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Unit 9 > Kantak - Basal Gang/Sara Bellum > Flashcards

Kantak - Basal Gang/Sara Bellum Flashcards

1
Q

What are the four parts/functional nuclei of the basal ganglia and what are their respective divisions? Which of these parts makes up the lentiform nucleus? Which of these parts makes up the striatum?

A

Caudate Nucleus
Globus Pallidus (External/Internal)
Substantia Nigra (Pars Reticulata/Compacta)
Subthalamic Nucleus

Lentiform Nucleus = Putamen + Globus Pallidus

Striatum = Caudate Nucleus + Putamen

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2
Q

What are the four roles of the basal ganglia?

A

Action Selection, Cognition, Mood + Vigor, Motor + Non-motor Habit Formation aka, Reward Based Behavior OR the anticipation of reward

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3
Q

Where does the BG receive afferent input from?

A

Cortex, Thalamus, Brain Stem

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4
Q

Where does efferent output from the BG go?

A

Thalamus, Brain Stem

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5
Q

What are the two major output nuclei of the BG?

A

Globus Pallidus Internus + Substantia Nigra Pars Reticulata

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6
Q

What part of the BG is the major receiver of input?

A

Striatum

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7
Q

Describe the Direct Pathway and name what receptor directs it.

A

D1 Receptors on the Substantia Nigra Pars Compacta are activated through the Direct Pathway.

Info from the Thalamus goes to the Cortex, this excites the Striatum (Putamen), inhibits the Gpi and therefore inhibits the thalamus. The some total of this is that the thalamus is disinhibited and facilitation of movement occurs.

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8
Q

Describe the inDirect Pathway and name what receptor directs it.

A

D2 Receptors on the Substantia Nigra Pars Compacta are activated through the Direct Pathway.

Info from the Thalamus goes to the Cortex, this excites the Striatum (Putamen), inhibits the Gpe, inhibits the Gpi, and therefore inhibits the thalamus and inhibits movement.

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9
Q

What is the effect of dopamine on the direct pathway?

A

all channels facilitated, more mvmt.

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10
Q

What is the effect of dopamine on the indirect pathway?

A

inhibits the indirect pathway = more mvmt.

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11
Q

Which neurotransmitter is released where in the basal ganglia circuit?

A 
Cortex: Glutamate (facilitatory)
Striatum (Putamen): GABA (inhibitory)
GPi + Pars Reticulata: GABA
Pars Compacta: Dopamine (either fac/inhib)
Subthalamic nucleus: Glutamate
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12
Q

What are the parallel circuits for the BG?

A

Skeletomotor: Motor Planning: Putamen
Oculomotor: Saccadic Eye Mvmt: Caudate
Executive: Associative: Caudate
Limbic: Emotion/Motivation: Ventral Striatum

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13
Q

What is more used at the beginning of learning vs. acquisition as far as parallel circuits within the BG? What parts of the striatum does this entail?

A

Pre-frontal Cortical-Basal Ganglia @ Beginning THEN Skeletomotor once automaticity has occurred. The shift moves from caudate to putamen.

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14
Q

What is the difference between hypokinetic and hyperkinetic basal ganglia pathologies?

A

Hypokinetic involved slow movement (akinesia/rigidity), reduced tone, and examples of this are PD, drug-induced PD, multiple systems atrophy, progressive palsy.

Hyperkinetic involve excessive uncontrolled movement (dyskinesias) and examples of this are chorea, myoclonus, tics.

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15
Q

What 3 things is Parkinsonism characterized by?

A
  1. Bradykinesia
  2. Resting Tremor / Rigidity
  3. Postural Instability
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16
Q

What are the diagnostic criteria for PD and how many of them do you need to have?

A

You need to have 3.

  1. Resting Tremor
  2. Unilateral Onset (though, can be bilateral)
  3. Progressive
  4. Good response to L-dopa
  5. Severe L-dopa induced chorea
  6. L-dopa response for +5 years
  7. Clinical Course > 10 years
17
Q

What are the negative symptoms of PD? Positive?

A

Negative: Bradykinesia/Akinesia, Postural Instability

Positive: Resting Tremor (suppressed to initiate movement), Rigidity (not velocity dependent!)

18
Q

What are the scales used to classify PD?

A

Hoehn Yahr (Stage 1 = unilateral, Stage 2 = bilateral)

UPDRS (4 parts)

19
Q

What are the pharmacological agents used to treat PD and how do they generally act?

A
  1. Increase amount of available dopamine (L-dopa, Carbidopa / Sinemet) - these can also cause hallucinations, chorea, and an increase in postural sway.
  2. Dopamine Agonists (these act like dopamine)
  3. Anticholinergics (block Glutamate)
    or. .. ultimately surgery (DBS)
20
Q

Where does the cerebellum receive input from?

A

1) Cortex
2) Brain Stem
3) Spinal Cord

21
Q

Where does the cerebellum send info to?

