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BB 2 > Basal Ganglia > Flashcards

Basal Ganglia Flashcards

1
Q

What 3 structures make up the basal ganglia

A

Subthalamus
Substantia nigra
Striatum

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2
Q

What 3 structures make up the striatum

A

Caudate nucleus
Putamen
Globus Pallidus

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3
Q

Describe the structure/ path of the head of the caudate

A

Fits into concave recess

Forms a long tapering rod on side of ventricle entering the temporal lobe

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4
Q

Where is the putamen located

A

Lateral to caudate

Linked to the caudate by spokes of the grey matter

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5
Q

Where is the accumbens located

A

Lies at anterior inferior junction of caudate and putamen

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6
Q

What makes up the dorsal striatum

A

Caudate and putamen

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7
Q

What makes up the ventral striatum

A

Nucleus accumbens

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8
Q

Where does input to basal ganglia come from

A

The whole body via the substantia nigra pars compacta

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9
Q

Where does output to basal ganglia come from

A

Thalamus, cortex and globus pallidus interna/ externa

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10
Q

4 functions of basal ganglia

A

Motor programme switch
Regulates intensity of slow/ stereotyped movements
Inhibit antagonistic and unecessary movements
Regulates attention and cognition

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11
Q

What are medium spiny neurons

A

Special type of GABAergic inhibitory neurones

95% of neurones with the human body

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12
Q

What is meant by convergence

A

Large dendritic trees of striatal output neurons

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13
Q

Is the direct pathway excitatory or inhibitory

A

Excitatory

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14
Q

At rest is the thalamus excited or inhibited

A

Inhibited

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15
Q

What is the aim of the direct pathway

A

To remove inhibition of the thalamus

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16
Q

Describe the steps of the direct motor cortex (not including the ‘extra bits’)

A

1) Excitatory (glutamate) output from the motor cortex synapses with an inhibitory neurone on striatum
2) Inhibition (GABA) of the GPi from striaum
3) Normally the GPi inhibits the thalamus, so when the GPi is inhibited, can’t inhibit thalamus anymore. Thalamus excitatory
4) Thalamus excitatory to the motor cortex
5) Excitation of muscles

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17
Q

Why does excitation of striuatum lead to inhibition of GPi

A

Striatum is inhibitory to GPi, so more excitation of inhibitory effect- more inhibition

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18
Q

Which 2 structures are involved in the fine tuning of the direct pathway

A

Substantia nigra and subthalamic nucleus

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19
Q

How does substantia nigra fine tune the direct pathway

A

Inhibitory neurones to striatum
Synapse with inhibitory neurones from striatum to GPi
Increased activity so increased dopamine to inhibit neurones in striatum
Further excites inhibitory neurones so more inhibition

20
Q

Describe the steps of the indirect pathway

A

Motor cortex releases glutamate, excitatory to striatum
Excitation of striatum means more inhibition to GPe
GPe normally inhibits subthalamic nucleus, no more inhibition to Gpe means excitation of STN
STN excites GPI
GPi inhibitory to thalamus- excited GPi= more inhibition to thalamus

21
Q

In repetitive movement, which pathway is active and which is inactive

A

Indirect=active

Direct= inactive

22
Q

In changes of movement which pathway is active and which is inactive

A 
Indirect= inactive
Direct= active
23
Q

Which type of dopamine receptor is involved in which pathway

A 
D1= direct
D2= indirect
24
Q

What happens when dopamine binds to D1 receptor

A

Increased synthesis of cAMP
Increases sensitivity of striatal cells to glutamate
Projects to GPi directly

25
Q

What is the overall function of dopamine

A

Allows motor programme to stop and start at will

26
Q

How do the subthalamic nucleus and substantia nucleus work in the background for the indirect pathway

A

STN excites SN
DOpamine neurones from SN go to striatum
Dopamine binds to D2 receptors reducing activity in excitatory neurones

27
Q

Where in the brain is there a loss of dopaminergic input in PD

A

Caudate and putamen

28
Q

Where are cells lost from in PD

A

Substantia Nigra

29
Q

What % of cells in the substantia nigra have to be dead before clinical signs of PD show themselves

A

80

30
Q

What are the 4 cardinal motor signs of PD

A

Tremor at rest
Rigidity
Bradykinesia
Loss of postural reflexes

31
Q

How do you treat early PD with cardinal symptoms but no other complications

A

Levodopa
Dopamine agonists
MAO-B inhibitors

32
Q

How do you treat motor and non motor complications, medications and side effects

A

Levodopa
Dopamine agonists
MAO-B inhibitors
COMT inhibitors

33
Q

How do you treat life limiting PD with significant disability

A

Deep brain stimulation

34
Q

Signs and symptoms of Huntingtons

A

Hyperkinesis
Extra involuntary movements
Dementia

35
Q

What changes in the brain change in Huntingtons

A

loss of GABA-ergic neurones in the striatum

36
Q

Define ballismus

A

Involuntary sudden jerky movement

37
Q

Define athetosis

A

Involuntary smooth sinuous movement

38
Q

How can Huntingtons be managed

A

Neuroleptics (dopamine antagonists)
Atypical antipsychotics
SSRI for depression

39
Q

Define disinhibition

A

When there are 2 inhibitory neurones in sequence- inhibition of inhibition= overall excitation

40
Q

Inputs from where to where are degenerated in parkinsons

A

From substantia nigra to caudate/ putamen

41
Q

Is there more of less tonic inhibition of the thalamus in parkinsons

A

More

42
Q

Is there increased or decreased excitation of the frontal cortex in PD

A

Decreased

43
Q

Input from where to where is degenerated in Huntingtons disease

A

Caudate to GPe

44
Q

Is there more or less tonic inhibition of thalamus in huntingtons

A

Less

45
Q

Is there increased or decreased excitation of frontal cortex

A

Increased

BB 2 (28 decks)

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