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Peripheral
Nerve
Injuries
Dr. YASIM
Dept. of Orthopaedics
LNH MAMC
Clefts of Schmidt -lantermann
 Incisures , oblique discontinuities in my myelin
 Function as an Interchange pathway between axon
internally and ECF externally.
Internal topography
Fascicular arrangement constantly change
the course
 Funiculi are numerous and small near joints except
ulnar nerve behind MEP and axillary nerve beneath
shoulder joint, where these two nerves frequently
composed of single funiculus.
 More epineurial tissue where cross joints
 Fibroblast, collagen fibre, mast cell common to all
three but mesothelial cells special feature of
perineurium.
Arteriae nervorum
Interfunicular arterioles
Nervi nervorum
 Originates from fibers in the nerve and form the
perivascular plexuses.
 Distributed to epi- , peri- , endonerium
 Sympathetic and sensory fibers
Classification of nerve injuries
Seddon Classification
1.Neuropraxia:
1.Minor contusion or compression with preservation of axis –
cylinder of myelin sheath.
2.Impulse transmission physiologically interrupted.
3.Complete recovery in a few days to weeks
2.Axonotemesis :
1.More significant injury
2.Breakdown of axon and distal Wallerian degeneration but with
preservation of schwann cell & endoneurial tubes
3.Spontaneous regeneration with good functional recovery can be
expected
3.Neurotmesis
1.More severe injury
2.Complete anatomical severance, avulsion or crushing of nerve
3.Axon, Schwann cell & endoneurial tubes are completely
disrupted
4.Spontaneous recovery cannot be expected unless explored
Sunderland Classification


Each degree of injury suggesting a greater anatomical
disruption with its correspondingly altered prognosis
Anatomically various degrees (1st– 5th) represent injury
to





Myelin
Axon
Endoneurial tube & it’s content
Perineurium
Entire nerve trunk


Sixth degree (Mackinson) or mixed injuries occur in
which a nerve trunk is partially severed and
remaining part of trunk sustains 1stto 4thdegree
injury.
Mixed recovery pattern depending on degree of
injury to each portion of nerve.
Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
damage
Axon
+
Endo
damage
Axon
+
Endo
+
Peri
damage
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
damage
Type Type
A B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis
(Division of a nerve)
Conduction block
 Arterial sleeve around nerve trunks blocks all fibers in
10 minutes ( Weiss and Davis 1943)
 Causes: compression/ traction/ ischemia / cold
 Differential sensitivity of motor and sensory fibers to
compression
 Damaged fibers more sensitive to ischemia than
normal fibers
 Large fibers more sensitive than fine fibers
Degeneration
 At site of injury:
 when sheath is preserved -crushed segment is
hyperaemic, endoneurial edema in 1-2 hours. By third day
schwann cell occupied tubes in crushed region and
regenerating axon sprouts .
 When sheath is ruptured- formation of retraction bulb.
Exudate btwn ends of fibre, bridging connective tissue
 Retrograde changes:
 When sheath intact- few mm
 When sheath ruptured – sevral cm nerve fibre reaction ,
nerve cell reaction, trans-synaptic neuronal reaction.
 Below site of injury: axon and myelin degenerate and
removed by phagocytosis, schwann cells proliferate
and the enodoneurial sheath is left encircling a column
of schwann cells.
 all traces of axon are lost by two weeks and precedes
degeneration of myelin
 Myelin fragments and paranodal and incisures act as
foci for physical distintegration by 8 th day and then
chemical degradation.
 Centrifugal failure: degeneration in terminal part of
intramuscular nerve fibre when more proximal part of
same fiber is normal.
