Neuro Exam 4.4

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  1. 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
  2. What are the different modulatory descending motor tracts?
    • rubrospinal tract
    • tectospinal tract
    • vestibulospinal tract
    • reticulospinal tract
  3. Where are the cell bodies of the UMN of the rubrospinal tract?
    red nucleus of midbrain
  4. Where does the UMN of the rubrospinal tract decussate?
  5. Where do the UMN of the rubrospinal tract terminate?
    ventral horns of SC
  6. What does the rubrospinal tract do?
    excite flexor activity and inhibit extensor activity
  7. Where are the cell bodies of UMN of tectospinal tract?
    superior colliculus of tectum of midbrain
  8. What is the superior colliculus involved with?
    visual reflexes
  9. Where does teh UMN of the tectospinal tract decussate?
  10. Where does the UMN of the tectospinal tract terminate?
    ventral horns of upper cervical SC
  11. What does the tectospinal tract do?
    reflex postural movements of the head, neck, and upper extremities in response to visual stimulus
  12. Where are the cell bodies of UMN of vestibulospinal tract?
    vestibular nuclei in tegmentum of pons
  13. Where does the UMN of the vestibulospinal tract decussate?
    no decussation
  14. Where does the UMN of the vestibulospinal tract terminate?
    ventral horns of SC
  15. What does the vestibulospinal tract do?
    involved w/ "righting refelxes" (from equilibrium issues in vestibular system)
  16. Where are the cell bodies of the UMN of the reticulospinal tract?
    multiple reticular nuclei throughout the tegmentum of the brainstem
  17. Is the function of the reticulospinal tract contralateral or ipsilateral?
    primarily ipsilateral function
  18. What does the reticulospinal tract do?
    excites extensor activity and inhibits flexor activity (stabilizes)
  19. Where does the reticulospinal tract descend to?
    ventral horns of spinal cord
  20. Which tract is the reticulospinal tract the opposite of?
    rubrospinal tract
  21. What are the LMN referred to as?
    alpha and gamma motor neurons
  22. Which tracts cause the most damage?
    corticospinal and corticobulbar
  23. Where can damage occur?
    • anywhere along the routes (corticospinal pathways)
    • several association areas (pre-motor cortex and supplemental motor cortex)
  24. 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)
  25. Where does the corticobulbar pathway receive LMN from?
    corticobulbar nuclei
  26. 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
  27. Paresis:
    weakness b/c skeletal mm are receiving less input (LMN doesn't receive input from damaged UMN)
  28. 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
  29. exaggerated DTR:
    • deep tendon reflex (violent, forceful, reflex)
    • hyperreflexia
  30. clonus:
    • spasms w/ alterations of contractions and relaxation in rapid succession of antagonistic and agonistic mm
    • hyperreflexia of spinal reflexes
  31. spastic paralysis:
    • characterized by involuntary contraction of 1 or more mm w/ loss of function
    • Hallmark of UMN lesion
  32. 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)
  33. hypertonia:
    increased muscle tone
  34. contralateral effects:
    prior to decussation and ipsilateral effects after decussation
  35. What is the reference point for contralateral v. ipsilateral effects with UMN damage?
    cell body of UMN
  36. What accounts for spastic paralysis, hypertonia, hyperreflexia, and clonus?
    • damage to UMN
    • LMN is still intact w/ reflex arc
    • babinski test for UMN lesion
  37. 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
  38. Which type of damage has a greater impact, gamma or alpha?
    gamma damage impact is greater than alpha
  39. 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)
  40. What is the Babinski test for UMN lesion?
    run an object up the lateral side of the foot
  41. What is a normal Babinski result?
    toes will plantarflex
  42. What is a positive Babinski result?
    toes will dorsiflex and the great toe fans (abnormal)
  43. Corticobulbar tract (CN w/ UMN) have what type of input?
  44. Which CNs have bilateral input?
    CN III, IV, V, VI, VII (only top half of orbits), IX, X, XI
  45. Which parasympathetic CN LMN (preganglionic) are not a part of the corticobulbar tract?
    CN III, VII, IX, X
  46. Compensatory mechanism:
    damage to one side and sill getting info from the other side b/c of bilateral input
  47. 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)
  48. What are the two CN exceptions to the bilateral input?
    CN VII and XII
  49. What type of input does CN XII have?
    unilateral innervation pattern
  50. What does CN XII innervate?
    extrinsic and intrinsic tongue mm
  51. Where are the cell bodies of CN XII?
    hypoglossal motor nucleus in medulla
  52. 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
  53. Does spastic paralysis occur when CN XII is damaged?
    yes, b/c UMN event
  54. 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
  55. 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
  56. With UMN lesion to CN XII which side does damage occur on?
  57. Damage to CN VII affects:
    facial mm (facial expression)
  58. What is the function of CN VII?
    dilating and constricting openings in face
  59. Where is the CN VII nucleus located?
  60. How is the CN VII nucleus divided?
    • into halves
    • superior half has bilateral input
    • inferior half has unilateral input from contralateral corticobulbar tract
  61. 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)
Card Set:
Neuro Exam 4.4
2013-04-28 21:44:25
neurology neuroscience neuroanatomy

review of neuro part 4 for exam 4
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