motor Flashcards

1
Q

what is the only neurotransmitter involved in causing muscles to contract

A

Ach

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2
Q

are voluntary movements open or closed loop

A

open loop (reflex movement closed)

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3
Q

what is the highest level in the hierarchy of movement control

A

cerebullum, basal ganglia, motor cortex- planning, coordination, desire to move

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4
Q

what is the middle level in the hierarchy of movement control

A

descending systems and brainstem

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5
Q

what is the lowest level in the hierarchy of movement control

A

from spinal cord from motor neurone to muscle

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6
Q

what allows refinement of movement and accuracy

A

feedback at every level

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7
Q

what happens in lesions to level 1 (hierarchy)

A

apraxia- can’t carry out movement even though able to by muscle, after stroke/neuro degeneration

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8
Q

what happens in lesions to level 3 (hierarchy)

A

muscle weakness, in disorders of spinal cord disease, neuropathy, muscle disease eg dystrophy

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9
Q

what is a motor unit

A

motor neurone and the muscle it innervates

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10
Q

where do lesions occur in lower motor neurone lesions

A

between ventral horn and muscle

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11
Q

what are central pattern generators

A

in thoracic and lumbar parts of spinal cord, dont require constant afferent input for an output

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12
Q

what pathways run medially originating in the brainstem

A

vestibulospinal, reticulospinal, tectospinal

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13
Q

what pathways run laterally originating in brainstem

A

rubrospinal

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14
Q

what systems make up the aminergic system and where do they originate

A

noradrenergic system (from locus coeruleus) and serotonergic system (from raphe nucleus)

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15
Q

what pathways are involved in planning and initiation

A

corticobulbar and corticospinal

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16
Q

what are the 2 divisions of the corticospinal pathway

A

lateral corticospinal tract (3/4 fibres cross over to travel here) and ventral tract (those that don’t cross)

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17
Q

does the basal ganglia have direct connection to neurones

A

no has to travel through the cortex

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18
Q

which tracts are motor

A

descending tracts

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19
Q

what does damage to the basal ganglia lead to

A

apraxia, huntingtons, parkinsons, hemiballismus (involuntary movements)

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20
Q

what is classed as an upper motor neurone lesion

A

damage to descending tracts

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21
Q

what are the signs of upper motor neurone lesions

A

spinal cord reflexes left in tact, loss cortical inhibition, mild weakness, increased tone, exaggerated reflexes

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22
Q

what is involved in the coordination of movement

A

cerebellum

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23
Q

what is the function of the cerebellum

A

compares intended with actual movement. stores movement info and can learn new movements, store timing

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24
Q

what happens if the cerebellum is damaged

A

incoordination, jerky movements, impaired balance

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25
Q

where does the cerebellum receive info from

A

copy of info from cortex (intended movement), info from muscle spindles, other receptors (actual movement)

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26
Q

where does the cerebellum send its adjustments to

A

cortex

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27
Q

what happens if sensory feedback is disturbed, what is this called

A

impaired proprioception and touch. Large sensory input neuropathy- can’t sense position of limbs in space

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28
Q

what are the 2 mechanisms of postural adjustments

A

compensatory and anticipatory

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29
Q

how rapid is the compensatory mechanism of postural adjustment

A

rapid, automatic, stereotyped, refined by learning

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30
Q

what happens in anticipatory mechanism postural adjustment

A

predict disturbances before voluntary action. improve by learning

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31
Q

what is the postural set

A

collection of responses- integrate adjustments with voluntary actions

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32
Q

are postural refexes triggered before or after feedback

A

before, then scaled to reach stability

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33
Q

how are postural reflexes different to simple reflexes

A

triggered before feedback, scaled to acheive stability, rapid and slower responses (like simple reflexes- rapid and stereotyped)

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34
Q

what are vestibular nuclei involved in

A

balance

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35
Q

what is the corticoreticular tract involved in

A

postural adjustments

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36
Q

what tracts are important for rapid responses to change in posture

A

transcortical tracts

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37
Q

which info travels fastest (proprioceptive, vestibular, visual)

