Lecture 6 - Movement Flashcards

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1
Q

What are the 3 types of muscle?

A
  1. Smooth
  2. Cardiac
  3. Skeletal
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2
Q

Describe smooth muscle

A
  • under involuntary control (ANS)
  • 2 types:
    • Single unit - contracts as one, e.g. hollow visceral organs (but not heart), like digestive tract
    • Multi-unit - individual cells are innervated, allowing gradual responses, e.g. lining of airways, and arrector pilli muscle in skin
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3
Q

describe cardiac muscle

A
  • Found in walls of heart - rhythmic contractions
  • Under involuntary control (ANS) - from neural inputs (stimulation) or hormons (adrenaline)
  • mix of striped and smooth muscle
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4
Q

Describe skeletal muscle

A
  • Under voluntary control/ reflexes
  • attaches to bones via tendons
  • Striated/striped muscle
  • 2 main casus of movements
    • Flexion - bending joint towards body
    • Extention - relaxing joint
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5
Q

What are the 2 main types of skeletal muscle?

A
  1. Extrafusal muscle fibers
    - outside muslce spindle
    - causes muscle contraction
  2. Intrafusal muscle fibers
    - Inside muscle spindle
    - Functions as a stretch receptor
    - regulates muscle contraction by stopping unwanted stretch
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6
Q

What is the neuro-muscular junction

A

Synapse between motor neuron and muscle fibre

  • Motor neuron synapses motor endplates on surface of muscle fibre - this regulates muscle contraction
  • muscle fibre contains myofibril
  • Where muscular contraction occurs
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7
Q

Describe the physical basis of muscular contraction

A
  • Endplate potentials: axon fires, motor neuron releases ACH -> depolarises muscle fibre
  • rate of firing = strenght of contraction
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8
Q

How do we avoid muscle damage?

A
  1. Intrafusal muscle fibers
    - sensory endings detect strength and tells brain if theres too much contraction, or too much relaxation
  2. Tendons
    - GOLGI TENDON ORGAN - contains stretch receptors that detec tension - then tells brain same things
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9
Q

How is movement controlled by the brain?

A

Involves the motor cortex, which includes:
- Primary motor cortex
- Frontal association cortex (Suppplementary motor area)
- Pre-motor cortex
-

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10
Q

Describe the primary motor cortex

A

Main player in execution of movement

  • ORganised somatotopically (motor homunculus) - so each part is mapped to a body part
  • Not every body part is equally sized, some need larger areas, e.g. fingers, hands tounge need more
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11
Q

What are the inputs to the primary motor cortex?

A

Include:

  • Frontal association cortex
  • Supplementary motor area
  • pre-motor cortex
  • as well as Primary Somatosensory Cortex (S1)
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12
Q

Outline S1

A
  • concerned with experience of bodily sense - so we can respond to environment
  • S1 neurons are in a particiular location - sends info to primary motor cortex about the specific muscules its responsibile for
  • provides rapid feedback to motor system - heart and reflexes for protecive function
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13
Q

Outline the Supplementary Motor area

A
  • responsibile for learning, planning and performing behaviours, consisting of sequences of movements
  • e.g. walking
  • SMA & PRE-SMA = urge to move, or anticipation that a movement will occur (thoughts before moving)
  • PRE-SMA = Control of spontaneous movement
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14
Q

What can damage to the SMA do?

A

Cant execute well learned sequences of responses

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15
Q

Outline the premotor cortex

A
  • involved in learning and executing complex movements
  • individual movements, not sequence movements
  • movement when stimuli indirectly indicates what to do, “do you like that dress”?
  • Contains mirror neurons
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16
Q

Define apraxia and the types there are

A
  • difficulty carrying out purposeful movements, but no an issue of paralysis, muscule weakness, faulty PNS, spinal cord damage etc - only cos of dysfunction in motor areas
  • often caused by damage to corpus callosum, frontal lobe, or parietal lobe
    1. Limb apraxia
    2. Constructional apraxia
    3. Occulomotor apraxiq
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17
Q

Outline limb apraxia

A

Problems with movements of arms, hands, fingsers

  • wrong body part, wrong movement, or wrong sequence
  • caused by damage to:
  • anterior corpus callosum, left frontal or left parietal lobe
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18
Q

Outline constructional apraxia

A
  • Problems drawing 3d objects, making geometrical contstructions (brikcs etc), and map reading
  • damage to: right parietal lobe
  • cant make movements based on visual representation of angles/ lines
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19
Q

Outline oculomotor apraxia

A
  • problems making controlled, voluntary and purposeful eye movements, especially moving eyes horizontally
  • damage to corpus callosum
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20
Q

How does movement command from brain reach muscles?