 Nmj is affected before nerve and muscle
 Failure at nmj is delayed by 45 min per cm increase in
length of section of nerve
 If not reinnervated, or delayed too much the funiculi
are replaced with fibrous tissue
 Changes appear more rapidly in child
 Large myelinated fiber degenerate early
 greater the length of distal severed axon longer it will
survive
Regeneration
 Schwann cells forerunner of regenerative process
 Axon tip
 Initial delay: time to reach injured zone
 Scar delay: time taken by axon to cross injury zone
 Period of functional recovery: time for recovery in
sufficient number of fibers and appropriate
combinations
 Terminal delay: due to atrophic changes in skin, muscle
fibers
 Reinervation is precisely same if tube is intact, below
lesion earliest 4- 10 days from injury
 Axon tip shows amoeboid activity, growth cone 50 sprouts from
one
 Time axon reach tube will be free of debris
 Nerves retain capacity to sprout for several year from original
injury
 After suture repair axon crosses distaly in 3-20 days
 Single axon may branch and reinervate more than one tube.
 No increase in number of tubes in distal stump and preserves
original pattern of innervation
 Hoffman- tinel sign: radiating tingling sensation felt in cutaneous
distribution of injured nerve on light percussion

SystemicDiseases
IdiopathicNeuropathies
EntrapmentSyndromes
InfectiousCauses
Primary injury
– Results from same trauma that injures a bone or
joint
– Radial nerve is the most commonly injured. Of
humeral shaft fractures, 14 % is complicated by
radial nerve injuries
– Displaced osseous fragments
– Stretching
– Manipulation
Secondary injury
– Results from involvement of nerve by infection, scar,
callous or vascular complications which may be
hematoma, AV fistula, Ischemia or aneurysm
Diagnosis of Peripheral nerve
injuries
• History
– Which nerve ?
– What level ?
– What is the cause ?
– What degree of injury ?
– Old or fresh injury ?
Diagnosis of Peripheral nerve
injuries
1. Motor:
– All muscles distal to the injury – paralyzed
& atonic
–
–
Atrophy : 50 -70 % in 1sttwo months
Striations & motor end plate configurations
retained for 12 – 18 months (critical limit
of delay)
2. Sensory :
• Sensory loss usually follows a definite
anatomical pattern, although factor of
overlap from adjacent nerves may be
present
• Autonomous zone
• Tinel’s sign
(3) Reflex
• Abolishes all reflexes transmitted by that
nerve, either afferent or efferent arc.
• Complete & incomplete lesion. So , not a
reliable guide to injury severity.
(4) Autonomic :
• Loss of sweating
• Loss of pilomotor response and
• Vasomotor paralysis in autonomous zone
(5) Others:
• Trophic Changes
•
•
Esp. hand and feet
Skin – thin, glistening, breaks easily to form
ulcers that heal slowly
• Fingernails
• Ridged, distorted and brittle
• Osteoporosis (Reflex sympathetic dystrophy)
Test for peripheral nerves of upper limb
• Radial nerve injury
– very high / high / low injury
– Wrist drop / finger drop / thumb drop
– Test for triceps/ /Brachioradialis/ wrist extensors /
extensor digitorum / EPL
• Median nerve
– High / low injury
– Test for FPL / FDS / FDP (lat. half) / FCR / Abd.
Pollicis brevis ( pen test) / Oppenens pollicis
– See for pointing index / complete claw hand
• Ulnar nerve
– High / low palsy –ulnar paradox
– Test for FCU / Abd. digiti minimi / Interossei (dorsal -
Egawa’s test ; palmar – card test ) / lumbricals /Add.
Pollicis (Froment’s sign / book test )
– Ulnar claw hand
Time of Surgery
• Primary repair : First 24 hours
• Delayed primary repair : First 1 – 18 days
• Secondary repair : 18 days- 3months
Indications for surgery
1. When a sharp injury has obviously divided a
nerve.
2. When abrading, avulsing or blast wounds have
rendered the condition of nerve unknown
3. When a nerve deficit follows a blunt or closed
trauma & no clinical or electrical evidence of
regeneration has occurred after an appropriate
time
4. When a nerve deficit follows a penetrating wound
as stab or low velocity gunshot wound, part
observed for evidence of nerve regeneration for
appropriate time.
