In one breath
Sensation from the trunk and limbs reaches the spinal cord along pseudounipolar neurons whose cell bodies sit in the dorsal root ganglia: their fibers come in by the dorsal root, while motor fibers leave by the ventral root (the Bell–Magendie law). Afferents come in three sizes: large myelinated Aα and Aβ for mechanoreception, small myelinated Aδ for fast pain and cold, and unmyelinated C for slow pain and temperature. Size decides which fibers fail first: ischemia and compression take touch before pain, while local anesthetics take pain before touch. Inside the cord an afferent climbs the dorsal column, relays in the dorsal horn onto a neuron that crosses to the anterolateral system, or reaches motor neurons; the dorsal horn itself is layered into Rexed laminae I–VI, each taking a different kind of input.
Builds on: Sensory receptors and their classification · Neurons and glial cells · Leads to: Ascending tracts: dorsal column and anterolateral system · Pain pathways and perception · Stretch reflex
Peripheral nerve
- Sensory signals from the body reach the CNS through the peripheral nerves.
- Each sensory axon belongs to a pseudounipolar neuron whose cell body lies in a dorsal root ganglion (DRG).
- A fiber’s diameter and conduction velocity depend on the receptor it serves and the sensation it carries.
- The sensory nerve of each cord segment supplies its own patch of skin, a dermatome. Together the dermatomes make up the body’s somatosensory map.
Applied: reading the sensory map
Because each segment, root and nerve has a fixed skin territory, a lesion of any one of them numbs a predictable area. Mapping the numb skin tells you which nerve or cord segment is diseased.
Afferent fibers in a skin nerve
| Fiber | Myelin, size | Carries |
|---|---|---|
| Aα, Aβ | Myelinated, large | Mechanoreceptor signals |
| Aδ | Myelinated, small | Fast pain, cold; some mechanoreceptors |
| C | Unmyelinated, small | Slow pain, temperature; a few mechanoreceptors |
Worth knowing, though not in your pages: the sizes and speeds that MCQs ask for (Ganong’s values).
| Fiber | Diameter | Speed |
|---|---|---|
| Aα | 12–20 µm | 70–120 m/s |
| Aβ | 5–12 µm | 30–70 m/s |
| Aδ | 2–5 µm | 12–30 m/s |
| C | 0.4–1.2 µm | 0.5–2 m/s |
- Worth knowing, though not in your pages: in the numbered system used for sensory fibers, groups Ia and Ib are Aα, group II is Aβ, group III is Aδ and group IV is C.
Four ways a nerve is damaged
Your book names four disease processes of peripheral nerves: axotomy, demyelination, ischemia and compression.
Axotomy
- Axotomy is cutting through a nerve fiber, usually in a cut injury.
- Distal to the cut: the detached axon degenerates. This is Wallerian degeneration (your book covers it in Chapter 24).
- Proximal to the cut: the neuron reacts too. The cell body swells, the soma shows chromatolysis, and the axon pulls back from the injury site.
- Repair: new fibers sprout from the proximal axon.
- Speed of regrowth: peripheral axons regrow faster than central axons, and sensory fibers faster than motor fibers.
- Worth knowing, though not in your pages: chromatolysis is the dispersal of the Nissl granules in the cell body, usually with the nucleus pushed to one side.
Demyelination
- Loss of myelin is a feature of many neuropathies.
- Under this heading your book places distal axonopathy: degeneration of the far ends of peripheral axons, common in diabetes and chronic alcoholism.
- It shows as sensory loss that starts in the distal limbs, a distal sensory neuropathy.
- Worth knowing, though not in your pages: strictly, distal axonopathy is loss of axons rather than of myelin. The classic demyelinating neuropathy is Guillain–Barré syndrome, in which conduction slows or blocks.
Ischemia
- Ischemia lasting more than 15 minutes abolishes touch, temperature and fast pain.
- Slow pain usually survives, because unmyelinated C fibers stand hypoxia better than myelinated fibers.
- Acute ischemia halts axoplasmic transport and impulse propagation: a conduction block.
- Chronic ischemia makes the fibers degenerate.
Compression
- Damage from pressure on a nerve is compressive neuropathy.
- Large fibers (over 5 µm across) are hit earlier and harder than small unmyelinated fibers, so slow pain is usually spared at first.
- Example: the median nerve trapped in the carpal tunnel, carpal tunnel syndrome.
