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PERIPHERAL NERVE INJURY
ASSESSMENT AND TENDON
TRANSFERS IN RADIAL NERVE PALSY
MODERATOR: DR.G.RAMESH
ASSOCIATE PROFESSOR ORTHOPAEDICS, GANDHI HOSPITAL
PRESENTER: DR.G.SAI.SUCHITRA
PG 3RD YEAR, GANDHI MEDICAL COLLEGE
PERIPHERAL NERVE
• “Peripheral nerve” is a term used synonymously to describe the
peripheral nervous system.
• The peripheral nervous system is a network of 43 pairs of motor and
sensory nerves that connect the brain and spinal cord (the central
nervous system) to the entire human body.
• These nerves control the functions of sensation, movement and
motor coordination.
STRUCTURE OF A PERIPHERAL NERVE
• The peripheral nerve is composed of the axons enclosed in Schwann’s
sheaths and their supporting endoneural tissues.
• Groups of axons are arranged in bundles called fascicles.
• The intraneural tissue around the microscopic Schwann’s tubes is
called the endoneurium, and a fibrous sheath of each fascicle is
called the perineurium.
• The perineurium is only four or five cell layers thick and therefore is
visible only with the aid of a microscope.
• The abundant macroscopic fibrous tissues incorporating all of the
fascicles of well- defined bundles constitute the epineurium.
• FASCICLES(AXONS)
• EACH FASCICLE
WRAPPED BY
ENDONEURIUM
• GROUP OF FASCICLES
BY PERINEURIUM
• INNER EPINEURIUM
LOOSELY WRAPPING
AROUND INNER
FASCICULAR GROUPS
AND OUTER
EPINEURIUM CLOSELY
APPOSED TO
PERIPHERAL NERVE
SHEATH CALLED
“ADVENTITIA”
• A certain amount of gliding motion occurs between the elastic
adventitia and the epineurium, which gives the nerve mobility for
crossing joints without suffering stretch injuries
• Nerve cells are called neurones.
• A neurone consists of a cell body (with a nucleus and cytoplasm), dendrites
that carry electrical impulses to the cell, and a long axon that carries the
impulses away from the cell
• Generation of a nerve impulse (action potential) of a sensory neurone
occurs as a result of a stimulus such as light, a particular chemical, or
stretching of a cell membrane by sound.
• Conduction of an impulse along a neurone occurs from the dendrites to the
cell body to the axon.
• Transmission of a signal to another neuron across a synapse occurs via
chemical transmitter. This substance causes the next neurone to be
electrically stimulated and keeps the signal going along a nerve.
ANATOMY:
Neuron:
Cell body:
Motor: anterior horn of spinal cord
Sensory: dorsal root ganglion
Axon:
• Myelinated: wrapped in double basement membrane of Schwann cell
• Non myelinated
Transport of intracellular components[vesicles]: 410 mm/day
• Structural proteins : 1-6 mm /day, limiting factor in nerve regeneration
• Individual nerve fibers vary widely in diameter and may also be
myelinated or unmyelinated.
• Myelin in the peripheral nervous system derives from Schwann cells,
and the distance between nodes of Ranvier determines the
conduction rate.
• A ganglion is a cluster of neuron cell bodies enveloped in an
epineurium continuous with that of a nerve. A ganglion appears as a
swelling along the course of a nerve.
• The spinal ganglia or posterior or dorsal root ganglia associated with
the spinal nerves contain the unipolar neurons of the sensory nerve
fibers that carry signals to the cord. The fiber passes through the
ganglion without synapsing.
• However, in the autonomic nervous system, a preganglionic fiber
enters the ganglion and in many cases synapses with another neuron.
The axon of the second neuron leaves the ganglion as the
postganglionic fiber.
PATHOPHYSIOLOGY OF NERVE INJURY
• All the functions distal to the point of severance are interrupted
• At the end of proximal nerve segment axons multiply and attempt to grow
distally
• A connective tissue growth envelopes the end of the nerve and obstructs
the path of these fibrils
• This connective tissue and fibrillar growth is called neuroma
• Distal nerve segment swells to double its original size and undergoes
Wallerian degeneration.
• This process is complete in about one month
• Occasionally the connective tissue growths at the end of each segment
may successfully penetrate the mass and grow distally restoring partial
functions
TINEL’S SIGN
Rate of nerve regeneration: 1-4.5 mm/day
• Tinels rate : 1-2 mm/day.[ 2-3 times in children]
“When percussion is lightly applied to the injured nerve tissue , we find the cutaneous
region of the nerve, a creeping sensation usually compared by the patient to that
caused by electricity”
 Reserve only for traumatic neuropathy
 Strongly positive Tinels over lesion after injury indicated severance or rupture
 Centrifugally moving Tinels sign persistently stronger than at the suture line-repair
that is going to be successful
 Tinels at the suture line stronger than at the growing end- repair that is going to fail
 Failure of distal progression of Tinels in a closed lesion – rupture or lesion impeding
regeneration
CLASSIFICATION OF NERVE INJURIES
• Classification of nerve injuries is useful in understanding their
pathological basis, making decisions on management, and predicting
the prognosis for recovery.
• Seddon described a classification of localized injuries to peripheral
nerves after study of large numbers of casualties during the second
world war, which is still widely used.
• Neurapraxia-
• Axonotmesis
• Neurotmesis
• LIMITATIONS OF SEDDON’S CLASSIFICATION-
• Seddon’s classification doesn’t distinguish between all grades of intraneural
damage.
• Lesions classified as axonotmesis have been observed to have variable
recovery. This is because variable degrees of damage to the connective
tissue layers of the nerve, including the endoneurium and perineurium, as
well as disruption of the axons are possible without loss of continuity of
the nerve trunk.
