Block 6 · CNS · CNS13 · Rev 1.2 · Updated Oct 23, 2026
CNS13 · Neuroscience · Study Guide
Proprioception & Spinal Reflexes
Learning objectives
- LO 1Follow the corticospinal tract on cross-sections from the internal capsule through midbrain, pons, medulla and cervical cord; know where it crosses; and predict what an upper vs lower motor neuron lesion looks like.
- LO 2Name the receptors that sense body position (muscle spindle, Golgi tendon organ) and the afferent fiber groups (Ia, II, Ib) that carry their signals.
- LO 3Trace and sketch how conscious position sense from the body and the face reaches somatosensory cortex, including where each pathway crosses.
- LO 4Trace and sketch how non-conscious position sense from the body and the face reaches the cerebellum, including where (and whether) each pathway crosses and which cerebellar peduncle it enters.
- LO 5Explain step by step how the knee-jerk (stretch) reflex, the withdrawal reflex and the crossed extensor reflex are wired.
- LO 6Predict the position-sense deficits produced by damage to the DCML and spinocerebellar systems in the spinal cord or brainstem.
★ Step 1 HY
⚠ Step 1 trap
✎ Memory tool
“ Buzzwords
MAPBig picture
- Proprioception → where body parts are + how they move
- Two sensors → muscle spindle (stretch) · Golgi tendon organ (tension)
- Same signal → three destinations
- → α motor neuron in cord → reflexes
- → DCML → cortex → conscious position sense (3 neurons, crosses)
- → spinocerebellar tracts → cerebellum → non-conscious coordination (2 neurons, same side)
- Brain controls reflexes via corticospinal tract (UMN)
- UMN lesion → reflexes ↑
- LMN / root / nerve lesion → reflexes ↓ or absent
- Localize → which pathway? which side? crosses where?
LO 1The corticospinal tract & UMN vs LMNWhere the motor command runs, where it crosses, and what breaks when it is cut.
By the end: you can name each level the lateral corticospinal tract passes, point to the pyramidal decussation, and sort any weakness into an UMN or LMN pattern within seconds.
Q1. What does the corticospinal tract do, and what is a "2-neuron relay"?
- The lateral corticospinal tract (LCST) controls voluntary limb movement, especially fine distal movement of the hands and fingers.
- It is a 2-neuron relay:
- Upper motor neuron (UMN): cell body in primary motor cortex (precentral gyrus) → axon all the way down to the cord.
- Lower motor neuron (LMN): α motor neuron in the ventral horn → axon out the ventral root and peripheral nerve → skeletal muscle. The LMN is the "final common pathway": every reflex and every voluntary command ends on it.
- Everything below the chin is moved by corticospinal fibers (the face uses corticobulbar fibers to cranial nerve nuclei).
CheckIs the α motor neuron in the ventral horn an upper or a lower motor neuron?
Lower motor neuron. Its cell body is in the spinal cord (or brainstem nucleus) and its axon leaves the CNS to reach muscle.
Q2. What route does the tract take, level by level, and where does it cross?
| Level | Where the CST sits on a cross-section | Lesion → weakness on |
|---|---|---|
| Internal capsule | Posterior limb (between thalamus and lentiform nucleus) | Contralateral face (lower), arm, leg |
| Midbrain | Middle ⅗ of the cerebral peduncle (crus cerebri), ventral | Contralateral body (± ipsilateral CN III = Weber) |
| Pons | Broken into bundles in the basis pontis (ventral pons) | Contralateral body (± CN VI/VII signs) |
| Medulla | Pyramids (ventral), then cross at the pyramidal decussation | Contralateral body (± ipsilateral tongue CN XII = medial medullary) |
| Spinal cord | Lateral funiculus (lateral CST), synapse on ventral horn α MN | Ipsilateral body below the lesion |
- Route to know cold: motor cortex → posterior limb of internal capsule → cerebral peduncle → pons → medullary pyramids → decussation → lateral CST → LMN in ventral horn.
- The lateral CST is a 2-neuron relay (UMN + LMN) that controls limb movement.
- The internal capsule is a stroke hot-spot:
- Fed by the thin lenticulostriate branches of the MCA.
- Infarct → contralateral hemiparesis (still above the decussation).
CheckA lesion in the left lateral funiculus at C6 weakens which side?
The left side (ipsilateral). The fibers have already crossed in the medulla, so in the cord the tract carries commands for the same-side body.
Step 1 HY — lacunar stroke
Pure motor hemiparesis (face, arm and leg equally, no sensory loss) = lacunar infarct of the posterior limb of the internal capsule from hypertensive lipohyalinosis of lenticulostriate arteries. Cortical (MCA surface) strokes give face/arm > leg plus cortical signs (aphasia, neglect).
Memory tool
"C-I-C-P-P-D-L": Cortex → Internal capsule → Cerebral peduncle → Pons → Pyramid → Decussation → Lateral column. Above the D = opposite side; below the D = same side.
Q3. How do you tell an upper motor neuron lesion from a lower motor neuron lesion?
- UMN lesion: the reflex arc in the cord is intact but has lost the brain's descending inhibition → the LMN over-responds → everything goes UP.
- LMN lesion: the arc itself is broken (ventral horn, root, nerve) → muscle has no input → everything goes DOWN.
| Sign | UMN lesion | LMN lesion |
|---|---|---|
| Weakness | Spastic paralysis (after an initial phase of "spinal shock") | Flaccid paralysis |
| Deep tendon reflexes | ↑ Hyperreflexia, clonus | ↓ / absent (areflexia) |
| Tone | ↑ (spasticity, clasp-knife) | ↓ (hypotonia) |
| Babinski | Present (upgoing big toe) | Absent (toes down) |
| Atrophy | Mild (disuse only) | Marked |
| Fasciculations | No | Yes |
CheckWhy does the knee jerk get brisker after a UMN lesion but disappear after an L4 root lesion?
