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BMS1052 > MOVEMENT > Flashcards

MOVEMENT Flashcards

1
Q

What is the NMJ?

A

The neuromuscular junction - synapse between nerve and muscle fibre (acetlycholine released)

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2
Q

Where do some acetlycholine receptors bind?

A

To nicotinic receptors (proteins embedded in muscle fibre)

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3
Q

What happens when Ach binds?

A

It binds and simultaneously lets Na+ in

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4
Q

How many subunits does a nicotinic receptor contain?

A

5 subunits

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5
Q

What needs to occur for the channel to open?

A

One molecule of Ach binding to each alpha subunit

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6
Q

What is another term for postsynaptic membrane?

A

Motor end plate

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7
Q

Where are lower motor neurons found ?

A

Ventral horn of spinal cord

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8
Q

What do lower motor neurons do?

A

Directly command muscle contraction

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9
Q

Are lower M.Ns distributed evenly throughout the body?

A

NO! Innervation of more than 50 muscles of arm originates from C3-T1 (ventral horn is ‘swollen’ )

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10
Q

Where are the motor neurons that innervate distal and proximal musculature found?

A

C and L-S segments of spinal cord

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11
Q

What is the first way the CNS controls muscle contraction?

A

By varying the firing rate of motor neurons

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12
Q

How does the alpha neuron communicate with the muscle fibre?

A
  • By releasing neurotransmitter Ach at NMJ
  • Ach released from presynaptic terminal causes response (EPSP-but not the same as in normal neuron-neuron synapses) in muscle fibre- end plate potential
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13
Q

What does one poostsynaptic AP cause?

A

A twitch (rapid contraction and relaxation of muscle fibre)

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14
Q

What does a sustained contraction require?

A

Continual barrage of APs

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15
Q

What does high frequency presynaptic activity cause?

A

Temporal summation of postsynaptic responses

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16
Q

What is the second way the CNS grades muscle contraction?

A

-Recruitment (recruiting additional synergistic motor units)

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17
Q

What can occur in a muscle with a large number of SMALL motor units (small alpha motor neurons) ?

A

The muscles can be more finely controlled by the CNS

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18
Q

What are small neurons more exited by?

A

Signals descending from brain

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19
Q

What is orderly recruitment of motor neurons due to?

A

The variation in motor neuron size

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20
Q

What are the three main sources of input to alpha motor neurons?

A
  1. Dorsal root ganglion
  2. Upper motor neurons in motor cortex and brain stem
  3. Interneurons in spinal cord (largest input and could be excitatroy or inhibitory, for motor programs)
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21
Q

What do the dorsal root ganglion cells do?

A

Innervate the muscle spindle- sensory and muscle length feedback

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22
Q

What are the upper motor neurons in the motor cortex and brain stem important for?

A
  • Initiation and control of voluntary movement
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23
Q

What are slow twitch muscle fibres?

A
  • Dark red
  • Large number of motochondira
  • Fatigue resistant
  • Slow to contract
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24
Q

Where are slow twitch muscles found?

A

Antigravity muscles (gastrocnemius soleus) of legs, the torso, and wings of birds

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25
Q

What are fast twitch fibres?

A
  • Contract rapidly
  • Fatigue faster
  • Fewer mitochondria
  • Anaerobic metabolism e.g. arm muscles
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26
Q

What are the two types of fast twitch muscles?

A
  • fatigue resistant (FR) and fast fatigable (FF) q
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27
Q

What are FR (fatigue resistant) fibres classified by?

A

Moderately strong and fast contractions and relatively resistant to fatigue
- Intermediate size

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28
Q

What are FF (fast fatiguable)fibres classified by?

A
  • They generate the stronges, fastest contractions but are quickly exhausted when stimulated at high frequency for long periods
  • Largest diameter so fastest conducting
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29
Q

Do different types of muscle fibres coexist in muscles?

A

YES!

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30
Q

Do different types of motor neurons coexist in muscles?