•
SUNDERLAND’S CLASSIFICATION-
Sixth degree [ Mac kinnon]:
combination or several degrees with various pattern of injury and
recovery.
Nerve trunk is partially severed, and the remaining part of the trunk
sustains fourth-degree, third-degree, second-degree, or rarely even first-
degree injury
ASSESSMENT OF NERVE INJURY
• CLINICALLY-
• SYMPTOMS FOLLOWING COMPLETE NERVE INJURY-
• Loss of stereognosis
• Loss of superficial pain, touch and temperature
• Loss of deep sensation to muscle and joint movements, position,
deep pressure and vibration
• Loss of motor supply to muscle results in muscle atrophy and fibrous
degeneration
• Deep tendon reflexes are diminished or absent
• Electrical stimulation of the nerve no longer causes the muscle to
contract but muscle can be individually stimulated by Faradic current
until two weeks after which even Faradism doesn’t elicit any response
• But the muscle continues to respond to Galvanic current with slow
contraction , greater in amplitude followed by slow relaxation
• This phenomenon is known as ”REACTION OF DEGENERATION” and
is characteristic feature of peripheral nerve injury
• Trophic influence is lost
• Neurophysiological studies form a relevant and well-established part in the
diagnosis and work-up of nerve injuries
• Does a nerve lesion exist?
• Where precisely is the lesion located?
• Are other nerves involved, which may explain patient’s signs and symptoms?
• What type of lesion is it –axonal or a demyelinating?
• Is there a generalized lesion of peripheral nerves, e.g. polyneuropathy?
• Is the lesion acute, subacute or chronic?
• What is the severity of the lesion?
• Additional questions, which can only partially be answered, are:
• What is the prognosis of untreated nerve injury or entrapment syndrome?
• What treatment modality is necessary –surgery or conservative treatment?
• Was the treatment effective?
GENERAL PRINCIPLES OF NCS
• Motor and sensory nerve conduction studies (NCS) are performed .
• The type of study depends on the nerve studied (motor, sensory or
mixed nerve) and on the site of recording
• In NCS the nerve is electrically stimulated by a bipolar surface
stimulator.
• As a general rule, only myelinated nerve fibres can be investigated.
• Skin temperature should be measured and the extremity be warmed
if the temperature is <32°C.
• Nerve conduction gets slightly slower at ages above 75 ys.
• Motor nerve conduction studies (mNCS)
• In mNCS compound motor action potentials (CMAP) are recorded
from a muscle innervated by the nerve under investigation. Surface
electrodes are used and the “active” (recording) electrode is placed
over the muscle belly, the other (reference) electrode over the
tendon at the insertion of the muscle (belly-tendon electrode
placement).
Figure 1: Median nerve motor nerve conduction study.
Standard electrode placement over the abductor pollicis
brevis muscle and stimulation of the median nerve at the
wrist are displayed.
• Sensory nerve conduction studies (sNCS)
• Orthodromic or antidromic nerve conduction studies are performed
to study sensory nerves.
• In antidromic studies amplitudes are usually higher than in
orthodromic studies, otherwise both methods are comparable.
• In antidromic studies of e.g. the median or ulnar nerves, the sensory
nerve action potential (SNAP) may be recorded using ring electrodes
placed around a finger, and the nerves are stimulated at the wrist.
• In orthodromic studies, surface electrodes are placed over the nerve
at the wrist, and finger nerves are stimulated by ring electrodes
Standard electrode placement for A) antidromic and B)
orthodromic median nerve sensory nerve conduction
studies. In A) stimulation is at the wrist, in B) at the index
finger.
• An NCV test shows the condition of the best surviving nerve fibers,
so in some cases the results may be normal even if there is nerve
damage
GENERAL PRINCIPLES OF NEEDLE
ELECTROMYOGRAPHY (EMG)
• Electric potentials produced by muscle fibres can also be recorded
using intramuscular needle electrodes
• Pathologic EMG findings are only seen in axonal nerve lesions.
• Typically, EMG is recorded when the muscle is at rest, during a weak
contraction and during a strong contraction.
• With the muscle at rest, spontaneous activity is assessed.
• In a healthy muscle there is only a brief burst of EMG signal when the
needle is moved within the muscle. This is called insertional activity.
• Following an axonal injury, several forms of pathological spontaneous
activity may be found.
• Fibrillation potentials (fibs) and positive sharp waves (psw) are seen
14-21 days following an axonal nerve lesion.
• They usually persist for 6-12 month, although some spontaneous
activity may persist for many years. Complex repetitive discharges and
myokymic discharges are sometimes seen in chronic lesions.
• However, all types of spontaneous activity can occur in other
disorders of nerve or muscle as well
• In general the neurophysiology tests can distinguish between injuries
where axons have not degenerated (neurapraxia) and those where
axons have degenerated distally (axonotmesis and neurotmesis)
• If axonotmesis has affected all the fibres in a nerve then the findings
will be indistinguishable neurotmesis.
• If there is a mixed lesion with some fibres intact detection of these
will imply the nerve trunk has not been disrupted.
MAGNETIC RESONANCE IMAGING (MRI)
• Normal nerves can be visualised on MRI although their signal
characteristics are not distinct from other tissues.
• A technique called magnetic resonance neurography, which enhances
neural tissue on images, was reported by Filler.
• In the zone of injury signals are affected by oedema and haemorrhage
in the surrounding tissues.
• MRI has proved effective in imaging peripheral nerve tumours.
