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SMP - Neurophysio Exam 1 > Lecture 11 - Somatic Motor System: Subcortical Systems > Flashcards

Lecture 11 - Somatic Motor System: Subcortical Systems Flashcards

1
Q

What are subcortical motor systems? Name the 3.

A

Motor systems below the motor cortex in the brain:

  • Basal ganglia
  • Pons
  • Cerebellum
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2
Q

How does the motor cortex interact with subcortical motor systems? What is the purpose of this?

A

There are reciprocal connections between the 2 creating feedback loops

Purpose: to modify the activity in the motor cortex to regulate initiation of movement or refine it

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3
Q

Describe the pathway from the basal ganglia to the motor cortex.

A

Through the the ventral lateral pars oralis of the thalamus

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4
Q

Describe the pathway from the pons and cerebellum to the motor cortex.

A

Through the the ventral lateral pars caudalis of the thalamus

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5
Q

What is the main purpose of the feedback of the basal ganglia on the motor cortex?

A

Inhibit unwanted movement

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6
Q

List the 5 structures of the basal ganglia.

A
  1. Caudate nucleus 2. Putamen 3. Globus pallidus 4. Subthalamic nucleus 5. Substantia nigra
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7
Q

What does the striatum of the basal ganglia contain?

A
  1. Caudate nucleus 2. Putamen
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8
Q

Label the basal ganglia.

A
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9
Q

Cortex to striatum of basal ganglia: excitatory or inhibitory?

A

Excitatory

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10
Q

What are the 2 parts of the globus pallidus?

A
  1. Internus
  2. Externus
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11
Q

Striatum to globus pallidus internus AND externus: excitatory or inhibitory?

A

Inhibitory

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12
Q

Globus pallidus externus of basal ganglia on subthalamic nucleus: excitatory or inhibitory?

A

Inhibitory

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13
Q

Globus pallidus internus of basal ganglia on thalamus: excitatory or inhibitory?

A

Inhibitory

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14
Q

Subthalamic nucleus of basal ganglia on globus pallidus internus: excitatory or inhibitory?

A

Excitatory

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15
Q

Subthalamic nucleus of basal ganglia on substantia nigra excitatory or inhibitory?

A

Excitatory

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16
Q

Substantia nigra of basal ganglia on thalamus: excitatory or inhibitory?

A

Inhibitory

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17
Q

Thalamus on cortex: excitatory or inhibitory?

A

Excitatory

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18
Q

What is the input nucleus of the basal ganglia?

A

Striatum

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19
Q

What is the output nucleus of the basal ganglia?

A

Globus pallidus internus

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20
Q

What 2 inputs does the striatum of the basal ganglia receive?

Type and source

A
  1. Glutamergic input from corticostriatal tract
  2. Dopaminergic from substantia nigra
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21
Q

What output does the globus pallidus internus of the basal ganglia send out?

Type, target, and pathway

A

Gabaergic output to the motor cortex via the ventral lateral pars oralis of the thalamus

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22
Q

What output does the striatum of the basal ganglia send out?

Type and targets?

A

Gabaergic to:

  • Globus pallidus internus
  • Globus pallidus externus
  • Substantia nigra
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23
Q

What are the consequences of the activation of the DIRECT pathway of the basal ganglia?

A

GPi inhibition → Decrease in basal ganglia output → Increase in motor behavior

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24
Q

What are the consequences of the activation of the INDIRECT pathway of the basal ganglia?

A

GPi activation → Increase in basal ganglia output → Decrease in motor behavior

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25
Q

Describe the direct pathway of the basal ganglia.

A

Subthalamic nucleus stimulates substantia nigra → Motor cortex and substantia nigra stimulate striatum → Striatum inhibits GPi → Decreased GPi inhibition of the the ventral lateral pars oralis of the thalamus → Thalamus stimulates motor cortex

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26
Q

Describe the indirect pathway of the basal ganglia.

A

Motor cortex stimulates striatum → Striatum inhibits GPe → Decrease of GPe inhibition of subthalamic nucleus → Subthalamic nucleus stimulates GPi → GPi inhibits ventral lateral pars oralis of the thalamus → Decreased stimulation of motor cortex by thalamus

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27
Q

Describe what happens in the basal ganglia pathways in Parkinson’s disease.

