What is the difference between Lower Motor Neuron (LMN) and Upper Motor Neuron (UMN) lesions?

Distinguishing Upper Motor Neuron (UMN) from Lower Motor Neuron (LMN) Lesions

Upper motor neuron lesions produce hyperreflexia, spasticity, and increased tone, while lower motor neuron lesions cause hyporeflexia/areflexia, fasciculations, muscle atrophy, and flaccid paralysis. 1, 2

Lower Motor Neuron (LMN) Signs

LMN damage affects the anterior horn cells, nerve roots, or peripheral nerves, producing a characteristic constellation of findings:

Primary Clinical Features

• Fasciculations: Spontaneous discharges of entire motor units appearing as irregular muscle twitches, described as sounding like "raindrops on a tin roof" 1, 2
• Muscle weakness and atrophy: Progressive loss of muscle bulk and strength due to denervation 2
• Hypotonia: Decreased muscle tone from interruption of normal neural input 1, 2
• Hyporeflexia or areflexia: Diminished or absent deep tendon reflexes 1, 2
• Flaccid paralysis: Decreased muscle tone accompanied by weakness 1, 2

Key Diagnostic Indicators

• Fasciculations are considered a "red flag" sign when evaluating neuromotor dysfunction and may indicate degenerative conditions affecting anterior horn cells 1, 2
• Creatine phosphokinase (CK) levels should be measured, as they may be significantly elevated (>1000 U/L) in certain LMN disorders like Duchenne muscular dystrophy 1
• Electromyography (EMG) and nerve conduction studies are cornerstone diagnostic tests for confirming LMN involvement 3

Upper Motor Neuron (UMN) Signs

UMN damage affects the corticospinal tract from the motor cortex to the spinal cord, producing distinctly different findings:

Primary Clinical Features

• Hyperreflexia: Brisk or exaggerated deep tendon reflexes 1, 2
• Spasticity: Increased muscle tone with velocity-dependent resistance to passive movement 1, 2
• Hypertonicity: Increased muscle tone 1, 4
• Clonus: Rhythmic muscle contractions in response to sudden, maintained stretch 1, 2
• Abnormal plantar reflex (Babinski sign): Upgoing toe response indicating corticospinal tract dysfunction 1

Distinguishing Characteristics

• UMN lesions do not produce fasciculations or muscle atrophy (at least not early in the disease course) 1, 2
• Weakness in UMN lesions follows a pyramidal pattern (extensors weaker than flexors in upper extremities; flexors weaker than extensors in lower extremities) 1

Mixed UMN and LMN Presentations

Amyotrophic Lateral Sclerosis (ALS)

ALS uniquely presents with both UMN and LMN signs simultaneously, representing degeneration at both levels of the motor system 1, 3, 4:

• UMN signs: Hypertonicity and hyperreflexia 1, 4
• LMN signs: Muscle fasciculations, weakness, and atrophy 1, 4
• The disease typically begins focally in one body region, with both UMN and LMN signs maximal in the same region, then spreads contiguously 5, 6
• Median survival is 3-4 years after symptom onset 1, 3, 4

Other Motor Neuron Disease Variants

• Primary Lateral Sclerosis (PLS): Predominantly UMN involvement with rapidly progressive cortical thinning in motor regions 3, 7
• Progressive Muscular Atrophy: Isolated LMN degeneration without UMN signs 3

Diagnostic Approach Algorithm

Step 1: Neuromotor Examination

Assess for the presence and distribution of UMN versus LMN signs in each body region 1, 2:

• Test deep tendon reflexes (hyperreflexia vs. hyporeflexia)
• Evaluate muscle tone (spasticity vs. flaccidity)
• Observe for fasciculations
• Assess muscle bulk for atrophy
• Check plantar reflexes

Step 2: Laboratory Testing

When LMN signs predominate with weakness 1:

• Measure serum creatine phosphokinase (CK) concentration
• Obtain thyroid-stimulating hormone (TSH) levels

Step 3: Electrodiagnostic Studies

EMG and nerve conduction velocity studies are essential for confirming LMN involvement and characterizing the pattern of denervation and reinnervation 1, 3

Step 4: Neuroimaging

MRI of the brain and spine without IV contrast is the optimal initial imaging modality 1, 3:

• For suspected ALS: Look for abnormal T2/FLAIR signal in corticospinal tracts and "snake eyes" appearance in anterior horns of the spinal cord 1, 3
• Imaging primarily excludes other conditions rather than confirms motor neuron disease 1, 3

Critical Clinical Pitfalls

• Do not confuse spasticity with rigidity: Spasticity is velocity-dependent (UMN sign), while rigidity is constant throughout range of motion (extrapyramidal sign) 1, 2
• Fasciculations require careful interpretation: They must be distinguished from benign fasciculations, which occur in isolation without weakness, atrophy, or reflex changes 1, 2
• Early ALS may mimic pure LMN disease: Some patients initially present with predominantly LMN signs before UMN signs become apparent 5, 6
• Sensory involvement argues against pure motor neuron disease: The presence of sensory deficits should prompt consideration of alternative diagnoses 1, 3