• It is also useful in assessment of brachial plexus injuries where
avulsion of nerve roots can be defined
• In addition to imaging the nerves themselves, information may be
obtained from MRI of muscle innervated by damaged nerves.
• On T2 and STIR images changes may be seen in denervated muscle as
early as two weeks after injury.
• The exact relationship between severity of nerve injury and the early
signal changes in muscles seen on MRI is not clear.
• More prolonged denervation of muscle leads to wasting and fatty
infiltration which can be seen on T1 waited MR images
Sagittal T2 weighted magnetic resonance image of the
shoulder showing increased signal in deltoid and teres
minor as a result of axillary nerve injury
ULTRASOUND
• Modern ultrasound scanners have improved to the extent that resolution is
now greater than MRI.
• Ultrasound is being used increasingly to examine nerves damaged by
closed trauma.
• It may be able to confirm continuity of a nerve, or diagnose rupture or
entrapment, for example, in a fracture.
• Fascicular disruption within a nerve trunk may be visualised.
• Use of ultrasound to examine the radial nerve injured in an association
with fractures of the humerus been reported and for diagnosis of median
nerve entrapment in the forearm.
• However, ultrasound is operator dependent and requires experience for
optimal interpretation
PRINCIPLES OF MANAGEMENT OF NERVE INJURY
• While the classifications of nerve injury provide a basis for prognosis
and management, in reality it can be difficult to diagnose the grade of
injury to a nerve in the early stages.
• The situation may only become clear in retrospect.
• Therefore a practical approach to management is recommended.
• It is useful to divide injuries into those which are open and closed.
OPEN NERVE INJURIES
• When there is evidence of loss of function in a nerve associated with a
wound, then in most circumstances exploration of the wound and the
affected nerve should be carried out.
• The only exception to this would be, if expert assessment indicates that the
patient is unlikely to benefit from repair of the nerve or if the patient is
unfit for operation.
• Uncertainty can occur when a nerve is partly divided since some function
will be preserved.
• Therefore lacerations associated with any neurological deficit should be
explored on the assumption that affected nerves are either partly or
completely divided rather than assuming than there is some form of lesion
in-continuity.
• Usually nerve repair should be carried out early at the same time as
other injured structures.
• Therefore fracture fixation, tendon repairs and skin closure is carried
out simultaneously, providing adequate vascularised skin and cover
can be provided.
• Full thickness vascularised skin cover is necessary over a nerve repair
rather than split skin graft.
CLOSED INJURIES-
• When a nerve has been injured as a result of blunt trauma there is likely to
be more uncertainly regarding the grade of injury.
• In general an assessment should be made of the probability that a nerve
has been disrupted or is under continuing compression.
• If the injury has been caused by high energy trauma then the chance of
disruption of the nerve is higher and early exploration should be
considered. If operation is required in any case, for example, for fracture
fixation, then the opportunity should not be missed to explore damaged
nerves and confirm continuity.
• Early exploration is best carried out within the first 2 weeks following
injury.
• If there has been lower energy trauma and a lesion in-continuity seems
likely then expectant management may be pursued.
• However, progress of nerve recovery should be monitored carefully
looking for return of muscle function and an advancing Tinel’s sign.
• If there is no improvement by 2 to 3 months from injury then surgical
exploration should be considered.
• Urgent neurophysiology assessment and imaging may help at this
stage
ACUTE NERVE COMPRESSION
• Nerves may be compressed by displaced fragments of fractures, dislocation of joints, or
expanding hematoma.
• The onset of loss of nerve function may be delayed after the injury although this may be
difficult to ascertain.
• Typically there is severe pain associated with the nerve palsy.
• This situation requires urgent management with reduction of fractures and dislocations.
• If closed reduction does not relieve the situation then open reduction with exploration of
the affected nerves should be performed.
• If there is suspicion of arterial injury, for example, false aneurysm, then angiography
should be arranged.
• Haematoma with sufficient pressure to cause nerve compression is likely to have been
caused by arterial haemorrhage.
• Drainage of the haematoma and vessel repair is required as an emergency.
A NERVE PALSY OCCURRING AFTER A
MEDICAL OR SURGICAL PROCEDURE
• This is an unfortunate and sometimes disastrous complication of
treatment.
• It is important to examine the function of nerves related to a surgical
procedure and document the findings before and afterwards.
• If a patient is found to have a new loss of nerve function after a
procedure then a prompt, careful and objective assessment needs to
be made.
• Since the clinician who has performed the procedure may have an
emotional attachment to the situation, it is often best to involve
another clinician
EXPLORING THE DAMAGED NERVE AT AN EARLY
STAGE TAKING INTO ACCOUNT THE FOLLOWING
FACTORS
• The events during the procedure should be reviewed to check whether the
nerve was identified and what the likely mechanism of injury is, including
laceration or compression.
• Whether the nerve palsy was present immediately after the procedure or
developed after a delay.
• If there is a possibility that the nerve is being subjected to continuing
compression, by haematoma or an implant then urgent re-operation
should be carried out
• Urgent investigations, including ultrasound, MRI, and neurophysiology may
be helpful
• The risks and benefits of carrying out a second procedure, including the
patient’s general condition, the risk of infection, and whether repair of the
affected nerve is likely to lead to useful functional recovery.
TENDON TRANSFERS
PREREQUISITES TO TENDON TRANSFER-
• OPEN WOUNDS
• A patient is not a candidate for a tendon transfer if he or she has
open wounds that could predispose to a disastrous postoperative
infection
• SOFT TISSUE COVERAGE
• Tendon transfers will glide only if transplanted through mobile,
unscarred, healthy tissues.
• Meeting this requirement usually entails subcutaneous rerouting of
the tendon out of contact with scar and fixed structures.
