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Brain And Behaviour > The Basal Ganglia > Flashcards

The Basal Ganglia Flashcards

1
Q

What is the function of the basal ganglia (BG)

A

Involved in setting the amplitude of movement (set the scale)

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2
Q

What structures form the striatum?

A

Caudate nucleus and the putamen

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3
Q

What structures from the lentiform nucleus?

A

Putamen and the globus pallidus internus and externus

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4
Q

What are the two components of the substantia nigra?

A

Pars compacta

Pars reticulata

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5
Q

What are the inputs into the striatum?

A

Mainly the SMA but also M1 and S1
Even the limbic system
Inputs from the frontal eye fields

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6
Q

What are the outputs of the BG?

A

To the Venteroanterior and lateral thalamus to the cortex
Superior Colliculus
Extrapyramidal tracts

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7
Q

What si the inhbitory path from the Gpi to the thalamus called?

A

The ansa lenticular fasiculus

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8
Q

What striatum is formed from two compartments…what are they?

A 
The striasome (small compartment) which receives inputs from the limbic system
The matrix (larger compartment) which receives inputs from sensory and motor cortex and projects to GP
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9
Q

Outputs from the striatum are?

A

Inhibitory

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10
Q

The thalamus is tonically ……. by the Gpi/SNr?

A

Inhibited

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11
Q

What neurons mediate the the excitation and inhibition within the BG?

A

Glutamatergic

GABAerigic

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12
Q

The SNc does what to the striatal outputs?

A

Stimulates striatal inhibitory outputs to the Gpi/SNr 9Via D1 receptors)
Inhibits inhibitory outputs to the GPe (via D2 receptors)

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13
Q

What are the different pathways within the BG?

A

The direct
The indirect
The hyperdirect

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14
Q

What is the function of the direct pathway?

A

The direct pathway inhibits the Gpi/SNr thus relieving thalamic inhibition via the ansa lenticular fasiculus. This allows the thalamis to stimulate the cerebral cortex and facilitate movement

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15
Q

What is the function of the indirect pathway?

A

Striatum inhibits the Gpe which intern inhibits the STN. The STN stimulates the Gpi/SNr potentiating inhibition of the thalamus. When the GPe is inhibited the su thalamic outputs are disinhibited. Since these outputs are excitatory the Gpi/SNr is stimulated. Increases thalamic inhibition. This decreases movement

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16
Q

At rest what inhibits movement?

A

The hyperdirect pathway which stimulates stimulatory outputs of the STN to the gpi/SNr (starts in cerebral cortex)

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17
Q

What is the net effect of the modulator dopamine?

A

Facilitation of movements as it inhibits the indirect pathway and stimulates the direct
Thus decreases inhibition on thalamus and allows cerebral cortex stimulation

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18
Q

How does the basal ganglia use the direct and indirect pathways to regulate movement amplitude?

A

It is hypothesised that movement amplitude requires a sequence of direct responses balance by other inhibitory responses mediated through the indirect pathway.

19
Q

What is the evidence which supports the hypothesis the BG set movement amplitude

A

Imaging studies using positron emission tomography (PET) in heathy subjects show that there is an increase in blood flow and thus metabolic activity in the BG when subjects were given an amplitude pressure to movement compared to no precue to movement

20
Q

When comparing patients with Parkinson’s disease and healthy controls, what is the effect of an amplitude, directional and null precue on mean reaction times to movement?

A

PD patients in general show an increase in reaction time for all parameters compared to controls. Within controls AP and DP reduces the reaction time for movement equally. However, in PD patients there was a smaller reduction in reaction time with the AP compared to the DP. The reaction time decrease, compared to NP, when given AP was larger in controls than that of PD patients. The decrease in reaction time for controls and PD patients for the DP was about the same. This shows that Pd patients did not use the AP as efficiently as directional precue meaning amplitude processing was impaired.

21
Q

What is Parkinson’s disease?

A

PD is a neurodegenerative disease of the substantia nigra which causes a decrease in dopamingeric neurons within the nigrostriatal pathway

22
Q

What are some epidemiological facts about PD?

A

2nd most common neurodegenerative condition
16-19 new cases per 100,000 person years
Disease of elderly with incidence between 70-79 rising to 93 per 100,000 person years
Age of onset on average ~65
5-10% monogenetic causes

23
Q

How many neurons have to be lost in the nigrostriatal pathway for clinical symptoms to manifest?

