closed (traction, fall, MVC) vs other mechanism; low vs. high velocity
  • Arm position at time of injury
  • Arm pulled down – C5 & C6 roots injuries
  • Arm abducted to 90o – middle plexus injured, especially C7 (iatrogenic intraop injuries)
  • Arm abducted > 90o – lower plexus injured, C8 & T1 are more severely injured
  • Symptoms: ispilateral motor/sensory deficits, pain (quality, quantity etc); Presence of paresthesia / weakness in other extremities – head or C-spine (complete and incomplete) injuries


what to do on physical / how do you approach physical for acquired BPI?

  • ABCs, vitals, general examination, vascular exam/pulses
  • Ideal to remove shirt; examine entire forequarter (extremity, back, chest, neck) of ipsi & contra-lateral
  • Assess for Horner’s (present 3-4 days post injury) – strongly correlates with avulsion C8/T1 or traction injury very close to cord (sympathetic fibres divide from the spinal nerve and emerge from T1 & T2 foramen), poor prognostic sign of recovery
  • Motor
  • Inspection – fasciculations, atrophy, position (waiter tip [upper plexus] - shoulder adduction, internal rotation; elbow extension; forearm pronation; wrist flexion)
  • All muscle groups tests in detailed & objective manner (MRC 0-5)
  • Proximal to distal following organization of plexus in terms of MOVEMENTS (for plexus) and MUSCLES (for peripheral nerves) and including trapezius, paraspinal muscles (head position)
  • AROM/PROM – look for glenohumeral joint stability (axillary nerve)
  • Reflexes
  • Sensory  (each dermatome and terminal branches)
  • MRC scale in all distributions (S0-S4)
  • Innervation density (S2PD, D2PD) & threshold (monofilament/vibration)
  • Tinel
  • Histamine triple response test
    • Histamine injected dermally à vasodilation, wheal, flare
    • Response = axonal reflex involving the sympathetic ganglion & DRG
    • Skin denervation + intact triple response à pre-ganglionic lesion
  • Serial exams over time


describe classic patterns of BPI (by cervical root) muscles affected, and motor functions /sensory loss


Muscles Affected

Functional Loss

Sensory Loss

C 5-6

Erb-Duchenne palsy

  • Deltoid, supraspinatus & infraspinatus, biceps, brachialis, coracobrachialis, brachioradialis ± radial wrist extensors, clavicular pectoralis major
  • Shoulder ext/int rotation, abduction & forward flexion, elbow flexion ± wrist extension, supination
  • Shoulder, lateral arm + thumb & index finger


Erb’s Plus deformity

  •  As above, plus triceps, ECRL & ECRB, FCR, EDC, EPL, EPB, APL
  • As above plus elbow, wrist, finger & thumb extensors
  • As above, plus middle finger

C(7), 8, T1 Klumpke’s palsy

  • (EDC, EPL) FDS, FDP, FPL, Lumbricals & interossei, thenars & hypothenars
  • (Finger extension) Finger & thumb flexion, median & ulnar intrinsics
  • Anterior and medial arm, (middle finger), Little & ring fingers

C5 - T1

  • All above
  • All above (flail arm)
  • Anaesthesia


discuss when, how and why diagnostic imaging is used in acquired BPI?

  • Plain X-rays
  • Cervical spine, chest, clavicle, shoulder girdle & humerus
  • CXR – inspiration / expiration AP – to assess diaphragm activity: elevation hemi-diaphragam = upper roots & phrenic n
  • Arteriogram
  • Penetrating injury to region of brachial plexus
  • Abnormal pulses associated with blunt or penetrating trauma
  • Normal initial exam followed by ↑ brachial plexus neurologic deficit that may be due to an expanding haematoma
  • CT / myelogram
  • Perform at 3-4 weeks to r/o pseudomeningocele: dye extrudes thru rupture of root/meningeal tear
  • Absence of 1 or both ventral/dorsal rootlets seen with a pseudomeningocele increases the specificity for root avulsion
  • Sensitivity 74-95 %, specificity – 90-98% [institution dependent]
  • MRI
  • High field strength MRI with mutliplanar views for distal plexus lesions; gold standard for non-traumatic BP palsy
  • 3D MR myelography – intradural rootlets
  • Both sensitivity and specificity lower than that reported for CT/Myelogram


