Basal Ganglia Flashcards

(47 cards)

1
Q

what is the definition of the basal ganglia

A

refers to structures that yield movement disorders when damaged

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2
Q

what is the striatum made up of

A

caudate nucleus

putamen

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3
Q

what is the lentiform nucleus made up of

A

putamen

globus pallidus

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4
Q

what are the two parts of the globus pallidus

A

globus pallidus interna (GPi)

globus pallidus externa (GPe)

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5
Q

what part of the basal ganglia is C-shaped w/a long tail that swings laterally

A

caudate

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6
Q

what part of the basal ganglia is just medial and coincides with the insula

A

putamen

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7
Q

what is the key “output” of the basal ganglia and where do most of the projections go

A

globus pallidus

-thalamus

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8
Q

where is the nucleus accumbens in reference to the basal ganglia structures

A

anterior, medial and inferior

only see in cross section at HEAD level of caudate

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9
Q

what seperates the putamen from the GPe

A

external medullary laminae

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10
Q

what does the internal medullary laminae separate

A

GPe from GPi

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11
Q

the substantia nigra is apart of the basal ganglia, what part of the brainstem can it be seen in cross section

A

rostral midbrain

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12
Q

the subthalamic nuclues is a part of the basal ganglia, where is it typically located in reference to the substantia nigra at midbrain cross section level

A

just on top and lateral to substantia nigra

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13
Q

what are the 2 parts of the substantia nigra ?

A

Compact - densely packed pigmented neurons

Reticular - nonpigmented neurons (more lateral)

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14
Q

what is the function of the compact part of substantia nigra ? What about the reticular part ?

A

Compact - DA projections to striatum

Reticular - output of Basal ganglia (like GP)

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15
Q

what limb of the internal capsule separates the caudate from the lenticular nucleus

A

anterior limb

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16
Q

what limb of the internal capsule separates the thalamus from the globus pallidus

A

posterior limb

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17
Q

what is the broad function of the basal gangli

A

modulate cortical output especially motor control

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18
Q

what are the 4 key players in the basal ganglia circuit or loop

A

cortex –> striatum –> globus pallidus –> thalamus —-> back to cortex

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19
Q

what are the main inputs of the BG circuit

A

cortical afferents to striatum

20
Q

what are the main outputs of the BG circuit

A

Globus pallidus interna and reticular part of substantia nigra

21
Q

The basal ganglia circuit or motor loop cannot influence the motor cortex directly. What does this mean ?

A

It must go through the thalamus, which is not apart of the BG its apart of the diencephalon

22
Q

excitatory connections of the BG motor loop use what nuerotransmitter

23
Q

inhibitory connections of the BG motor loop use what nuerotransmitter

24
Q

T/F in the striatum there is only one neurochemical territory

A

F, there are many nuerochemicla territories in the striatum

25
expain the direct or principal circuit of the basal ganglia
1 - excitatory input from cortex to striatum 2 - striatum sends inhibitory output to GPi 3 - GPi sends inhibitory output to VA/VL of thalamus 4 - thalamus sends excitatory input back to cortex
26
How could you manipulate the direct pathway to increase motor cortical output ?
Increase inhibition on GPi (GPi is now less active)
27
how does increasing inhibition on GPi result in increased cortical output
If increase inhibition on GPi, its less active so puts LESS inhibition on thalamus = more excitation to cortex = greater output
28
how would you decrease motor cortical output in the direct BG pathway
Increase excitation on GPi (now more active) = increased inhibition on thalamus = decreased excitation to cortex = decreased cortical output
29
the degeneration of ______ leads to huntington's disease
striatum
30
what is the main sign of huntingtons disease
chorea - rapid, rigid dance like movements of face and limbs
31
T/F Huntingtons disease is autosomal recessive disease
F, Autosomal dominant (meaning more number the repeats the faster the onset)
32
what are the 2 new additional BG structures involved in the indirect BG pathway that are not a factor in the direct pathway
subthalamus and GPe
33
explain the indirect pathway of the basal ganglia
1 - excitation input from cortex to A) striatum or B) subthalamus 2 - A) striatum inhibitory to GPe = inhibition of subthalamu B) subthalamus excitatory output to GPi 3 - GPi inhibitory output to thalamus 4 - thalamus excitatory input back to cortex
34
if you decrease the output of GPe in the basal ganglia indirect pathway, what will be the result ?
Decrease GPe inhibitory output on subthalamus = increased excitatory output to GPi=increased inhibition on thalamus = decreased excitatory input to cortex = decreased cortical output
35
if you were to increase the inhibitory output from GPe in the indirect BG pathway what would be the end result
decreased thalamic inhibition = increase cortical output
36
in strokes it is very common for the subthalamus to be damaged, how would this affect the indirect BG pathway
results in less excitatory input to GPi=decreased inhibition on thalamus= excessive increased excitatory input to cortex = TOO much cortical output
37
what is the dramatic movement disorder where limbs, usually on one side of the body, are flailing and rotating that is the result of a damaged subthalamus
hemiballismus
38
hemiballismus is the result of damage to what vessel ?
Posterior cerebral a. (PCA)
39
what is the role of the substantia nigra in the basal ganglia
Substantia nigra compact - sends DA input to striatum | Substantia nigra reticulata - sends output to thalamus
40
what part of the substantia nigra is similar to GPi in terms of their function
SNr similar to GPi b/c both are main outputs to thalamus of basal ganglia
41
what are the 3 cardinal features of Parkinson's disease
1 - bradykinesia 2 - resting tremors 3 - rigidity ***Need 2 of the 3 for diagnosis***
42
The loss of ______ neurons is a major characteristic of Parkinsons disease
Substantia nigra compacta
43
How does the loss of substantia nigra compacta affect cortical output in parkinsons disease
no DA projections to striatum = little inhibitory output to GPi (making more active) = increased inhibitory output to thalamus = decreased excitatory input to cortex = decreased cortical output = bradykinesia
44
what is the drug commonly used to treat parkinsons disease and how does it function
levodopa - precursor for DA so it acts to replace lost DA projections from degeneration of nigrostriatal fibers
45
if you were to treat parkinsons disease through a surgical approach, what part of the brain would you destroy and why ?
- remove GPi | * ** removes massive inhibition on thalamus****
46
if you were to treat parkinsons disease by deep brain stimulation where would you implant the electrodes in the brain ?
subthalamus
47
if you were trying to treat parkinsons disease that affected the right limbs of the body, what side of pallidotomy would help reduce symptoms ?
Left side pallidotomy | **L basal ganglia controls L cortex which controls contralateral musculature***