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brain & behaviour 2 > Advanced Movements > Flashcards

Advanced Movements Flashcards

1
Q

why do humans have complex nervous systems?

A

as a way to navigate through an environment which is constantly changing

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2
Q

how do sea squirts nervous systems work?

A
  • sea squirt larvae = more complex than its adult form
  • has motor cord and brain-like ganglia
  • upon finding a rock/stationary object, sea squirts become sessile, absorb much of its own brain and return to a rather primitive condition
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3
Q

what does cerebellum mean in Latin?

A

little brain

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4
Q

Graded and Competitive Goal Selection (selecting goals for actions) [Roitman and Shadlen]
-> looking at how our brains may respond to different quality of signal - we can look at the neurological activity and see what kind of quality of signal was received
-> wanted to see premotor areas responding to sensory cues which are enhanced or diminished based on the sensory cues involved

What happened in this experiment?

A
  • Juice monkeys trained to respond visual signal and then choose a course of action in order to get a juice reward
  • presented with two targets (T1 and T2) and they are presented with a target (loads of dots), they have to look at the correct location to get a juice reward
  • In motion condition, you can vary the quality of the stimuli (no useful information, or subtle change indicating a direction which may indicate some kind of a reward (25% motion coherence (move in the right direction) or 50% motion coherence))
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5
Q

how can dispute the idea of free-will?

A

our brains particularly the premotor area, get ready to perform a motor act before we consciously decide to do something

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6
Q

what differences can we see in the monkey’s posterior parietal cortex? (Roitman and Shadlen, 2002)

A

when you differentiate brain activity based on the coherence of the signal
-> 50% highest firing rate, 25%, 5% chance level (and then 0% is last)
-> so any given time, more quality of information can prime your ultimate decision making on what to do next

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7
Q

what is sensorimotor transformation?

A

the process in which sensory stimuli are converted into motor commands
-> something needed to move, navigate the world and react to the environment

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8
Q

what requires a sensorimotor transformation?

A

a reflex -> gets converted in your nervous system into an actionable signal that your body makes
-> there are many types to: responds to sound, vision nd smell

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9
Q

what are two motor commands which require sensorimotor transformation and use the visual system?

A

reaching and grasping

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10
Q

how does reaching link to sensorimotor transformation?

A

system responsible for transforming visual information about the location of objects in extra personal space into the direction of a reaching movement
-> A path connects the parieto-occipital extrastriate area (PO) and the dorsal motor area (PMd)

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11
Q

how does the reaching system work?

A

PO connects with MDP (medial dorsal parietal), and MIP [codes the location of target you’re reaching for] (medial interparietal areas), eventually reach the PMD and allow you to reach in an appropriate direction

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12
Q

how does grasping link to sensorimotor transformation?

A

this system is responsible for transforming visual information about the properties of obkects, such as shape and size, into commands for effective grasping.
-> A path connects the dorsal and extrastriate (ES) cortext and the ventral premotor area (PMv)

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13
Q

how does the grasping system work?

A

Information fed back into primary motor cortex, and dorsal ES area and AIP (focus on shape size, orientation, including orientation of your hand), pre-motor area specifically works on grasping + a reminder that this is a constant flow of information

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14
Q

if the parietal area is damaged, there may be some issues. what is this condition called?

A

Optic Ataxia
-> anything behind the central sulcus seperating the frontal and parietal lobe can cause issues with this type of sensori-motor transformation

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15
Q

What is Optic Ataxia?

A
  • an inability to reach and orientate your grip accurately under visual guidance (often like they’re reaching out in the dark)
  • reaching accurately involves reaching in the right direction with the correct grip, scaling and grip orientation/finger placement
  • visual guidance means being able to see both the target and the hand throughout
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16
Q

what is optic ataxia an issue with?

A

converting visual feedback into well actionable actions
-> not due to any basic sensory or motor deficit

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17
Q

what limbs can optic ataxia affect?

