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UMN LMN
LMN:
Motor neurons which innervate the skeletal muscles. These form the final common pathways to skeletal muscles. If any motor impulse has to pass to skeletal muscle, it has to pass to LMN.
These neurons include: Alpha motor neuron in ventral horn of spinal cord & also motor neurons in nuclei of cranial nerves in brain stem.
UMN:
These are present above the level of LMN. These control motor activity through separate pathways. These neurons may be located in cerebral cortex, basal ganglia & also in brain stem.
FEATURES:
Only a few muscles are involved in LMN lesion. Flaccid paralysis in LMN lesion, i-e, loss of voluntary movements with hypotonia or atonia. Loss of superficial reflexes. Loss of deep reflexes / tendon jerks. Muscle atrophy (*main cause is loss of trophic actions of motor nerves, supplying skeletal muscles). Disuse is minor cause.
There are fasiculations (when bundles of muscle fibers contract) & fibrillations (individual muscle fibers contract) seen when there is slow degeneration of LMNs. Shortening of paralyzed muscles contractures. Reaction of degeneration: response to faradic stimulation & galvanic stimulation. In LMN lesion, muscles respond to faradic stimulation upto 7 days & to galvanic stimulation upto 10 days. After 10 days, no response (faradic = interrupted current stimulation & galvanic = direct current stimulation). Babinski sign is not present.
A) SPASTIC PARALYSIS:
Loss of voluntary movements with increased muscle tone. In this lesion large no. of muscles are involved. It may be hemiplegia.
D) TENDON JERKS:
They become brisk or exaggerated due to facilitation of stretch reflex.
DIFFERENCES BETWEEN:
LMN LESION: UMN LESION (Pyramidal & Extrapyramidal) LEVEL OF LESION: Level is above alpha motor neuron in cerebral cortex, basal ganglia & brain stem.
LMN LESION: TONE: Loss of voluntary movements with hypotonia / atonia. No. OF MUSCLES INVOLVED: Small no. of muscles are involved. TYPE OF PARALYSIS: Flaccid paralysis.
UMN LESION: TONE: Loss of voluntary movements with hypertonia. No. OF MUSCLES INVOLVED: Large no. of muscles involved. TYPE OF PARALYSIS: Spastic paralysis (clasp knife rigidity).
LMN LESION: CAUSE OF ATROPHY: Due to loss of trophic action of nerves mainly. REFLEXES: Loss of deep reflexes. No ankle / knee clonus. Negative babinski sign.
UMN LESION: CAUSE OF ATROPHY: Due to disuse & only slight atrophy. REFLEXES: Reflexes become exaggerated due to facilitation of stretch reflex. ankle / knee clonus. Positive babinski sign.
LMN LESION: CONTRACTURE: Present. FASCICULATION / FIBRILLATION: Present (slow degeneration of LMNs).
UMN LESION: CONTRACTURE: Absent. FASCICULATION / FIBRILLATION: Absent . There is loss of skilled movements of peripheral limbs.
LMN LESION: HEMIPLEGIA: Not a common feature. SUPERFICIAL REFLEXES: Lost. CONTROL OF MOTOR ACTIVITY: Final common pathway to skeletal muscles.
UMN LESION: HEMIPLEGIA: Common SUPERFICIAL REFLEXES: Lost. (abdominal, cremasteric). CONTROL OF MOTOR ACTIVITY: Controls motor activity through separate pathways.