Upper Motor Neuron vs. Lower Motor Neuron: Key Differences
Upper motor neurons (UMN) are located in the brain and spinal cord and produce spasticity, hyperreflexia, and extensor plantar responses when damaged, while lower motor neurons (LMN) are peripheral neurons that cause flaccidity, hyporeflexia/areflexia, fasciculations, and muscle atrophy when injured. 1, 2
Anatomical Location
Upper Motor Neurons:
- Located in the motor cortex, brainstem, and corticospinal tracts within the central nervous system 3
- Extend from the cerebral cortex through the internal capsule and cerebral peduncles down to the spinal cord 1
Lower Motor Neurons:
- Located in the anterior horns of the spinal cord and cranial nerve nuclei in the brainstem 3
- Extend peripherally through nerve roots and peripheral nerves to directly innervate muscle fibers 3
Clinical Signs of Damage
Upper Motor Neuron Lesions Produce:
- Spasticity: Increased muscle tone with velocity-dependent resistance to passive movement 1, 2
- Hyperreflexia: Brisk or exaggerated deep tendon reflexes 1, 2
- Clonus: Rhythmic muscle contractions in response to sudden, maintained stretch 1, 2
- Extensor plantar response (Babinski sign): Upgoing great toe with fanning of other toes when the sole is stroked 1, 2
- No muscle atrophy (or only mild disuse atrophy) 4
- Preserved or increased muscle bulk 4
Lower Motor Neuron Lesions Produce:
- Fasciculations: The most characteristic sign—spontaneous discharges of entire motor units appearing as irregular muscle twitches, sounding like "raindrops on a tin roof" 3, 5, 2
- Flaccid paralysis: Decreased muscle tone with weakness 1, 5, 2
- Hyporeflexia or areflexia: Diminished or absent deep tendon reflexes 1, 5, 2
- Progressive muscle atrophy: Loss of muscle bulk due to denervation 1, 2
- Hypotonia: Decreased muscle tone from interruption of neural input 5
Diagnostic Approach
For Lower Motor Neuron Involvement:
Electrodiagnostic studies are mandatory—clinical examination alone is insufficient: 1
- EMG findings: Fibrillation potentials, positive sharp waves, fasciculations, and complex repetitive discharges indicating denervation 3, 1, 2
- Nerve conduction studies: Normal or low compound muscle action potential amplitudes with relatively normal conduction velocities 1, 2
- Creatine phosphokinase (CK): Should be measured when LMN involvement with weakness is identified 1, 2
For Upper Motor Neuron Involvement:
- MRI brain without IV contrast is the optimal initial imaging modality 1, 2
- UMN findings on MRI: Abnormal T2/FLAIR signal in the corticospinal tracts, particularly in the posterior limb of the internal capsule and cerebral peduncles 1, 2
- Transcranial magnetic stimulation (TMS): Can detect UMN dysfunction through measures like reduced short interval intracortical inhibition (SICI) 6
For Combined UMN and LMN Disease:
- Spine MRI: May show abnormal T2/STIR signal in the anterior horns ("snake eyes" appearance) for LMN involvement, though this appears late and is not specific 1, 2
- Both UMN and LMN signs can begin in the same body region but progress independently according to neuronal anatomy 7, 8
Critical Clinical Pitfalls
Do not rely on clinical examination alone to establish LMN involvement—electrodiagnostic studies are mandatory. 1
- Sensory symptoms should prompt reconsideration of pure motor neuron disease, as sensory pathways are not involved in typical UMN or LMN lesions 1
- In diseases like ALS, UMN and LMN degeneration can be independent processes despite affecting the same body regions 7, 8
- Missing the distinction can delay diagnosis of treatable conditions versus progressive motor neuron diseases 9, 4
Pathophysiological Independence
The degeneration of UMN and LMN can occur independently at their respective anatomical levels, even when affecting the same peripheral body region 7, 8. Motor manifestations typically begin focally in one body region (98% of cases), with both UMN and LMN signs maximal in that region but progressing independently according to neuronal anatomy 7.