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Motor Neuron Lesions

Upper Motor Neuron (UMN) Lesions Cell body in motor cortex  or brainstem → long axon running laterally in spinal cord → synapse with LMN

Lower Motor Neuron (LMN) Lesions Cell body in the ventral horn of spinal cord → enters periphery to innervate skeletal muscle

  • UMN Lesions:
    • Stroke is a common cause of UMN signs as ischaemia can affect the function of UMNs
  • LMN Lesions:
    • Damage can occur anywhere between the LMN cell body in the ventral horn and the skeletal muscle it innervates
  • UMN Lesions:
    • Damage to an UMN would cause weakness/paralysis of movement for the group of muscles it innervates
  • LMN Lesions:
    • Damage to a LMN would affect the regulation of voluntary movement, reflexes and tone of muscle it innervates
Clinical Presentation
  • UMN Lesions:
    • Hypertonia (increased muscle tone)
      • UMN have a role in descending inhibition of muscle tone, therefore loss of UMN input leads to loss of inhibition of muscle tone and therefore causes hypertonia
    • Spasticity
      • Muscles are tight/stiff during passive movement, and the amount of resistance is proportional to the speed of passive movement
    • Clasp knife reflex
      • A decrease in muscle tone following a sudden increase in resistance, allowing the muscle to be easily stretched
    • Hyperreflexia (brisk reflexes)
      • UMN also have a role in descending inhibition of the stretch reflex, therefore, loss of UMN leads to hyperreflexia
    • Positive Babinski sign
      • Large toe extends and other toes abduct when lateral border of the plantar surface of the foot is stroked
    • Clonus
      • Contractions occurring in a muscle when it is suddenly stretched and held in that position 
    • Disuse Atrophy
      • Long-term disuse of a muscle due to paralysis can result in muscle atrophy
  • LMN Lesions:
    • Hypotonia/atonia (reduced or absent muscle tone)
      • LMN damaged, therefore, inability to elicit deep tendon reflexes
    • Flaccid paralysis
      • Muscles will receive a weakened/lack of signal to contract when attempting voluntary movement  
    • Hyporeflexia/areflexia (reduced or absent reflexes)
      • Due to loss of an efferent portion of stretch reflex
    • Fasciculations
      • Damaged LMN can fire spontaneous action potentials causing small involuntary muscle contractions    
    • Muscle atrophy
      • Pronounced muscle atrophy (best seen in distal muscles or muscle adjacent to bony structures) due to loss of neurotrophic factors from the LMN nerve terminal
  • UMN Lesions:
    • Often see hypotonia and hyporeflexia immediately following UMN damage – hypertonia and hyperreflexia are long term consequences of UMN damage
  • LMN Lesions:
    • Spinal muscular atrophy (SMA) = autosomal recessive disorder resulting in the loss of motor neurons in the ventral horn of spinal cord – presents with same signs and symptoms seen in LMN lesions
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