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

Lecture 11 - Somatic Motor System: Subcortical Systems Flashcards

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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
Describe the direct pathway of the basal ganglia.
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
26
Describe the indirect pathway of the basal ganglia.
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
27
Describe what happens in the basal ganglia pathways in Parkinson's disease.
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**
28
What are D1 and D2? Describe how they work.
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
29
What are the 4 symtoms of Parkinson's?
1. Hypokinesia/Akinesia 2. Rigidity 3. Tremor 4. Bradykinesia
30
What is ataxia? What is it due to?
Loss of coordination Cerebellum damage
31
Treatment for Parkinson's? Potential side effect?
L-dopa to increase dopamine levels Side effects: unintended overproduction of norepi/epi
32
Describe what happens in the basal ganglia pathways in Huntington's disease.
**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
What is bradykinesia?
Slow movements
34
What is the rigidity symptom due to in Parkinson's?
UMN damage ⇒ increased muscle tone
35
Which cells of the substantia nigra synthesize dopamine?
Pars compacta cells
36
What are the 2 subtypes of Parkinson's disease?
1. Tremor dominant 2. Non-tremor dominant
37
When are tremors seen in tremor dominant Parkinson's disease?
* At rest * During postural holding * During intentional movements
38
Which subtype of Parkinson's patients respond well to L-dopa treatment?
Non-tremor dominant
39
Is the cognitive performance of patients better in tremor dominant or non-termor dominant Parkinson's patients?
Tremor dominant
40
Which Parkinson's subtype includes the dementia symptom?
Non-tremor dominant
41
Describe the tremor progression and characteristics in tremor dominant Parkinson's disease.
Distinct temporal progression compared to other common symptoms Tremors appear on contralateral side
42
Which Parkinson's subtype is a marker of "begnin Parkinson's"? What does this mean?
Tremor dominant Milder cell loss in substantia nigra pars compacta aka less dopamine loss
43
What are the 3 symptoms in non-tremor dominant Parkinson's disease? Where can they be confined?
Triad: resting tremor, dyskinesia, and muscular rigidity May be dominant in extremities, postural muscles, or on one side of the body
44
What other type of cells are lost in tremor dominant Parkinson's disease?
Cell loss in retrorubral midbrain
45
What is another name for the retrorubral midbrain?
Red nucleus
46
What % of dopaminergic cells are pars compacta cells?
76%
47
What % of dopaminergic cells are red nucleus cells?
10%
48
How are serotonin levels impacted in tremor dominant Parkinson's disease?
Low serotonin levels
49
Standard state of the thalamus: activated or inhibited?
Inhibited
50
How is Huntington's disease passed on?
Autosomal dominant
51
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?
100%, meaning that everyone who has the gene/allele for the phenotype actually shows it 50% chance of kids having it
52
Describe the genetic basis of Huntington's disease.
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
What are the 2 types of symptoms of Huntington's disease?
* Choreiform movements = unintentional purposeless rapid flicking movements * Dementia, personality changes, and cognitive impairments
54
What is the treatment for Huntington's disease? How does it work?
**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
How can Huntington's be diagnosed post-mortem?
Post mortem autopsy shows destruction of striatum
56
How can Parkinson's be diagnosed post-mortem?
Post-mortem autopsy shows loss of pigmentation in substantia nigra
57
What is the black pigmentation of the substantia nigra due to?
Neuromelanin
58
What % of the neurons in the brain does the cerebellum contain? What % of the brain volume does it comprise?
50% of neurons 10% of brain volume
59
Describe the descending input to the cerebellum.
Contralateral sensory and motor information from the cortex via the pons
60
Describe the ascending input to the cerebellum.
Ipsilateral sensory input from the medulla and spinal cord
61
What is the target of the cerebellum's output?
Thalamus
62
What are the 2 components of the cerebellum? Which one is the outermost layer? For each: * Input or output function? * From or to where?
* 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
Label that shit aka the cerebellum
64
Describe the corticopontocerebellar pathway: * Pathway from cerebral cortex to cerebellar cortex * Pathway from deep cerebellar nuclei to thalamus
* 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
What does damage to the cerebellum cause? 6 things
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
What is apraxia? What is it due to?
Inability to execute skilled movement on cue Due to SMA or PMA damage
67
What is dysdiadochokinesia?
Diffilculty performaing rapidly alternating movements
68
What are the 2 types of dysmetria?
1. Hypermetria (overshoot) 2. Hypometria (undershoot)
69
What are the effects of alcohol on the cerebellum?
* 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
What is fetal alcohol syndrome?
Maternal consumption of alcohol inhibits BDNF release and cell growth in the fetus­ resulting in cognitive deficits in fetus
71
What part of the brain is dynsfunctional in Wernicke’s encephalopathy and Korsakoff psychosis syndrome?
Cerebellum
72
How do alcoholic and WKS brains look like on an MRI? What is this indicative of?
Enlarged ventricles Indicative of damage to the deep structures of the brain
73
What deficiency does alcoholism cause? Which cells are most sensitive to this?
Alcoholism causes a VB1 (thiamine) deficiency Cerebellar granular cells are the most sensitive to this deficiency
74
Globus pallidus externus target(s)? Type of signal?
Subthalamic nucleus Inhibitory
75
What is dyskinesia? What is this a symptom for?
Abnormal or impaired voluntary movement seen in non-tremor dependent Parkinson's disease patients

SMP - Neurophysio Exam 1 (13 decks)

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