Lecture 4b-descending pathways Flashcards
what is the pyramidal motor system used for
how we make voluntary movements
-sometimes we want voluntary contract head muscles (facial expressoin) and sometimes we want voluntary contract body muscles (biceps)
each voluntary motor pathway (pyramidal) requires how many neurons? what are they
2-upper motor neuron and lower motor neuron
the LMN projects directly to what?
to muscle to cause muscle contraction via spinal nerves, etc (body) and motor CN (for head)
what kind of neurons are the alpha and gamma motor neurons at the ventral horn gray
LMN
-they leave the cord as the ventral rootlets/roots which join the spinal nerve and go out to the periphery to innervate striated skeletal muscle
what is are the 2 main UMN to consider
corticospinal tract and corticobulbar tract
what does the corticospinal tract do
-conveys impulses from motor areas of cortex down to the LMN in the spinal cord
- large bundle of fibers (axons) that start in cell bodies in motor areas of the cerebral cortex,
- descends through the brainstem and lateral white columns of the spinal cord, and
- terminates in the spinal cord’s ventral horn gray.
what does the corticobulbar tract do
conveys impulses from motor areas of cortex; but instead of projecting to the cord, it sends impulses down to LMNs in the brainstem
-brainstem=bulbar
what are extrapyramidal tracts
other UMNs since they also synapse on LMNs
why can single neurons w/ very long axons project all the way from motor cortex to the contralateral half of the spinal cord?
bc a relay in thalamus is not required for outputs from the cortex
where does the corticospinal tract begin?
where is that located?
arises/starts in the motor cortex, primarily in the primary motor cortex which is in the precentral gyrus of the frontal lobe
what is the motor homunculus
the distorted map of the body
“FUTL”
face, upper ext, thorax, lower extrem
when the fibers of the CST descend, where do they coalesce
post limb of the internal capsule
-V shaped white matter
what happens when there is a lesion at the PLIC
contralateral spastic paralysis of the body
after the PLIC, the CST descends through the brainstem, specifically where in the brainstem?
wehre in midbrain
wehre is pons
where in medulla
ventral brainstem
- crus cerebri (of the cerebral peduncles)
- base of pons aka basis pontis
- medullary pyramids
how much of the CST axons will cross to the other side of the body? where will they do that?
90% -but for this course consider this a crossed tract.
-medullary pyramids of the low medulla
where is the CST while it is in the spinal cord?
when does the CST reach the cord?
the lateral funiculus
1-2mm caudal to the motor decussation
what is the goal of the UMN?
to synapse on the LMN
the LMN goes out to innervate striated skeletal muscles of the body
if your brain wnats to impact upper extremities (ex. flex biceps), it leaves the lateral funiculus where?
where will it synapse at
at the level of cervical enlargement and will synapse on the corr. LMNs in the ventral horn gray
where is the lateral corticospinal tract in the cord?
in the dorsal aspect of the lateral funiculus
diff. from brainstem-CST is in ventral brainstem but in lateral cord
what are the steps to the corticospinal tract
- begins in the primary motor cortex in the precentral gyrus of the frontal lobe
- fibers of the CST descend and coalesce in the PLIC
- after PLIC, the CST descends through the ventral brainstem (crus cerebri (midbrain), basis pontis (pons), medullary pyramids (medulla))
- CN 3 and CN6 - vast majority of CST axons cross to the other side in the medullary pyramids
- about 1-2mm caudal to the motor decussation, we are now in the cord -called the lateral corticospinal tract now in the lateral funiculus
- “exit the highway” and synpase ventral horn cells.
- LMN to directly innervate striated skeletal muscle. ex. if you want to impact upper extremities it leaves the lateral funiculus at the level of the cervical enlargement and synapse on corres. LMNs in the ventral horn gray.
what is the function of the corticospinal tract?
what does it do to alpha motor neurons and gamma motor neurons?
control of VOLUNTARY skilled movements of the distal muscles, particularly the distal flexor musculature
- activates alpha motor neurons (excitatory drive)
- also has inhibitory influence on certain spinal reflexes; influences muscle tone and deep tendon reflex
- inhibitory to gamma motor neurons
waht do alpha motor neurons go out to innervate? via what?
what do gamma motor neurons innervate
extrafusal striated skeletal muscle
via ventral roots, etc
intrafusal muscle fibers
what happens when the UMN is lesioned
increased firing of the gamma motor neurons resulting in more contraction of the poles of the muscle spindle making them hypersensitive to further changes in muscle length
-hyperreflexia and hypertonicity/spasticity
where is the lateral CST located
in the dorsal-lateral funiculus of white just medial to the dorsal spinocerebellar tract
does the CST directly innervate muscles of the arms or legs?
no. the CST is an UMN which synapses on the LMN. it is the LMN itself which will go out to directly innervate muscle
when a UMN lesion (visualize the entire course of the CST in the brain and cord) occurs (ex. stroke) what happens to: weakness muscle tone stretch reflexes (DTRs) fascifuations atrophy babinski sign
weakness: yes, decreased strenght
muscle tone: increased (hypertonic, spastic)
stretch reflexes (DTRs): increased (hyperreflexia)
fascifuations: no
atrophy: mild (atrophy of disuse)
babinski sign: yes
when a LMN lesion (ventral horn gray, ventral roots, etc) occurs (ex. polio) what happens to: weakness muscle tone stretch reflexes (DTRs) fascifuations atrophy babinski sign
weakness: yes, decreased strenght
muscle tone: decreased (hypotonic, flaccid)
stretch reflexes (DTRs): decreased or absent (hyporeflexia or areflexia)
fascifuations: yes, possibly
atrophy: severe
babinski sign: no
UMN damage =
LMN damage =
spastic paresis
flaccid paralysis
what is spastic paresis
waht is flaccid paralysis
type of weakness characterized by hypertonicity and hyperreflexia, partial weakness
type of weakness accopanied by hyporeflexia and hypotonicity, total weakness
UMN lesions =
LMN lesions =
atrophy of disuse
wasting atrophy
in UMN lesion, what do you lose inhibitory control over?
why do you not get as much muscle atrophy (except of disuse)?
gamma motor neurons
-still have extrapyramidal inputs
whay do you have flaccid paralysis in an LMN lesion
bc the LMNs are dead, you have marked muscle atrophy, no deep tendon reflexes, no muscle tone
- connection btwn nervous system and striated skeletal muscle is cut off => atrophy and arefelxia
- inputs into the ventral horn cells don’t matter now cause the LMNs of the final common pathway (LMNs) are dead
what is the CST (pyramidal system) importnat for
what are extrapyrmaidals used for
- fine movements of distal flexor muscles
- locomotion (ex walking), posture and balane, orienting towards a sensory stimuli
