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BRS YEAR 2 > Motor Cortical Control > Flashcards

Motor Cortical Control Flashcards

1
Q

what kind of organisation exists in the motor system?

A

functional segregation
Motor system organized in a number of different areas that control different aspects of movement
hierarchical organisation depending on complexity of tasks (higher order control programme and decide movement and lower excecute tasks)

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2
Q

where does information from the primary motor cortex pass to?

A

basal ganglia, cerebellum, thalamus, spinal cord and brainstem

  • brainstem → muscles of head, neck, facespinal cord → rest of muscles
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3
Q

what muscles do motor information in the brainstem get passed to? what about the spinal cord?

A

brainstem → muscles of head, neck, face

spinal cord → rest of muscles

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4
Q

what do the basal ganglia and cerebellum do?

A

adjust the commands received from other parts of the motor control system

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5
Q

what are the pyramidal tracts?

A

corticospinal and corticobulbar

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6
Q

extrapyramidal tracts?

A

vestibulospinal, tectospinal, reticulospinal, rubrospinal

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7
Q

Are extrapyramidal tracts ascending or descending

A

Descending

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8
Q

what makes something pyramidal/extrapyramidal?

A

either pass through pyramids of medulla or don’t

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9
Q

functional differences - what do pyramidal do?

A

voluntary movements of body and face (motor cortex → cranial nerve nuclei or spinal cord)

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10
Q

functional differences - what do extrapyramidal do?

A

involuntary movements for posture, balance and locomotion
Brainstem nuclei to spinal cord

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11
Q

Corticospinal tract

A

Passes down lateral corticospinal tract or anterior corticospinal tract
Decussation occurs where most go to lateral
Lateral control limb muscles anterior control trunk

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12
Q

corticobulbar function?

A

movements of face and neck → cranial nerve nuclei

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13
Q

vestibulospinal function?

A

stabilise head during body movement , coordinate head movement with eye movement, postural adjustments

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14
Q

reticulospinal function?

A

Muscle tone changes with voluntary movement
postural stability
Primitive descending tact
From medulla and pons

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15
Q

tectospinal function?

A

orientation of head and neck during eye movements
From superior colliculus of midbrain

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16
Q

Rubrospinal

A

Innervate lower motor neurons of flexors of the Upper limb
From red nucleus of the
Mainly taken over by corticospinal tract

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17
Q

negative signs of upper motor neuron lesion?

A

loss of voluntary motor function
paresis (graded weakness of movements)
paralysis-complete loss of movement

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18
Q

Positive signs of upper motor lesions

A
  • spasticityincreased muscle tone
  • hyperreflexiaexaggerated reflexes
  • clonusabnormal oscillatory muscle contraction
  • babinski’s signabnormal upward curling of big toe (normal in infants but not adults) on stimulation

increased abnormal motor function due to loss of inhibitory descending inputs

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19
Q

Apraxia

A

Loss of skilled movement (loss of info is not paretic)
Have lost info about how to perform skilled movement

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20
Q

Common cause of apraxia

A

Stroke and dementia
Lesions of inferior parietal lobe ,frontal lobe (premotor cortex,supplementary motor area)

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21
Q

signs of lower motor tract lesion

A

hypotonia, hyporeflexia, muscle atrophy,weakness

  • fasciculationsdamaged motor units → spontaneous action potentials → visible twitch
  • fibrillationstwitching of individual muscle fibres recorded during needle electromyography
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22
Q

what are dysarthria and dysphagia?

A

Difficulty speaking or swallowing

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23
Q

what is motor neuron disease?

A

progressive neurodegenerative disorder of motor system → spectrum
Also known as amyotrophic lateral sclerosis
UMN-spasticity,brisk limb and jaw reflex,babinski sign,loss of dexterity,dysarthria,dysphagia
LMN-weakness,muscle wasting,tongue fasicukation,nasal speech,dysphagia

24
Q

basal ganglia main structural elements?

A

caudate nucleus
lentiform nucleus
substantia nigra (midbrain)
nucleus accumbens
subthalmic nuclei

25
Q

basal ganglia main function?

A

decision to move

performing associated movements e.g. changing facial expression in reaction, swinging arms while walking

suppressing unwanted movements

performing movements in order

26
Q

what is the striatum?

A

Caudate nucleus and putamen

27
Q

what is parkinson’s disease?

A

degeneration of dopaminergic neurons from substantia nigra to striatum

Symptoms include bradykinesia, expressionless face → hypomimic, akinesia (difficulty in initiation of movements), rigidity, tremor at rest

28
Q

Huntingtons disease

A

degeneration of GABAergic neurons in striatum caudate and then putamen

Symptoms involve jerky involuntary movement,difficulty swallowing,gait disorder and cognitive decline/dementia

Choreic movement

29
Q

What is ballism

A

Contralateral flinging of extremities
Caused by stroke affecting the subthalamic nucleus
Symptoms occur contralaterally

30
Q

What separates the cerebrum and cerebellum

A

Tentorium cerebelli

31
Q

broad function of cerebellum?

A

Coordinates and predictions of movement

32
Q

Three main parts of cerebellum

A

vestibulocerebellum (central strip), spinocerebellum (medial vertical stripe), cerebrocerebellum (lateral stripe)

  • vestibulocerebellumregulate gait, posture and equilibrium, coordinate head and eye movements. Damage (tumour) causes gait ataxia and tendency to fall even when sitting with eyes open
  • spinocerebellumcoordinate speech, coordinate limb movements, adjust muscle tone. Damage (degeneration and atrophy associated with chronic alcoholism) affect leg causing abnormal gait and stance (wide)
  • cerebrocerebellumcoordinate skilled movements, cognitive function & attention, process language, emotional control. Damage affects mainly arms/skilled coordinated movements and speech
33
Q

main signs of cerebellar dysfunction?

A
  • ataxiagait disturbance
  • dysmetriainappropriate force and distance for target oriented movement
  • intention tremoroscillatory limb trajectory in target directed movement
  • dysdiadochokinesiainability to perform rapidly alternating movements
  • scanning speechstaccato bc impairment of speech muscle coordination
  • lower motor neurons of brainstem and spinal cord
34
Q

Alpha motor neurons

A

Lower motor neurons of brainstem and spinal cord
Innervate extrafusal muscle fibres if skeletal muscle

35
Q

Activation of alpha motor neurons

A

Causes muscle contraction

36
Q

what is a motor unit?

A

single motor neuron along with all the muscle fibres it innervates

37
Q

different types of motor unit?

A

slow (type I)- small dendritic trees cell bodies and axons
fast & fatigue resistant (type IIA)-large dendritic trees cell bodie and axons
fast & fatiguable (type IIB)-large dendritic trees cell bodies and axons

38
Q

difference in force produced by IIA and IIB?

A

IIA is weaker, IIB (fatiguable) is stronger

39
Q

Order of motor unit recruitment

A

Small first to allow slow twitch units (fine movement allowed)

40
Q

Rate coding

A

Way for brain to regulate force a muscle produces
The higher the firing rate the more force produced

41
Q

Summation

A

unit fires at too fast a frequency to allow muscle relaxation between contractions → recruitment of other motor units

-

42
Q

what are neurotrophic factors?

A

growth factors that prevent neuron death and promote growth after injury

43
Q

what does cross innervation of muscle fibres do?

A

some properties are switched e.g. muscle fibres can become faster or slower dependent on nerve

44
Q

What change does aging cause

A

preferential loss of type II fibres → slower contraction times

45
Q
  • what determines the magnitude and timing of reflex functions?
A

Intensity and onset stimulus

46
Q

reflexes can’t be controlled but can be influenced e.g. by Jendrassik manoeuvre → what is that?

A

pulling against locked fingers to increase magnitude of knee jerk reflex
Can also bite down teeth or clench fist

47
Q

supraspinal control of reflex arcs under normal conditions?

A

Inhibitory

48
Q

what reveals the excitatory control?

A

Decerebration

49
Q

how can brain damage affect reflexes?

A

rigidity and spasticity from brain damage can result in over-active stretch reflexes

50
Q

hyperreflexia is associated with what kind of lesion?

A

upper motor neuron lesion → loss of descending inhibition

51
Q

defining features of clonus?

A

involuntary and rhythmic muscle contractions

52
Q

hyporeflexia is associated with what kind of disorder?

A

Lower motor neurone disease

53
Q

Descending supraspimal control of reflex

A
  1. Activating alpha motor neurons
    2.activating inhibitory interneurons
    3.activating propriospinal neurons
    4.activating gamma motor neurons
    5.actuvating terminal of afferent fibres
54
Q

Primary motor cortex

A

Located in pre central gyrus anterior to central sulcus
Controls fine discrete precise voluntary movement
Provide descending signal to execute movement

55
Q

Premotor area

A

Located anterior to primary motor cortex
Involved in planning movement
Regulates externally cued movement
Eg seeing an apple and reaching out for it

56
Q

Supplementary motor area

A

Located anterior and medial to primary motor cortex
Plans complex movement eg internally cued speech
Becomes active prior to voluntary movement

BRS YEAR 2 (43 decks)

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