• MAXIMUM JOINT MOBILIZATION ESTABLISHED
• One never gains more active range of motion from tendon transfers
than the preoperative passive range of motion.
• Therefore, it is important that good joint mobility precede tendon
transfers. With disrupted motor nerves or muscle–tendon losses, the
imbalance of forces acting across the joints occurs immediately (with
the exception of total paralysis, in which there is no imbalance).
• In contrast, joint stiffening and deformity develop as the result of the
imbalance. Attention to joint stiffening and deformity with
appropriate therapy and splinting can substantially prevent these
complications.
• SKELETAL STABILIZATION
• RESTORED SENSIBILITY
• When possible, restoration of at least protective sensibility should
precede tendon transfers.
• Skin sensibility is not absolutely required for tendon transfers to be
useful, but it is always desirable
• POWER AND CONTROL
• To be a candidate for tendon transfer, a muscle must have adequate
power for the new function, be nonspastic, and be under good
volitional control.
• It also needs to be an independently functioning muscle unit, such as
a finger superficial flexor or the EIP, in contrast to the flexor digitorum
communis (FDC), whose four tendons originate from a common
muscle.
• In general, only muscles having a power grade of 4 or 5 (on the 0 to 5
scale) are suitable candidates for transfer.
• AMPLITUDE OF EXCURSION
• The muscle to be transferred must have an adequate amplitude of
excursion for its new function or be so situated that its effective
amplitude can be enhanced by tenodesis as it crosses an actively
controlled joint. Most often this joint will be the wrist
• ANATOMICALLY FAESIBLE LOCATION OF THE MUSCLE
• The surgical rerouting of a muscle and tendon should be in as direct a
line of pull as possible between the muscle’s origin and its new
insertion. Otherwise, as it begins to function, it will work into a
straight line of pull and become too slack.
• SYNERGISM
• Muscles that simultaneously and automatically contract to work
together are referred to as synergistic. An example is wrist extension
with finger flexion, as has already been discussed.
• Synergism was once considered important in selecting muscles for
transfer, but it is much less important today
• EXPENDABILITY
• Obviously, if a muscle is to be transferred for a new duty, the surgeon
must be certain that this will be of more benefit to the patient than
the muscle is in its normal situation.
• POTENTIAL PIP JOINT COMPLICATIONS
• The surgeon should be constantly aware of the possibilities of creating
secondary problems.
• If the proximal interphalangeal (PIP) joint of the finger from which the
flexor digitorum superficialis (FDS) is to be taken is hyperextensible from an
incompetent or ruptured volar plate, taking its FDS tendon can cause a
distressing recurvatum deformity.
• If the hyperextensibility is slight, simply leaving one slip of the FDS long so
it can adhere proximally in the tendon sheath is all that is necessary.
However, with gross hyperextensibility of the PIP joint, suturing a long
distally attached slip of the FDS to its proximal sheath is necessary for
tenodesis control of the joint.
• If any two of the three nerves are irreparably lost, a major functional
impairment is inevitable, and reconstruction must entail a substantial
simplification of the hand’s mechanical design if useful function is to
be restored.
• At the same time, wrist extension–flexion, as emphasized by White
(1960), is of such fundamental importance that its arthrodesis should
be done only as a last resort
TENDON TRANSFERS IN RADIAL NERVE PALSY
POST OPERATIVE CARE
• PROTECTIVE PHASE (SURGERY – 3-5 WEEKS)
• OBJECTIVES- Edema control, protective splinting, mobilise uninvolved joints
• MOBILISATION PHASE
• Begun when tendon healing is adequate for mobilisation
• OBJECTIVES-
• Mobilise transferred tendons
• Immobilise soft tissue
• Continue mobilisation of uninvolved joints
• Reinforce pre operative teaching and patient education
• Begin home rehabilitation
• Day time dynamic splinting and night time static splinting
• INTERMEDIATE PHASE(5-8 WEEKS POST OP)
• Gradually increase hand activities and passive ROM
• Limited functional movements permitted
• RESISTIVE PHASE (8-12 WEEKS POST OP)
• Resistance exercises started
• Therapeutic objective is increasing endurance and strength
• Work related tasks are begun
BIBLIOGRAPHY
• TUREK’S TEXT BOOK OF ORTHOPAEDICS
• BEASLEY’S TEXT BOOK OF HAND SURGERY
• LIVING TEXT BOOK OF HAND SURGERY
• TEXT BOOK OF PLASTIC SURGERY
• CAMPBELL’S 12TH EDITION
• JOHN HOPKIN’S NEUROLOGY AND NEUROSURGERY
Peripheral nerve injuries-ASSESSMENT AND TENDON TRANSFERS IN RADIAL NERVE PALSY

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Peripheral nerve injuries-ASSESSMENT AND TENDON TRANSFERS IN RADIAL NERVE PALSY

  • 1. PERIPHERAL NERVE INJURY ASSESSMENT AND TENDON TRANSFERS IN RADIAL NERVE PALSY MODERATOR: DR.G.RAMESH ASSOCIATE PROFESSOR ORTHOPAEDICS, GANDHI HOSPITAL PRESENTER: DR.G.SAI.SUCHITRA PG 3RD YEAR, GANDHI MEDICAL COLLEGE
  • 2. PERIPHERAL NERVE • “Peripheral nerve” is a term used synonymously to describe the peripheral nervous system. • The peripheral nervous system is a network of 43 pairs of motor and sensory nerves that connect the brain and spinal cord (the central nervous system) to the entire human body. • These nerves control the functions of sensation, movement and motor coordination.
