week 7 Movement Flashcards

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1
Q

What are the functions of muscles?

A

to create movement. movement are behaviours.

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2
Q

Understand the three categories of muscle.

A

Smooth muscle:gi system
Striated muscle; (skeletal muscle). Mix of fast-twitch fibres (fast contractions, fatigues rapidly,anaerobic) and slow-twitch fibres (less vigorous contractions, slow to fatigue, aerobic, uses oxygen).. Use slow-twitch for walking, talking etc, things we can do for hours. Anaerobic muscle use spares glucose for the brain but build up an oxygen debt and utilises fatty acids. Still fatigue in time. Training and genetics determines the ratio of fast and slow twitch fibres.
Each muscle fibre receives info from just 1 axon, but 1 axon may innervate many muscle fibres. The more axons, the finer the movement control. eg eye has approx 1 axon per 3 muscle fibres, cf biceps has 1 axon to more than 100 fibres.
Heart muscle;

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3
Q

What is a neuromuscular junction, and which neurotransmitter is most important at this junction?

A

a neuromuscular junction is the synapse b/n neuron axon and muscle fibre. In skeletal muscle neuromuscular junctions, it is always acetylcholine acting as neurotransmitter. Acetylcholine causes muscle contracture.

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4
Q

What is a motor unit?

A

A motor unit is a nerve and all the muscle fibres it innervates.

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5
Q

Know the difference between a flexor and extensor muscle, and how they act in concert to produce effective movements of limbs.

A

Flexor muscle brings limb closer to body or decreases angle between 2 bones and extensor further away (or increases angle between 2 bones).
If there is a flexor and an extensor muscle/s operating on the same joint, one will be relaxed when the other contracts. Contraction is determined by acetylcholine and relaxation is an absence of acetylcholine.

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6
Q

Understand the function of the muscle spindle organ. How does the muscle spindle achieve this function?

A

A proprioceptor is a receptor cell detecting movement or position. Muscle spindle receptor is a type of proprioceptor which is in parallel to muscle fibres and responds when the muscle is stretched MORE THAN THE ANTAGONISTIC muscle. This results in a message via the spinal cord, such that the muscle then contracts. This is an example of a STRETCH reflex and it helps to maintain balance. An example is the knee jerk.

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7
Q

Understand the function of the Golgi tendon organ. How does the Golgi tendon organ achieve this function?

A

Golgi tendon organs are also proprioceptors. These are located in the tendons, at the ends of muscles.They respond to muscle tension. They serve to prevent excessive contraction, via the spinal cord, resulting in some interneurons inhibiting some muscle fibre contraction.

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8
Q

Compare and contrast the actions of these two types of proprioceptor. How are they similar? How are they different?

A

Muscle spindle organ located mid muscle, acts to counterbalance antagonistic muscle. Golgi tendon organ at ends of muscle acts to prevent overexertion of individual muscle.

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9
Q

Proprioception is not necessarily a conscious exercise involving higher levels of the nervous system such as the brain. In fact, many of the most important functions are carried out at an unconscious level and involve spinal reflex arcs. What is a reflex? Understand several types of reflex and suggest reasons why these reflexes have evolved in us.

A

A reflex is a muscle movement which is not under conscious control, which is the same response, given the same stimulus. Examples include the stretch reflex, pupillary light response ,gag reflex etc.Reflexes are fast due to mimimal units involved. Have evolved as likely immediate-survival aids.
A reflex is a ballistic movement-once launched it is unalterable. Other movements such as threading a needle have many feedbacks checks and adjustments.

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10
Q

What is a central pattern generator?

A

Central pattern generator-neural mechanism within spinal cord which generates rhythmic patterns of motor output. eg wing flapping etc.

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11
Q

Locate the primary motor area and premotor area on the lateral surface of a sketch of the human cerebral hemisphere. Note the relationship between cortical representation and precision of motor activity.

A

11

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12
Q

Know the role of each of the following areas near the primary motor cortex (it is no accident that each of these movement- and body-relevant areas is nearby):
posterior parietal,
cortex, primary,
somatosensory,
cortex, prefrontal,
cortex,
premotor cortex,
supplementary,
motor cortex.

A

Posterior Parietal;planning of movement. Monitors body in relation to rest of world. Damage here and may have difficulty finding objects in space despite being able to describe them.
Primary somatosensory cortex; awareness of body parts.
Prefrontal cortex:complex movements such as writing. Also involved in inhibiting movements, which develop as mature.Complex goal planning etc. Stores sensory info re target. most active immediately prior to a movement.
Premotor cortex most active just prior to a movement.
Supplementary motor cortex-involved in organization of rapid sequence of movement.

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13
Q

Understand the role of the motor cortex in movement generation.

A

Main source of brain input into spinal cord which results in movement. Produces patterns which represent the intended outcome.

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14
Q

Understand the location of the cerebellum, its motor functions.

A

Cerebellum involved in smoothing out muscle movement, sensory perception of non moving areas,violations of sensory perceptions (ie unexpected feeling), vital for precise timing of short intervals.Damage here may result in intention tremor, jerky movements, ability to judge loudness of sound without ability to judge its duration, difficulty maintaining attention, takes longer to be able to shift attention.
Cells arranged in efficient arrays of parrallel fibres and purkinje cells. Purkinje cells are inhibitory on certain movements. The arrangement is perfect for efficient rapid flow of information which is utilised to perform predictive error correction by comparing goal movement with path movement.

