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BMB Test 2 > B7.038 Central Motor Systems > Flashcards

B7.038 Central Motor Systems Flashcards

1
Q

motor tracts within the lateral column of the cord

A

lateral corticospinal
rubrospinal
lateral reticulospinal

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2
Q

motor tracts within the ventral column of the cord

A

vestibulospinal
ventral reticulospinal
ventral corticospinal
tectospinal

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3
Q

how do descending systems inhibit spinal cord reflexes

A

can switch them on/off or change the strength
synapse with and inhibit/excite interneurons within the reflex pathways (reflexes can be suppressed with voluntary effort)

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4
Q

corticospinal/corticobulbar systems

A 
called pyramidal tracts
originate in motor and sensory cortex
terminate on CN nuclei (corticobulbar) or a and gamma motoneurons controlling distal limb muscles as well as interneurons (corticospinal)
-90% in lateral column
-10% in ventral column
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5
Q

sensory component of the corticospinal system

A

originates from primary somatosensory cortex (postcentral gyrus) and terminates in dorsal column nuclei and dorsal horn of spinal cord
can excite or inhibit dorsal column neurons
modulates activity in ascending systems and can screen out routine stimulation of the skin (from clothes)

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6
Q

extrapyramidal tracts

A 
rubrospinal
reticulospinal
-pontine
-medullary
vestibulospinal
tectospinal
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7
Q

rubrospinal tract

A 
originates in red nucleus
travels in lateral column
terminates on interneurons in spinal cord
largely crossed
controls distal limb muscles
stimulates flexors, inhibits extensors
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8
Q

red nucleus input

A

contralateral deep cerebellar nuclei

motor cortex bilaterally

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9
Q

reticulospinal tracts

A

originate from reticular formation of medulla and pons

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10
Q

pontine reticulospinal tract

A

travel in ventral column

stimulate muscles, primarily extensors

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11
Q

medullary reticulospinal tract

A

travel in lateral column

inhibit muscles, primarily extensors

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12
Q

vestibulospinal tract

A

originates from vestibular nuclei
terminates on interneurons and motoneurons in anterior horn, mostly ipsilateral
facilitates anti-gravity muscles
maintains posture

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13
Q

reticulospinal and vestibulospinal tract role in movements

A

limited role in extremities

main influence on trunk

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14
Q

tectospinal tract

A

originates from superior colliculus in midbrain
travels in ventral column, primarily crosses
terminates on interneurons and motoneurons in cervical spinal cord, mostly crossed
plays role in reflexive control of neck muscles in response to visual stimuli

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15
Q

alpha gamma coactivation

A

in voluntary movement, both alpha and gamma motoneurons are activated by descending systems
increases spindle afferent activity to assist with movement
results in automatic load compensation (bc gamma motoneurons sense changes in load)

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16
Q

spindle load compensation mechanism

A

increase in external load > increased spindle afferent activity > increased alpha motoneuron excitation > increased muscle tension > overcomes load

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17
Q

effect of corticospinal lesion

A

loss of fine motor control

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18
Q

effect of rubrospinal lesion

A

little or no deficit or corticospinal is intact

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19
Q

effect of reticulospinal lesion

A

severe impairment of axial and proximal muscles; loss of righting reflexes

20
Q

effect of vestibulospinal lesion

A

severe impairment of axial and proximal muscles; loss of righting reflexes

21
Q

decerebrate posture

A

results from damage to the upper brain stem (upper pons severed)
arms are adducted and extended
wrists pronated
fingers flexed
legs stiffly extended with plantar flexion of the foot

22
Q

decorticate posture

A

results from damage to corticospinal tracts
arms are adducted and flexed
wrists and fingers flexed on the chest
legs stiffly extended and internally rotated with plantar flexion of the foot

23
Q

why are motor cortex lesions worse than pyramidal tract lesions?

