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PS1003 > PS1003 Andrew: Central Control of Movement > Flashcards

PS1003 Andrew: Central Control of Movement Flashcards

1
Q

What is a simple reflex?

A

Stretch reflex, knee jerk etc. It is mediated at the level of the spinal cord rather than the level of the brain

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2
Q

What is posture and postural change?

A

standing and balancing

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3
Q

What is locomotion?

A

walking, running- when limbs are used in order to perform tasks

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4
Q

What is sensory orientation?

A

head turning, eye fixation

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5
Q

What is species specific action patterns?

A

ingestion, courtship, escape/defence, grooming, gestures. A lot seems to be innate- controlled by the motor outputs. It shows itself differently in different animals.

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6
Q

What are acquired skills?

A

speech, dressing, painting, driving, sports, etc. e.g. chimpanzees, crows and such use tools to retrieve food

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7
Q

Where do motor outputs come from?

A

From the motor cortex, where they project through pyramidal tracts to spinal cord, where it synapses with peripheral motor neurones (within the spinal cord) connect to the nerones that go to the other limbs

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8
Q

What are the other pathways which relate to motor outputs?

A

Basal ganglia and cerebellum via brainstem and spinal cord.

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9
Q

What is the difference between the pyramidal tracts and the basal ganglia/cerebellum?

A

They run parallel from cortex, and outside the pyramidal tract and are called extrapyramidal system. They do no originate from the primary motor cortex.

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10
Q

Spinal motor pathways: what is the pyramidal tract responsible for?

A

Controls most of our fine movements and main control

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11
Q

Spinal motor pathways: what is the Tectospinal responsible for?

A

Co-ordinates head and eye movements as part of the optic reflexes. From the superior colliculus.

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12
Q

Spinal motor pathways: what is the Vestibulospinal responsible for?

A

Influences postural muscles. From the vestibular nucleus. It is very important to balance and detection of head movement.

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13
Q

Spinal motor pathways: what is the Reticulospinal responsible for?

A

projects from reticular formation. Inhibition or facilitation of movement (fine tuning of the main movement)

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14
Q

What does the primary motor cortex do?

A

Source of pyramidal tract neurones (cell body region). Located in pre-central gyrus (in front of central sulcus)

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15
Q

What does the supplementary motor cortex do?

A

Conception and initiation of movement (going to the primary motor cortex and being told what to do). Lesions here would cause involuntary movement or speech (Broca’s area)

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16
Q

What does the premotor cortex do?

A

Important in motor coordination. Lesions cause impairments in stability of stance, gait and hand coodination.

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17
Q

What does the motor homunculus show?

A

can do really fine control of certain things e.g. fingers/face but not of the leg. so the number of motor neurones going to an area determines how fine movement you can do in one area

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18
Q

What are the areas of that the motor primary cortex (most sensitive and least sensitive)

A

jaw, face, fingers, tongue vs shoulder, elbow, hip

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19
Q

What does the cerebellum (outside the cortex) do?

A

Controls neural ‘programs’ for the execution of skilled movements. So when we learn a new skill we are training the cerebellum. Lies at the back of the head- top of the spine

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20
Q

What does the basal ganglia (outside the cortex) do/

A

A group of subcortical forebrain nuclei (caudate nucleus, putamen (=striatum), Globus palludus, subthalamic nucleus). Modulates patterns of motor acitivty

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21
Q

Where does the visual cortex feed into when it comes to movement?

A

Cerebellum and premotor cortex

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22
Q

Where does the cerebellum feed into?

A

Motor nuclei of the thalamus

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23
Q

Where does the basal ganglia feed into?

A

Motor nuclei of the thalamus

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24
Q

Where does the motor nuclei of the thalamus feed into?

A

the supplementary motor cortex and the primary motor cortex

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25
Q

Where does the prefrontal cortex feed into?

A

The premotor cortex

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26
Q

Where does the supplementary motor cortex feed into?

A

the premotor cortex

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27
Q

Where does the premotor cortex feed into?

A

The primary motor cortex, the pyramidal tract and the brainstem

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28
Q

Where does the primary motor cortex feed into?

A

The pyramidal tract and the brainstem

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29
Q

Where does the brainstem feed into?