discuss use of EMG in BPI

  • Useful to assess muscles which are difficult to assess clinically (rhomboids, serratus anterior, paraspinal muscles)
  • Denervation paraspinals = strong indicator of root avulsion
  • First few days: no change
  • 5-7 days: reduced recruitment - fewer MUPS;
  • 6-12 weeks 
  • Denervation: Fibrillations indicate axonal injury (2nd – 5th) – present at > 6 wks; absent MUPs w/ volunt. effort @ 12 wks
  • Signs of spontaneous recovery/reinnervation @ 12 wk assessment (2nd, 3rd degree injury): MUPS, nascent units, giant MUPS ( higher amplitude and longer duration)


discuss use of NCS in BPI

·   Sensory Nerve Action Potentials (SNAPs) most helpful to determine pre/postganglionic level of injury

o  preganglionic injuries à DRG separated from the CNS causing anaesthesia, however the cell body of the peripheral nerve which is located within the DRG is intact so Wallerian degeneration does not occur and the SNAP is maintained

o  Positive SNAP in the presence of anaesthesia is pathognomonic of preganglionic injury (= root avulsion)


summarize use of imaging and EDS in BPI

CT myelogram & EMG/NCS at 4 wks

o root avulsion or high energy total plexus palsy: operate as early as 6 weeks

o otherwise, r/a at 3 months with physical exam & EMG/NCS --> if no return of function, no ­ MUPs then plan for OR

o if function returning, r/a at 6 months with possible repeat EMG/NCS – OR if no/minimal improvement in function or nonanatomic return of function, otherwise continue to wait


list indications for operative intervention in BPI

Open injuries

Strong suspicion of significant damage with poor likelihood of spontaneous recovery

o  Laceration in close proximity to plexus

o  Clear indication of injury to roots

Lack of functional recovery after initial period of observation


discuss contraindications to operative management of BPI

  • Absolute – unrealistic patient goals, unwillingness to undergo operation, clear progress with non-operative management
  • Relative – Advanced age, medical comorbidity, traumatic brain injury, associated spinal cord injury

o  Occasionally isolated proximal C8-T1 due to inability of nerve regeneration to reach hand – but candidate for n. transfer!

o  > 1 year since initial injury for NERVE surgery (except paeds; not a c/i for TT)


when considering timing of intervention for BPI, what are the guiding principles?

o  Better functional outcomes in patients with spontaneous recovery vs. surgery

o  Surgery indicated for patients with absent or inadequate spontaneous recovery

o  Outcomes improved if patients who will require surgery receive it early

o  Timing is dictated by mechanism


discuss general approach to timing in BPI and peripheral nerve injury

  • Immediate / early exploration and repair (within days): open, sharp injuries & deficit
  • Immediate / early exploration, identify and tag nerve ends and delayed/subacute repair at ~ 3 weeks
  • Initial assessment in OR – level of injury, continuity, mapping, tagging nerves if unable to perform primary repair
  • Sub-acute repair allows for delineation of ZOI, surgical plan includes excision of neuroma and nerve grafting: open injury with crush/contusion, vascular injury, avulsion, (blast)
  • Early Surgery ~ 6/52 to ~ 6/12 
  • Expectant management until 12 weeks: closed injuries, gunshot, blast, radius # (management scenarios are controversial)


discuss priorities of repair in total BPI

  • Elbow flexion by biceps/brachialis muscle reinnervation
  • If additional motor nerves available for transfer, the triceps is restored next to allow greater control of elbow and stability with forearm extension
  • Shoulder stabilization & abduction, and external rotation by suprascapular and axillary nerve reinnervation
  • Hand Sensation below the elbow in C6, C7 distribution by reinnervation of the lateral cord
  • Wrist extension and finger flexion
  • Wrist flexion and finger extension
  • Intrinsic hand function


list and briefly describe standard surgical options available to BPI

Neurolysis: Indicated for a post-traumatic neuroma-in-continuity with a positive NAP

o  External neurolysis – lysis of adhesions between epineurium and surrounding structures

o  Internal neurolysis – longitudinal incisions made in epineurium & fascicles lysed from surrounding scar tissue within the nerve