A

proprioceptive info travels 2x as fast as vestibular and visual info (visual slowest)

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38
Q

what happens when muscle spindles are activated

A

alpha motor neurones activity increases so muscle contracts

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39
Q

what coactivation is important when alpha motor neurones are activated and what is the action

A

gamma coactivation- which allows the spindles to remain taut and sensitive in contraction

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40
Q

what does the vestibular reflex respond to

A

in response to head movement changing wrt neck and limbs

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41
Q

what is decerebrate rigidity

A

arms and legs EXTEND

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42
Q

what is decerebrate rigidity due to

A

complete bilateral lesion just above the reticular formation below red nucleus. action of reticulospinal and vestibulospinal areas on alpha and gamma nuclei on the spinal cord predominantly extensors

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43
Q

what is decorticate rigidity

A

arms FLEX

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44
Q

what happens in decorticate rigidity

A

lesion is higher- above the midbrain red nucleus.

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45
Q

what does the brainstem have in control of posture

A

reticular formation. reticulospinal tracts involved

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46
Q

what does stimulation of the anterior lobe of the cerebellum lead to

A

decrease in decerebrate activity

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47
Q

what happens if you cut the vestibular nerve (wrt decerebrate rigidity)

A

decrease decerebrate rigidity

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48
Q

what damage to sensory structures can be postural disorders

A

blind (increase postural sway), vestibular disease (menieres), somatosensory injury/peripheral neuropathy

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49
Q

what damage to motor structures can be postural disorders

A

brainstem damage, cerebellar and basal ganglia damage

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50
Q

what are pyramidal tracts?

A

corticobulbar and corticospinal

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51
Q

what does the basal ganglia contain

A

putamen, caudate nucleus, globus pallidus, substantia nigra, subthalamic nucleus

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52
Q

what is the caudate nucleus part of (BG)

A

putamen

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53
Q

what are the caudate and putamen together names (BG)

A

striatum or neostriatum

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54
Q

what are basal ganglia disorders characterised by

A

involuntary movements, change in posture, balance and muscle tone, slowness of movement without weakness

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55
Q

what are most of the cell types in striatum and in what condition are cells lost from here

A

medium spiny projections. lose cells in Huntingtons

56
Q

what are the cell types in substantia nigra and in what condition are cells lost from here

A

dopaminergic, lost in Parkinsons

57
Q

what is the main input pathway for the basal ganglia

A

striatum

58
Q

what is the main output pathway for the basal ganglia

A

globus pallidus through substantia nigra

59
Q

in the direct pathway what does the striatum act on

A

globus pallidus and substantia nigra (overall pathway is excitatory on cortex)

60
Q

what is the normal effect of globus pallidus and substantia nigra on the thalamus

A

inhibitory, so by the striatum inhibiting the GPi and SN, this has a disinhibitory effect on the thalamus

61
Q

which pathway helps to inhibit unwanted motor movement

A

indirect basal ganglia pathway

62
Q

what does the striatum act on in the indirect pathway

A

on globus pallidus external then subthalamic nucleus then to globus pallidus internal

63
Q

what pathway leads to the disinhibition of the thalamus and so increased muscle movement

A

direct pathway

64
Q

how is the direct pathway mediated

A

DA D1

65
Q

how is the indirect pathway mediated

A

DA D2

66
Q

what effect does dopamine have on the basal ganglia

A

increases cortical stimulation- increases activity in direct pathway, decreases activity in the indirect pathway

67
Q

what happens in Parkinsons

A

dopamine neurones from the substantia nigra are lost

68
Q

what is the putamen responsible for

A

motor control

69
Q

what is the caudate responsible for

A

recognition, and eye movements

70
Q

what is the ventral striatum responsible for

A

limbic function

71
Q

what are some of the loops within the basal ganglia that specific parts of the cortex project to specific parts of the striatum

A

oculomotor loops ( frontal/supplementary eye fields), cognitive loops (dorsolat and orbitofrontal prefrontal cortex), behavioural loops (anterior cingulate cortex)