  • 3. STRUCTURE OF A PERIPHERAL NERVE • The peripheral nerve is composed of the axons enclosed in Schwann’s sheaths and their supporting endoneural tissues. • Groups of axons are arranged in bundles called fascicles. • The intraneural tissue around the microscopic Schwann’s tubes is called the endoneurium, and a fibrous sheath of each fascicle is called the perineurium. • The perineurium is only four or five cell layers thick and therefore is visible only with the aid of a microscope. • The abundant macroscopic fibrous tissues incorporating all of the fascicles of well- defined bundles constitute the epineurium.
  • 4. • FASCICLES(AXONS) • EACH FASCICLE WRAPPED BY ENDONEURIUM • GROUP OF FASCICLES BY PERINEURIUM • INNER EPINEURIUM LOOSELY WRAPPING AROUND INNER FASCICULAR GROUPS AND OUTER EPINEURIUM CLOSELY APPOSED TO PERIPHERAL NERVE SHEATH CALLED “ADVENTITIA”
  • 5.
  • 6. • A certain amount of gliding motion occurs between the elastic adventitia and the epineurium, which gives the nerve mobility for crossing joints without suffering stretch injuries
  • 7. • Nerve cells are called neurones. • A neurone consists of a cell body (with a nucleus and cytoplasm), dendrites that carry electrical impulses to the cell, and a long axon that carries the impulses away from the cell • Generation of a nerve impulse (action potential) of a sensory neurone occurs as a result of a stimulus such as light, a particular chemical, or stretching of a cell membrane by sound. • Conduction of an impulse along a neurone occurs from the dendrites to the cell body to the axon. • Transmission of a signal to another neuron across a synapse occurs via chemical transmitter. This substance causes the next neurone to be electrically stimulated and keeps the signal going along a nerve.
  • 8.
  • 9. ANATOMY: Neuron: Cell body: Motor: anterior horn of spinal cord Sensory: dorsal root ganglion Axon: • Myelinated: wrapped in double basement membrane of Schwann cell • Non myelinated Transport of intracellular components[vesicles]: 410 mm/day • Structural proteins : 1-6 mm /day, limiting factor in nerve regeneration
  • 10. • Individual nerve fibers vary widely in diameter and may also be myelinated or unmyelinated. • Myelin in the peripheral nervous system derives from Schwann cells, and the distance between nodes of Ranvier determines the conduction rate.
  • 11. • A ganglion is a cluster of neuron cell bodies enveloped in an epineurium continuous with that of a nerve. A ganglion appears as a swelling along the course of a nerve. • The spinal ganglia or posterior or dorsal root ganglia associated with the spinal nerves contain the unipolar neurons of the sensory nerve fibers that carry signals to the cord. The fiber passes through the ganglion without synapsing. • However, in the autonomic nervous system, a preganglionic fiber enters the ganglion and in many cases synapses with another neuron. The axon of the second neuron leaves the ganglion as the postganglionic fiber.
  • 12.
  • 13. PATHOPHYSIOLOGY OF NERVE INJURY • All the functions distal to the point of severance are interrupted • At the end of proximal nerve segment axons multiply and attempt to grow distally • A connective tissue growth envelopes the end of the nerve and obstructs the path of these fibrils • This connective tissue and fibrillar growth is called neuroma • Distal nerve segment swells to double its original size and undergoes Wallerian degeneration. • This process is complete in about one month • Occasionally the connective tissue growths at the end of each segment may successfully penetrate the mass and grow distally restoring partial functions
  • 14.
  • 15. TINEL’S SIGN Rate of nerve regeneration: 1-4.5 mm/day • Tinels rate : 1-2 mm/day.[ 2-3 times in children] “When percussion is lightly applied to the injured nerve tissue , we find the cutaneous region of the nerve, a creeping sensation usually compared by the patient to that caused by electricity”  Reserve only for traumatic neuropathy  Strongly positive Tinels over lesion after injury indicated severance or rupture  Centrifugally moving Tinels sign persistently stronger than at the suture line-repair that is going to be successful  Tinels at the suture line stronger than at the growing end- repair that is going to fail  Failure of distal progression of Tinels in a closed lesion – rupture or lesion impeding regeneration
  • 16. CLASSIFICATION OF NERVE INJURIES • Classification of nerve injuries is useful in understanding their pathological basis, making decisions on management, and predicting the prognosis for recovery. • Seddon described a classification of localized injuries to peripheral nerves after study of large numbers of casualties during the second world war, which is still widely used. • Neurapraxia- • Axonotmesis • Neurotmesis
  • 17.
  • 18. • LIMITATIONS OF SEDDON’S CLASSIFICATION- • Seddon’s classification doesn’t distinguish between all grades of intraneural damage. • Lesions classified as axonotmesis have been observed to have variable recovery. This is because variable degrees of damage to the connective tissue layers of the nerve, including the endoneurium and perineurium, as well as disruption of the axons are possible without loss of continuity of the nerve trunk. •
  • 20. Sixth degree [ Mac kinnon]: combination or several degrees with various pattern of injury and recovery. Nerve trunk is partially severed, and the remaining part of the trunk sustains fourth-degree, third-degree, second-degree, or rarely even first- degree injury
  • 21. ASSESSMENT OF NERVE INJURY • CLINICALLY- • SYMPTOMS FOLLOWING COMPLETE NERVE INJURY- • Loss of stereognosis • Loss of superficial pain, touch and temperature • Loss of deep sensation to muscle and joint movements, position, deep pressure and vibration • Loss of motor supply to muscle results in muscle atrophy and fibrous degeneration • Deep tendon reflexes are diminished or absent
  • 22. • Electrical stimulation of the nerve no longer causes the muscle to contract but muscle can be individually stimulated by Faradic current until two weeks after which even Faradism doesn’t elicit any response • But the muscle continues to respond to Galvanic current with slow contraction , greater in amplitude followed by slow relaxation • This phenomenon is known as ”REACTION OF DEGENERATION” and is characteristic feature of peripheral nerve injury • Trophic influence is lost
  • 23.