Direct repair: Rarely possibly following traumatic brachial plexus injury (only in sharp injury)

Direct repair with graft (length of gap + 10%)

o  Indicated for Neuroma-in-continuity with no NAP; Nerve rupture

o  Non-vascularized Nerve Grafts – most common

o  Vascularized nerve Grafts: Graft length >15cm or large diameter (superior ulnar collateral art/vein)

Neurotization (direct to motor end-plate)

Nerve transfer

Tendon transfer

Free functional muscle transfer


what are complications of BP exploration / repair?

·   nerve injury: phrenic, spinal accessory 

·   vascular injury (scalene triangle, subclavian vessels) 

·   skeletal injury (iatrogenic clavicle osteotomy then mal/non-union)

·   pneumothorax

·   wound complications


list indications for nerve transfer

o  High nerve injury

o  Lack of available proximal nerve for repair (ex: very proximal, root avulsions)

o  Require delayed repair (but still intside timeline to maintain motor endplate)

o  Inadequate tissue bed to facilitate regeneration or to avoid operating in severely scarred bed

o  Partial nerve injury with well-defined functional deficit (avoids downgrading)

o  Unclear level of injury (ex: idiopathic neuritides, radiation neuritis)

o  Reinervation of FFMTs


list contraindications to nerve transfer

: different procedure will provide equal or better outcome with less morbidity or shorter recovery time

- duration of injury greater than 12-18 mos


discuss intraplexal donors for nerve transfer (options, adv, disadv)

o  Options – ipsilateral C5 (strongest donor), ipsilateral C7 (can sacrifice in C5/6 avulsions), branches of peripheral nerves

o  Advantages – greater # of axons, less need for re-education

o  Disadvantages – involved in initial injury, may need interposition graft


discuss extraplexal donors for nerve transfer (options, adv, disadv)

  • Spinal Accessory Nerve
    • Uses – to SSN, axillary or free gracilis
    • Posterior to SCM, transverse incision over clavicle (leave branch to mid/distal trapezius intact)
  • Intercostal nerves
    • 9 available (T3-11), may need multiple donors for neurotisation, challenging and lengthy dissection
    • Uses – innervate FFMT for elbow flexion, T4/5 for thoracodorsal and long thoracic neurotization
  • Phrenic Nerve
    • Suprascapular harvest with coaptation to SSN or nerve graft to musculocutaneous, axillary, median
    • Advantage – within surgical field, C3/4 often intact, large number motor axons
    • Disadvantage – nerve graft required, paralysis diaphragm, pneumothorax, intrathoracic approach
  • Contralateral C7
    • Used in multiple avulsions lacking intra/extraplexal donors (can use full or partial C7) – use with vascularized ulnar n
    • Advantage – many axons, can neurotize many recipients
    • Transient motor and sensory deficits (resolve <6/12), long distance to end target, functional recovery not ideal (better <18yo), chronic pain, violating normal limb
  • Motor branches of cervical plexus


discuss general principles of motor and sensory nerve transfer



Functional donor nerve

Functional donor nerve

Expendable or redundant donor

Expendable, non-critical sensory distribution

Large number of purely motor axons

Large number of purely sensory axons

Proximal to motor end-plate (donor distal, recipient proximal)

Proximal to sensory end-organ (donor distal, recipient proximal)

Synergistic (preferable)


Ideal end-to-end unless ongoing re-innervation (then end-to-side with small breach in recipient axon – ie AIN to DMB)

Ideal end-to-end for critical sensation; end-to-side for less critical or “pull” sensory fibres

Uniform pre-requisites for motor and sensory nerve transfer:

  • Stable skeleton
  • Supply overlying soft tissue
  • Full/near-full passive ROM (more important for tendons)


Compare nerve transfer to tendon transfer


Nerve Transfer

Tendon Transfer


Restore a lost function by transferring a less critical nerve to a non-functional nerve