A

2 groups of descending motor tracts from brain to periphery

  1. lateral group - 3 tracts including basal ganglia
    - Controls voluntary independent limb movements
  2. Ventromedial group - 4 tracts
    - controls automatic movements (e.g. keeping us balanced when walking)
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21
Q

What 3 brain areas are involed in modulation of movement?

A
  1. Basal ganglia (telenhcephalon)
  2. Cerebellum (hindbrain)
  3. Reticular formation
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22
Q

How does basal ganglia modulate movement?

A
  • Voluntary movement under control of primary motor cortex and ventromedial stream
    -Motor nuclei of BG include:
    • Caudate nucleus (input nuclei)
    • Putamen (input nuclei)
    • Globus pallidus (output)
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23
Q

What are BG’s inputs and outputs?

A

Inputs:

  • Cerebral cortex (primary motor cortex & primary somatosensory cortex)
  • Midbrain substantia nigra

Outputs:
- Motor cortex (primary motor cortex, premotor cortex and supplementary motor area) (via thalamus)

24
Q

What are the two disorders of the BAsal ganglia?

A
  • huntingdons and parkinsons disease
25
Q

Outline causes of parkinsons diseasee

A

Caused by:

  • damage to nigrostriatal bundle - which normally secrete dopamine
  • you therefore have an inbalance of excitatory and inhibitory neurons
26
Q

What are the symptoms of parkinsons

A
  • muscular rigidity
  • slowness of movement
  • resting tremor (pill rolling hands)
  • posutral instability (Cant sit upright)
27
Q

How can parkinsons be treated?

A

L-DOPA (dopamine precursor)

- sid effects - involuntary movements/ postures - festination, stalling movements

28
Q

Outline causes of huntingdons disease

A

Degeneration of caudate nuclueas and putamen, which should normally inhibit globus pallidus
- hereditary with no known treatment

29
Q

Define huntingdons

A

fatal in 10-15 years, usually starts in 30s/40s

30
Q

What are symptoms of huntingdons?

A
  • Cognitive & emotional change

- uncontrollable jerky movement

31
Q

what is the function of the cerebeluum?

A

to Smooth, and intergrate on going movement (riding a bike)

  • integrates moveemtn sequences
  • indepedent, rapid, slilled movements (e.g. catching a ball
  • postural reflexes
32
Q

What are the inputs/ outputs to cerebellum?

A

inputs:

  • vestibular system and audio/ visual systems - when controlling postural reflexes and catching a ball for instance
  • motor and somatosensory cortex - when controlling independent limb movement
33
Q

What are the outputs to cerebellum?

A

outputs:

  • vestibular system and audio/ visual systems - when controlling postural reflexes and catching a ball for instance
  • motor and somatosensory cortex - when controlling independent limb movement (fine movements)
34
Q

What are symptoms of ataxia?

A
  • Disturbance in balance/ posture
  • Decomposition of movement - separate, not smooth movements
  • Impaired timing of ballistic movements
  • trouble with independent limb movement
35
Q

What are causes of ataxia?

A
Stroke,
Haemmorrahge,
alcoholism
tumour
chronice, degenerative conditions
physical trauma
36
Q

cheese

A

crackers

37
Q

How does reticular formation modulate movement?

A

important in variety of motor functions

  • regulates muscle tone (how much muscles contract, i.e whats there resting positiong?)
  • controls autoomatic and semi-automatic movement (dont need to think about it but can inhibit it)
  • posture
  • locomotion
38
Q

What are somatosenses?

