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Neurology > Basal ganglia > Flashcards

Basal ganglia Flashcards

1
Q

In what way does the basal ganglia regulate movement?

A
  1. regulates the intensity of slow movement
  2. inhibits antagonist and unnecessary movements
  3. switch motor programs
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2
Q

Name the neural structures that make up the basal ganglia.

A

Caudate
Putamen
(make the corpus striatum)
Globus pallidus internal + external
(makes the lenticular nucleus with the putamen)
Also has motor associations with subthalamic nucleus + substantia nigra

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3
Q

In what region/s is the caudate nucleus located?

A

Frontal lobe and temporal lobe

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4
Q

In what region is the putamen located?

A

Forebrain

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5
Q

What two structures does the internal capsule separate?

A

Lentiform nucleus and caudate nucleus

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6
Q

What artery/ies supply the putamen?

A

MCA and ACA (penetrating branches such as the recurrent artery of Heubner)

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7
Q

What artery/ies supply the caudate?

A

MCA (body) and ACA (anterior)

also supplied by lenticulostriate arteries

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8
Q

What artery/ies supply the thalamus?

A

Branches of posterior cerebral and basilar arteries –> posterior choroidal, thalamogeniculate, and thalamoperforator arteries

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9
Q

What artery/ies supply the globus pallidus?

A

Anterior choroidal artery and middle cerebral artery

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10
Q

What artery/ies supply the internal capsule?

A

MCA (middle), ACA (anterior limb), anterior choroidal (posterior limb)

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11
Q

Which pathway involves projections from the cerebral cortex to the putamen and caudate? What NT is involved?

A

Corticostriatal pathway

Glutamate (excitatory)

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12
Q

Which pathway involves projections from the substantia nigra pars compacta to the putamen and caudate? what NT is involved?

A

Nigrostriatal pathway

Dopamine

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13
Q

What NT is involved with the local circuit neurones within the corpus striatum?

A

Gamma-AminoButyric Acid (inhibitory)

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14
Q

Describe how initiation of volitional movement occurs through the direct pathway.

A
  1. cerebral cortex projects to the corpus striatum via excitatory glutamate neurones
  2. when the corpus striatum is ‘excited’ it releases GABA
  3. corpus striatum projects to the GPi and inhibits it via GABA
  4. this prevents GPi from inhibiting the VA/VL complex (therefore it is disinhibited)
  5. there is excitation of UMNs in the frontal cortex
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15
Q

Describe how the indirect pathway works.

A

Acts to antagonise the activity of the direct pathway

  1. output from the caudate and putamen goes through the GPe and the subthalamic nucleus (before GPi)
  2. tonic inhibitory actions of the GPi are increased by excitatory input from subthalamic nucleus
  3. Motor thalamus remains fixed and supplementary motor cortex output remains fixed
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16
Q

During rest or repetitive movement, what is the state of the direct and indirect pathways? (i.e. active or inactive?)

A

direct pathway = inactive

indirect pathway = active

17
Q

What is the effect of dopamine on the direct and indirect pathways?

A

Dopamine increases the action of the direct pathway (via D1 receptors)

Dopamine decreases the action of the indirect pathway (via D2 receptors)

18
Q

How are D1 receptors able to increase the action of the direct pathway?

A

The D1 receptor increases cAMP
this increases the sensitivity of the corpus striatum neurones to glutamate
increases the inhibition of the GPi

19
Q

What would happen if there was no dopamine in this system? (i.e. as in hypo kinetic disorders)

A

There would be no activation of D1 receptors and no depression of D2 receptor - system is ‘stuck’ = unable to stop/start movement properly

20
Q

What are the characteristics of Parkinson’s?

A

resting tremor
slowness of movement (bradykinesia)
muscular rigidity
minimal facial expressions

21
Q

In PD, what causes the defects in motor function?

A

Loss of dopaminergic neurones in the substantial nigra pars compacta - shift to indirect pathway

22
Q

What kinds of drugs are used to treat early PD?

A

Levodopa
Dopamine agonists
MAO-B inhibitors

23
Q

What kinds of drugs are used to treat PD with motor and non-motor complications?

A

COMT inhibitors
Apomorphine
Amantadine

24
Q

What treatment method is used to treat life-limiting PD?

A

DBS

25
Q

What gene is mutated in Huntington’s disease?

A

Hungtingtin

26
Q

What is responsible for the hyperkinetic movements seen in Huntington’s?

A

Loss of GABAergic neurones in the corpus striatum

27
Q

What is chorea?

A

rapid, involuntary, jerky-type movements that are more distal

28
Q

What is athetosis?

A

slow, involuntary, smooth, writhing-type movements that are more distal

29
Q

What is ballismus?

A

rapid, involuntary, wild-flinging type movements that are more proximal

30
Q

What drugs would you use to treat a Huntington’s patient with no other symptom but chorea?

A

Tetrabenazine

Amantadine

31
Q

What drugs would you use to treat a Huntington’s patient with chorea and weight loss?

A

Olanzapine

Cannabinoids

32
Q

What drugs would you use to treat a Huntington’s patient with chorea, psychosis, aggression/impulsivity?

A 
Aripiprazole
Haloperidol
Olanzapine
Risperidone
(+ many others)
33
Q

What is the inheritance pattern of Huntington’s?

A

Autosomal dominant

Neurology (46 decks)

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