Block 6 · CNS · CNS15 · Rev 1.2 · Updated Oct 23, 2026
CNS15 · Neuroscience · Study Guide
Motor Cortex and Descending Pathways
Learning objectives
- LO 1For each part of the motor cortex (M1, supplementary motor area, lateral premotor cortex, posterior parietal cortex), predict what a small lesion there does, and tell apraxia and neglect apart from true weakness at the bedside.
- LO 2Follow the corticospinal tract from cortex down to the lower motor neuron (internal capsule → cerebral peduncle → pyramid → decussation), and use the internal capsule's body map and blood supply to predict which body parts a capsular stroke will weaken.
- LO 3Compare the four brainstem motor tracts (rubrospinal, vestibulospinal, reticulospinal, tectospinal): where each starts, which muscles it drives, what it does, and how each one shapes posture once corticospinal control is gone.
- LO 4Explain why a hemiplegic patient holds the arm flexed but the leg extended: the red nucleus takes over in the arm, and the vestibular nuclei take over in the leg.
- LO 5Tell decorticate from decerebrate posturing, and place each one above or below the red nucleus.
- LO 6Given an unlabeled motor case, place the lesion in cortex/internal capsule, brainstem, or spinal cord by combining pyramidal vs extrapyramidal signs with the sensory findings, including the split pattern of Brown-Séquard syndrome.
★ Step 1 HY
⚠ Step 1 trap
✎ Memory tool
“ Buzzwords
MAPBig picture
- Plan → SMA + premotor (with parietal spatial map) → command → M1
- Pyramidal route (corticospinal, corticobulbar) → straight to LMNs → fine, voluntary, distal control
- Brainstem routes (rubro-, vestibulo-, reticulo-, tectospinal) → posture · tone · balance · orienting
- Corticospinal cut → surviving brainstem tracts shape the limbs
- Capsular stroke → flexed arm, extended leg
- Brain injury → decorticate (above red nucleus) vs decerebrate (below)
- Bedside pattern → UMN vs LMN · face vs body · sensory loss → where the lesion is
Memory tool — the company analogy
SMA/premotor = the planners, M1 = the CEO who signs the order, corticospinal tract = the express courier (direct, precise), brainstem tracts = the regional managers (keep you upright and toned without asking). Fire the CEO's courier and the managers run things their own way: crude, stiff, and predictable.
LO 1The motor cortex and what each part's lesion looks likeM1 = weakness; SMA, premotor and parietal = can't plan or aim, but strength is normal
By the end: you can name each motor area, say what it does with an everyday example, predict the deficit from a lesion there, and tell apraxia and neglect from paralysis at the bedside.
Q1. Where are the motor areas, and which Brodmann numbers go with them?
- Primary motor cortex (M1) = precentral gyrus, Brodmann area 4; wraps onto the medial surface as the paracentral lobule (leg/foot).
- Premotor areas = Brodmann area 6, just in front of M1:
- Supplementary motor area (SMA) = the medial part (medial surface, ACA territory).
- Lateral premotor cortex (PMC) = the lateral part on the convexity (MCA territory).
- Frontal eye field = area 8, in front of premotor cortex: voluntary saccades to the opposite side.
- Behind the central sulcus but still part of the "motor" team: primary somatosensory cortex (areas 3,1,2) and posterior parietal cortex (areas 5, 7).
Where do the descending axons come from? Layer V pyramidal neurons of M1, premotor and S1. The giant ones in M1 are Betz cells (large, glutamatergic, excitatory).
CheckWhich cortical layer gives rise to corticospinal axons, and what are its biggest neurons called?
Layer V; Betz cells. Layer V is the main output layer of cortex to subcortical targets.
Q2. What does each area do, and what happens when it is damaged?
| Area | Job (with an everyday example) | Lesion → what you see |
|---|---|---|
| Primary motor cortex (M1), area 4 | The executor. Projects directly to LMNs of brainstem and cord. Encodes force, direction, extent and speed of movement. | Contralateral paralysis/weakness (UMN signs) in the body part mapped there. |
| Supplementary motor area (medial premotor) | The internal planner: plans, sequences and times complex, often two-sided movements from memory (piano from memory, typing). | Can't do complex sequences (brushing teeth, tying shoes); can't sequence a plan or describe how to use an object. Strength normal. |
| Lateral premotor cortex | Like SMA but driven by external cues (playing piano by reading music, braking at a red light). Shapes the hand (ventral part) and aims the reach (dorsal part). | Loss of fluency handling objects, can't adjust movement to external cues, can't mimic a movement. Strength normal. |
| Primary somatosensory cortex | Its descending fibers synapse in the DCML nuclei (gracilis/cuneatus) and dorsal horn, tuning incoming sensation to limb position and force. | Contralateral loss of fine touch/position sense; clumsy, poorly-guided movement. |
| Posterior parietal cortex | Merges proprioception (S1) and vision into a spatial map: egocentric (where is my hand vs my shoulder?) and allocentric (where is my hand vs the cup?). | Apraxia (like premotor). Right-sided lesion → left hemispatial neglect (hemineglect). |
Ideaassociation cortex
→
PlanSMA (internal) / PMC (external cue)
→
ExecuteM1 → CST
→
CheckS1 + parietal feedback
CheckA pianist can still play pieces she knows by heart but can't play from new sheet music. Which area?
Lateral premotor cortex. Externally cued movement is lost; internally generated (SMA) sequences are spared.
Memory tool — In vs Out
SMA = Self-generated (inside your head). Premotor (lateral) = Prompted from outside (light, music, a demonstration).
Q3. Apraxia, neglect, or paralysis? How do I tell them apart at the bedside?