Skeletal stability
Healthy tissue bed
Healthy nerve ends
No undue tension
Adequate soft tissue coverage
Types of Nerve Repair
1. Endoneurolysis
2. Partial Neurorrhaphy
3. Neurorrhaphy
1. Epineural
2. Epi-perineural
3. Perineural
4. Nerve grafting
Epineurial
Less exact
Simple
Group Fascicular
Better alignment
More dissection (scarring)
The functional results of group fascicular repair
has not been shown to be more superior than that
of epineurial repair.
Method of closing gap between nerve ends
1. Nerve grafting
2. Transposition
3. Bone resection
1. Mobilization ( critical nerve gap distance – value
of Grantham)
2. Positioning of extremity
–
–
Flex knee and elbow < 90°
Flex wrist < 40°
Motor
Proprioception
Touch
Temperature
Pain
Sympathetic
Recovery
Injury
Prognostic Factors of Outcomes
Patient
factor •Age
• Level of injury (distal vs
proximal)
• Type of nerve (pure vs mixed
functions)
• Condition of nerve ends
Injury
factors
• Delay to repair
• Length of gap
Surgical
factors
Evaluationof Patientwith
Neuropathy
History
• The diagnostic process begins with the physician
obtaining acareful history.
• The family, social, and occupational histories are
important for identifying familial occurrences or
toxic exposures.
History
KeyQuestions:
•Isthe onset sudden or gradual?
• Isthe progression rapid orslow?
• Isthe predominant manifestation sensory, motor, orboth?
•Isthe distribution focal or generalized, distal orproximal,
symmetric or asymmetric?
• Isthere autonomic involvement?
• Doesthe patient have any associateddiseases?
Relative predisposition to injury to peroneal
component than tibial
More superficial
Greater disability becoz of over stretched muscles
Poorer blood supply single funiculus with major nutrient
artery exposed on surface
Large and tighty packed funiculi with less connective tissue
Oblique course ,fixed at sciatic notch and neck of fibula
NERVE CRITICAL DELAY
High ulnar nerve lesions 9 months
Low ulnar nerve lesions 15 months
High median nerve lesions 9 months
Low median nerve lesions 12 months
Common peroneal nerve 12 months
EMG
 Can distinguish a recent from old injury in medico –
legal cases
 At initial post injury- normal or recruitment at this
point depends on injury pattern
 10 to 14 day- abnormal spontaneous rest potential ,
positive sharp waves in denervated myotome
 14 to 18 days- fibrillations appear
 3 months – polyphasic potentials / motor unit
potential increase progressively
Brachial plexus
 Erbs – C 5 6 with or without c7 dysfunction
 Extended elbow, adducted internally rotated
 If serratus ant, levator scapulae, rombiods gone
indicating lesion medial to dorsal scapular and long
thorasic
 Denervation potention in segmental paraspinous
muscles inervated by post rami
 Myelography- pseudo meningocele
 Klumpke-C8 T1 with or without C 7 dysfunction
 Intrinsic of hand / flexors of wrist and finger
 Horner syndrome -ptosis /anhydrosis /miosis
enopthalmos / loss of cilio spinal reflex
radial nerve
 In closed humeral fracture normal function may return
in 3-6 months
 In absence of nerve recovery and advancing tinel
exploration can be done after 3 months
 Tendon transfer can be done after 6 months
Median nerve
 Flexion of index and middle finger- side to side suture
with ulnar inervated fdp
 Fpl – brachioradilis / ECRL / ECU
 Thumb opposition- EIP
Ulnar nerve
restoration of intrinsic
If wrist extensors are strong to prevent flexion of wrist
and intrinsics are weak not paralyzed – bunnell transfer ( 4
fds, modified 1 ring finger fds split)
If wrist flexion is chronic habit- Riordan
Brand- ECRB/ 4 tailed free graft - volar to deep tansverse
metacarpal lig – lumbrical canal- radial side of extensor
apponeurosis except index finger difficult to re-educate
if wirst ext stronger than flex – brand – ECRL volarward 4
tail free graft
 If fds /wrist flex /ext not available- fowlers – EIP or
riordan modification of fowler- EIP + PL free plantaris
 If n0 muscle/ joint supple – zancolli capsulodeisis
 Bouvier test- if ext at ip present then static procedure
if ext not present dynamic procedure required
 Thumb adduction- omer- ring fds split brown- EIP in
palm near 3rd metacarpal
Thank You

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peripheral nerve injury concepts and management

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  • 6. Clefts of Schmidt -lantermann  Incisures , oblique discontinuities in my myelin  Function as an Interchange pathway between axon internally and ECF externally.
