UMN vs LMN Lecture Notes Flashcards

UMN vs LMN

Overview

  • The presentation discusses the differences between Upper Motor Neurons (UMNs) and Lower Motor Neurons (LMNs).

Motor Pathways

  • Pyramidal Tract:

    • Primary tract for voluntary movement.

    • Provides a direct pathway between the cerebral cortex and the spinal cord.

    • Named from the medullary pyramids of the medulla oblongata.

    • Divides into the corticospinal and corticobulbar tracts.

      • Corticospinal tract fibers synapse with spinal nerves.

      • Corticobulbar fibers synapse with cranial nerves.

    • Majority of corticospinal tract axons decussate at the pyramidal decussation; axons continue their descent contralateral from their cell bodies of origin and enter the spinal cord at the lateral funiculus; tract is now the lateral corticospinal tract.

    • About 10% of the corticospinal tract axons do not decussate and continue their descent down the brain ipsilateral to their cell bodies of origin; enter the ventral aspect of the spinal cord and are known as the anterior corticospinal tract

    • UMN lesions above the pyramidal decussation- symptoms contralateral to the site of the lesion

    • UMN lesions below the decussation present symptoms ipsilateral to the lesion

    • Causes of UMN lesion: cerebrovascular accidents, traumatic brain injury, anoxic brain injury, malignancy, infections, inflammatory disorders, neurodegenerative disorders, and metabolic disorders

  • Extrapyramidal Tracts:

    • Provide indirect pathways for the coordination of movement.

    • Important for maintaining posture and regulating involuntary motor functions.

    • Examples:

      • Reticulospinal tract from reticuluar formation

      • Vestibulospinal tract from vestibular nuclei

      • Rubrospinal tract from the red nucleus

      • Tectospinal tract from the superior colliculus

    • Functions:

      • Postural tone adjustment.

      • Preparation of predisposing tonic attitudes for involuntary movements.

      • Performing movements that make voluntary movements more natural and correct.

      • Control of automatic modifications of tone and movements.

      • Control of the reflexes that accompany the responses to affective and attentive situations.

      • Control of movements that are originally voluntary but become automatic through exercise and learning.

      • Inhibition of involuntary movements (hyperkinesias), particularly evident in extrapyramidal disease.

Upper Motor Neurons (UMN)

  • First-order neurons responsible for carrying electrical impulses that initiate and modulate movement.

  • Pyramidal neurons in the precentral gyri (primary motor area) form the corticospinal tract.

  • UMNs synapse in the anterior horn with LMNs.

Corticospinal Tract
  • Majority of axons decussate (cross) at the pyramidal decussation.

  • Axons descend contralaterally in the lateral funiculus, forming the lateral corticospinal tract.

  • Lateral corticospinal tract axons control distal extremities and synapse directly on lower motor neurons.

    • Responsible for precise, agile, and highly skilled movements (e.g., buttoning a shirt, playing the piano).

  • About 10% of corticospinal tract axons do not decussate and descend ipsilaterally as the anterior corticospinal tract.

    • Terminate in skeletal muscles that control movements of the trunk and proximal parts of the limbs.

UMN Lesions
  • Damage to motor neurons above the nuclei of cranial nerves or anterior horn cells of the spinal cord.

  • Symptoms (Upper Motor Neuron Syndrome):

    • Weakness (affects extensors of the arm and flexors of the leg).

    • Spasticity.

    • Clonus.

    • Hyperreflexia.

    • Babinski sign (extension of the large toe and fanning of other toes upon stroking the sole of the foot).

    • Hoffman sign (flexion and adduction of the thumb when flicking the middle finger).

  • UMN Lesion Location and Symptoms:

    • Above the pyramidal decussation: symptoms contralateral to the lesion (e.g., right lesion causes left-sided weakness).

    • Below the decussation: symptoms ipsilateral to the lesion (e.g., left-sided spinal cord lesion causes left-sided weakness).

