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Block 5; Week 3 > Basal Ganglia > Flashcards

Basal Ganglia Flashcards

1
Q

How does the basal ganglia communicate with the LMN? Is this ipsilateral or contralateral?

A

communicates w/ LMN via the cortex. Then those UMN end up communicating with the LMN.
This is contralateral.

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2
Q

How does the cerebellum communicate with LMNs-ipsilaterally or contra laterally?

A

ipsilaterally

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3
Q

Which structures make up the striatum?

A

the caudate & putamen

  • *this is the receiving zone
  • *both of these parts have similar inputs & outputs, give output to GP
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4
Q

Which structures make up the lenticular nucleus?

A

the putamen & globus pallidus

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5
Q

What makes up the efferent zone of the basal ganglia?

A

globus pallidus

substantia nigra

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6
Q

Which part of the substantia nigra is a part of the basal ganglia?

A

the pars reticulata-this is the outer portion

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7
Q

What are some other structures that are a part of the basal ganglia that we haven’t talked about yet?

A

the sub thalamic nucleus

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8
Q

Describe the loop of the basal ganglia communicating with the outside world.

A

Basal Ganglia–Thalamus-Cortex–>Basal Ganglia

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9
Q

Where do you find the substantia nigra?

A

you find it in the midbrain sitting right above the cerebral peduncles

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10
Q

Which part of the internal capsule are you looking at when you see the thalamus & the lenticulate nucleus?

A

you are looking at the posterior limb

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11
Q

What are the 2 parts of the substantia nigra?

A

compacta (internal part)
reticulata (external part)
**one deals with input & one with output

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12
Q

Is the subthalamic nucleus located rostrally or caudally in relation to the substantia nigra?

A

it is located rostrally

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13
Q

What composes the basal ganglia proper?

A

caudate
putamen
globus pallidus

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14
Q

T/F Caudate and putamen are the receiving zone of the BG, are functionally similar in terms of their afferents, but they receive slightly different efferents.

A

False. They are similar in their efferents, but vary in their afferents.

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15
Q

The striatum is called the receiving zone. Where does it receive information from?

A

all areas of the cortex except: primary visual & auditory areas.
**this is made anatomically possible b/c the caudate is everywhere!!

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16
Q

The striatum gets dopaminergic input from a part of the substantia nigra. Which part?

A

it gets input from the compacta (internal) part.

**Note the reticulata part is a part of the basal ganglia’s efferent division.

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17
Q

The caudate follows the course of which structure?

A

the lateral ventricles

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18
Q

Describe the direct pathway in detail.

A

The cortex stimulates a neuron in the striatum. The nerve in the striatum inhibits the nerve in the GPinternal. the nerve in the GP internal inhibits the nerve in the VA/VL motor thalamus. The nerve in the thalamus is then free to activate the motor cortex. The motor cortex sends down commands via the corticospinal trunk. The CST decussates @ the pyramids. It turns into the lateral corticospinal tract & synapses w/ LMN eventually. The LMN stimulates muscles.

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19
Q 
What type of a neuron are the following:
Neuron from Cortex-->Striatum
Neuron from Striatum-->GPint
Neuron from GPint-->VA/VL motor thalamus
Neuron from VA/VL-->Motor Cortex
A

Neuron from Cortex–>Striatum: excitatory by nature
Neuron from Striatum–>GPint: inhibitory by nature–gabanergic.
Neuron from GPint–>VA/VL motor thalamus: inhibitory by nature–>gabanergic.
Neuron from VA/VL–>Motor Cortex: excitatory by nature.

20
Q

What are 2 names for the special structure that the neuron passes thru to get from GPint to VA/VL?

A

the lenticular fasciculus or ansa lenticularis

21
Q

What is the end result of the direct pathway of the basal ganglia?

A

it increases the transmission from VA/VL to the motor cortex. Therefore, it increase motor activity. : )

22
Q

If you have too much activity of the direct pathway…what happens?

A

you get a hyperkinetic syndrome

23
Q

Which of the following lesions of the basal ganglia would increase motor activity via the direct pathway?
A lesion to the GP internal
A lesion to the VA/VL motor thalamus

A

The lesion to the GP internal would increase motor activity. It would destroy the cell body of the inhibitory neuron of the thalamus.
The lesion to the VA/VL would actually destroy the cell body of the neuron that activates the motor cortex. Therefore, it would turn down motor activity.

24
Q

Describe in detail the indirect pathway of the basal ganglia.

A

The cortex sends an excitatory neuron to the striatum. This activates the next neuron, which is inhibitory, and goes to the GP external. This inhibits the next neuron, which is inhibitory, and ends up at the sub thalamic nucleus. This activates the next neuron, which is excitatory, and goes to the GP internal. This activates the next neuron, which is inhibitory, and goes to the VA/VL motor thalamus. This inhibits the next neuron, which is excitatory, and goes to the motor cortex. Less activation of the next neuron which descends via the corticospinal trunk & decussates @ the pyramids. Then it continues descending via the lateral corticospinal tract. It synapses w/ a LMN (activating it) & stimulating muscles.