  • 7. Internal topography Fascicular arrangement constantly change the course
  • 8.  Funiculi are numerous and small near joints except ulnar nerve behind MEP and axillary nerve beneath shoulder joint, where these two nerves frequently composed of single funiculus.  More epineurial tissue where cross joints  Fibroblast, collagen fibre, mast cell common to all three but mesothelial cells special feature of perineurium.
  • 9.
  • 12. Nervi nervorum  Originates from fibers in the nerve and form the perivascular plexuses.  Distributed to epi- , peri- , endonerium  Sympathetic and sensory fibers
  • 13. Classification of nerve injuries Seddon Classification 1.Neuropraxia: 1.Minor contusion or compression with preservation of axis – cylinder of myelin sheath. 2.Impulse transmission physiologically interrupted. 3.Complete recovery in a few days to weeks 2.Axonotemesis : 1.More significant injury 2.Breakdown of axon and distal Wallerian degeneration but with preservation of schwann cell & endoneurial tubes 3.Spontaneous regeneration with good functional recovery can be expected 3.Neurotmesis 1.More severe injury 2.Complete anatomical severance, avulsion or crushing of nerve 3.Axon, Schwann cell & endoneurial tubes are completely disrupted 4.Spontaneous recovery cannot be expected unless explored
  • 14. Sunderland Classification   Each degree of injury suggesting a greater anatomical disruption with its correspondingly altered prognosis Anatomically various degrees (1st– 5th) represent injury to      Myelin Axon Endoneurial tube & it’s content Perineurium Entire nerve trunk   Sixth degree (Mackinson) or mixed injuries occur in which a nerve trunk is partially severed and remaining part of trunk sustains 1stto 4thdegree injury. Mixed recovery pattern depending on degree of injury to each portion of nerve.
  • 16.
  • 17. Conduction block  Arterial sleeve around nerve trunks blocks all fibers in 10 minutes ( Weiss and Davis 1943)  Causes: compression/ traction/ ischemia / cold  Differential sensitivity of motor and sensory fibers to compression  Damaged fibers more sensitive to ischemia than normal fibers  Large fibers more sensitive than fine fibers
  • 18. Degeneration  At site of injury:  when sheath is preserved -crushed segment is hyperaemic, endoneurial edema in 1-2 hours. By third day schwann cell occupied tubes in crushed region and regenerating axon sprouts .  When sheath is ruptured- formation of retraction bulb. Exudate btwn ends of fibre, bridging connective tissue  Retrograde changes:  When sheath intact- few mm  When sheath ruptured – sevral cm nerve fibre reaction , nerve cell reaction, trans-synaptic neuronal reaction.