UMN lesion: arc intact, descending inhibition lost → hyperreflexia. L4 root lesion: the afferent/efferent limb of the arc itself is cut → hypo/areflexia.
Step 1 HY — UMN vs LMN diseases
- ALS: UMN + LMN signs together (spastic, hyperreflexic limbs with atrophy and fasciculations); no sensory loss. Riluzole.
- Polio / spinal muscular atrophy: pure LMN (ventral horn) → flaccid, areflexic, fasciculating.
- Babinski is normal in infants (up to ~1 yr) because the corticospinal tract is not yet fully myelinated.
- Acute cord injury: first spinal shock (flaccid, areflexic) for days–weeks, then UMN signs emerge.
Step 1 trap
Atrophy alone does not mean LMN: long-standing UMN weakness causes mild disuse atrophy. The discriminators are fasciculations, reflexes, tone and Babinski. Also, the acute flaccid phase after a cord injury is spinal shock, not an LMN lesion.
Buzzwords
"clasp-knife" / velocity-dependent tone → UMN spasticity"upgoing toe" → Babinski, UMN"fasciculations + atrophy" → LMN"pure motor hemiparesis" → lacune, posterior limb IC
ApplyLO 1 application questions
A1A 66-year-old with long-standing hypertension wakes with weakness of the right face, arm and leg, brisk right reflexes and a right Babinski sign. Sensation is normal. Where is the lesion?
Left posterior limb of the internal capsule (lacunar infarct). UMN pattern, contralateral, face + arm + leg equally, no sensory or cortical signs → lenticulostriate lacune above the decussation.
A2A man has wasting and twitching of the left hand intrinsics, an absent left triceps reflex, and brisk reflexes with an upgoing toe in both legs. What two neuron types are affected?
LMN at the cervical level (hand) + UMN for the legs. Mixed UMN/LMN with no sensory loss → think ALS (or a cervical cord lesion compressing ventral horn + descending CST).
A3Predict: a tumor compresses the left medullary pyramid just above the decussation. Which limbs are weak, and what reflex change do you expect?
Right arm and leg; hyperreflexia with a right Babinski (once the acute phase passes). Above the crossing → contralateral UMN signs.
LO 2Proprioceptors & their afferent fibersSpindle (stretch) vs Golgi tendon organ (tension); Ia, II, Ib.
By the end: you can draw a muscle with a spindle in parallel and a GTO in series, label Ia, II, Ib, α and γ, and match each fiber to its skin-nerve equivalent and speed.
Q1. What are the fiber classes, and which ones carry proprioception?
- DRG neurons send axons of different thickness. Thicker + more myelin = faster.
- Skin nerves use letters (Aα, Aβ, Aδ, C); muscle nerves use Roman numerals (I, II, III, IV). Same sizes, two naming systems.
- Muscle proprioception rides on Group I and II fibers: Ia and II from the spindle, Ib from the Golgi tendon organ.
| Skin name | Muscle name | Diameter / speed | Carries |
|---|---|---|---|
| Aα | Group I (Ia, Ib) | Thickest (13–20 µm), fastest (80–120 m/s) | Proprioception: spindle (Ia), Golgi tendon organ (Ib) |
| Aβ | Group II | Thick, myelinated (6–12 µm, 35–75 m/s) | Spindle length (II); touch/pressure from skin |
| Aδ | Group III | Thin, lightly myelinated (1–5 µm, 5–30 m/s) | Fast (sharp) pain, cold |
| C | Group IV | Unmyelinated (0.2–1.5 µm, 0.5–2 m/s) | Slow (burning) pain, warmth, itch |
CheckWhich fiber drives the withdrawal reflex when you step on a tack, and which drives the knee jerk?
Withdrawal: Aδ (fast pain). Knee jerk: Ia (spindle).
Memory tool
Biggest numbers are slowest: I is the fastest "first class" fiber, IV (C) is the slow back-of-the-bus fiber. "Alpha is the A-team; C is the Crawler."
Q2. What is a muscle spindle, and what do Ia and II endings each report?
- A muscle has two kinds of fibers:
- Extrafusal fibers = the ordinary working skeletal muscle → innervated by α motor neurons.
- Intrafusal fibers = tiny fibers inside a capsule = the muscle spindle → innervated (at their contractile ends) by γ motor neurons.
- The spindle lies in parallel with the extrafusal fibers → when the muscle is stretched, the spindle is stretched too → its afferents fire. Spindle = stretch (length) detector.
- Two types of sensory endings wrap the intrafusal fibers:
- Annulospiral (primary) endings → Group Ia: coil around the middle of nuclear bag and chain fibers; fire during the dynamic phase (rate of stretch).
- Flower-spray (secondary) endings → Group II: fire in proportion to static length (more stretch → more firing).
- Ia/II afferents also send collaterals up the dorsal columns → DCML damage removes spindle input from conscious position sense.
CheckYou pull a muscle quickly to a new length and hold it there. Which ending bursts during the pull, and which keeps firing during the hold?
Ia (annulospiral) bursts during the pull (rate of change); II (flower-spray) keeps firing during the hold (static length).
Q3. What is the Golgi tendon organ, and how is it different from the spindle?
- The Golgi tendon organ (GTO) sits in the tendon, at the muscle–tendon junction, in series with the muscle fibers.
- When the muscle contracts, it pulls on the tendon → collagen strands squeeze the nerve endings → Group Ib fires. GTO = tension (contraction) detector.
- It has no efferent (motor) supply of its own.
| Feature | Muscle spindle | Golgi tendon organ |
|---|---|---|
| Location | Inside the muscle belly, parallel to extrafusal fibers | Tendon, in series with muscle |
| Detects | Stretch (length + rate of change) | Tension / active contraction |
| Afferent | Ia (annulospiral) + II (flower-spray) | Ib |
| Efferent control | γ motor neurons (set sensitivity) | None |
| Reflex | Stretch (myotatic) reflex → same muscle contracts | Inverse myotatic / autogenic inhibition → same muscle relaxes |
| During active contraction | Unloaded (goes slack) unless γ co-activated | Fires strongly |
CheckDuring a strong voluntary contraction, which receptor's firing rises sharply even without any γ drive?
