The peripheral endings of DRG neurons either stay bare (free nerve endings) or are wrapped in a specialized structure (encapsulated receptors, plus the Merkel cell complex).
| Receptor | Sensation | Adapts | Where / look | Fiber → pathway |
|---|---|---|---|---|
| Meissner corpuscle | Light (fine) touch, low-frequency vibration / flutter | Fast | Dermal papillae of hairless skin (fingertips, lips); small receptive field | Aβ → DCML |
| Pacinian corpuscle | Vibration (high-frequency) and deep pressure | Fast | Deep dermis, joints, ligaments; "onion-skin" lamellar capsule; large field | Aβ → DCML |
| Merkel disc (cell) | Pressure and texture, sustained static touch, shape | Slow | Basal epidermis, fingertips; small field | Aβ → DCML |
| Ruffini ending | Skin stretch, joint angle, slippage | Slow | Dermis, joint capsules (encapsulated); large field | Aβ → DCML |
| Free nerve ending | Pain and temperature (and itch) | Slow / none | All skin, most tissues | Aδ, C → anterolateral (spinothalamic) |
"Pacinian = Pulsing (vibration), Meissner = Mild touch, Merkel = Maintained pressure, Ruffini = Rubber-band stretch." The two that end in -cian/-sner (corpuscles) adapt fast; the disc and the ending (Merkel, Ruffini) adapt slow.
Adaptation = how a receptor's firing changes during a constant stimulus.
"Slow adapting" does not mean slow conduction. Merkel and Meissner both use the same fast Aβ fiber; adaptation is a property of the receptor ending, conduction speed is a property of the axon.
Rule: bigger + more myelin = faster. Touch and proprioception get the express lane; pain and temperature take the local.
| Fiber | Diameter (µm) | Myelin | Speed (m/s) | Carries | Pathway |
|---|---|---|---|---|---|
| Aα (group Ia, Ib) | 13–20 | Heavy | 80–120 | Muscle spindle (Ia), Golgi tendon organ (Ib) → proprioception | DCML (conscious) / spinocerebellar (non-conscious) |
| Aβ (group II) | 6–12 | Heavy | 35–75 | Mechanoreceptors of skin: touch, pressure, vibration | DCML |
| Aδ (group III) | 1–5 | Thin / light | 5–30 | Pain, temperature: "fast", sharp, well-localized pain; cold | Anterolateral |
| C (group IV) | 0.2–1.5 | None | 0.5–2 | Pain, temperature, itch: "slow", dull, aching pain; warmth | Anterolateral |
Local anesthetics block small, myelinated fibers first (Aδ pain), then C, then Aβ touch, then Aα motor/proprioception. Boards like "patient feels pressure but no pain after lidocaine."
A-β = "Big touch", A-δ = "Darn, that's hot!", C = "Crawling slow". Alphabet order = shrinking size = slowing speed: α > β > δ > C.
ACA stroke → contralateral leg/foot sensory + motor loss (medial surface). MCA stroke → contralateral face and arm > leg. Loss of two-point discrimination, vibration and position = dorsal column problem.
Touch, pressure, vibration, conscious proprioception (fine, discriminative)
Aβ + Aα · crosses in the medulla
Pain and temperature (+ crude touch)
Aδ + C · crosses in the cord
Non-conscious proprioception → cerebellum
Spindles, tendon organs
Crude touch travels with pain/temp in the anterior spinothalamic part of the anterolateral system. So a patient with dorsal column loss still feels a cotton swab, but cannot localize it or tell two points apart. Do not answer "total loss of touch" for a dorsal column lesion.
"Big guys walk down the middle aisle." Large Aβ fibers go medial into the dorsal column; small fibers stay lateral.
Boards phrase it as: gracilis = T7 and below (legs), cuneatus = T6 and above (arms). Same line, different wording.
"Graceful legs walk down the middle; the cuneiform arms reach out." Gracilis = legs = medial; cuneatus = arms = lateral. "Legs in, arms out."
| Neuron | Cell body | Axon travels in | Synapses in |
|---|---|---|---|
| 1st order | Dorsal root ganglion | Ipsilateral dorsal column (gracilis / cuneatus) | Nucleus gracilis / cuneatus, caudal (closed) medulla |
| 2nd order | Nucleus gracilis / cuneatus | Internal arcuate fibers (cross) → contralateral medial lemniscus | VPL of thalamus |
| 3rd order | VPL | Posterior limb of the internal capsule | Primary somatosensory cortex (postcentral gyrus; "sensorimotor cortex") |
The DCML is a 3-neuron relay that transmits touch, pressure and conscious proprioception. Body chain: DRG → fasciculus gracilis/cuneatus → synapse in nucleus gracilis/cuneatus (closed medulla) → decussate via internal arcuate fibers → medial lemniscus → synapse in VPL → sensory cortex.
