Peripheral nerve injuries

DIPLOMA IN PHYSIOTHERAPY
NEUROLOGY SYSTEM–II (PDPT 4623)
 Learning objectives
Students shall learn and understand
about:
– The structure & functions of nerve
– The causes of nerve lesion
– The clinical features & typical deformity of
peripheral nerve lesion
– The types and classification of nerve lesion
– The physiotherapy treatments for nerve
lesion
 LEARNING OUTCOMES
• At the end of the session, students will be able
to:
– Identify the structure & functions of nerve
– Describe on the causes of nerve lesions, clinical
features & typical deformities, doctors and
physiotherapy management of peripheral nerve
lesion
– Demonstrate on physiotherapy management for
peripheral nerve lesions
 Anatomy review
• A peripheral nerve consists of a bundle or bundles of axons
whose cell bodies are in the spinal cord or ganglia just outside
the spinal cord
• Motor nerve fibers originate in the anterior column of the spinal
cord
• Sensory nerve fibers originate in the dorsal root ganglia
• Sympathetic fibers are axons of cell bodies in the sympathetic
ganglia of the autonomic nervous system.
 Structure of a nerve
• It has an outer covering
which forms a sheath
around the nerve, called
the epineurium.
• Nerve fibers, which are
axons, organize into
bundles known as fascicles
with each fascicle
surrounded by the
perineurium.
• Between individual nerve
fibers is an inner layer of
endoneurium.
 NERVE STRUCTURE AND
FUNCTION
• In the peripheral nerves, all motor axons and the large
sensory axons serving touch, pain and proprioception
are coated with myelin
• Every few millimeters the myelin sheath is
interrupted, leaving short segments of bare axon
called the nodes of Ranvier.
• Nerve impulses leap from node to node at the speed
of electricity, much faster than would be the case if
these axons were not insulated by the myelin sheaths.
• Consequently, depletion of the myelin sheath causes
slowing - and eventually complete blocking - of axonal
conduction.
• Most axons -in particular the small-diameter fibres
carrying crude sensation and the efferent sympathetic
fibres -are unmyelinated but wrapped in Schwann cell
cytoplasm.
• Damage to these axons causes unpleasant bizarre
sensations and various sudomotor and vasomotor
effects.
 Causes of injury to peripheral nerves
• Trauma (crush injury, traction, gunshot wounds, laceration,
electrical burn)
• Compression (entrapment)
• Irritation
• Metabolic disorders
• Burn
• Inflammatory (neuritis)
• Virus
• Age related changes

 Damage varies in severity from transient and quickly

recoverable loss of function to complete interruption and
degeneration.
 There may be a mixture of types of damage in the various
fascicles of a single nerve trunk.
CLASSIFICATION OF NERVE
INJURIES
 Seddon's classification

Neurapraxia
• temporary paralysis of a nerve caused by lack of
blood flow or by pressure on the affected nerve with
no loss of structural continuity.
Axonotmesis
• neural tube intact, but axons are disrupted.
• nerves are likely to recover.
Neurotmesis
• the neural tube is severed.
• Injuries are likely permanent without repair.
Seddon’s classification
 Sunderland`s classification
• Grade I
– Same as Seddon's neuropraxia.
• Grade II
– Same as Seddon's axonotmesis.
• Grade III
– Neurotmesis with preservation of the perineurium.
• Grade IV
– Neurotmesis with preservation of the epineurium. Everything
else is disrupted.
– Nerve grossly appear edematous.
– Nerve grafting is required.
• Grade V
– Complete transection of the nerve trunk.
• The peripheral nerve damage may also be classified
depending upon the number of nerves involved and site of
the lesion on the nerve.
• Mono-neuropathy or neuritis is the lesion involving a single
nerve
• Multiple mono-neuropathy or mono-neuritis multiplex is
the lesion involving two or more nerves
• Poly-neuropathy or neuritis is the lesion involving many
nerves throughout the body.
• Radiculopathy is the lesion involving a nerve root, at the
point of its origin from the spinal cord.
• Neuronopathy is the lesion involving the nerve cell, usually
the motor neuron or anterior horn cell in the spinal cord.
• Bulbar palsy refers to the motor weakness or paralysis of
muscles of tongue, larynx and pharynx due to involvement of
cranial nerve nuclei located in the brainstem.
 PHASES
Nerve response to injury in two phases:
1. Wallerian degeneration
2. Neural regeneration
 PHASE 1 :
WALLERIAN DEGENERATION
• It is a process that results when a nerve fibre is cut or
crushed, in which the part of the axon separated
from the neuron's cell body degenerates distal to the
injury
• Distal axon degeneration, following section or severe
injury, with degeneration of the myelin.
• Degeneration occurs distal to the level of injury,
including motor & sensory end receptors
• Distally remains empty Schwann sheaths &
endoneurial tubes: Shrinkage & collapse.
• This is also known as anterograde or
orthograde degeneration
• The process occurs within 7-10 days of injury
and this portion of the nerve is inexcitable
electrically.
 Axon degeneration
• Distal degenerated nerve is inexcitable
electrically.
• Regeneration can occur since the basement
membrane of the Schwann cell survives and
act as a skeleton along which tha axon
regrows up to a rate of about 1mm per day.
 Demyelination
• Segmental destruction of the myelin sheath
occurs without axonal damage
• The primary lesion affects the Schwann cell
and causes marked slowing of conduction or
conduction block
• Associated with minor neuropraxia injury of
axons
• Local demyelination is caused by
inflammation, eg: Guillain-Barre syndrome.
 Dying back neuropathy

