LEC 23- Basal Ganglia Flashcards

1
Q

Describe the topographical anatomy and the names of the neurotransmitters of nuclei related to basal ganglia

A

(I) Striatum (caudate nucleus + putamen), located in telencephalon, utilize GABA and acetyl choline

(II) Globus pallidus (external & internal), located in telencephalon, utilize GABA

(III) Subthalamic nucleus, located in diencephalon, utilizes Glutamate

(IV) Substantia nigra (pars compacta [dopamine] & pars reticulata [GABA]), located in midbrain

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2
Q

Describe the role of the basal ganglia in motor control.

A
  • do not maintain direct connections with the spinal cord (input or output)
  • have an input into extrapyramidal pathways
  • work closely with supplementary motor cortex rather than premotor cortex
  • by acting on supplementary cortex, basal ganglia indirectly modulate the function of pyramidal pathway
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3
Q

Describe the major components of the basal ganglia.

A

The basal ganglia consist of four major interconnected subcortical nuclei:

  1. Striatum (Caudate nucleus + putamen),
  2. Globus pallidus (external and internal),
  3. Subthalamic nucleus
  4. Substantia nigra (pars compacta and reticulata).

Forebrain (1&2), diencephalon (3), midbrain (4)

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4
Q

Describe the role of the basal ganglia in movement control.

A

The basal ganglia participate in the control of voluntary movement by facilitating wanted motor plans and suppressing unwanted motor plans.

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5
Q

How do the basal ganglia interact with other motor pathways?

A

The basal ganglia modulate the functions of both pyramidal and extrapyramidal pathways.

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6
Q

Define the connection of the basal ganglia with the spinal cord.

A

The basal ganglia do not have direct connections with the spinal cord for input or output.

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7
Q

What is the primary source of input to the basal ganglia?

A

The basal ganglia receive major input from the prefrontal cortex and send their output back to supplementary motor cortex via the thalamus

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8
Q

Explain the consequences of damage to the basal ganglia.

A

Damage to the basal ganglia can result in movement disorders, such as excessive involuntary movements seen in Huntington’s disease or reduced voluntary movement seen in Parkinson’s disease.

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9
Q

Describe the structure of the basal ganglia.

A

The basal ganglia consist of the internal capsule, caudate nucleus, putamen, and globus pallidus - external and internal and Subthalamic nucleus (STN), Substantia nigra (SN)

  • caudate nucleus (head & body), putamen, globus pallidus in the frontal and parietal lobes
  • caudate nucleus (tail) in temporal lobes

The internal capsule passes between the caudate nucleus and the putamen

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10
Q

How is the striatum divided?

A

The striatum is divided into the caudate nucleus and putamen by the internal capsule.

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11
Q

Describe the structure and connections of the caudate nucleus.

A

Located in the lateral wall of the lateral ventricle, following a C-shaped course.

Absent in the posterior horn of the lateral ventricle.

Connected to the putamen by gray matter (cell) bridges.

Has a large head in the frontal lobe, primarily receiving input from the prefrontal cortex.

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12
Q

How are the caudate, putamen, and amygdala connected?

A

The caudate tail is nearly continuous with the amygdala in the temporal lobe.

Ventral parts of the caudate and putamen merge to form the nucleus accumbens (ventral striatum).

Only the dorsal striatum (caudate and putamen) is part of the basal ganglia.

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13
Q

How does the basal ganglia contribute to motor plan selection?

A

The basal ganglia contribute to motor plan selection by facilitating required motor plans and suppressing unwanted motor plans, working in conjunction with the supplementary motor cortex (SMC).

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14
Q

Define the role of the internal and external globus pallidus in the basal ganglia.

A

The internal globus pallidus (GPi) and external globus pallidus (GPe) are involved in regulating the output of the basal ganglia, with GPi primarily providing inhibitory signals to the thalamus and GPe modulating the activity of other basal ganglia components.

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15
Q

Do the basal ganglia have a role in voluntary movement regulation?

A

Yes, the basal ganglia play a crucial role in the regulation of voluntary movement, influencing the selection and execution of motor plans.

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16
Q

How do the basal ganglia interact with extrapyramidal pathways?

A

The basal ganglia also regulate movements controlled by extrapyramidal pathways, which are involved in the coordination and modulation of involuntary movements.

