Neuro-Basal Ganglia

Front 1

How are the basal ganglia involved with movement?

Back 1

They are involved in the control of movement

Front 2

What are the five subcortical nuclei of the basal ganglia?

Back 2

1. Caudate
2. Putamen
3. Globus Pallidus (internal and external segments)
4. Subthalamic nuclei
5. Substantia nigra

Front 3

The striatum is composed of what two structures? How else are they related?

Back 3

The caudate and putamen; they have similar function

Front 4

What is another name for the globus pallidus?

Back 4

Pallidum

Front 5

The term 'pallidum' sometimes refers to what?

Back 5

Internal segment of the globus pallidus and pars reticulata of the substantia nigra (they have similar output function)

Front 6

What are the three outputs of the basal ganglia?

Back 6

1. Substantia nigra (pars reticulata) to thalamus (VA and VL)
2. Globus pallidus (internal segment) to thalamus (VA and VL)
3. Substantia nigra (pars reticulata) to superior colliculus and pedunculopontine nuclei

Front 7

Fibers from the substantia nigra travel to the thalamus, then where?

Back 7

To the premotor cortices

Front 8

Fibers from the globus pallidus travel to the thalamus, then where?

Back 8

To the premotor cortices

Front 9

What is the function of the pedunculopontine nuclei?

Back 9

They are the locomotor area of the brainstem

Front 10

In the cortex loop of the basal ganglia, transmitters and synaptic actions result in disinhibition of what?

Back 10

Neurons in the premotor and supplementary motor cortex

Front 11

Are corticostriate connections excitatory or inhibitory? What neurotransmitter is used?

Back 11

Excitatory; glutamate

Front 12

Are striatopallidal and striatonigral connections excitatory or inhibitory? What neurotransmitter is used?

Back 12

Inhibitory; GABA

Front 13

Are pallidothalamic connections excitatory or inhibitory? What neurotransmitter is used?

Back 13

Inhibitory; GABA

Front 14

Are thalamocortical connections excitatory or inhibitory?

Back 14

Excitatory

Front 15

Where are dopaminergic cells located in the substantia nigra?

Back 15

In the pars compacta

Front 16

The dopaminergic nigrostriatal pathway has projections to what part of the brain?

Back 16

The striatum

Front 17

What happens to the substantia nigra in persons with Parkinson's disease?

Back 17

There is a loss of dopamine containing cells in the substantia nigra

Front 18

What are the effects of the dopaminergic nigrostriatal pathways?

Back 18

1. May have excitatory effects on some striatal neurons
2. May have inhibitory effects on other striatal neurons

Front 19

What is the indirect basal ganglia pathway?

Back 19

The subthalamic nucleus

Front 20

The subthalamic nucleus receives input from what part of the brain?

Back 20

The external segment of the globus pallidus

Front 21

The subthalamic nucleus has outputs to what part of the brain?

Back 21

1. Internal segment of the globus pallidus
2. Pars reticulata of the substantia nigra

Front 22

Is the subthalamic output excitatory or inhibitory? What does it do?

Back 22

Excitatory; inhibits the thalamus indirectly through the internal segment of globus pallidus

Front 23

A lesion of the subthalamic nucleus results in what?

Back 23

-Disinhibition of the thalamus
-Violent, involuntary movements of the opposite side of the body (hemiballismus)

Front 24

Is the basal ganglia active before cells in the cortex during voluntary movement?

Back 24

No

Front 25

Is the basal ganglia primarily responsible for stimulus-triggered movement?

Back 25

No

Front 26

Is the basal ganglia involved in self-initiated movement?

Back 26

Possibly

Front 27

Are diseases of the basal ganglia well understood?

Back 27

No

Front 28

Why are symptoms caused by diseases of the basal ganglia poorly understood?

Back 28

They include motor and cognitive deficits, and cognitive symptoms are not well defined

Front 29

What are three diseases of the basal ganglia?

Back 29

1. Parkinson's disease
2. Huntington's disease
3. Tardive dyskinesia

Front 30

What are the symptoms of tardive dyskinesia? What is it caused by?

Back 30

Involuntary movements; caused by anti-psychotic drugs

Front 31

What is the etiology of Parkinson's disease?

Back 31

Unknown etiology

Front 32

When do symptoms of Parkinson's disease apear?

Back 32

In the 5th or 6th decade

Front 33

What are the symptoms of Parkinson's disease?

Back 33

-Akinesia
-Bradykinesia
-Paucity of movement
-Resting tremor
-Rigidity
-Disturbances of postural reflexes
-Short steps when walking
-Mask-like face
-General loss of affect

Front 34

What is akinesia?

Back 34

Difficulty initiating movement

Front 35

What is bradykinesia?

Back 35

Movements that are slower than normal

Front 36

What is paucity of movement?

Back 36

Not moving as much as normal

Front 37

What is a resting tremor?

Back 37

Alternating movements at rest, 'pill rolling'

Front 38

What are the symptoms of rigidity in Parkinson's disease?

Back 38

-Increased resting muscle tone
-Present in muscles on both sides of joint
-Not velocity dependent

Front 39

What is the cause of Parkinson's disease?

Back 39

-Loss of dopaminergic cells in substantia nigra (pars compacta)
-Decreased amount of dopamine available as neurotransmitter in the striatum

Front 40

Does dopamine in the nigrostriatal pathway have an excitatory or inhibitory effect on the striatum?

Back 40

Excitatory

Front 41

Is the striatal-pallidal pathway excitatory or inhibitory?

Back 41

Inhibitory

Front 42

The loss of dopamine causes what to happen in the striatal cells?

Back 42

-Decreased activity of striatal cells
-Causes cells in GP to be more active
-Thalamus is more inhibited

Front 43

The loss of dopamine in the nigrostriatal pathway ultimately causes what to happen in the cerebral cortex?

Back 43

Less activity in the cerebral cortex, consistent with symptoms of akinesia and bradykinesia

Front 44

Does dopamine in nigrostriatal cells have an excitatory or inhibitory effect on a subset of cells in the striatum?

Back 44

Inhibitory

Front 45

How does dopamine have both inhibitory and excitatory effects?

Back 45

-Different target cells in striatum respond to dopamine differently
-Decreased dopamine in nigrostriatal pathway could cause both
-Akinesia and bradykinesia or resting tremor and rigidity

Front 46

What happens to patients with Parkinson's disease when they are given L-dopa orally?

Back 46

-Symptoms reduced
-Allows the patient to function better
-Does not cure the disease
-Symptoms typically worsen over time as L-dopa becomes less effective

Front 47

What are some interventions for Parkinson's disease?

Back 47

-L-dopa
-Transplantation of embryonic tissue into the striatum
-Pallidotomy
-Transplantation of stem cells
-Stimulation of the globus pallidus

Front 48

How is Huntington's disease spread?

Back 48

Genetic disorder transmitted by a dominate gene

Front 49

When do symptoms of Huntington's disease first appear?

Back 49

Fourth decade of life

Front 50

What are the symptoms of Huntington's disease?

Back 50

Rapid, jerky involuntary movements of the face, arms and legs

Front 51

What is the pathology of Huntington's disease?

Back 51

-Reduced number of GABAergic projection neurons in the caudate and putamen
-Changes in indirect pathway via subthalamic nucleus ultimately results in disinhibition of the thalamocortical pathways

Front 52

Is there a treatment for Huntington's disease?

Back 52

No