  • 24. • Neurophysiological studies form a relevant and well-established part in the diagnosis and work-up of nerve injuries • Does a nerve lesion exist? • Where precisely is the lesion located? • Are other nerves involved, which may explain patient’s signs and symptoms? • What type of lesion is it –axonal or a demyelinating? • Is there a generalized lesion of peripheral nerves, e.g. polyneuropathy? • Is the lesion acute, subacute or chronic? • What is the severity of the lesion? • Additional questions, which can only partially be answered, are: • What is the prognosis of untreated nerve injury or entrapment syndrome? • What treatment modality is necessary –surgery or conservative treatment? • Was the treatment effective?
  • 25. GENERAL PRINCIPLES OF NCS • Motor and sensory nerve conduction studies (NCS) are performed . • The type of study depends on the nerve studied (motor, sensory or mixed nerve) and on the site of recording • In NCS the nerve is electrically stimulated by a bipolar surface stimulator. • As a general rule, only myelinated nerve fibres can be investigated. • Skin temperature should be measured and the extremity be warmed if the temperature is <32°C. • Nerve conduction gets slightly slower at ages above 75 ys.
  • 26. • Motor nerve conduction studies (mNCS) • In mNCS compound motor action potentials (CMAP) are recorded from a muscle innervated by the nerve under investigation. Surface electrodes are used and the “active” (recording) electrode is placed over the muscle belly, the other (reference) electrode over the tendon at the insertion of the muscle (belly-tendon electrode placement).
  • 27. Figure 1: Median nerve motor nerve conduction study. Standard electrode placement over the abductor pollicis brevis muscle and stimulation of the median nerve at the wrist are displayed.
  • 28. • Sensory nerve conduction studies (sNCS) • Orthodromic or antidromic nerve conduction studies are performed to study sensory nerves. • In antidromic studies amplitudes are usually higher than in orthodromic studies, otherwise both methods are comparable. • In antidromic studies of e.g. the median or ulnar nerves, the sensory nerve action potential (SNAP) may be recorded using ring electrodes placed around a finger, and the nerves are stimulated at the wrist. • In orthodromic studies, surface electrodes are placed over the nerve at the wrist, and finger nerves are stimulated by ring electrodes
  • 29. Standard electrode placement for A) antidromic and B) orthodromic median nerve sensory nerve conduction studies. In A) stimulation is at the wrist, in B) at the index finger.
  • 30.
  • 31.
  • 32.
  • 33.
  • 34.
  • 35. • An NCV test shows the condition of the best surviving nerve fibers, so in some cases the results may be normal even if there is nerve damage
  • 36. GENERAL PRINCIPLES OF NEEDLE ELECTROMYOGRAPHY (EMG) • Electric potentials produced by muscle fibres can also be recorded using intramuscular needle electrodes • Pathologic EMG findings are only seen in axonal nerve lesions. • Typically, EMG is recorded when the muscle is at rest, during a weak contraction and during a strong contraction. • With the muscle at rest, spontaneous activity is assessed. • In a healthy muscle there is only a brief burst of EMG signal when the needle is moved within the muscle. This is called insertional activity.
  • 37. • Following an axonal injury, several forms of pathological spontaneous activity may be found. • Fibrillation potentials (fibs) and positive sharp waves (psw) are seen 14-21 days following an axonal nerve lesion. • They usually persist for 6-12 month, although some spontaneous activity may persist for many years. Complex repetitive discharges and myokymic discharges are sometimes seen in chronic lesions. • However, all types of spontaneous activity can occur in other disorders of nerve or muscle as well
  • 38. • In general the neurophysiology tests can distinguish between injuries where axons have not degenerated (neurapraxia) and those where axons have degenerated distally (axonotmesis and neurotmesis) • If axonotmesis has affected all the fibres in a nerve then the findings will be indistinguishable neurotmesis. • If there is a mixed lesion with some fibres intact detection of these will imply the nerve trunk has not been disrupted.
  • 39.
  • 40. MAGNETIC RESONANCE IMAGING (MRI) • Normal nerves can be visualised on MRI although their signal characteristics are not distinct from other tissues. • A technique called magnetic resonance neurography, which enhances neural tissue on images, was reported by Filler. • In the zone of injury signals are affected by oedema and haemorrhage in the surrounding tissues. • MRI has proved effective in imaging peripheral nerve tumours. • It is also useful in assessment of brachial plexus injuries where avulsion of nerve roots can be defined
  • 41. • In addition to imaging the nerves themselves, information may be obtained from MRI of muscle innervated by damaged nerves. • On T2 and STIR images changes may be seen in denervated muscle as early as two weeks after injury. • The exact relationship between severity of nerve injury and the early signal changes in muscles seen on MRI is not clear. • More prolonged denervation of muscle leads to wasting and fatty infiltration which can be seen on T1 waited MR images
  • 42. Sagittal T2 weighted magnetic resonance image of the shoulder showing increased signal in deltoid and teres minor as a result of axillary nerve injury
  • 43. ULTRASOUND • Modern ultrasound scanners have improved to the extent that resolution is now greater than MRI. • Ultrasound is being used increasingly to examine nerves damaged by closed trauma. • It may be able to confirm continuity of a nerve, or diagnose rupture or entrapment, for example, in a fracture. • Fascicular disruption within a nerve trunk may be visualised. • Use of ultrasound to examine the radial nerve injured in an association with fractures of the humerus been reported and for diagnosis of median nerve entrapment in the forearm. • However, ultrasound is operator dependent and requires experience for optimal interpretation
  • 44. PRINCIPLES OF MANAGEMENT OF NERVE INJURY • While the classifications of nerve injury provide a basis for prognosis and management, in reality it can be difficult to diagnose the grade of injury to a nerve in the early stages. • The situation may only become clear in retrospect. • Therefore a practical approach to management is recommended. • It is useful to divide injuries into those which are open and closed.
