NERVE INJURY, REPAIR, AND

HEALING
PRESENTER: TEAM I (FH/ET/PI)
SUPERVISOR: DR. JAINAL ARIFIN, M.KES, SP.OT(K)SPINE
REFERENCES

• Orthopedic Basic Science : Biology and Biomechanics of the Musculoskeletal

System 2nd edition - AAOS
• Campbell’s Operative Orthopaedics 12th edition – Canale, S.T.., et al
TRAUMATIC NERVE INJURY
• Those causing a temporary block of nerve conduction at the site of
injury without loss of axon continuity
• Those in which axons are damaged and cause axonal degeneration
• Disintegration of axon and myelin sheath distal to and proximal from the injury
site (Wallerian degeneration) with the end result of denervation
• The cell body may respond by regeneration or degeneration (cell death)
CLASSIFICATION OF NERVE INJURIES

• Prior to World War II

• Contusion, concussion, stretch, compression, laceration, division

• 1943
• 3 divisions (neurapraxia, axonotmesis, neurotmesis)

• 1951
• 5 degree injury
• Based on histopathological findings
• May be caused by mechanical, thermal, chemical, and ischemic
FIRST-DEGREE INJURY

• Corresponds to neurapraxia and characterized by interruption of conduction at the site

of injury
• Principal cause include mild compression and ischemia which alters the ionic
composition, nutrient supply, energy metabolism, and/or axonal transport
• Motor fibers more susceptible to injury than sensory fibers (failure occurs sequentially :
motor, proprioceptor, touch, temperature, and pain. Recovery occurs in a reverse order)
• Full restoration of function may take as long as 3 to 4 months after the injury
SECOND-DEGREE INJURY

• Corresponds to axonotmesis and involve severe damage or

severance of the axon, leading to wallerian degeneration.
• Axon generally regenerates within its original endoneurial tube
• Causes complete loss of motor and sensory functions
• Fibrillation and denervations are evident in muscles
THIRD-DEGREE INJURY

• Degeneration of the axons and loss of endoneurial tube continuity

• Complete loss of motor and sensory functions
• Healing takes longer than second-degree injury due to more severe
retrogrades disturbances to the cell body
• Axons may be misdirected and reinnervate inappropriate targets
• Poor functional recovery occurs when reinnervation occur in functionally
different axon and target
FOURTH-DEGREE INJURY

• Continuity of nerve trunk is preserved but the fascicles are ruptured or so

disorganized that they can no longer be demarcated from the epineurium
• Retrograde neuronal effects are more severe than in third-degree injuries
with higher incidence of neuronal cell-body degeneration and axon loss
• Complete loss of motor and sensory functions in the region served by the
nerve
• Requires excision of the damaged segment and surgical repair of the nerve
FIFTH-DEGREE INJURY

• Complete loss of continuity of the nerve trunk

• Nerve ends remain separated, and varying amounts of scar tissue form
between the cut ends
• Chances of restoring function are minimal because of the few numbers
of axons that regenerates across the lesion
CAUSES OF NERVE INJURIES

• COMPRESSION NERVE INJURY (open VS closed)

• A force applied to the nerve that results in an alteration in the cross-sectional dimensions of
the nerve

• STRETCH INJURY (open VS closed)

• A deforming force applied along the long axis of the nerve, resultin in increases in its length

• FRICTION (closed)
• Occurs when a nerve rubs across a rough surface or structure

• ISCHEMIA
COMPRESSION INJURIES
COMPRESSION INJURIES
• DOUBLE CRUSH SYMDROME ?
• Clinical Implications in daily orthopedic practice
• “In a study of 48 arthrotomy patients where the cuff pressure was between 350 and
450 mmHg, more than 50% had EMG changes postsurgery. In those surgeries that
exceeded 1 hour, 85% of the patients has abnormal EMGs postsurgery.”
• “To minimize the effects of tourniquet ischemia on muscle and nerve, it is recommended that
the pressure in the cuff used for upper extremity surgery be no more than 50 to 100 mmHg
above the systolic pressure. For lower extremity surgery, twice the systolic pressure is

