motor Flashcards
(136 cards)
1
Q
what is the only neurotransmitter involved in causing muscles to contract
A
Ach
2
Q
are voluntary movements open or closed loop
A
open loop (reflex movement closed)
3
Q
what is the highest level in the hierarchy of movement control
A
cerebullum, basal ganglia, motor cortex- planning, coordination, desire to move
4
Q
what is the middle level in the hierarchy of movement control
A
descending systems and brainstem
5
Q
what is the lowest level in the hierarchy of movement control
A
from spinal cord from motor neurone to muscle
6
Q
what allows refinement of movement and accuracy
A
feedback at every level
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
8
Q
what happens in lesions to level 3 (hierarchy)
A
muscle weakness, in disorders of spinal cord disease, neuropathy, muscle disease eg dystrophy
9
Q
what is a motor unit
A
motor neurone and the muscle it innervates
10
Q
where do lesions occur in lower motor neurone lesions
A
between ventral horn and muscle
11
Q
what are central pattern generators
A
in thoracic and lumbar parts of spinal cord, dont require constant afferent input for an output
12
Q
what pathways run medially originating in the brainstem
A
vestibulospinal, reticulospinal, tectospinal
13
Q
what pathways run laterally originating in brainstem
A
rubrospinal
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)
15
Q
what pathways are involved in planning and initiation
A
corticobulbar and corticospinal
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)
17
Q
does the basal ganglia have direct connection to neurones
A
no has to travel through the cortex
18
Q
which tracts are motor
A
descending tracts
19
Q
what does damage to the basal ganglia lead to
A
apraxia, huntingtons, parkinsons, hemiballismus (involuntary movements)
20
Q
what is classed as an upper motor neurone lesion
A
damage to descending tracts
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
22
Q
what is involved in the coordination of movement
A
cerebellum
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
24
Q
what happens if the cerebellum is damaged
A
incoordination, jerky movements, impaired balance
25
where does the cerebellum receive info from
copy of info from cortex (intended movement), info from muscle spindles, other receptors (actual movement)
26
where does the cerebellum send its adjustments to
cortex
27
what happens if sensory feedback is disturbed, what is this called
impaired proprioception and touch. Large sensory input neuropathy- can't sense position of limbs in space
28
what are the 2 mechanisms of postural adjustments
compensatory and anticipatory
29
how rapid is the compensatory mechanism of postural adjustment
rapid, automatic, stereotyped, refined by learning
30
what happens in anticipatory mechanism postural adjustment
predict disturbances before voluntary action. improve by learning
31
what is the postural set
collection of responses- integrate adjustments with voluntary actions
32
are postural refexes triggered before or after feedback
before, then scaled to reach stability
33
how are postural reflexes different to simple reflexes
triggered before feedback, scaled to acheive stability, rapid and slower responses (like simple reflexes- rapid and stereotyped)
34
what are vestibular nuclei involved in
balance
35
what is the corticoreticular tract involved in
postural adjustments
36
what tracts are important for rapid responses to change in posture
transcortical tracts
37
which info travels fastest (proprioceptive, vestibular, visual)
proprioceptive info travels 2x as fast as vestibular and visual info (visual slowest)
38
what happens when muscle spindles are activated
alpha motor neurones activity increases so muscle contracts
39
what coactivation is important when alpha motor neurones are activated and what is the action
gamma coactivation- which allows the spindles to remain taut and sensitive in contraction
40
what does the vestibular reflex respond to
in response to head movement changing wrt neck and limbs
41
what is decerebrate rigidity
arms and legs EXTEND
42
what is decerebrate rigidity due to
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
43
what is decorticate rigidity
arms FLEX
44
what happens in decorticate rigidity
lesion is higher- above the midbrain red nucleus.