A

The extrapyramidal motor pathways

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30
Q

What does the thalamus act as?

A

The gate that filters information, feeds into the different areas and modulates their behaviour

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31
Q

At what level are spinal reflexes mediated?

A

At the spinal cord, as these reflexes need to respond quickly e.g. when skin meets something hot

32
Q

How does the brain find out about the reflexes that happen?

A

It works backwards to the brain, so the action takes place first and then the brain finds out the reason why- this allows for quicker reflexes. Does not require cortical input.

33
Q

What happens within a knee jerk reflex?

A

tapping the knee tendon stimulated tendon stretch receptors

34
Q

How are the sensory neurones synapses connected to motor neurone?

A

Directly

35
Q

How is limb extension caused?

A

The muscles contract

36
Q

Examples of neurological disease of the motor system:

A 
●	Paralysis
●	 Apraxia
●	 Decomposition of movement
●	 Parkinson’s disease
●	 Huntington’s disease
●	 Duchenne’s muscular dystrophy
●	Myesthenia gravis
●	Multiple sclerosis
●	Diseases of peripheral rather than central origin
37
Q

Paralysis: how is it caused?

A

There is damage to motor neurones

38
Q

Paralysis: What does it mean to be viral?

A

of the nature of, caused by, or relating to a virus or viruses.

39
Q

Paralysis: What is an example of viral within paralysis?

A

poliomyelitis – leads to destruction of spinal motor neurones

40
Q

Paralysis: What type of damage to motor neurones can happen to cause paralysis?

A

Viral, toxins, hereditary, polio injury and damage to primary motor cortex

41
Q

Paralysis: what is an example of toxins and/or hereditary?

A

amyotrophic lateral sclerosis – degeneration of motoneurons in the brainstem and spinal cord

42
Q

Paralysis: what is polio?

A

no motor neurones moving out- so can cause death as even the motor neurone for breathing stopped

43
Q

Paralysis: what type of injury would be permanent?

A

severing of spinal cord

44
Q

Paralysis: what type of injury would be transient?

A

Bruising or compression of spinal cord

45
Q

Paralysis: What makes injuries transient?

A

The swelling can dissipate allowing neurones to heal. Therpay- make it transient than permanent- allow recovery of neurones

46
Q

Paralysis: what happens if there is damage to primary motor cortex?

A

(partial) paralysis of movement on one side of the body (contralateral to damage). Extent of paralysis depends on damage, and often accompanied by spasticity and abnormal reflexes.

47
Q

What is apraxia?

A

Inability to carry out movements in response to commands

48
Q

What is apraxia not due to?

A

paralysis, loss of comprehension or loss of motivation

49
Q

What is apraxia due to?

A

disconnection of primary motor cortex from supplementary motor areas and premotor cortex. So the motor patterns (instructions) are being genreated but not passed onto primary motor cortex where output goes

50
Q

What is the decomposition of movement?

A

The inability to perform “motor patterns” e.g. walking. No longer automatic, movement requires thought- broken individual segments instead of smooth exectuion

51
Q

Why does the decomposition of movement happen?

A

May be due to cerebellar damage, indicates what it does in motor control- produces complex motor patterns and involved in learning it

52
Q

What influence does the cerebellum have in movement?

A

The visual cortex and somatosensory cortex feeds into it, with in then feeding into the motor nuclei of the thalamus

53
Q

What are the symptoms of Parkinson’s disease?

A

tremors, muscle rigidity, akinesia (loss of voluntary movement), stooped posture, shuffling gait, excessive sweating/salvation, micrographia (small handwriting), deficits in extra-pyramidal motor pathways, altered cognitive function e.g. dementia

54
Q

What is a consequence/symptom of Parkinson’s disease?

A

Altered cognitive function, depression- these could e reactive than a pathology

55
Q

What is neuropathology of Parkinson’s diseases?

A

Degeneration of the nigro-striatal pathway which leads to a depletion of striatal dopamine.

56
Q

Neuropathology of Parkinson’s diseases: what happens to dopamine?

A

some degeneration of other dopamine pathways too- may account for some of the psychological deficits. Not clear to the extent however.

57
Q

Neuropathology of Parkinson’s diseases: What is the nigro-striatal pathway?

