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All descending tracts other than cortico-spinal / pyramidal are included in it.
1) RUBRO-SPINAL TRACT:
ORIGIN: Red nucleus (midbrain). Fibers cross over to opposite side & descend through pons & medulla lat white column of spinal cord. Fibers terminate on inter-neurons. Inter-neurons synapse with alpha & gamma motor neurons.
RED NUCLEUS
Red nucleus receives fibers from: Cerebral cortex & Cerebellum. Rubro-spinal tract is an alternate pathway, through which cerebral cortex & cerebellum control activity of motor neurons in spinal cord.
This tract is excitatory for flexors & inhibitory for extensors (anti-gravity muscles).
2) TECTO-SPINAL TRACT:
ORIGIN: superior colliculus located in tectum of midbrain. Tract fibers descend without crossing. Fibers terminate onto motor neurons in ventral horn of upper cervical segments of spinal cord, through inter-neurons.
This tract controls reflex movements of head & neck, in response to visual stimuli, e.g, something shines behind reflex turning of head & neck back to the shining object.
RETICULO-SPINAL TRACT:
ORIGIN: Tract arises from reticular formation (groups of scattered neurons along with nerve fibers present in midbrain, pons & medulla). * Superiorly reticular formation is connected to cerebral cortex & inferiorly to spinal cord.
VESTIBULO-SPINAL TRACT:
ORIGIN: Vestibular nuclei in lower pons & medulla. Mostly fibers remain uncrossed. Then enter Ant. White column of spinal cord. Terminate on alpha & gamma motor neurons, through interneurons.
2 components of the tract: Major component Lat. V.S Tract Minor component Med. V.S Tract. Lat. V.S Tract lat. Vest. Nuclei. Med. V.S Tract med Vest. Nuclei.
Vest-spinal tract is excitatory for extensors (unlike rubro-spinal). Vestibular nuclei cerebellar fibers Vestibular nuclei internal ear fibers (vestibular apparatus).
OLIVO-SPINAL TRACT:
ORIGIN: Inferior olivary nucleus in medulla. Fibers cross over to opposite side & descend into lat. White column of spinal cord. Fibers terminate onto motor neurons in ventral horn through interneurons.
This tract controls activity of motor neurons in spinal cord. Inferior olivary nucleus receives fibers from cerebral cortex, corpus striatum, reticular formation & spinal cord.
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.