A

1) Cortex
2) Brain Stem
NOT THE SPINAL CORD

22
Q

What connects the brain stem to the cerebellum bilaterally?

A

Superior, Middle, Inferior Cerebellar Peduncles

23
Q

The cerebellum plays a role in which three functions?

A
  1. Motor Control / monitoring/planning
  2. Motor Learning
  3. Cognitive Aspects of Human Behavior
24
Q

Which side of the body does the cerebellum control? For what regions of the cerebellum do tracts double cross to achieve this?

A

Ipsilateral.

Ventral Spinal Cerebellar Tract
Cerebrocerebellar

25
Q

Where do the inputs of the cerebellum come from? Howsabout the outputs?

A

Inputs:

The Cortex (usually, a movement plan).

Ventral Spinocerebellar Tract (how did the plan go?)

Outputs:

Motor / Premotor Cortex
Brainstem

26
Q

What are the different presentations for removal of the cerebellum vs. damage?

A

W/ removal there is no sensation or strength loss.

W/ damage, there is a loss of accuracy of movement, balance + tone, motor learning and cognitive function.

27
Q

What are the effects of BG lesions to each of these locations: Substantia Nigra, Putamen, Subthalamic Nucleus, and Caudate Nucleus.

A

PD
Chorea
Hemiballism
Emo/Cognitive Issues

28
Q

What are all the deep cerebellar nuclei and where are they located? What is their significance?

A

Vermis: Fastigial
Intermediate: Interposed
Lateral: Dentate

The Vestibular Nuclei are not in the cerebellum.

They are the main outputs of the cerebellum.

29
Q

What are the fxal roles of the regions of the cerebellum and where are they located structurally within the cerebellum?

A

Cerebrocerebellum: higher order planning, the lateral portion of the longitudinal fissures of the cerebellum.

Spinocerebellum: in the intermediate hemispheres more limb specific, in the vermis, more head and trunk specific.

Vestibulocerebellum: flocconodular lobe specific, controls balance, head/gaze control (so, smooth pursuit/saccade effected if damaged), proprio of neck and coordination of vision/head.

30
Q

What are the 3 main repercussions of damage to the spinocerebellum?

A

1) loss of planning/speed
2) feed forward w/ loss of timing of agonist/antagonist (intention/terminal tremor) #dysmetria
3) interactive torques #ataxia

31
Q

What are the 3 layers of the cerebellar cortex and how do these interact with the cerebral cortex?

A

1) Molecular
2) Purkinje
3) Granular

The Deep Cerebellar Nuclei send output to the Mossy Fibers constantly. This output arises from granule cells in the granular layer to the parallel fibers of the molecular layer. These parallel fibers effect the purkinje fibers at a constant state. Contrarily, the Purkinje Fibers directly synapse to the deep cerebellar nuclei and also have interactions with Climbing Fibers. Climbing Fibers arise from the inferior olivary nuclei and go directly to the molecular layer to effect the Purkinje Fibers with a complex signal that only fires when needed OR open recognition of discrepancy from Biomechanical Links to the Cortex.

32
Q

What is the difference between the dorsal spinocerebellar tracts and the ventral?

A

Dorsal is somatosensory info (mostly from legs).

Ventral is the state of SC during active movements.

33
Q

Which parts of the contemporary model of motor control are linked with the BG vs. the CB?

A

Action Selection:BG

Execution/Inverse/Forward Model: CB

34
Q

What are the differences in reactive postural control bw PD & CB?

A

PD have coactivation (and so experience rigidity or akinesia)

CB have magnified responses in either direction and a lack of coordination between agonists and antagonists.

35
Q

How do you distinguish cerebellar ataxia from sensory ataxia?

A

CB lesion: cannot stand w/ feet together with EO or EC.

DCML lesion: can stand together with EO, but not EC.

36
Q

What is the physiological effect of HIT training and how might we define HIT in the clinic?

A

The effect is that more D2 receptors arise on the striatum.

FITT (frequency, intensity, timing, type).

37
Q

What are the three primary functions of the thalamus?

A
  1. Weigh station for all sensory info - olfactory.
  2. Voluntary Motor Activity (given connections to the BG/CB)
  3. Limbic System Connections
38
Q

What is the function of the Internal Medullary Lamina and External Medullary Lamina of the Thalamus?

A

Internal serves to 1) separate thalamus into anterior/medial/lateral sections, 2) connects fibers that connect thalamic nuclei together.

External serves to 1) separate the reticular nucleus from the thalamic mass, and 2) contains the thalamocortical and corticothalamic fibers.

39
Q

What are the differences between the Ventral Anterior Nucleus, Ventral Lateral Nucleus, and Ventral Posterior Nucleus?

A

VAN = motor activity based, receives info from GPi and SN, sends info to premotor and supp motor cortex.

VLN = motor activity based, receives info from GPi and SN, also dentate nucleus and primary motor cortex, sends info to primary motor cortex.

VPN = chief sensory relay station, receives info from contralateral head/neck/body, sends to primary somatosensory info.

Unit 9 (2 decks)

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