motor systems 2 Flashcards
(89 cards)
1
Q
which lobe is involved in motor control?
A
all of the frontal lobe
parietal lobe
2
Q
what is the relationship between the position on the cortical region and the complexity of movement?
A
the more anterior the cortical region, the more complex role in movement
3
Q
what is area 4?
A
primary motor cortex
4
Q
where is the primary motor cortex?
A
immediately anterior to the central sulcus
5
Q
what do lesions of the primary motor cortex cause?
A
cause initial paralysis or paresis of specific muscle groups
6
Q
why is some recovery of function possible after lesions of the primary motor cortex?
A
bc of cortical plasticity
7
Q
why is there a smaller chance of recovery with bigger lesions?
A
more muscle groups are involved
8
Q
what part of the brain do strokes with MCA occlusion affect? what effect does this have and why?
A
- affects almost all of one side of the frontal lobe
- leads to severe motor disability in the contralateral body (apart from lower limb bc lower limb is supplied by the anterior cerebral artery)
9
Q
what does an MI of the proximal MCA affect the blood supply to?
A
o Basal ganglia via lenticulostriate arteries
o Motor cortex
10
Q
what is area 6?
A
premotor cortex
11
Q
what is area 8?
A
supplementary motor cortex
12
Q
what does damage to area 6 or 8 cause?
A
motor apraxia
13
Q
how does motor apraxia present?
A
o Normal reflexes + no muscle weakness
o Difficulty performing complex motor tasks e.g. tying shoelace
14
Q
why does damage to one side of the brain cause minimal symptoms?
A
bc the contralateral area can take over some functions of the damaged tissue
15
Q
what are areas 7 and 19?
A
posterior parietal cortex
16
Q
what does damage to areas 7 and 19 cause?
A
sensory apraxia
17
Q
what is sensory apraxia?
A
Difficulty performing complex motor tasks when triggered by sensory input (e.g. when asked verbally to do something)
18
Q
where are the FEFs and Broca’s area?
A
adjacent to the premotor area
19
Q
what do the FEFs do?
A
motor control of extraocular eye muscles - controls voluntary eye movements
20
Q
what is the function of Broca’s area?
A
muscles regulating speech
21
Q
what does damage to Broca’s area cause?
A
motor aphasia
22
Q
what is motor aphasia?
A
patient struggles w motor programmes to construct meaningful word sequences
23
Q
what is oculomotor apraxia?
A
difficulty moving eyes horizontally + quickly
- Either have to turn head to follow object or use peripheral vision
24
Q
what causes oculomotor apraxia?
A
bilateral lesions of the FEFs
25
what causes sensory apraxia?
caused by damage to connections from posterior parietal lobe to premotor cortex
26
what are areas 1, 2 and 3?
somatosensory cortex
27
where do 40% of corticobulbospinal tract axons come from? what do the axons do?
somatosensory cortex
Axons send instruction to spinal cord that modulate sensory input – modulate spinal reflexes (e.g. suppress nociceptive reflexes)
28
what are areas 9 and 10?
dorsolateral prefrontal cortex
29
what are the functions of areas 9 and 10?
Areas 9 & 10 – executive functions;
o Plan movement
o Evaluate possible future actions and decide which is best
o Involved in problem solving, judgement
30
what do lesions of the dorsolateral prefrontal cortex cause?
apathy, personality changes and lack of ability to plan or to sequence actions/tasks
31
what difference does it make if the dorsolateral prefrontal cortex lesion affects the left lobe vs the right lobe?
o Left hemisphere mainly affected – poor memory for verbal info
o Right hemisphere mainly affected – poor memory for spatial info
32
what is the wisconsin card sorting test?
common test for frontal lobe function - tests perseverence
33
what can cause frontal cortex damage?
impact w frontal bone e.g. road traffic accident or blow to the head that causes contusions
34
what are contusions?
brain bruising
35
what is area 11?
orbitofrontal cortex
36
what does the orbitofrontal cortex control?
control (inhibition) of motor responses associated w the limbic system
o E.g. responses to hunger, thirst, sexual drives etc
37
what does damage to the orbitofrontal cortex cause?
pesudopsychopathic behaviour
38
what is pseudopsychopathic behaviour?
impulsiveness, puerility, a jocular attitude, sexual disinhibition, and complete lack of concern for others
39
what is an orbital personality?
people with pseudopsychopathic behaviour
40
what does stroke damage to the motor thalamus cause?
severe paralysis
41
what does the corticobulbospinal tract pass through on its way to the brainstem?
internal capsule
42
what does the corticobulbar component of the CBS tract terminate on?
o CN nuclei V + VII for cortical control of the head muscles
o Occulomotor nuclei III, IV + VI for control of eye movements
o Pontine nuclei
o Reticular formation
o Red nucleus
43
what is the red nucleus?
large nucleus in the midbrain next to the oculomotor nuclei
44
where does the corticospinal component of the tract decussate and what does it become?