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15
Q

Understand the role of the basal ganglia in modulating movement.

A

Basal ganglia are strongly involved in self-initiated movement. Caudate nucleus plus Putamen = Dorsal Striatum (or Striatum).
Striatum receives input from cerebral cortex and substantia nigra, and sends output toglobus pallidus. Globus pallidus sends output to thalamus and frontal cortex.
Direct Pathway from Striatum inhibits globus pallidus which inhibits thalamus (direct effect is to likely stimulate specific movement).
The Indirect Pathway has additional back and forth connections within the globus pallidus to the subthalamus andthe net effect is likely to be suppression of unwanted movement. The Indirect Pathway is important in learning (movements/behaviours).
Both the Direct and Indirect Pathways are very active just before a movement and both are inactive when the animal is at rest.

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16
Q

What are the anatomical constituents of the basal ganglia?

A

Large subcortical structures within the forebrain. Includes Caudate Nucleus, Putamen, Globus Pallidus.
Ventral Striatum = Nucleus accumbens + Olfactory tubercle and this plus Ventral palladium, Substantia nigra and Subthalamic nucleus are by some classified as part of Basal ganglia also.

17
Q

Be familiar with the Lateral and Medial corticospinal tracts and be able to compare and contrast their respective functions.

A

Lateral Corticospinal Tract;pathway of axons from Primary motor cortex, some surrounding areas and Red nucleus , crossover to contralateral side in the medulla (at Pyramids)to their target organs which are especially hands and feet. Controls movement of more lateral muscles. Also called Pyramidal tract.
The Medial Corticospinal Tract; axons from many parts of cerebral cortex plus from Tectum, Reticular formation and Vestibular nucleus. These axons progress down both sides of the spinal cord to muscles of neck, trunk shoulders etc. Mainly controls movements such as walking, turning, bending etc.

18
Q

Understand the possible consequences of disorder of the cerebellum (including some problems other than movement disorder).

A

Problems when cerebellar damage present include: imbalance, incoordination, trouble tapping or following rhythyms, aim problems, difficulty with speech and writing.
Continuous motion is ok eg drawing a circle-no start or finish (presumably difficulty with the start and finish though).
Difficulty with saccades (moving eyes from 1 spot quickly to another) (many short movements are made until by trial and error arrive at desired point).

19
Q

Know the main signs and symptoms of Parkinson’s Disease.

A

Affects 1-2 % of over 65’s.Gradual loss of dopamine-releasing axons from the Substantia nigra. Results in increase in inhibitory input to Thalamus, causing rigidity, muscle tremors, slow movements and difficulty initiating voluntary movements. Also reduced motivation and pleasure. Some have cognitive deficits also.

20
Q

Understand the causes of Parkinson’s disease and how the main treatments work.

A

Cause is damage to Substantia nigra. Likely combination of causal factors;
a) genetic, at least 28 variants found that increase risk, and having multiple variants increases risk even more
b) chemical exposure. Possibly to some pesticides, fungicides, drug use (eg MPTP-similiar to heroin), and increased risk with genetic variants
c). Decreased risk if heavy smoker or coffee drinker (but these have other risks)
Treatments;
a) L-Dopa-pre-cursor to dopamine. Daily pill.Increases dopamine release in all axons (those that were impaired and those that were not). Does not replace other neurotransmitters which have also been depleted. Does not slow progression but ameliorates symptoms. side effects of nausea, restlessness, low bp, repetitive movements, difficulty sleeping, hallucinations.
b)other drugs which either stimulate dopamine receptors or block the breakdown of dopamine.
c) deep brain electrode stimulation. Not fully understood but thought might be excessive synchrony of firing within the basal ganglia, and electrode stimulation disrupts such unhealthy rhythms.
d)Transplant of brain tissue from aborted foetuses. Takes multiple foetuses for 1 transplant.
e).Stem cell harvest, differentiate to produce L-dopa and transplant. Ongoing re esearch.

21
Q

Know the main signs and symptoms of Huntington’s Disease.

A

Affects 17 per 100000 Americans of European ancestry, fewer in Europe and v rare African/Asian ancestry. Progressive, fatal. tremors, writhing. Gradual extensive progressive brain damage.Damaged basal ganglia thus less inhibition on thalamus and increased activity in motor areas of thalamus. Also often have apathy, depression, poor judgement, alcoholism, hallucinations, sexual disorder (range from non response to promiscuity). These psychological disorders often present many years prior to the recognisable motor tremors. May start at any age but most likely between age 30 and 50.

22
Q

Understand the causes of Huntington’s disease and how the main treatments work

A

Caused by one autosomal dominant gene. Fault on chromosome 4. In the area of concern, are repetitions of C-A-G bases. Normal number of repetitions is 11-24. 36-40 is fairly safe, if do develop dz will not be until much older, but more than 40 repeats will get dz. The more repeats, the younger are when onset occurs.
The protein coded for by this sequence is Huntingtin. The mutant form impairs neurons and glia by effects on mitochondria and potassium channels.
Tx is Tetrabenazine which reduces dopamine, serotonin and norepinephrine in the brain. Helps re muscle writhing/tremors but does not halt dz progression.Side effects fatigue, somnolence, suicidal thoughts, depression, nausea.
Physiotherapy can be helpful. Talk therapy for other psychological components.