Which fibers fail first
| Insult | Lost first | Lasts longest |
|---|---|---|
| Ischemia | Touch | Slow pain (C) |
| Compression | Touch | Slow pain (C) |
| Local anesthetic | Pain | Touch |
The orders are opposite
Ischemia and pressure remove touch before pain; a local anesthetic removes pain before touch. The small unmyelinated fiber is the most sensitive to the drug but the most resistant to hypoxia and pressure.
- Worth knowing, though not in your pages: Ganong ranks the fiber classes by sensitivity, most sensitive first: to hypoxia B, A, C; to pressure A, B, C; to local anesthetics C, B, A.
Dorsal root
- Afferents that run in a peripheral nerve enter the cord through the dorsal root.
- The DRG cell body has two axons: the distal one is the peripheral nerve fiber, and the proximal one is the dorsal root fiber that enters the cord.
- The skin supplied by one DRG is a dermatome.
- Your book says adjacent dermatomes usually overlap little, which is what lets a band of sensory loss be pinned to one segment.
- The supply of muscles (myotomes) and bones (sclerotomes) by single ganglia is looser, with more overlap.
A slip in your book
Your book says neighbouring dermatomes barely overlap. Standard texts (Guyton, for one) stress the opposite: adjacent dermatomes overlap a good deal, and the sharp borders drawn on dermatome charts are a simplification. Use the book’s point in the exam, but don’t claim sharp borders in a viva.
Clinical significance
- A dorsal root can be compressed, cut or attacked by disease. What the patient notices depends on how severe the injury is and which fibers it reaches.
- Mild compression irritates the root; heavier compression damages it.
Compression of the dorsal root
- Not rare. The usual cause is a herniated intervertebral disc.
- It causes pain in every dermatome whose root is caught.
| Degree | Result in the dermatome |
|---|---|
| Irritation | Paresthesia or hyperesthesia |
| Damage | Frank segmental anesthesia |
Other diseases of the dorsal root
- Traction
- Inflammation
- Ischemia
- Infection: tabes dorsalis
- Degeneration
Worth knowing, though not in your pages: tabes dorsalis is late neurosyphilis that destroys the dorsal roots and the dorsal columns, so position sense is lost and Romberg’s sign is positive (see Abnormalities of dorsal column sensations).
Spinal cord: the Bell–Magendie law
- Afferent fibers enter the cord by the dorsal root; efferent fibers leave it by the ventral root.
- So the dorsal root is sensory and the ventral root is motor. This is the Bell–Magendie law.
- The exception: a few afferents do run in the ventral root. Most are small unmyelinated nociceptors from the viscera.
The two names behind the law:
- Charles Bell (1774–1842), anatomist and neurosurgeon, showed that the ventral roots are motor. He was the first to study the sensory and motor roles of the roots separately.
- François Magendie (1783–1855), a physiologist of the same era, made the functions of both roots clear. Your book also credits him with work on vomiting, absorption and where drugs act, with noting anaphylaxis, and with treating pathology as part of physiology.
- Both reached the same conclusion, so the law carries both names.
- Worth knowing, though not in your pages: the dates usually quoted are Bell 1811 and Magendie 1822. The ventral-root afferents are one reason why cutting dorsal roots (rhizotomy) does not always relieve pain.
Where an afferent goes in the cord
Your book lists these destinations for a primary afferent (the first-order neuron) once it enters the cord:
- Straight up the dorsal column, with no relay in the cord, to its second-order neuron in the medulla. This is the dorsal column pathway.
- A relay in the dorsal horn of the same segment and side. The second-order neuron crosses to the other side and ascends in the anterolateral system.
- A few segments up or down the cord before it meets its second-order neuron.
- Onto motor neurons: afferents from muscle spindles, Golgi tendon organs and joint receptors reach the matching anterior horn cells, mostly directly and sometimes through interneurons (see Muscle spindle and Stretch reflex).
- Onto interneurons of the segment, or onto the endings of descending fibers from the brain.
The key point: a dorsal-root afferent ends either on an ascending sensory neuron or on a segmental motor neuron.
Somatotopic organization
The afferents are laid out by body part:
| Fibers from | Position in the cord |
|---|---|
| Distal limbs, ventral trunk | Medial |
| Proximal limbs, dorsal trunk | Lateral |
Rexed laminae
- Rexed described the layers of the spinal grey matter in 1954, from their cell architecture. They are the Rexed laminae.
- Laminae I–VI form the dorsal horn. They are the sensory laminae, because the afferents end there.