A

can affect one limb in one or both hemispheres (not purely visual or spatial) or can affect both or one limb in one hemisphere (not purely motor)

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18
Q

how does co-ordination work to reach a visual target?

A
  • parietal cells represent location of visual stimuli]
  • brain must transform between multiple coordinate systems to generate reaching to a visual target
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19
Q

double dissociations can tell us which part of the brain gets damaged in relation to visual tasks like this? what dies evidence help to tell us?

A

the parietal cortex helps the coordination of visual and position information for pre-motor areas

  • dorsal ‘where’ stream is a pathway that allows us to form visually guided behaviour
  • ventral ‘what’ pathway helps us with the ability to remember and identify things (ventral has strong connections with long term memory in the medial temporal lobe)
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20
Q

what can happen if you damage a specific parietal area

A

like optic ataxia
-> can describe what something is but not guide your hand towards it

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21
Q

what happens if your posterior parietal cortex is untouched, yet you damage the medial temporal lobe

A

your ability to describe would be severely disrupted

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22
Q

chains of movements are strung together with the intent to do what? (and what component is important for this)

A

to achieve a goal (and the supplementary motor cortex is important for this)

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23
Q

what is the supplementary motor cortex/area essential for?

A

self-generating movements
-> can draw on your stored repertoire of movements at any given point, irrespective of what’s going on in the environment

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24
Q

without the SMA what would happen?

A

we would no longer be able to perform well learned movements and rely on external cues to get things done

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25
Q

what could deactivation of SMA prodce?

A

severe disruption of learned sequences

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26
Q

what must there be a functional dissociation between to produce cued and uncued movements?

A

the pre-motor cortex and supplementary motor cortex

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27
Q

in the absence of explicit sensory cues, what is crucial?

A

for temporal structure of movement (SMA region)
-> And multiple movements or multiple motor programs can be relayed in a pre-determined (or determined) order

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28
Q

how can we measure the impact of knocking the system (SMA) out?

A

muscolo injections (an inhibitor of brain activity providing a temporal lesions in monkeys)

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29
Q

Cued sequences and learned sequences after a muscolo injection which is inhibiting this particular brain region

A

can see monkeys might learn an acute sequences (push, pull), show them a light to cue them and they will be able to do those actions in the correct sequence BUT if you ask them to perform a sequence they’ve learned previously, that has become reliant on the SMA then they create a lot more errors and we assume the size of the lesion/injection size would correlate with decreased performance on this task
-> functionable association here between the primates area, the supplementary motor areas and we can measure it depending on the particular tools and techniques we use

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30
Q

what size is the cerebellum?

A

small but highly folded and large surface area because of the sulci and gyri

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31
Q

can you read the cerebellum with fMRI?

A

difficult
-> relatively understudied for its importance and intrinsic role in certain aspects of our movement (due to the difficulty studying it)

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32
Q

what happens to the cerebellum if it’s damaged?

A

issues with co-ordination and voluntary motor movements, and ability to maintain balance and equilibrium

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33
Q

what is the basal ganglia?

A

group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions

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34
Q

where is the cerebellum?

A

at the back of the brain, immediately inferior to the occipital and temporal lobes, and within the posterior cranial fossa.
-> It is separated from these lobes by the tentorium cerebelli, a tough layer of dura mater

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35
Q

where is the basal ganglia?

A

nuclei embedded deep in the brain hemispheres

36
Q

what is the striatum?

A

a cluster of interconnected nuclei that form a part of the basal ganglia. It is involved in decision making functions, such as motor control, emotion, habit formation, and reward

37
Q

what is error correction?

A

when we make a movement, we receive a signal from our cortex on what we’re meant to do as well as information on what we’ve done (where our body is in space and time -> info is co-ordinated in the cerebellum)

38
Q

what does the cerebellum compare in error correction?

A

compares what you did and what you intended

39
Q

what happens if there is a mismatch?