Paralysis (M1 / CST)
- Weak on strength testing
- UMN signs: ↑ reflexes, spasticity, Babinski
- Can't do it because muscles won't fire
Apraxia (SMA, PMC, parietal)
- Strength, sensation and understanding intact
- Can't perform a learned, purposeful act on command or by imitation
- Movement possible but poorly planned
Hemineglect (right parietal)
- Strength normal
- Ignores the left side of space and body: eats only the right half of the plate, shaves half the face
- Often denies deficit (anosognosia)
CheckA man with 5/5 strength cannot show you how to comb his hair, either on command or by copying you. Paralysis or apraxia?
Apraxia. Full strength rules out paralysis; the problem is planning a learned act.
Step 1 HY — the homunculus and stroke territory
- Leg/foot = medial surface → ACA stroke → contralateral leg > arm weakness (± SMA apraxia, abulia, urinary incontinence).
- Face, hand, arm = lateral convexity → MCA stroke → contralateral face + arm > leg, + aphasia (dominant) or neglect (nondominant).
- Hand and face/lips get the most cortex (fine control).
Step 1 HY — frontal eye field
Area 8 drives saccades to the opposite side. Destructive lesion (stroke) → eyes look toward the lesion (away from the weak side). Seizure focus → eyes look away from the focus.
Step 1 trap — weakness is not apraxia
If the stem says "strength is normal" but the patient can't do a task, don't pick M1 or internal capsule. Look for SMA (internal sequences), lateral premotor (cued/imitation) or parietal (spatial). Neglect = right parietal; ideomotor apraxia classically = left (dominant) parietal.
Buzzwords
"can't tie shoes, full strength" → SMA apraxia
"can't copy a gesture" → lateral premotor
"ignores left side of plate" → right posterior parietal
"Betz cells" → layer V of M1
"eyes deviate toward lesion" → destroyed frontal eye field
ApplyLO 1 application questions
A1After an ACA-territory stroke, a 70-year-old has a weak right leg and, although his arms are strong, he cannot carry out the steps of making a cup of tea or explain how to use a spoon. Which two cortical areas are hit?
Left M1 leg area (paracentral lobule) and left SMA. Both sit on the medial surface supplied by the ACA; the SMA lesion explains the sequencing apraxia.
A2A woman with a right parietal stroke has normal strength but leaves the left side of her hair uncombed and bumps into door frames on the left. Diagnosis?
Left hemispatial neglect from a right posterior parietal lesion. The parietal spatial map (egocentric/allocentric) is lost for the left side of space.
A3A stroke affects only the left precentral gyrus over the lateral convexity, at the hand knob. Predict the deficit.
Weakness of the right hand with loss of fine finger movement (UMN type). M1 maps contralaterally; the hand area is on the lateral convexity (MCA).
A4A driver keeps missing red lights. He can do sequences from memory perfectly and his strength is normal. Which region best fits?
Lateral premotor cortex. It starts and adjusts movement in response to external cues like a traffic light.
LO 2The corticospinal tract, cortex to muscleRoute, crossing point, internal capsule map and blood supply, UMN vs LMN
By the end: you can draw the tract level by level, say where it crosses, predict the side of weakness from the lesion level, use the internal capsule's map and arteries to predict a capsular stroke, and sort UMN from LMN signs.
Q1. What path does the corticospinal tract take?
M1 layer VUMN
→
Posterior limb IC
→
Cerebral pedunclemiddle 3/5
→
Basis pontis
→
Pyramidmedulla
→
Decussation~90% cross
→
Lateral CST→ LMN
CheckA lesion of the left medullary pyramid (above the decussation) weakens which side?
Right side. Above the decussation = contralateral weakness; below it (in the cord) = ipsilateral.
Q2. How do the lateral and anterior corticospinal tracts differ?
| Feature | Lateral CST | Anterior CST |
|---|---|---|
| Share of fibers | ~90% | ~10% |
| Crossing | At the pyramidal decussation (lower medulla) | Not in the brainstem; many cross at their target level (anterior white commissure) → bilateral effect |
| Muscles | Distal limb: voluntary, fine movement; drives whole-limb movement via pattern-generator interneurons | Proximal / axial (trunk, neck): postural adjustment |
| Extent | Whole cord | Upper cord only; does not go below L2 (no trunk muscles below that) |
| Position in cord | Lateral funiculus | Anterior funiculus, by the anterior median fissure |
- ~90% cross → lateral CST (distal, fine, voluntary); ~10% uncrossed → anterior CST (proximal, bilateral, not below L2)
- Path → motor cortex → internal capsule → cerebral peduncles → pyramids → decussation → contralateral ventral horn LMN → muscle
CheckWhy does a unilateral CST lesion barely weaken the trunk?
Trunk muscles get bilateral control (anterior CST plus brainstem tracts), so the other hemisphere covers them.
Step 1 trap — where the anterior CST stops
The in-house number is "not below L2." Many board texts simply say the anterior CST serves neck and trunk and ends in the cervical/upper thoracic cord. Either way, the point is the same: axial muscles, bilateral. Don't let the level distract you.
Q3. How is the internal capsule organized, and what supplies it?
| Part | Fibers | Arteries |
|---|---|---|
| Anterior limb | Corticopontine; thalamocortical (DM, anterior nuclei) | ACA branches (medial striate/Heubner), MCA branches |
| Genu | Corticobulbar (face, tongue) | ACA, MCA branches, internal carotid |
| Posterior limb | Corticospinal (arm → trunk → leg); thalamocortical sensory (VPL/VPM) behind; optic and auditory radiations at the very back | MCA lenticulostriate branches, anterior choroidal |
Because the face, arm and leg fibers are packed into a few millimeters, one small capsular lesion gives contralateral face + arm + leg weakness all at once. A cortical lesion usually spares part of the map.
CheckA small lacune hits only the front of the posterior limb. Predict the deficit.
Pure motor hemiparesis of the contralateral arm > leg (± face if it reaches the genu), without sensory loss, since thalamocortical fibers lie farther back.
Step 1 HY — internal capsule stroke
- Lenticulostriate arteries = thin end-branches of the MCA → hypertension → lipohyalinosis → lacunar infarct; or Charcot-Bouchard microaneurysm rupture → putamen/capsule hemorrhage.