Restore a lost function by transferring a functioning musculotendinous unit


No timing restrictions; generally reserved for > 12 mos or pts present delayed

Early; ideal < 6 mos; up to 12-18 mos after injury


  • Avoid surgery through zone of injury
  • Shorter time to re-innervation
  • > 1 muscle restored per transfer
  • Motor and sensory recover
  • No disruption to muscle-tendon unit balance
  • Fast recovery and return to function (after short post-op immobilization)
  • Reliable results


  • Delayed return of function (axon re-innerv’n)
  • Must present early
  • Potential for incomplete recovery
  • Need motor re-education
  • Often consider downgrade by 1 MRC
  • Operate through injured tissues
  • Donor site morbidity
  • Disruption to muscle-tendon unit balance (too tight/loose); tendon adhesions
  • 1 function per transfer
  • No sensory return


Delayed presentation

Equivalent/superior functional outcome with less morbidity or recovery w/ alternate



discuss nerve transfer for elbow flexion


Donor Nerve

Recipient Nerve


Elbow Flexion (1st priority)

  • MCN
  • Biceps brachii, brachialis


  • UN Fascicle to FCU (Oberlin)
  • MN Fascicle to FDS/PL/FCR
  • Biceps, Brachialis branches of MCN
  • Double fascicular = MN fascicle FDS/FCR to biceps & ulnar FCU fascicle to brachialis; not proven over single fasicle
  • If present > 9-12 mos better result may be w/ FFMT
  • Medial Pectoral Nerve Branches
  • Thoracodorsal Nerve
  • Spinal Acessory Nerve
  • Intercostal Nerve
  • MCN
  • Motor axons are lost when plugging directly into MCN (vs to a muscle motor branch)



discuss nerve transfers for shoulder abduction and external rotation

  • Donor SAN to SSN for supraspinatous (abduction, stabilization) and infraspinatous (external rotation)
    •  ICN
  • Donor medial triceps branch of radial nerve to axillary nerve for deltoid (abd) and teres minor (ext rot)
    • alternate ICN, TDN, medial pectoral nerve


discuss nerve transfer for radial neuropathy / wrist & finger & thumb extension

Wrist, Finger extension

(radial neuropathy)

  • Pronator Teres br. of MN
  • FDS or FCR/PL br. of MN*
  • FCU of UN
  • ECRB br of RN, PIN
  • (FCR or FCU to PIN; FDS to ECRB)
  • TT are more reliable and fast
  • NT can theoretically sacrifice a potential TT option
  • *NT are often paired with PT to ECRB TT as an internal splint; confounds results of studies


discuss nerve transfer for median neuropathy / finger & wrist & thumb flexion

Finger Flexion / median neuropathy

  • Brachialis br. of MCN or BR, Supinator br. of RN
  • ECRB of RN
  • AIN


  • PT branch of MN
  • NT not as well established, but if using specific motor branches doesn't appreciably impair ability for late TT


discuss nerve transfer for ulnar neuropathy / intrinsic hand fxn

Intrinsic Hand Function / Ulnar neuropathy (3rd priority)

  • Terminal AIN (to PQ)
  • Deep motor branch of UN
  • NT does not prohibit eventual TT


what are the advantages for posterior approach to plexus for upper trunk injuries / for nerve transfer for shoulder function?

o  Allows SAN to be divided at most distal point, preserving function to upper trapezius

o  Release of SSN from suprascapular notch removes potential point of compression

o  Allows for proximal dissection of AN to include the branch to teres minor, restoring external rotation and glenohumeral stability

o  Allows for adherence to principle of transferring nerve as close to target as possible


discuss sensory nerve transfer




MN – Thumb & IF

  • MN – Common sensory branch to 3rd WS
  • UN – Common sensory branch to 4th WS
  • UN - Dorsal cutaneous branch
  • MN – common sensory branch to 1st WS & radial digital nerve to thumb

MN – Noncritical sensory

  • UN – Common sensory branch to 4th WS (end-to-side)
  • MN – common sensory branch to 2nd, 3rd WS

UN – Ring & Small Fingers

  • MN – common sensory branch/fascicle to 3rd WS
  • UN – commons sensory branch/fascicle to 4th WS, ulnar digital nerve to small finger

Ulnar border of hand

  • LABC
  • MN sensory branch to distal forearm (end-to-side)
  • UN – Dorsal cutaneous branch