72
Q

what else is basal ganglia involved in apart from movement

A

cognition and behaviour

73
Q

how are the medium spiny neurones in the striatum organised

A

patches (striosomes) and matrix

74
Q

what is the neocortex (striatum)

A

newer, many layers. specific/ highly processed. projects to matrix then cortex

75
Q

what is the allocortex (striatum)

A

older, fewer layers. olfactory cortex, hippocampus. less specific projects to patches then more diffuse areas

76
Q

what is ACh release dependent on

A

Ca2+

77
Q

drugs that act presynaptically to negatively modulate neurotransmitter a

A

Mg2+ as this negatively modules Ca2+ channel; local and general anaesthetics- inhibit propagation; antibiotics; tetracycline (bind Ca2+)

78
Q

how do toxins such as tetradoxin and maculotoxin work?

A

decrease voltage gated Na+ channel

79
Q

what toxins act on vesicles

A

B bungarotoxin and atraxotoxin, initial massive release ACH, eventual depletion of stores leading to paralysis

80
Q

what is myasthenia gravis

A

autoimmune disease leading to depletion in nicotinic receptors. muscle fatigue and weakness

81
Q

what can use to treat myasthenia gravis

A

neostigmine, pyrimidostigmine. reversible ACHEIs

82
Q

what are non depolarising blockers

A

block the receptor (competitive antagonist)

83
Q

what are depolarising blockers

A

fit into the receptor (agonist)

84
Q

do the neuromuscular blockers lead to muscle contraction

A

no neither type do

85
Q

when would depolarising blockers be used

A

if need rapid paralysis as have a rapid speed of onset. non depolarising have a longer duration of action

86
Q

examples of non depolarising blockers and how do they work.

A

vecuronium, pancuronium. antagonise nicotinic receptors.

87
Q

what is the only depolarising blocker used. how does it work

A

suxamethonium. prolonged depolarisation of skeletal muscle, stays in synaptic cleft longer as metabolised by plasma cholinesterase (slower than ACH)

88
Q

what are the initial effects of depolarising blocker

A

fasiculations

89
Q

what are the side effects of depolarising blocker

A

hyperkalaemia- due to prolonged opening of the channel. can lead to arrhythmias, and asystole. bradycardia, increased gastric tone

90
Q

what is denervation supersensitivity

A

if denervated or severly damaged muscle, nACHRs don’t localise to motor endplate, spread along surface of muscle. prolonged open time and depolarise more readily

91
Q

what can suxamethonium trigger

A

malignant hyperpyrexia

92
Q

whats the difference between a depolarisation block and desensitisation block

A

depolarisation- inactivation VGNa+ channels. desensitisation- no mEPP so no activation of VGNa+

93
Q

what is the prefrontal cortex involved in

A

processing for cognition, initiation of movement

94
Q

what is the role of cortex in movement

A

calculate target, initiation, cessation, timing, speed, balance, identify, plan, execute

95
Q

what area of motor cortex involved in identifying target

A

posterior parietal cortex

96
Q

what brodmann area is the pre motor area

A

6 alpha

97
Q

what brodmann area is the supplementary motor area and action

A

6 beta. programming, planning, initiation

98
Q

how is the primary motor cortex organised

A

somatotopically (motor homunculus)

99
Q

which has more complex movements primary or supplementary motor areas

A

supplementary- more complex and bilateral movements

100
Q

what is 50% of the motor cortex output from

A

primary motor cortex. the other 50%from premotor and somatosensory cortices

101
Q

what does powerful excitation of alpha motor neurones lead to

A

muscle tone

102
Q

what neurones go to muscle spindle and provide sensory feedback to the brain

A

gamma neurones

103
Q

what are the inputs to the motor cortex

A

from periphery (directly through ventral posterolat nuc of thal, indirectly from primary sensory cortex and sensory association cortex); from cerebellum ( through VPLo of thalamus, ventrolat complex, and area X of thalamus); from globus pallidus (via VPLo and VLC)