45
what does the brainstem have in control of posture
reticular formation. reticulospinal tracts involved
46
what does stimulation of the anterior lobe of the cerebellum lead to
decrease in decerebrate activity
47
what happens if you cut the vestibular nerve (wrt decerebrate rigidity)
decrease decerebrate rigidity
48
what damage to sensory structures can be postural disorders
blind (increase postural sway), vestibular disease (menieres), somatosensory injury/peripheral neuropathy
49
what damage to motor structures can be postural disorders
brainstem damage, cerebellar and basal ganglia damage
50
what are pyramidal tracts?
corticobulbar and corticospinal
51
what does the basal ganglia contain
putamen, caudate nucleus, globus pallidus, substantia nigra, subthalamic nucleus
52
what is the caudate nucleus part of (BG)
putamen
53
what are the caudate and putamen together names (BG)
striatum or neostriatum
54
what are basal ganglia disorders characterised by
involuntary movements, change in posture, balance and muscle tone, slowness of movement without weakness
55
what are most of the cell types in striatum and in what condition are cells lost from here
medium spiny projections. lose cells in Huntingtons
56
what are the cell types in substantia nigra and in what condition are cells lost from here
dopaminergic, lost in Parkinsons
57
what is the main input pathway for the basal ganglia
striatum
58
what is the main output pathway for the basal ganglia
globus pallidus through substantia nigra
59
in the direct pathway what does the striatum act on
globus pallidus and substantia nigra (overall pathway is excitatory on cortex)
60
what is the normal effect of globus pallidus and substantia nigra on the thalamus
inhibitory, so by the striatum inhibiting the GPi and SN, this has a disinhibitory effect on the thalamus
61
which pathway helps to inhibit unwanted motor movement
indirect basal ganglia pathway
62
what does the striatum act on in the indirect pathway
on globus pallidus external then subthalamic nucleus then to globus pallidus internal
63
what pathway leads to the disinhibition of the thalamus and so increased muscle movement
direct pathway
64
how is the direct pathway mediated
DA D1
65
how is the indirect pathway mediated
DA D2
66
what effect does dopamine have on the basal ganglia
increases cortical stimulation- increases activity in direct pathway, decreases activity in the indirect pathway
67
what happens in Parkinsons
dopamine neurones from the substantia nigra are lost
68
what is the putamen responsible for
motor control
69
what is the caudate responsible for
recognition, and eye movements
70
what is the ventral striatum responsible for
limbic function
71
what are some of the loops within the basal ganglia that specific parts of the cortex project to specific parts of the striatum
oculomotor loops ( frontal/supplementary eye fields), cognitive loops (dorsolat and orbitofrontal prefrontal cortex), behavioural loops (anterior cingulate cortex)
72
what else is basal ganglia involved in apart from movement
cognition and behaviour
73
how are the medium spiny neurones in the striatum organised
patches (striosomes) and matrix
74
what is the neocortex (striatum)
newer, many layers. specific/ highly processed. projects to matrix then cortex
75
what is the allocortex (striatum)
older, fewer layers. olfactory cortex, hippocampus. less specific projects to patches then more diffuse areas
76
what is ACh release dependent on
Ca2+
77
drugs that act presynaptically to negatively modulate neurotransmitter a
Mg2+ as this negatively modules Ca2+ channel; local and general anaesthetics- inhibit propagation; antibiotics; tetracycline (bind Ca2+)
78
how do toxins such as tetradoxin and maculotoxin work?
decrease voltage gated Na+ channel
79
what toxins act on vesicles
B bungarotoxin and atraxotoxin, initial massive release ACH, eventual depletion of stores leading to paralysis
80
what is myasthenia gravis
autoimmune disease leading to depletion in nicotinic receptors. muscle fatigue and weakness
81
what can use to treat myasthenia gravis
neostigmine, pyrimidostigmine. reversible ACHEIs
82
what are non depolarising blockers
block the receptor (competitive antagonist)
83
what are depolarising blockers
fit into the receptor (agonist)
84
do the neuromuscular blockers lead to muscle contraction
no neither type do
85
when would depolarising blockers be used
if need rapid paralysis as have a rapid speed of onset. non depolarising have a longer duration of action
86
examples of non depolarising blockers and how do they work.
vecuronium, pancuronium. antagonise nicotinic receptors.
