Basal Ganglia

Question 1

What are the two main parts of the Basal Ganglia?

Answer 1

Striatum
Globus Pallidus (pallidum)

Question 2

where is the readiness potential processed?

Answer 2

striatum and pallidum, is then relayed back to the motor cortex by the thalamus

Question 3

What two important structures do the basal ganglia make contact with?

Answer 3

Substantia Nigra

Subthalamic nucleus

Question 4

Which basal ganglia structure is the substantia nigra in contact with?

Answer 4

Striatum

Question 5

Which basal gangliar structure is the subthalamic nucleus in contact with?

Answer 5

Pallidum

Question 6

What two things are associated with disease of the basal ganglia?

Answer 6

difficulty starting voluntary actions

Difficulty stopping unwanted movements

Question 7

What disease of the basal ganglia is characterised by akinesia?

Answer 7

Parkinson’s disease

Question 8

Parkinson’s disease is described as having hypokinetic features, what are some of these?

Answer 8

Dead pan face
'reptilian' stare
loss of asspociated movements (arm swinging)
Shuffling gait
Stooped posture

Question 9

Does movement exacerbate or relieve hyperkinetic features of parkinson’s disease?

Answer 9

relieves - tremor completely disappears when moving

Question 10

Apart from tremor, what is another hyperkinetic feature of Parkinson’s?

Answer 10

Rigidity, either ‘lead pipe’ or spastic. An increase in muscle tone that affects ext/flexors

Question 11

What are some of the main Hyperkinetic disorders?

Answer 11

Huntington’s chorea
Athetosis
Ballism

Question 12

What is Huntington’s chorea?

Answer 12

Jerky, spasmodic movements at rest and in voluntary movements

Question 13

How do Huntington’s chorea and Parkinson’s chorea tremor differ?

Answer 13

Parkinson’s only at rest, Huntington’s all of the time, even during voluntary movement

Question 14

What is athetosis?

Answer 14

Slow, writhing movements usually affecting the extremities.

NB if trunk affected, torsion spasm and grotesque posture noticed.

Question 15

What is Ballism?

Answer 15

Violent flailing limb movements

Question 16

What is a necessity of movement control with regard to the pallidum?

Answer 16

Voluntary reglulation of the spontaneity of the pallidum cells.

Question 17

How does the striatum affect the pallidum? What neurotransmitter allows this?

Answer 17

Profound inhibition, mediated by GABA neurotransmitter

Question 18

What part of the BG does the cortical input arrive in?

Answer 18

striatum

Question 19

At rest, is the pallidum being inhibited or stimulated ?

Answer 19

inhibited. Via the cortico-striatal pathway excitation.

Question 20

during a voluntary action, is the corticostriatal pathway being inhibited or stimulated?

Answer 20

inhibited, this is via the readiness potential.

Question 21

What effect does the substantia nigra have on the striatum and consequently the motor response?

Answer 21

It inhibits the striatum, which leads to an increase in motor activity due to lack of pallidum inhibition.

Question 22

What causes huntington’s chorea?

Answer 22

degeneration of Striatum, meaning that the cortical input i that keeps things organised is lost. Essentially unchecked motor gibberish ensues

Question 23

How is voluntary control achieved?

Answer 23

The actions of the cortex on the striatum allow control of motor function.

Question 24

What does the substantia nigra do?

Answer 24

Inhibits the striatum, keeping it in check to avoid over suppression of motor function in pallidum

Question 25

What causes Parkinson's disease?

Answer 25

The nigrostriatal pathway is destroyed, meaning the striatum overinhibits the pallidum making it very difficult to start a movement

Question 26

What neurotransmitter is used in the nigrostriatal pathway?

Answer 26

Dopamine

Question 27

What percentage of nigrostriatal pathway fibres are lost before symptoms ensue?

Answer 27

80%

Question 28

What is the proposed theory for Parkinsonian tremors/rigidity?

Answer 28

Disruption in pathway from the BG to the brainstem

Question 29

What do Striatal interneurones do?

Answer 29

Excite the projection from the Striatum to the pallidum.

Question 30

Name an important pharmacological feature of striatal interneurones

Answer 30

Cholinergic

Question 31

What is the treatment for parkinsons and how does it work?

Answer 31

L-DOPA. It is the precursor of DA but DA can't cross the blood brain barrier. LDOPA becomes DA in the brain and restores some functionality to Substantia nigra.

Question 32

What is a problem with L-DOPA?

Answer 32

Only 0,01% of dose reaches S nigra.

Question 33

What can be used in cmombination with L-DOPA to increase efficacy and how does it do this.

Answer 33

Decarbocylase inhibitor (carbidopa). This stops L-Dopa being decarboxylated to DA outside of the BBB. Carbidopa doesn't cross so can't interfere in the target area.

Question 34

What is the less common Parkinsons treatment?

Answer 34

Dopamine Agonists such as Apomorphine

Question 35

Do the inputs to the striatum synapse onto the striatum itself or the interneurones?

Answer 35

Interneurones. | Both the cortical input and the Nigrostrital input. These are excitatory.

Question 36

Does the subthalamic nucleus inhibit or stimulate the pallidum?

Answer 36

Inhibit

Question 37

What gets damaged to cause Ballism?

Answer 37

Subthalamic nucleus

Question 38

What is a side effect of long term L-DOPA or DA agonists?

Answer 38

Psychosis

Question 39

What are some possible new treatments for Parkinsons?

Answer 39

Autotransplantation of adrenal medulla (Da is precursor of adrenaline) Stem cells Deep Brain Stimulation

Question 40

What are some treatments for Huntington's chorea?

Answer 40

ACh Mimetics | DA blockers

Question 41

What is a possible side effect of Huntington's Pharma treatment?

Answer 41

Parkinsonism may be produced

Question 42

What does dopamine stimulate?

Answer 42

Substantia Nigra

Question 43

What does ACh Stimulate?

Answer 43

Striatum (interneurones)