A

will send advice out to the cortex to correct your movement, resulting in a fairly smooth movement (cerebellum allows us to smooth our movement)

  1. signals leave the motor cortex and go through the cerebellum
  2. also get a signal on what the body is doing from the spinal cord
  3. compares the two and adjusts what you do to produce smooth movement
    ^ stabiliser
40
Q

how does motor learning work?

A

we learn through practice or experiencing a certain skill

41
Q

how does the cerebellum help you when learning a skill?

A
  1. start learning a new skill -> mismatch in what you intended but the cerebellum will help you reduce the amount of error in these signals
  2. cerebellar neuronal circuits learn to make more accurate movements progressively over time
  3. after motor act has been repeated many times (.e. motor training), the successive steps of the motor act become gradually more precise over time and ultimately established in their own right
  4. results in changes in the nervous system and the production of a new motor skill in its own right -> procedural memory
  5. once the cerebellum has perfecly learned its role in different patterns of movement, it establishes a specific motor program for each of the learned movements
42
Q

what are ballistic movements?

A
  • movements include writing, typing, talking, running etc. (so fast/rapid that there is no way you can physically alter its trajectory until once its been conducted) -> beyond the realms of sensory feedback

-> These movements occur so rapidly that it is almost impossible to depend for their control on the sensory feed-back.
-> Once the movement is activated there is no way to modify its present course by any sensory feed-back control mechanism

43
Q

what does ballistic mean?

A

grow

44
Q

Cerebellum: Input and Output

A

INPUT: frontal motor and parietal cortices going to the pons and then crossing the midline (one side of the body to another) [brain informing the cerebellum of what you’re planning to do].
- you have a number sub-systems feeding into the cerebellum, telling it what you actually did

Midline: when you cross from one side of the body to the other - for integration reasons. This is information on what you intend to do, informing the cerebellum what you plan to do

If there’s a mismatch: Cerebellum talks to the deep cerebellar nuclei and moves that information back across the midline through the ventrolateral complex (known as the thalamus - common output for the basal ganglia and the cerebellum) to the primary motor and premotor cortices to enact that corrective movement

45
Q

you have a number of subsystems feeding into the cerebellum, telling it what you actually did, what are these?

A
  • Inferior Olive: senses from vision and hearing
  • Vestibular Nucleus: movement of the head, trunk and limbs
  • Spinal Cord: what your body is doing right now (what your muscles have done and what they’ve intended to do
46
Q

what happens if there’s some sort of mismatch?

A

need to do some sort of error correction and this is what is happening in the output
-> cerebellum talks to the deep cerebellar nuclei and moves that information back across the midline through the ventrolateral complex (known as the thalamus - common output for the basal ganglia and the cerebellum) to the primary motor and premotor cortices to enact that corrective movement

47
Q

the thalamus is a common output for what?

A

basal ganglia and cerebellum -> provides a route back to the primary cortex from two different areas

48
Q

How does Motor Error Correction Work?

A
  1. Information from the motor cortex (left, what your body has done. Right, what you’ve predicted).
  2. Spinal cord and musculoskeletal system feeds forwards to the motor output and sensory consequences - one half of the comparative function
  3. Cerebellum predicts sensory consequences )and this is the other half of the comparative function) generating an error signal which is punted from the cerebellum up to the thalamus and allows you to correct a given movement
49
Q

what did original research (prior to 1990s) did they say was the primary role of the cerebellum?

A

motor functions

50
Q

what has more recent evidence suggest about the cerebellum and error correction?

A

involved in cognition

51
Q

what might the cognitive error correction occur?

A
  • functionality of the cerebellum may be co-opted (in terms of it way of correcting our motor errors)
    -> We might see the prefrontal cortex, prefrontal target areas feeding information about the consequences of your cognition (one half comparative function and the cerebellum is giving the other half of the comparative function, your predictive cognitive consequences were of this particular act you’ve made
    -> This generates error signal, which is punted from the cerebellum to the thalamus to the prefrontal cortex, like motor area connection
52
Q

types of cerebellar dysfunction: how can cerebella ataxia be acquired?