  • 45. OPEN NERVE INJURIES • When there is evidence of loss of function in a nerve associated with a wound, then in most circumstances exploration of the wound and the affected nerve should be carried out. • The only exception to this would be, if expert assessment indicates that the patient is unlikely to benefit from repair of the nerve or if the patient is unfit for operation. • Uncertainty can occur when a nerve is partly divided since some function will be preserved. • Therefore lacerations associated with any neurological deficit should be explored on the assumption that affected nerves are either partly or completely divided rather than assuming than there is some form of lesion in-continuity.
  • 46. • Usually nerve repair should be carried out early at the same time as other injured structures. • Therefore fracture fixation, tendon repairs and skin closure is carried out simultaneously, providing adequate vascularised skin and cover can be provided. • Full thickness vascularised skin cover is necessary over a nerve repair rather than split skin graft.
  • 47.
  • 48.
  • 49. CLOSED INJURIES- • When a nerve has been injured as a result of blunt trauma there is likely to be more uncertainly regarding the grade of injury. • In general an assessment should be made of the probability that a nerve has been disrupted or is under continuing compression. • If the injury has been caused by high energy trauma then the chance of disruption of the nerve is higher and early exploration should be considered. If operation is required in any case, for example, for fracture fixation, then the opportunity should not be missed to explore damaged nerves and confirm continuity. • Early exploration is best carried out within the first 2 weeks following injury. • If there has been lower energy trauma and a lesion in-continuity seems likely then expectant management may be pursued.
  • 50. • However, progress of nerve recovery should be monitored carefully looking for return of muscle function and an advancing Tinel’s sign. • If there is no improvement by 2 to 3 months from injury then surgical exploration should be considered. • Urgent neurophysiology assessment and imaging may help at this stage
  • 51. ACUTE NERVE COMPRESSION • Nerves may be compressed by displaced fragments of fractures, dislocation of joints, or expanding hematoma. • The onset of loss of nerve function may be delayed after the injury although this may be difficult to ascertain. • Typically there is severe pain associated with the nerve palsy. • This situation requires urgent management with reduction of fractures and dislocations. • If closed reduction does not relieve the situation then open reduction with exploration of the affected nerves should be performed. • If there is suspicion of arterial injury, for example, false aneurysm, then angiography should be arranged. • Haematoma with sufficient pressure to cause nerve compression is likely to have been caused by arterial haemorrhage. • Drainage of the haematoma and vessel repair is required as an emergency.
  • 52. A NERVE PALSY OCCURRING AFTER A MEDICAL OR SURGICAL PROCEDURE • This is an unfortunate and sometimes disastrous complication of treatment. • It is important to examine the function of nerves related to a surgical procedure and document the findings before and afterwards. • If a patient is found to have a new loss of nerve function after a procedure then a prompt, careful and objective assessment needs to be made. • Since the clinician who has performed the procedure may have an emotional attachment to the situation, it is often best to involve another clinician
  • 53. EXPLORING THE DAMAGED NERVE AT AN EARLY STAGE TAKING INTO ACCOUNT THE FOLLOWING FACTORS • The events during the procedure should be reviewed to check whether the nerve was identified and what the likely mechanism of injury is, including laceration or compression. • Whether the nerve palsy was present immediately after the procedure or developed after a delay. • If there is a possibility that the nerve is being subjected to continuing compression, by haematoma or an implant then urgent re-operation should be carried out • Urgent investigations, including ultrasound, MRI, and neurophysiology may be helpful • The risks and benefits of carrying out a second procedure, including the patient’s general condition, the risk of infection, and whether repair of the affected nerve is likely to lead to useful functional recovery.
  • 55.
  • 56. PREREQUISITES TO TENDON TRANSFER- • OPEN WOUNDS • A patient is not a candidate for a tendon transfer if he or she has open wounds that could predispose to a disastrous postoperative infection • SOFT TISSUE COVERAGE • Tendon transfers will glide only if transplanted through mobile, unscarred, healthy tissues. • Meeting this requirement usually entails subcutaneous rerouting of the tendon out of contact with scar and fixed structures.
  • 57. • MAXIMUM JOINT MOBILIZATION ESTABLISHED • One never gains more active range of motion from tendon transfers than the preoperative passive range of motion. • Therefore, it is important that good joint mobility precede tendon transfers. With disrupted motor nerves or muscle–tendon losses, the imbalance of forces acting across the joints occurs immediately (with the exception of total paralysis, in which there is no imbalance). • In contrast, joint stiffening and deformity develop as the result of the imbalance. Attention to joint stiffening and deformity with appropriate therapy and splinting can substantially prevent these complications.
  • 58. • SKELETAL STABILIZATION • RESTORED SENSIBILITY • When possible, restoration of at least protective sensibility should precede tendon transfers. • Skin sensibility is not absolutely required for tendon transfers to be useful, but it is always desirable
  • 59. • POWER AND CONTROL • To be a candidate for tendon transfer, a muscle must have adequate power for the new function, be nonspastic, and be under good volitional control. • It also needs to be an independently functioning muscle unit, such as a finger superficial flexor or the EIP, in contrast to the flexor digitorum communis (FDC), whose four tendons originate from a common muscle. • In general, only muscles having a power grade of 4 or 5 (on the 0 to 5 scale) are suitable candidates for transfer.