A

NO!! Each motor unit contains muscle fibres of only a single type
e.g. one type of slow motor unit that contains only slowly fatiguing red fibres

  • also two types of motor units containing EITHER FR FF
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31
Q

What can too muhc Ach lead to?

A

Desenistisation of receptors and block of nueromuscular transmission

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32
Q

What are myofibrils surrounded by?

A

Sarcoplasmic reticulum (sac that stores Ca2+)

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33
Q

How do APs gain access to the SR?

A

T tubules (network of tunnels)

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34
Q

What are T tubules?

A
  • Like inside out axons
  • membrane contains voltage sensitive clusters of 4 Ca2+ channels called tetrads
  • T tubule membrane linked to calcium release channel in SR membrane
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35
Q

What is the molecular basis of muscle contraciton?

A

Myofibril divided into disks (z lines)

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36
Q

What is a sarcomere?

A

Segment composed of two z lines with myofibril between

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37
Q

What is anchored to Z lines?

A
  • thin filaments (actin)

- the actin proteins face one another and never come into contact

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38
Q

What is between the thin filaments?

A

THICK filaments (myosin protein)

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39
Q

When does muscle contraction occur?

A

When thin filaments slide along thick filaments and bring Z lines toward one another

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40
Q

In contraction the sarcomere…

A

Becomes shorter in length

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41
Q

What do the myosin heads do?

A
  • ‘walk along’ the actin filament
  • binds actin molecules and conformational change occurs that causes them to pivot (causes thick filament to move with respect to the thin filament)
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42
Q

How does the myosin head ‘unlock’?

A

ATP binds to the myosin heads and heads disengage and unlock so process can repeat

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43
Q

What happens when muscle is at rest?

A

Myosin can’t interact with actin

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44
Q

How does Ca2+ initiate contraction with respect to the complex?

A
  • Binds to TROPONIN which then shifts tropomyosin position and then exposes sites where myosin can bind to actin
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45
Q

How long does contraction continue?

A

Based on amount of Ca2+ and ATP being available

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46
Q

Why do muscles become stiff after death?

A
  • Because muscle cells starved of ATP
  • No ATP prevents detachment of myosin heads and leaves myosin attachment sites on actin filaments exposed for binding (permanent attachments for thick and thin filaments form)
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47
Q

What are the critical steps in contraction?

A
  1. AP
  2. Ach release
  3. Na+ entry triggers Navs
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48
Q

What happens when AP propagates in muscle fibre?

A
  • The T tubules allow AP to reach all parts of the muscle fibre simultaneously
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49
Q

What is a DHP receptor?

A
  • Voltage gated Ca2+ channel
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50
Q

What happens when the AP reaches the DHP receptor?

A
  • There is physical coupling between DHP receptor and ryanodine receptor
  • When DHP opens in response to voltage gradient, also causes ryanodine receptor to open (ca2+ channel on the lateral sac of the SR)
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51
Q

Why do your muscles get ‘warm’ when you exercise?

A

Energy demands associated with ATP pumping Ca2+ back in

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52
Q

What occurs in crossbridge cycling?

A
  • 4 states
  • The RATE at which this occurs depends on the ATP (e.g. muscle cells with lots of mitochondria will go through it quicker)
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53
Q

What is Ca2+ critical for?

A

Cross bridge cycling

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54
Q

What is the latent period known as?

A

Gap between when the AP has arrived and when you start seeing force

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55
Q

What does the latent period depend on ?

A
  • AP conduction time

- Time for Ca2+ to be released

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56
Q

Why does force last for so long?

A

Takes some time for troponin to move off tropomyosin (1st step)

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57
Q

What limits the maximum force generation?

A
  • takes time for cross bridging to occur
  • Passive muscle tension
    (fused and unfused tetanus)
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58
Q

What effect does a nicotinic Ach receptor antagonist have?

A
  • nicotinic receptors on skeletal muscle
  • weakness and inability to generate contractions
  • competitive antagonist prevents Ach binding
  • So flaccid paralysis
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59
Q

What effect does massive release of acetylcholine, norepinephrine and GABA have?