The GTO (Ib). It is in series, so it feels the force. The spindle, in parallel, would go slack as the muscle shortens.
Step 1 HY
- GTO → Ib → inhibitory interneuron → relaxes the same muscle (autogenic inhibition, "inverse myotatic reflex"): protects the tendon from excessive force. Contributes to the clasp-knife phenomenon in spasticity (resistance suddenly gives way).
- Spindle sensitivity is reset by γ motor neurons; increased γ drive is one contributor to spasticity after UMN lesions.
Step 1 trap
Don't flip them: stretch → spindle, tension → GTO. A question that describes "sudden relaxation when straining" is the GTO/Ib, not the spindle. And γ motor neurons go to the spindle, never to the GTO.
Memory tool
Spindle = Stretch = Side-by-side (parallel). Golgi = Grip force = in a line (series), like a link in a chain. "Ia = Initial (dynamic) burst; II = It's still stretched."
Buzzwords
"intrafusal" → spindle, γ MN"annulospiral" → Ia"flower-spray" → II"in series with the tendon" → GTO, Ib"nuclear bag / chain" → spindle fiber types
Image drill · Michigan SecondLook
How to use: name what you see, then tap the card to check. Images credited to the Michigan SecondLook Anki Deck (University of Michigan Medical School).
1 · What is inside the green dashed capsule? (tap for answer)
Muscle spindle: a connective-tissue capsule (green) around small intrafusal fibers (blue outline in the answer image). The large surrounding fibers are extrafusal fibers (ordinary skeletal muscle, purple).
It is a stretch receptor lying in parallel with the extrafusal fibers: it signals muscle length and rate of stretch via group Ia (and II) afferents.
It is a stretch receptor lying in parallel with the extrafusal fibers: it signals muscle length and rate of stretch via group Ia (and II) afferents.
Image: Michigan SecondLook Anki Deck · SecondLook Neuroanatomy (Michigan Virtual Microscopy Slide Collection), University of Michigan Medical School · CC BY-NC-SA 4.0
ApplyLO 2 application questions
A1A weightlifter holds a maximal load; suddenly his arm "gives way" and relaxes. Which receptor and fiber explain this?
Golgi tendon organ → Ib. High tension activates Ib → inhibitory interneuron → α MN of the same muscle inhibited (autogenic inhibition).
A2A toxin selectively destroys γ motor neurons. Predict what happens to spindle Ia firing during a voluntary contraction.
Ia firing falls silent ("spindle unloading"). Without γ drive the intrafusal fibers go slack as the muscle shortens, so the CNS loses length feedback and tone drops.
A3A demyelinating neuropathy that preferentially hits large fibers will impair which two bedside tests first?
Deep tendon reflexes and vibration/position sense. Both depend on large myelinated Ia/II (Aα/Aβ) fibers; pain and temperature (Aδ, C) are relatively spared.
LO 3Conscious proprioception: body & face → cortexDCML for the body; main sensory nucleus of V for the face.
By the end: you can draw the 3-neuron DCML and trigeminal (main sensory) pathways, name each nucleus, and state where each one crosses.
Q1. Which pathway carries conscious position sense from the body, and how is it wired?
- Conscious proprioception (joint position, movement = "kinesthesia") travels with fine touch, pressure and vibration in the dorsal column–medial lemniscus (DCML). It is a 3-neuron relay.
1st orderDRG neuron; axon enters cord and ascends ipsilaterally in the dorsal column (gracilis = leg, medial; cuneatus = arm, lateral)
→
2nd orderNucleus gracilis / cuneatus (caudal medulla) → axons cross as internal arcuate fibers
→
Medial lemniscusascends through medulla, pons, midbrain (contralateral)
→
3rd orderVPL of thalamus → posterior limb IC → S1 (postcentral gyrus)
CheckIn the spinal cord, is the DCML carrying information from the same or the opposite side of the body?
Same side (ipsilateral). It does not cross until the caudal medulla.
Q2. How does conscious position sense from the face reach the cortex?
- Facial expression muscles have few or no spindles, so facial "proprioception" travels with facial touch in the trigeminal system.
- Where each pathway crosses: DCML in the medulla (internal arcuate fibers); face pathway after the main sensory nucleus, in the pons.
1st orderCell body in trigeminal ganglion; axon enters pons in CN V
→
2nd orderMain (principal) sensory nucleus of V in the pons → crosses
→
VTTTventral trigeminothalamic tract ascends contralaterally
→
3rd orderVPM of thalamus → face area of S1
CheckWhich thalamic nucleus is the 3rd-order neuron for the face, and which for the body?
Face → VPM ("M for Mouth/Mug"); body → VPL.
Step 1 HY
- Bedside test of conscious proprioception = joint position sense (big toe up/down, eyes closed) and the Romberg test; vibration uses a 128-Hz tuning fork.
- Medial lemniscus lies next to the CST in the medial medulla → medial medullary syndrome (anterior spinal artery): contralateral hemiparesis + contralateral loss of position/vibration + ipsilateral tongue deviation.
Step 1 trap
The main (principal) sensory nucleus handles facial touch/conscious position; the spinal trigeminal nucleus handles facial pain and temperature; the mesencephalic nucleus handles jaw-muscle spindle input. Don't swap them.
Memory tool
"Gracilis = Ground (legs), medial; Cuneatus = Ceiling (arms), lateral." "Internal Arcuate = Across."
ApplyLO 3 application questions
A1A small infarct destroys the right VPL. With eyes closed, which side's toe position does the patient misjudge?
Left. VPL is 3rd order, after the medullary crossing, so it carries the contralateral body.
A2A lesion of the left medial lemniscus in the pons: which side loses position sense, and is the face affected?
Right body loses position/vibration sense. The face is largely spared (it rides in the nearby VTTT, which may be involved if the lesion is larger).
