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Neuroscience > Unit 3 - Motor Control > Flashcards

Unit 3 - Motor Control Flashcards

0
Q

Lower motor neurons

A

Motor neuron projecting from spinal cord to the motor end plate on muscle,
Synapses with upper motor neuron in ventral horn

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1
Q

Upper motor neuron

A

Projects from cortical areas to spinal cord, synapses with lower motor neuron

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2
Q

Higher cortical areas

A

–> no direct contact with spinal cord, so influence = indirect.
ie: association cortex, basal ganglia, and cerebellum
(Signal via thalamus)

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3
Q

Spinal circuit reflex

A

Most simple motor circuit,
Sensory receptors –> spinal grey matter –> muscle
(Cutaneous, pain or muscle spindles)
ie: stretch reflex

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4
Q

Central pattern generator (CPG)

A

Moderately complex motor circuit;
Generated at brainstem or spinal cord,
INdependent of descending input, but turned on/off by cortex
Ex: walking or breathing

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5
Q

ballistic movement

A

rapid movement that MUST go to completion
(can’t withdraw action once started)
ie: saccades (eyes), hemiballismus

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6
Q

organization of motor neurons in spinal cord

A

Medial: axial muscles – control balance/stability
Lateral: distal muscles – fine motor control
dorsal: flexor mm.
ventral: extensor, mm.

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7
Q

motor unit

A

a single alpha motor neuron, along with all muscle fibers innervated by it (3-1,000)

    • small size = fine motor control
  • increase muscle force by recruiting motor units
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8
Q

2 types of alpha motor neurons (+ function)

A

“red” (small): slow, low force, fatigue-resistant

“pale” (large): fast, fatiguable

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9
Q

monosynaptic/myotactic reflex

A
  1. passive stretch of tendon
  2. a) contract muscle (via muscle spindle Rs)
    b) relax opposing muscle (“reciprocal inhibition”)
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10
Q

nocioceptive withdrawal reflex

A 
1. nocioRs sense pain (ie: step on tack)
(--> Lissauer's tract)
2. a) ipsilateral flexor contracts
    b) contralateral extensor contracts
* provides support for opp. limb to "escape"
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11
Q

Muscle proprioceptive pathway

A
  1. muscle spindle (stretch R)
  2. ipsilateral dorsal column - spinal cord
  3. dorsal column nucleus
    * decussate!*
  4. contralateral medial lemmniscus
  5. VPL of thalamus –> S1 (cortex)
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12
Q

muscle spindle

A

in parallel with mm., w/ stretch Rs;

  • -> passive stretch/increase muscle length
  • 1a and II axons
    • gamma mns change length to increase sensitivity (via intrafusal fibers)
  • stimulated by vibration (lengthening illusion)*
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13
Q

Golgi tendon

A

in series w/ mm (at end, inside collagen);

  • -> isometric contraction (tension on muscle)
  • 1b axons to inhib. interneurons, compensate for fatigue
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14
Q

Lesion to posterior parietal cortex

A
  1. apraxia (loss of learned/skilled movements)

2. optic ataxia (mis-reaching)

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15
Q

Lesion to premotor/supplementary motor cortex

A

poor planning and sequencing,
decreased spatial organization
* feet = medial, head = lateral

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16
Q

lesion to basal ganglia

A
  1. akinesia/bradykinesia (slowed mvmt)
  2. ballismus
    (responsible for selection and initiation of mvmt)
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17
Q

lesion to cerebellum

A

ataxia (uncoordinated mvmt)

* normally responsible for mvmt smoothness and coordination

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18
Q

Cortical circuits involved in voluntary movement

A

Direct to spinal neurons:
1. corticospinal tract; 2. corticobulbar (*bilateral!)
INdirect to spinal neurons:
1. corticorubral tract; 2. corticoreticular tract

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19
Q

Thalamic motor control

A
  1. VPL = somatosensory (proprioceptive/cutaneous info)