Somatotopy is kept the whole way (S-L-T-C in the cord → leg/arm bands in the lemniscus → homunculus).
Conscious proprioception rides the same route: large myelinated fibers from muscle spindles (Ia, II) and Golgi tendon organs (Ib). The non-conscious copy of that data goes to the cerebellum (spinocerebellar tracts).
DCML: up first, cross in the medulla. Spinothalamic: cross first (anterior white commissure, within 1–2 segments), then up. This one difference generates every Brown-Séquard question.
The DCML does not cross at the pyramidal decussation — that is the corticospinal (motor) tract. Sensory decussation (internal arcuate fibers) sits slightly rostral and dorsal to it in the caudal medulla.
Every sensory system except olfaction relays through the thalamus before reaching cortex.
| Nucleus | Relays | Input pathway |
|---|---|---|
| VPL (ventral posterolateral) | Body sensation | Medial lemniscus (DCML) + spinothalamic |
| VPM (ventral posteromedial) | Face sensation + taste | Trigeminothalamic tracts; solitary nucleus |
| LGN (lateral geniculate) | Vision | Optic tract |
| MGN (medial geniculate) | Hearing | Inferior colliculus |
VPM = "Makeup goes on the face (and in the Mouth)" → face + taste. VPL = Limbs. LGN = Light, MGN = Music.
A small VPL/VPM lacunar infarct → pure contralateral hemisensory loss (face + body). Weeks later: thalamic pain syndrome (Dejerine-Roussy) — burning contralateral pain and allodynia.
| Sensory nucleus of V | Location | Modality |
|---|---|---|
| Mesencephalic | Midbrain → upper pons | Jaw proprioception (jaw-jerk reflex) |
| Principal (main, chief) sensory | Mid-pons, lateral to the motor nucleus of V | Discriminative touch, pressure, vibration (DCML equivalent) |
| Spinal trigeminal | Pons → caudal medulla → upper cervical cord | Pain and temperature (crude touch) |
| Neuron | Cell body | Axon / tract | Synapses in |
|---|---|---|---|
| 1st order | Trigeminal (semilunar) ganglion | CN V root, enters at mid-pons | Principal sensory nucleus of V (pons, ipsilateral) |
| 2nd order | Principal sensory nucleus | Most cross → VTTT (contralateral); some stay → DTTT (ipsilateral) | VPM of thalamus |
| 3rd order | VPM | Posterior limb of internal capsule | Face area of postcentral gyrus (lateral) |
Trigeminal exits: "Standing Room Only" → V1 Superior orbital fissure, V2 foramen Rotundum, V3 foramen Ovale. VTTT = Via the other side (crossed); DTTT = Doesn't cross.
One rule: before the crossing → ipsilateral deficit; after the crossing → contralateral deficit. In the cord, a lesion hits fibers entering at that level and all those coming up from below; higher segments have not entered yet.
| Lesion site | Side of deficit | Region affected |
|---|---|---|
| Peripheral nerve / dorsal root | Ipsilateral | That nerve's / dermatome's territory (all modalities) |
| Dorsal column (cord) | Ipsilateral | Dermatomes at and below the lesion |
| Nucleus gracilis / cuneatus | Ipsilateral | Leg (gracilis) or arm (cuneatus) |
| Medial lemniscus (rostral medulla, pons, midbrain) | Contralateral (already crossed) | Whole body below the face |
| VPL / internal capsule / S1 | Contralateral | Body (VPL) ± face (VPM); cortex follows homunculus |
| CN V or principal sensory nucleus | Ipsilateral face | Face touch |
| VTTT alone | Little / no loss | DTTT backup |
Right hemisection at T10: right loss of vibration/position below T10 (DCML), right UMN weakness below (corticospinal), left loss of pain/temp starting 1–2 levels below (spinothalamic already crossed), right LMN signs and all-modality loss at the level. Above T1 → ipsilateral Horner.
Romberg tests proprioception, not the cerebellum. A patient who falls only with eyes closed has a sensory ataxia (dorsal columns or large-fiber neuropathy); a cerebellar patient is wobbly regardless.
Dorsal columns + lateral corticospinal + spinocerebellar (demyelination; ↑ methylmalonic acid).
Bilateral vibration/position loss, positive Romberg, spastic paresis, Babinski, ± macrocytic anemia. Pernicious anemia, vegans, metformin, gastrectomy, N₂O abuse.
Tertiary neurosyphilis → degeneration of dorsal roots and dorsal columns.
Positive Romberg, stomping gait, lightning (shooting) pains, Argyll Robertson pupils (accommodate, don't react), absent DTRs, Charcot joints.