25
Q

What is the overall effect of the indirect pathway of the basal ganglia?

A

it decreases the activity of the neuron from the VA/VL motor thalamus–>motor cortex. Thus, there is less motor activity.

26
Q

The neuron from the cortex that activates the neuron in the striatum goes thru which structure on its journey?

A

corticostriate

27
Q

Describe in detail the indirect & direct pathways in relation to the substantia nigra.

A

Cortex–> Striatum (+)
Substantia Nigra–>Direct Path (+)
Substantia Nigra–>Indirect Path (-)
direct: striatum–>GPint (-)
indirect striatum–>GPext (+ but less so)
Subthalamic Nucleus: GPext–>SN (- but stimulates b/c itself inhibited)
SN–>GPint (+)
So, now…the direct pathway is trying to inhibit the next neuron in the GPi & the indirect pathway is trying to stimulate the next neuron in the GPi. But since the substantia nigra activates the direct & inhibited the indirect…the direct wins!
Inhibition of inhibitory neuron to VA/VL.
More stimulation allowed of VA/Vl.
More communication to Motor Cortex. Then descends w/ CST & then pyramidal decussation & descent w/ LCST. Synapse w/ LMN & activation of muscles.

28
Q

What is the overall effect of the direct & indirect pathways with substantia nigra input?

A

activation of direct pathway.
inactivation of the indirect pathway.
More motor output.

29
Q

Which receptors are there on the neurons of the direct pathway in the striatum that receive the dopaminergic input from the substantia nigra?

A

D1 receptors. They increase cAMP levels in response to Dopamine & are activated.

30
Q

Which receptors are there on the neurons of the indirect pathway in the striatum that receive dopaminergic input from the substantia nigra?

A

D2 receptors. They decrease cAMP levels in response to dopamine & are inhibited.

31
Q

Which part of the substantia nigra gives the dopaminergic input to the basal ganglia that we have been talking about?

A

compacta

32
Q

If you didn’t have the substantia nigra…what would be the result?

A

an increase in the indirect pathway & a decrease in the direct pathway

33
Q

What’s the deal with ACh Striatal component of the basal ganglia?

A

Within the striatum is a neuron that can synapse on neurons of the direct & indirect pathway. It releases ACh. this has an inhibitory effect on the direct pathway & an excitatory effect on the indirect pathway. The motor activity, therefore, increases.

34
Q

What are the 2 categories of disorders of the basal ganglia?

A

hypokinetic & hyperkinetic syndromes

35
Q

What is the classic hypo kinetic syndrome? What are its features?

A 
Parkinson's disease
Tremor at rest
Masked facies
Rigidity (cogwheel)
Retropulsion
Festinating gait
Shuffling gait
Loss of postural reflexes
Depression, anxiety and dementia
36
Q

What causes Parkinson’s?

A

well…you lose dopamine projecting cells from the substantia nigra to the striatum.
you get less activation of the direct pathway & less inhibition of the indirect pathway
thus, you get a hypo kinetic deal.
the small ACh cells become dominant.

37
Q

What happens if you lose D2 receptors?

A

Then you get less inhibition of the indirect pathway
The indirect pathway is enhanced.
Then, you get less motor activity.

38
Q

What are 2 examples of hyperkinetic syndromes?

A

Huntington’s Chorea

Hemiballismus

39
Q

What is hemiballismus/hemiballism?

A

this is caused by a lesion to or destruction of the sub thalamic nucleus…
this takes out the indirect pathway–get more movement.
causes wild, flinging movements of the body (usu extremities)

40
Q

What is the potential problem of treating Parkinson’s with L-DOPA?

A

Well, it is the right thing to treat it with dopamine.

But sometimes super sensitivity can result.

41
Q

What should you treat Huntington’s disease with?

A

ACh

42
Q

When does Huntington’s disease usu show up?

A

4th or 5th decade

43
Q

Describe what happens in Huntington’s disease, including the progression.

A

Starts w/ a movement disorder (usu in the extremities, a rapid, jerky dance-like movement)
Leads to dementia
Leads to death

44
Q

What causes Huntington’s disease in terms of the basal ganglia?

A

loss of striatal cells
less activation of the indirect pathway–>movement goes up.
With progression of the disease, also less inhibition of the direct pathway–>movement goes up.
Hyperkinetic movement disorder.

45
Q

Describe the characteristics of a lower motor neuron syndrome.

A

paralysis
muscle atrophy
areflexia & atonia
ipsi deficit in the spinal cord

46
Q

Describe the characteristics of an upper motor neuron syndrome.

A

paresis (weakness)
no atrophy
hyper-reflexia, hypertonia, spasticity
contra deficit above decussation, ipsi deficit below decussation

47
Q

Describe the characteristics of the basal ganglia.

A 
no paralysis
no atrophy
Parkinsons: rigidity, resting tremor
Huntington's: chorea, hyperkinesia
contra deficits

Block 5; Week 3 (9 decks)

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