- Classic: pure motor hemiparesis (face, arm, leg equally) with no sensory loss, no aphasia, no visual field cut.
- Bigger posterior-limb lesion → adds hemisensory loss (± homonymous hemianopia if optic radiation).
Memory tool — "FAT Leg" walks backwards
Front to back in the capsule: Face (genu) → Arm → Trunk → Leg. In the cord's lateral CST: legs Lateral, arms medial.
Q4. What are UMN vs LMN signs, and why does each happen?
| Sign | UMN (pyramidal) lesion | LMN lesion |
|---|---|---|
| Paralysis | Spastic, after an initial floppy phase (spinal shock) | Flaccid: no nerve, no contraction |
| Tone | ↑ Spasticity: "clasp-knife", velocity-dependent | ↓ Hypotonia (loss of γ motor drive) |
| Reflexes | ↑ Hyperreflexia, clonus: spindle arc intact but LMN has no descending brake so it over-responds | ↓ Areflexia: the reflex arc itself is broken |
| Babinski | Present (upgoing big toe, fanning) | Absent |
| Atrophy | Minimal (mild disuse over time) | Marked ("use it or lose it") |
| Fasciculations / fibrillations | No | Yes: spontaneous firing of surviving axons / denervated muscle fibers |
| Pattern of weakness | "Pyramidal" pattern: arm extensors and leg flexors weakest | Matches a root, nerve or segment |
Day 0UMN injury
→
Spinal shockflaccid, areflexic (days–weeks)
→
ReleaseLMNs disinhibited; antigravity muscles dominate
→
Chronicspastic, hyperreflexic, Babinski
CheckWhy is the Babinski sign normal in a 6-month-old?
The corticospinal tract is not mature yet. A healthy CST suppresses this primitive toe-extension reflex; pyramidal damage releases it in adults.
Step 1 HY — ALS and other "pure" motor diseases
- ALS: degeneration of both UMNs and LMNs → mixed signs (atrophy + fasciculations next to spasticity, hyperreflexia, Babinski). Sensation, eye movements, bladder spared. SOD1 / C9orf72; TDP-43 inclusions; riluzole, edaravone.
- Polio, spinal muscular atrophy (Werdnig-Hoffmann, SMN1, "floppy baby", tongue fasciculations) = pure LMN (anterior horn).
- B12 deficiency (subacute combined degeneration) = lateral CST + dorsal columns.
Memory tool — ALS spares the ALS
Amyotrophic Lateral Sclerosis does not touch the Anterolateral System (pain/temp). It is a motor-only disease.
Step 1 trap — acute UMN lesion looks like LMN
Right after a cord transection or big stroke, limbs are flaccid and areflexic (spinal shock). Don't call it an LMN lesion; spasticity and hyperreflexia appear over days to weeks. Fasciculations and early marked atrophy point to LMN.
Buzzwords
"clasp-knife" → UMN spasticity
"fasciculations + atrophy" → LMN
"both, sensation normal" → ALS
"pure motor hemiparesis, hypertensive" → lacune, posterior limb IC
"Charcot-Bouchard" → lenticulostriate hemorrhage
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 · Name the triangle-marked cells and their layers. (tap for answer)
Pyramidal neurons, concentrated in layers III and V.
Layer III pyramidal cells project mainly to other cortex. Layer V pyramidal cells give rise to the corticospinal (and corticobulbar) tract; the giant layer V pyramidal cells of M1 are Betz cells.
Layer III pyramidal cells project mainly to other cortex. Layer V pyramidal cells give rise to the corticospinal (and corticobulbar) tract; the giant layer V pyramidal cells of M1 are Betz cells.
Image: Michigan SecondLook Anki Deck · SecondLook Neuroanatomy (Michigan Virtual Microscopy Slide Collection), University of Michigan Medical School · CC BY-NC-SA 4.0
2 · Locate the lateral and anterior corticospinal tracts. (tap for answer)
Lateral CST (purple, in the lateral funiculus; ~85–90% of fibers, crossed at the pyramidal decussation) synapses on LMNs and interneurons of the lateral ventral horn, mostly in the cervical and lumbar enlargements (limb muscles).
Anterior CST (pink, ventral funiculus beside the anterior median fissure; uncrossed in the medulla, crosses in the cord) synapses on the medial motor group (axial/trunk muscles).
Anterior CST (pink, ventral funiculus beside the anterior median fissure; uncrossed in the medulla, crosses in the cord) synapses on the medial motor group (axial/trunk muscles).
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 64-year-old with long-standing poorly controlled hypertension wakes with weakness of the left face, arm and leg. Sensation, language and vision are normal. Lesion and vessel?
Right posterior limb (± genu) of the internal capsule; lenticulostriate branches of the MCA. Pure motor hemiparesis is the classic lacunar picture.
A2A knife wound cuts the right lateral funiculus at T8. Which leg becomes spastic?
The right leg. In the cord the lateral CST has already crossed, so the deficit is ipsilateral.
A3A 58-year-old has weak, wasted hands with fasciculations, brisk biceps reflexes and upgoing toes. Pinprick and vibration are normal. Diagnosis?
ALS. LMN signs (wasting, fasciculations) plus UMN signs (hyperreflexia, Babinski) with sensation intact.
A4Two hours after a C6 cord injury, the legs are flaccid with absent reflexes. A student calls it an LMN lesion. What is the better explanation?
Spinal shock. The UMN injury first causes flaccid, areflexic paralysis; spasticity and hyperreflexia follow.
LO 3The brainstem motor tractsRubrospinal, vestibulospinal, reticulospinal, tectospinal: origin, target, job
By the end: for each brainstem tract you can give its nucleus, whether it crosses, its muscle group (flexor vs extensor, distal vs axial), its job, and what it does when the CST is gone.
Q1. What do "pyramidal" and "extrapyramidal" mean?