A
  • Cramps, muscle contractions. Rarely death, only death in small animals, also spasms
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60
Q

What happens if you prevent Ach release?

A

Flaccid paralysis with cramps (e.g in Botox)

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61
Q

What does the titin filament account for?

A

PASSIVE TENSION

- has spring like properties

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62
Q

What is active tension?

A

The amount of tension generated on the sarcomere

- Depends on the length

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63
Q

What is the optimal length dependent on?

A
  • The overlap between actin and myosin
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64
Q

What is the max length dependent on?

A

No overlap of actin/myosin

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65
Q

What is the min length limited by?

A
  • Thin filament overlap

- Overlap of thick filaments and Z disks

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66
Q

What is isotonic contraction?

A

Muscle changes length whilst maintaining constant tension

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67
Q

What is isometric contraction?

A
  • Muscles develops tension without changing length
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68
Q

Most muscle contractions are…

A

neither isotonic nor isometric

69
Q

What happens at the molecular level?

A
  • Cross ridging occurs when APs reach the muscle fibres

- If NO LENGTHENING OCCURS then cross-bridges rebind in the same place

70
Q

How is there no shortening when cross bridge cylcing is typically associated with shortening?

A
  • Cycling can continue but myosin cross bridges repeatedly attach and detatch from the same protein
71
Q

What does force generation with no shortening equal?

A
  • Isometric contraction
72
Q

Which two factors are part of isotonic muscle contraciton?

A

Concentric (muscle shortening) and eccentric (muscle lengthening) contraction

73
Q

What is isometric contraction?

A
  • Force generation begins from time of first cross bridge attachment (few ms)
  • To
74
Q

What is isotonic contraction?

A
  • Evidence of shortening is delayed until enough crossbridges have attached to conunteract load (15ms)
  • shortening period ends once load returns to resting position (70ms)
75
Q

What can types of skeletal muscle be defined by?

A
  1. Maximum shorteining velocity

2. ATP pathway

76
Q

What is type 2a fibres?

A

Type 2 meaning fast fibres

- a meaning Oxidative- so lots of mitochondria, good blood supply, lots of myoglobin

77
Q

What is type 2b fibres?

A

Type 2 meaning fast fibres

  • ‘b’ meaning glycolytic
  • Large glycogen stores, few mitochondria, generally thicker, WHITE in appearance
78
Q

Do slow glycolytic fibres exist?

A

no!!

79
Q

Which type of fibres does the body recruit first?

A
  • Uses the small SLOW fibres first, as they can sustain force for long amounts of time, then recruit the fast oxidative, then lastly recruit the fast glycolytic which are the most rapid
80
Q

Type I fibres have motor units that..

A
  • Have smaller cell bodies and smaller diameter axons

- Steady, low frequency activity (slow oxidative)

81
Q

Type II fibres have motor units that..

A
  • Have large cell bodies and diameter axons

- occasional high frequency bursts (30-60hz)

82
Q

What did the experiment on the muscle type show?

A

That the muscle phenotype depends on the RATE of APs coming from the motor neuron
(Fast pattern: 30-60Hz) (slow pattern- 10-20 Hz)

83
Q

What does Area 4 contain and what is it responsible for?

A
  • primary motor cortex
  • contains cortical inputs from A.6 and somatosensory A1,2,3.
  • ## Responsible for generating neural responses for EXECUTION of movement
84
Q

When is Area 4 active?

A

Only when executing movements

85
Q

What has the lowest electrical thresholds for stimulating movement?

A

Primary motor cortex (Area 4)

86
Q

What two functionally distinct regions does area 6 contain?

A
  1. PMA (premotor area)

2. SMA- supplementary motor area (two divisions)

87
Q

What is the PMA responsible for?

A

Sensory guided movements e.g. visual info- picking up phone and also partly postural adjustments

88
Q

What are the two divisions of the SMA (supplemenraty motor area in A6)?

A
  1. SMA proper (caudal)

2. pre- SMA (rostral)

89
Q

What is the function of the SMA proper subdivision?

