Chapter 7 - Movement Flashcards

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1
Q

What is the primary motor cortex?

A

The cerebral cortex

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2
Q

What does stimulation of neurons result in?

A

Outcomes (i.e. moving hand to mouth).

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3
Q

Where does planning of a movement occur?

A

Posterior parietal cortex. It monitors the position of the body relative to the world.

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4
Q

What areas are responsible for a rapid sequence of movements?

A

The PFC and supplementary motor cortex are responsible for planning and organising a rapid sequence of movements.

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5
Q

What area of the brain is important for considering probable outcomes of possible movements?

A

PFC

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6
Q

What are corticospinal tracts?

A

Paths from the cerebral cortex to the spinal cord. There is the lateral corticospinal tract and the medial corticospinal tract.

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7
Q

What is the lateral corticospinal tract?

A

Pathway of axons from the primary motor cortex and red nucleus (midbrain area responsible for arm movements). In bulges in the medulla (pyramids) the lateral tract crosses to the contralateral side. It controls movement in peripheral areas.

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8
Q

What is the medial corticospinal tract?

A

Axons from many parts of the cerebral cortex. The medial pathway includes axons from the midbrain tectum, reticular formation and the vestibular nucleus (brain area that receives input from vestibular system). The tract goes to both sides of spinal cord and controls muscles of neck, shoulders, trunk and therefore bilateral movements like running, walking, standing and sitting.

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9
Q

What role does the cerebellum play in movement?

A

Cerebral damage results in trouble with rapid movements that require aim, timing and alternations of movements. Cerebellum responds to sensory information even when not moving. People with cerebellum damage need longer to shift their focus.

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10
Q

What is the cerebellar cortex?

A

The surface of the cerebellum.

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11
Q

How are neurons arranged in the cerebellar cortex?

A

In a precise geometrical pattern, with multiple repetitions of the same units.

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12
Q

What are Purkinje cells?

A

Flat (2-D) cells in sequential plans, parallel to one another. Found in the cerebellar cortex.

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13
Q

What are parallel fibres?

A

Axons parallel to one another and perpendicular to the planes of the Purkinje cells.

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14
Q

How do Purkinje cells work?

A

Action potentials in parallel fibres excite one Purkinje cell after another. Each Purkinje cell transmits an inhibitory message to cells in the nuclei of the cerebellum (clusters of cell bodies in the interior of the cerebellum) and the vestibular nuclei in the brainstem, which in turn sends information to the midbrain and the thalamus.

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15
Q

How do Purkinje cells impact on the duration of the response?

A

Depending on which and how many parallel fibres are active, they might only stimulate the first few Purkinje cells or a long series of them. Because the parallel fibres’ messages reach different Purkinje cells one after another, the greater the number of Purkinje cells, the greater their collective duration of response. The less Purkinje cells results in a brief message to the target cells; the more Purkinje cells, the message lasts longer. The output of Purkinje cells controls the timing of a movement, including its onset and offset.

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16
Q

What role does the basal ganglia play in movement?

A

The basal ganglia is a group of subcortical structures - caudate nucleus, putamen and globus pallidus.

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17
Q

What makes up the striatum?

A

Caudate nucleus and putamen.

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18
Q

Where does the striatum receive input from?

A

The cerebral cortex and substantia nigra.

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19
Q

Where does the striatum output to?

A

The globus pallidus which then sends output to the thalamus, which connects to the frontal cortex.

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20
Q

What is the direct path?

A

The direct path from the striatum inhibits the globus pallidus, which inhibits part of the thalamus. By inhibiting an inhibitor, the net effect is excitation. Direct path enhances selected movement.

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21
Q

What is the indirect path?

A

Essential for learned performance and inhibits inappropriate competing movements. The indirect path has extra connections within the globus pallidus and back and forth to the subthalamus.

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22
Q

What is the basal ganglia important for?

A

Self-initiated, spontaneous behaviours. Self-initiated behaviours are slower than those of stimulus-initiated. It regulates the vigour of movements and responds well to the reward value of possible action.

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23
Q

What are the symptoms of Parkinson’s disease?

A

Rigidity, muscle tremors, slow movements, difficulty initiating physical and mental activity. May have problems with attention, language and memory.

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24
Q

When does Parkinson’s start and what symptoms start?

A

More common as people age. Starts with olfaction and psychological depression.

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25
Q

What is the cause of Parkinson’s symptoms in the brain?

A

Loss of neurons in the substantia nigra. This creates a loss of dopamine-releasing axons to the striatum. The decreased activity in the striatum results in a decreased inhibition of the globus pallidus which increases inhibitory inputs to the thalamus. The results are slow and weak spontaneous movements and less vigorous voluntary movements.

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26
Q

What causes Parkinson’s?