- Pyramidal tracts = the ones that travel in the medullary pyramids: corticospinal and corticobulbar (direct cortex → LMN).
- Extrapyramidal tracts = the brainstem pathways: rubrospinal, vestibulospinal, reticulospinal, tectospinal (cortex → brainstem nucleus → cord, or no cortex at all).
- Extrapyramidal systems = basal ganglia and cerebellum: they don't send axons to the cord but tune the motor cortex and brainstem centers.
Lateral (voluntary, flexor) system
- Lateral CST + rubrospinal
- Distal limb muscles, flexor bias
- Fine, skilled movement of limbs and fingers
Ventromedial (involuntary, antigravity) system
- Vestibulospinal, reticulospinal, tectospinal (+ anterior CST)
- Axial and proximal muscles, extensor bias
- Posture, tone, balance, head/neck orienting
Check"Pyramidal symptoms" refers to the pyramidal cells of cortex or to the medullary pyramids?
The medullary pyramids, i.e., the corticospinal/corticobulbar route. Cortical pyramidal neurons feed both systems.
Q2. Where does each tract run in the spinal cord?
CheckA small lesion in the right lateral funiculus of the cervical cord would hit which two descending motor tracts?
Lateral CST and rubrospinal tract, which lie next to each other; the small rubrospinal tract is often damaged along with the CST.
Q3. What does each brainstem tract do?
| Tract | Origin | Crossed? | Ends / muscles | Function |
|---|---|---|---|---|
| Rubrospinal | Red nucleus (midbrain); input from cortex (corticorubral) and cerebellum (interposed, dentate) | Yes, right away: ventral tegmental decussation | Cervical cord; upper-limb flexors only | Facilitates flexors, inhibits extensors of the arm. In humans outweighed by the lateral CST. Red nucleus = key relay of cerebellar output. Visible in decorticate posturing. |
| Lateral vestibulospinal | Lateral vestibular nucleus (Deiters', pons/medulla junction) | No (ipsilateral) | Whole cord; extensor (antigravity) muscles, esp. legs | Balance, upright posture. Visible in decerebrate posturing. |
| Medial vestibulospinal | Medial vestibular nucleus (medulla) | Bilateral (via MLF) | Cervical/upper thoracic; neck | Stabilizes the head as the body moves; coordinates head with eye movements. |
| Reticulospinal | Reticular formation: pontine (medial RST) and medullary (lateral RST) | Mostly ipsilateral (medullary partly bilateral) | Whole cord; proximal flexors and extensors | Driver of muscle tone; primitive orienting toward/away from stimuli, non-dexterous movement; "emotional" posture (hunched in depression, jumpy when excited). Pontine ⊕ extensors; medullary ⊖ extensors. |
| Tectospinal | Superior colliculus (tectum) | Yes: dorsal tegmental decussation | Upper cervical cord; neck | Integrates eye and head movement: orients head/neck toward a sudden sight or sound. |
- Rubrospinal → upper-limb flexors only; the red nucleus integrates cerebellar output
- Vestibulospinal → medial: stabilizes the head, links head + eye movement; lateral: extensors, balance
- Reticulospinal → driver of muscle tone; primitive orienting, "emotional" motor responses
- Tectospinal → superior colliculus; integrates eye and head movement
- Corticospinal + rubrospinal = flexor system, fine limb movement; vestibulospinal + reticulospinal = antigravity, posture, balance
CheckWhich brainstem tract crosses at the ventral tegmental decussation, and which at the dorsal?
Ventral = rubrospinal; dorsal = tectospinal. Both cross in the midbrain right after leaving their nucleus.
Step 1 trap — corticorubral vs rubrospinal
The corticorubral projection is what synapses in the red nucleus; the rubrospinal tract starts there and crosses in the ventral tegmental decussation (not the "ventral tegmental area," which is a dopamine nucleus). Also: the lateral vestibulospinal and pontine reticulospinal tracts are uncrossed.
Memory tool — tract hooks
- Rubro = Red = aRm flexion (only reaches the cervical cord).
- Vestibulo = Vertical: keeps you standing (extensors).
- Reticulospinal: Pons = Plus (excites extensors), Medulla = Minus (inhibits extensors).
- Tecto = "look at that!": head follows the eyes.
Q4. Once the corticospinal tract is lost, what can the brainstem tracts still do?
- Rubrospinal can partly take over arm movement: gross flexion and grasping, but not fine, independent finger movement. That skill belongs to the CST alone.
- Vestibulospinal and reticulospinal keep posture, tone and balance, and now act unopposed → antigravity muscles dominate → spasticity.
- Which tracts survive decides the shape of a paralyzed limb: that is LO 4 and LO 5.
CST lostno fine/distal control
→
Rubrospinalarm: gross flexion only
→
Vestibulo/reticulolegs, trunk: extensor tone
CheckA monkey with a pure pyramid lesion can still grab food with its whole hand. What can't it do?
Pick up a small object with independent finger movement (precision grip). Only the CST gives that.
Step 1 HY — what boards ask about these tracts
- Boards rarely ask the tracts in isolation; they ask them through posturing (decorticate = red nucleus intact; decerebrate = vestibulospinal unopposed).
- Medial longitudinal fasciculus carries the medial vestibulospinal fibers; MLF lesion = internuclear ophthalmoplegia (MS).
- Holmes (rubral) tremor = midbrain red nucleus lesion: rest + postural + action tremor.
Buzzwords
"red nucleus" → rubrospinal, arm flexors
"Deiters' nucleus" → lateral vestibulospinal, extensors
"superior colliculus → neck" → tectospinal
"muscle tone, hunched in depression" → reticulospinal
ApplyLO 3 application questions
A1Someone yells your name from the left and your head snaps toward the sound before you decide to look. Which tract?
Tectospinal. The superior colliculus turns head and neck toward a sudden visual or auditory stimulus.
A2A cat with its cerebrum removed has a lesion added in the left lateral vestibular nucleus. Which limbs lose their extensor rigidity?
