Overview of the Nervous System & Nerve Injury

Central Nervous System (CNS)

• Components: Brain & spinal cord
• Protection: Protected by bones and blood-brain barrier

Peripheral Nervous System (PNS)

• Components: Nerves & ganglia outside CNS
• Characteristics:
  • Not protected by bones and blood-brain-barrier
  • Exposed to toxins and mechanical injuries
  • Capacity to regenerate - re-grow if cut (unlike CNS)

Nerve Structure

Connective Tissue Layers

• Epineurium: Outermost connective tissue layer
• Perineurium: Middle connective tissue layer surrounding fascicles
• Endoneurium: Innermost connective tissue layer surrounding individual nerve fibers

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Nerve Fiber Components

• Motor axons: Transmit motor signals
• Sensory axons: Transmit sensory signals
• Myelin coating:
  • Lipoprotein layer produced by Schwann cells
  • Facilitates rapid nerve conduction

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Classification of Nerve Injuries

Types of Injury

• Neuropathies: Degenerative nerve disorders
• Ischemia: Reduced blood supply to nerve tissue
• Mechanical Injury:
  • Compression: Prolonged pressure on nerve
  • Traction: Stretching or pulling forces
  • Laceration/Cut: Sharp or penetrating injuries
  • Burn: Thermal or chemical damage

Extent of Damage

• Transient Injury:
  • Recoverable loss of function
  • Usually temporary conduction block
• Complete Injury:
  • Irreversible structural damage
  • Complete or permanent loss of function

Pathophysiology of Nerve Injury

Degeneration Process

When a peripheral nerve is cut:

• Distal axon segments undergo Wallerian degeneration (cell death)
  • Wallerian degeneration: Progressive destruction of distal axon segments
  • Retrograde degeneration extends to the first Node of Ranvier
• Proximal axon segments undergo regeneration (attempt regrowth)
  • Regeneration rate: Approximately 1mm/day

Regeneration Challenges

If muscles remain paralyzed for extended periods:

• Muscle atrophy and degeneration of motor end plates
• Joint stiffness and contracture development
• Clinical implication: Need to maintain muscle readiness and joint flexibility through physical therapy

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Complications of Regeneration

1. Misdirected axonal growth in mixed nerves
   • Motor-to-sensory and sensory-to-motor inappropriate connections
2. Axonal loss during regeneration process
   • Some axons fail to reach target destinations
3. Time-dependent challenges:
   • Motor end plate degeneration in denervated muscles
   • Joint stiffness from prolonged immobilization

Seddon Classification of Mechanical Nerve Injuries

Overview

Type	Severity	Structural Damage	Recovery Potential
Neuropraxia	Mild	Conduction block without structural damage	Excellent (days-weeks)
Axonotmesis	Moderate	Axonal damage with intact connective tissue	Good (weeks-months)
Neurotmesis	Severe	Complete transection of nerve	Poor (requires surgery)
Z

Neuropraxia (First Degree)

Pathophysiology:

• Result of blunt trauma or overstretching without structural damage
• Transient localized physiological conduction block
• No anatomical disruption of nerve fibers
• No distal Wallerian degeneration occurs

Clinical Features:

• Presents primarily as motor paralysis
• Some residual sensory or autonomic function typically preserved
• Nerve conduction studies: Show conduction block at injury level

Prognosis and Management:

• Complete recovery typically occurs within days to weeks
• Usually diagnosed by exclusion of more severe injuries
• Conservative management with observation

Axonotmesis (Second Degree)

Pathophysiology:

• Result of more severe blunt injury, traction, or overstretch
• Axonal damage within intact connective tissue framework
• Endoneural tubes remain intact and provide pathway for regeneration
• Distal Wallerian degeneration occurs distal to injury

Clinical Features:

• Significant motor and sensory deficits
• More complete functional loss than neuropraxia

Prognosis and Management:

• Expected spontaneous recovery
• Recovery may take weeks to months
• May leave residual deficits due to imperfect regeneration
• Physical therapy to maintain joint mobility and muscle readiness

Neurotmesis (Third Degree)

Pathophysiology:

• Complete transection of nerve:
  • All nerve components severed (axons, myelin, endoneurium, perineurium, epineurium)
• Neuroma formation at injury site
  • Disorganized mass of regenerating axons, Schwann cells, and fibroblasts

Clinical Features:

• Complete loss of motor and sensory function
• Permanent functional deficit without intervention

Prognosis and Management:

• Function never returns to normal without surgical intervention
• Surgical repair required:
  • Epineural repair: Suturing of outer nerve sheath
  • Endoneural repair: Microscopic repair of individual fascicles
  • Cable grafting: Using donor nerve (commonly sural nerve) for gaps
  • Tube scaffolds: Synthetic conduits for nerve regeneration

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Clinical Assessment of Nerve Injuries

Comprehensive Evaluation

Medical History

• Thorough history collection:
  • Symptoms indicating nerve dysfunction
  • Mechanism and timing of injury
  • Progression of symptoms
  • Associated medical conditions

Physical Examination

• Systematic neurological examination:
  • Motor function assessment (strength testing)
  • Sensory examination (light touch, pinprick, temperature)
  • Reflex testing
  • Special tests for specific nerve injuries

Diagnostic Investigations

• Electrodiagnostic studies:
  • Nerve conduction studies:
    • Localizes injury site
    • Determines severity of injury
    • Assesses recovery progress
  • Electromyography (EMG): Evaluates muscle denervation and reinnervation
• Imaging studies: MRI or ultrasound when indicated