A3Predict: why is the right fasciculus cuneatus absent from a section of the lumbar cord?
Cuneatus carries T6 and above, so it is only added in the upper thoracic and cervical cord. In the lumbar cord the dorsal column is all gracilis.
LO 4Non-conscious proprioception → cerebellumCuneocerebellar, dorsal & ventral spinocerebellar, mesencephalic V.
By the end: for each tract you can state the body region, the 2nd-order nucleus, whether it crosses, and which cerebellar peduncle it uses.
Q1. What is non-conscious proprioception, and what rule makes it different from the DCML?
- Proprioceptive information sent to the cerebellum, which uses it to adjust balance, posture and movement. We are unaware of it.
- 2-neuron relay (DRG → 2nd-order nucleus → cerebellum, no thalamus).
- The cerebellum works ipsilaterally: the right cerebellum handles the right body. Every spinocerebellar route ends on the same side it started, even the one that crosses twice.
| Conscious (DCML) | Non-conscious (spinocerebellar) | |
|---|---|---|
| Destination | Somatosensory cortex (via VPL) | Cerebellum |
| Neurons | 3 | 2 |
| Side | Crosses (medulla) → contralateral cortex | Ends ipsilateral |
| Awareness | Yes: "where is my toe?" | No: automatic coordination |
CheckProprioception from the left leg ends up in which cerebellar hemisphere?
Left. Non-conscious proprioception always ends ipsilaterally.
Q2. How does each spinocerebellar tract run?
- Clarke's nucleus (nucleus dorsalis) is a column of cells in the medial base of the dorsal horn (lamina VII) that exists only from C8 to L2. Its presence or absence decides which tract a fiber uses.
- Net result: cerebellar information is ipsilateral for the body (dorsal and cuneocerebellar tracts never cross; the ventral tract crosses twice).
| Tract | Region / receptors | 2nd-order nucleus | Crossing | Peduncle |
|---|---|---|---|---|
| Dorsal (posterior) spinocerebellar | Lower body & leg; spindles + GTOs | Clarke's nucleus (C8–L2). Afferents entering below L2 climb in the fasciculus gracilis to reach it | Uncrossed: ascends ipsilaterally in the lateral funiculus | Inferior (restiform body) |
| Cuneocerebellar | Upper body & arm (above C8) | Accessory (lateral) cuneate nucleus in the medulla; 1st-order axons get there via the fasciculus cuneatus | Uncrossed | Inferior |
| Ventral (anterior) spinocerebellar | Lower body; mainly GTOs | Spinal border cells at the base of the dorsal horn | "Double crossed": crosses in the anterior white commissure, ascends contralaterally, crosses back in the cerebellum | Superior |
| Face (mesencephalic V) | Jaw (masticatory) muscle spindles | Mesencephalic nucleus of V (midbrain); see Q3 | Uncrossed | Mainly superior |
CheckWhy doesn't the arm use the dorsal spinocerebellar tract?
Clarke's nucleus is absent above C8. Arm afferents ascend in the fasciculus cuneatus to the accessory cuneate nucleus in the medulla instead (cuneocerebellar tract), which is the "upper-limb version" of Clarke's.
Step 1 HY — peduncles
| Peduncle | Main traffic |
|---|---|
| Inferior (ICP, restiform body) | In: dorsal spinocerebellar, cuneocerebellar, olivocerebellar (climbing fibers), vestibulocerebellar |
| Middle (MCP) | In: pontocerebellar (cortex → pontine nuclei → contralateral cerebellum) |
| Superior (SCP) | Out: dentate → red nucleus/VL thalamus (main output). In: ventral spinocerebellar (the exception) |
Step 1 trap
"Crosses" does not mean "contralateral cerebellum." The VSCT crosses twice, so it still delivers ipsilateral body information. Also, the cuneocerebellar 2nd-order nucleus is the accessory (lateral/external) cuneate nucleus, not the nucleus cuneatus of the DCML.
Memory tool
"Ventral = V-shaped path: down-across-up-across" (double crossed) and "Ventral goes up top (superior)". Everything else enters "Inferior = Ipsilateral and Immediate."
Buzzwords
"nucleus dorsalis, C8–L2" → Clarke's → DSCT"restiform body" → inferior cerebellar peduncle"double crossed" → VSCT, SCP"accessory cuneate" → cuneocerebellar
Q3. How does position sense from the face reach the cerebellum?
- The mesencephalic nucleus of V (midbrain, alongside the periaqueductal gray) carries non-conscious proprioception from the face/jaw to the cerebellum.
- It is unique: its cells are pseudounipolar primary sensory neurons whose cell bodies sit inside the CNS rather than in a ganglion. In effect it is a "DRG living in the brainstem."
- It receives spindle afferents from the muscles of mastication (and periodontal stretch receptors) and also projects to the motor nucleus of V → the jaw-jerk reflex (CN V in, CN V out).
ReceptorMasseter / temporalis spindle
→
Mesencephalic n. Vprimary cell body in the midbrain
→
Cerebellumnon-conscious
+
Motor n. Vjaw jerk
CheckWhere are the cell bodies of the afferent limb of the jaw-jerk reflex?
Mesencephalic nucleus of V (midbrain), not the trigeminal ganglion.
Step 1 HY
The mesencephalic nucleus is the only place where primary sensory neuron cell bodies live inside the CNS. A brisk jaw jerk points to an UMN lesion above the pons (e.g., bilateral corticobulbar disease, pseudobulbar palsy); a normal jaw jerk with brisk limb reflexes points below the pons (e.g., cervical myelopathy).
ApplyLO 4 application questions
A1A mass compresses the right superior cerebellar peduncle. Which ascending proprioceptive tract is interrupted, and from which side of the body?
Ventral spinocerebellar tract, carrying the right lower body (its fibers ascended on the left, enter via the right SCP, and cross back into the right cerebellum). The SCP also carries major cerebellar output, so expect ipsilateral limb ataxia.