The left limbs. The lateral vestibulospinal tract is ipsilateral and drives extensors.
A3Predict the effect of stimulating the medullary reticular formation on leg extensor tone.
Extensor tone ↓. The medullary (lateral) reticulospinal tract inhibits extensors; the pontine one excites them.
A4Why do brainstem tracts control mostly proximal and axial muscles, while the CST controls distal ones?
Their terminations: medial tracts end on medial motor pools (axial/girdle), lateral CST and rubrospinal on lateral pools (distal limb).
LO 4Why the arm flexes and the leg extends after a strokeRubrospinal wins in the arm; vestibulospinal wins in the leg
By the end: you can explain every finding in the classic hemiplegic patient (lower face, body, flexed arm, extended leg, circumduction) from which tracts are lost and which survive.
Q1. What does the classic patient look like?
Case: sudden paralysis. Left side normal. Right side:
| Finding | Why |
|---|---|
| Right lower face weak | Loss of corticobulbar fibers (genu) to the lower facial nucleus |
| Right body weak | Loss of CST (posterior limb) |
| Arm flexed | CST gone; rubrospinal (flexor) dominant in the arm |
| Leg extended | CST gone; no rubrospinal input to the leg, so vestibulospinal (extensor) is dominant |
Lesion: left internal capsule (lenticulostriate MCA), above the red nucleus, so the red nucleus is still working.
Q2. Why does each limb take a different shape?
- The rubrospinal tract ends in the cervical cord → it can only pull the arm into flexion.
- The lateral vestibulospinal tract (with pontine reticulospinal) runs the whole cord and drives antigravity extensors → it wins in the leg.
- Result when walking: the stiff, long leg can't bend at the knee/ankle, so the patient swings it out in an arc = circumduction.
The four-line answer
- Lower face paralysis = loss of corticobulbar
- Body paralysis = loss of CST
- Flexed arm = loss of CST, rubrospinal dominant in arms (flexor)
- Extended leg = loss of CST, no rubrospinal in legs, so vestibulospinal dominant (extensor)
CheckWhy doesn't the leg flex the way the arm does?
There is no rubrospinal input to the lumbar cord, so nothing pulls the leg into flexion; the extensor (vestibulospinal) drive wins.
Step 1 HY — hemiplegic gait
Chronic UMN hemiparesis → circumduction gait: arm flexed/adducted, leg extended with foot plantarflexed and inverted, leg swung laterally. Contrast: scissor gait (bilateral UMN, e.g., cerebral palsy), steppage gait (LMN foot drop, common peroneal nerve), shuffling (Parkinson), wide-based ataxic (cerebellum).
Step 1 trap — "pyramidal weakness" vs posture
The weakest muscles in UMN weakness are arm extensors and leg flexors. The posture (flexed arm, extended leg) is the mirror image: the stronger antigravity groups win. Both facts describe the same patient.
Memory tool — "Red arm, Vertical leg"
Red nucleus pulls the arm up toward the chest; vestibular nuclei keep the leg straight and vertical.
ApplyLO 4 application questions
A1A woman has a left hemiplegia with flexed left arm and extended left leg, plus left lower-face weakness with a normal forehead. Where is the lesion?
Right internal capsule (genu + posterior limb) or right motor cortex/corona radiata. Same-side face and body weakness, forehead spared = UMN above the brainstem.
A2If the rubrospinal tract reached the lumbar cord in humans, how would the hemiplegic leg look?
It would tend toward flexion, like the arm. The leg extends only because no rubrospinal flexor drive reaches it.
A3Why does the patient swing the leg outward instead of lifting it straight forward?
The leg is held extended and can't flex at hip/knee/ankle, so it is functionally too long; circumduction clears the toes.
LO 5Decorticate vs decerebrate posturingIs the red nucleus still connected?
By the end: you can recognize both postures, place each lesion relative to the red nucleus, give the GCS motor score, and say which is worse.
Q1. What do the two postures look like, and where is the lesion?
- Decorticate → lesion above the red nucleus → rubrospinal function shows (arm flexion)
- Decerebrate → lesion below the red nucleus → lateral vestibulospinal function shows (extension); tectospinal activity is also credited for the arched neck
- GCS motor: 6 obeys · 5 localizes pain · 4 withdraws · 3 abnormal flexion · 2 extension · 1 none
CheckIn both postures the fingers stay curled. Why?
The CST is lost in both, so there is no fine finger control in either.
Step 1 HY — boards' version
Boards phrase decerebrate rigidity as unopposed vestibulospinal and pontine reticulospinal extensor drive after a lesion at or below the midbrain (classically from transtentorial (uncal) herniation compressing the midbrain). A switch from decorticate to decerebrate = the lesion is moving down the brainstem → worsening.
Memory tool — "cor" = heart
De-COR-ticate: hands pulled up to the cor (heart). DecErEbrate: Extended Everything, and it's Even worse.
Step 1 trap — "decerebrate" sounds higher
"Decerebrate" sounds like the bigger cortical lesion, but it means the lesion is lower (brainstem). Lower lesion → fewer surviving tracts → worse posture and prognosis.
Q2. What are primitive reflexes, and why do they matter here?
Primitive (neonatal) reflexes are innate, need no planning, and start in utero or early life. They are suppressed as the descending cortical motor pathways mature. If they persist or return in an adult, something is wrong (cerebral palsy, frontal lobe or CST damage).
| Reflex | Stimulus → response | Typically gone by |
|---|---|---|
| Rooting | Stroke cheek → turns head, opens mouth (feeding) | ~4 months |
| Sucking | Touch the mouth → sucks | ~4 months |
| Moro (startle) | Sudden drop of head → arms fling out, then come together | ~3–4 months |
| Palmar grasp | Object in palm → grips | ~6 months |
| Stepping | Held upright, feet touch surface → walking movements | ~2 months |
| Swimming | Placed face-down in water → paddling, breath-holding | ~6 months |
| Babinski (plantar) | Stroke lateral sole → big toe up, other toes fan | ~12 months (up to 2 yr) |
CheckA 75-year-old with frontal dementia grips the examiner's fingers whenever the palm is stroked. What does this mean?
