Spinal Cord & Spinal Nerves

Fig. 1.40 — Basic anatomy of a (thoracic) spinal nerve: posterior (sensory) root with spinal ganglion + anterior (motor) root unite to form the spinal nerve, which splits into posterior and anterior rami.

Gray's Anatomy for Students, 4e

Grey matter = H-butterfly · White matter = tracts · Grey:White ratio highest in cervical enlargement (limb innervation)

Fig. 2.11 — Vertebral canal, spinal cord and spinal nerves: the cord ends at L1–L2 (conus medullaris); below it the lumbosacral roots form the cauda equina within the subarachnoid space.

Gray's Anatomy for Students, 4e

The spinal cord is the great cable of the nervous system — a finger-wide column that extends from the foramen magnum down to the L1/L2 vertebral level in adults, where it tapers into the conus medullaris. Think of it as a relay station: sensory signals race up, motor commands race down, and the H-shaped grey matter in the middle is where neurons actually live. Two enlargements — cervical (C4–T1) and lumbosacral (L1–S3) — exist because more neurons are needed to serve the limbs; the grey-to-white ratio is highest there. A single blood supply rule governs the most devastating strokes: the anterior spinal artery feeds the anterior two-thirds of the cord (motor + pain/temperature tracts), while two posterior spinal arteries supply only the posterior columns — knowing this one fact explains the entire clinical picture of anterior cord syndrome.

Two questions dominate spinal tract anatomy: where does each tract cross, and what modality does it carry? Pain and temperature fibres enter the cord, cross within 1–2 segments in the anterior white commissure, and travel up as the contralateral spinothalamic tract — that crossing within the cord is the key to Brown-Séquard syndrome. Fine touch, vibration, and proprioception travel ipsilaterally all the way to the medulla before crossing at the sensory decussation — which is why a unilateral cord lesion produces opposite-sided sensory deficits for different modalities. Motor commands from cortex cross at the medullary pyramids as the corticospinal decussation, then descend as the lateral corticospinal tract. The TMU 2019 exam asked for the full "superficial sensory pathway of trunk and limbs" (8 marks) — that is the spinothalamic tract in its entirety, from receptor to cortex.

Every spinal nerve is a merger of two roots: the dorsal (sensory) root carrying signals in from the periphery via the dorsal root ganglion, and the ventral (motor) root carrying commands out from anterior horn cells. They unite in the intervertebral foramen and immediately divide into dorsal ramus (paravertebral muscles and back skin) and ventral ramus (limbs and anterior trunk). The key counting rule to memorise: there are 8 cervical nerves but only 7 cervical vertebrae, because C1–C7 exit above their vertebra while C8 exits below C7. Below that, every nerve exits below its vertebra — and this numbering gap is why C8 radiculopathy comes from the C7/T1 disc, not from a non-existent C8 vertebra.

31 pairs of spinal nerves: 8 cervical (C1–C8) + 12 thoracic (T1–T12) + 5 lumbar + 5 sacral + 1 coccygeal. Each formed by union of dorsal (posterior) root (sensory, DRG) + ventral (anterior) root (motor). Unite in intervertebral foramen → spinal nerve → immediately divides into dorsal ramus (posterior structures, paravertebral muscles + skin) + ventral ramus (limbs + anterior trunk). Note: C1 has a ventral root but usually no dorsal root (no sensory dermatome for C1).

Fig. 8.188 — Cervical plexus (C1–C4): cutaneous branches (lesser occipital, great auricular, transverse cervical, supraclavicular) and motor branches including the phrenic nerve (C3–C5).

Gray's Anatomy for Students, 4e

The cervical plexus (C1–C4) is clinically dominated by one nerve: the phrenic. "C3, 4, 5 keeps the diaphragm alive" is the most tested mnemonic in anatomy — damage above C3 (e.g., high cervical cord injury) stops breathing entirely, while damage below C5 spares the diaphragm. The phrenic nerve also has a sensory component to the central diaphragm and pericardium, which is why diaphragmatic irritation (subphrenic abscess, ectopic pregnancy rupture) refers pain to the shoulder tip via the C3/C4 supraclavicular dermatome. The great auricular nerve (C2/C3) is the most commonly injured cutaneous nerve in parotidectomy — numbness over the ear and parotid region is the expected post-operative finding surgeons warn patients about.