A

Genetics - genes make little difference to late-onset Parkinson’s. They impact early-onset forms of the disease. More than 20 genes identified.
Toxins - Drug MPTP (chemical that body converts to MPP, which accumulates in and then destroys neurons that release dopamine, partly by impairing the transport of mitochondria from the cell body to the synapse). Postsynaptic neurons react to loss of dopamine by increasing their number of dopamine receptors. Exposure to chemicals that damage the substantia nigra.
Traumatic head injury - increases risk of developing Parkinson’s.

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27
Q

What reduces the risk of developing Parkinson’s?

A

Smoking cigarettes and drinking coffee (10 or more cups a day).

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28
Q

What treatments to Parkinson are there?

A

L-dopa - a precusor to dopamine that crosses the blood-brain barrier. L-dopa is converted by the brain to dopamine and is an effective treatment. It has side effects of nausea, restlessness, sleep problems, low BP, repetitive movements, and sometimes hallucinations and delusions.

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29
Q

What are the symptoms of Huntington’s disease?

A

Motor symptoms - arm jerks and facial twitches. Spreads into writhing. Tremors interfere with walking, speech and other voluntary movements.
Psychological disorders - depression, sleeplessness, hallucinations and delusions, memory impairments, anxiety, poor judgement, alcohol and drug abuse, sexual disorders.
(1 in 10,000 people)

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30
Q

What areas of the brain are related to Huntington’s disease?

A

Extensive damage in the basal ganglia and cerebral cortex. The output of the basal ganglia is inhibitory to the thalamus and this increases the output from the thalamus resulting in involuntary jerky movements.

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31
Q

What causes Huntington’s disease?

A

An autosomal dominant gene. The chromosome 4-C-A-G sequence of bases that repeats 11-24 times. More than 39 repetitions means likely to the get the disease and the earlier the onset.

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32
Q

What does Huntington’s disease often get misdiagnosed as in the early stages?

A

Schizophrenia.

33
Q

What increases the risk of early onset Huntington’s disease?

A

Alcohol and drug abuse.

34
Q

How does the Huntington gene cause damage?

A

The Huntington gene codes a protein - Huntingtin, which the mutant form occurs inside neurons. It impairs neurons through increasing neurotransmitter release, impairs mitochondria and transport of chemicals down the axon.

35
Q

The reason why a dopamine pill is ineffective for treating Parkinson’s disease is that:

A

dopamine does not cross the blood-brain barrier.

36
Q

A saccade is initiated by impulses from the ____.

A

cerebellum

37
Q

MPTP and some chemicals in herbicides:

A

can damage cells of the substantia nigra.

38
Q

The posterior parietal cortex ____.

A

keeps track of the position of the body relative to the world​

39
Q

The motor cortex can become active when imagining movement. T or F

A

True

40
Q

What is a common symptom of Huntington’s disease?

A

Twitches, tremors, and writhing that interfere with voluntary movement

41
Q

The prefrontal cortex ____.

A

responds to lights, noises, and other signals for a movement

42
Q

Movements near the midline of the body, such as bending and turning of the trunk, are controlled by which motor system?

A

medial tract

43
Q

In Huntington’s disease, earlier onset is associated with slower deterioration over time. T or F

A

False

44
Q

At least some cases of Parkinson’s disease are apparently linked to what cause?

A

A toxic substance found in a heroin substitute

45
Q

The part of the cortex that is most active during preparations for a movement and less active during the movement itself is the ____.

A

premotor cortex

46
Q

Which of the following is NOT common in people with Parkinson’s disease?
Select one:
a. Rigidity and tremors
b. Slowness of movements
c. Outbursts of emotions
d. Difficulty initiating voluntary movements

A

c. Outbursts of emotions

47
Q

​In order to elicit movement, the motor cortex ____.

A

sends axons to the brainstem and spinal cord

48
Q

Most of the axons of the medial tract go to which side of the body?

A

bilateral

49
Q

A brief stimulation of the motor cortex, less than 50ms, produces what kind of result?

A

Isolated muscle twitches

50
Q

Why do we move the eye muscles with greater precision that the biceps muscle?

A

Each axon to the biceps muscles innervates about 100 fibres, therefore, it is not possible to change the movement by a small amount. In contrast, an axon to the eye muscle only innervates about three fibres.

51
Q

Which transmitter causes a skeletal muscle to contract?

A

Acetylcholine. A muscle only contracts.

52
Q

In what way are fish movements impaired in cold water?

A

A fish can move rapidly in cold water, but it fatigues easily.

53
Q

Duck breast muscles are red (dark meat), whereas chicken breast muscles are white. Which species can probably fly for a longer time before fatiguing?

A

Ducks can fly great distances as they often do during migration. The white muscle of a chicken breast has the power necessary to get heavy body off the ground but it fatigues rapidly. Chickens seldom fly far.

54
Q

Why is an ultra marathoner probably not impressive at short-distance races?

A

An ultra marathoner builds up large numbers of slow-twitch fibres at the expense of fast-twitch fibres. Therefore, endurance is great but maximum speed is not.

55
Q

If you hold your arm out straight and someone pulls it down slightly, it quickly bounces back. Which proprioceptor is responsible?