2. VA/VL = timing/coordination

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20
Q

Major cortical motor areas

A

1.Primary motor cortex (BA 8)
2. Supplementary motor cortex (BA 6)
3. Premotor cortex (BA 6)
4. Cingulate Motor area (BA 24)
Req’s: thin granular layer (IV), & electrical stim. to area –> mvmt

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21
Q

Neurons in primary motor cortex (M1)

A

each = directionally tuned,

fire: just before & during mvmt, (latency = 100-150 ms)
* population vector of neurons matches direction of mvmt*
- - increase firing rate = increase force

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22
Q

lesion to pyramidal tract

A

decrease in hand control, ie:

  1. thumb-finger opposition
  2. precise grip (=> “scoop hand”)
  3. single digit extension
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23
Q

lesion to primary motor cortex

A
  • -> spastic paresis (bc = upper motor neurons)
  • lose fine motor control
  • increase tone/hyper-reflexia
  • adjacent representations fill in void! (modified by use/experience)
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24
Q

Function of Premotor cortex (BA 6)

A

1) learned visual stimulus-response associations

2) rule-based actions
3) motor planning (to instructional cue)
* ventral (PMv) = hand grasp & mirror neurons
* dorsal (PMd) = arm reach

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25
Q

Supplementary motor area function (SMA):

A

self-initiated mvmts, mental mvmt rehearsal, and learned motor sequences.

  • single neurons = selective for specific mvmt sequences (Bop-it);
  • – “bereitshift potential” = from EEG over SMA.
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26
Q

“distributed processing” for motor cortex:

A

Multiple distinct cortical areas responsible for motor processing,
* all areas have different but overlapping function*
–> damage to 1 area = mild/transient,
BUT damage to >1 area = severe, persistant

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27
Q

input to inferior cerebellar peduncle:

A
  1. vestibular nuclei
  2. brainstem
  3. spinal cord
    * output = vestibular nuclei
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28
Q

input to Middle Cerebellar Peduncle:

A
  1. Pontine Relay Nuclei
  2. Cerebral cortex
    (output = cerebellum)
29
Q

Cellular organization of the cerebellum

A

3 layers, 5 total cell types.

  1. Purkinje layer: 1 cell thick (purkinje cell bodies)
  2. Molecular layer: purkinje dendrites, parallel fibers, and interneurons
  3. Granular layer: granule cells (= cell bodies of parallel fibers),
    * inhibited by Golgi cells (interneurons, NT = GABA)
30
Q

synapses on Purkinje cells

A

all use glutamate as excitatory NT,
1. Climbing fibers (from Inf. Olive) –> short AP burst
= motor error signal (teaching)
2. Granule cells (become parallel fibers) –> single AP
= sensory feedback/motor commands
** Purkinje cells = INhibitory to Deep Cerebellar Nuclei **

31
Q

Climbing fibers

A

neurons connecting Inferior Olive to Purkinje Cells (excitatory),
for signaling motor errors;
input to Inf.O. from:
Cerebral cortex, Red Nucl., Spinal Cord, Deep Cerebellar Nuclei

32
Q

Mossy Fibers

A

neurons in cerebellum connecting input to Purkinje cells (excit.),
via Granule cells/parallel fibers.
Input from: Cerebral cortex, Brainstem and Spinal cord.

33
Q

Long-term Depression

A

phenomenon where parallel fiber signaling is weakened by simultaneous firing of climbing fibers.

34
Q

Output from cerebellum

A

info from cerebellum to a) motor thalamus, b) Red Nucleus

via Superior Cerebellar Peduncle.

35
Q

Inferior Olive (relation to cerebellum)

A

Receives input from Cortex, Red Nucleus, Spinal Cord, and Deep Cerebellar Nuclei (“Loop Circuit”).
* sends to CONTRAlateral cerebellar hemisphere.
Inferior Olive –> Climbing Fibers –> Purkinje Cell(s)

36
Q

unilateral lesions in cerebellum cause…

A

Hypotonia (if decrease gamma motor neuron activity via thalamus),
= IPsilateral deficits bc cross twice (in SCP and after M1)

37
Q

Vestibulocerebellum

A

= vermis and flocculonodular lobe.
controls balance and eye mvmts,
Inputs: vestibular nuclei, visual cortex, motor cortex (for posture)
Output: Vestibular nucleus
Lesion deficits:
- balance: fall to side of lesion,
- Eyes: spontaneous nystagmus, poor smooth pursuit (eyes(

38
Q

Spinocerebellum

A

= vermis and medial hemispheres;
Receives somatosensory info.
Input: spinal cord (ipsilateral limb tracts)
Output: to Reticular Formation (via Fastigial nucleus)
Lesion Deficits:
Ataxia, dysmetria (poor coordination), hypotonia, tremor, poor rapid alt. mvmts/decomposed mvmt.

39
Q

Cerebrocerebellum

A

= lateral hemisphere; helps w/ voluntary mvmt.
Input: Motor cortex, somatosensory cortex, Association cortex
Output: Motor thalamus (via dentate nucleus)
Lesion Deficits: fine mvmt ataxia, cognitive deficits

40
Q

Basal Ganglia

A

“Gates” mvmt (selection and initiation); somatotopic organization.
= Striatum, Globus Pallidus, Subthalamic nucl, and Substancia Nigra.
– Direct Path: suppress inhibition –> increase motor output.
— Indirect: inhibit direct path –> decrease motor output.

41
Q

lesion to caudate nucleus

A

deficit = robotic walking

42
Q

Lesion to putamen

A

deficit = vulgar and impulsive personality shift, hypersexuality

43
Q

striatum neurons

A

= medium spiny neurons (“MSNs”) –> inhibitory projections to globus pallidus, NT = GABA.
(+ some interneurons)
* somatotopic organization

44
Q

Nigrostriatal pathway

A

from STN (subthalamic nucleus) to Striatum;
D1 Rs: + to MSNs in Direct path.
D2 Rs: - to MSNs in INdirect path
==> promote movement (aka motor output)
** Dopamine deficit in Parkinson’s limits this pathway.

45
Q

Parkinson’s Disease

A

–> akinesia, bradykinesia, slow rest tremor
= Dopamine deficit to nigrostriatal pathway,
From oxidative stress, mimicked by MTPT drug.
Treatment: L-DOPA, Pallidotomy (decrease inhibitory GPi output), DeepBrain Stimulation

46
Q

Huntington’s Disease

A

autosomal dominant mutation (CAG repeat on chrom.4 short arm)
-> MSNs and cerebral cortical neurons die
==> chorea, athetosis (slow writing), Dementia, and personality changes.
* 30-50 yr. onset

47
Q

Direct Basal ganglia pathway

A

Cortex –> (+) striatum –I (-) GPi/SNr -/-I Thalamus

==> suppress inhibition = increase motor output

48
Q

INdirect Basal Ganglia pathway

A

Cortex–> striatum–I GPe -/-I (-)STN –> (+)GPi/SNr –I Thalamus
==> inhibit direct pathway = Decrease motor output

49
Q

Lesion to Globus pallidus

A

–> dystonia (sustained muscle contractions, abnormal postures, etc.)

50
Q

lesion to Subthalamic Nucleus (STN)

A

–> hemiballismus (involuntary flinging motion in extremities)
bc lesion causes LOSS in mvmt inhibition (via INdirect pathway)

51
Q

Muscle groups used for postural tone

A

(tonic activity in muscles opposing gravity)

  • Upper limb flexors
  • Lower limb extensors
52
Q

2 routes for postural control

A
  1. Direct: via vestibulospinal tract to alpha mns
  2. Reflex Route: via corticospinal or reticulospinal tracts to gamma mns
    ==> act on muscle spindles to increase tone via alpha mns
53
Q

Reticulospinal tract and postural control:

A

to modulate gamma mns –> affect alpha mns;
a) Cortex –I Pontine Reticular Formation –> + gamma mns
= increase m. tone.
b) Cortex –> Medullary Reticular Formation –I - gamma mns
= DEcrease tone.