A

Damage to dopaminergic cells of the substantia nigra:

  • Substantia nigra cannot activate the direct pathway through dopamine D1 receptors to cause increased motor activity (PRIMARILY)
  • Substantia nigra cannot inhibit the indirect pathway through dopamine D2 receptors

RESULT: decreased voluntary muscle movements

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28
Q

What are D1 and D2? Describe how they work.

A

2 dopamine receptor subtypes on the striatum:

  • D1 + dopamine = stratium stimulation to inhibit GPi MORE = more muscle movements
  • D2 + dopamine = striatum inhibition = stratium stimulation to inhibit GPe = less muscle movements
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29
Q

What are the 4 symtoms of Parkinson’s?

A
  1. Hypokinesia/Akinesia
  2. Rigidity
  3. Tremor
  4. Bradykinesia
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30
Q

What is ataxia?

What is it due to?

A

Loss of coordination

Cerebellum damage

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31
Q

Treatment for Parkinson’s? Potential side effect?

A

L-dopa to increase dopamine levels

Side effects: unintended overproduction of norepi/epi

32
Q

Describe what happens in the basal ganglia pathways in Huntington’s disease.

A

Morphological change in striatum: loss of D2 receptors:

  • Substantia nigra cannot stimulate the striatum to inhibiting GPe, so GPe is active leading to failure of the indirect pathway

RESULT: increased involuntary muscle movements: hyperkinesia

33
Q

What is bradykinesia?

A

Slow movements

34
Q

What is the rigidity symptom due to in Parkinson’s?

A

UMN damage ⇒ increased muscle tone

35
Q

Which cells of the substantia nigra synthesize dopamine?

A

Pars compacta cells

36
Q

What are the 2 subtypes of Parkinson’s disease?

A
  1. Tremor dominant
  2. Non-tremor dominant
37
Q

When are tremors seen in tremor dominant Parkinson’s disease?

A
  • At rest
  • During postural holding
  • During intentional movements
38
Q

Which subtype of Parkinson’s patients respond well to L-dopa treatment?

A

Non-tremor dominant

39
Q

Is the cognitive performance of patients better in tremor dominant or non-termor dominant Parkinson’s patients?

A

Tremor dominant

40
Q

Which Parkinson’s subtype includes the dementia symptom?

A

Non-tremor dominant

41
Q

Describe the tremor progression and characteristics in tremor dominant Parkinson’s disease.

A

Distinct temporal progression compared to other common symptoms

Tremors appear on contralateral side

42
Q

Which Parkinson’s subtype is a marker of “begnin Parkinson’s”? What does this mean?

A

Tremor dominant

Milder cell loss in substantia nigra pars compacta aka less dopamine loss

43
Q

What are the 3 symptoms in non-tremor dominant Parkinson’s disease? Where can they be confined?

A

Triad: resting tremor, dyskinesia, and muscular rigidity

May be dominant in extremities, postural muscles, or on one side of the body

44
Q

What other type of cells are lost in tremor dominant Parkinson’s disease?

A

Cell loss in retrorubral midbrain

45
Q

What is another name for the retrorubral midbrain?

A

Red nucleus

46
Q

What % of dopaminergic cells are pars compacta cells?

47
Q

What % of dopaminergic cells are red nucleus cells?

48
Q

How are serotonin levels impacted in tremor dominant Parkinson’s disease?

A

Low serotonin levels

49
Q

Standard state of the thalamus: activated or inhibited?

50
Q

How is Huntington’s disease passed on?

A

Autosomal dominant

51
Q

What is the penetrance of Huntington’s disease? What does this mean?

So if you have one affected and one non-affected parent, what are the chances of the kids having it?

A

100%, meaning that everyone who has the gene/allele for the phenotype actually shows it

50% chance of kids having it

52
Q

Describe the genetic basis of Huntington’s disease.

A

Huntington gene (HTT) with expanded CAG repeats

Codes for huntingtin protein (Htt)

Mutated protein is toxic in neurons and affects D2 receptors in striatum first

  • Increased number of CAG repeats = low age of onset
  • Number of CAG repeats increase with generations
53
Q

What are the 2 types of symptoms of Huntington’s disease?