A
  • Planning of motor actions, especially when guided from memory. e.g. serving in tennis
90
Q

Which area of the A6 is responsible for serving in tennis?

A
  • SMA proper subdivision of SMA
91
Q

What is the function of the pre-SMA subdivison?

A
  • Acquiring new motor sequences (piano chord playing)
92
Q

What is the differene between PMA and SMA in general?

A

PMA- premotor area incorperates sensory info
SMA- internally generated movements, performing already learned sequence (retrieval) or linking multiple known sequences e.g. serving at tennis match)

93
Q

Which area do SIMPLE finger movements involve?

A

Mainly the PRIMARY MOTOR CORTEX (also primary somatosensory for sensory)

94
Q

Which areas are active when doing sequential finger movement such as piano chord plaing?

A

Supplementary Motor Area (pre-SMA) -guided from memory

95
Q

What happens if you mentally rehearse playing the piano?

A

Only activity in the SMA and pre SMA will occur (NOTHING IN THE MOTOR AREA OR SOMATOSENSORY CORTEX)

96
Q

What is an open loop system?

A
  • You don’t have feedback to modify what is happening in that system e.g. don’t need to monitor a bicep curl
97
Q

What type of activity is the cerebellum involved in?

A
  • It is like a dog catching a frizbee which is closed loop as the dog must MODIFY behaviour in response to frizbee
  • It integrates sensory feedback on a range of timescales with awareness of body position into closed loop system for modifying cortical control of movement
98
Q

Which types of muscles does the cerebellum help to coordiante?

A
  • Adjusts posture and gait
  • Refines movements IN PROGRESS (evaluates disparities between INTENTION and ACTION)
  • Adapts and improves REPETITIONS of the same movement (trial and error) (like catching the orange behind the back)
99
Q

What are the 3 functional regions of the cerebellum that map onto the anatomical regions?

A
  • Vestibulocerebellum
  • Spinocerebellum
  • Cerebrocerebellum (lateral hemisphere)
100
Q

Where do OUTPUTS originate in?

A
  • Either in deep nuclei or flocculondular lobe
101
Q

What are the SOLE OUTPUTS of the cerebellar cortex?

A

Purkinje cells

102
Q

What do purkinje cells do?

A

Inhibit neurons in the cerebellar deep nuclei which are the sole outputs of the cerebellum

103
Q

Where do the majority of outputs prokect via?

A
  • cerebellar peduncles (superior peduncles only)
104
Q

What is the general loop of events?

A
  • sensory inputs and efferent copy of motor commands
  • processing in cerebellar cortex
  • purkinje cells in cerebellar cortex prokect to deep nuclei
  • deep nuclei projections leave cerebellum
105
Q

What happens when you have a lesion to the vestibulocerebellum (flocculondular lobe) ?

A
  • can’t incorperate vestibular info.
  • difficulty controlling eye position when moving head
  • Hard to keep balanced BUT can move arms and legs fine if laying on a bed - don’t have to worry about postural adjustments.
106
Q

What happens when there is a lesion in the cerebrocerebellum (lateral hemisphere) ?

A
  • Affects control of IPSILATERAL MOVEMENTS
  • Delays in initiating movement
  • Irregularities in timing movement components (decomposition) e.g. moving fingers whilst changin arm position.
  • lose cognitive functions such as walking, memory, abstract reasoning, spatial cognition
107
Q

What side of the body does the CEREBELLUM control?

A
  • The right side of the body
108
Q

What does the spinocerebelllum do?

A
  • Critical for coordinating movements
  • compares efferent copy and somatosensory information
  • regulates movements in progress and modulates descending commands
109
Q

What happens if you have an electrical prosthetic placed into body?

A
  • no longer has intact proprioception (no spindles, stretch receptors, golgi tendon organs
  • Can only tell where prosthetic arm is in space by LOOKING AT IT therefore missing out on the spinocerebellum movements (so difficult type of prosthetic)
110
Q

What are the symptoms of spinocerebellar damage?