A

Nigrostriatal pathway is the efferent connection between the susbtantia nigra and corpus striatum. Nigrostriatal pathway is one of the major dopamine pathways in the brain. Nigrostriatal pathway is particularly involved in the production of movement, as part of a system called the basal ganglia motor loop.

58
Q

Neuropathology of Parkinson’s diseases: What is the corpus striatum?

A

part of the basal ganglia of the brain, comprising the caudate and lentiform nuclei.

59
Q

What is the striatum?

A

is one of the nuclei in the subcortical basal ganglia of the forebrain. The striatum is a critical component of the motor and reward systems

60
Q

Neuropathology of Parkinson’s diseases: What is substantia-nigra?

A

It is a black substance (appears darker than neighbouring areas). Located in the mesencephalon (midbrain) and is important to reward and movement

61
Q

Neuropathology of Parkinson’s diseases: What is striatal dopamine?

A

a catecholamine neurotransmitter and is especially important in the regulation of movement. The responsible set of dopamine-producing neurons has cell bodies in a region of the brain called the substantia nigra, which projects to the striatum.

62
Q

Neuropathology of Parkinson’s diseases: What is Amyotrophic lateral sclerosis?

A

one of a group of diseases often called motor-neurone disease

63
Q

What is the GABA neurotransmitter?

A

GABA contributes to motor control, vision, and many other cortical functions. It also regulates anxiety.

64
Q

What happens to dopamine if there is damage to the primary motor cortex?

A

Dopamine modulates movement, but if there is damage it causes motor deficiencies as it should feed into the striatum alongside glutamate to produce GABA but it does not.

65
Q

what were early treatments for Parkinson’s Disease?

A

Prior 1960s there was no effective treatment. One symptom was salivation, 1930s gave patients belladonna (alleviated salivation but also motor deficient symptoms). First treatment: belladonna atropine

66
Q

How was dopamine used to cure Parkinson’s disease?

A

Dopamine’s involvement led to drugs increasing brains dopamine, however it cannot cross from the blood to the brain tissues so they used the precursor, L-DOPA, which entered the brain and converted into dopamine there

67
Q

What were the severe side effects of using L-DOPA/dopamine to treat Parkinson’s Disease?

A

dyskinetic movements (involuntary muscle movement), psychoticism. control of symptoms were not good.

68
Q

What is the future of Parkinson’s Disease treatments?

A

Surgical interventions and neural transplantation are under investigation as alternative therapies

69
Q

What is Huntington’s disease?

A

It is a progressive disease causing involuntary muscle jerks, affects the whole body. involves intellectual deterioration, depression and occasional psychoticism

70
Q

What is the age of onset for Huntington’s disease?

A

30-45years. Many people have children before this, so ethical when to tell people as their children may inherit genes.

71
Q

How is Huntington’s disease determined?

A

It is genetically determined (single dominant gene)

72
Q

What does Huntington’s disease cause?

A

Degeneration of the output neurones from the striatum, reducing inhibitory modulation of motor function

73
Q

What treatment is there for Huntington’s disease?

A

No effective treatment. GABA replacement or dopamine antagonists provide some relief

74
Q

What is the ethical dilemma surrounding Huntington’s disease?

A

Not being able to halt the progression of the disease so issues to do with allowing them to pass genes on

75
Q

What is the influence of basal ganglia in the motor system?

A

It feeds into the motor nuclei of the thalamus

76
Q

What is the basal ganglia?

A

Situated at the base of the forebrain. strongly connected with cerebral cortex, brainstem and thalamus. involved in voluntary movement, learning, and routine movements such as eye movement, walking and even emotion.

77
Q

Summary:

A

● Pyramidal motor system:
● Neurones originate in primary motor cortex
● Source of primary motor neurones to spinal cord in pyramidal tract
● Receives input from supplementary motor cortex and premotor cortex
● Also receives input from basal ganglia and cerebellum
● Extrapyramidal motor system:
● Neurones originate in mid brain and hind brain (brain stem)
● Control non-conscious motor control
○ Ocular reflex
○ Balance
○ Fine motor tuning
● Damage to motor areas produce varying degrees of motor deficit, depending on localisation and extent of the damage.

PS1003 (6 decks)

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