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From Flashcardlet > PHYSIOL [B] motor > Flashcards

PHYSIOL [B] motor Flashcards

0
Q

role of cerebellum in voluntary movements:

A

compares planned action to actual action and helps correct disparity

  • think touching your nose diagram!!
  • drunk symptoms when it screws up
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1
Q

describe descending projection pathway:

A

primary motor cortex receives input from premotor areas
projects info to spinal cord through corticospinal tract
info goes to motor neurons and interneurons

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2
Q

what is the hierarchy of motor control?

A 
premotor and non-motor cortical area 
basal ganglia
cerebellum
motor cortex 
brainstem 
spinal cord - execution
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3
Q

describe the path sensory info takes from skin to muscle:

A

receptors in the skin pick up sensory info -> dorsal ganglion(cell bodies) -> interneuron in spinal cord -> afferent pathway -> thalamus -> primary somatic sensory cortex -> primary motor cortex -> efferent pathway -> spinal cord -> muscle!

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4
Q

what info does the somatosensory cortex provide?

A

sensory info required for specific planning, initiation and ongoing movement

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5
Q

explain the concept of “plasticity” of the brain

A

brain can remodel itself in response to varying demands
eg. phantom limb, cortex normally dedicated to hand was dedicated instead to face
expansion due to training

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6
Q

2 main areas of sensory cortex?

A

primary somatosensory cortex

posterior parietal cortex

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7
Q

function of posterior parietal cortex(more towards back of brain):

A

encodes complex sensory info to ensure planned movement is matched to the external environment
guides movements of eyes, head, arms and hands

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8
Q

what areas does the posterior parietal cortex receive input from?

A

visual, auditory, somatosensory

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9
Q

3 mains areas of the motor cortex:

A

premotor cortex
supplementary motor area
primary motor cortex

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10
Q

function of premotor cortex:

A

involved with planning and coordination of movements in response to SENSORY MOVEMENTS

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11
Q

function of supplementary motor area:

A

active during planning and coordinating INTERNALLY-GUIDED movements

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12
Q

function of primary motor cortex:

A

controls simple features of movement

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13
Q

what does EMG stand for?

A

ElectroMyoGraphic

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14
Q

where do afferent fibres enter spinal cord?

A

through dorsal root

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15
Q

where do efferent fibres exit spinal cord?

A

ventral root

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16
Q

how are motor nuclei are interconnected across segments of the spinal cord?

A

by propriospinal neurons (interneurons?)

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17
Q

how are the motor nuclei of the spinal cord arranged?

A

along medial-lateral axis according to function
ie.
most medial nuclei => innervate proximal muscles
most lateral nuclei => innervate distal muscles

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18
Q

function of spinal cord?

A

integration of many basic reflexes, such as the withdrawl reflex

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19
Q

pathway of pain reflex:

A

pain receptor -> afferent pathway -> interneuron -> efferent pathway -> flexor/extensor muscles -> withdrawal response

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20
Q

where are voluntary movements organised?

A

cortex - primary motor cortex controls simple features of movement

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21
Q

what neurotransmitter is deficient in Parkinson’s disease?

A

dopamine

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22
Q

define voluntary movement:

A

continuous spectrum of movements ranging from most automatic to least automatic

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23
Q

what is muscle excitation-contraction coupling?

A

series of events linking muscle excitation to muscle contraction

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24
Q

what is the synapse between neuron and muscle called?

A

neuromuscular junction

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25
Q

what is the response in the muscle called?

A

EPSP = Excitatory Post-Synaptic Potential

or End Plate Potential

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26
Q

where is the end plate region?

A

plate of muscle fibre neuron attaches itself to

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27
Q

describe steps of “excitation” at NMJ:

A

1) AP propagation in motor neuron
2) Ca2+ voltage gated channel open
3) tiggers Ach to be released into synapse
4) binding of neurotransmitter to receptor
5) receptor opens, allows positively charged ions to enter(Na) and exit(small K) ..triggers post synaptic cell depolarisation => EPP
6) moves along postsynaptic cell until hits more Na+ channels
7) Na+ enters as wave of depolarisation hits
8) AP propagation in muscle fibre
9) enzyme destroys excess Ach (neurotransmitter)

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28
Q

As Ca+ enters axon terminal, what does it trigger the release of? and how?

