Courtesy: Dr Rishi Dhir, Consultant Orthopaedic Surgeon, UK

Introduction

This video lecture provides a comprehensive overview of peripheral nerve injuries, with emphasis on:

• Basic nerve anatomy

• Mechanisms and causes of nerve injury

• Clinically relevant classification systems

• Nerve conduction studies and EMG

• Practical exam scenarios and real-world clinical decision-making

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1. Overview of Nerve Anatomy

Components of the Nervous System

• Central Nervous System (CNS)

  • Brain, brainstem, and spinal cord

• Peripheral Nervous System (PNS)

  • Transmits sensory and motor signals between the body and CNS

• Autonomic Nervous System (ANS)

  • Controls involuntary functions

  • Includes sympathetic and parasympathetic systems

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Structure of a Neuron

Each neuron consists of:

• Axon – conducts electrical impulses

• Myelin sheath – fatty insulating layer produced by Schwann cells, increases conduction velocity

• Cell body – contains nucleus and controls neuronal function

• Dendrites – receive incoming signals

• Synaptic terminal – transmits signals to muscles or other neurons

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Supporting Structures of Peripheral Nerves

• Glial cells – provide support and nutrition

• Connective tissue layers:

  • Endoneurium – surrounds individual axons

  • Perineurium – surrounds fascicles; forms the blood–nerve barrier

  • Epineurium – surrounds entire nerve, providing mechanical protection

The perineurium is critical for maintaining the blood–nerve barrier and regulating nutrient exchange.

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2. Causes of Nerve Injury

A useful mnemonic to recall common causes is “DATING ME”:

• D – Diabetes (diabetic neuropathy)

• A – Autoimmune (e.g., Guillain–Barré syndrome)

• T – Trauma (fractures, lacerations)

• I – Inflammatory (vasculitis)

• N – Neoplasms (tumor compression)

• G – General systemic disorders (malnutrition, metabolic disease)

• M – Motor neuron diseases (e.g., ALS)

• E – Electrical or thermal injuries (burns, electrocution)

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3. Classification of Nerve Injuries

Seddon Classification (1943)

• Neuropraxia

  • Temporary conduction block

  • No structural damage

  • Common in compression injuries (e.g., carpal tunnel syndrome)

• Axonotmesis

  • Axonal disruption with intact connective tissue

  • Good potential for recovery

• Neurotmesis

  • Complete disruption of nerve and sheath

  • Requires surgical repair

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Sunderland Classification (1951)

• Grade 1 – Neuropraxia

• Grade 2 – Axon damage, intact endoneurium

• Grade 3 – Axon damage with disrupted endoneurium

• Grade 4 – Axon damage with disrupted perineurium

• Grade 5 – Complete nerve transection (neurotmesis)

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Birch & Bonney Classification (Clinically Oriented)

• Conduction block – equivalent to neuropraxia

• Degenerative lesion – includes axonotmesis and neurotmesis

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4. Mechanisms of Nerve Injury & Healing

Mechanisms

• Compression injuries – reversible conduction block

• Stretch injuries – damage to connective tissue layers with scarring

• Lacerations – severe injuries requiring surgical repair

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Wallerian Degeneration

• Occurs in axonotmesis and neurotmesis

• Distal axonal segment degenerates due to loss of nutrient supply

• Cleared by macrophages, leaving Schwann cells behind

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Nerve Regeneration

• Schwann cells align to form Bands of Büngner

• Release neurotrophic factors guiding axonal growth

• Axonal growth rate ? 1 mm/day

• Cell body response includes:

  • Nuclear displacement

  • Increased mitochondrial activity

  • Phenotypic shift toward regeneration

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5. Conduction Block & Blood–Nerve Barrier

• The blood–nerve barrier lies between perineurium and endoneurium

• Compression leads to:

  • Microvascular compromise

  • Edema and inflammatory cell infiltration

  • Protein leakage ? vicious cycle of swelling

• Prolonged compression may progress to Wallerian degeneration

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6. Clinical Examination & Diagnostic Tools

Clinical Assessment

• Detailed history (motor vs sensory symptoms)

• Focused physical examination

Special Tests

• Tinel’s sign

• Phalen’s test (for carpal tunnel syndrome)

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Nerve Conduction Studies (NCS)

• Measure:

  • Latency

  • Amplitude

  • Conduction velocity

• Not reliable in isolation

• Must be compared with the contralateral side

• Not performed in the first 6 weeks after injury

Key Findings

• Prolonged latency

• Reduced amplitude

• Slowed conduction velocity

Examples

• Carpal tunnel syndrome ? slowed conduction at wrist

• Cubital tunnel syndrome ? slowed conduction at elbow

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Electromyography (EMG)

• Resting EMG should be electrically silent

• Denervation shows:

  • Fibrillation potentials

  • Positive sharp waves

• Reinnervation shows:

  • Polyphasic motor units

  • Increasing amplitude with recovery

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7. Tinel’s Sign & Its Variants

• Advancing Tinel’s sign

  • Indicates active nerve regeneration

• Pseudo-Tinel’s sign

  • Seen in chronic compressive neuropathies

  • Due to myelin damage, not regeneration

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8. Treatment Principles

Based on Severity

• Neuropraxia

  • Observation and physiotherapy

• Axonotmesis

  • Monitoring; surgery if no recovery

• Neurotmesis

  • Surgical repair mandatory

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9. Surgical Management: Ladder of Reconstruction

• Neurolysis

• Direct nerve repair (low tension)

• Nerve grafting (auto/allograft)

• Nerve transfer

• Tendon transfer

• Free muscle transfer

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Tendon Transfers

• Used when nerve recovery is not possible

• Key principles:

  • Adequate tendon excursion

  • Synergistic muscle action

  • Patient motivation and rehabilitation compliance

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10. Timing of Surgical Exploration

• Consider surgery if:

  • No clinical or electrophysiological recovery by 6 weeks to 3 months

  • Persistent pain, compression, or expanding hematoma

  • No advancing Tinel’s sign or EMG evidence of reinnervation

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11. Clinical Applications

Carpal Tunnel Syndrome (CTS)

• Risk factors: pregnancy, hypothyroidism, manual labor

• Examination:

  • Tinel’s sign

  • Phalen’s test

  • Durkan’s test

• Important to rule out proximal pathology (cervical spine)

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Radial Nerve Injury

• Common after trauma (e.g., motorbike accidents)

• Features:

  • Wrist drop

  • Dorsal hand sensory loss

• Management prioritizes fracture stabilization

• Many injuries recover spontaneously

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Ulnar Nerve Injury

• Features:

  • Clawing of fingers

  • Intrinsic muscle wasting

  • Reduced grip strength

• Requires thorough hand and neurological assessment

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12. Summary: Practical Clinical Approach

• Use triple assessment:

  • Clinical

  • Radiological

  • Neurophysiological

• NCS and EMG support—but do not replace—clinical judgment

• Management decisions depend on:

  • Severity of injury

  • Presence of fractures or compression

  • Evidence of recovery