A

The muscle spindle.

56
Q

What is the function of Golgi tendon organs?

A

Golgi tendon organs respond to muscle tension and thereby prevent excessively strong muscle contractions.

57
Q

In what way doe the brain anatomy facilitate communications between body sensations and body movements?

A

The motor cortex represents muscular control of body areas in close alignment to the way the somatosensory cortex, just posterior to the motor cortex, represents sensations from those areas.

58
Q

What evidence indicates that cortical activity represents the “idea” of the movement and not just muscle contractions?

A

Activity in the motor cortex leads to a particular outcome, such as movement of the hand to the mouth, regardless of what muscle contractions are necessary given the hand’s current location.

59
Q

How does the posterior parietal cortex contribute to movement?

A

It is important for perceiving the location of objects and the position of the body relative to the environment. It is also active for planning a movement

60
Q

How does the premotor cortex contribute to movement?

A

It is active in preparing for a movement shortly before it occurs.

61
Q

How does the supplementary motor cortex contribute to movement?

A

It is active in preparing for a movement shortly before it occurs. The supplementary motor cortex inhibits a habitual action when it is appropriate.

62
Q

How does the prefrontal cortex contribute to movement?

A

It stores sensory information relevant to a movement and considers possible outcomes of a movement.

63
Q

When expert pianists listen to familiar, well-practiced music, they imagine the finger movements, and the finger area of their motor cortex becomes active, even if they are not moving their fingers. If we regard those neurons as another kind of mirror neuron, what do these results imply about the origin of mirror neurons?

A

These neurons must have acquired these properties through experience. That is, they did not enable pianists to copy what they hear; they developed after pianists learned to copy what they hear.

64
Q

What kinds of movements does the lateral tract control? The medial tract?

A

The lateral tract controls detailed movements in the periphery on the contralateral side of the body. The medial tract controls trunk movements bilaterally.

65
Q

What kind of perceptual task would be most impaired by damage to the cerebellum?

A

Damage to the cerebellum impairs perceptual tasks that depend on accurate timing.

66
Q

How are the parallel fibres arranged relative to one another and to the Purkinje cells?

A

The parallel fibres are parallel to one another and perpendicular to the Purkinje cells.

67
Q

If a large number of parallel fibres are active, what is the effect on the collective output of the Purkinje cells?

A

As a larger number of parallel cells become active, the Purkinje cells increase their duration of response.

68
Q

In general, do the basal ganglia have more effect on responses to a stimulus or on self-initiated movements?

A

The basal ganglia have more influence on self-initiated movements, which are generally slower.

69
Q

What aspect of movement do the basal ganglia control?

A

The basal ganglia control the vigour of movements.

70
Q

What kind of learning depends most heavily on the basal ganglia?

A

The basal ganglia are essential for learning motor habits that are difficult to describe in words.

71
Q

Explain the evidence that someone’s conscious decision to move does not cause movement.

A

Researchers recorded responses in people’s cortex that predicted the upcoming response. Those brain responses occurred earlier than the time people reported as “when they made the decision”.

72
Q

On what basis are some researchers skeptical of this evidence?

A

The studies assume that people accurately report the times of their intentions. However, people’s responses are influenced by events after the movement and therefore we cannot be confident of their accuracy.

73
Q

Is the genetic basis stronger for early-onset or late-onset of Parkinson’s disease?

A

Early-onset.

74
Q

How does MPTP exposure influence the likelihood of Parkinson’s disease? What are the effects of cigarette smoking?

A

Exposure to MPTP can include symptoms of Parkinson’s disease. Cigarette smoking is correlated with decreased prevalence of the disease.

75
Q

How does L-dopa relieve the symptoms of Parkinson’s disease?

A

L-dopa enters the brain, where neurons convert it to dopamine, thus increasing the supply of a depleted neurotransmitter.

76
Q

In what ways is L-dopa treatment disappointing?

A

L-dopa increases dopamine activity in spurts and in all neurons, not steadily and not just in those that need help. It does not stop the loss of neurons. It has unpleasant side effects.

77
Q

Why is transfer of metal tissue more successful in animal models of Parkinson’s than it is with human patients?

A

In laboratory animals, researchers use young animals at an early stage of the disease. In humans, this is and option when all else has failed, and as a result the patient already has extensive brain damage at the time of surgery.

78
Q

Why does damage to the basal ganglia lead to involuntary movements?

A

Output from the basal ganglia to the thalamus is inhibitory. After damage to the basal ganglia, the thalamus and therefore the cortex, receive less inhibition. Thus, they produce unwanted actions.

79
Q

What procedure enables physicians to predict who will or will not get Huntington’s disease and to estimate onset of age?

A

Physicians can count the number of consecutive repeats of the combination C-A-G on one gene on chromosome 4. If the number is fewer than 36, the person will not develop Huntington’s disease. For repeats of 36 or more, the larger the number, the more certain the person is to develop Huntington’s and the earlier the probable age of onset.