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Neuroscience > L44 Movement Disorders Basal Ganglia > Flashcards

L44 Movement Disorders Basal Ganglia Flashcards

1
Q

what does the BG receive info about motor commands from?

A

prefrontal cortex
premotor cortex
primary motor cortex

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2
Q

does the BG have any direct synaptic connections with motor neurons?

A

NO - through the thalamus, the BG participates in the initiation and control of voluntary movement

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3
Q

what is the role of the BG?

A

initiation an control of voluntary movement through the thalamus

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4
Q

what are the 4 nuclei of the BG?

A

straitum - caudate n. + putamen
globus pallidus - GPm, GPl
subthalamic n.
substantia nigra - pars reticulata and pars compacta

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5
Q

are the motor neurons in the BG excitatory or inhibitory?

A

inhibitory

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6
Q

what type of receptors are D1 receptors in the striatum?

A

excitatory

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7
Q

what type of receptors are D2 receptors in the striatum?

A

inhibitory

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8
Q

what is the effect of the direct pathway on movement?

A

facilitate movement

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9
Q

what is the effect of the indirect pathway on movement?

A

inhibits movement

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10
Q

describe Parkinson’s disease

A

bilateral degeneration of dopaminergic cells in SN

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11
Q

what type of disorder of Parkinson’s disease?

A

HYPOkinetic

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12
Q

what are the sx/sx of Parkinson’s disease?

A 
bilateral...
akinesia 
bradykinesia
resting tremors
muscular rigidity 
.. see notes on video lecture
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13
Q

describe Huntington’s Chorea?

A

bilateral degeneration/loss of strial GABA neurons that EXPRESS D2 receptors

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14
Q

what type of disorder is Hungtinton’s Chorea?

A

HYPERkinetic

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15
Q

what are the sx/sx of Huntington’s Chorea

A

irregular bilateral movements
dyskinesia
involuntary movement of head, arms, legs
marked change in mental status

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16
Q

describe hemiballismus

A

lesion of the subthalamic n. usually from stroke

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17
Q

what type of disorder is hemiballismus?

A

HYPERkinetic

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18
Q

what are the sx/sx of Hemiballismus?

A

irregular movements of the limbs and trunk on contralateral side
involuntary flinging arms and writhing movements of the leg ON ONE SIDE

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19
Q

what is parkinsonism?

A

describes symptoms involving any combo of resting tremors, muscular rigidity, bradykinesia, impaired postural reflex

20
Q

what are the 4 things that can look like parkinson’s disease (perhaps differential dx)?

A 
drug induced 
vascular 
repetitive head trauma
postencephalitic 
neoplastic
21
Q

describe drug induced parkinsonism?

A
  • antipsychotic drugs (DA receptor blockers)
  • depletors of DA stores (reserpine - old BP med)
  • toxic contaminants (MPTP) - homemade drugs toxin…
22
Q

describe vascular parkinsonism

A

strokes affecting the BG (nigrostriatal path)

affects lower body and gait

23
Q

describe reptitive head truma

A

boxing-like injury associated with dementia because of damage to the midbrain

24
Q

describe postencephalitic parkinsonism

A

virally induced degenerations of substantia nigra

25
Q

describe Sydenham’s chorea

A

linked to childhood rheumatic fever

transient, but preg women are susceptible for recurrence

26
Q

describe drug induced chorea

A

caused by L-dopa, anticonvulsants or antipsychoics as a result of enhancing dopaminergic transmission within the BG

27
Q

what are drug therapies for parkinson’s disease?

A 
L-dopa
dopamine agonist
drugs that enhance dopamine release
MAO inhibitors
COMT inhibitors
anticholinergic drugs
28
Q

what does L-dopa do?

A

increases rate of dopamine synthesis in the still functional SNc
given orally with cabidopa to prevent dopamine synthesis outside of CNS
effectiveness decreases over time as SNc neurons die out

29
Q

what do dopamine receptor agonists do?

A

D2 agonist - bromocriptine
D1 and D2 agonist - pergolide

bypass degenerating nigrostriatal neurons and acts directly on postsynaptic receptors

30
Q

what are drugs that enhance dopamine release?

A

anti-viral drug
amantadine - good effect on akinesia and rigidity, but PSYCHO

may promote release of dopamine or block ACh receptors

31
Q

what do MAO inhibitors do?

A

selegiline - block dopamine breakdown

may delay the need for other therapies

32
Q

what do COMT inhibitors do?

A

inhibit dopamine breakdown– increase dopamine effects

may be given in addition to L-dopa and carbidopa

33
Q

what makes up the lentiform nucleus?

A

putamen and globus pallidus

34
Q

what makes up the striatum?

A

caudate n. + putamen

35
Q

what provides vital modulation to the direct and indirect pathways?

A

substantia nigra — dopamine producing cells projects into the striatum to release DA

36
Q

what is the function of DA in the direct and indirect pathways?

A

regulates BG function – thus, indirectly regulating cortical control of movement

ALWAYS cortical excitation = increased movement!

37
Q

what type of feedback is seen in direct BG loop

A

positive - cortical input increases cortical activity

38
Q

what type of feedback in seen in indirect BG loop?

A

negative - cortical input supresses cortical activity

39
Q

describe neoplastic parkinsonism

A

tumors can disturb the nigrostriatal system

40
Q

describe athetosis

A

striatal or thalamic injury can yield continuous writhing

41
Q

what do anticholinergic drugs do?

A

muscarinic antagonists - suppress ACh mediated excitation of striatal neurons

ACh makes parkinsonism WORSE!

42
Q

what sites are ablated (burned) in surgical ablation?

A

subthalamus
medial globus pallidus
both of them are way overactive = hyperkinesis

43
Q

what sites are involved in deep brain stimulation

A

thalamus
golbus pallidus
subthalamus

44
Q

what happens when you increase DA transmission (maybe from L-dopa drug)?

A

PSYCHOSIS

45
Q

what is therapeutically given for brain degeneration?

A

block D2 receptors

Neuroscience (54 decks)

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