  • 60. • AMPLITUDE OF EXCURSION • The muscle to be transferred must have an adequate amplitude of excursion for its new function or be so situated that its effective amplitude can be enhanced by tenodesis as it crosses an actively controlled joint. Most often this joint will be the wrist • ANATOMICALLY FAESIBLE LOCATION OF THE MUSCLE • The surgical rerouting of a muscle and tendon should be in as direct a line of pull as possible between the muscle’s origin and its new insertion. Otherwise, as it begins to function, it will work into a straight line of pull and become too slack.
  • 61. • SYNERGISM • Muscles that simultaneously and automatically contract to work together are referred to as synergistic. An example is wrist extension with finger flexion, as has already been discussed. • Synergism was once considered important in selecting muscles for transfer, but it is much less important today • EXPENDABILITY • Obviously, if a muscle is to be transferred for a new duty, the surgeon must be certain that this will be of more benefit to the patient than the muscle is in its normal situation.
  • 62. • POTENTIAL PIP JOINT COMPLICATIONS • The surgeon should be constantly aware of the possibilities of creating secondary problems. • If the proximal interphalangeal (PIP) joint of the finger from which the flexor digitorum superficialis (FDS) is to be taken is hyperextensible from an incompetent or ruptured volar plate, taking its FDS tendon can cause a distressing recurvatum deformity. • If the hyperextensibility is slight, simply leaving one slip of the FDS long so it can adhere proximally in the tendon sheath is all that is necessary. However, with gross hyperextensibility of the PIP joint, suturing a long distally attached slip of the FDS to its proximal sheath is necessary for tenodesis control of the joint.
  • 63. • If any two of the three nerves are irreparably lost, a major functional impairment is inevitable, and reconstruction must entail a substantial simplification of the hand’s mechanical design if useful function is to be restored. • At the same time, wrist extension–flexion, as emphasized by White (1960), is of such fundamental importance that its arthrodesis should be done only as a last resort
  • 64. TENDON TRANSFERS IN RADIAL NERVE PALSY
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  • 74. • PROTECTIVE PHASE (SURGERY – 3-5 WEEKS) • OBJECTIVES- Edema control, protective splinting, mobilise uninvolved joints • MOBILISATION PHASE • Begun when tendon healing is adequate for mobilisation • OBJECTIVES- • Mobilise transferred tendons • Immobilise soft tissue • Continue mobilisation of uninvolved joints • Reinforce pre operative teaching and patient education • Begin home rehabilitation • Day time dynamic splinting and night time static splinting
  • 75. • INTERMEDIATE PHASE(5-8 WEEKS POST OP) • Gradually increase hand activities and passive ROM • Limited functional movements permitted • RESISTIVE PHASE (8-12 WEEKS POST OP) • Resistance exercises started • Therapeutic objective is increasing endurance and strength • Work related tasks are begun
  • 76.
  • 77. BIBLIOGRAPHY • TUREK’S TEXT BOOK OF ORTHOPAEDICS • BEASLEY’S TEXT BOOK OF HAND SURGERY • LIVING TEXT BOOK OF HAND SURGERY • TEXT BOOK OF PLASTIC SURGERY • CAMPBELL’S 12TH EDITION • JOHN HOPKIN’S NEUROLOGY AND NEUROSURGERY

Editor's Notes

  1. NEUROPRAXIA -caused by transient compression or stretch. Loss of nerve function results from conduction block. Paralysis of muscles innervated by the nerve is complete but some sensation may be preserved. Autonomic function may also be preserved. This type of injury will recover completely providing the cause, for example, ongoing compression, is removed.  Recovery does not follow a proximal to distal progression as occurs with axon regeneration. As long as there is no ongoing insult cases of neurapraxia can be managed without operation. Axonotmesis results from a more severe blunt injury to a nerve. This is sufficient to cause axon degeneration but the connective tissue layers of the nerve including the endoneurial tubes remain intact. Radial nerve injury associated with fracture of the humeral shaft is often an axonotmesis. Clinical examination reveals complete loss of motor, sensory, and autonomic function. Since axons distal to the site of injury have undergone Wallerian degeneration conduction is lost both at and distal to the site of injury. Providing the cause is removed, uncomplicated regeneration of axons occurs along the same pathway will occur, with recovery of function progressing from proximal to distal. Tinel’s sign can be elicited initially at the site of the injury and will advance distally over time. There is usually near normal recovery. Neurotmesis is the situation where a nerve is completely divided or so badly disorganized that recovery cannot occur. All the connective tissue layers of the nerve as well as the axons are disrupted. There is axon degeneration distal to the injury. Neurotmesis may be caused by laceration or high energy traction injuries sufficient to rupture the nerve. In addition injection of noxious drugs or ischaemia can destroy a nerve.  Recovery can only occur after appropriate surgical repair of the nerve and relies on axonal regeneration. Because  disruption and mixing of fibres at the site of the repair results in failure of correct distal connections,  recovery is never perfect. In general the outcome is worse after repair of a nerve ruptured by severe traction rather than direct repair of a clean laceration. It should be emphasized that the findings on clinical examination and neurophysiology assessment may be   the same for axonotmesis and neurotmesis, yet there is a clear difference in prognosis and management.
  2. Normally muscle contracts strongly to faradic current and twitches to galvanic current