87
what is the only depolarising blocker used. how does it work
suxamethonium. prolonged depolarisation of skeletal muscle, stays in synaptic cleft longer as metabolised by plasma cholinesterase (slower than ACH)
88
what are the initial effects of depolarising blocker
fasiculations
89
what are the side effects of depolarising blocker
hyperkalaemia- due to prolonged opening of the channel. can lead to arrhythmias, and asystole. bradycardia, increased gastric tone
90
what is denervation supersensitivity
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
what can suxamethonium trigger
malignant hyperpyrexia
92
whats the difference between a depolarisation block and desensitisation block
depolarisation- inactivation VGNa+ channels. desensitisation- no mEPP so no activation of VGNa+
93
what is the prefrontal cortex involved in
processing for cognition, initiation of movement
94
what is the role of cortex in movement
calculate target, initiation, cessation, timing, speed, balance, identify, plan, execute
95
what area of motor cortex involved in identifying target
posterior parietal cortex
96
what brodmann area is the pre motor area
6 alpha
97
what brodmann area is the supplementary motor area and action
6 beta. programming, planning, initiation
98
how is the primary motor cortex organised
somatotopically (motor homunculus)
99
which has more complex movements primary or supplementary motor areas
supplementary- more complex and bilateral movements
100
what is 50% of the motor cortex output from
primary motor cortex. the other 50%from premotor and somatosensory cortices
101
what does powerful excitation of alpha motor neurones lead to
muscle tone
102
what neurones go to muscle spindle and provide sensory feedback to the brain
gamma neurones
103
what are the inputs to the motor cortex
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
what % of corticospinal tracts arise from brodmanns 4
31%
105
if you stimulate the primary motor cortex where is the motor action
in the other side of the body
106
what else does the primary motor cortex code for
force and direction (more complex)
107
if the primary motor cortex was destroyed would stimulation of the association cortex produce movement
no
108
does the primary motor cortex always fire
no not for crude movements. not all movements controlled by this, can be triggered by emotion or semi automatic responses
109
what is the role of the pre motor area
process info before movement
110
what do lesions to the pre motor area lead to
apraxia
111
what are the reaction times in the pre motor area
slower here- 120-150 ms
112
where is the principle input from to pre motor area and the output
input- from post parietal cortex. output- medial descending systems
113
role of the supplementary cortex
programmes sequences, posture, voluntary movement coordinates bilateral movement
114
does the cerebellum have direct connection to lower motor neurones
no
115
what happens in damage to the cerebellum
disrupt coordination, speech, balance, decrease motor tone
116
what are the areas of the cerebellum
vestibulocerebellum, spinocerebellum, cerebrocerebellum
117
what is the function of the vestibulocerebellum
balance
118
what is the function of the spinocerebellum
posture
119
what is the function of the cerebrocerebellum
planning, evaluate sensory info, cognitive functions
120
what are the inputs to the cerebellum
mossy fibres and climbing fibres
121
how do the mossy fibres work
enter the granular layer, make synapses then to the molecular layer, parallel fibres which then intersect with the Purkinje fibres
122
are the parallel fibres strong in terms of excitatory
not by themselves but thousands of them produce a sufficient excitatory stimulus
123
how do the climbing fibres work and where do they come from
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
what are the deep nuclei in the cerebellum
fastigial, interposed (globus and emobilliform), dentate
125
what are the nodes of the cerebellum
anterior, posterior, flocculonodular lobe
126
what are the cerebellar peduncles
superior, middle, inferior. input and output runs in these
127
what is the function of the superior peduncle of cerebellum
efferents from dentate, globose and embolliform nuclei. proprioceptive info. afferents- proprioceptive info from the lower body
128
what is the function of the middle peduncle of the cerebellum
mainly afferents, copy of info for muscle movement. pyramidal tract carrying down LMNs
129
what is the function of the inferior peduncle
connect cerebellum to medulla, vestibular nuclei, and cells of reticular formation. proprioceptive info from upper body
130
function of vestibulocerebellum
flocculonodular lobe directly connects to vestibular nuclei. influences eye movements, and body equilibrium, walking and standing
131
what would happen if the vestibulocerebellum was damaged
disturbances in posture and gait, nystagmus
132
function of the spinocerebellum
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
function of the cerebrocerebellum
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
other functions cerebellum
motor learning (storage learned tasks, make fine adjustments); non motor learning (cognition, processing of language and music)
135
what happens if there is a cerebellar lesion
deficit in cognition, behavioural changes
136
what are associated with cerebellar disease
hypotonia, pendular reflexes, ataxia, dysmetria (lack of rhythm), action tremor, balance and posture, ipsilateral signs