Radial sensory nerve

  • LABC
  • RN – sensory branch.


duscuss secondary / late reconstructive options for shoulder in BPI

·   Pedicled muscle transfer --> 1) Trapezius to humerus (deltoid tuberosity) for abduction; 2) L’Episopo Procedure - latissimus dorsi & teres major are transposed posterolaterally for ext rotation; 3) pec major sternoclavicular head transferred for flexion

·   Rotation osteotomy of humerus (static option)

·   Arthrodesis glenohumeral joint


discuss secondary / late reconstructive options for elbow flexion / function in BPI

  • Pedicled muscle transfer
  • Latissimus Dorsi: bipolar transfer (humeral insertion transferred to coracoid process, distally to biceps tendon),
  • Pec major/minor: humeral insertion transferred to acromion, origin to biceps tendon; need stable shoulder (leads to chest asymmetry); used in C5,6 paralysis or MCN injury)
  • Triceps to Biceps Transfer (not advisable if crutches needed)
  • Modified Steindler Flexorplasty
  • Indications - Upper plexus lesion with inadequate elbow flexion; >6-9 months since injury; Patients with good power (M4/5) in forearm flexor-pronator muscles; Good shoulder stability
  • Flexor-pronator muscles released on a bone fragment from medial epicondyle and transposed proximally onto anterior aspect of humerus

Functioning free gracilis muscle transfer


discuss secondary options for hand/wrist function in BPI


·   Tendon transfers

·   Free gracilis muscle to forearm for finger flexion or extension (single muscle function); or finger extension + elbow flexion (double muscle function)

·   Arthrodesis


·   Extension and stabilization

·   Pronator Teres transfer

·   Arthrodesis


what are the indications for FFMT?

  • A - dysfunction - major functional muscle loss
  • Common: loss of muscle: direct trauma/crush, electrical burn, Volkman’s ischemic contracture, tumour extirpation
  • Less common: loss of nerve: BPI, tumour extirpation, isolated peripheral nerve injury
  • Plus B - for which alternative and simpler reconstructions are not available
  • no available tendon or nerve transfer, tenodesis or fusion
  • examples: forearm flexors, extensors, elbow flexion, shoulder flexors, anterior compartment lower leg


discuss principles of FFMT

  • Available uninjured recipient neurovascular structures outside zone of injury
  • Full / near full pROM
  • Stable soft-tissue bed
  • Stable and supple soft tissue for coverage of FFMT* 
  • Intact recipient muscle origin and insertion
  • For forearm flexors (ex: FDS/FDP/FPL): sensate digits, functioning intrinsic muscles, finger / wrist flexion


what are ideal features of FFMT?

·   Similar strength of contraction (proportional to x-sectional area)

·   Similar or slightly greater excursion

·   Single dominant blood supply 

·   Single innervation easier than multiple innervating fascicles

·   Appropriate location and length of NV pedicle for recipient bed


list common donor muscles utilized in FFMT

·   gracilis

·   latissimus dorsi

·   split pectoralis major

·   hemi-gastrocnemius

·   tensor fascia lata


discuss radiation neuritis

·   Radiation neuritis caused by intrinsic and extrinsic nerve factors

·   Intrinsic – fibrosis of epineurial, perineurial and endoneurial connective tissue and of the intra-neural vascular network

·   Extrinsic – dense fibrosis of tissue investing plexus

  • goals of treatment
    • Relieve constriction
    • ·   Free the nerves

      ·   Replace fibrosed tissue with healthy vascular tissue

      ·   Selective neurolysis recommended as soon as possible


discuss treatment of pain syndromes in BPI

·   Early aggressive physiotherapy and pain control

·   Early referral to a pain specialist

·   Drugs: gabapentin, amytriptyline, phenytoin, carbamazepine

·   TENS

·   Posterior dorsal column stimulation

·   Thalamic stimulation

·   Neurosurgical coagulation of the dorsal root entry zone

·   Surgery: Neurolysis, neuroma resection, nerve grafting


discuss factors for history of obstetrical BPI

·   Maternal factors (DM, pre-ecclampsia), Prenatal course, Labour (duration)