GAA repeat in frataxin (FXN, chr 9) → mitochondrial iron overload.
Teen with ataxia, dorsal column + spinocerebellar + corticospinal loss, pes cavus, kyphoscoliosis, diabetes; death from hypertrophic cardiomyopathy.
Mimics B12 SCD (myelopathy with dorsal column signs). Think after bariatric surgery or excess zinc intake.
Rare. Ipsilateral vibration/position loss below the lesion; motor largely spared (see LO 4).
Folate deficiency gives the same megaloblastic anemia as B12 but no dorsal column disease and normal methylmalonic acid. Giving folate alone to a B12-deficient patient fixes the blood and lets the cord keep degenerating.
Boards show a cord section with one region shaded and ask the deficit. Dorsal = DCML (ipsilateral vibration/position), lateral = corticospinal (ipsilateral UMN) + spinocerebellar, anterolateral = spinothalamic (contralateral pain/temp), ventral horn = LMN.
| Level | Landmarks to identify it | DCML structures | Trigeminal touch |
|---|---|---|---|
| Closed (caudal) medulla | No 4th ventricle (central canal); pyramids ventral | Nucleus gracilis + cuneatus dorsally (capped by their fasciculi); internal arcuate fibers sweeping ventromedially; start of ML | — (spinal V nucleus here, for pain) |
| Open (rostral) medulla | 4th ventricle on top; inferior olives; pyramids | Medial lemniscus = vertical band beside the midline, just dorsal to the pyramid. Arm dorsal, leg ventral. | — |
| Upper / mid pons | Bulky basilar pons with transverse pontine fibers; middle cerebellar peduncles; 4th ventricle | ML turns horizontal at the tegmentum–basilar border. Arm medial, leg lateral. | Principal (chief) sensory nucleus dorsolateral, lateral to motor V; crossed VTTT joins the ML |
| Midbrain (superior colliculus) | Cerebral aqueduct; superior colliculi; cerebral peduncles | ML moved dorsolaterally in the tegmentum, heading for VPL | VTTT alongside, heading for VPM |
The medial lemniscus is a person standing beside the midline in the medulla (head = arm dorsal, feet = leg ventral), who lies down in the pons (arm medial, leg lateral) and then walks out to the side in the midbrain.
Don't confuse the medial lemniscus (sensory, beside midline, dorsal to pyramid) with the MLF (medial longitudinal fasciculus — eye movements, just under the 4th ventricle floor) or with the pyramid (motor, most ventral).
Open each card after you commit to an answer.
| Artery | Supplies | Infarct → loses | Spares |
|---|---|---|---|
| Anterior spinal (1, midline) | Anterior 2/3: ventral horns, lateral corticospinal, spinothalamic | Bilateral weakness (LMN at level, UMN below) + bilateral pain/temp loss below; bladder dysfunction | Dorsal columns (vibration, position) |
| Posterior spinal (2) | Posterior 1/3: dorsal columns, dorsal horns | Ipsilateral vibration / position loss below the lesion | Motor largely spared; pain/temp spared |
Sudden bilateral paralysis + loss of pain/temperature, with preserved vibration and proprioception. Classic triggers: aortic aneurysm repair/dissection, aortic cross-clamping, hypotension. Watershed: upper-mid thoracic cord.
"Preserved vibration" points away from the dorsal columns. Don't pick B12 deficiency or tabes when the tuning fork is still felt; pick anterior spinal artery / anterior cord syndrome.
General pattern: paramedian branches → medial structures (motor tracts, medial lemniscus, motor CN nuclei); circumferential branches → lateral structures (spinothalamic, spinal V, cerebellar peduncles, sympathetics).
| Level | Medial (paramedian) | Lateral |
|---|---|---|
| Midbrain | PCA paramedian branches (+ top of basilar) | PCA circumferential, superior cerebellar |
| Pons | Basilar paramedian branches | AICA (caudal), superior cerebellar (rostral) |
| Rostral (open) medulla | Anterior spinal + vertebral | PICA + vertebral (+ posterior spinal, dorsal) |
| Caudal (closed) medulla | Anterior spinal | Vertebral + posterior spinal (dorsal: gracile/cuneate nuclei) |
Pyramid → contralateral hemiparesis. ML → contralateral vibration/position loss. CN XII → tongue deviates toward lesion.
DCML hit ✔
Ipsilateral face pain/temp loss + contralateral body pain/temp loss, dysphagia, hoarseness (n. ambiguus), ipsi Horner, vertigo/nystagmus, ipsi limb ataxia.
DCML spared ✘ (ML is medial)
Corticospinal → contralateral hemiparesis; ML → contralateral vibration/position loss; ± ipsilateral CN VI (eye can't abduct).