Some times wallerian degeneration begins in the most

peripheral tissue and progress centrally from that point –
common in trigeminal system caused by metabolic intoxication
like metal poisoning, isoniazid and penicillin therapy
 PHASE 2:
NEURAL REGENERATION
• Neuronal regeneration with sprouting of the axon.
• For nerve regeneration to be successful:
– The axon must cross the injury site
– Enter the same endoneurial tube
• The rate of regeneration is 1 – 3 mm/day after an
initial latency of 3 to 4 weeks with additional delays
at the injury site & at the end organ
• Nerve regeneration is complicated by many factors
which may include:
– Shrinkage of the endoneurial tube (preventing
reentry of the sprouting axons)
– Scaring at the site of injury (short-circuiting the
progress of the sprouting axon)
• Mismatching of the motor, sensory, & sympathetic
fibers.
• Degeneration of motor & sensory end receptors.
• In most favorable conditions: severance of a
peripheral nerve injury usually results in some
degree of residual deficit.
 Neurotrophic effect
• If the tissue deinnervated for a long period of time , certain
clinical changes may take place, which are called as
neurotophic effect.
• Skeletal muscles – early spontaneous muscle spasm, flaccid
paralysis,with progressive atrophy and lack of muscle
definition and tone.
• Skin & mucosa –cold, dry and inelastic, susceptibility to injury,
poor healing, irregular keratinization, scaly , cracked skin.
 FACTORS AFFECTING
PROGNOSIS FOR RECOVERY

• Type of lesion • Size of gap

• Level of lesion • Delay in suture
• Type of nerve • Associated lesion
– Mixed versus unmixed • Surgical skill
nerves
– Motor versus sensory
recovery
• Age
 CLINICAL FEATURES
• pain in the affected area
• burning sensations or tingling muscle, numbness
• Loss of sensation
• Loss of motion
• Loss of power
• Loss of reflexes
• Wasting
• Trophic changes
• Contractures
 Typical deformities :
• Wrist drop ---- radial nerve injury