A 
triggers the release of Acetylcholine
via EXOCYTOSIS (from vesicles into synapse)
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29
Q

What actually happens during an End Plate Potential?

A

local current flow occurs between the depolarised end plate and the adjacent membrane

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30
Q

why is excess Ach destroyed by enzymes in the synapse?

A

to terminate the response

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31
Q

what is a single muscle cell called?

A

muscle fiber

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32
Q

what is a sarcomere?

A

functional unit of skeletal muscle (2.5 um wide)

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33
Q

where is a sarcomere found?

A

between the Z lines(connects thin filaments of two adjoining sarcomeres)

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34
Q

describe and explain the appearance of sarcomeres:

A

displays alternating dark(thick filament-myosin) and light(thin filament-actin, troponin, tropomyosin) lines
giving appearance of striations

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35
Q

during contraction, what aspects of the sarcomere changes in length?

A

filaments remain the same length
slide over each other to a greater extent
dark band remains the same,
light band shortens,
H zone(middle of sarcomere, only think filaments) also shortens

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36
Q

what do thick filaments in muscle fibres consist of?

A

myosin

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37
Q

what do the thin filaments in muscle fibres consist of?

A

actin, troponin and tropomyosin

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38
Q

what is meant by the cross bridge interaction?

A

sliding filament mechanism by action of actin and myosin interactions

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39
Q

how is the cross-bridge link broken?

A

fresh ATP must attach itself to myosin in order for cross-bridge to be broken at the end of the cycle.
eg. when someone dies there is not fresh ATP to attach to myosin, so cross-bridge within muscles between actin and myosin cannot be broken, hence why stiffness occurs

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40
Q

what is Tropomyosin?

A

covers actin sites

allows muscle to contract with Ca2+ binding site

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41
Q

what is tropomyosin?

A

blocks myosin binding in resting

tropomyosin will move out of the way when Ca2+ binds to troponin

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42
Q

what is the source of Ca2+ in muscle?

A

sarcoplasmic reticulum

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43
Q

how does action potential enter muscle cell?

A

transverse tubule

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44
Q

what happens to CA2+ is released from sarcoplasmic reticulum following AP entering T-tubules?

A

Ca2+ bind to troponin on actin filaments, which makes tropomyosin move aside
this opens cross-bridge binding sites on actin

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45
Q

how is cross-bridge bending/pulling powered?

A

ATP

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46
Q

what happens after Ca2+ is no longer needed for binding?

A

its reused!

pumped back into sarcoplasmic reticulum using extra ATP

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47
Q

muscle enlargement is the result of:

A

increased diameter of muscle fibres

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48
Q

where does fibre thickening come from?

A

increased content of myosin and actin, which permits a greater opportunity for cross-bridge interaction and increases the muscles contractile strength

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49
Q

how are signals passed between the nerve terminal and the muscle?

A

by chemical messenger acetylcholine (ACh)

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50
Q

what element is the link between excitation and contraction?

A

calcium

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51
Q

what are the types of muscle contraction?

A

concentric
eccentric
isometric

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52
Q

how do different types of muscle contraction occur?

A

through altering amount of force produced in the muscle RELATIVE to the external load

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53
Q

what equation helps define the different muscle types?

A

muscle torque/load torque
> 1 = concentric(greater muscle torque eg. load LIFTED by arm)
< 1 = eccentric(greater load torque eg. load LOWERED by arm)
= 1 = isometric(equal)

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54
Q

what are the 2 main factors that affect force muscle can exert?

A

excitation (stimulated by nervous system)

properties of muscle (muscular + mechanical) eg. size, fiber type, velocity of shortening

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55
Q

what neural factors influence muscle force?

A
  • number of muscle fibres contracting within a muscle(recruitment)
  • twitch summation of each contracting fiber by increasing rate of APs (rate modulation)
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56
Q

what are the muscular and mechanical factors that influence muscle force?

A 
size, 
fiber type/length
velocity of muscle shortening
muscle torque (torque produced at the joint)
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57
Q

what technique allows muscle fiber potentials to be recorded?

