6. Motor disorders Flashcards

1
Q

source of dopamine in midbrain

A

substation nigra pars compacta

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2
Q

how do basal ganglia communicate with motor cortex?

A

thalamus

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3
Q

basal ganglia lesions
-ipsi or contraleteral? why?

-bilateral? why?

A

contralateral: decussation of CST from ipsilateral motor cortex

yes: neurodegeneration is the common cause, and usually this is symmetrical e.g Parkinson’s

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4
Q

functions of basal ganglia

A

direct pathways reinforce appropriate movements (excitatory to motor cortex)

indirect pathways remove inappropriate movements (inhibitory to motor cortex)

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5
Q

cause of Parkinson’s

A

degeneration of dopaminergic neurones in SNc

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6
Q

explain why Parkinson’s causes tremor

A

dysfunction of indirect pathway which would normally suppress unwanted movements

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7
Q

explain why Parkinson’s causes rigidity

A

lack or coordination between agonists and antagonists i.e. opposing each other

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8
Q

explain why Parkinson’s causes bradykinesia

A

loss of cortical excitation = slow movements

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9
Q

cause of Huntington’s chorea

A

loss of inhibitory projections from striatum to GPe

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10
Q

does Huntington’s chorea cause hyper or hypokinesia? why?

A

hyper
‘brakes’ taken off thalamus

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11
Q

cause of hemiballismus

A

damage to subthalamic nucleus which normally inhibits thalamus via GPi

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12
Q

function of cerebellum

A

sequencing and coordinating movement

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13
Q

where does the cerebellum receive sensory inputs from

A

contralateral sensory cortices
ipsilateral spinal cord
proprioceptive neurones

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14
Q

how might cerebellar lesions present

A

vomiting
vertigo (poor coordination of extra ocular muscles)
difficulty walking

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15
Q

explain why cerebellar lesions cause dysdiadochokinesia

A

cant sequence pronation, supination….

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16
Q

explain why cerebellar lesions cause ataxia

A

difficulty sequencing lower limb muscle contractions, and loss of unconscious proprioception from lower limbs

17
Q

explain why cerebellar lesions cause nystagmus

A

poor coordination of extra ocular eye muscles

18
Q

explain why cerebellar lesions cause dysarthria

A

poor coordination of laryngeal and tongue musculature

19
Q

basal ganglia corticospinal pathway

A

instructs muscles what to do, from motor cortex UMN, decussate at medulla, synapse on LMN, goes to muscle

20
Q

basal ganglia corticostriatal pathway

A

motor cortex sends motor plan to basal ganglia

21
Q

basal ganglia pallidothalamocortical pathway

A

basal ganglias assessment of motor plan sent back to motor cortex via thalamus

22
Q

basal ganglia nigrostriatal pathway

A

source of dopamine to basal ganglia from Sac

23
Q

hypothetically, where would the signs be if basal ganglia were damaged unilaterally. why?

A

contraleteral

basal ganglia pathways all communicate with ipsilateral motor cortex, then corticospinal pathway decussates at medulla to contralateral side

24
Q

relevance of cerebellar tonsils

A

in raised ICP, can be forced down through foramen magnum and compress medulla

25
Q

cerebellar pathways: corticopontocerebellar

A

motor cortex communicates its motor plan through cerebellum, decussates in pons to contralteral cerebellar hemisphere

26
Q

cerebellar pathways: cerebellothalamocortical

A

projects from cerebellar hemisphere to contralateral thalamus then to motor cortex same side as thalamus

27
Q

cerebellar pathways: spinocerebellar

A

primary sensory neurones carry info from muscle spindles to ipsilateral cerebellar hemisphere

28
Q

why are cerebellar damage signs ipsilateral?

A

-double decussation of corticopontocerebellar and cerebellothalamocortical pathways

-ipsilateral sensory pathway via spinocerebellar pathway