A
  • send info about events occuring on surface and inside body to brain
  • Cutaneous sense = skin senses (touch, pain, temperature etc)
  • Prioprioception - (stretch receptors- muscles and tendons) and kinesthiasia - collectively provide sensory info about bodily position and movement
  • organic sense provide info about pleasant and unpleasant sensations (cold drink on hot day)
39
Q

What are the 4 skin receptors

A
  1. Merkels sdics - indentation, just glaborous
  2. Ruffini copuslces - indentiation, both hair and glaborous
  3. Pancinian corpuscles - rapid vibrations of skin, both
  4. Mueisnners corpuscles - low frequency vibrations. taps, just glaborous
40
Q

What are the layers of skin?

A

Subcutaneous tissue, dermis and epidermis

41
Q

Which type of skin has the most receptors>

A

glabourous - hands and feet interact with env more

42
Q

How is touch perceived?

A

Through MECHANORECEPTORS - sensitive to pressure and vibration - caused by skin stretching, moving dendrites of mechanoreceptors

43
Q

What are the 4 types of mechano receptors and what do they do?

A
  1. Merkels discs - pressure, slow adaptation
  2. Ruffini copuslces - maintaining grip, slow adaptation
  3. Pancinian corpuscles - surface roughnuss, very small vibrations/ machines - rapid adaptation
  4. Mueisnners corpuscles - fine mechanical sensitive (e.g. insects on skin), moderate adaptation
44
Q

Define adaptation

A

How long it takes receptor cells to stop respondingin to a stimuli - to look for change

45
Q

How is temperature perceived?

A

Temp receptors = thermoreceptors

- Have free nerve endings in skin

46
Q

What are the 2 types of thermoreceptors

A
  1. warm receptors - signal conveyed in unmyelinated c fiber
  2. Cold reeceptros - signal conveyed in lightly myleinated Adelta and unmyelinated c fibers

Some also respond to chemicals (e.g. menthol)

47
Q

How is pain perceived?

A

Pain receptors = nocireceptors, detect noxious stimuli

- also have free nerve endings

48
Q

What are the 3 types of nocireceptors

A
  1. Heat sensitive (burning and imflammation)
  2. High-threshold mechanoreceptors (intense presure - pinch)
  3. ATP sensitive (reduced tissue blood supply - sleeping on arm), involved in angina, migraine, muscle damage, ATP is an energy source
49
Q

What are the 3 perceptual and behavioural effects of pain?

A
  1. Sensory (pain intensity) - invovolves pathway up to S1 and S2 pathway
  2. Immediate emotional consequences - unpleasantness of stimulus - involves insular cortex and anterior cingulate cortex
  3. Long-term implicatinos of chronic pain - involves pathways reaching to PFC
50
Q

What are the two ways that impulses generated by tissue damage are modified?

A
  1. ascending regulation of pain

2. Descending regulation of pain

51
Q

Outline ascending regulation of pain

A
  • modification of afferent info from env
  • MEZLACK & WALL - Gate theory of pain
    • Both tacticle and nocireceptive fibres synapse projection nureouns that carry pain info to brain
    • but can only carry 1 signal
    • Noxious input excites projection neuron -> more pain
    • Tacticle inhibits -> less pain
52
Q

Outside descending regulation of pain

A
  • endogenous opiods (natural painkillers), increase periaquiductal grey acitivity - reducing pain
  • Without them, periaquiductal grey gets input from fonrtal cortex, amygdala, hypothalamus - learning and emotion affect pain (important in chronic pain & knowing it wont hurt us)
  • Rostroventral medulla also reduces pain
53
Q

Define phantom limb syndrome

A

Sensation of continued presence of amputated limb - often feels like hand is clenched/ nails digging in

54
Q

What is the theory of phantom limb syndrome?

A

Crosswiring - as S1 is somatotopically arranged input from hand is near arm, but also near face
- areas near hand take over/ remap hand regiion thats no longer in use - so stroking face may feel like hand

55
Q

Outline somatosensory cortex

A

2 main areas:

  • primary somatosensory cortex (s1)
  • Secondary somatosensory cortex (s2)

Somatotopicly arranged - maintains spatial organisation within cns - like motor cortex (somatosensoty homunculus)
- important areas have bigger area

56
Q

what are the pyschological factors that influence pain?

A
  • early experiences - decreases sensitivity
  • Perceived self-efficacy “ i can take it”
  • Attention to pain
  • Anxiety, depression and perceived helplessness - leads to more pain