A
  • Choreiform movements = unintentional purposeless rapid flicking movements
  • Dementia, personality changes, and cognitive impairments
54
Q

What is the treatment for Huntington’s disease? How does it work?

A

VMAT inhibitors

Inhibiting VMAT inhibits packaging of biogenic amines (aka dopamine) in NT vesicles → less dopamine released by substantia negra → less dopamine binding to D1 receptors → less movements through the direct pathway (since we don’t have a viable indirect pathway, we can’t control movements so best to just calm the direct pathway)

55
Q

How can Huntington’s be diagnosed post-mortem?

A

Post mortem autopsy shows destruction of striatum

56
Q

How can Parkinson’s be diagnosed post-mortem?

A

Post-mortem autopsy shows loss of pigmentation in substantia nigra

57
Q

What is the black pigmentation of the substantia nigra due to?

A

Neuromelanin

58
Q

What % of the neurons in the brain does the cerebellum contain? What % of the brain volume does it comprise?

A

50% of neurons

10% of brain volume

59
Q

Describe the descending input to the cerebellum.

A

Contralateral sensory and motor information from the cortex via the pons

60
Q

Describe the ascending input to the cerebellum.

A

Ipsilateral sensory input from the medulla and spinal cord

61
Q

What is the target of the cerebellum’s output?

62
Q

What are the 2 components of the cerebellum? Which one is the outermost layer?

For each:

  • Input or output function?
  • From or to where?
A
  • Cerebellar cortex (outermost layer)
    • Input from:
      • Motor cortex via pons
      • Inferior olive of medulla
      • Spinal cord
      • Vestibular nucleus
  • Deep cerebellar nuclei
    • Output to contralateral motor cortex via ventral lateral pars caudalis of the thalamus
63
Q

Label that shit aka the cerebellum

64
Q

Describe the corticopontocerebellar pathway:

  • Pathway from cerebral cortex to cerebellar cortex
  • Pathway from deep cerebellar nuclei to thalamus
A
  • Pathway from cerebral cortex to cerebellar cortex:
    • Frontal/parietal cortex → pons → middle cerebellar peduncle (at midline) → cerebellar cortex
  • Pathway from deep cerebellar nuclei to thalamus
    • Deep cerebellar nuclei → superior cerebellar peduncle → (crossing midline) → ventral lateral pars caudalis of thalamus → M1 and PMA
65
Q

What does damage to the cerebellum cause? 6 things

A
  1. Ataxia on ipsilateral side of body
  2. Decomposition of multi-joint movements (aka robot like movement)
  3. Dysmetria
  4. Unintentional tremor
  5. Dysdiadochokinesia
  6. Impaired motor learning
66
Q

What is apraxia? What is it due to?

A

Inability to execute skilled movement on cue

Due to SMA or PMA damage

67
Q

What is dysdiadochokinesia?

A

Diffilculty performaing rapidly alternating movements

68
Q

What are the 2 types of dysmetria?

A
  1. Hypermetria (overshoot)
  2. Hypometria (undershoot)
69
Q

What are the effects of alcohol on the cerebellum?

A
  • Increases GABA signaling
  • Inhibits NMDA receptor activity
    • Inhibits BDNF release (brain derived neurotrophic factor), which stimulates cell growth
    • Stimulates caspase activity which stimulates apoptosis
70
Q

What is fetal alcohol syndrome?

A

Maternal consumption of alcohol inhibits BDNF release and cell growth in the fetus­ resulting in cognitive deficits in fetus

71
Q

What part of the brain is dynsfunctional in Wernicke’s encephalopathy and Korsakoff psychosis syndrome?

A

Cerebellum

72
Q

How do alcoholic and WKS brains look like on an MRI? What is this indicative of?

A

Enlarged ventricles

Indicative of damage to the deep structures of the brain

73
Q

What deficiency does alcoholism cause? Which cells are most sensitive to this?

A

Alcoholism causes a VB1 (thiamine) deficiency

Cerebellar granular cells are the most sensitive to this deficiency

74
Q

Globus pallidus externus target(s)? Type of signal?

A

Subthalamic nucleus

Inhibitory

75
Q

What is dyskinesia? What is this a symptom for?

A

Abnormal or impaired voluntary movement seen in non-tremor dependent Parkinson’s disease patients

SMP - Neurophysio Exam 1 (13 decks)

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