continues to the lower medulla and decussates at C1-C5 to form large lateral CST and small medial CST
45
what deficit occurs with a brain injury above the spinal cord/medulla junction?
contralateral motor deficit
46
what deficit occurs with a brain injury in the spinal cord?
motor deficit on the same side
47
where does the lateral CST run?
in the dorsolateral cord near motor neurons supplying distal muscles
48
what does the CST have monosynaptic connections with?
thumb and the digits
49
what is inhibition of flexion reflexes mediated by?
corticospinal tract
50
where does the anterior corticospinal tract run?
in the medial ventral cord
51
what does the lateral corticospinal tract control?
voluntary movements of the neck
52
what does damage to the CST cause? why?
loss of control of hands and fingers but not loss of posture or locomotion and gait (bc these are controlled by the extra-pyramidal systems (descending motor tracts)
53
where do the extra pyramidal systems originate?
from groups of cell bodies in the brainstem
54
what are the main components of extrapyramidal systems?
lateral vestibulospinal tract and reticulospinal tracts
55
where does the lateral vestibulospinal tract originate?
vestibular nuclei in the upper medulla/lower pons
56
what does the lateral vestibulospinal tract do?
controls posture and balance
| tonically active during upright posture
57
where does the reticulospinal tract originate?
reticular formation of pons and medulla
58
what is the reticulospinal tract responsible for?
o Autonomic control – drives sympathetic preganglionic neurons
o Drive to respiration (phrenic nerve)
59
what is the origin of the rubrospinal tract?
red nucleus in the brainstem
60
what does the red nucleus mainly receive input from?
the cerebellum
61
what is the red nucleus?
large nucleus in the midbrain
62
what is the function of the rubrospinal tract?
needed for control of movement velocity and transmitting motor commands from cerebellum to the musculature
63
what do lesions of the rubrospinal tract cause?
movement slowness
64
what does the tectospinal tract do?
coordinates voluntary head and eye movements
activates reflex movements of the head in response to visual and auditory stimuli
65
where does the tectospinal tract originate and where does it project and terminate?
- originates in the superior colliculus
| - projects to the contralateral cervical spinal cord to terminate in the rexed laminae VI, VII and VIII
66
what is the medial vestibulospinal tract a continuation of?
medial longitudinal fasciculus
67
what does the medial vestibulospinal tract mediate?
reflex co-ordination of the head and neck muscles with the extraocular eye muscles to maintain objects in view even if the body moves
68
what do major descending motor tracts do?
modulates strength and activity of reflex pathways in the spinal cord
69
which motor neurons are the ones driving the muscles of the thumb and fingers and lips and tongue?
Only UMNs that act directly on LMNs in the spinal cord
70
define spasticity
abnormally increased muscle tone
| o Spastic muscles have increased tendon reflexes
71
what is characteristic of UMN lesions?
spasticity
72
what is clonus?
series of jerky contractions of a particular muscle following sudden stretching of the muscle
73
what is hyperreflexia?
pathologically brisk tendon reflex is seen in one or more muscles
74
what is decorticate posturing?
arms are adducted and flexed w wrists and fingers flexed on the chest
o Legs may be internally rotated and stiffly extended w plantar flexion of the feet
75
what does decorticate posturing indicate?
Indicates damage to the corticospinal tract in the midbrain
76
describe decerebrate posturing?
adducted and extended arms w wrists pronated + fingers flexed. Legs internally rotated and stiffly extended, with plantar flexion of the feet
77
what causes decerebrate posture?
bc of excessive activity (disinhibition) in extrapyramidal system esp vestibulospinal tract
• If red nucleus is damaged by severe midbrain injury decerebrate posturing
78
what keeps the vestibulospinal tract under tonic inhibition?
corticobulbospinal tract
| red nucleus
79
what patients show decerebate posturing?
ONLY unconscious patients
80
what patients show decorticate posturing?
usually seen in unconscious patients
81
what do discrete acute lesions cause?
initial paralysis followed by variable degree of recovery
82
what occurs during recovery from a lesion?
weakness, clumsiness and fatigue of movements
83
what is hemiplegic dystonia?
persistent flexion of arms and extension of the legs
84
what can cause hemipleic dystonia?
• If there’s persistent spasticity following a motor cortex lesion, spasticity is invariably combined w motor weakness
85
what is the clasp knife reflex?
characteristic of chronic cerebral motor lesions
86
what is spinal shock?
clinical condition that occurs after acute damage to the spinal cord that includes any damage to the descending tracts
87
how long can spinal shock last for?
Can last for days, weeks or months depending on severity
88
what are the acute effects of lesions of the motor tracts in the cord?
paralysis or paresis and reduced reflex responses in all muscles below the region of injury
89
what are the chronic effects of lesions of motor tracts in the cord?
spinal shock wears off and monosynaptic reflexes reappear
o Crossed extensor reflexes may also recover
o In severe injury, these reflexes aren’t controlled by the brain and may become exaggerated and hyperactive
o Clonus may be present
o Babinski sign will normally be present.