A

can be acquired through bleeding of the cerebellum (strokes), mercury exposure, lead or another toxin, viral bacterial infections (incl Lyme disease) and chicken poxs

53
Q

what are some symptoms of cerebella ataxia?

A
  • Errors in range and direction of movement
  • Uncontrolled eye movements.
  • Unsteady gait.
    Slurred speech and more.
54
Q

how can we test whether an individual has cerebella ataxia?

A

taking your finger out and pointing it to your nose as individuals with cerebellar dysfunction will struggle to actually touch their nose/land it properly

55
Q

types of cerebellar dysfunction: what is hypometria and response delays?

A
  • Delayed response.
  • Hypometria: movements short of intended goal.
56
Q

types of cerebellar dysfunction: what is Dysdiadoch Kinesia?

A

Impairment of ballistic ability to perform rapid alternating movements

57
Q

how do alcohol and field sobriety tests work?

A
  • FST allows police to gauge how much you’ve been drinking -> cerebellum is sensitive to the ethanol found in alcohol
  • People will have trouble co-ordinating their feedback
58
Q

Cerebellum reliant aspects of the FST include:

A

▪ Walking in a line.
▪ Touching the tip of the nose with eyes closed.
▪ Quality control on bad ideas…

59
Q

what does the basal ganglia do?

A

inhibit actions generated by the motor cortex
-> motor cortex is in a state of excitation and is constantly trying to move and the way that we gate movement is between degrees of inhibition in the basal ganglia loop

60
Q

what is the role of the basal ganglia?

A

action selection

61
Q

How does the basal ganglia loop work?

A
62
Q

Caudate and Putamen

A

receiving zones (get signals from the cortex and collectively you might see them sometimes known as the straitum)

63
Q

Globus pallidus and substania nigra para reticulata

A

provides the principal output

64
Q

what are the Globus pallidus and substania nigra para reticulata modulated by?

A

substania nigra pars compacta
-> latin for black substance (melanin makes it appear darker and we think it has a protective function for this particular brain region)

65
Q

what two regions does the substance nigra pars compacta

A

pars compacta and the pars raticulta
-> producing dopamine which modulates the whole system

66
Q

where is the sub thalamic nuclei?

A

sits below the thalamus

67
Q

what connections is the thalamus in?

A

constant state of excitation to the cortex
-> (constant flow of excitation up to the cortical structures)

68
Q

what relationship does the cortex have with the caudate and putamate?

A

excitatory

69
Q

what relationship does the caudate and putamen have with globus pallid us and substantially nigra pars compacta??

A

inhibitory
-> this releases the thalamus from any kind of pressure - - generate more excitatory information that goes up to the cortex (this is like the direct and indirect pathway)

70
Q

what happens during an excitatory connection?

A

do it’s job stronger

71
Q

what is hypokinesia?

A
  • Insuffient direct pathway output
  • Excess indirect pathway output

-> excessive slowing / diminished ability to move

72
Q

what is hyperkinesia?

A
  • Excess direct pathway output
  • Insufficent indirect pathway output
    -> people making too much movement
73
Q

Direct Pathway: Stimulate Movement

A

Cortex (stimulates) -> striatum (inhibits) SNr-Gpi (less inhibition of thalamus - doing there job not so much- and will generate more movement in your muscles) -> Thalamus (stimulates) -> cortex.

  • Cortex then stimulates the corticalspinal tract via upper motor neurones -> lower motorneurones -> muscles = movement.
74
Q

Indirect Pathway: Inhibit Movement

A

Cortex (stimulates) -> striatum (inhibits) -> GPe (less inhibition of STN) -> STN (stimulates) -> SNr-Gpi (inhibits) -> Thalamus (is stimulating less) -> Cortex

  • Cortex (is stimulating less) -> Upper motorneurones -> Stimulated less -> Lower motorneurones (stimulated less) -> Muscles (stimulated less) = flaccid muscles and less movement.
75
Q

What is Parkinson’s disease?

