Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4 BAB > 10 The Basal Ganglia and Cerebellum > Flashcards

10 The Basal Ganglia and Cerebellum Flashcards

1
Q

What are the 3 key functions of the cerebellum?

A

sensorimotor coordination
control of muscle tone
motor learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 anatomical components of the cerebellum?

A

Spino-cerebellum (medial)
Vestibulo-cerebellum (caudal)
Cerebro-cerebellum (lateral hemispheres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the spino cerebellum do?

A

receives sensory input from the spinal cord
output to the reticular formation and red nucleus

controls axial musuclature and posture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the vesitbulo-cerebellum do?

A

input from and output to vestibular nucleus

control over posture/balance, eye movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the cerebro-cerebellum do?

A

instructs the primary motor cortex (movement direction, timing, and force)
compares intended movements with actual movements, sending compensatory instructions to M1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is ataxia and what functional components are involved?

A

unsteady, staggering gait

spino-cerebellum
cerebro-cerebellum
vestibulo-cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is dysmetria and which funcitonal ocmponents are involved?

A

inaccurate termination of movement

spino-cerebellum
cerebro-cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What symptom is associated with damage to the spino-cerebellum only?

A

hypotonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What symptom if associated with vestibulo-cerebellum damage only?

A

Nystagmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What symptom is associated with cerebro-cerebellum damage only?

A

dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does excitatory sensory information reach the cerebellum?

A

mossay fibres

climbing fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does the purkinje cell send information to?

A

deep cerebellar nuclei (inhibitory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do deep cerebellar nuclei cells do?

A

compare input from mossay and climbing input

before and after cerebellar processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the basal ganglia outflow like at rest?

A

inhibitory and constant

inhibits the thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does the cortex do to the basal ganglia when we want to move?

A

excites it, so it switches off outflow

this means the thalamus is no longer inhibited (functions through disinhibition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which part of the basal ganglia receives cortical excitatory input?

A

striatum (STR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the parts of the striatum?

A

Caudate nucleus
putamen
nucleus accumbens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the STN?

A

subthalamic nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the parts of the Globus Pallidus (GP)?

A 
External segment (GPe)
Internal segment (GPi)
20
Q

What are the parts of the substantia nigra?

A 
reticulata (SNr)
pars compacta (SNc)
21
Q

Name a shared property of GPi and SNr

A

GABAergic

22
Q

What does the striatum communicate with?

A

SNr/GPi

direct and indirect pathway

23
Q

What is the indirect pathway from the striatum to SNr/GPi?

A

GPe -> STN
GPe inhibitory to STN which is excitatory

essentially inhibits SNr/GPi directly, and indirectly

24
Q

How does the SNr/GPi communicate with the thalamus?

A

it inhibits it

therefore, if the cortex exictes the striatum, themthe SNr/GPi is inhibited, and hence the thalamus is excited by disinhibition

25
Q

What excitatory neurotransmitter is associated with the basal ganglia?

A

glutamate

26
Q

What inhibitory neurotransmitter is associated with the basal gnaglia?

A

GABA

27
Q

What does the SNc do with the basal ganglia?

A

modulates striatum function
dopaminergic
makes sure the direct and indirect pathways are in balance

28
Q

What does dopamine from SNc do?

A

acts on direct pathway (D1 receptors) and indirect pathway (D2 receptors via striatum, decreasing BG output

29
Q

Are dopamine receptors excitatory or inhibitory?

A

D1 - excitatory (direct pathway)

D1 - inhibitory (indirect pathway)

30
Q

Imbalance between direct and indirect pathways can cause what kinds of disorders?

A

Hypokinetic (Parkinson’s)

Hyperkinetic (Huntington’s, Hemiballism, Tardive Dyskinesia)

31
Q

What are the 3 characteristics of Parkinson’s disease?

A

tremor
bradykinesia
rigidity

32
Q

What is the primary pathology of Parkinson’s disease?

A

degeneratice loss (>80%) of nigro-striatal dopaminergic pathway

Lewy bodies are the pathological hallmark

33
Q

How would you treat parkinson’s?

A

replace dopamine despite loss of SNc

L-DOPA

34
Q

What problems are associated with L-DOPA?

A

effectiveness diminishes over 2-5 years
due to progressive disease

decreased DA-ergic nerve terminals
decreased capacity to convert L-DOPA to dopamine

resulting increase in L-DOPA dose frequency
causes the development of movement abnormalities

35
Q

What are the key characteristics of huntington’s Disease?

A

XS movement
unconttrollable motor patterns
psychiatric disturbance, dementia

36
Q

is Huntinton’s AD or AR?

A

AD

37
Q

What is the peak age of onset for Huntington’s disease?

A

40-45yrs

38
Q

What is the primary pathology of Huntington’s disease?

A

loss of striatal output neurons in indirect pathway

39
Q

Name 3 drugs used to treat Huntington’s

A

Tetrabenazine
Chlorpromazine
Baclofen

40
Q

What is the MOA of tetrabenazine?

A

VMAT inhibitor, decreases DA storage, and release

41
Q

What is the MOA of Chlorpromazine?

A

DA antagonist

42
Q

What is the MOA of Baclofen?

A

GABA-B agonist

decreased spinal reflexes

43
Q

What causes Hemiballismus?

A

damage to STN (stroke, unilateral)

44
Q

What is the effect of Hemiballismus?

A

contralateral violent flailing movements of limbs

45
Q

WHat causes tardive dyskinesia?

A

increased DA receptor sensitivity, due to long-term exposure to antipsychotic drugs (DAR antagonists)

46
Q

What is the effect of Tardive Dyskinesia?

A

uncontrolled movement of facial and trunk muscles

extrapyramidal effects

47
Q

Name an antipsychotic which can cause tardive dyskinesia

A

chlorpromazine

4 BAB (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions