motor II Flashcards

1
Q

what part of the brain compensate for any body postural change

A

brainstem vestibular nuclei and reticular formation nuclei

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2
Q

when does a feedforward anticipatory adjustment happen

A

just before movement begins to stabilise posture

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3
Q

where in the brain initiates the feedforward anticipatory adjustments

A

brainstem reticular formation nuceli

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4
Q

what is the babinski sign

A

an upward extensor plantar response

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5
Q

what does the babinski sign indicate

A

an upper motor neuron lesion

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6
Q

what is spasticity

A

increased muscle tone, or hyperactive stretch reflex or clonus

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7
Q

why does an UMN lesion cause spasticity

A

there is removal of the cortical inhibitory influences

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8
Q

true/false UMN lesions cause spasticity immediately

A

false - it takes a few days. for the first few days there is flaccidity until spinal circuits regain function

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9
Q

input to area 6 comes from…

A

the ventral lateral nucleus in dorsal thalamus

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10
Q

input to ventral lateral nucleus comes from…

A

basal ganglia

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11
Q

input from basal ganglia comes from…

A

prefrontal, motor and sensory cortexes

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12
Q

loop of basal ganglia, ventral lateral nucleus and cortexes

A

ventral lateral nucleus –> cortex (esp area 6) –> basal ganglia –> ventral lateral nucleus

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13
Q

corpus striatum is part of what brain group

A

basal ganglia

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14
Q

components of corpus striatum

A

caudate and putamen

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15
Q

what part of the basal ganglia are the input regions

A

caudate and putamen (corpus striatum)

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16
Q

an inhibitory synapse releases glutamine/GABA

A

GABA

17
Q

which axons of the basal ganglia are GABAergic (inhibitory)

A

putamen and caudate projecting to the globus pallidus and substantia nigra

18
Q

which parts of the corpus striatum fire before which movements

A

putamen fires before limb and trunk movements

caudate fires before eye movements

19
Q

which tract of the brain is responsible for keeping eyes stable through movements

A

tectospinal tract

20
Q

cortex to putamen is excitatory/inhibitory

A

excitatory

21
Q

putamen to globus pallidus is excitatory/inhibitory

A

inhibitory

22
Q

globus pallidus to ventral lateral nuclei is excitatory/inhibitory

A

inhibitory

23
Q

ventral lateral nuclei to SMA is excitatory/inhibitory

A

excitatory

24
Q

cascade of cortical excitation

A

cortex excites the putamen –> putamen inhibits the globus pallidus –> releases ventral lateral nuclei from inhibition –> ventral lateral nuclei excites the SMA

25
Q

what part of the positive feedback loop that happens basal ganglia and cortex will trigger the GO for movement

A

when the SMA is boosted beyond a certain threshold

26
Q

if going via the corpus striatum is the direct pathway - what does the indirect pathway go via

A

the subthalamic nucleus

27
Q

disorders of the basal ganglia

A

parkinson’s disease and huntington’s disease

28
Q

pathophysiology of huntington’s

A

atrophy of basal ganglia –> loss if inhibitory effects of basal ganglia –> hyperkinesia and uncontrolled movement and ticks

29
Q

pathophysiology of parkinson’s

A

degeneration of neurones in substantia nigra –> loss of excitatory input to striatum –> hypokinesia, slow and rigid

30
Q

function of cerebellum in movement

A

coordination

31
Q

motor loop of cerebellum

A

cerebellum –> ventral lateral nuclei –> motor cortex (esp area 4) –> sensory cortex –> cerebellum

32
Q

presentation of cerebellar lesions

A

ataxia
uncoordinated, inaccurate movements/finger-nose test)
staggers when walking

33
Q

causes of cerebella damage

A

alcohol, MS, paraneoplastic syndrome

34
Q

cerebellar disorders have increased/decreased tone

A

decreased tone