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Neuro Block 4 > Motor Systems 4 Basal Ganglia - Ebner > Flashcards

Motor Systems 4 Basal Ganglia - Ebner Flashcards

1
Q

A female in her early thirties has begun developing uncontrolled voluntary movements. It seems to be getting worse. She is adopted so you do’t have ny a family history.
Her partner is especially worried about her loss of mental function.
What might be the diagnosis?

A

Maybe could be mutliple things, but sounds a lot like Huntington’s

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2
Q

What are the 4 parts of the basal ganglia?

A

Neostriatum
Globus Pallidus
Substantia Nigra
Subthalamic Nucleus

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3
Q

Neostriatum consists of what two structures?

A

Caudate and putamen

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4
Q

What are the primary output neurons of the neostriatum?

they also receive inputs FYI

A

Spiny neurons

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5
Q

What neurotransmitters do spiny neurons use?

A

Mostly GABA
1 group is GABA and Substance P
1 group is GABA and Enkephalin

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6
Q

Describe the afferent projection to the striatum:

A

Corticostriate projection - Cortex to striatum

Originates in many areas - ex Premotor and Motor
Excitatory and Glutamate

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7
Q

Describe the striatum’s direct pathway:

A

Striatum GABA/SP project to inhibit GPi
GPi projects to inhibit VL and VA of thalamus

Striatum GABA/SP also project to inhibit SNr
SNr also inhibits VA/VL of thalamus and brainstem

Thalamus (VA/VL) activates cortex
Brainstem (superior colliculus for eye movements and pedunculopontine nuclei for locomotion)

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8
Q

What is the indirect pathway of the striatum?

A

Striatum GABA/ENK cells inhibit the GPe
GPe inhibits STh (with GABA)
STh excites GPi and SNr (with glutamate)

(Like before, GPi and SNr go on to inhibit the thalamus)

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9
Q

What is the hyperdirect pathway?

A

Pathway that uses glutamate, the cortex directly activates the STh (subthalamic nucleus)

Briefly mentioned in class….

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10
Q

Describe the Substantia Nigra Pars Compacta pathway? (SNc)

A

So the SNc uses dopamine to both stimulate and inhibit depending on the target’s receptors

It activates the GABA/SP neurons of the Striatum through D1 receptos.
It inhibits the GABA/ENK neurons of the Striatum via D2 receptors

GABA/SP neurons go on to inhibit the SNc and GPi/SNr
GABA/ENK neurons go on to inhibit the GPe in the indirect pathway

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11
Q

So what part of the basal ganglia is sort of tonically keeping motor movement from happening?

What has to happen to make motor movement occur?

A

GPi is inhibiting the thalamus and motor activity

GPi must be inhibited for motor to happen

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12
Q

Use eye movement to show what happens in the basal ganglia to make movement happen:

A

Caudate receives excitatory signal from frontal eye fields
Direct and indirect pathways decrease SNr activity
Thalamus is activated and disinhibits superior colliculus
Saccades produced!

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13
Q

How would a crazy increase of Dopamine affect the basal ganglia?

A

DA will decrease GABA/ENK activity, so GPe stays active. GPe inhibits STh so that it cannot excite GPi/SNr at all

GABA/SP cells are activated and directly inhibit GPi and SNr a lot.

GPi/SNr is now out of the picture, causing the thalamus to stimulate cortex motor activity A LOT!
Lots of involuntary motor movements.

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14
Q

What’s a great way to get full of dopamine activity?

A

Cocaine or meth

I mean, that’s not great, but that’s what happens

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15
Q

What will result from a Subthalamic nucleus lesion?

Why?

A

Ballismus!
Wild exaggerated limb movements

Getting rid of STH is going to decrease major stimulus to GPi/SNr
Thalamus and cortex hyperactive

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16
Q

What kind of problem creates Parkinson’s disease?

A

Main pathology behind disease is loss of pigmented cells in substantia nigra pars compacta (SNc).

SNc can’t inhibit GABA/ENK, so they inhibit GPe, which sets STh free to activate GPi/SNr

SNc can’t excite GABA/SP cells to inhibit GPi/Snr

SO. Thalamus stays inactivated so movements are very slow

17
Q

4 main clinical findings of Parkinson’s?

A

Bradykinesia (slow movement and reflex)
Rigidity
Resting tremor
Postural Instability

18
Q

Treatment for Parkinson’s?

A

Restore dopamine using L-dopa

dopamine can’t pass BBB

19
Q

What happens if you get a lesion in your globus pallidus?
Symptoms?
Why?

A

Dystonia: sustained twisting and repetitive muscle contractions
Caused by an increase in motor activity because the GPi can no longer inhibit thalamus activity

20
Q

What will striatal lesions in the two different regions cause?

A
  1. Putamen
    - Associated with motor cortical areas
    - Get stereotypic motor hyperactivity
  2. Caudate
    - related to prefrontal cortex/premotor /SMA
    - Changes in more “complex behavior”
    * Vulgarity
    * Increased appetite/polydipsia
    * Hypersexuality
21
Q

What is the pathology of Huntington’s Disease?

Including genetics.