104
Q

what % of corticospinal tracts arise from brodmanns 4

A

31%

105
Q

if you stimulate the primary motor cortex where is the motor action

A

in the other side of the body

106
Q

what else does the primary motor cortex code for

A

force and direction (more complex)

107
Q

if the primary motor cortex was destroyed would stimulation of the association cortex produce movement

A

no

108
Q

does the primary motor cortex always fire

A

no not for crude movements. not all movements controlled by this, can be triggered by emotion or semi automatic responses

109
Q

what is the role of the pre motor area

A

process info before movement

110
Q

what do lesions to the pre motor area lead to

A

apraxia

111
Q

what are the reaction times in the pre motor area

A

slower here- 120-150 ms

112
Q

where is the principle input from to pre motor area and the output

A

input- from post parietal cortex. output- medial descending systems

113
Q

role of the supplementary cortex

A

programmes sequences, posture, voluntary movement coordinates bilateral movement

114
Q

does the cerebellum have direct connection to lower motor neurones

A

no

115
Q

what happens in damage to the cerebellum

A

disrupt coordination, speech, balance, decrease motor tone

116
Q

what are the areas of the cerebellum

A

vestibulocerebellum, spinocerebellum, cerebrocerebellum

117
Q

what is the function of the vestibulocerebellum

A

balance

118
Q

what is the function of the spinocerebellum

A

posture

119
Q

what is the function of the cerebrocerebellum

A

planning, evaluate sensory info, cognitive functions

120
Q

what are the inputs to the cerebellum

A

mossy fibres and climbing fibres

121
Q

how do the mossy fibres work

A

enter the granular layer, make synapses then to the molecular layer, parallel fibres which then intersect with the Purkinje fibres

122
Q

are the parallel fibres strong in terms of excitatory

A

not by themselves but thousands of them produce a sufficient excitatory stimulus

123
Q

how do the climbing fibres work and where do they come from

A

come from the inferior olivary nucleus on the contralateral side of the brainstem. they split into branches (10) which then innervate Purkinje fibres. they wind round the purkinje fibres ‘climbing’ so there is a large response

124
Q

what are the deep nuclei in the cerebellum

A

fastigial, interposed (globus and emobilliform), dentate

125
Q

what are the nodes of the cerebellum

A

anterior, posterior, flocculonodular lobe

126
Q

what are the cerebellar peduncles

A

superior, middle, inferior. input and output runs in these

127
Q

what is the function of the superior peduncle of cerebellum

A

efferents from dentate, globose and embolliform nuclei. proprioceptive info. afferents- proprioceptive info from the lower body

128
Q

what is the function of the middle peduncle of the cerebellum

A

mainly afferents, copy of info for muscle movement. pyramidal tract carrying down LMNs

129
Q

what is the function of the inferior peduncle

A

connect cerebellum to medulla, vestibular nuclei, and cells of reticular formation. proprioceptive info from upper body

130
Q

function of vestibulocerebellum

A

flocculonodular lobe directly connects to vestibular nuclei. influences eye movements, and body equilibrium, walking and standing

131
Q

what would happen if the vestibulocerebellum was damaged

A

disturbances in posture and gait, nystagmus

132
Q

function of the spinocerebellum

A

between ant and post lobes (consists of vermis and intermed lobes).output/input via fastigial and interposed nuclei. somatosensory info from spinocerebellar tracts. fine tunes ongoing movements. influences the medial and lateral descending pathways

133
Q

function of the cerebrocerebellum

A

consists of lateral hemispheres and dentate nucleus. predominant cortical input via corticopontine nucleus then dentate gyrus. output to dentate nucleus to thalamus, then to motor and pre motor. also red nucleus. planning

134
Q

other functions cerebellum

A

motor learning (storage learned tasks, make fine adjustments); non motor learning (cognition, processing of language and music)

135
Q

what happens if there is a cerebellar lesion

A

deficit in cognition, behavioural changes

136
Q

what are associated with cerebellar disease

A

hypotonia, pendular reflexes, ataxia, dysmetria (lack of rhythm), action tremor, balance and posture, ipsilateral signs