A primitive (frontal release) sign: cortical inhibition of the grasp reflex has been lost.
Buzzwords
"arms flexed on chest, legs extended" → decorticate, above red nucleus
"all four limbs extended, arms pronated" → decerebrate, below red nucleus
"GCS motor 3 vs 2" → flexion vs extension
"blown pupil, then extensor posturing" → uncal herniation
ApplyLO 5 application questions
A1A TBI patient's arms were flexed on admission; 6 hours later the arms extend and pronate with painful stimuli and the right pupil is dilated. Interpret.
Decorticate → decerebrate: lesion progressing below the red nucleus, most likely uncal herniation compressing the midbrain (CN III). Worse prognosis; emergency.
A2GCS motor score for a patient who extends all limbs to a sternal rub?
2. Extension = decerebrate.
A3A large bilateral thalamic hemorrhage. Which posture do you expect?
Decorticate. Thalamus is above the red nucleus, so rubrospinal arm flexion survives.
A4Predict the posture if a lesion destroyed the brainstem below the vestibular nuclei too (e.g., lower medulla).
Flaccid, no posturing (GCS motor 1). With vestibulospinal and reticulospinal tracts also cut, no descending tract is left to drive extensor tone.
LO 6Where is the lesion? Localizing a motor casePyramidal vs extrapyramidal, face vs body, and the sensory clues
By the end: from a vignette you can decide pyramidal vs extrapyramidal, then place a pyramidal lesion in cortex/capsule, brainstem or cord using the face and the sensory pattern (including Brown-Séquard).
Q1. Step one: is it pyramidal or extrapyramidal?
| Feature | Pyramidal (corticospinal) lesion | Extrapyramidal lesion (basal ganglia / cerebellum) |
|---|---|---|
| Weakness | Spastic paresis/paralysis, often hemiparesis; arm extensors and leg flexors weakest | No true paralysis; bradykinesia / akinesia instead |
| Tone | Spasticity: "clasp-knife", velocity-dependent | Rigidity: "lead-pipe" or "cogwheel", not velocity-dependent (basal ganglia); hypotonia (cerebellum) |
| Deep tendon reflexes | Hyperreflexia, clonus | Normal or mildly ↑ |
| Involuntary movements | Usually absent (clonus may occur) | Resting tremor, intention tremor, chorea, athetosis, dystonia, tics |
| Babinski | Present | Absent |
| Muscle bulk | Preserved acutely; mild diffuse atrophy over time | No significant atrophy |
| Gait | Hemiplegic / circumducted | Shuffling, festinating, stooped (BG); ataxic (cerebellum) |
- Pyramidal → spastic, hyperreflexic, Babinski, circumducted gait
- Extrapyramidal → no paralysis, rigidity, tremor/involuntary movements, normal reflexes, no Babinski
Tremor types
| Tremor | When | Site |
|---|---|---|
| Resting | At rest, improves with movement ("pill-rolling") | Basal ganglia (Parkinson) |
| Intention (kinetic) | Worse as the hand nears the target | Cerebellum |
| Postural / essential | Holding a posture; often familial, better with alcohol | No structural lesion |
| Holmes (rubral) | Rest + postural + action combined | Red nucleus (midbrain) |
CheckClasp-knife or lead-pipe: which one changes with how fast you move the limb?
Clasp-knife (spasticity) is velocity-dependent; lead-pipe/cogwheel rigidity is the same at any speed.
Step 1 trap — spasticity vs rigidity
Both are "increased tone." Spasticity = UMN, velocity-dependent, gives way (clasp-knife), with hyperreflexia. Rigidity = basal ganglia, constant through the range (lead-pipe), cogwheeling if tremor rides on it, reflexes normal.
Q2. Step two: use the face. Cortex/capsule, brainstem, or cord?
| Level | Motor pattern | Helpful company |
|---|---|---|
| Cortex | Contralateral; often patchy (face + arm in MCA, leg in ACA) | Aphasia, neglect, apraxia, field cut, cortical sensory loss, seizures |
| Internal capsule | Contralateral face + arm + leg equally (lower face only) | Often pure motor; no cortical signs |
| Brainstem | Crossed: ipsilateral cranial nerve (LMN) + contralateral body (UMN) | Diplopia, dysarthria, vertigo, ataxia; e.g., Weber (CN III + contralateral hemiparesis, midbrain), medial medullary (CN XII + contralateral hemiparesis) |
| Spinal cord | Ipsilateral UMN below the level, face spared; LMN signs at the level | A sensory level; bladder/bowel; dissociated sensory loss |
CheckRight arm and leg weakness plus LEFT facial weakness (forehead included). Level and side?
Left pons (brainstem). Crossed signs: left facial nucleus/nerve (LMN, whole face) + left CST before it crosses.
Step 1 HY — corticobulbar fibers and the face
- Central (UMN) facial palsy: contralateral lower face only, forehead wrinkles normally (cortex, genu of IC).
- Bell palsy (LMN): ipsilateral entire face, can't close eye or raise brow (± hyperacusis, taste loss).
- CN XII also gets mainly contralateral input: cortical lesion → tongue deviates away from the lesion; LMN XII lesion → tongue deviates toward the lesion with atrophy/fasciculations.
- Most other cranial motor nuclei get bilateral corticobulbar input, so a one-sided UMN lesion barely affects jaw, palate, swallowing. Bilateral corticobulbar lesions → pseudobulbar palsy: dysarthria, dysphagia, brisk jaw jerk, emotional lability (pathological laughing/crying), no tongue atrophy. Contrast bulbar palsy (LMN: tongue atrophy, fasciculations), as in ALS.
Memory tool — face decides the level
- Face with body, same side → above the brainstem (cortex/capsule).