A

EMG - ElectroMyoGraphy

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58
Q

single motor unit refers to?

A

single motor neuron + all the muscle fibers it innervates

59
Q

what is a motor neuron pool?

A

group of motor neurons that innervate one muscle

60
Q

what is the innervation ratio?

A

number of muscle fibers per motor unit

61
Q

for areas involved in small precise movements is the innervation ratio big or small?

A

small-er
as there are more motor neurons present, each motor neuron controls less muscle fibres creating more precise movements
eg. eye and hands

62
Q

what is the “size” principle?

A

the orderly recruitment from smallest to largest motor units in increasing motor unit force

63
Q

simple model explaining increasing force production? THINK OF

A

water tank with 4 exiting pipes at different levels

where water flow = excitatory drive!

64
Q

what is the result of increasing frequency of APs?

A

allows twitch force to summate, due to higher availability of Ca2+ in cytosol

65
Q

what is Tetanus?

A

it occurs if the muscle fiber is stimulated so rapidly that is doesnt have a chance to relax between stimuli
- fatigue follows this OR stimulation ceases

66
Q

what does the max force a muscle can exert depend on?

A

its physiological cross-sectional area (PCSA)

67
Q

wtf is the PCSA (Physiological Cross-Sectional Area)?

A

its a measure of the number of cross-bridges in parallel

68
Q

what 3 physiological properties(of the muscle fibers they innervate) classify motor units?

A

twitch characteristics
tension characteristics
fatiguability

69
Q

describe the likely classification of a greater exercise intensity motor unit:

A

more fast twitch fibers
high force
fast fatigue

70
Q

what is “optimum length”?

A

length at which max number of cross bridges can be formed

sarcomere

71
Q

state the relationship between velocity of contraction and force produced:

A

as speed goes up, amount of force produced goes down

72
Q

what is the equation for calculating torque?

A

force (N) x moment arm (m)

..wtf is moment arm? ..the length of leaver

73
Q

what does torque produce?

A

rotation about a joint

74
Q

when is the feedforward control used?

A

during rapid movements and Anticipatory Postural Adjustments

75
Q

What are Anticipatory Postural Adjustments?

A

any task that you do that involves changes in center of gravity
adjustment preformed by the CNS to compensate
eg. raising one arm, compensatory muscles activated to maintain balence

76
Q

function of receptors in motor control?

A

take info from periphery and translate into neural code that CNS can use

77
Q

which of our senses is the “dominant” one?

A

vision

78
Q

where else does visual input go in the brain? and what do they control?

A

thalamus - visual perception
superior colliculus - saccades
midbrain - pupillary reflexes

79
Q

what are saccades?

A

very fast eye movements to track different objects

80
Q

what is the overall function of the superior colliculus?

A
  • receives and maps sensory inputs from; visual, auditory, somatosensory and motor
  • integrates all sensory info
81
Q

what fibers do muscle spindles consist of?

A

2 sensory afferent
1 motor efferent
intrafusal muscle

82
Q

function of muscle spindle:

A
  • detects, responds to and modulates changes in the length of skeletal muscle fibers
  • to provide an important regulatory function for movement and maintenance of posture
83
Q

describe path of stretch reflex pathway:

A

afferent input from sensory endings of muscle spindle fiber ->
alpha motor neuron output connecting directly to regular skeletal muscle fiber

84
Q

example of stretch reflex?

A

tendon tap reflex!

85
Q

explain why the tendon tap results in knee jerk response:

A

tapping patellar tendon with a rubber mallet stretches muscle spindle(sensory afferent endings within muscle spindle connect with alpha motor neuron)
resulting in contraction of EXTENSOR muscle

86
Q

what are articular receptors?

A

proprioceptors that reside in joints

87
Q

what is the function of articular receptors?

A

signal potentially damaging states of the joints

eg. high joint capsule tension, joint angles close to anatomical limits, joint inflammation

88
Q

function of mechanoreceptors in the skin?

A

respond to pressure, play particularly important role in motor control

89
Q

what are the 2 superficial mechanoreceptors of the skin?

