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What are the modulatory descending motor tracts?
pathways that subserve the corticospinal tract in that they refine and finesse tha activity of LMN receiving input from UMN
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What are the different modulatory descending motor tracts?
- rubrospinal tract
- tectospinal tract
- vestibulospinal tract
- reticulospinal tract
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Where are the cell bodies of the UMN of the rubrospinal tract?
red nucleus of midbrain
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Where does the UMN of the rubrospinal tract decussate?
midbrain
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Where do the UMN of the rubrospinal tract terminate?
ventral horns of SC
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What does the rubrospinal tract do?
excite flexor activity and inhibit extensor activity
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Where are the cell bodies of UMN of tectospinal tract?
superior colliculus of tectum of midbrain
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What is the superior colliculus involved with?
visual reflexes
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Where does teh UMN of the tectospinal tract decussate?
midbrain
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Where does the UMN of the tectospinal tract terminate?
ventral horns of upper cervical SC
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What does the tectospinal tract do?
reflex postural movements of the head, neck, and upper extremities in response to visual stimulus
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Where are the cell bodies of UMN of vestibulospinal tract?
vestibular nuclei in tegmentum of pons
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Where does the UMN of the vestibulospinal tract decussate?
no decussation
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Where does the UMN of the vestibulospinal tract terminate?
ventral horns of SC
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What does the vestibulospinal tract do?
involved w/ "righting refelxes" (from equilibrium issues in vestibular system)
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Where are the cell bodies of the UMN of the reticulospinal tract?
multiple reticular nuclei throughout the tegmentum of the brainstem
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Is the function of the reticulospinal tract contralateral or ipsilateral?
primarily ipsilateral function
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What does the reticulospinal tract do?
excites extensor activity and inhibits flexor activity (stabilizes)
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Where does the reticulospinal tract descend to?
ventral horns of spinal cord
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Which tract is the reticulospinal tract the opposite of?
rubrospinal tract
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What are the LMN referred to as?
alpha and gamma motor neurons
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Which tracts cause the most damage?
corticospinal and corticobulbar
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Where can damage occur?
- anywhere along the routes (corticospinal pathways)
- several association areas (pre-motor cortex and supplemental motor cortex)
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Where does the corticobulbar pathway terminate?
- with motor nuclei with CNs that have a motor function
- association areas (pre-motor cortex and supplemental motor cortex which influence precentral gyrus and have own UMN)
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Where does the corticobulbar pathway receive LMN from?
corticobulbar nuclei
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What are the classical signs of UMN damage?
- paresis
- paralysis
- exaggerated DTR
- clonus
- spastic paralysis
- hypertonia
- contralateral effects prior to decussation and ipsilateral after decussation
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Paresis:
weakness b/c skeletal mm are receiving less input (LMN doesn't receive input from damaged UMN)
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Paralysis:
- loss of movement
- large range of loss b/c of less input
- most of the time means loss of function as well
- often called UMN paralysis
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exaggerated DTR:
- deep tendon reflex (violent, forceful, reflex)
- hyperreflexia
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clonus:
- spasms w/ alterations of contractions and relaxation in rapid succession of antagonistic and agonistic mm
- hyperreflexia of spinal reflexes
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spastic paralysis:
- characterized by involuntary contraction of 1 or more mm w/ loss of function
- Hallmark of UMN lesion
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When you have an UMN lesion, it doesn't get to the LMN to tell it when to fire and it does what it wants to and:
fires (spastic paralysis)
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hypertonia:
increased muscle tone
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contralateral effects:
prior to decussation and ipsilateral effects after decussation
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What is the reference point for contralateral v. ipsilateral effects with UMN damage?
cell body of UMN
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What accounts for spastic paralysis, hypertonia, hyperreflexia, and clonus?
- damage to UMN
- LMN is still intact w/ reflex arc
- babinski test for UMN lesion
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Damage to UMN causes spastic paralysis, hypertonia, hyperreflexia and clonus because:
LMN is getting no supraspinal instruction (corticospinal tract is no longer influencing LMN activity
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Which type of damage has a greater impact, gamma or alpha?
gamma damage impact is greater than alpha
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How does the LMN still being intact with reflex arc cause spastic paralysis, hypertonia, hyerreflexia, and clonus?
- skeletal m is still innervated
- reflex arc runs amuck due to lack of superior control (causing increased DTR and hypertonicity)
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What is the Babinski test for UMN lesion?
run an object up the lateral side of the foot
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What is a normal Babinski result?
toes will plantarflex
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What is a positive Babinski result?
toes will dorsiflex and the great toe fans (abnormal)
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Corticobulbar tract (CN w/ UMN) have what type of input?
bilateral
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Which CNs have bilateral input?
CN III, IV, V, VI, VII (only top half of orbits), IX, X, XI
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Which parasympathetic CN LMN (preganglionic) are not a part of the corticobulbar tract?
CN III, VII, IX, X
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Compensatory mechanism:
damage to one side and sill getting info from the other side b/c of bilateral input
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Why don't you see spastic paralysis in CN if you you have a stroke on one side or the other?
bilateral input (compensatory mechanism)
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What are the two CN exceptions to the bilateral input?
CN VII and XII
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What type of input does CN XII have?
unilateral innervation pattern
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What does CN XII innervate?
extrinsic and intrinsic tongue mm
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Where are the cell bodies of CN XII?
hypoglossal motor nucleus in medulla
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What happens when there is damage to the corticobulbar tract associated with CN XII?
- problems w/ tongue
- genioglossus muscle doesn't work on one side and tongue sticks out to the side
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Does spastic paralysis occur when CN XII is damaged?
yes, b/c UMN event
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Stroke on R side of CN XII affects:
- L side of tongue; it is not getting any input from R tract (corticobulbar)
- Person can stick tongue out but will deviate to L b/c of spastic paralysis on L
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Which way does the tongue deviate with damage to CN XII?
deviates to paralyzed side b/c healthy side pushes the tongue to paralyzed side b/c there is no resistance on that side
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With UMN lesion to CN XII which side does damage occur on?
contralateral
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Damage to CN VII affects:
facial mm (facial expression)
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What is the function of CN VII?
dilating and constricting openings in face
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Where is the CN VII nucleus located?
pons
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How is the CN VII nucleus divided?
- into halves
- superior half has bilateral input
- inferior half has unilateral input from contralateral corticobulbar tract
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What occurs with damage to R corticobulbar (CN VII)?
- superior (bilateral) will not be damaged
- inferior 1/2 will have L facial spastic paralysis (unilateral)
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