  • Causes:

    • Cerebrovascular accidents.

    • Traumatic brain injury.

    • Anoxic brain injury.

    • Malignancy.

    • Infections.

    • Inflammatory disorders.

    • Neurodegenerative disorders.

    • Metabolic disorders.

Lower Motor Neurons (LMN)

  • Directly innervate skeletal muscle.

  • Cell bodies are in the anterior horn of the spinal cord and at cranial nerve nuclei.

  • Cholinergic.

Types of Motor Neurons
  • Branchial Motor Neurons:

    • Located in the brainstem; form LMNs of the cranial nerve nuclei.

    • Innervate muscles formed by the branchial (pharyngeal) arch; includes muscles innervated by cranial nerves V, VII, IX, and X.

  • Visceral Motor Neurons:

    • Component of the autonomic nervous system (ANS).

    • Regulate smooth muscles and glands.

    • Divided into sympathetic and parasympathetic nervous systems.

  • Somatic Motor Neurons:

    • Located in the ventral horn of the spinal cord.

    • Directly innervate skeletal muscle.

    • Receive stimuli from UMNs.

    • Subtypes:

      • Alpha motor neurons: Innervate extrafusal muscle fibers (primary means of skeletal muscle contraction).

      • Beta motor neurons: Innervate both extrafusal and intrafusal fibers (poorly characterized).

      • Gamma motor neurons: Innervate muscle spindles and dictate their sensitivity; fine-tune muscle contraction (alpha-gamma coactivation).

LMN Lesions
  • Presentation:

    • Muscle atrophy.

    • Fasciculations (muscle twitching).

    • Decreased reflexes (hyporeflexia).

    • Decreased tone.

    • Negative Babinski sign.

    • Flaccid paralysis.

  • Examples:

    • Poliomyelitis.

    • Spinal muscular atrophy.

Extrapyramidal Tracts and Related Diseases

  • Diseases/Conditions:

    • Parkinson's disease (PD).

    • Huntington's chorea (HC).

    • Sydenham chorea.

    • Multiple systemic atrophy (MSA).

    • Progressive supranuclear palsy.

  • Clinical Features:

    • Hypokinesias (scarcity of movement).

    • Akinesia (absence of movement).

    • Bradykinesia (slowness in the execution of voluntary movements).

  • Hyperkinesias:

    • Abnormal involuntary movements.

      • Choreic movements: Sudden, irregular, incomplete, aimless, variable movements.

      • Athetotic movements: Arrhythmic, slow, exaggerated, tentacular movements.

      • Hemiballism: Intense choreic-like movements that persist during sleep.

      • Tics: Rapid muscle contractions reproducing stereotyped movements, can be voluntarily inhibited.

      • Tremors: Rhythmic, slow pace (4-5 oscillations per second), more pronounced at rest, attenuates during voluntary movements.

      • Spasms: Involuntary movements (tonic or clonic).

      • Myoclonus: Rapid, sudden contractions involving isolated muscles or bundles of muscle fibers.

Bilateral Injuries at the Brainstem Level

  • Can cause quadriplegia.

  • Hypertonia (decerebrate or decorticate rigidity) can be observed, depending on the level of injury.

Descending (Efferent) Pathways:

Pyramidal Tracts
  • Lateral corticospinal tract

  • Anterior corticospinal tract

Extrapyramidal Tracts
  • Rubrospinal tract

  • Reticulospinal tracts

  • Olivospinal tract

  • Vestibulospinal tract

Sensory and Ascending (Afferent) Pathways

Dorsal Column Medial Lemniscus System
  • Gracile fasciculus

  • Cuneate fasciculus

Spinocerebellar Tracts
  • Posterior spinocerebellar tract

  • Anterior spinocerebellar tract

Anterolateral System
  • Lateral spinothalamic tract

  • Anterior spinothalamic tract

  • Spino-olivary fibers