A

1) meissner corpuscles - rapidly conducts AP

2) merkel disks - slowly adapting to AP

90
Q

name the 2 deep mechanoreceptors of the skin:

A

1) pacinian corpuscles (rapidly adapting)

2) ruffini endings

91
Q

voluntary movements are ______ directed and improve with ______ as a result of ________ and ________ mechanisms

A

goal
practice
feedback AND feedforward

92
Q

what receptors are important for motor control?

A 
eyes
muscle spindles
golgi tendon organs
joint receptors
cutaneous receptors
93
Q

what is the sensory receptor for the stretch reflex?

A

muscle spindle

94
Q

what is the magnitude of muscle strength determined by?

A

muscular factors
mechanical factors
neural factors

95
Q

describe mechanical factors that determine magnitude of muscle strength:

A

moment arms associated with the different forces

96
Q

what evidence is there to suggest some differences in strength depend on the nervous system?

A
  • strength can be increased WITHOUT activating the muscle

- dissociation between changes in muscle size and strength

97
Q

name sites of potential neural adaption to training

A

1) cortical control
2) antagonist activity
3) descending drive
4) interlimb coupling
5) motor unit activity
6) motor neuron excitability

98
Q

describe neural adaption in cortical control:

A

this is adaption of neurons in cortical map, which only occurs for NEW motor skills
eg. guitar playing - a new skill

99
Q

describe neural adaption of descending drive with training:

A

increase in amount of drive through greater input from brain to motor neurons
increase in motor neurons - increase in force

100
Q

describe what interlimb coupling is:

A

when one side is trained and there is a significant increase in muscle on the otherside
mechanism not yet completely understood

101
Q

describe what neural adaption happens to motor unit activity with training:

A

increase in discharge rates

102
Q

define fatigue:

A

a reduction of the force generating capacity of the neuromuscular system that occurs with muscle activity
any exercise-induced reduction in maximal voluntary force or power output

eg. increased effort needed to maintain submaximal contractile force

103
Q

what are the possible sites for fatigue?

A

peripheral fatigue

central fatigue

104
Q

describe peripheral fatigue:

A

due to sustained max contractor

-> change in muscle fibers themselves

105
Q

describe central fatigue:

A

its the progressive reduction in voluntary activation of muscle
-> due to sustained weak contraction

106
Q

name possible sites from brain to muscle where fatigue may occur:

A

1) input to motor cortex 5) excitation contraction coupling
2) CNS drive to lower motor neuron 6) availability metabolic substrates
3) activation of muscles and motor units 7) intracellular milieu
4) neuromuscular transmission 8) contractile apparatus
CENTRAL 9) muscle blood flow
PERIPHERAL

107
Q

main effect of CNS fatigue:

A

decline in motor unit (motor neuron and muscle fibres) activity throughout a fatiguing task

108
Q

describe muscle twitch after fatigue:

A

decrease in force
increase in duration
more chance for summation

109
Q

repeated bout of the same eccentric exercise causes what(in terms of muscle damage)?

A

results in reduced symptoms of damage and soreness compared with initial bout
eg. footballers, first game is sore but after training games no longer make them sore

110
Q

general mechanisms for the repeated-bout effect:

A 
initial bout of eccentric exercise
muscle damage
adaption 
neural theory - connective tissue theory - cellular theory
repeated bout of eccentric exercise
less muscle damage
111
Q

describe 3 locations within CNS that may adapt with strength training:
AND HOW:

A

cortical control -
antagonist activity - decrease in antagonist activity
descending drive - increase in amount(greater input from brain to motor neurons)

112
Q

describe 4 potential sites of central fatigue:

A

1) input to motor cortex
2) CNS drive to lower motor neuron
3) activation of muscles and motor units
4) neuromuscular transmission

113
Q

describe neural theory that is thought to contribute to the repeated bout effect:

A

increased motor unit activity
increased slow-twitch fiber recruitment
increased motor unit synchronisation

114
Q

describe connective tissue theory that is thought to contribute to the repeated bout effect:

A

increased intramuscular connective tissue

intermediated filament remodelling

115
Q

describe cellular theory that is thought to contribute to the repeated bout effect:

A

strengthening of cell membranes
removal of weak muscle fibres
longitudinal addition of sarcomeres

116
Q

via WHAT does the basal ganglia influence the motor cortex to facilitate movement?