A
  • ATAXIA- uncoordinated/innacurate movements
  • DYSYNERGIA- decomposition of synergistic multijoint movements (touching finger to nose)
    DYSMETRIA- lack of coordination resulting in overshoot or undershoot (e.g. trouble changing directions or drawing square)
111
Q

What is the difference between ganglia and nuclei?

A

Ganglia- Clusters of cell bodies in PNS

Nuclei- Clusters of cell bodies in CNS ( gray matter)

112
Q

What are the basal ganglia?

A
  • Deep in the brain (four collections of cell bodies)
  • Encode reward
  • Help choose between possible movements
113
Q

What are the four collections of cell bodies that make up the basal ganglia?

A

STRIATUM (caudate + pudamen)

  • GLOBUS PALLIDUS (external and internal)
  • SUBTHALMIC NUCLEUS
  • SUBSTANSIA NIGRA
114
Q

What is the direct pathway of the basal ganglia?

A
  • Positive feedback loop
  • Increased inhibitory of globus palitus (inhibitory projection to VLo) -this disinhibition raises activity which then raises activity in the cortex.
115
Q

What is the indirect pathway of the basal ganglia?

A
  • negative feedback loop (next supressive effect on cortex)
  • Small activity increase will be pushed back down if propagated through indirect pathway of group
  • so there is competition-tension between excitation and depression.
116
Q

What is the dopaminergic projections from SNc to striatum?

A
  • Dopamine has a DUAL effect

- Mode of action depends on receptors D1+ and D2-

117
Q

What do D1 receptors lead to?

A

Depolarisation of neurons

118
Q

What is the size of the End Plate Potential (depolarisation in muscle) directly related to?

A
  • End Plate Potential is directly related to the amount of Ach that binds to the post- synaptic Acetylcholine receptors.
119
Q

Why does the depolarisation for the MUSCLE action potential last longer than the nerve AP?

A
  • Because Na+ isn’t the only ion moving into the cell’ Ca++ is ALSO moving in and it is the Ca++ that hangs around for longer (sequesteration is longer) so depolarisation lasts for longer (positive charge)
120
Q

During neuromuscular transmission:

(a) There is a decrease in the permeability of the motor end plate membrane to Ca++.
(b) Acetylcholine binds to receptors on the motor end plate membrane
(c) Ca++ is released from vesicles located in the motor nerve terminal
(d) Acetylcholinesterase depolarises the muscle membrane adjacent to the motor end plate
(e) Re-uptake of acetylcholine into the motor nerve terminal terminates the action of this transmitter

A

(b) Acetylcholine binds to receptors on the motor end plate membrane

121
Q

Signal transmission from motor nerves to skeletal muscle at the neuromuscular junction:

(a) Requires temporal summation of several end plate potentials to trigger a muscle action potential
(b) Is excitatory when the muscle is required to contract and inhibitory when the muscle is required to relax
(c) Is faster than at other synapses because of direct contacts between the nerve terminal membrane and the motor end plate membrane on the muscle cell
(d) Normally has a high ‘safety factor’, ensuring that each nerve action potential always produces a muscle action potential
(e) Is highly efficient because each muscle cell receives simultaneous input from several nerve axons

A

(d) Normally has a high ‘safety factor’, ensuring that each nerve action potential always produces a muscle action potential

122
Q

Myasthenia gravis is an autoimmune disease resulting in a loss of functional acetylcholine receptors and severe muscle weakness. Which of the following drugs might be useful in treating this condition?

(a) A drug that inhibits acetylcholinesterase
(b) A drug that inhibits release of acetylcholine
(c) A blocker of cation channels in the motor end plate
(d) An anabolic steroid that increases muscle mass
(e) A drug that inhibits the uptake of choline into motor nerves

A

(a) A drug that inhibits acetylcholinesterase

123
Q

All of the following are involved in neuromuscular transmission, EXCEPT:
(a) An increase in the movement of Na+ and K+ into the motor end plate membrane

(b) An influx of Mg++ into the motor axon terminal
(c) Binding of acetylcholine to receptors on the motor end plate membrane
(d) Depolarisation of the muscle membrane adjacent to the motor end plate
(e) Re-uptake of acetylcholine into the motor axon terminal

A

(b) An influx of Ma++ into the motor axon terminal (does not occur!!!)

124
Q

What is the threshold?

A
  • The lowest current needed to either produce a reliably measurable force or a reliably measurable change in voltage (for EMGs)
125
Q

What can the threshold be influenced by?

A
  • How well you place the electrode
  • How much conductive gel you have on the electrode
  • whether you are stimulating at the elbow or on the forearm
126
Q

What happens when Ca++ is sequestered ?

A

The binding sites are no longer available (so actin and myosin can no longer bind)

127
Q

What should we expect with the force when two pulses are searated by less than 150ms ?

A
  • That the force for the second force is larger than the first
128
Q

In the practical, how was the force summation different to the EPSP in neurons?

A
  • In muscles, it was the measure of all the electrical activity in the motor unit because APs can’t sum.
  • Summation of total amount of APs which was the electrical activity (because this was not an intracellular recording)
129
Q

If we have an interpulse interval of 50ms what will occur?

A

It will appear as if only one pulse has occured, however they have just summed from temporal summation. Each force will add to the EXISTING force

130
Q

What is the physiological limit of force summation?

A

When all of the Ca++ is released inracellularly and kept there so all the myosin binding sites are epxosed

131
Q

Why are small motor units recruited first?

A

Small cell bodies–> so higher membrane resistance (R) and if I is fixed and R is large, then it will be easier to get to AP spiking threshold

132
Q

What occurs in the eccentric contraction, in terms of the myosin head?

A
  • Myosin head binding sites are in the OPPOISTE direction to the power stroke of the myosin head
133
Q

Which pathway works to maintain posture when standing?

A

Ventromedial pathways

134
Q

What is another name for a muslce spindle?

A

A stretch receptor

135
Q

What does a muscle spindle contain?

A

Specialised skeletal muscle in a fibrous capsule

  • Middle third of capsule is swollen
  • Type Ia axons-sensory (meaning it is the thickest so conducts well)
136
Q

What do proprioceptros do?

A
  • Detect changes in muscle length (stretch)

- Ones own body sense

137
Q

What are intrafusal muscle fibres responsible for?

A

Changing spindle length and so sensitivity

138
Q

What are extrafusal muscle fibres responsible for?

A

Force generation

139
Q

Where do the alpha motor neurons form a connection to?

A

The extrafusal muscle fibres (NMJ)

140
Q

Where do the gamma motor neurons form a connection to?

A

The intrafusual muscle fibres

141
Q

What does alpha motor neuron activation do to Ia fibres ?

A

Decreases the Ia activity

142
Q

What does the gamma motor neuron activation do to Ia fibres?

A
  • Increases the activity
143
Q

What are gamma motor neurons?

A

A type of LOWER motor neuron like alpha but slightly different

144
Q

What do you need to inhibit for flexion to occur?

A

Need to inhibit the alpha neurons

145
Q

What is a golgi tendon organ?

A
  • A sensory of skeletal muscle embedded in the tendon
  • Monitors muscle tension or the force of contraction
  • Innervateed by Ib motor axons (muscle tension information)
  • situated IN SERIES with muscle fibres (helps to distinguish Ia activity coding muscle length info from Ib;muscle tension info)
146
Q

What happens to muscle spindle after contraction of extrafusal muscle fibres?

A
  • Spindle is slack (so can’t signal muscle length)
147
Q

What is gamma coactivation?

A
  • Where the gamma neurons are activated after extrafusal muscle shortens to increase Ia activity so that the muscle spindle can detect changes in muscle length.
148
Q

What does the myotactic reflex involve (neurons)?

A

Single synapse at NMJ and involves two motor neurons (alpha)

149
Q

What is reciprocal inhibition?

A

Sensory inputs from Ia axons are used to inhibit contraction of antagonist (so contraction of one muscle automatically relaxes the second)

150
Q

What does reciprocal inhibition prevent?

A

Myotactic reflex from resisting intentional movement

151
Q

What are the steps in the reflex action of Ia (sensory) fivre activation?

