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.

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).

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