Basal Ganglia

Question 1

Basal ganglia

Answer 1

A group of nuclei located (bilaterally) deep in the telencephalon, diencephalon, and midbrain
Primarily located between the cerebral cortex and thalamus, but also in midbrain & near thalamus

Question 2

Function of basal ganglia

Answer 2

To modify initiation and execution of motor activity
-also cognitive and limbic connections

Helps refine movement signal from cortex by inhibiting “incorrect” motor activity

Question 3

Brake hypothesis works by Disinhibition. What is disinhibition?

Answer 3

Release from ongoing inhibition
Inhibit the ongoing inhibition

Question 4

Striatum

Answer 4

-Caudate nucleus
-Nucleus accumbens
-Putamen

Question 5

Globus pallidus

Answer 5

-External segment (GPe)
-Internal segment (GPi)

Question 6

Subthalamic nucleus (STN)

Answer 6

-

Question 7

Sustantia nigra

Answer 7

-Compact part (SNc) - dopaminergic
-Reticular part SNr) - output nuclei

Question 8

Lenticular nucleus
(aka lentiform nucleus)

Answer 8

-Putamen
Globus pallidus
-External segment (GPe)
-Internal segment (GPi)

Question 9

Effect of dopamine (on GPe) varies

Answer 9

▪ Excitatory on putamen neurons that are part of the direct pathway (see below)
▪ Inhibitory on putamen neurons that are part of the indirect pathway
➢ basically, dopamine facilitates movement (see Parkinson’s disease below)

Question 10

Thalamic drive

Answer 10

a theoretical proposal that attempts to predict the motor effects of specific changes within the
basal ganglia – thalamic – cerebral cortical circuitry
a far from perfect
▪ e.g., fails to predict neuronal discharge changes in the thalamus (VA/VL) in various diseases

Question 11

What is the basic idea behind the thalamic drive?

Answer 11

Basic idea is to understand which regions of the circuit are excitatory or inhibitory and be able
to predict whether damage to those areas will result in increased cortical motor activity
(hyperkinetic; increased thalamic drive) or decreased cortical motor activity (hypokinetic;
decreased thalamic drive)

Question 12

Direct Pathway

Answer 12

Motor cortex → striatum => GPi/SNr => thalamus → motor cortex
Facilitates movement
Disinhibits the thalamus
▪ increased thalamic drive (thus, damage to this pathway = hypokinetic [Parkinson’s])

Question 13

Indirect Pathway

Answer 13

Motor cortex → striatum => GPe => STN → GPi => thalamus→ motor cortex
Inhibits movement
Inhibits the thalamus
▪ decreased thalamic drive (thus, damage to this pathway = hyperkinetic [Huntington’s])

Question 14

Hyperkinetic movement disorders

Answer 14

Extraneous, unwanted movements
e.g., Huntington’s disease, athetosis

Question 15

Chorea

Answer 15

involuntary, constant, rapid, complex body movements that flow from one body part to
another

Question 16

Choreiform

Answer 16

resembling chorea
involuntary “dance like” movement of the limbs

Question 17

Athetosis

Answer 17

slow, writhing movements of the fingers and hands, and sometimes of the toes

Question 18

Ballismus

Answer 18

violent, flailing movements
damage to subthalamic nuclei of basal ganglia results in hemiballismus

Question 19

Dystonia

Answer 19

a persistent spasm/posture of a body part which can result in grotesque movements and
distorted positions of the body

Question 20

Tremor

Answer 20

rhythmic, involuntary, oscillatory movements

Question 21

Resting tremor

Answer 21

Resting tremor occurs when a body part is at complete rest against gravity
▪ tremor amplitude decreases with voluntary activity

Question 22

Postural tremor

Answer 22

postural tremor occurs during maintenance of a position against gravity and
increases with action

Question 23

Essential tremor (familial)

Answer 23

▪ most common form of tremor
▪ tremors occur in a person who is moving or trying to move and no cause can be identified

Question 24

Intentional tremor

Answer 24

manifests as a marked increase in tremor amplitude during a terminal portion of
targeted movement.
➢ examples of intention tremor include cerebellar tremor/pathology

Question 25

Hypokinetic movement disorders

Answer 25

difficulty or absence of intended movements
b e.g., Parkinson’s disease

Question 26

Bradykinesia

Answer 26

slowing of voluntary movement

Question 27

Difficult initiating movement

Answer 27

use center of gravity to compensate: initiate walking or sit-stand

Question 28

Increased muscle tone: Rigidity
Lead-pipe rigidity

Answer 28

resistance persists throughout the range of movement of a particular joint

Question 29

Increased muscle tone: Rigidity
Cogwheel rigidity

Answer 29

periodic resistance at different points throughout the range of movement

Question 30

Spasticity (speed dependent)

Answer 30

move slow and can move limb through ROM
- often pyramidal system; unidirectional (e.g., only flexion)

Question 31

Rigidity (not influenced by speed)

Answer 31

move fast or slow and still can’t move limb through ROM
- often extra-pyramidal system; bidirectional

Question 32

Parkinson’s disease

Answer 32

degenerative hypokinetic disorder
B Extremely common (100-200 per 100,000) >60 yrs old
C Primary symptoms
1 bradykinesia, difficulty initiating movement
a often assume flexed posture
▪ lean forward to compensate for difficultly starting/continuing walking
2 increased muscle tone (rigidity)
3 resting tremor
4 decreased voluntary movement
a micrographia, decreased facial expression “masked expression”, monotone speech
5 potential dementia/depression changes
6 dysautonomic symptoms
a e.g., urge incontinence (loss of bladder control), constipation
D Pathology
1 cell loss in substantia nigra – compact part (SNc)
a reduced dopamine production
▪ inhibits direct pathway = increases inhibition of thalamus = decreases thalamic drive
➢ indirect pathway now dominant (also decreases thalamic drive)
2 note that many other brain regions are involved (e.g., hippocampus, neocortex, brainstem
nuclei)

Question 33

Huntington’s disease

Answer 33

genetic degenerative hyperkinetic disorder
B Prevalence: 5 per 100,000
a autosomal dominant (children have 50% chance of inheriting)
C Primary symptoms
a appear in adulthood (30-50 yrs)
b gradual onset
2 dementia
a progressive loss of attention & executive function
▪ poor ability to plan, organize, and sequence
▪ short term memory deficits
3 chorea
a initially appears as fidgeting or restlessness
b eventually becomes severe
▪ begins in face & arms; progresses to whole body
D Pathology
1 loss of GABA-ergic neurons in GPe
b eventually includes much of striatum (caudate & putamen)
▪ inhibits indirect pathway = increases thalamic drive
➢ = hyperkinesis
▪ loss of neurons in cortex & striatum also decreases stimulation of direct pathway
➢ = decreased thalamic drive (may result in slowing of the hyperkinetic movements)
2 loss of cortical neurons (esp. prefrontal cortex)
▪ role in attentional and executive symptoms

Question 34

Emotional

Answer 34

Ventral striatum
- nucleus accumbens
- head of the caudate
- putamen
Limbic connections
- amygdala
- hippocampus
- orbital, cingulate, & entorhinal cortex
- MD thalamus → cingulate cortex

Question 35

Cognitive

Answer 35

caudate nucleus
- from association cortical areas to prefrontal cortex

Question 36

Motor

Answer 36

putamen
- from somatosensory cortex to motor cortex