- Face and body on opposite sides → brainstem (crossed).
- Face spared, sensory level → spinal cord.
Q3. Step three: use the sensory findings. What does Brown-Séquard look like?
Case (ladder fall):
Right leg
- Voluntary motor control ✓, normal reflexes
- Feels cotton swab (light touch) ✓
- Can't feel pin-prick or hot/cold
Left leg
- No motor control, exaggerated reflexes
- Can't feel cotton swab
- Feels pin-prick and hot/cold ✓
→ Left hemisection of the cord (thoracic): Brown-Séquard syndrome.
| Finding (below the lesion) | Side | Why |
|---|---|---|
| Spastic paralysis, hyperreflexia, Babinski | Ipsilateral | Lateral CST already crossed (medulla) |
| Loss of fine touch, vibration, proprioception | Ipsilateral | Dorsal columns cross later (medulla) |
| Loss of pain and temperature (starting 1–2 levels below) | Contralateral | Anterolateral fibers crossed at entry (anterior white commissure) |
| At the level: band of all-modality loss + LMN signs | Ipsilateral | Roots and ventral horn destroyed |
| Horner syndrome (lesion above T1) | Ipsilateral | Descending sympathetic fibers |
- Hemisection → ipsilateral touch/pressure loss, contralateral pain/temp loss, spastic paralysis, hyperreflexia, Babinski (ipsilateral)
- ALS → corticospinal tract degeneration (UMN + LMN); does NOT affect the anterolateral system
- Localizing figures
- Spinal cord → ipsilateral body, face spared
- Brainstem → crossed (face one side, body the other)
- Cortex / internal capsule → face + body same side
CheckWhich leg has lost pain/temperature after a right hemisection at T10?
The left leg. Pain/temp fibers crossed right after entering the cord.
Step 1 HY — incomplete cord syndromes
| Syndrome | Cause | Lost | Spared |
|---|---|---|---|
| Anterior cord | Anterior spinal artery infarct (aortic surgery/dissection) | Bilateral motor (CST) + pain/temp below | Dorsal columns |
| Central cord | Neck hyperextension in elderly; syringomyelia | Arms > legs (arm fibers medial in lateral CST); cape-like pain/temp loss | Legs relatively, sacral sensation |
| Posterior cord | Tabes dorsalis, B12 | Vibration, proprioception | Motor, pain/temp |
| Brown-Séquard | Hemisection (stab, tumor) | Ipsi motor + DC; contra pain/temp | — |
Step 1 trap — which side is "the lesion side"?
In Brown-Séquard the weak leg is the lesion side. The leg that "can't feel pain" is the opposite side. Students often put the lesion on the side with the pain/temp loss; don't.
Buzzwords
"stab wound, one leg weak, other leg numb to pin" → Brown-Séquard
"crossed hemiplegia" → brainstem
"forehead spared" → UMN facial palsy
"pathological laughing/crying + dysarthria" → pseudobulbar palsy
"cogwheel, pill-rolling" → basal ganglia
"arms worse than legs after hyperextension" → central cord
Q4. How does the whole motor hierarchy fit together for localization?
Planningassociation cortex, basal ganglia (direct/indirect), cerebrocerebellum → VA/VL thalamus
→
Premotor + M1build the command
→
ExecutionCST + brainstem pathways → muscle
→
FeedbackDCML to cortex; non-conscious proprioception to spinocerebellum
- Lesion in the execution line (M1, capsule, brainstem, cord, LMN) → weakness, with UMN or LMN signs.
- Lesion in the planning/modulating loops (basal ganglia, cerebellum) → no paralysis; abnormal speed, tone, tremor, coordination.
- Lesion in planning cortex (SMA, premotor, parietal) → apraxia or neglect with normal strength.
ApplyLO 6 application questions
A1Right hemiparesis with left eye "down and out," ptosis and a dilated left pupil. Localize.
Left midbrain (Weber syndrome): left CN III fascicles + left cerebral peduncle (CST before crossing) → crossed signs.
A2A patient has weak spastic legs with Babinski signs bilaterally and loss of pinprick below the umbilicus, but vibration and position sense are normal. Localize.
Anterior spinal artery infarct (~T10). Bilateral lateral CST + anterolateral system lost; dorsal columns (posterior spinal arteries) spared.
A3A man has slow movements, a shuffling gait, and resistance that is equal throughout passive elbow flexion. Reflexes normal, toes downgoing. Pyramidal or extrapyramidal?
Extrapyramidal (basal ganglia, Parkinson). Rigidity (not velocity-dependent), no paralysis, normal reflexes, no Babinski.
A4After bilateral strokes, a patient cries without feeling sad, has slurred speech and trouble swallowing, a brisk jaw jerk, and no tongue atrophy. Diagnosis?
Pseudobulbar palsy from bilateral corticobulbar (UMN) lesions; bulbar LMN palsy would show tongue atrophy and fasciculations.
MCQPractice questionsClick an answer to see the explanation.
Score: 0 / 0
1A 68-year-old man has an infarct in the territory of the left anterior cerebral artery. His right leg is weak. His arms have full strength, and he understands commands, yet he cannot carry out the steps of buttoning a shirt or tying his shoes and cannot explain how a toothbrush is used. Damage to which area best explains the inability to perform these tasks?
B. Supplementary motor area. The SMA (medial area 6, ACA territory) plans and sequences internally generated movements; lesions cause apraxia for multi-step tasks with normal strength. A: hand area is on the lateral convexity (MCA) and would cause weakness. C: lateral premotor is MCA territory and handles externally cued movement/imitation. D: right parietal causes neglect. E: S1 loss causes sensory deficits.
2A 61-year-old man with long-standing poorly controlled hypertension develops sudden weakness of the left lower face, left arm and left leg, equal in severity. Sensation, language, visual fields and eye movements are normal. Occlusion of which vessel most likely caused this?