A2Predict: a lesion destroys Clarke's nucleus bilaterally at T4–T10. Whose non-conscious proprioception is lost, and whose is spared?
Lower body/leg input through the DSCT is lost; arm input is spared (cuneocerebellar via the accessory cuneate nucleus). The VSCT still carries some lower-body GTO information.
A3A section shows a lightly stained nucleus at the medial base of the dorsal horn. What level of the cord is this likely from?
C8–L2 (usually thoracic): that is Clarke's nucleus.
LO 5Spinal reflexes: stretch, withdrawal, crossed extensorThe wiring and the logic of each arc.
By the end: you can trace each reflex from receptor to muscle, count its synapses, explain reciprocal inhibition and α–γ co-activation, and give the root level for each bedside reflex.
Q1. What is a spinal reflex?
- An involuntary, instantaneous response to a stimulus.
- Mediated through the spinal cord; it does not need the brain (the brain only modulates it).
- Basic unit: afferent sensory neuron → (± interneurons) → efferent α motor neuron → muscle.
- Three you must know: stretch (myotatic), flexion (withdrawal), crossed extensor.
Q2. How does the knee jerk (stretch / myotatic reflex) work?
StretchTap patellar tendon → quadriceps stretched
→
Spindleintrafusal fibers stretched → Ia fires
→
Ia → cordcell body in DRG; excitatory synapse on homonymous α MN
→
Contractsame muscle contracts → leg kicks
- Monosynaptic: only one synapse (2 neurons: Ia afferent + α MN). It is the simplest segmental reflex.
- Homonymous = the α MN that supplies the same muscle the spindle sits in.
- Reciprocal inhibition: an Ia collateral excites an inhibitory interneuron (glycine) → inhibits the α MN of the antagonist (hamstrings) so it relaxes and doesn't fight the kick.
- Ia/II collaterals also ascend in the dorsal columns (conscious) and feed the spinocerebellar tracts (non-conscious).
- Full sequence: stretch → spindle → Ia fires → Ia synapses on α MN (and on the γ MN via an excitatory interneuron) → α contracts extrafusal fibers + γ contracts intrafusal fibers → spindle no longer detects extra stretch → reflex ends.
CheckHow many neurons and how many synapses are in the core stretch-reflex arc? How many in the reciprocal-inhibition branch?
Core arc: 2 neurons, 1 synapse (monosynaptic). Reciprocal inhibition: 3 neurons, 2 synapses (Ia → inhibitory interneuron → antagonist α MN).
Q3. Why are γ motor neurons co-activated, and what happens without them?
- When the extrafusal muscle shortens, the parallel spindle would go slack → Ia goes silent → the CNS goes "blind" to length mid-movement.
- γ motor neurons contract the ends of the intrafusal fibers, re-tightening the central region → the spindle stays taut and keeps reporting.
α firesextrafusal fibers shorten
+
γ firesintrafusal poles contract
→
Spindle stays tautIa keeps firing
→
Continuous feedbacktone and smooth control maintained
CheckWhat happens to muscle tone if γ co-activation is lost?
Tone decreases, because spindle feedback drops out during contraction.
Step 1 HY
- Boards phrase it as α–γ co-activation driven by descending (UMN) commands: the brain fires α and γ together during voluntary movement.
- Renshaw cells: α MN collaterals excite these ventral-horn interneurons, which release glycine to inhibit the same α MN (recurrent inhibition). Tetanus toxin blocks glycine/GABA release from Renshaw and other inhibitory interneurons → spastic paralysis, trismus, risus sardonicus. Strychnine blocks glycine receptors.
Step 1 trap
Reciprocal inhibition requires an interneuron. Primary afferents are always excitatory (glutamate); a sensory fiber can never directly inhibit a motor neuron.
Q4. Which stretch reflexes are tested at the bedside, and at what levels?
| Reflex (muscle) | In-house level | Boards "single root" |
|---|---|---|
| Jaw jerk (masseter) | CN V | CN V (in and out) |
| Muscles of facial expression | CN VII | (not a routine board reflex) |
| Biceps | C5, C6 | C5 |
| Brachioradialis | C5, C6 | C6 |
| Triceps | C7 | C7 |
| Finger flexors | C8 | C8 |
| Quadriceps (knee jerk / patellar) | L2, L3, L4 | L4 (L3–L4) |
| Gastrocnemius–soleus (ankle jerk / Achilles) | S1 | S1 |
| Grade | 0 | 1+ | 2+ | 3+ | 4+ |
|---|---|---|---|---|---|
| Meaning | Absent | Hypoactive | Normal | Brisk / hyperactive | Clonus |
CheckA disc herniation abolishes the ankle jerk. Which root?
S1 (typically an L5–S1 disc).
Memory tool
Count up from the foot: "S1, 2 buckle my shoe (Achilles); 3, 4 kick the door (patellar); 5, 6 pick up sticks (biceps/brachioradialis); 7, 8 lay them straight (triceps)."
Step 1 HY — hypo vs hyperreflexia
- Hyporeflexia/areflexia: LMN lesion, radiculopathy, peripheral neuropathy (diabetic: ankle jerks lost first, length-dependent), Guillain–Barré, tabes dorsalis, hypothyroidism (slow relaxation phase).
- Hyperreflexia, clonus, Babinski: UMN lesion (stroke, MS, cord compression, ALS, B12 deficiency).
- Jendrassik maneuver: have the patient hook fingers and pull (or clench teeth) to reinforce a weak reflex before calling it absent.
- Superficial reflexes: cremasteric L1–L2, anal wink S3–S4.
Step 1 trap
A reduced reflex in a nervous patient is not "absent" until reinforced (Jendrassik). And a few beats of ankle clonus that fade can be normal; sustained clonus is UMN.
Q5. How do the withdrawal and crossed extensor reflexes work?
- Flexion (withdrawal) reflex: step on a tack → cutaneous Aδ (fast pain) fibers → excitatory interneurons (spread over several segments) → α MNs of flexors fire; inhibitory interneurons silence the extensors → the limb pulls away. Polysynaptic, ipsilateral.
