Corticospinal Tract - The Main Highway
- Principal pathway for voluntary, skilled, and fine motor control, originating from the primary motor cortex (precentral gyrus).
- Decussation: ~90% of fibers cross in the medulla to form the lateral tract; the remaining 10% form the anterior tract.
⭐ Clinical Pearl: Lesions above the decussation (e.g., stroke) cause contralateral motor deficits. Lesions below the decussation (e.g., spinal cord injury) cause ipsilateral deficits.

Extrapyramidal Tracts - The Side Roads
- Function: Modulate motor activity, especially posture, balance, and reflexes, without direct cortical input.
- Key Tracts & Roles:
- Vestibulospinal: From vestibular nuclei; crucial for balance and head position.
- Reticulospinal: From reticular formation; governs postural control and muscle tone.
- Rubrospinal: From red nucleus; facilitates upper limb flexion.
- Tectospinal: From superior colliculus; coordinates head/neck movements in response to visual stimuli.

⭐ Clinical Pearl: Lesions above the Red Nucleus can cause decorticate (flexor) posturing. Lesions at or below it cause decerebrate (extensor) posturing, which typically indicates a more severe brainstem injury.
Lesion Clues - UMN vs LMN
| Feature | UMN Lesion | LMN Lesion |
|---|---|---|
| Weakness | Spastic paralysis | Flaccid paralysis |
| Reflexes | ↑ Hyperreflexia | ↓ Hyporeflexia |
| Tone | ↑ Hypertonia | ↓ Hypotonia |
| Babinski | Positive (Upgoing) | Negative (Downgoing) |
| Atrophy | Late (disuse) | Severe & early |
| Fasciculations | Absent | Present |
⭐ The Babinski sign (dorsiflexion of the big toe with fanning of other toes) is a key indicator of UMN damage, specifically to the corticospinal tract.

Clinical Syndromes - Pathway Problems
-
Brown-Séquard Syndrome (Hemicord Lesion)
- Ipsilateral loss of UMN motor control, proprioception, and vibration below the lesion.
- Contralateral loss of pain and temperature, starting 1-2 levels below the lesion.
-
Amyotrophic Lateral Sclerosis (ALS)
- Combined UMN (spasticity, ↑reflexes) and LMN (atrophy, fasciculations) signs.
- Sensation and cognition are typically spared.
⭐ Superoxide dismutase 1 (SOD1) gene mutation is a well-known cause of familial ALS.
-
Anterior Cord Syndrome
- Bilateral loss of motor function, pain, and temperature.
- Spares dorsal columns (proprioception, vibration).

High‑Yield Points - ⚡ Biggest Takeaways
- The corticospinal tract is the principal pathway for voluntary movement, decussating at the medullary pyramids.
- Upper Motor Neuron (UMN) lesions cause spastic paralysis, hyperreflexia, and a positive Babinski sign.
- Lower Motor Neuron (LMN) lesions result in flaccid paralysis, fasciculations, and severe muscle atrophy.
- The basal ganglia modulate movement; lesions lead to disorders like Parkinson's or Huntington's disease.
- The cerebellum coordinates movement and balance; damage causes ataxia and intention tremors.
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