Seddon's and Sunderland's Classification of Nerve Injury

Also includes information from pages 130-131 in the textbook from Final Frontier

Which Sunderland grade corresponds to Seddon's classification of Neuropraxia?

Sunderland 1^∘

What is the primary pathological mechanism of Neuropraxia?

Segmental demyelination (without loss of axonal continuity).

In Neuropraxia, how is action potential conduction affected relative to the lesion site?

slowed or blocked at the point of demyelination, but remains normal both above and below the point of compression.

What is the primary cause/etiology of Neuropraxia?

Mild ischemia resulting from nerve compression or traction.

What degree of muscle wasting is seen in Neuropraxia?

No or minimal muscle wasting.

What is the typical recovery time frame for Neuropraxia?

Minutes to days.

What signs and symptoms characterize Neuropraxia?

Pain, muscle weakness, numbness, and affected proprioception (with no or minimal muscle wasting).

Which Sunderland grades are categorized under Seddon's classification of Axonotmesis?

Sunderland 2^∘ and 3^∘

What structural nerve defect defines Axonotmesis?

Loss of axonal continuity while the surrounding connective tissue coverings remain intact.

What cause leads to Axonotmesis?

Prolonged compression or stretch causing infarction and necrosis.

What direction does Wallerian degeneration occur to the lesion site in Axonotmesis?

Distal

At what rate do regenerating axons grow during recovery from Axonotmesis?

1 mm/day (or approximately 1 inch/month).

In Axonotmesis recovery, which function is restored first: sensation or motor function?

Sensation

What functional losses occur in Axonotmesis?

Complete loss of motor, sensory, and sympathetic functions, along with evident muscle wasting and pain.

Which Sunderland grades correspond to Seddon's classification of Neurotmesis?

Sunderland 3^∘, 4^∘, and 5^∘

What is the structural definition of Neurotmesis?

Complete severance of the nerve fiber along with disruption of its connective tissue coverings.

What direction does Wallerian degeneration occur to the lesion site in Neurotmesis?

Distal

What typical severe trauma mechanisms cause Neurotmesis?

Gunshot or stab wounds, avulsions, and ruptures.

How does pain presentation in Neurotmesis differ from that in Neuropraxia and Axonotmesis?

Neurotmesis presents with no pain (anesthesia), whereas pain is present in both Neuropraxia and Axonotmesis.

What recovery requirement distinguishes Neurotmesis from Axonotmesis?

Neurotmesis requires surgical repair for recovery, whereas Axonotmesis can regenerate spontaneously.

What is represented in A

Neuropraxis

What is represented in B

Axomotmesis

What is represented in C

Neurotmesis

True or False: axons that undergo regeneration remyelinate to their pre-injury levels

False

What is collateral sprouting and what is the result

When intact axons pick up denervated terminal targets

Results in switching of the muscle fiber types

Mononeuropathy

Involvement of a single nerve

Mononeuropathy multiplex

Involvement of 2 or more nerves without clear pattern of polyneuropathy

Radiculopathy

Involvement of nerve roots

Plexopathy

Involvement of brachial or lumbosacral plexus

Segmental demyelination

Primarily impacts myelin

Axonal degeneration

Impacts axons to a greater degree than myelin

In what direction does axonal degeneration progress

Distal to proximal

True or False: most polyneuropathic conditions impact both myelin and axons

True

Polyneuropathic conditions are more ACUTE/CHRONIC in nature

Chronic

What are acute and rapidly progressing polyneuropathic conditions typically related to

Toxins (poison) or Autoimmune conditions (GBS)