A

lesions of the pyramidal tract only destroy the direct influence of the motor cortex on motor neurons
motor cortex lesions destroy both direct and indirect influences of motor cortex on motor neurons (rubrospinal and reticulospinal)

24
Q

function of the basal ganglia

A

integrate multimodal (sensory, cognitive) cortical information (Glu) in the context of motivational information (DA) to initiate and maintain meaningful behavior

25
Q

receiving nuclei of BG

A

striatum
-putamen
-caudate
receives inputs from cerebral cortex

26
Q

globus pallidus

A

internal segment: output nucleus of BG

external segment

27
Q

striatal medium spiny neuron

A

receives input from: cerebral cortex (glu), substantia nigra(dopamine)
sends projections to GP (GABA)

28
Q

functions of BG

A 
selection of movements
gating motor function
motor learning
reward based conditioning
habit formation
29
Q

function of the BG in movement

A

disinhibits CNS structures and allows initiation of voluntary movements
normal output from BG is inhibitory and neurons have a high tonic firing rate

30
Q

direct route of BG

A

thalamic cells are released from inhibition (disinhibition)

  1. originates from cerebral cortex
  2. projects to striatum
  3. striatum projects to GPi or SN
  4. GPi projects to thalamus
  5. thalamus projects to cortex
31
Q

indirect route of BG

A 
corticostriatal excitation results in inhibition of GPe and disinhibition of STN
results in excitation of GPi, which inhibits the thalamus and decreases excitation in motor cortec
1. originates from cerebral cortex
2. projects to striatum
3. striatum projects to GPe
4. GPe projects to STN
5. STN projects to GPi
6. GPi projects to thalamus
7. thalamus projects to cortex
32
Q

effect of dopamine on direct/indirect routes

A

excited direct route, causing disinhibition of thalamus
inhibits the indirect rout, causing suppression of the STN and disinhibition of the thalamus
dopamine = increased motor activity

33
Q

excitatory components of the BG pathways

A
  1. cortical inputs to striatum
  2. pathways from STN to GPi
    mediated by glutamate
34
Q

inhibitory components of the BG pathways

A
  1. direct route from striatum to GPi
  2. GPi to thalamus
  3. indirect route from striatum to GPe
  4. pathways from GPe to STN
    mediated by GABA
35
Q

mixed components of the BG pathways

A

substantia nigra pathway has mixed effects, mediated by dopamine

36
Q

rigidity

A

increased resistance to passive joint movement

37
Q

Parkinsonian tremor

A

4-8 Hz oscillation occurring in absence of voluntary movement

38
Q

akinesia/bradykinesia

A

inability to initiate voluntary movement

most troubling motor symptom

39
Q

neuropathology of Parkinson’s

A
  1. degeneration of nigrostriatal dopamine neurons is the cardinal feature
  2. decrease in dopamine content in the striatum, symptoms appear when content drops below 20%
40
Q

abnormalities in neuronal activity in PArkinson’s

A

lack of SN dopamine results in an increased activation of the indirect pathway (inhibitory to cortex) and a decrease in activity of the direct pathway (excitatory to cortex)

41
Q

hemiballismus

A

high velocity, large amplitude involuntary slinging movements
generally involving the arms

42
Q

Huntington’s chorea

A

genetic disorder characterized by movement abnormalities and loss of GABA neurons projecting from striatum to GPe

43
Q

choreiform movements

A

involuntary, irregular, jerky movements that are slower and smaller amplitude than movements associated with ballismus

44
Q

athetosis

A

continuous writhing movements

45
Q

abnormalities in neuronal activity in Huntingtons

A

decreased inhibitory pathway activity in the BG leads to increase in excitatory stimulation to the cortex

46
Q

laterality of effects on movement from lesions of BG

A

lesions of the BG affect limb movements contralateral to the lesion
projections from BG to cortex are uncrossed
projections from motor cortex to the spinal cord are crossed

BMB Test 2 (22 decks)

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