posterior horn

**Anatomy** - Spinal gray matter is divided into the posterior (dorsal) horn (sensory), the intermediate zone/lateral horn (autonomic; T1–L2 sympathetic and S2–S4 parasympathetic), and the anterior (ventral) horn (somatic motor). - Primary afferent cell bodies lie in the dorsal root ganglia (pseudounipolar neurons). Their central processes enter via the dorsal root and synapse in the posterior horn (or ascend directly in the dorsal columns).

**Rexed laminae (posterior horn = laminae I–VI)** - Lamina I (posteromarginal nucleus): nociceptive and thermal input from Aδ and C fibers. Gives rise to the spinothalamic tract. - Lamina II (substantia gelatinosa): C-fiber input and interneurons. Key site of pain modulation (gate control theory) and opioid/enkephalin action. Descending input from the periaqueductal gray and the raphe nuclei (serotonin, norepinephrine) acts here. - Laminae III–IV (nucleus proprius): Aβ fibers (touch). Contain second-order neurons for the spinothalamic tract. - Lamina V–VI: wide dynamic range neurons that receive convergent visceral and somatic input. This convergence underlies referred pain. Lamina VI is prominent in the cervical and lumbar enlargements and receives proprioceptive input. - Clarke's nucleus (nucleus dorsalis, C8–L3) lies in lamina VII at the base of the posterior horn. It relays unconscious proprioception via the dorsal spinocerebellar tract.

**Fiber types and pathways** - Aδ (fast, myelinated) and C (slow, unmyelinated) fibers carry pain and temperature. They synapse in laminae I, II, and V, then the second-order neuron decussates via the anterior white commissure (within 1–2 segments) and ascends in the contralateral lateral spinothalamic tract to the VPL of the thalamus. - Aβ fibers carrying fine touch, vibration, and proprioception ascend ipsilaterally in the dorsal columns (fasciculus gracilis and cuneatus) without synapsing in the cord. They synapse in the medulla (nucleus gracilis and cuneatus), then cross as the medial lemniscus. - Lissauer's tract (dorsolateral fasciculus) is where pain and temperature fibers ascend or descend 1–2 segments before synapsing.

**Clinical correlations** - **Syringomyelia:** a cystic cavity expands in the central cord, typically C8–T1. It damages the crossing spinothalamic fibers in the anterior white commissure, causing a bilateral "cape-like" loss of pain and temperature with preserved light touch and vibration (dissociated sensory loss). It may extend to the anterior horn (hand weakness and atrophy) and the lateral horn (Horner syndrome). It is associated with Chiari I malformation. - **Tabes dorsalis (tertiary syphilis):** degeneration of the dorsal roots and dorsal columns causes loss of proprioception and vibration, sensory ataxia, a positive Romberg sign, lightning pains, and Argyll Robertson pupils. - **Brown-Séquard syndrome (hemisection):** ipsilateral loss of dorsal column function and ipsilateral UMN signs below the lesion. Contralateral loss of pain and temperature begins 1–2 levels below the lesion. Ipsilateral LMN signs and a band of sensory loss occur at the lesion level. - **Herpes zoster:** the virus reactivates in the dorsal root ganglion and causes dermatomal pain and vesicles. Postherpetic neuralgia reflects changes in dorsal horn processing. - **Pain pharmacology:** intrathecal and epidural opioids act on μ receptors in lamina II. This presynaptically inhibits substance P and glutamate release from primary afferents. Gabapentinoids act on α2δ calcium channel subunits in the dorsal horn. - **Substance P and glutamate** are the main neurotransmitters released by nociceptive primary afferents in the dorsal horn. Capsaicin depletes substance P. - **Vitamin B12 deficiency (subacute combined degeneration):** demyelination of the dorsal columns and lateral corticospinal tracts causes loss of vibration and proprioception plus spastic weakness.

**Mnemonic** "Dorsal = Detects" (sensory input) and "Ventral = Voluntary movement" (motor output). Dorsal root = afferent; ventral root = efferent (Bell–Magendie law).