17
Q

Excitatory neurotransmitters (e.g. glutamate): What activity do these have on post-synaptic cells?

A

Excites, increases activity, promote action potentials

18
Q

Inhibitory neurotransmitters (e.g. GABA): What activity do these have on post-synaptic cells?

A

Inhibit and reduce activity, suppress action potentials

19
Q

How do neurons communicate with each other at synapses?

A

Neurons communicate by releasing neurotransmitters from the tips of axons, which then bind to receptors on the post-synaptic cell.

20
Q

What are the main pathways in the basal ganglia?

A

Two pathways: Direct (GO) pathway and Indirect (NOGO) pathway.

Direct pathway facilitates movement; indirect pathway suppresses unwanted movements.

Both pathways help achieve smooth, coordinated movement.

21
Q

What is the role of the striatum in the basal ganglia?

A

The striatum (caudate + putamen) is the main input center for the basal ganglia.

Sends outputs to internal pallidum (GPi) and substantia nigra pars reticulata (SNr).

22
Q

What is the function of the direct pathway in the basal ganglia?

A

Acts as an accelerator to initiate and promote movement.

Disinhibits thalamic neurons, increasing thalamocortical activity.

All connections in this pathway are GABAergic (inhibitory).

23
Q

What is the function of the indirect pathway in the basal ganglia?

A

Acts as a brake to suppress unwanted movements.

Inhibits thalamocortical neurons, reducing activity in motor plans.

Subthalamic nucleus (STN) projection is excitatory (glutamatergic); others are inhibitory.

24
Q

How does the substantia nigra pars compacta (SNc) influence the direct pathway?

A

SNc releases dopamine, exciting D1-receptor neurons in the striatum.

Facilitates wanted motor actions by promoting disinhibition of thalamocortical neurons.

SNc modulation of the direct pathway helps initiate movement.

25
Q

How does the SNc influence the indirect pathway?

A

SNc dopamine release inhibits cholinergic interneurons (D2 receptors) in the striatum.

Reduces tonic inhibition on the thalamus, allowing movement initiation.

Balances indirect pathway to control unwanted movement suppression.

26
Q

What is the overall role of the SNc in motor function?

A

SNc maintains balance between direct and indirect pathways.

Facilitates motor control by modulating cortical inputs.

Reduces inhibition on thalamo-cortical neurons, allowing smooth movement.

27
Q

Do the direct and indirect pathways have the same or different effects on thalamo-cortical neurons?

A

Both pathways lead to the same effect of reducing inhibition of the thalamo-cortical neurons, despite their different synaptic actions.

28
Q

What are hyperkinetic disorders of the basal ganglia?

A

Characterized by excessive involuntary movement (dyskinesia).

Example: Huntington’s disease (degeneration of the striatum).

Associated with reduced activity in the indirect pathway.

29
Q

What are common symptoms of hyperkinetic dysarthria?

A

Involuntary movements may superimpose on voluntary speech, affecting clarity.

Vocal quality can be harsh, strained, or strangled, with voice stoppages.

Common symptom: hypernasality.

Severity ranges from mild intelligibility issues to complete speech disruption.

30
Q

What are hypokinetic disorders of the basal ganglia?

A

Characterized by reduced voluntary movement (bradykinesia or hypokinesia).

Example: Parkinson’s disease (degeneration of SNc).

Reduced direct pathway activity, increased indirect pathway activity.

Symptoms include stooped posture, rigidity, shuffling steps, mask-like face, and tremors.

31
Q

What is Parkinson’s and what are some clinical unmet needs

A

Parkinsons: degeneration of nigro-striatal dopaminergic neurons

Unmet needs: psychosis, neurodegeneration, cognitive impairment, depression, anxiety, motor fluctuation, dyskinesia

32
Q

What are the speech characteristics of hypokinetic dysarthria in Parkinson’s disease?

A

Cause: Lesions in the substantia nigra; sometimes from medications or head trauma.
Phonation: Hoarseness, low volume, affecting clarity.
Resonance: Possible hypernasality.
Prosody: Monopitch, monoloudness, and palilalia (syllable repetition).
Articulation: Bradykinesia leads to slow, imprecise, and festinating (short, fast) speech.