Neuropraxia (Neurapraxia)

Definition

"The nerve conducts normally distal to but not across the lesion, resulting in conduction block, which is the electrophysiological correlate of neuropraxia." — Bradley and Daroff's Neurology in Clinical Practice

Pathophysiology

• Temporary mechanical distortion of myelin → segmental demyelination
• No Wallerian degeneration (axons and endoneurial tubes are intact)
• Results in a local conduction block at the injury site
• Nerve conduction is normal distal to the lesion but blocked across it
• Motor function is typically lost, but some sensation and autonomic function may be preserved (larger myelinated fibres are more susceptible than small unmyelinated fibres)

• Compression (e.g., "Saturday night palsy" — radial nerve compression causing wrist drop)
• Displaced fracture or dislocation (stretch/pressure on adjacent nerve)
• Tourniquet palsy
• Iatrogenic: needle trauma, injection pressure (e.g., mental nerve block)

Classification Context: Seddon & Sunderland

Clinical Features

• Complete motor paralysis of muscles innervated by the affected nerve
• Preserved or partially preserved sensation and autonomic function (compared to axonotmesis)
• No signs of Wallerian degeneration on nerve conduction studies
• Tinel's sign is absent (no axonal degeneration)

Electrodiagnostic Findings (EMG/NCS)

• Nerve conduction: Normal distal to the lesion; conduction block across the lesion
• EMG: No fibrillation potentials or positive sharp waves (no denervation, since axons are intact)
• Distal motor latency and conduction velocity: Normal distal to injury for 72–96 hours after injury (axons remain electrically viable distally before degeneration — but in neuropraxia, they remain permanently viable since there is no axonal injury)

Prognosis & Recovery

• Recovery is always complete if the causative compression/stretch is removed
• Timeline: days to 12 weeks (typically 6–12 weeks for full remyelination)
• Recovery pattern is not proximal-to-distal (unlike axonal regeneration in axonotmesis) — improvement can occur at any point along the nerve simultaneously, because axons are intact

Management

• Non-operative in most cases — remove the offending cause (reduce fracture, release compression, remove tourniquet)
• Physiotherapy to maintain joint mobility and prevent contractures during recovery
• Serial clinical and electrophysiological monitoring
• If no recovery by 3 months, re-evaluate (may indicate a worse injury grade than initially suspected)
• Surgical exploration is not indicated for isolated neuropraxia

Clinical Examples

Cervical Cord Neuropraxia (Special Context)

Axonotmesis

Definition

"Axonotmesis is the term used for a more severe blunt injury to a nerve, which causes disruption of the axons and myelin sheaths with consequent axonal degeneration." — Rockwood and Green's Fractures in Adults, 10e

Pathophysiology

Immediate events (at the injury site)

• Axonal continuity is lost at the injury site
• The severed axon undergoes retrograde die-back to the nearest node of Ranvier proximally
• The cell body (perikaryon) undergoes chromatolysis: nuclear peripheralization, rough ER fragmentation, and perikaryal swelling — a proregenerative response

Wallerian Degeneration (distal to injury)

• Occurs within 72–96 hours of axonal disruption
• The distal axon and myelin sheath fragment and degenerate
• Schwann cells and macrophages phagocytose myelin and cellular debris
• Distal end organs (muscle fibers, sensory receptors) become denervated
• The nerve does not conduct at or distal to the injury zone

Distal nerve tube changes

• Schwann cells proliferate and switch to a pro-regenerative phenotype (upregulate neurotrophic factors, form Bands of Büngner)
• However, if the distal stump remains denervated >1 month, Schwann cells begin to atrophy and lose this phenotype
• Endoneurial tube fibrosis and shrinkage progressively obstruct axonal regrowth

Denervated muscle changes

• ~30% of muscle weight lost in the first month

• 60% loss by the fourth month

• Muscle fiber atrophy, sarcoplasm loss, and denervation hypersensitivity (upregulation of nicotinic ACh receptors beyond the motor endplate)

Nerve Regeneration

• The proximal axon forms multiple growth cones (regenerative sprouting)
• Axons regrow through intact endoneurial tubes at 1–2 mm/day (~1 inch/month)
• Recovery proceeds proximal to distal
• Regenerating axons follow the same endoneurial pathway and reconnect with the same end organ (unlike neurotmesis)
• Full recovery, though slow, can approach near-normal

Sunderland Subclassification

"If the sprouting axons are unable to reach the distal endoneurium, then a neuroma in continuity will develop, and no spontaneous recovery will occur (Sunderland class IV)." — Current Surgical Therapy, 14e

Clinical Features

• Complete loss of motor, sensory, and autonomic function (unlike neuropraxia, where sensation/autonomic may be partially preserved)
• No conduction at or distal to the injury on nerve conduction studies
• Progressive denervation atrophy of target muscles
• Tinel's sign may be present and advance distally as regeneration proceeds — a positive prognostic sign

Electrodiagnostic Findings (EMG/NCS)

Studies are not diagnostically reliable for 3–6 weeks after injury due to the delay in Wallerian degeneration completion.

Prognosis

• Grade II: Excellent — complete recovery expected, axons follow intact endoneurial tubes to original targets
• Grade III: Fair — variable quality due to misdirected axons; some functional recovery but may be incomplete
• Grade IV: Poor — neuroma-in-continuity forms; surgical intervention needed

• Distance from injury to target organ (longer = worse)
• Age (younger patients regenerate better)
• Timing of decompression/repair
• Severity of Schwann cell and endoneurial tube atrophy

Management

• Peripheral nerve repair is best performed early (≤14 days), tension-free, in a clean wound bed
• Nerve gaps addressed with nerve conduit, decellularized nerve allograft, or autograft
• Nerve transfers considered for irreparable injuries (provide shorter reinnervation distance)

Classic Examples

Key Distinction: Axonotmesis vs. Neuropraxia vs. Neurotmesis

"The clinical features and neurophysiologic findings may be the same for axonotmesis and neurotmesis, yet there is a major difference in prognosis and management." — Rockwood and Green's Fractures in Adults, 10e