Upper Motor Neuron Vs. Lower Motor Neuron Paralysis

Upper Motor Neuron Vs. Lower Motor Neuron Paralysis


UPPER MOTOR NEURON Vs. LOWER MOTOR NEURON PARALYSIS

UPPER MOTOR NEURON (UMN):

  • Descending neurons from cerebral cortex, cerebellum & brainstem.
  • Terminate directly on neurons innervating muscle.
  • I.e., on α-motor neurons.

UMN TRACTS:

  • Corticospinal (Pyramidal)
  • Extrapyramidal tracts.
  • Cell axons of these pathways.
  • E.g. Giant pyramidal cells.
  • Betz cells of primary motor cortex.

UMN Lesion (UMNL):

  • Damaged corticospinal (pyramidal) & other descending tracts (extrapyramidal tract).

LOWER MOTOR NEURONS (LMN):

  • Neurons directly innervating muscle.
  • α-motor neurons – Axons of anterior/ventral horn cells of spinal cord.

LMN Lesion (LMNL):

  • Damaged lower motor neurons of spinal cord: α-motor neuron & brainstem.
UMN & LMN FOR SPINAL CORD AND BRAIN:

 

TYPE OF NEURON FOR SPINAL CORD FOR BRAIN
UMN
  • Corticospinal
  • Extrapyramidal tract
  • Corticobulbar tract 
LMN 
  • α-motor neuron (Ventral horn cells)
  • Motor cranial nerves with their nuclei.
FEATURES & SIGNS OF UMNL & LMNL:
 
FEATURE/SIGN UPPER MOTOR NEURON PARALYSIS LOWER MOTOR NEURON PARALYSIS

Paralysis

(Loss of voluntary control)

Present – Spastic paralysis

Present – Flaccid paralysis

Muscles affected Regional paralysis.

Segmental paralysis.

Muscle tone

Increased tone – SPASTICITY.

With “Clasp-Knife rigidity“.

Leading to “Hypotonia/flaccidity” muscle tone.
Deep tendon reflex Exaggerated  – Hyperreflexia.

Absent/Reduced

Areflexia/Hyporeflexia.

Superficial reflexes

Absent – 

Abdominal & cremasteric.

Only if particular neuron supplying muscle is affected.
Babinski sign

Positive – Extensor plantar response.

Indicates corticospinal tract involvement.

Absent –

Plantar reflex flexor.

Clonus Present Absent 
Fasciculations Absent

Present – Due to denervation hypersensitivity & spontaneous activity.

Wasting & contractures Absent Present

REASON FOR SPASTICITY IN UMN:

  • Due to extrapyramidal tract injury.
  • Removal of inhibition by ventral horn cell (α-motor neuron).
  • This produces exaggerated γ-motor neuron activity.
  • Hence, spasticity & exaggerated tendon reflexes (hyperreflexia).

Note:

  • Pure pyramidal (corticospinal) tract lesions:
  • Cause hypotonia & hyporeflexia.
  • (Rather than spasticity & hyperreflexia).
Exam Question
 

UPPER MOTOR NEURON Vs. LOWER MOTOR NEURON PARALYSIS

FEATURES & SIGNS OF UMNL & LMNL:
 
FEATURE/SIGN UPPER MOTOR NEURON PARALYSIS LOWER MOTOR NEURON PARALYSIS

Paralysis

 

Present – Spastic paralysis

Present – Flaccid paralysis

Muscle tone 

Increased – SPASTICITY.

With “Clasp-Knife rigidity”.

Leading to “Hypotonia/flaccidity” muscle tone.
Deep tendon reflexes Exaggerated  – Hyperreflexia.

Absent/Reduced 

(Areflexia/Hyporeflexia).

Superficial reflexes

Absent – 

Abdominal & cremasteric.

Only if specific neuron supplying muscle is affected.
Babinski sign

Positive – Extensor plantar response.

Indicates corticospinal tract involvement.

Absent –

Plantar reflex flexor.

Don’t Forget to Solve all the previous Year Question asked on Upper Motor Neuron Vs. Lower Motor Neuron Paralysis

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