recommended. Tourniquets should not be applied for more than 2 hours to minimize
neural and muscular injury.”
STRETCH INJURIES
• Although the epineurium assists
In maintaining the undulations
in the nerve trunk, the
component primarily
responsible for the tensile
strength and elasticity of the
nerve is the perineurium
NEURAL DEGENERATION
• Healing of nerve injuries consists of a process of cellular repair as opposed to tissue
repair
• The initial response to nerve injury is axonal degeneration followed by
regeneration
• Zone of Injury
• When a nerve trunk is severed, the 2 ends retract
• Within the first 24 hours, capillary permeability (serotonin and histamine) increased and
reaches a peak between days 7 and 14
• A swelling is composed of : disorganized edematous matrix of Schwann cells, fibroblasts,
capillaries, macrophages, and collagen fibers develops at the end of each nerve stump
• The growing tips of the proximal axons will enter this swelling and must navigate through this
matrix
• During surgical repair of an injury, this traumatized zone of injury is resected and the stumps
are reapposed with sutures or a nerve graft
NERVE RESPONSE
• Wallerian Degeneration : The series of metabolic and structural
events occurring in the segment distal to the lesion involves the axon,
myelin sheaths, Schwann cells, and endoneurial collagen.
• 1. Axonal degeneration
• Initiated within hours of injury
• Neural conductance within the distal segment is completely lost within 48 to 96
hours after the injury
• All traces of the axon debris are usually lost within 2 weeks of the injury
• Myelin debris is removed by macrophages and Schwann cells within 1 week-3
month period
NERVE RESPONSE

• 2. Schwann cell response

• Within 24 hours, Schwann cells throughout the distal segment udergo a series of mitoses and peaks ad day 3
• The newly divided Schwann cells maintain cytoplasmic processes that interdigitate and line up in rows beneath
the original basal lamina
• These tubes are referred to as the bands of Bunger.
• Also produces fibronectin and laminin which promote growth of neuritis in culture
• The cells also produce nerve growth factor and nerve growth factor receptors

• 3. Macrophage response
• After nerve injury (day 1-3), macrophage accumulate around the degenerating fibers
• Macrophage-derived interleukin-1 is required to stimulate Schwann cells to prduce nerve growth factor
NERVE RESPONSE

• 4. Nerve cell body response

• Alteration of metabolic priority
• From neurotransmitter to production of proteins needed for axonal repair and growth (also cytoskeletal
proteins such as tubulin and actin)
• Increase of growth-associated proteins (GAPs) which promote axonal growth and extension
• 5. Proximal segment response
• The fate of axons depends on whether the cell body survives and regenerates a new axon or
degenerates
• If the cell body degenerates, the entire proximal length of the axon undergoes wallerian degeneration.
If the cell body survives, the proximal nerve fibers undergo a reduction in axon diameter and myelin
thickness that proceeds distally from the cell body
FUNCTIONAL RECOVERY AFTER NERVE INJURY

• Age of the patient

• Type of nerve injured
• Distance the regenerating axons must grow to reach the target orgam
• Length of the injury zone
• Timing of the nerve repair
• For every delay of 6 days between injury and repair there is a variable loss of potential recovery that
averages about 1% of maximal performance

• Status of the target organ at the time it is reinnervated

• Technical expertise of the surgeon
MUSCLE RECOVERY AFTER DENERVATION

Obstacles :
• A loss of muscle fibers
• A loss of motor units
• The motor axons that reinnervate the muscle may have the capacity to sprout and
maintain synaptic connections with more fibers than they would in a normal muscle

• A loss in the ability to increase muscle fiber size and reverse the atrophy that
occurs after denervation
NERVE REPAIR INDICATIONS

• When a sharp injury has obviously divided a nerve, early exploration is indicated for diagnostic, therapeutic, and prognostic
purposes.
• When abrading, avulsing, or blasting wounds have rendered the condition of the nerve unknown, exploration is required for
identification of the nerve injury and for marking the ends of the nerve with sutures for later repair.
• When a nerve deficit follows blunt or closed trauma, and no clinical or electrical evidence of regeneration has occurred after
an appropriate time, exploration of the nerve is indicated.
• In situations in which a nerve has been intact before closed reduction and casting of a fracture, but a significant deficit is found immediately
after, we explore the nerve as soon as feasible.

• When a nerve deficit follows a penetrating wound, such as that caused by a low-velocity gunshot, the part is observed for
evidence of nerve regeneration for an appropriate time. If there is no evidence of regeneration, exploration is indicated.
NERVE REPAIR (METHODS)

• Primary repair (6-8 hours) VS Delayed primary repair (7-18 days)

• ENDONEUROLYSIS (Internal Neurolysis)
• PARTIAL NEURORRHAPHY
• NEURORRHAPHY & NERVE GRAFTING
EPINEURAL NEURORRHAPHY
PERINEURAL NEURORRHAPHY
INTERFASCICULAR NERVE GRAFTING
THANK YOU