- The ventral horn holds the motor laminae. The main one is lamina IX. Laminae VII and VIII also count as motor but contain mostly interneurons.
- Lamina X is the intercommissural lamina.
- Fibers of different diameters end mainly in different sensory laminae.
Lamina I
- Input: small nociceptive Aδ and C fibers, so its cells respond mainly to noxious stimuli.
- Output: to many spinal and supraspinal targets, among them the lateral cervical nucleus, the dorsal column nuclei and the thalamus.
Lamina II: substantia gelatinosa
- Input: mainly C fibers, so most of its cells respond to noxious or strong mechanical stimuli.
- Output: mostly local; a few cells project to other segments.
Laminae III–VI
- Input: mainly myelinated A fibers. The cells respond to fine touch, vibration and proprioception.
- Output: their axons ascend in the dorsal column pathway.
- Lamina V also receives input from nociceptors.
Worth knowing, though not in your pages:
- lamina I is also called the marginal zone, and laminae III–IV the nucleus proprius;
- lamina V holds wide-dynamic-range neurons on which skin and visceral afferents converge, one basis of referred pain;
- the substantia gelatinosa is where the pain “gate” works (see Endogenous pain control and gate control theory);
- lamina VII contains Clarke’s column and the intermediolateral (sympathetic) column; lamina IX holds the α and γ motor neurons; lamina X surrounds the central canal.
Draw it: a primary afferent and the Rexed laminae
Draw the cord in cross-section with its butterfly of grey matter. Number the dorsal horn from its tip inwards: I as a thin cap, II as a pale band under it (substantia gelatinosa), then III to VI down to the neck of the horn. Put VII in the intermediate grey, VIII in the medial ventral horn, IX as clumps of motor neurons in the ventral horn and X around the central canal. Outside the cord, draw a DRG with a pseudounipolar cell body. Bring its central branch in by the dorsal root and give it four endings: straight up the dorsal column; onto a dorsal horn cell whose axon crosses in front of the central canal into the opposite anterolateral white matter; onto an interneuron; and directly onto an anterior horn cell whose axon leaves by the ventral root.
Descending control of the laminae
- Descending input comes mainly from the cortex (corticospinal tract) and the brainstem (extrapyramidal tracts).
- Most of it ends, directly or through interneurons, on anterior horn motor neurons. A good share, though, ends on cells of the sensory laminae.
- Purpose: to adjust incoming sensory traffic to the body’s motor needs. This gives sensory–motor coordination and a feedback loop for sensory–motor regulation.
Where each tract ends in the laminae, sorted by lamina:
| Laminae | Descending tracts ending there |
|---|---|
| I, II | Raphespinal, medullary reticulospinal |
| III, IV | Corticospinal |
| V | All four: corticospinal, raphespinal, both reticulospinals |
| VI | Corticospinal, raphespinal, medullary reticulospinal |
| VII | Raphespinal, both reticulospinals |
| VIII | Pontine reticulospinal |
- Memory hook: raphespinal and medullary reticulospinal share one list (I, II, V, VI, VII), and they are the only two that reach the pain laminae I and II. Corticospinal keeps to III–VI. Pontine reticulospinal stays deep (V, VII, VIII).
- Worth knowing, though not in your pages: the raphespinal fibers use serotonin and start in the nucleus raphe magnus. They are part of the brain’s descending pain-control system (see Endogenous pain control and gate control theory).
Exam-answer skeleton: "Bell–Magendie law" (short note)
- State the law: afferents enter by the dorsal root, efferents leave by the ventral root, so the dorsal root is sensory and the ventral root motor.
- The anatomy behind it: the DRG’s pseudounipolar neuron, with its distal axon in the nerve and its proximal axon in the dorsal root; motor axons from anterior horn cells leave in the ventral root.
- The two scientists and what each showed: Bell (1774–1842), Magendie (1783–1855).
- The exception: a few small unmyelinated visceral nociceptors in the ventral root.
- Significance: the dorsal and ventral roots are the afferent and efferent limbs of spinal reflexes, and dermatomes let a sensory loss be traced to its root or segment.
- Applied: dorsal root compression by a disc (pain, paresthesia, segmental anesthesia) and tabes dorsalis.
Asked in exams
- Bell–Magendie law: May 2022, MCQ · Mar 2024, 5 marks
- Nerve fibre types and their conduction speeds: Mar 2024, MCQ