Anatomy-Basal Ganglia Flashcards

1
Q

Main components of the basal ganglia

A

Caudate, Putamen, Globus Pallidus, Subthalamic nucleus, Substantia Nigra

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2
Q

Lentiform nucleus

A

Putamen + Globus Pallidus

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3
Q

Corpus striatum

A

Caudate + Putamen + Globus Pallidus

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4
Q

Striatum

A

Caudate + Putamen

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5
Q

What CNS structure does the basal ganglia receive in put from and where does its output go to? What about the cerebellum?

A

Basal Ganglia: input from prefrontal cortex, output to thalamus and on to supplemental motor area. Cerebellum: input from prefrontal cortex, output to thalamus and on to lateral premotor area.

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6
Q

What is the role of the basal ganglia in movement?

A

Initiating and terminating movements. Regulating the amount of movement executed.

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7
Q

What is the role of the cerebellum in movement?

A

To compare the intended movement with the executed movement.

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8
Q

Which nuclei are the input and output nuclei of the basal ganglia? What nuclei are intrinsic to the basal ganglia?

A

Input: Striatum (caudate/putamen). Output: Medial pallidial segment & Substantia Nigra Pars Reticulata. Intrinsic: lateral pallidial segment and subthalamic nuclei only communicate with other basal ganglia.

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9
Q

What other symptoms do you see in patients with problems with their basal ganglia?

A

Motor dysfunction, oculomotor dysfunction, dementia, personality changes. This is because the oculomotor, prefrontal and limbic loops all run through the same basal ganglia pathway as the motor loop does.

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10
Q

Name 4 main inputs to the basal ganglia.

A

Cerebral cortex (glutamate), Substantia Nigra Pars Compacta (Dopamine), Centromedian nucleus (glutamate), Raphe nuclei (Serotonin)

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11
Q

Efferent fibers of the striatum

A

Spiny neurons. Axons leave the striatum and communicate with other nuclei of the basal ganglia. There are 2 types: neurons that produce GABA/Substance P and others that produce GABA/Enkephalin

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12
Q

Interneurons of the striatum

A

Aspiny neurons. They are completely confined to the striatum and modulate spiny neurons with different neurotransmitters, ACh being the most clinically important.

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13
Q

What are the excitatory and inhibitory connections in the basal ganglia?

A

Direct pathway is inhibitory. Indirect pathway: Excitatory

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14
Q

How does the direct pathway modify thalamus activity?

A

Cerebral cortex releases glutamate on striatum -> GABA/Substance P neurons activated -> GABA released on output nuclei (MPS & SNr) -> output nuclei activity reduced -> thalamus excitation -> glutamate activation of supplemental motor area -> facilitation of movement

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15
Q

How does the indirect pathway modify thalamus activity?

A

Cerebral cortex releases glutamate on striatum -> GABA/Enkephalin neurons activated -> inhibition of lateral pallidal segment -> less GABA released on STN -> increased STN activity -> more glutamate released onto output nuclei -> thalamus inhibited -> activity of SMA inhibited -> movement suppressed.

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16
Q

How do the direct pathway and indirect pathway work together?

A

Direct pathway activates the precise motor movement and the indirect pathway inhibits pathways that may interfere

17
Q

What is the overall effect of acetylcholine released by aspiny neurons on the basal ganglia?

A

Favors the indirect pathway. ACh binding to GABA/Substance P spiny neurons in the direct pathway inhibits them. ACh binding to GABA/Enkephalin spiny neurons in the indirect pathway activates them.

18
Q

What is the overall effect of dopamine released by the pars compact on the basal ganglia?

A

Favors the direct pathway. Dopamine binding to GABA/Substance P spiny neuron D1 receptors in the direct pathway activates them. Dopamine binding to D2 receptors on the GABA/Enkephalin spiny neurons and cholinergic aspiny neurons in the indirect pathway inhibits them.

19
Q

Different types of basal ganglia disorders (movement disorders)?

A

Hyperkinetic: more dopamine or less ACh, direct pathway imbalance. Hypokinetic: less dopamine or more ACh, indirect pathway imbalance.

20
Q

What are symptoms characteristic of Parkinson’s disease?

A

Bradykinesia, rigidity, resting tremor, postural/gate instability. Loss of dopaminergic neurons in the substantia nigra pushes the basal ganglia balance towards hypokinesia. Consequently patients also have a difficult time starting to walk because initiating movements is difficult with depressed basal ganglia function.

21
Q

Mutation in Huntington’s disease

A

CAG repeats that cause degeneration of the GABA/Enkephalin neurons in the striatum.

22
Q

Why do patients with Huntington’s disease develop chorea? What other symptoms do they present with?

A

Degeneration of the GABA/Enkephalin neurons pushes the basal ganglia towards hyperkinesia. They also present with hypotonia, psychiatric symptoms (depression, anxiety, irritability) and dementia.

23
Q

How do you treat Parkinson symptoms?

A

Supplement dopamine or stimulate the output nuclei

24
Q

How do you treat Huntington symptoms?

A

Dopamine depletion

25
Q

How does a vascular lesion in the subthalamic nucleus affect the basal ganglia?

A

Hemiballism. This pushes the basal ganglia towards hyperkinesia, this condition is especially associated with ballismus (flailing movements).