A

thalamus!

117
Q

what is the corticospinal tract?

A

largest descending fibre tract

118
Q

where does the corticospinal tract divide?

A

at the medullary pyramids -> into ventral and lateral tracts

119
Q

what are direct corticospinal connections responsible for?

A

fine control of digits

120
Q

what would be the effect of bilateral section of the corticospinal pathway?

A

instead of using small precise grip, entire hand is used

121
Q

what is the leading cause of damage to the corticospinal pathway?
and what does this result in?

A

stroke!

results in paralysis of the contralateral upper and lower limbs and facial muscles

122
Q

what does Parkinson’s disease result from?

A

loss of most of the neurons using dopamine as their neurotransmitter

123
Q

how much of the total brain dopamine does the BG contain?

A

80%!

124
Q

what characterises Parkinsons disease?

A

slowness
tremor(5-6 Hz)
rigidity (resistance to motion)
deficits in postural reactions

125
Q

what are the current treatments for Parkinson’s disease?

A

Drugs (L-DOPA)
Deep brain stimulation
stem cell therapy?

126
Q

what are the 3 functionally distinct parts of the cerebellum?

A

1) Vestibulocerebellum
2) spinocerebellum
3) cerebrocerebellum

127
Q

function of Vestibulocerebellum:

A

important for maintaining balance(VESTIBULAR IN EAR!!) and controls eye movements

128
Q

function of Spinocerebellum:

A

enhances muscle tone and coordinates skilled, voluntary movements

129
Q

function of cerebrocerebellum:

A

plays role in planning and initiating voluntary activity by input to cortical motor areas

130
Q

what are 3 typical defects observed in cerebellar diseases:

A

1) delay in movement initiation
2) inaccuracy in range/direction, decomposition of movement(shoulder first, elbow second), tremor increases on approaching nose
3) irregular pattern of alternating movements

131
Q

how many pairs of spinal nerves are there?

A

31 pairs

132
Q

what aspects of neural processing is limbic association cortex primarily responsible for?

A

motivation
emotion
memory

133
Q

what aspects of neural processing is Broca’s area primarily responsible for?

A

speech formation

134
Q

what aspects of neural processing is primary motor cortex primarily responsible for?

A

voluntary movements

135
Q

what aspects of neural processing is posterior parietal cortex primarily responsible for?

A

integration of somatosensory and visual input; important for complex movements

136
Q

what aspects of neural processing is Wernicke’s area primarily responsible for?

A

speech understanding

137
Q

what is agnosia?

A

defect in the ability to recognise sensory stimuli without a defect in the sense

138
Q

what is apraxia?

A

the inability to perform simple motor skills in the absence of paralysis

139
Q

does the location of a spinal lesion matter?

A

YASSS

location will produce muscle weakness and atrophy based on spinal location and somatotopic organisation in the brain

140
Q

what happens when the descending motor pathway is damaged?

A

can lead to spasticity, which is increased muscle tone cause by heightened stretch reflexes

141
Q

what is ALS?

A

Amyotrophic Lateral Sclerosis
leads to the progressive death of alpha-motor neurons, resulting in muscle denervation and a loss of voluntary muscle control

142
Q

true or false: Agnosia refers to the inability to perform simple motor skills in the absence of paralysis

A

FALSE!

thats Apraxia

143
Q

true or false: the Spinocerebellum is a part of the cerebellum that plays a role in planning and initiating voluntary activity by input to cortical motor areas

A

FALSE
thats the cerebocerebellum
the spinocerebellum enhances muscle tone and coordinates skilled, voluntary movements

144
Q

what is the condition of rigor mortis?

A

the locking in place of skeletal muscles that begins 3-4 hours after death

145
Q

why does rigor mortis occur?

A

an increase in intracellular calcium creates cross-bridge binding, and there is no ATP avaliable for cross-bridge detachment

146
Q

​Nerve gas poison is known to inactivate acetylcholinesterase (AChE) so that the AChE normally in the neuromuscular junction no longer removes the ACh released at the end plate. The result of this poison is?

A

Large amounts of ACh can accumulate and repetitively stimulate the muscle fibre, causing muscle spasm

From Flashcardlet (34 decks)

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