• Claw hand ---- ulnar nerve injury

• Foot drop ---- lateral popliteal nerve injury

• Ape thumb ---- median nerve injury

• Winging of scapula ---- thoracodorsal nerve injury

• Pointing index ---- median nerve injury

 INVESTIGATION
IMAGING
•Radiography - is primarily useful for
identifying other diagnoses, such as fracture
or cervical spondyloarthropathy.
•MRI (magnetic resonance imaging) - rarely
needed for initial evaluation of a typical
nerve injury, it may be helpful for specific
nerves.
•Ultrasonography - is a less expensive
modality to define anatomic entrapment,
but its use is limited by lack of
standardization of technique and
interpretation
ELECTRODIAGNOSTIC
TESTING
•Electromyography (EMG)
- records the electrical
activity of a muscle from a
needle placed into the
muscle, looking for signs of
denervation
• Nerve conduction studies
– differentiate axonal degeneration (reduced amplitude)
from demyelination (reduced conduction velocity)
– Characterize whether sensory motor fibres; localize
the sites of abnormality.
• Nerve biopsy: sural nerve is the one most commonly
biopsied provided that its conduction is abnormal.
• Cerebrospinal fluid (CSF) examination:
– Guillain-Barre syndrome or chronic inflammatory demyelinating
polyradiculoneuropathy: protein content is usually raised.
 TREATMENT
• Nonsurgical treatment for nerve injuries may
include:
– Acupuncture
– Massage therapy
– Medication : Steroid, methylcobalamine
– Orthotics
– Physical therapy and rehabilitation
– Weight loss management
• Surgical treatment
– may be needed if the individual has persistent
neurologic symptoms or if conservative therapies
have been unsuccessful.
 SURGERY
Primary Repair
• A divided nerve is best
repaired as soon as this can be
done safely.
• Primary suture at the time of
wound toilet has considerable
advantages: the nerve ends
have not retracted much; their
relative rotation is usually
undisturbed; and there is no
fibrosis.
 Nerve Grafting
• Used to bridge gaps.
Delayed Repair • Sural nerve most commonly
• Late repair -i.e. weeks or used (single\cable)
months after the injury - • Vascularised grafts also used
maybe indicated because
– a closed injury was left
alone but shows no sign Nerve Transfer
of recovery at the • Indicated for root avulsions of
expected time brachial plexus.
– the diagnosis was • Spinal accessory to
missed and the patient suprascapular nerve
presents late or • Intercostal nerves to
– primary repair has musculocutaneous nerve
failed.
Tendon Transfer
• Motor end plate must have
degenerated
(i.e. 18 – 24 months after
injury)
• Assess
– Muscles – lost
– Muscles – available
• Donor Muscle
– Expendable
– Adequate power
– Synergistic
• Transferred tendon
– Routed subcutaneously
– Straight pull
 Physiotherapy management?

• Ulnar nerve injuries

• Radial nerve injuries
• Sciatic nerve injuries
• Brachial plexus injuries
• Erb’s palsy
PHYSIOTHERAPY MANAGEMENT
 Assessment of peripheral nerve
injury
• Observation: attitude of the limbs,
wasting, trophic changes in skin, • Tone
edema
• Examination
• Functional
activities
– Range of motion
– Muscle girth
• Neural tension
– Hand functions: reaching,
test
grasping • Special tests
– Sensation
– Reflexes
 Physiotherapy treatment
• Bracing or splinting • Manual Therapy such as
• Ice or heat treatment soft tissue massage and
• Flexibility exercises • Sensory re-education
• Progressive exercises to • Activity modification
improve mobility and
strength
• Neural mobilization
• Nerve and muscle
stimulation
 Acute stage: stage of total paralysis
• To maintain the properties of the muscles
– Stimulating paralyzed muscle using interrupted
galvanic current (denervated muscle)
• To maintain joint range of motion
– positioning
– Passive range of motion
– Gentle sustain stretching
• To prevent any abnormal attitude of affected part
(splinting to prevent overstretching of the affected
muscle)
• To maintain the skin integrity (kept supple
using moisturizer or oil)
• Prevention of edema which is possible for
paralysis as brachial plexus & sciatic nerve
injury due to gravity dependent position &lack
of muscular tone
– elastocrepe bandage & elevation
 Recovery stage
Innervation has started & muscle begins to
show active contraction
•Muscle reeducation
•Faradic re-education &biofeedback
•Strengthening
•Functional retraining as gripping,walking or
stairs climbing
 Post-surgical physiotherapy
management
• Maintaining passive and active range of motion
• Pain management
• Motor and Sensory reeducation with reinnervation
or nerve transfers
• Wound, edema and scar management assistance
• Prevent/treat pain syndromes related to
musculoskeletal
• Provide devices to protect surgical repairs and
tendon transfers and to maximize function
 References
• Porter, S.B. (2008). Tidy’s physiotherapy. Amsterdam:
Elsevier Health Science
• Stokes, M. & Stack, E. (2013). Physical Management for
Neurological Conditions (3rd. Ed.). London: Elsevier
Health Sciences
• Martin, S. & Kessler, M. (2007). Neurologic
interventions for physical therapy (2nd. Ed.).
Philadelphia: Saunders.
• O’Sullivan, S.B. & Schmitz. T.J. (2008). Physical
Rehabilitation ( 5th ed.). Philadelphia: F.A. Davis.
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