- Crossed extensor reflex: the same Aδ input reaches interneurons that cross in the anterior white commissure → in the opposite leg they excite extensors and inhibit flexors → that leg stiffens to bear the body's weight and keep balance.
| Reflex | Afferent | Synapses | Effect |
|---|---|---|---|
| Stretch (myotatic) | Ia (spindle) | Monosynaptic onto homonymous α MN | Stretched muscle contracts; antagonist inhibited |
| Flexion (withdrawal) | Aδ (pain) | Polysynaptic, ipsilateral | Ipsilateral flexors contract, extensors relax |
| Crossed extensor | Aδ (pain) | Polysynaptic, crosses in AWC | Contralateral extensors contract, flexors relax |
| Inverse myotatic (GTO) | Ib | Disynaptic (inhibitory interneuron) | Same muscle relaxes |
CheckWhy must the withdrawal reflex be polysynaptic?
Interneurons let one input spread across several segments (whole-limb withdrawal), switch signs (excite flexors, inhibit extensors) and cross to the other side (crossed extensor). A single synapse can do none of that.
Buzzwords
"monosynaptic" → stretch reflex (Ia)"homonymous motor neuron" → same muscle"reciprocal inhibition" → antagonist relaxes"steps on a nail, other leg stiffens" → crossed extensor"autogenic inhibition" → GTO, Ib
Step 1 trap
The withdrawal reflex is driven by Aδ pain fibers, not Ia. The anterior white commissure is also where spinothalamic fibers cross, so a central cord lesion (syrinx) can hit both.
ApplyLO 5 application questions
A1Tapping the patellar tendon makes the quadriceps contract and the hamstrings relax. Name the transmitter at each central synapse.
Ia → quadriceps α MN: glutamate (excitatory). Inhibitory interneuron → hamstring α MN: glycine. Reciprocal inhibition needs that extra interneuron.
A2A diabetic patient has absent ankle jerks but normal knee jerks and stocking numbness. Explain.
Length-dependent peripheral neuropathy: the longest fibers (to the feet, S1 arc) fail first, breaking the Achilles reflex arc while the shorter L3–L4 arc survives.
A3Predict: a child steps on glass with the right foot. Describe all four muscle groups' responses.
Right flexors contract, right extensors relax (withdrawal); left extensors contract, left flexors relax (crossed extensor), via interneurons crossing in the AWC.
A4Three months after a cervical cord injury, tapping the Achilles tendon produces 8 rhythmic beats of plantarflexion. Grade and meaning?
4+ (sustained clonus) → UMN lesion. The S1 arc is intact but released from descending inhibition.
LO 6Predicting proprioceptive deficits from lesionsDorsal columns, spinocerebellar systems, hemisection.
By the end: given a lesion site, you can predict which position-sense deficits occur and on which side; given a pattern of deficits, you can find the lesion.
Q1. Where do the tracts sit in a cord cross-section?
Q2. What happens when the dorsal columns are damaged?
- Symptoms are ipsilateral to the damaged column, in the dermatomes at and below the lesion (the DCML has not crossed yet).
- Loss of tactile sense: vibration, deep touch, 2-point discrimination → can't identify/describe an object in the hand (astereognosis).
- Loss of kinesthetic sense (position and movement) → movements are clumsy and uncoordinated (sensory ataxia), worse in the dark or with eyes closed.
- Tabes dorsalis (late neurosyphilis, Treponema pallidum) is the classic dorsal-column disease:
- Appears ~20 years after infection, in about 30% of untreated patients.
- Spirochetes invade the large myelinated fibers → degeneration of the DCML (dorsal roots + dorsal columns).
- Signs: positive Romberg, abnormal (stomping) gait, numbness of toes, feet and legs.
- Treatable with penicillin. The Tuskegee study (1932–1972) withheld this known treatment from Black men with syphilis: a landmark failure of research ethics.
- Positive Romberg: balance needs 2 of 3 inputs (vision, vestibular, conscious proprioception). Patient is steady with eyes open, sways or falls with eyes closed.
CheckOnly the lateral part of the right dorsal column is damaged at C4. What is lost?
The fasciculus cuneatus → vibration, fine touch and position sense of the right arm/upper trunk (ipsilateral). The legs (gracilis, medial) are spared.
Step 1 HY — posterior cord diseases
| Disease | Cause | Tracts | Clues |
|---|---|---|---|
| Tabes dorsalis | Tertiary syphilis | Dorsal columns + dorsal roots | Romberg +, stomping gait, lightning pains, areflexia, Argyll Robertson pupil, Charcot joints |
| Subacute combined degeneration | Vitamin B12 (or copper) deficiency | Dorsal columns + lateral CST (+ spinocerebellar) | Vibration/position loss + spastic legs + Babinski; ↑ MMA |
| Friedreich ataxia | GAA repeat, frataxin (chr 9), AR | Spinocerebellar + dorsal columns + lateral CST + DRG | Teen with ataxia, absent DTRs, Babinski, pes cavus, kyphoscoliosis, hypertrophic cardiomyopathy, diabetes |
Step 1 trap — Romberg
A positive Romberg means sensory (proprioceptive) ataxia: stable with eyes open, unstable with eyes closed. Cerebellar ataxia is unsteady even with eyes open, so Romberg is not "positive" in the classic sense. Romberg tests standing balance, not limb coordination.
Buzzwords
"stomping gait, worse in the dark" → dorsal column / sensory ataxia"pupil accommodates but doesn't react" → Argyll Robertson, tabes"wide-based, eyes-open ataxia" → cerebellar"cannot identify a key in the hand" → astereognosis, DCML
Q3. What happens when non-conscious proprioception is lost?
- Pure lesions confined to the spinocerebellar tracts have not been reported (they sit on the cord rim next to other tracts).
