Pathophysiology · MU Sofia

43. Paresis and paralysis - classification, etiology, pathogenesis, clinical manifestations.

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Topic 43 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 276 words (2 min of reading), with 15 flashcards.

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  1. Paresis and paralysis - classification, etiology, pathogenesis, and clinical manifestations.

Paresis and paralysis - classification, etiology, pathogenesis, and clinical manifestations.

Paresis: Partial loss of voluntary motor function; means weakness.

Paralysis: Complete loss of voluntary motor function.

Classification

  1. 1 According to distribution
  1. 2 According to cause (neuroanatomical level)

Etiology (Causes)

Upper motor neuron (UMN) causes

  • Stroke (cerebral infarct or hemorrhage ).
  • Traumatic brain injury.
  • Multiple sclerosis.
  • Spinal cord injury (above anterior horn).

Lower motor neuron (LMN) causes

  • Poliomyelitis (anterior horn cell damage).
  • Peripheral nerve injury (trauma, compression).
  • Guillain- Barré syndrome (acute inflammatory demyelination).
  • Amyotrophic lateral sclerosis (affects both UMN and LMN).

Other causes

  • Neuromuscular junction disorders (e.g., myasthenia gravis).
  • Myopathies (muscle diseases, e.g., muscular dystrophy).

Pathogenesis

UMN lesion pathogenesis

  • Damage to corticospinal (pyramidal) pathways above anterior horn cell.
  • Loss of inhibitory control → overactivity of spinal reflexes.
  • Imbalance between excitatory and inhibitory signals.

LMN lesion pathogenesis

  • Damage to anterior horn cell or peripheral motor neuron.
  • Loss of direct innervation to muscles.
  • Leads to denervation and muscle fiber atrophy.

Clinical manifestations

UMN lesion features

  • Weakness: more pronounced in extensors of upper limbs and flexors of lower limbs (classic pyramidal pattern).
  • Hyperreflexia (exaggerated tendon reflexes).
  • Spasticity (increased muscle tone, velocity- dependent).
  • Clonus (rhythmic contractions after sudden stretch).
  • Babinski sign positive (toe extension when sole is stroked).
  • No significant muscle atrophy early.

LMN lesion features

  • Weakness: variable distribution depending on nerve.
  • Hyporeflexia or areflexia (decreased or absent reflexes).
  • Flaccidity (decreased tone).
  • Fasciculations (visible spontaneous muscle twitches).
  • Muscle atrophy (due to denervation).

Additional clinical patterns

  • Monoplegia/ monoparesis: often from cortical or peripheral nerve lesion (e.g., radial nerve palsy).
  • Hemiplegia/hemiparesis: usually from stroke or brain lesion affecting one hemisphere.
  • Paraplegia/paraparesis: often spinal cord injury below cervical level or bilateral cortical leg area lesion.
  • Tetraplegia/quadriparesis: high cervical cord injury or diffuse brainstem damage.

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