·   Delivery: vertex vs breech, vag vs. c/s; assisted delivery (forceps, vacuum); shoulder/head dystocia

·   Head, or shoulder dystocia – most common association

·   Birth weight, gestational age, Apgars (1,5,10 mins)

·   Complications: asphyxia, respiratory complication, clavicle fracture, rib fracture, humerus fracture, Horner’s syndrome, hemidiaphragm paralysis, shoulder subluxation, torticollis


discuss differential diagnosis of OBSTETRICAL BPI

·   Clavicle #, shoulder dislocation (e.g. not moving limb d/t pain)

·   Central/spinal injury (e.g. low tone in all extremities, spastic CP)

·   Arthrogryposis (can look very similar to C5-6 – shoulders adducted, int rotated with elbows extended and wrists flexed BUT also finger/thumb flexion deformity, wasting/atrophy of all involved muscles esp shoulder girdle, joints stiff on PROM, and symmetric bilaterally)

·   Delayed diagnosis septic glenohumeral joint (rare)


discuss components of physical exam in OBSTETRICAL BPI

  • Completely undressed
  • Inspection: posture of limb and head, any spontaneous movement, Horner's syndrome
  • Palpate: clavicle, humerus, ribs, scapula
  • Motor assessment: utilize the active movement scale (or alternate)
    • 5 motions evaluated: Shoulder: adbudction, extension, internal rotation, external rotation; Elbow: flexion, extension; Forearm: pronation, supination; Wrist, fingers, thumb: flexion, extension
    • AMS: TEST SCORE - Motions: FLEXION of elbow; EXTENSION of elbow, wrist, thumb, fingers
  • Sensory assessment: Child’s reaction to pinching the skin


discuss indications for operative intervention in obstetrical BPI

·   At 3 mos: complete BP palsy (flail extremity) or evidence C8-T1 avulsion (Horner’s syndrome, if unclear – consider CT myelogram) or failed Test score (<3.5, incorrect prediction for poor recovery of ~ 5% vs. elbow flxn alone ~ 12%)

·   At 6mos: C5-6 pattern with no improvement in function (failure of antigravity biceps function most often used as indication)

·   At 9mos: C5-6 pattern and failed “cookie test” (< grade 6 of biceps on the HSC scale- Dr. Clarke)


describe complications associated w/ operative intervention in obstetrical BPI


o  General: risks GA & prolonged procedure

o  Failure to extubate at end of case (e.g. fluid overload)

o  Wound healing problems/scar

o  Hematoma, Seroma

o  Injury to phrenic nerve (incr risk of URTIs in first 2 yrs)

o  Introp pneumo & need for chest tube

o  Risks of Tisseel (human fibrinogen + aprotonin [blocks proteolysis] and human thrombin + CaCl, from pooled human plasma): no reported transmission of virus, rare allergy


o  no or incomplete return of mvt; ongoing fxnl deficits (eg ext rotation shoulder & need for 2˚ reconstructive procedures

o  pain

o  Long term sequelae of OBPP = short limb (poorly understood)






  1. presence of inciting noxious event or immobilization
  2. abnormal pain response to stimuli:
    1. any of: allodynia, dysesthesia, hyperalgesia, hyperpathia
    2. disproportionate to inciting event
    3. not limited to single peripheral nerve distribution
  3. any / either of vasomotor instability or sudomotor instability
  4. absence of identifiable cause for degree of pain and dysfunction


what are 2 types of CRPS

  1. TYPE 1: (formerly RSD) - without known nerve injury
  2. TYPE 2: (formerly causalgia) - with known nerve injury


what are the foci of treatment for CRPS and give examples of each:

  •  Treatment is multi-disciplinary: OT/PT, anesthetist, hand/upper extremity surgeon, SW, psychologist/psychiatrist
  • Pain management:
    • Medications:
      • Opioids
      • Antiinflammatories: NSAIDS, COX, steroids
      • Membrane stabilizers: Gabapentin/valproic acid
      • Antidepressants: tricyclics - nortriptylline, amitriptylline
      • Sympatholytic - prazosin
      • Other: NMDA blocker (methadone), continuous sympathetic blockade infusion, topical therapy
    • Surgical: DRG implanted stimulator, sympathectomy, procedures to improve ROM or amputation / may or may not be helpful
  • Rehab: desensitization, aROM/pROM
  • Psycological therapy: CBT, stress management


discuss EDS findings after closed BPI

  • Neurotransmitters:
    • 0 - 72 hrs: motor nerve stimulation still possible as neurotransmitters still in NMJ and expressed
    • up to 1 week: time to complete neurotransmitter depletion
  • EDS
    • 72hrs to 3-6 wks: Wallerian degeneration down distal stump; EDS do not correlate to degree of nerve injury during this time
    • 7 days: CMAP nadir
    • 11 days: SNAP nadir
    • 3-5 weeks: appearance of fibirillations (marker of denervation)


describe the sequence of repair sensory touch sub-modalities after decompression

  1. Pain / temperature: small myelinated and unmyelinated
  2. Large myelinated touch/pressure:
    1. One point moving touch / low-frequency vibration - Meissner
    2. One point static touch - Merkel cell neurite complex
    3. High frequency vibration - Pacinian
    4. Two point moving touch
    5. Two point static touch


When should motor nerve transfers be used instead of nerve grafts

  1. Proximal brachial plexus injury with no suitable proximal stump
  2. Proximal injuries a very long distance from motor end plate
  3. Spinal cord root avulsion
  4. Large segmental loss of nerve
  5. Avoid operating in a scarred bed
  6. Partial nerve injury with a well-defined deficit
  7. Nerve injuries where level of injury is ill-defined (ex: radiation neuritis, idiopathic neuritis, multi-level injury)



Pair the term with its definition

  1. sensation of pain in absense of stimuli
  2. extreme sensation of pain disproportionate to a painful stimulus
  3. sensation of pain in response to a non-painful stimulus
  4. sensation of pain ongoing after removal/cessation of painful stimulus


  • A - 3
  • B - 4
  • C - 2
  • D - 1



  • pain / sensory dysfunction: allodynia, dysesthesia, hyperpathia, hyperesthesia
  • motor changes - decreased ROM, decreased function, tremor, weakness
  • trophic changes - nail (hypertrophy/hyperkeratosis, pitting), skeletal (osteopenia), skin (atrophy), extremity (thin, pencil fingertips), muscle (atrophy/wasting)
  • vasomotor instability - temperature asymmetry/changes, skin discolouration
  • sudomotor instability - edema, sweating asymmetry/changes


what is a suspected pathophysiology in CRPS?

  • nociceptor sensitization
  • neurogenic inflammation
  • vasomotor dysfunction
  • maladaptic neuroplasticity


what is a ddx for CRPS?

  • CNS/PNS pain syndrome, peripheral neuropathy, MS, ALS
  • normal response to trauma / injury
  • infection
  • neoplasm
  • vascular dysfunction
  • autoimmune disorder
  • degenerative or inflammatory arthritis


how do you diagnose CRPS

  • clinical diagnosis
    • inciting event
    • response disproportionate to inciting event
    • no ongoing pathology to cause pain / no alternate diagnosis
    • symptoms/signs from each of the following groups
      • sensory
      • motor/trophic
      • vasomotor
      • sudomotor
  • Adjuncts for diagnosis:
    • thermography
    • evaluation of autonomic control/response
    • evaluation of sympathetically mediated pain (local block temporaritly treats/diminishes symptoms)
    • imaging: XR & bone scan (uniformly abnormal)


how do you diagnose sympathetically mediated pain in CRPS?

  • positive response (symptom decrease/resolution; temporary_
  • phentolamine IV (chemical sympathectomy via non-specific alpha blockade)
  • nerve block (regional, stellate ganglion, peripheral n)


what is the approach to treatment of CRPS?

  • accurate diagnosis
  • pain management
    • medical - common
      • opioids, anti-inflammatory, anti-depressant, membrane stabilizing (ex gabapentin), sympathetic blockade, CCB
    • surgical
      • address a nociceptive foci (neurogenic, mechanical [like bone spur]), increase ROM, sympathetcomy, implantable electric stimulator of DRG, CNS ablation, amputation
  • physio & rehab
  • psychosocial assessments and support