54
Q

Lesion to “MRF” (medullary reticular formation):

A

INcreased tone bc DISinhibit gamma neurons

(so increase alpha mn work too)

55
Q

Median Vestibular tract (“MST”)

A

carries bilateral cervical information from semicircular ducts,
=> stabilize head position, influence alpha mns to neck muscles.
(maintain center of gravity)

56
Q

Lateral Vestibular tract (LVST)

A

ipsilateral to all levels of spinal cord,
=> stabilize stance/maintain balance and posture.
to alpha mns of legs
(anti-gravity and tilt reflexes)

57
Q

Lesion to vestibulospinal tracts

A

loss of balance,

will fall towards side of lesion

58
Q

Decortication

A

lesion above the red nucleus, so red nuc = DISinhibited;
(ie: cerebral cortex, internal capsule, thalamus)
Sx –> flex arms and extend legs

59
Q

decerebration

A

lesion below the red nucleus, disrupts the rubrospinal tract
(loss of tonic input from cortex –> hyperactive stretch reflex)
-> increase gamma mn activity = increase postural tone
Sx –> extend arms and legs, arch head back
Treatment: cut dorsal roots to decrease rigidity

60
Q

Reasons for return of sensation >2 months after lesion

to descending systems

A
  • -> hyperactive reflexes and hypertonic bc…
    1. denervation sensitivity (increase sensitivity to input)
    2. synaptic void filled by nearby neurons (increase strength of proximal circuits)
61
Q

saccade

A

ballistic mvmt to rapidly redirect fovea,
*not modifiable once started, = CPG reflex.
** CAN perform on verbal command**
During mvmt: blurry image and no f(x)al vision
Latency: 150-200 ms, Duration: 20-50 ms
Velocity: ~400 degrees/second

62
Q

Smooth pursuit (eye mvmt)

A

eye mvmt to follow moving target – eyes match speed of target;
“retinal slip” = speed mismatch
* canNOT perform on visual command (uses saccadic tracking)
DO have f(x)al vision while move eyes
= voluntary cortical modulation of reflex mech in brainstem

63
Q

Lesion to cortical eye fields and/or brainstem visual centers

A

1 or other: mild, transient saccade deficits

Both areas: severe and persistent saccade deficits

64
Q

Cortical eye fields

A

code direction and amplitude of eye movement,
each neuron = directionally tuned.
= frontal/supplementary eye fields and lateral intraparietal area;
*project to: a) brainstem (saccade reflex)
b) pontine relay nuclei/cerebellum (smooth pursuit)

65
Q

Superior colliculus

A

1 of 2 visual centers in brainstem, = on tectum of midbrain;
F(x): reflexive, contralateral saccades
- superficial layer: stimulus position
- deep layer: direction/amplitude of saccade

66
Q

reticular formation

A 
1 of 2 visual centers in brainstem,
= saccade central pattern generator
a) midbrain (riMLF) = vertical component
	- output: abducens nucleus
b) pons (PPRF) = horizontal component
	- output: occulomotor nucleus
 *output goes 1st to nucleus of IPsilateral eye!
67
Q

“Pulse-step” pattern for visual saccades

A

= firing pattern in abducens and occulomotor nuclei;

  1. pulse: burst –> saccade
  2. step: tonic activity –> fixation/tension
68
Q

pathway for smooth pursuit:

A
  1. cortical eye fields/extrastriate visual cortex
    - via Pontine Relay Nuclei -
  2. Cerebellum: Flocculum
  3. Vestibular nuclei
  4. Brainstem nuclei (direct to abducens, INdirect to occulomotor)
  5. Eye muscles
69
Q

Function of Vermis (cerebellum) in saccades

A

adjusts amplitude of saccade to match target
(so gaze lands accurately on target)
*Lesion ==> dysmetric saccades (miss/overshoot target)

70
Q

Lesion to flocculum (cerebellum)

A

–> smooth pursuit = abolished!
but saccades not affected.
(so use saccadic tracking to overcome deficit)

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