A
  • Resting tremor in limbs (~4-5 Hz) that disappears on movement or during sleep.
  • Muscle rigidity – resistance to passive movement: jerky (cogwheel) movement.
  • Akinesia – general paucity of involuntary movement.
  • Bradykinesia (slowness).
  • Can produce fatal complication and impact an individual’s quality of life
  • Microphasia: really small handwriting - symptom of the disease is handwriting gets smaller (smaller fine motor control)
76
Q

Neurologically, what system is disrupted in Parkinson’s disease?

A

dopamine system

77
Q

How is the dopamine system disrupted in Parkinson’s disease?

A

Dopamine system links to striatum -> more dopamine, more movement

  1. D1 receptors excited by dopamine in basal ganglia and favour a direct pathway - which is why they have trouble starting and stopping movement when this particular system is disrupted
    ^if you follow subsequent connections, you end up with a htypokinect disorder
78
Q

how can you address Parkinson’s disease?

A

Can address this through deep brain stimulation and L-dopa treatment

-> (but these people would become hypersexual, go gambling etc. because dopamine is also responsible for the reward system and an abundance of dopamine causes impulsivity)

79
Q

what is Huntington’s Disease?

A
  • Fatal / Progressive disease causing involuntary muscle jerks.
  • It will ultimately affect the whole body.
  • Also intellectual deterioration, depression and occasionally psychoticism.
  • Genetically determined (single dominant gene).
  • Excessive overstimulating of the basal ganglia loop resulting in excess movement (links between cognition and movement and motor control)
  • Causes degeneration of the output neurones from the striatum, reducing inhibitory modulation of motor function.
  • 10-20 years life span / Onset is usually 30-45 yrs old (usually have already have children, is a difficult decision)
  • Neurodegenerative disease that produces a characteristic movement known as chorea (produces unpurposeful movement)
  • Also causes mental disturbance: psychosis, irritability, depression
  • Cognitive impairments: dementia
  • Have really enlarged 4th ventricles - degenerations of caudate nucleus in the basal ganglia (therefore the ventricle next door becomes/appears much larger)
80
Q

what can help manage Huntington’s Disease symptoms?

A

dopamine antagonists and neuroleptics for the chorea

-> antipsychotics for psychosis

81
Q

what is the neural background with Huntington’s?

A

Excessive overstimulating of the basal ganglia loop resulting in excess movement (links between cognition and movement and motor control)
-> hyperkinesia

82
Q

what is SMA essential for?

A

linking complex movements

83
Q

what helps fine tune our movements?

A

cerebellum and basal ganglia

84
Q

advanced movements require what?

A

an intricate set of checks and balances contingent on feedback.

85
Q

Basal Ganglia Loop

A
  1. The caudate and putamen (orange) are the zones receiving the main inputs to the basal ganglia.
  2. The globus pallidus (purple) provides the principal output, which projects to the ventral anterior and ventrolateral (VA/VL) nuclear complex of the thalamus, which in turn projects to the motor cortex.
  3. The substantia nigra pars reticulata in the midbrain serves as the output nucleus for the basal ganglia circuits controlling eye movements.
  4. Pro-jections from the cortex excite neurons in the caudate and putamen, which then inhibit neurons in the globus pallidus and substantia nigra pars reticulata.
  5. This effect suppresses tonic inhibition of the thalamus by the globus pallidus, thereby further exciting the cortex.
  6. The substantia nigra pars compacta provides modulatory dopaminergic inputs to the basal ganglia, and a circuit through the subthalamic nucleus serves a secondary role in releasing movement.

brain & behaviour 2 (19 decks)

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