A

Genetic:

  • Abnormal short arm of Chromosome 4
  • CGA repeat creates gain of function
  • Onset 25-40 yrs old

Path:

  • Death of spiny neurons in Striatum
  • Especially GABA/ENK
  • Death of full Striatum and cortex follows
22
Q

Symptoms of Huntington’s Disease?

A

Involuntary movements as indirect pathway affected
Chorea - brief, repetitive, jerky, uncontrolled movements
Athetosis - slow, involuntary, convoluted, writhing

Dementia and personality changes

Akinesia as direct pathway is affected
- loss of voluntary movement

23
Q

Describe the striatum’s direct pathway:

A

Striatum GABA/SP project to inhibit GPi
GPi projects to inhibit VL and VA of thalamus

Striatum GABA/SP also project to inhibit SNr
SNr also inhibits VA/VL of thalamus and brainstem

Thalamus (VA/VL) activates cortex
Brainstem (superior colliculus for eye movements and pedunculopontine nuclei for locomotion)

24
Q

What is the indirect pathway of the striatum?

A

Striatum GABA/ENK cells inhibit the GPe
GPe inhibits STh (with GABA)
STh excites GPi and SNr (with glutamate)

(Like before, GPi and SNr go on to inhibit the thalamus)

25
Q

What is the hyperdirect pathway?

A

Pathway that uses glutamate, the cortex directly activates the STh (subthalamic nucleus)

Briefly mentioned in class….

26
Q

Describe the Substantia Nigra Pars Compacta pathway? (SNc)

A

So the SNc uses dopamine to both stimulate and inhibit depending on the target’s receptors

It activates the GABA/SP neurons of the Striatum through D1 receptos.
It inhibits the GABA/ENK neurons of the Striatum via D2 receptors

GABA/SP neurons go on to inhibit the SNc and GPi/SNr
GABA/ENK neurons go on to inhibit the GPe in the indirect pathway

27
Q

So what part of the basal ganglia is sort of tonically keeping motor movement from happening?

What has to happen to make motor movement occur?

A

GPi is inhibiting the thalamus and motor activity

GPi must be inhibited for motor to happen

28
Q

Use eye movement to show what happens in the basal ganglia to make movement happen:

A

Caudate receives excitatory signal from frontal eye fields
Direct and indirect pathways decrease SNr activity
Thalamus is activated and disinhibits superior colliculus
Saccades produced!

29
Q

How would a crazy increase of Dopamine affect the basal ganglia?

A

DA will decrease GABA/ENK activity, so GPe stays active. GPe inhibits STh so that it cannot excite GPi/SNr at all

GABA/SP cells are activated and directly inhibit GPi and SNr a lot.

GPi/SNr is now out of the picture, causing the thalamus to stimulate cortex motor activity A LOT!
Lots of involuntary motor movements.

30
Q

What’s a great way to get full of dopamine activity?

A

Cocaine or meth

I mean, that’s not great, but that’s what happens

31
Q

What will result from a Subthalamic nucleus lesion?

Why?

A

Ballismus!
Wild exaggerated limb movements

Getting rid of STH is going to decrease major stimulus to GPi/SNr
Thalamus and cortex hyperactive

32
Q

What kind of problem creates Parkinson’s disease?

A

Main pathology behind disease is loss of pigmented cells in substantia nigra pars compacta (SNc).

SNc can’t inhibit GABA/ENK, so they inhibit GPe, which sets STh free to activate GPi/SNr

SNc can’t excite GABA/SP cells to inhibit GPi/Snr

SO. Thalamus stays inactivated so movements are very slow

33
Q

4 main clinical findings of Parkinson’s?

A

Bradykinesia (slow movement and reflex)
Rigidity
Resting tremor
Postural Instability

34
Q

Treatment for Parkinson’s?

A

Restore dopamine using L-dopa

dopamine can’t pass BBB

35
Q

What happens if you get a lesion in your globus pallidus?
Symptoms?
Why?

A

Dystonia: sustained twisting and repetitive muscle contractions
Caused by an increase in motor activity because the GPi can no longer inhibit thalamus activity

36
Q

What will striatal lesions in the two different regions cause?

A
  1. Putamen
    - Associated with motor cortical areas
    - Get stereotypic motor hyperactivity
  2. Caudate
    - related to prefrontal cortex/premotor /SMA
    - Changes in more “complex behavior”
    * Vulgarity
    * Increased appetite/polydipsia
    * Hypersexuality
37
Q

What is the pathology of Huntington’s Disease?

Including genetics.

A

Genetic:

  • Abnormal short arm of Chromosome 4
  • CGA repeat creates gain of function
  • Onset 25-40 yrs old

Path:

  • Death of spiny neurons in Striatum
  • Especially GABA/ENK
  • Death of full Striatum and cortex follows
38
Q

Symptoms of Huntington’s Disease?

A

Involuntary movements as indirect pathway affected
Chorea - brief, repetitive, jerky, uncontrolled movements
Athetosis - slow, involuntary, convoluted, writhing

Dementia and personality changes

Akinesia as direct pathway is affected
- loss of voluntary movement

Neuro Block 4 (23 decks)

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