A

60-70%

Estimates vary to up to 80%

24
Q

Symptoms of PD?

A 
Resting tremor (pill rolling 4-6Hz)
Bradykinesia
Rigidity (cogwheeling/lead pipe)
Masked faces
Postural instability
Stooped shuffling gait
Sleep disturbances
Mood disorders
25
Q

what happens to the basal ganglia circuitry in PD?

A

SNc does not stimulate the direct (decrease of inhibition of Gpi/SNr from striatum)
SNc does not inhibit the indirect (Increased inhibited of Gpe, increased inhibition to STN, STN disinhibited = greater stimulation of Gpi/SNr
Greater inhibition to the thalamus thus thalamic outputs which facilitate movement are inhibited

26
Q

What does EEG activity in pd show?

A

Decreased readiness potential

27
Q

What does EMG activity show in PD?

A

Smaller initial peak to overcome inertia of limb. This decrease in output means movement is difficult to initiate and patients may fall for ward to initiate movement via reflex action

28
Q

what is the befit of visual cues to movement?

A

If patients do not have to rely on internal cues to movement they move more readily. External visual cues aid movement as directional cue reduce reaction time for movement. The cues are believed to involve cortical areas for planning where, for example, the foot should be rather than internal ones

29
Q

What types of movement are more greatly effected in PD?

A

Complex movements

30
Q

What is the treatment for PD?

A 
L-Dopa
Dopamine receptor agonists
COMT inhibitors
Anticholinergics
Deep brain stimulation (depolarising block to globus pallidus)
31
Q

What is needed when administrating DOPA?

A

Carbidopa (peripheral dopa decarboxylase inhibitors)
Increased amount of Dopa getting into CNS 9from 1% to 10%)
Reduces dose need
Reduces peripheral ADRs

32
Q

What are some motor complication of PD?

A

Freezing
Dyskinesia (at peak dose of diphasic)
Wearing off

33
Q

Other ADRs of dopamine therapy?

A

Psychosis, N+V, hypotension

34
Q

What is advanced Parkinson’s disease defined as?

A

PD with progressive motor impairment in spite of l dopa treatment with motor complications (50% at 5 years)

35
Q

Why does L-dopa eventually become uneffective?

A

Continual loss of dopaminergic neurons. L-Dopa needs to be converted into dopamine within the CNS by DOPA decarboxylase (as dopamine cannot pass through BBB). No neurons=no conversion

36
Q

What are some symptoms of Huntington’s disease?

A

Chorea (wild uncontrolled movements which are abrupt and jerky)
Mood change
Subcortical dementia

37
Q

What causes Huntington’s disease?

A

Autosomal domainat mutation in Huntington gene on chromosome 4
Forms Huntington protein with polyglutamine repeats. Normally there are 20 but in HD >60
Onset is 50/60’s decade but this is variable depending on the number of polyQ repeats an individual has

38
Q

When happens to the circuitry in the BG in HD?

A

Degeneration of GABAergic and cholingeric neurons in the striatum means that there is a loss of inhibitory striatal outputs to the Gpe. This means the the STN is more greatly inhibited which relieves the Gpi/SNr from STN stimulation. Increase in thalamic outputs

39
Q

What are two types of dystonia?

A

Spasmodic tortillas

Idiopathic torsion dystonia (ITD)

40
Q

What causes idiopathic torsion dystonia?

A

Autosomal dominant mutations in DYT1 or DYT6

41
Q

What are the characteristics of ITD? What causes it?

A

It is a progressive disorder which manifests in childhood. It causes severe disability within 10 years
Caused by degeneration of striatum

42
Q

symptoms of ITD?

A

Spasmodic contracture in muscles

Dystonia spasms in legs, trunk and neck on walking

43
Q

What is spasmodic torticolis? Age of onset?

A

Spasmodic twisting it the neck due to spasm of the sternocleidomastoid muscle
50-60

44
Q

Treatment for spasmodic torticolis?

A

Botulinum toxin which causes paralysis at the NMJ and causes muscle to relax
Is temporary as body develops antibodies to toxin

Brain And Behaviour (12 decks)

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