dorsal root ganglion

**Anatomy/Histology** - Located in the dorsal root of each spinal nerve, in the intervertebral foramen (just proximal to the union with the ventral root to form the mixed spinal nerve). - Contains cell bodies of first-order (primary afferent) sensory neurons. These are **pseudounipolar**: a single process bifurcates into a peripheral branch (to skin, muscle, joints, viscera) and a central branch (to the spinal cord via the dorsal root). - Surrounded by **satellite glial cells** (the PNS analog of astrocytes); neurons are enclosed in a connective tissue capsule continuous with the epineurium/perineurium. - **No synapses** occur in the DRG (no interneurons, no dendrites) - it is just a station of cell bodies. It has no blood-nerve barrier (fenestrated capillaries), making it vulnerable to toxins and immune attack. - Ventral root = motor (efferent) axons; cell bodies are in the ventral horn (anterior horn), not the DRG. Mnemonic: "Dorsal = Direct to cord/Afferent/Sensory; Ventral = Voluntary/Efferent/Motor" (Bell-Magendie law: dorsal roots sensory, ventral roots motor).

**Sensory pathways** - Large myelinated Aα/Aβ fibers (proprioception, vibration, fine touch) enter and ascend ipsilaterally in the **dorsal columns** (fasciculus gracilis/cuneatus) - first-order neuron cell bodies in DRG, synapse in the medulla (nucleus gracilis/cuneatus), then decussate as medial lemniscus. - Small fibers: Aδ (fast pain, temperature) and C (slow pain, temperature, itch) synapse in the dorsal horn (Rexed laminae I, II, V), then decussate via the anterior white commissure and ascend in the **spinothalamic tract**. - Cell bodies of DRG neurons also contain cranial nerve analogs: the trigeminal ganglion (CN V), geniculate ganglion (CN VII), and superior/inferior ganglia of CN IX and X.

**Embryology** - Derived from **neural crest cells** (as are satellite cells, Schwann cells, sympathetic chain ganglia, adrenal medulla, melanocytes). Motor neurons and the dorsal horn derive from the neural tube (alar plate = sensory/dorsal; basal plate = motor/ventral).

**Clinical correlations** - **Herpes zoster (shingles)**: Varicella-zoster virus (VZV) lies latent in DRG (and cranial nerve ganglia, e.g., trigeminal) after primary varicella (chickenpox). Reactivation causes a painful vesicular rash in a single dermatome; postherpetic neuralgia is a complication. HSV-1 latency is in the trigeminal ganglion; HSV-2 in sacral ganglia. - **Sensory neuronopathy (ganglionopathy)**: Damage to DRG neurons causes a non-length-dependent sensory loss with prominent sensory ataxia and areflexia, with preserved strength. Causes: paraneoplastic (anti-Hu/ANNA-1 antibodies, classically small cell lung cancer), Sjögren syndrome, cisplatin toxicity, pyridoxine (vitamin B6) excess toxicity, and others. - **Tabes dorsalis (tertiary syphilis)**: Degeneration of dorsal roots/DRG and dorsal columns, causing loss of proprioception and vibration sense, sensory ataxia, positive Romberg, Argyll Robertson pupils, lancinating pain, and Charcot joints. - **Friedreich ataxia** (GAA trinucleotide repeat expansion in frataxin gene, chromosome 9, autosomal recessive): degeneration of DRG neurons, dorsal columns, spinocerebellar tracts, and corticospinal tracts; also hypertrophic cardiomyopathy (most common cause of death), diabetes, and kyphoscoliosis. - **Vitamin B12 deficiency / subacute combined degeneration**: dorsal columns, lateral corticospinal tracts, spinocerebellar tracts (cord pathology rather than DRG). - **Lesion location contrast**: A lesion of the dorsal root/DRG causes dermatomal sensory loss (all modalities) in the ipsilateral dermatome and loss of reflex (afferent limb); radiculopathy (e.g., disc herniation compressing the root) produces dermatomal pain/paresthesia and diminished reflexes. - **Wallerian degeneration**: A peripheral nerve injury causes degeneration distal to the injury; the DRG's peripheral branch can regenerate, but the central branch (in the CNS) regenerates poorly. Conditioning peripheral lesions improve central regeneration experimentally. - **Pain/therapeutics**: DRG neurons express voltage-gated sodium channels (Nav1.7, Nav1.8, Nav1.9) - gain-of-function Nav1.7 mutations cause erythromelalgia and paroxysmal extreme pain disorder; loss-of-function causes congenital insensitivity to pain. TRPV1 (capsaicin receptor) is expressed on nociceptive DRG neurons. Local anesthetics block Na+ channels; gabapentinoids bind the α2δ subunit of voltage-gated Ca2+ channels, upregulated in DRG after nerve injury. Pulsed radiofrequency and DRG stimulation are used for chronic pain (e.g., CRPS). - **Diabetic neuropathy** and **chemotherapy-induced neuropathy** (e.g., cisplatin, paclitaxel) also involve DRG neuron injury. - **Hereditary sensory and autonomic neuropathies (HSAN)**: loss of DRG neurons (e.g., familial dysautonomia/Riley-Day, HSAN III, IKBKAP/ELP1 mutation, in Ashkenazi Jews).

**High-yield pearls** - DRG = cell bodies of first-order sensory neurons; pseudounipolar; no synapses; neural crest-derived. - VZV latency site (along with cranial nerve sensory ganglia). - Ganglion (PNS cluster of cell bodies) vs. nucleus (CNS cluster of cell bodies). - Dorsal root = sensory afferent; ventral root = motor efferent (Bell-Magendie law).