Overview

Axons myelinated per cell1 (one internode)

Internode length≈0.2–2 mm

Regeneration rate≈1–3 mm/day

Myelinating Schwann cells line up along a peripheral axon, each forming one internode (≈0.2–2 mm) by spirally wrapping its plasma membrane around the axon and compacting it. The nucleus and cytoplasm are pushed to the outside as the neurilemma (sheath of Schwann), and each Schwann cell–axon unit is enclosed by a basal lamina, which CNS oligodendrocytes lack. PNS myelin contains P0 (myelin protein zero), PMP22 and MBP. Non-myelinating (Remak) Schwann cells embed many small C fibres in troughs of their cytoplasm (Remak bundles). Terminal (perisynaptic) Schwann cells cap the neuromuscular junction.

After a nerve is cut or crushed, the distal axon and its myelin break down within days (Wallerian degeneration). Schwann cells dedifferentiate into "repair cells": they proliferate, phagocytose myelin with recruited macrophages, secrete neurotrophic factors (NGF, BDNF, GDNF), and line up within the preserved basal lamina tubes as bands of Büngner. These bands guide the regenerating axon sprouts. Axons regrow at about 1–3 mm per day (≈1 inch per month), which is used to predict the timing of recovery. This regenerative environment is the main reason why peripheral nerves, unlike CNS tracts, can regenerate.

Anatomy

Histology: Elongated nuclei along nerve fibres. In transverse section, myelinated fibres look like rings with a dark outline (osmium) or "empty" spaces (H&E). Schmidt–Lanterman incisures and the nodes of Ranvier are visible. S-100 positive.
Development: Derived from the neural crest, through Schwann cell precursors. Axonal neuregulin-1 type III levels determine whether an axon is myelinated.

Function

Myelinate peripheral axons, one internode per cell, for saltatory conduction.
Ensheathe and support unmyelinated C fibres (Remak bundles).
Guide and promote axon regeneration after injury (bands of Büngner, neurotrophins).
Clear myelin debris during Wallerian degeneration.
Maintain the neuromuscular junction (terminal Schwann cells).

Clinical significance

Guillain–Barré syndrome

An acute immune-mediated polyradiculoneuropathy, often 1–3 weeks after Campylobacter jejuni or viral infection (molecular mimicry with gangliosides). The classic demyelinating form (AIDP) targets Schwann cell myelin. It presents with ascending symmetrical flaccid weakness, areflexia, mild sensory symptoms and autonomic instability, and respiratory failure is a risk (monitor FVC). CSF shows albuminocytological dissociation (raised protein, normal cells). Treat with IVIG or plasma exchange; steroids are not used.

Schwannoma and neurofibromatosis type 2

Benign, encapsulated, S-100-positive Schwann cell tumours (Antoni A and B areas, Verocay bodies). The vestibular schwannoma (acoustic neuroma) at the cerebellopontine angle causes unilateral sensorineural hearing loss and tinnitus. Bilateral vestibular schwannomas are diagnostic of NF2 (merlin, chromosome 22).

Nerve injury (Seddon classification)

Neurapraxia: focal demyelination or conduction block with the axon intact; recovery in days to weeks. Axonotmesis: the axon is divided but the endoneurial tubes are intact; Wallerian degeneration follows, then good regeneration at ≈1–3 mm/day. Neurotmesis: complete transection of nerve and sheaths, needing surgical repair, and recovery is incomplete. Other Schwann cell disorders: Charcot–Marie–Tooth 1A (PMP22 duplication) and leprosy (Mycobacterium leprae infects Schwann cells).

Compiled from standard anatomy and physiology references — see the Nervous System sources. For education only; not medical advice.