- But damage to the spinocerebellar regions of the cerebellum or to the cerebellar peduncles causes a wide, broad-based gait and loss of muscle tone (hypotonia), on the ipsilateral side.
- Key contrast: patient is aware of where the limb is (DCML intact) but movements are poorly coordinated.
| Lesion site | Conscious position sense (DCML) | Non-conscious (to cerebellum) |
|---|---|---|
| Dorsal column, spinal cord | Lost ipsilateral, at/below lesion | Mostly spared (DSCT/VSCT are lateral); below-L2 leg fibers climbing in gracilis to Clarke's may be hit |
| Lateral funiculus, spinal cord | Spared | DSCT (ipsilateral) and VSCT (contralateral fibers) hit; usually masked by CST signs |
| Medial lemniscus, pons/midbrain | Lost contralateral | Spared (already in cerebellum) |
| Inferior cerebellar peduncle | Spared | DSCT + cuneocerebellar lost → ipsilateral ataxia |
| Superior cerebellar peduncle | Spared | VSCT input lost; plus major cerebellar output → ipsilateral ataxia |
CheckLesion of the left medial lemniscus in the pons: is non-conscious proprioception from the right leg affected?
No. Spinocerebellar fibers have already entered the cerebellum (ICP in the medulla) or travel separately (VSCT to the SCP).
Q4. How do you solve the classic hemisection (Brown-Séquard) case?
- Hemisection = one half of the cord is cut. Use the crossing rules:
- DCML crosses in the medulla → loss of touch, vibration, position on the same side.
- Lateral CST crossed in the medulla → same-side UMN weakness (spastic, hyperreflexic, Babinski) below the lesion.
- Spinothalamic crosses in the cord (AWC) within 1–2 segments → opposite-side pain and temperature loss, starting 1–2 levels below.
- At the lesion level: ipsilateral LMN signs and ipsilateral loss of all sensation in that dermatome.
Ladder fall: LEFT leg
No motor control · exaggerated reflexes (UMN) · can't feel Q-tip (DCML) · can feel pin-prick and hot/cold
Ladder fall: RIGHT leg
Normal motor and reflexes · can feel Q-tip · can't feel pin-prick or hot/cold (spinothalamic from the left cord, already crossed)
Answer
Left hemisection of the cord at L1 (Brown-Séquard). Motor + DCML loss is on the lesion side; pain/temp loss is opposite.
CheckWhy is the answer not "a right dorsal column lesion"?
A right dorsal column lesion would cause right touch/position loss only, with no motor or pain/temp findings. The ladder patient has left touch loss + left UMN weakness + right pain/temp loss → a left hemisection.
Step 1 HY — cord syndromes
- Anterior spinal artery infarct: everything lost (motor, pain/temp) except dorsal columns → vibration/position spared.
- Posterior spinal artery / dorsal columns: only vibration/position lost.
- Syringomyelia: AWC → bilateral "cape" pain/temp loss; touch spared.
- Brown-Séquard: ipsilateral DCML + motor, contralateral pain/temp.
Memory tool
"DCML and CST cross in the Medulla → lesion below the medulla is the Same side. Spinothalamic crosses in the Spine → Swapped side." Whichever leg can't feel pin-prick is the opposite side from the lesion.
Image ID drillName what you see
Image 1: which disease, which tracts?
Tabes dorsalis. The dorsal columns (between the dorsal horns, top) are pale = demyelinated/degenerated; dorsal roots also affected.
Image 2: arrow and green tracts?
Arrow = Clarke's nucleus (C8–L2). Light green = dorsal spinocerebellar (ICP, uncrossed). Dark green = ventral spinocerebellar (SCP, double crossed).
Image 3: outlined lesion?
Hemisection → Brown-Séquard syndrome: ipsilateral DCML + UMN signs, contralateral pain/temperature.
ApplyLO 6 application questions
A1A man damages the left dorsal column at the L1 cord level. What is lost and where?
Vibration, fine touch and position sense from L1 down on the left. The DCML stays uncrossed until the caudal medulla.
A2A 58-year-old vegan has paresthesias, loss of vibration in both feet, a positive Romberg, spastic legs and bilateral Babinski signs. Which tracts and why?
Dorsal columns + lateral corticospinal tracts (subacute combined degeneration, B12 deficiency). Sensory ataxia (Romberg) plus UMN signs.
A3A patient falls when she washes her face in the shower with eyes closed, but walks steadily in a lit room. Is this cerebellar or sensory ataxia?
Sensory ataxia (dorsal columns). Vision compensates for lost proprioception; closing the eyes removes the second input (positive Romberg).
A4Predict: a stab wound hemisects the right side of the cord at T8. Map the deficits.
Right leg: UMN weakness, hyperreflexia, Babinski, loss of vibration/position. Left side from ~T10 down: loss of pain/temperature. At T8 on the right: band of total sensory loss ± LMN signs.
MCQPractice questionsClick an answer to see the explanation.
Score: 0 / 0
1A 64-year-old man with poorly controlled hypertension develops sudden weakness of the right side of the face, right arm and right leg. Right-sided reflexes are 3+ with an upgoing right toe. Sensation, language and visual fields are normal. Which structure is most likely infarcted?
B. Pure motor hemiparesis of face, arm and leg with UMN signs and no cortical signs = lacunar infarct of the contralateral posterior limb of the internal capsule (lenticulostriate branches). A: medial precentral gyrus (ACA territory) gives mainly leg weakness. C: wrong side. D: a cord lesion causes ipsilateral weakness and spares the face. E: a right pyramid lesion would give left-sided weakness.
2A 45-year-old woman has 4 months of progressive weakness of the left hand. Exam shows wasting of the intrinsic hand muscles with visible twitching and an absent left finger-flexor reflex. Sensation is normal. Which additional finding is most consistent with the lesion type affecting her hand?
D. Atrophy, fasciculations and areflexia = LMN lesion (C8 ventral horn/root), which also produces hypotonia. A, B, C and E are UMN signs (Babinski, spasticity, clonus, hyperreflexia).
