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Where can damage to the LMN occur?
cell body or axon
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Which CNs are invovled with LMN paralysis?
any CN w/ motor function
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What are the types of neurons that can be LMN?
alpha or gamma motor neurons
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Where are LMN found?
- motor nuclei of CN
- ventral horns of SC
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Damage of LMN in Sc damage:
ventral horns, ventral root, spinal nerve or peripheral nerve
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Damage of LMN in CN damages:
motor nucleus in brainstem or facial nerve itself
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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)
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What are the clinical signs of LMN damage?
- paresis
- flaccid paralysis
- hypotonia
- decreased or absent DTR
- atrophy
- fibrillations/fasciculations
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Paresis:
- weakness; not innervating skeletal muscle resulting in dramatic weakness
- also occurs w/ UMN damage
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When peripheral nerve is cut, NMJ is no longer functioning, therefore:
skeletal muscle function is lost (paresis)
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Flaccid paralysis:
- total loss of muscle tone with resultant loss of function
- lost instructions from LMN
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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)
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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)
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Decreased or absent DTR:
wiped out LMN part of reflex arc
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atrophy:
reduction in size of skeletal muscle as a result of decreased tone (decreased actin and myosin fibers)
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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
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Is there atrophy with UMN damage?
no b/c muscle cells are still contracting but it is spastic
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Fibrillation/fasciculations:
- spontaneous activity of skeletal muscle
- physiological (chemical) response, not neurological (neuron is not telling muscle to contract)
- disturbance of pH
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Are symptoms of LMN damage contralateral or ipsilateral?
always ipsiltateral
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For LMN damage, what is the reference point for ipsilateral and contralateral?
the lesion
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Where is the cell body of LMN?
ventral horn of SC or motor nucleus of CN w/ motor function
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Do LMN decussate?
no, therefore damage is always ipsilateral
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Which CN are involved with LMN paralysis?
CN III, IV, V, VI, VII, IX, X, XI, XII
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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!
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What happens during LMN paralysis?
- ipsilateral damage
- loss of parasympathetic activity
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What are the categories of collective responses of normal LMN physiology?
- spinal reflex responses
- brainstem reflexes
- posture and muscle tone
- rhythmic patterned movements
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What are spinal reflex responses?
- noxious stimulation reflexes
- DTR
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What are brainstem reflexes?
- counterpart of SC reflexes
- noxious reflexes
- DTR
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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
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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
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What do rhythmic patterned movements become?
central pattern generators (CPG)
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What are central pattern generators?
- used to delineate rhythmic patterns (generate motor activity)
- neural networks that produce rhythmic patterned outputs w/o sensory feedback
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Where are CPGs maintained?
- basal ganglia
- spinal cord
- brainstem
- cerebellum
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What are reciprocal inhibitory neural circuits?
physiological substrates for rhythmogenesis in CPG systems
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CPGs are hardwired systems set up:
above structures
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When do you make new central pattern generators?
each time you learn a new motor task (like learning to play violin)
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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
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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
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Research shows that humans have central pattern generators in:
their SCs
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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)
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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
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Normal infants make walking movements even though they have never experienced walking before:
inherited CPGs allow this!
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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
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Are spinal cord reflexes segmental in nature?
yes; may involve 1 segment or several adjacent segments
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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
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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
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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)
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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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