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1

CLASSIFY AND LIST AND OUTLINE FACTORS THAT MODIFY (POSITIVE, NEGATIVE) NERVE HEALING AND REPAIR

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

2

WHAT ARE THE PRINCIPLES OF NERVE REPAIR?

  • 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)

3

DISCUSS THE TYPES OF NERVE REPAIR

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)

4

DESCRIBE TECHNIQUES USED TO AID IN FASICULAR MATCHING

·   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

5

LIST MECHANISMS TO INCREASE LENGTH TO FACILITATE PRIMARY REPAIR

·   mobilization - affords 1-2cm

·   transposition - ie ulnar nerve anterior transposition

·   bone shortening

(+neurotization)

6

DISCUSS INTERNAL TOPOGRAPHY OF PERIPHERAL NERVES IN UPPER EXTREMITY

Radial

  • 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

Ulnar

  • 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

7

DESCRIBE NERVE GRAFT HEALING

·   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

8

CLASSIFY TYPES OF NERVE GRAFTS REPAIR

·   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

9

DESCRIBE SOURCES OF NON VASCULARIZED AND VASCULARIZED AUTOGENOUS NERVE GRAFT

·   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)

 

10

DESCRIBE SOURCES OF GRAFT MATERIAL FOR NERVE GAP

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

11

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

12

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

13

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

14

WHAT HAPPENS IN THE PROXIMAL STUMP DURING NERVE HEALING?

  • 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

15

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

16

DEFINE NEUROTROPISM

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

17

DEFINE NEUROTROPHISM

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

18

HOW DO YOU DEFINE NEUROMA?

·   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

19

DESCRIBE CLINICAL PRESENTATION OF 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

20

LIST NON OPERATIVE TREATMENTS OF NEUROMA

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

21

CLASSIFY NEUROMA

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

22

DESCRIBE OPERATIVE TREATMENT OF NEUROMA

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

23

WHAT IS A GLIOMA

o  no regeneration in distal stump therefore neuroma does not form

o  glioma is the minor fibroblast and schwann cell response

24

what is the etiology of brachial plexopathy?

Congenital

 

 

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

Acquired (vitamin)

 

Vascular

  • Aneurysm of subclavian artery

Infectious

  • ?viral Parsonage-Turner

Inflammatory

  • Multiple neuritis, post-radiation

Trauma (most common)

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

Toxic

 

Allergic

  • Allergic plexopathy

Metabolic

 

Idiopathic

  • Plexopathy of unknown origin

Iatrogenic

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

Immunologic

  • Post Vaccination

Neoplastic

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

25

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

26

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

27

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

28

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

29

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

                  Roots

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

C5-7

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

30

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