3A patient with a hereditary neuropathy that selectively destroys the largest, fastest-conducting myelinated afferents has absent knee jerks, but pain and temperature sensation are normal. Loss of which afferent class best explains the absent reflex?
C. The afferent limb of the stretch reflex is the Ia (annulospiral) spindle afferent, the thickest and fastest class (Aα equivalent). Aδ/Group III and C carry pain and temperature (preserved here). γ efferents are motor, not afferent.
4During a maximal arm-wrestling effort, a competitor's biceps suddenly relaxes and his arm drops, although he is not fatigued. Activation of which receptor and afferent is most responsible?
E. The GTO lies in series in the tendon and senses tension. High force → Ib → inhibitory interneuron → relaxation of the same muscle (autogenic inhibition, inverse myotatic reflex). A and B are spindle afferents that signal stretch and excite the same muscle. C and D are cutaneous receptors.
5When the patellar tendon is tapped, the quadriceps contracts and the hamstrings relax. Which mechanism produces the hamstring relaxation?
A. Reciprocal inhibition: an Ia collateral excites an inhibitory (glycine) interneuron onto the antagonist's α MN. B: primary afferents are always excitatory. C: Renshaw cells provide recurrent inhibition of the α MN that drives them. D: the hamstring tendon is not loaded by the tap. E: the reflex is spinal and too fast for cortical involvement.
6A barefoot child steps on broken glass with the right foot. The right leg flexes while the left leg extends to support her weight. The interneurons that produce the left-leg response cross the midline in which structure?
D. The crossed extensor reflex uses commissural interneurons that cross in the anterior white commissure of the cord. A and B are medullary crossings (CST and DCML). C is a midbrain commissure (pupillary pathways). E links the cerebral hemispheres; the reflex needs no brain.
7In an experimental animal, γ motor neurons to the soleus are selectively silenced while α motor neurons remain intact. During a voluntary contraction of the soleus, what happens to Ia afferent firing from soleus spindles?
B. The spindle is in parallel; as the muscle shortens it unloads. Without γ co-activation to tighten the intrafusal poles, Ia firing pauses and length feedback (and tone) is lost. C confuses the spindle with the GTO. D: GTO activity travels in Ib, not Ia. E is not a thing.
8A 52-year-old man reports that his left foot feels "like it belongs to someone else." With eyes closed he cannot tell whether his left great toe is moved up or down, and a tuning fork is not felt on the left foot. Pinprick and temperature are normal on both sides, strength and reflexes are normal. Which lesion best explains these findings?
E. Loss of position and vibration in the left foot with nothing else = left dorsal column (gracilis carries the leg). The DCML is ipsilateral in the cord. A: wrong side. B: pain/temperature pathway. C: non-conscious; the patient would not report loss of position awareness. D: the medial lemniscus has crossed, so a left pontine lesion affects the right body.
9A 61-year-old man has a stamping, wide-based gait, lancinating leg pains and pupils that constrict to near objects but not to light. He stands steadily with eyes open but falls when he closes them. Knee and ankle jerks are absent. Which structures are primarily degenerated?
C. Tabes dorsalis (tertiary syphilis): spirochetes damage large myelinated dorsal root fibers → dorsal column degeneration → sensory ataxia, positive Romberg, lightning pains, areflexia (Ia limb of the arc lost), Argyll Robertson pupils. A and B would give weakness. D: pure spinocerebellar lesions are not reported. E: cerebellar ataxia is unsteady with eyes open.
10A tumor selectively compresses the left superior cerebellar peduncle. Which ascending proprioceptive pathway is most directly interrupted?
A. The VSCT is the only spinocerebellar tract that enters via the superior cerebellar peduncle (after crossing in the AWC, then crossing back). B, C and E enter via the inferior cerebellar peduncle. D goes to the thalamus, not the cerebellum.
11A researcher traces muscle spindle afferents from the forearm. Unlike afferents from the leg, these fibers never synapse in Clarke's nucleus. Where do they synapse to reach the cerebellum?
E. Clarke's nucleus exists only from C8 to L2, so upper-limb afferents ascend in the fasciculus cuneatus to the accessory (lateral) cuneate nucleus → cuneocerebellar tract → ipsilateral ICP. A is the DCML relay for the leg. B is the VSCT origin. C is conscious proprioception. D gives climbing fibers, not proprioceptive relay from the arm.
12A neurologist taps the patient's chin with the mouth slightly open and the jaw closes briskly. The cell bodies of the afferent neurons for this reflex are located in which structure?
D. Jaw-muscle spindle afferents are pseudounipolar neurons whose cell bodies lie in the mesencephalic nucleus, the only primary sensory cell bodies inside the CNS. They also carry non-conscious facial proprioception to the cerebellum. A holds most other trigeminal afferent cell bodies. B and C are 2nd-order nuclei (touch; pain/temperature). E is CN VII.
13After a knife wound to the back, a man cannot move his right leg, which has brisk reflexes and an upgoing toe. He cannot feel vibration in the right foot. He cannot feel pinprick or cold on the left leg. Where is the lesion?
B. Brown-Séquard: the lesion side has UMN weakness and DCML loss (both cross in the medulla), while pain/temperature loss is contralateral (spinothalamic crosses in the cord). A is the mirror image. C spares the dorsal columns. D lacks motor and pain findings. E would affect the right face/arm too and not split sensory modalities by side.
14A 15-year-old boy has a progressive staggering gait, absent ankle and knee jerks, loss of vibration sense in the feet, bilateral extensor plantar responses, high-arched feet and an echocardiogram showing concentric left ventricular hypertrophy. Which genetic finding is most likely?
C. Friedreich ataxia (autosomal recessive): spinocerebellar + dorsal columns + lateral CST + DRG degeneration (hence absent reflexes with Babinski), pes cavus and hypertrophic cardiomyopathy. A: Huntington disease (chorea). B: myotonic dystrophy. D: fragile X. E: spinal muscular atrophy (pure LMN, no sensory loss).