Neuro Exam 4.5

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brau2308
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216422
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Neuro Exam 4.5
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2013-04-28 18:56:46
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neurology neuroanatomy neuroscience
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review of neuro part 5 for exam 4
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  1. Where can damage to the LMN occur?
    cell body or axon
  2. Which CNs are invovled with LMN paralysis?
    any CN w/ motor function
  3. What are the types of neurons that can be LMN?
    alpha or gamma motor neurons
  4. Where are LMN found?
    • motor nuclei of CN
    • ventral horns of SC
  5. Damage of LMN in Sc damage:
    ventral horns, ventral root, spinal nerve or peripheral nerve
  6. Damage of LMN in CN damages:
    motor nucleus in brainstem or facial nerve itself
  7. How do LMN get damaged?
    • lesion or trauma (viral infection/disease)
    • can damage ventral horn itself
    • can damage a peripheral nerve (will probably also damage sensory nerve)
  8. What are the clinical signs of LMN damage?
    • paresis
    • flaccid paralysis
    • hypotonia
    • decreased or absent DTR
    • atrophy
    • fibrillations/fasciculations
  9. Paresis:
    • weakness; not innervating skeletal muscle resulting in dramatic weakness
    • also occurs w/ UMN damage
  10. When peripheral nerve is cut, NMJ is no longer functioning, therefore:
    skeletal muscle function is lost (paresis)
  11. Flaccid paralysis:
    • total loss of muscle tone with resultant loss of function
    • lost instructions from LMN
  12. How is flaccid paralysis in LMN damage different from UMN damage?
    still have innervation from LMN but you have lost the control (not communicating with skeletal m)
  13. Hypotonia:
    • decreased muscle done (reflex arc broken)
    • no reason for muscle to contract b/c it lost the source that makes the muscle contract
    • opposite of UMN (hypertonia)
  14. Decreased or absent DTR:
    wiped out LMN part of reflex arc
  15. atrophy:
    reduction in size of skeletal muscle as a result of decreased tone (decreased actin and myosin fibers)
  16. Cut a peripheral nerve you no longer contract the muscle (not in use), therefore:
    the actin and myosin start to deteriorate b/c you don't need it anymore
  17. Is there atrophy with UMN damage?
    no b/c muscle cells are still contracting but it is spastic
  18. Fibrillation/fasciculations:
    • spontaneous activity of skeletal muscle
    • physiological (chemical) response, not neurological (neuron is not telling muscle to contract)
    • disturbance of pH
  19. Are symptoms of LMN damage contralateral or ipsilateral?
    always ipsiltateral
  20. For LMN damage, what is the reference point for ipsilateral and contralateral?
    the lesion
  21. Where is the cell body of LMN?
    ventral horn of SC or motor nucleus of CN w/ motor function
  22. Do LMN decussate?
    no, therefore damage is always ipsilateral
  23. Which CN are involved with LMN paralysis?
    CN III, IV, V, VI, VII, IX, X, XI, XII
  24. CN can have LMN paralysis or UMN paralysis, therefore you must:
    make sure you know which one you are dealing with b/c they are completely separate things!
  25. What happens during LMN paralysis?
    • ipsilateral damage
    • loss of parasympathetic activity
  26. What are the categories of collective responses of normal LMN physiology?
    • spinal reflex responses
    • brainstem reflexes
    • posture and muscle tone
    • rhythmic patterned movements
  27. What are spinal reflex responses?
    • noxious stimulation reflexes
    • DTR
  28. What are brainstem reflexes?
    • counterpart of SC reflexes
    • noxious reflexes
    • DTR
  29. Describe posture and muscle tone:
    • stabilization and setting a foundation for other movements
    • results from constant adjustments by your mm to the shifts in gravity; proprioception
  30. What are rhythmic patterned movements?
    • born w/ some due to embryonic hardwiring
    • begin as voluntary movement patterms
    • ultimately maintained as reflexive and involuntary patterns
    • many acquired throughout life
  31. What do rhythmic patterned movements become?
    central pattern generators (CPG)
  32. What are central pattern generators?
    • used to delineate rhythmic patterns (generate motor activity)
    • neural networks that produce rhythmic patterned outputs w/o sensory feedback
  33. Where are CPGs maintained?
    • basal ganglia
    • spinal cord
    • brainstem
    • cerebellum
  34. What are reciprocal inhibitory neural circuits?
    physiological substrates for rhythmogenesis in CPG systems
  35. CPGs are hardwired systems set up:
    above structures
  36. When do you make new central pattern generators?
    each time you learn a new motor task (like learning to play violin)
  37. Example of reciprocal inhibitory neural circuits:
    a cat w/ a transected SC can still walk on a treadmill when SC is electrically stimulated (no supraspinal input)
    • there are still afferent fibers available to enter SC and effect LMN to execute activity
    • sensory input from treadmill initiates a reflex arc at SC
    • central pattern generator is located in SC, so cat can still walk
    • treadmill touches receptors that initiate CPG in SC
  38. Another example of reciprocal inhibitory neural circuits:
    Can also make a lesion at base of medulla to deafferentate the SC (dorsal root rhizotomy)
    • eliminates afferent sensory input
    • cat still walks on treadmill
    • reinforces that CPG is in SC
  39. Research shows that humans have central pattern generators in:
    their SCs
  40. W/ cat example: Deafferentation of spinal nn (cut dorsal roots --contain sensory neurons--no afferent input) and SC lesion:
    • no input when feet touch treadmill
    • no reflex
    • electrode below SC lesion: stimulating here begins gait (current activates CPGs)
  41. Anencephalic children (no brain=no supraspinal input) do have patterned flexion/extension movement while just lying there (genetic hardwiring):
    • anencephaly: cephalic disorder that results from neural tube defect that occurs when cephalic (head) of neural tube fails to close; resulting in the absence of a major portion of the brain, skull and scalp
    • still make walking movements b/c of CPG
  42. Normal infants make walking movements even though they have never experienced walking before:
    inherited CPGs allow this!
  43. So why can't people with SC injuries above the lumbar spine walk?
    • more complex to walk on 2 extremities instead of 4 (integration issues w/ equilibrium and balance)
    • most central pattern generators are learned, but gait is innate
    • humans require more supraspinal input
  44. Are spinal cord reflexes segmental in nature?
    yes; may involve 1 segment or several adjacent segments
  45. Spinal cord reflexes may involve propriospinal loops or circuits (neural circuitry):
    • located close to midline of SC
    • communicate b/w different levels
    • located in gray matter
  46. Spinal cord reflexes can be modulated by supraspinal influences:
    • rubrospinal tract (bias flexor activity)
    • reticulospinal tract (bias extensor activity)
    • Both influence LMN going to mm
  47. What are the 4 fundamental anatomical parts to a SC reflex?
    • receptor organ on distal end of sensory organ
    • afferent sensory neuron w/ receptor at distal end
    • efferent motor neuron w/ effector organ at distal end
    • effector organ (NMJ)
  48. Where must damage occur to lose reflex?
    damage to any part of the fundamental anatomical parts can cause pt to lose reflex

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