  • 19.  Below site of injury: axon and myelin degenerate and removed by phagocytosis, schwann cells proliferate and the enodoneurial sheath is left encircling a column of schwann cells.  all traces of axon are lost by two weeks and precedes degeneration of myelin  Myelin fragments and paranodal and incisures act as foci for physical distintegration by 8 th day and then chemical degradation.  Centrifugal failure: degeneration in terminal part of intramuscular nerve fibre when more proximal part of same fiber is normal.  Nmj is affected before nerve and muscle  Failure at nmj is delayed by 45 min per cm increase in length of section of nerve
  • 20.  If not reinnervated, or delayed too much the funiculi are replaced with fibrous tissue  Changes appear more rapidly in child  Large myelinated fiber degenerate early  greater the length of distal severed axon longer it will survive
  • 21. Regeneration  Schwann cells forerunner of regenerative process  Axon tip  Initial delay: time to reach injured zone  Scar delay: time taken by axon to cross injury zone  Period of functional recovery: time for recovery in sufficient number of fibers and appropriate combinations  Terminal delay: due to atrophic changes in skin, muscle fibers  Reinervation is precisely same if tube is intact, below lesion earliest 4- 10 days from injury
  • 22.  Axon tip shows amoeboid activity, growth cone 50 sprouts from one  Time axon reach tube will be free of debris  Nerves retain capacity to sprout for several year from original injury  After suture repair axon crosses distaly in 3-20 days  Single axon may branch and reinervate more than one tube.  No increase in number of tubes in distal stump and preserves original pattern of innervation  Hoffman- tinel sign: radiating tingling sensation felt in cutaneous distribution of injured nerve on light percussion 
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  • 30. Primary injury – Results from same trauma that injures a bone or joint – Radial nerve is the most commonly injured. Of humeral shaft fractures, 14 % is complicated by radial nerve injuries – Displaced osseous fragments – Stretching – Manipulation Secondary injury – Results from involvement of nerve by infection, scar, callous or vascular complications which may be hematoma, AV fistula, Ischemia or aneurysm
  • 31. Diagnosis of Peripheral nerve injuries • History – Which nerve ? – What level ? – What is the cause ? – What degree of injury ? – Old or fresh injury ?
  • 32. Diagnosis of Peripheral nerve injuries 1. Motor: – All muscles distal to the injury – paralyzed & atonic – – Atrophy : 50 -70 % in 1sttwo months Striations & motor end plate configurations retained for 12 – 18 months (critical limit of delay)
  • 33. 2. Sensory : • Sensory loss usually follows a definite anatomical pattern, although factor of overlap from adjacent nerves may be present • Autonomous zone • Tinel’s sign
  • 34. (3) Reflex • Abolishes all reflexes transmitted by that nerve, either afferent or efferent arc. • Complete & incomplete lesion. So , not a reliable guide to injury severity. (4) Autonomic : • Loss of sweating • Loss of pilomotor response and • Vasomotor paralysis in autonomous zone
  • 35. (5) Others: • Trophic Changes • • Esp. hand and feet Skin – thin, glistening, breaks easily to form ulcers that heal slowly • Fingernails • Ridged, distorted and brittle • Osteoporosis (Reflex sympathetic dystrophy)
  • 36. Test for peripheral nerves of upper limb • Radial nerve injury – very high / high / low injury – Wrist drop / finger drop / thumb drop – Test for triceps/ /Brachioradialis/ wrist extensors / extensor digitorum / EPL • Median nerve – High / low injury – Test for FPL / FDS / FDP (lat. half) / FCR / Abd. Pollicis brevis ( pen test) / Oppenens pollicis – See for pointing index / complete claw hand
  • 37. • Ulnar nerve – High / low palsy –ulnar paradox – Test for FCU / Abd. digiti minimi / Interossei (dorsal - Egawa’s test ; palmar – card test ) / lumbricals /Add. Pollicis (Froment’s sign / book test ) – Ulnar claw hand
  • 38. Time of Surgery • Primary repair : First 24 hours • Delayed primary repair : First 1 – 18 days • Secondary repair : 18 days- 3months
  • 39. Indications for surgery 1. When a sharp injury has obviously divided a nerve. 2. When abrading, avulsing or blast wounds have rendered the condition of nerve unknown 3. When a nerve deficit follows a blunt or closed trauma & no clinical or electrical evidence of regeneration has occurred after an appropriate time 4. When a nerve deficit follows a penetrating wound as stab or low velocity gunshot wound, part observed for evidence of nerve regeneration for appropriate time.
  • 40. Skeletal stability Healthy tissue bed Healthy nerve ends No undue tension Adequate soft tissue coverage
  • 41. Types of Nerve Repair 1. Endoneurolysis 2. Partial Neurorrhaphy 3. Neurorrhaphy 1. Epineural 2. Epi-perineural 3. Perineural 4. Nerve grafting
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  • 45. Epineurial Less exact Simple Group Fascicular Better alignment More dissection (scarring) The functional results of group fascicular repair has not been shown to be more superior than that of epineurial repair.
  • 46.
  • 47. Method of closing gap between nerve ends 1. Nerve grafting 2. Transposition 3. Bone resection 1. Mobilization ( critical nerve gap distance – value of Grantham) 2. Positioning of extremity – – Flex knee and elbow < 90° Flex wrist < 40°
  • 48.
  • 50. Prognostic Factors of Outcomes Patient factor •Age • Level of injury (distal vs proximal) • Type of nerve (pure vs mixed functions) • Condition of nerve ends Injury factors • Delay to repair • Length of gap Surgical factors
  • 52. History • The diagnostic process begins with the physician obtaining acareful history. • The family, social, and occupational histories are important for identifying familial occurrences or toxic exposures.
  • 53. History KeyQuestions: •Isthe onset sudden or gradual? • Isthe progression rapid orslow? • Isthe predominant manifestation sensory, motor, orboth? •Isthe distribution focal or generalized, distal orproximal, symmetric or asymmetric? • Isthere autonomic involvement? • Doesthe patient have any associateddiseases?
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  • 71. Relative predisposition to injury to peroneal component than tibial More superficial Greater disability becoz of over stretched muscles Poorer blood supply single funiculus with major nutrient artery exposed on surface Large and tighty packed funiculi with less connective tissue Oblique course ,fixed at sciatic notch and neck of fibula
  • 72. NERVE CRITICAL DELAY High ulnar nerve lesions 9 months Low ulnar nerve lesions 15 months High median nerve lesions 9 months Low median nerve lesions 12 months Common peroneal nerve 12 months
  • 73.
  • 74. EMG  Can distinguish a recent from old injury in medico – legal cases  At initial post injury- normal or recruitment at this point depends on injury pattern  10 to 14 day- abnormal spontaneous rest potential , positive sharp waves in denervated myotome  14 to 18 days- fibrillations appear  3 months – polyphasic potentials / motor unit potential increase progressively
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  • 80. Brachial plexus  Erbs – C 5 6 with or without c7 dysfunction  Extended elbow, adducted internally rotated  If serratus ant, levator scapulae, rombiods gone indicating lesion medial to dorsal scapular and long thorasic  Denervation potention in segmental paraspinous muscles inervated by post rami  Myelography- pseudo meningocele
  • 81.  Klumpke-C8 T1 with or without C 7 dysfunction  Intrinsic of hand / flexors of wrist and finger  Horner syndrome -ptosis /anhydrosis /miosis enopthalmos / loss of cilio spinal reflex
  • 82. radial nerve  In closed humeral fracture normal function may return in 3-6 months  In absence of nerve recovery and advancing tinel exploration can be done after 3 months  Tendon transfer can be done after 6 months
  • 83.
  • 84. Median nerve  Flexion of index and middle finger- side to side suture with ulnar inervated fdp  Fpl – brachioradilis / ECRL / ECU  Thumb opposition- EIP
  • 85. Ulnar nerve restoration of intrinsic If wrist extensors are strong to prevent flexion of wrist and intrinsics are weak not paralyzed – bunnell transfer ( 4 fds, modified 1 ring finger fds split) If wrist flexion is chronic habit- Riordan Brand- ECRB/ 4 tailed free graft - volar to deep tansverse metacarpal lig – lumbrical canal- radial side of extensor apponeurosis except index finger difficult to re-educate if wirst ext stronger than flex – brand – ECRL volarward 4 tail free graft
  • 86.  If fds /wrist flex /ext not available- fowlers – EIP or riordan modification of fowler- EIP + PL free plantaris  If n0 muscle/ joint supple – zancolli capsulodeisis  Bouvier test- if ext at ip present then static procedure if ext not present dynamic procedure required  Thumb adduction- omer- ring fds split brown- EIP in palm near 3rd metacarpal
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