A
  1. Monosynaptic excitation of homoynmous muscle
  2. Excitation of synergist muscles
  3. Inhibition of antagonist muscles
  4. Restricted to muscles in the same “myotactic unit” (effect at that single joint)
152
Q

What is autogenic inhibition in the golgi tendon organ?

A

Maintains muscle tension within an optimal range

Increases muscle tension (inhibition of alpha motor neuron and reduced rate of muscle contracton)

153
Q

What are the steps in the reflex action of the Ib fibre activation?

A
  1. Disynaptic inhibition of homoynmous muslce
  2. Inhibtion of synergist muscles
  3. Excitation of antagonist muscles
  4. Affects other myotactic units (more widespread than Ia fibres)
  5. Context dependent (autogenic inhibition is suppresed during locomotion)
154
Q

What is a summary of muscle spindles?

A
  • signal info about muscle LNEGTH
  • innervated by type Ia sensory neruosn
  • in PARALLEL with extrafusal muscle fibres
  • gamma co activation maintains sensitivity
155
Q

WHat is a summary of the golgi tendon organs?

A
  • SIgnal information about muscle TENSION
  • Innervated by type Ib sensroy neurons
  • In SERIES with muscle fibres
  • NO direct motor innervation
156
Q

What do upper motor neurons do?

A

Control voluntary movements

  • do not directly innervate the muscle
  • cell bodies in brain, project down spinal cord to lower motor neurons
157
Q

Where does the lateral corticospinal tract start in the spinal cord and then end up?

A

It starts in the white matter (lateral corticospinal tract) then ends in the anterior gray matter horn of spinal cord

158
Q

Which areas in the homonculous map are the largest for the motor region (M1-Area4) ?

A
  • the face and the hand (legs are the smallest)
  • motor cortex goal is to OVERALL movement
  • SA in cortex is proportional to level of fine muscle control
159
Q

Is there a sequentially ordered representation of adjacent muscles?

A

NO!!! It controls multiple muscles for an overall response

160
Q

What occurs in a unilateral lesion of the UMN (upper motor neurons) ABOVE the pyramidal desucssation point?

A

If would affect the contralateral side as signal not able to pass through decussating bit as it is severed

161
Q

What occurs in a unilateral lesion of the UMN BELOW the decussation point?

A

It will affect the ipsilateral side

162
Q

What does a unilateral lesion in the LMN (lower motor neuron) produce?

A

Ipsilateral paralysis and atrophy

163
Q

What are lower motor neuron lesion symptoms?

A

Flaccid paralysis (loss of motor control, lesion in brain-> contralateral paralysis lesion below decussation-> ipsilateral) e.g. paraplegia

  • Paresis (weakness/incomplete paralysis, voluntary power is impaired)
  • Muscle atrophy (Muscle fibres lose contractile proteins
  • Arefglexia (loss of reflexes due to missing circulatory)
164
Q

Are symptoms for upper motor neuron lesions the same over time?

A

-NO THERE ARE BOTH SHORT AND LONG TERM SYMPTOMS

165
Q

What occurs on the first day of an UMN lesion?

A
  • Flaccidity
  • Hypotonia (decreased s.c. activity)
  • Areflexia (loss of muscle tone)
166
Q

What are the long term symptoms for a UMN lesion?

A
  • Loss of fine /fractionated movements
  • Spasticity (hyper-reflexia and hyper-tonia)
  • Babinski sign
167
Q

What is hyper-reflexia? (the long term symptom for UMN damage)

A
  • Exaggerated reflexive control
  • Loss of descending inhibition
  • e.g exaggerated and rapid tendon jerk and flexion reflexes
    (also Clonus is sustained stretch leading to rhythmic cycles of contraction and relaxation)
168
Q

What is hypertonia (long term symptom for UMN damage)?

A
  • Increased RESISTANCE to passive muscle stretch
  • reflects ongoing contractile activity in muscle
  • due to hyper-excitability and tonic input from muscle stretch receptors

BMS1052 (14 decks)

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