Overview

Every spinal nerve except usually C1 has a dorsal root ganglion. It sits on the dorsal root just proximal to its junction with the ventral root, normally in the intervertebral foramen. Lumbosacral ganglia lie within the canal, and the C1 and C2 ganglia lie on the vertebral arches. It contains thousands of pseudounipolar neurons. Each has a single stem process that divides in a T shape: a peripheral branch to receptors in skin, muscle, joints or viscera, and a central branch that enters the cord through the dorsal root. Impulses run directly from the peripheral to the central branch, bypassing the soma, so the ganglion is a site of cell bodies only and contains no synapses.

Each neuronal soma is enveloped by a complete capsule of flattened satellite glial cells. Neuron size correlates with fibre type: large cells give Aα/Aβ fibres (proprioception, touch) and small cells give Aδ and C fibres (pain, temperature, itch). Cranial nerve sensory ganglia (trigeminal, geniculate, superior and inferior ganglia of IX and X, spiral and vestibular) are homologues.

Location: On the dorsal root of each spinal nerve within the intervertebral foramen, lateral to the dural sleeve. It lies close to the posterolateral intervertebral disc and the facet joint.

Anatomy

Histology: Large rounded neuronal somata (≈20–100 µm) with central nuclei and prominent nucleoli, each ringed by satellite cells. These are separated by bundles of myelinated fibres. Autonomic ganglia, by contrast, have smaller multipolar neurons with eccentric nuclei and incomplete satellite coverings.
Development: Derived from the neural crest, which also forms its satellite cells and the Schwann cells of the root.

Function

Houses the cell bodies of all somatic and visceral primary afferent neurons of the spinal nerves.
Provides the metabolic (trophic) support for very long sensory axons.
Its satellite glia regulate the neuronal microenvironment; changes in them contribute to chronic pain.

Clinical significance

Herpes zoster (shingles)

Varicella-zoster virus lies latent in DRG and cranial sensory ganglion neurons after chickenpox. On reactivation, often with age or immunosuppression, it travels down the peripheral axon and causes a painful vesicular rash confined to one dermatome, most often thoracic or V1. Post-herpetic neuralgia is a common sequel.

Sensory neuronopathy (ganglionopathy)

Destruction of DRG neurons causes non-length-dependent sensory loss and severe sensory ataxia. Causes include paraneoplastic anti-Hu (small-cell lung cancer), Sjögren syndrome, cisplatin, pyridoxine toxicity and Friedreich ataxia.

Radiculopathy

Disc herniation or foraminal stenosis compresses the DRG and root. The result is dermatomal pain and paraesthesia, myotomal weakness and loss of the corresponding reflex.

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