Basal Ganglia Flashcards

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

A

glutamate

23
Q

inhibitory connections of the BG motor loop use what nuerotransmitter

A

GABA

24
Q

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

A

F, there are many nuerochemicla territories in the striatum

25
Q

expain the direct or principal circuit of the basal ganglia

A

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
Q

How could you manipulate the direct pathway to increase motor cortical output ?

A

Increase inhibition on GPi (GPi is now less active)

27
Q

how does increasing inhibition on GPi result in increased cortical output

A

If increase inhibition on GPi, its less active so puts LESS inhibition on thalamus = more excitation to cortex = greater output

28
Q

how would you decrease motor cortical output in the direct BG pathway

A

Increase excitation on GPi (now more active) = increased inhibition on thalamus = decreased excitation to cortex = decreased cortical output

29
Q

the degeneration of ______ leads to huntington’s disease

A

striatum

30
Q

what is the main sign of huntingtons disease

A

chorea - rapid, rigid dance like movements of face and limbs

31
Q

T/F Huntingtons disease is autosomal recessive disease

A

F, Autosomal dominant (meaning more number the repeats the faster the onset)

32
Q

what are the 2 new additional BG structures involved in the indirect BG pathway that are not a factor in the direct pathway

A

subthalamus and GPe

33
Q

explain the indirect pathway of the basal ganglia

A

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
Q

if you decrease the output of GPe in the basal ganglia indirect pathway, what will be the result ?

A

Decrease GPe inhibitory output on subthalamus = increased excitatory output to GPi=increased inhibition on thalamus = decreased excitatory input to cortex = decreased cortical output

35
Q

if you were to increase the inhibitory output from GPe in the indirect BG pathway what would be the end result

A

decreased thalamic inhibition = increase cortical output

36
Q

in strokes it is very common for the subthalamus to be damaged, how would this affect the indirect BG pathway

A

results in less excitatory input to GPi=decreased inhibition on thalamus= excessive increased excitatory input to cortex = TOO much cortical output

37
Q

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

A

hemiballismus

38
Q

hemiballismus is the result of damage to what vessel ?

A

Posterior cerebral a. (PCA)

39
Q

what is the role of the substantia nigra in the basal ganglia

A

Substantia nigra compact - sends DA input to striatum

Substantia nigra reticulata - sends output to thalamus

40
Q

what part of the substantia nigra is similar to GPi in terms of their function

A

SNr similar to GPi b/c both are main outputs to thalamus of basal ganglia

41
Q

what are the 3 cardinal features of Parkinson’s disease

A

1 - bradykinesia
2 - resting tremors
3 - rigidity
Need 2 of the 3 for diagnosis

42
Q

The loss of ______ neurons is a major characteristic of Parkinsons disease

A

Substantia nigra compacta

43
Q

How does the loss of substantia nigra compacta affect cortical output in parkinsons disease

A

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
Q

what is the drug commonly used to treat parkinsons disease and how does it function

A

levodopa - precursor for DA so it acts to replace lost DA projections from degeneration of nigrostriatal fibers

45
Q

if you were to treat parkinsons disease through a surgical approach, what part of the brain would you destroy and why ?

A
  • remove GPi

* ** removes massive inhibition on thalamus**

46
Q

if you were to treat parkinsons disease by deep brain stimulation where would you implant the electrodes in the brain ?

A

subthalamus

47
Q

if you were trying to treat parkinsons disease that affected the right limbs of the body, what side of pallidotomy would help reduce symptoms ?

A

Left side pallidotomy

L basal ganglia controls L cortex which controls contralateral musculature*