Fig. 7.52 — Brachial plexus (C5–T1): roots → trunks (upper, middle, lower) → divisions → cords (lateral, posterior, medial) → terminal branches (musculocutaneous, axillary, radial, median, ulnar).

Gray's Anatomy for Students, 4e

The brachial plexus (C5–T1) is the wiring harness for the entire upper limb — five roots reorganise into trunks, divisions, cords, and finally named branches. The mnemonic "Real Texans Drink Cold Beer" locks the order in. Clinically, two birth injury patterns dominate: Erb's palsy (C5/C6 upper trunk — "waiter's tip" arm from loss of deltoid, biceps, and supinators) and Klumpke's palsy (C8/T1 lower trunk — intrinsic hand wasting and claw hand, often with Horner's syndrome from T1 sympathetic damage). In the adult, the three most-tested nerve injuries are: radial nerve at the spiral groove (wrist drop, sensory loss at 1st web space), median nerve at the carpal tunnel (thenar wasting, LOAF muscles, night-time tingling), and ulnar nerve at the medial epicondyle (claw hand of ring/little fingers, hypothenar wasting). Each has a unique autonomous sensory zone that confirms the diagnosis at the bedside.

Fig. 4.173 — Lumbar plexus (L1–L4): iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, femoral and obturator nerves emerging around the psoas major.

Gray's Anatomy for Students, 4e

The lower limb is served by two overlapping plexuses: lumbar (L1–L4) and sacral (L4–S3). Three nerves dominate clinically. The femoral nerve (L2–L4) extends the knee via quadriceps and is tested by the knee jerk (L3/L4) — damage in the femoral triangle or from psoas abscess causes inability to climb stairs. The sciatic nerve (L4–S3) is the largest nerve in the body and supplies everything below the knee; its safe injection zone is the upper outer quadrant of the buttock. The common peroneal nerve, as it winds around the fibular neck, is the most vulnerable peripheral nerve in the lower limb — a simple leg cross or fibular neck fracture causes foot drop, and the key bedside test is whether inversion is preserved (tibial nerve intact → pure peroneal lesion, not sciatic or L5 root). The pudendal nerve (S2/S3/S4) is the nerve of the perineum — "S2, 3, 4 keeps the penis off the floor."

Fig. 1.38 — Dermatomes. A. Anterior view. B. Posterior view — the area of skin supplied by a single spinal nerve (e.g. T4 nipple, T10 umbilicus, L1 groin).

Gray's Anatomy for Students, 4e

Dermatomes are the body's postcode system — each patch of skin reports back to a specific spinal level, and knowing the landmarks lets you localise a cord or root lesion precisely. The trunk landmarks confirmed in the TMU anatomy notes: T2 = sternal angle, T4 = nipple, T6 = xiphoid process, T10 = umbilicus (also where appendicitis pain begins as referred visceral pain), T12 = anterior superior iliac spine. For the limbs, the C6 autonomous zone is the tip of the thumb (carpal tunnel tingling), C7 is the middle finger (most common cervical disc level), L5 is the big toe and dorsum of foot (L4/5 disc), and S1 is the lateral foot and sole (L5/S1 disc, ankle jerk). Myotomes give you the reflex ladder: biceps = C5/C6, triceps = C7, knee = L3/L4, ankle = S1/S2 — one absent reflex places the lesion precisely.

Identifying a spinal cord lesion pattern is one of the highest-yield clinical skills in anatomy — the TMU 2019 exam devoted 9 marks to a single question about the internal capsule alone. The key is always: which tracts are hit, and how do they decussate? UMN lesions (above the anterior horn) give spasticity + hyperreflexia + Babinski; LMN lesions (at or below the anterior horn) give flaccidity + wasting + fasciculations + areflexia. Cauda equina syndrome (L2–S5 roots) is a surgical emergency — saddle anaesthesia + urinary retention + bilateral flaccid leg weakness demands urgent MRI and decompression within 48 hours. Subacute combined degeneration (B12 deficiency) is the classic "combined" lesion: dorsal columns + corticospinal tracts simultaneously, producing the paradox of absent ankle jerks (peripheral neuropathy) with extensor plantar responses (UMN cord involvement) — virtually pathognomonic.

An intervertebral disc is a hydraulic shock absorber — gelatinous nucleus pulposus contained by the annulus fibrosus — and when the annulus tears, the nucleus herniates posterolaterally (because the posterior longitudinal ligament is strongest centrally) to compress the exiting nerve root. The L+1 rule for the lumbar spine is the clinical shortcut: the L4/L5 disc compresses the L5 root, L5/S1 compresses S1. For the cervical spine: C5/C6 disc → C6 root (thumb tingling, weak biceps), C6/C7 disc → C7 root (middle finger, weak triceps — the most common cervical level). The straight leg raise (SLR) test stretches the sciatic nerve; pain below 60° of elevation is positive for L4/L5/S1 radiculopathy. Red flags — saddle anaesthesia, bilateral symptoms, urinary/bowel dysfunction — mean central disc prolapse causing cauda equina syndrome until proven otherwise: MRI spine urgently.

16.9.1 — Intervertebral Disc Anatomy & Prolapse

Fig. 2.70 — MRI of the lumbar spine: posterior herniation of the L2–L3 disc (nucleus pulposus through the annulus fibrosus) compressing the cauda equina.

Gray's Anatomy for Students, 4e

Disc structure: Nucleus pulposus (gelatinous, high water content in youth — 90%, decreases with age → disc degeneration) surrounded by annulus fibrosus (concentric rings of fibrocartilage). Disc receives nutrition by diffusion (avascular). Prolapse types: Protrusion (nucleus herniates but annulus intact) → extrusion (nucleus herniates through annulus) → sequestration (free fragment in spinal canal). Most common direction: posterolateral (posterior longitudinal ligament strongest centrally → disc bulges to side) → compresses exiting nerve root.

◆ Which Disc → Which Root? (the L+1 rule for lumbar)

In the lumbar spine: the L4/L5 disc (between L4 and L5 vertebral bodies) compresses the L5 root (the traversing root at that level). The L5/S1 disc compresses the S1 root. In the cervical spine: the C5/C6 disc compresses C6 root; C6/C7 disc compresses C7 root. Exception: central disc prolapse → cauda equina syndrome (bilateral).

Syringomyelia is the cord destroying itself from within — a fluid-filled cavity (syrinx) expands outward from the central grey matter, hitting structures in a predictable inside-out sequence. First to go: the anterior white commissure, where pain and temperature fibres from both sides are crossing. This produces the signature bilateral cape distribution of dissociated sensory loss (pain/temperature gone bilaterally over arms and shoulders, fine touch preserved). Then the anterior horn cells are damaged (LMN signs in arms — wasting, fasciculations, areflexia), then the corticospinal tracts (UMN signs in legs — spasticity, hyperreflexia). The commonest cause is Arnold-Chiari type I malformation (cerebellar tonsillar herniation >5 mm below foramen magnum), and the treatment — posterior fossa decompression — often causes the syrinx to collapse. The key MRI finding: a sausage-shaped T2-hyperintense central cavity on sagittal imaging.

Meralgia paraesthetica is a purely sensory mononeuropathy — no motor weakness, no reflex change — caused by entrapment of the lateral femoral cutaneous nerve (LFCN, L2/L3) under the inguinal ligament near the ASIS. The name itself is the diagnosis: "meralgia" = thigh pain, "paraesthetica" = abnormal sensation. The key bedside differentiator is that quadriceps strength and the knee jerk are completely normal — the moment you find motor weakness or a depressed knee jerk, the diagnosis switches to L3 radiculopathy or femoral nerve compression. Obesity is the most common risk factor (abdominal girth increases the angulation of the nerve at the inguinal ligament), and weight loss alone often resolves symptoms. The treatment ladder is conservative first: loose clothing, weight loss, NSAIDs/gabapentin; then steroid + LA injection at the ASIS; surgical decompression or neurectomy only for refractory cases.