D. Pure motor hemiparesis involving face, arm and leg equally = lacune in the right posterior limb/genu of the internal capsule, supplied by lenticulostriate arteries (hypertensive lipohyalinosis). A: ACA weakens mainly the leg. B: PCA gives a visual field cut/thalamic sensory loss. C: PICA gives lateral medullary syndrome (crossed sensory loss, no hemiparesis). E: ASA gives bilateral cord signs and spares the face.
3Three months after a left internal capsule stroke, a 70-year-old woman walks with her right arm held flexed against her chest and her right leg stiffly extended, swinging it outward with each step. The flexed posture of the right arm is mainly driven by a tract that begins in which structure?
A. Red nucleus. With the CST lost, the rubrospinal tract (crossed, cervical cord, upper-limb flexors) dominates the arm. B: lateral vestibulospinal drives extensors and explains the extended leg. C: tectospinal orients head/neck. D: medullary reticulospinal inhibits extensors but does not set arm flexion. E: the right cortex controls the left side.
4A 24-year-old man is brought in after a motorcycle crash. On arrival his arms flex onto his chest and his legs extend to painful stimulus. One hour later his right pupil is fixed and dilated, and painful stimulus now causes extension and pronation of all four limbs. The change in posture indicates a lesion at which level?
E. Decorticate → decerebrate means the lesion (here uncal herniation compressing the midbrain, with CN III palsy) has moved below the red nucleus; rubrospinal flexion is lost and vestibulospinal/pontine reticulospinal extension is unopposed. A–C are above the red nucleus and give decorticate posture. D: a cervical cord lesion produces flaccid/spastic quadriparesis, not decerebrate posturing; it would also cut the vestibulospinal tracts.
5A 55-year-old man has 8 months of progressive hand weakness. Exam shows wasting of the intrinsic hand muscles with visible fasciculations, spastic legs, brisk reflexes in all limbs and bilateral upgoing toes. Which additional finding would be least expected?
C. This is ALS: degeneration of both UMNs and LMNs with sensation spared (it does not affect the anterolateral system). A, B, D, E are expected bulbar (LMN: tongue fasciculations) and pseudobulbar (UMN: brisk jaw jerk) features with dysarthria and dysphagia.
6A 40-year-old roofer falls from a ladder onto a metal rail. His right leg moves normally, has normal reflexes and feels a cotton swab, but he cannot feel pin-prick or hot and cold on it. His left leg cannot move, has exaggerated reflexes and an upgoing toe, cannot feel the cotton swab, yet feels pin-prick normally. Where is the lesion?
B. Brown-Séquard: ipsilateral (left) UMN paralysis and dorsal column loss, contralateral (right) pain/temperature loss. A: would reverse the sides. C: anterior cord gives bilateral weakness and pain loss with dorsal columns spared. D: central cord hits arms more than legs. E: a left capsular lesion causes right-sided weakness with no dissociated sensory loss.
7A 72-year-old woman suddenly cannot smile on the right side and her right arm is weak. She wrinkles her forehead and closes both eyes symmetrically. Where is the lesion most likely located?
A. Lower-face weakness with forehead sparing = UMN (corticobulbar) lesion; the upper face gets bilateral cortical input. Same-side arm weakness puts it above the brainstem on the left. B, C: LMN lesions (Bell palsy, nucleus) paralyze the whole ipsilateral face including forehead. D: would affect the left face. E: would weaken the left side.
8A 66-year-old man cannot close his left eye or raise his left eyebrow, and the left corner of his mouth droops. His right arm and leg are weak with brisk reflexes and an upgoing right toe. Where is the lesion?
D. Crossed signs = brainstem. Whole left face (LMN: left facial nucleus/fascicle) + right hemiparesis (left CST before the pyramidal decussation) → left ventral/caudal pons. A, B: cortical/capsular lesions spare the forehead and put face and body on the same side. C: would give right face + left body. E: would spare the face and weaken the left body.
9A 67-year-old man has a 2-year history of slow movements. He has a 5-Hz tremor of the right hand at rest that stops when he reaches for a cup, ratchet-like resistance at the wrist that is the same at any speed, and a stooped, shuffling gait. Strength is normal, reflexes are 2+ and plantar responses are flexor. Where is the primary lesion?
E. Resting tremor, cogwheel rigidity (not velocity-dependent), bradykinesia, normal reflexes and no Babinski = extrapyramidal (basal ganglia) disease, i.e., Parkinson disease. A–C: pyramidal lesions give weakness, spasticity, hyperreflexia and Babinski. D: cerebellar lesions give intention tremor, ataxia and hypotonia.
10After a stroke, a 74-year-old right-handed woman has normal strength in all limbs. She eats only from the right half of her plate, does not dress her left arm, and draws a clock with all the numbers crowded on the right side. Which area is most likely damaged?
C. Left hemispatial neglect with normal strength = right (nondominant) posterior parietal lesion; this region builds the spatial map (egocentric and allocentric). A: left parietal lesions give apraxia/aphasia-related deficits, rarely dense neglect. B: would cause left weakness. D: SMA gives sequencing apraxia. E: lateral premotor gives loss of cue-guided movement and imitation.
11A 19-year-old is admitted after a diving accident with a complete C7 cord injury. On day 1 both legs are completely flaccid with absent knee and ankle reflexes and mute plantar responses. Which best explains these findings?
A. An acute UMN lesion first produces flaccid, areflexic paralysis (spinal shock); spasticity, hyperreflexia and Babinski signs appear over days to weeks. B, C: LMN damage would be at the lumbar level, not C7. D: loss of extensor inhibition would produce increased tone, not flaccidity. E: disinhibition would raise tone and reflexes.
12In an experimental animal, a small lesion destroys the deep layers of the right superior colliculus and their descending output. Which response will be most impaired?
D. The tectospinal tract (superior colliculus → crosses in the dorsal tegmental decussation → upper cervical cord) orients head and neck toward visual/auditory stimuli. A: lateral CST. B: lateral vestibulospinal. C: rubrospinal. E: reticulospinal.