Bilateral basilar → locked-in syndrome.
Like Wallenberg plus facial paralysis (CN VII nucleus), hearing loss (VIII), ↓ lacrimation/salivation.
DCML spared.
Ipsilateral CN III palsy (down and out, ptosis, dilated pupil) + contralateral hemiparesis (cerebral peduncle).
Medial brainstem stroke = motor + medial lemniscus + medial CN motor nucleus (crossed hemiparesis, "alternating" syndrome). Lateral = pain/temp crossed pattern + Horner + cerebellar + the level's CN, with power and vibration preserved.
"Don't PICK a horse (hoarse) that can't eat (dysphagia)" — nucleus ambiguus signs = PICA. "Facial droop means AICA's pooped." Medial medullary: "lick your wounds" — tongue points toward the lesion.
Wallenberg gives sensory loss but the DCML is spared — vibration and position remain normal on both sides. If the vignette has contralateral vibration loss + hemiparesis, it is medial, not lateral.
| Nerve | Taste region | 1st-order cell body (ganglion) |
|---|---|---|
| Facial (VII) — chorda tympani | Anterior 2/3 of tongue | Geniculate |
| Glossopharyngeal (IX) | Posterior 1/3 of tongue | Inferior (petrosal) |
| Vagus (X) | Minor role: soft palate / epiglottis region | Inferior (nodose) |
Nucleus solitarius = visceral sensory: taste, baroreceptors (IX carotid sinus, X aortic arch), gut distension. Nucleus ambiguus = motor to pharynx/larynx (IX, X). Dorsal motor nucleus of X = parasympathetic to the viscera. VPM handles face sensation and taste.
"Solitary = Sensory; Ambiguus = Action (motor)." Taste is the "head" of the solitary nucleus (rostral); the gut is the "tail" (caudal).
1A 68-year-old woman has 6 months of tingling feet and unsteadiness that is worse in the dark. Vibration and joint-position sense are absent at the toes bilaterally. She stands steadily with eyes open but sways and nearly falls with eyes closed. Knee reflexes are brisk and plantar responses are extensor. Hemoglobin is 9.8 g/dL with MCV 112 fL. Which is the most likely diagnosis?
2A 60-year-old man has sudden loss of vibration and position sense in the right arm and right leg. Pain and temperature are normal. Strength is normal, and the face is unaffected. Where is the single lesion most likely located?
3A researcher records from a cutaneous receptor in the deep dermis of the palm. The receptor responds briskly to a 250-Hz vibration and at the onset and offset of steady pressure, but is silent while the pressure is held. Histology shows concentric lamellae around a single nerve ending. Which receptor is this?
4Nerve conduction studies of the sural nerve show a sensory conduction velocity of 48 m/s in a healthy volunteer. The fibers generating this response most likely carry which information, by which axon class?
5A 25-year-old man is stabbed in the back. He has weakness of the right leg with a right Babinski sign. Which additional sensory findings are expected if the lesion is a right hemisection of the cord at T10?
6A 72-year-old man undergoes open repair of a thoracoabdominal aortic aneurysm. On waking he cannot move either leg and has lost pinprick and temperature sensation below the umbilicus bilaterally. Which modality is most likely preserved in his legs?
7A 66-year-old woman suddenly develops right arm and leg weakness and loss of vibration and position sense on the right side. On protrusion, her tongue deviates to the left. Facial sensation and pain/temperature sensation are normal. Occlusion of which vessel best explains this?
8Second-order neurons in the principal sensory nucleus of the trigeminal nerve send most of their axons across the midline in the ventral trigeminothalamic tract. In which thalamic nucleus do these axons terminate?
9After surgery for chronic otitis media on the left, a 40-year-old woman notes that food tastes bland on the front of the left side of her tongue. Light touch and pinprick on the same area are normal, and facial movements are symmetric. Which structure was most likely injured?
10The central processes of taste fibers from the posterior third of the tongue make their first synapse in which structure?
11A 55-year-old man has episodes of sudden stabbing leg pain, a wide-based stomping gait and a positive Romberg sign. Knee and ankle reflexes are absent. His pupils are small and irregular; they constrict on near focus but not to light. Degeneration of which structures explains his gait?
12A 14-year-old girl has 2 years of progressive clumsiness and falls. Exam shows absent ankle reflexes, loss of vibration sense in the feet, bilateral Babinski signs, high-arched feet and kyphoscoliosis. ECG shows left ventricular hypertrophy. Which genetic mechanism is most likely?
13A 70-year-old man has sudden numbness and weakness of the left foot and leg. His left arm and face are normal. Two-point discrimination on the left sole is impaired. Infarction in the territory of which artery best explains this?