Difference between upper and lower motir neyron lesion
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Upper Motor Neuron (UMN) vs Lower Motor Neuron (LMN) Lesions
Anatomy First
Upper motor neurons (UMN) are neurons in the cerebral cortex (primary motor cortex) whose axons descend via the corticospinal tract (for limbs/trunk) and corticobulbar tract (for cranial nerve motor nuclei) to synapse on lower motor neurons. Any lesion from the cortex down to - but not including - the anterior horn of the spinal cord is a UMN lesion.
Lower motor neurons (LMN) are the final common pathway - they sit in the anterior horn of the spinal cord (or motor cranial nerve nuclei) and their axons travel via peripheral nerves directly to skeletal muscle. Any lesion from the anterior horn outward is a LMN lesion.
Key Comparison Table
| Feature | UMN Lesion | LMN Lesion |
|---|---|---|
| Weakness | Yes | Yes |
| Muscle atrophy | No (mild disuse atrophy only) | Yes - prominent, early |
| Fasciculations | No | Yes |
| Muscle tone | Increased (spasticity) | Decreased (flaccidity) |
| Deep tendon reflexes | Increased (hyperreflexia) | Decreased/absent (hyporeflexia/areflexia) |
| Babinski sign | Present (positive) | Absent |
| Clonus | May be present | Absent |
| Hoffmann sign | May be present | Absent |
| Paralysis type | Spastic paralysis | Flaccid paralysis |
- Neuroanatomy through Clinical Cases, 3rd Ed. (Table 6.4) and Ganong's Review of Medical Physiology, 26th Ed.
Important Nuances
1. Acute UMN Lesion - "Spinal Shock"
With acute UMN lesions (e.g., a fresh stroke or acute spinal cord injury), the initial picture can look like an LMN lesion:
- Flaccid paralysis
- Decreased tone and hyporeflexia
This is because the spinal cord circuits have lost their supraspinal input suddenly. Over hours to months, this transitions into the classic spastic picture with hyperreflexia. This acute phenomenon is called spinal shock in the spinal cord context.
2. Why UMN lesions cause spasticity
Pure corticospinal tract lesions in animals do NOT cause spasticity. Spasticity is thought to arise from damage to descending inhibitory pathways that run alongside the corticospinal tract. Loss of these inhibitory influences increases excitability of anterior horn motor neurons, causing brisk reflexes and increased tone.
3. Babinski sign (Plantar Extensor Response)
In UMN lesions: stroking the lateral sole causes dorsiflexion of the great toe + fanning of other toes (positive Babinski). In adults this is always pathological. (In infants whose corticospinal tracts are not fully myelinated, it is a normal finding.)
Signs by Category
UMN Lesions produce:
- Weakness (predominantly affects flexors in lower limbs, extensors in upper limbs)
- Spasticity + hypertonia
- Hyperreflexia, sustained clonus
- Pathological reflexes: Babinski sign, Hoffmann sign, loss of abdominal reflexes
- Pseudobulbar palsy (when bilateral corticobulbar involvement)
- No fasciculations, no significant atrophy
LMN Lesions produce:
- Weakness + flaccid paralysis
- Hypotonia / atonia
- Hyporeflexia / areflexia
- Fasciculations (spontaneous firing of denervated motor units)
- Muscle atrophy (denervation atrophy - muscle loses trophic input)
- No pathological reflexes
Facial Nerve - A Special Case
The facial nerve (CN VII) demonstrates the UMN vs LMN distinction beautifully:
- UMN lesion (e.g., stroke): Only the lower face is weak on the contralateral side. The upper face is spared because it receives bilateral cortical input (both hemispheres contribute to upper face movement).
- LMN lesion (e.g., Bell's palsy): Entire ipsilateral half of face is paralyzed - both upper and lower face affected.
Classic Disease Examples
| Disease | Type | Reason |
|---|---|---|
| Stroke, brain tumor | UMN | Cortex/internal capsule lesion |
| Spinal cord compression (below lesion) | UMN | Descending tracts interrupted |
| Poliomyelitis | LMN | Anterior horn cell destruction |
| Peripheral neuropathy | LMN | Peripheral nerve (LMN axon) damaged |
| Bell's palsy | LMN | CN VII peripheral lesion |
| ALS (Lou Gehrig's) | Both UMN + LMN | Simultaneous degeneration of both |
- Neuroanatomy through Clinical Cases, 3rd Ed.; Ganong's Review of Medical Physiology, 26th Ed.; Bradley and Daroff's Neurology in Clinical Practice
Memory Aid
"ULNAR" for LMN - think Unatrophy reversed - LMN = Atrophy, Fasciculations, Flaccid, Areflexia ("3 Fs": Flaccid, Fasciculations, wasting)
UMN = "SHIRE" - Spasticity, Hyperreflexia, Increased tone, Reflexes brisk, Extensor plantar response (Babinski)
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