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Basal Ganglia Flashcards

1
Q

5 basal ganglia?

A 
Caudate
Putamen
Globus Pallidus
Subthalamic nucleus
Substantia nigra
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2
Q

Damage to basal ganglia lead to?

A

Movement disorders that are distinct from damage to motor cortex/projections

Damage to BG produces involuntary movements or inability to initiate movements

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3
Q

2 motor systems?

A

Pyramidal

Extapyramidal

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4
Q

BG does what to output of cortex?

A

Modulates it

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5
Q

Pyramidal vs extrapyramidal symptoms

A

Pyramidal - damage to descending pathways, paralysis, paresis

Extrapyramidal - damage to BG

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6
Q

Caudate and putamen?

A

Two parts of the same nucleus

Split by internal capsule

Known collectively as the neostriatum or striatum

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7
Q

Describe the caudate?

A

Head, body, and tail

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8
Q

Cell bridges of the striatum?

A

Penetrating fibers of the internal capsule connecting the caudate and putamen

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9
Q

What happens to the striatum rostroventrally?

A

Caudate and putamen verge and become the ventral striatum which is part of the nucleus accumbens which connects to the limbic system

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10
Q

Two neuronal types of the striatum?

A

Spiny stellates - 95%, dominant receipient of inputs, major output

Aspiny interneurons

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11
Q

Spiny stellate NT?

A

Inhibitory GABA projection cells

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12
Q

Aspiny interneurons NT?

A

Cholinergic

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13
Q

The lentiform or lenticular nucleus is comprised of

A

Putamen and Globus pallidus

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14
Q

Where is the substantia nigra?

A

Ventral to subthalamic nuclues

Mediodorsal to basis pedunculi

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15
Q

Two parts of the substantia nigra?

A

Pars compacta

Pars reticulata

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16
Q

Describe the pars compacta?

A

Pigmented cells, meanin, byproduct of dopamine metabolism

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17
Q

Describe the pars reticulata?

A

Located more ventrally, GABA

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18
Q

GPPIn is very similar to?

A

The pars reticulata

Same nuclear group, separated by fibers of the internal capsule

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19
Q

Inputs to the striatum?

A

Corticostriate

Pars compacta

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20
Q

Describe corticostriate to striatum

A

From all parts of the cerebral cortex

Glutaminergic

Excitatory

Terminates on teh spins of spiny stellates

Topographically organized

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21
Q

Describe the pars compacta to the striatum

A

Dopaminergic on both spiny stellates and interneurons

Destroyed in parkinsons!

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22
Q

5 structures of basal ganglia

A

caudate, putamen, globus pallidus, subthalamic nucleus and substantia nigra

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23
Q

striatum=

A

caudate + putamen

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24
Q

What is part of the same nucleur group as SNPR?

A

GPPI (separated by internal capsule)

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25
Q

lentiform nucleus=

A

putamen + globus pallidus

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26
Q

Outputs of basal ganglia project to?

A

ventral lateral nucleus of thalamus

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27
Q

Caudate runs on the lateral aspect of which ventricle?

A

lateral ventricle

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28
Q

Damage to BG produces?

A

involuntary movements or inability to initiate movements

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29
Q

Damage to BG leads to movement disorders which _________ (are or are not) distinct from those following damage to motor cortex and its projections.

A

ARE

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30
Q

Pyramidal system

A

Lateral motor systems (lateral CST) and medial motor systems (reticulo-spinal & tectospinal tracts)

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31
Q

Extrapyramidal system

A

BG

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32
Q

Pyramidal symptoms

A

Damage to descending pathways, paralysis and paresis

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33
Q

Extrapyramidal symptoms

A

Damage to BG

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34
Q

BG lesions

A

hyperkinetic or hypokinetic movement disorders

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35
Q

Caudate and Putament

A

Two parts of the same nucleus, split by the internal capsule

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36
Q

Cell bridges

A

Penetrating fibers of the internal capsule, connecting the caudate and putamen

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37
Q

Ventral striatum or mostly nucleus accumbens

A

Rostroventral merging of caudate and putamen.

38
Q

Ventral striatum is important connections with ______________ system.

39
Q

2 neuronal types of the striatum

A

spiny stellates and aspiny interneurons

40
Q

Spiny stellates

A

Inhibitory GABAergic projection cells

41
Q

Aspiny interneurons

A

Cholinergic. These cholinergic interneurons preferentially form excitatory synapses onto striatal neurons of the indirect pathway.

42
Q

Where is the Substantia Nigra located?

A

Ventral to subthalamic nucleus, mediodorsal to basis pedunculi

43
Q

What are the two parts of the Substantia Nigra?

A

SNPC (pars compacta), SNPR (pars reticulata)

44
Q

SNPC

A

pigmented cells from melanin which is a byproduct of dopamine metabolism

45
Q

SNPR

A

located more ventrally than SNPC is GABAergic

46
Q

Corticostriate projections

A

From essentially all parts of cerebral cortex; glutamatergic, excitatory, terminates on spines of spiny stellates

47
Q

Centromedian nucleus of thalamus receives inputs from

A

motor cortex

48
Q

centromedian nucleus of thalamus projects onto

A

spiny stellates of striatum

49
Q

Interconnections between components of BG

A

SNPC to Striatum: Dopaminergic (both on spiny stellates and interneurons)

50
Q

Which neurons are destroyed in Parkinson’s?

A

Dopaminergic interconnections between SNPC to Striatum

51
Q

Direct striato-pallidal pathway

A

Striatal spiny stellates (D1) project directly to GPPIn/SNPR

52
Q

Indirect striato-pallidal pathway

A

Striatal spine stellates (D2) project to GPPEx, which project to subthalamic nucleus, which then projects to the GPPIn/SNPR

53
Q

D1 dopamin receptors

A

GABA/substance P/dynorphin

54
Q

D2 dopamin receptors

A

GABA/enkephalin

55
Q

D1 receptors are excitatory or inhibitory on the direct striatal neurons?

A

excitatory

56
Q

D2 receptors or excitatory or inhibitory on the indirect striatal neurons?

A

inhibitory

57
Q

All connections in the Striato-Pallidal pathway are GABAergic except

A

subthalamic to GPPIn/SNPR which is excitatory glutamatergic

58
Q

Output from BG

A

GPPIn/SNPR to the VL/VA thalamus which project to the cortex

59
Q

Direct pathway increases or decreases activity of cortical cells?

60
Q

Direct pathway

A

Striatum to GPPIn/SNPR - inhibitory: GPPIn/SNPR to VA/VL - inhibitory: VA/VL to cortex - excitatory

61
Q

Direct pathway

A

Increase activity in striatum of neurons which project through the direct pathway: Increase inhibition of GPPIn/SNPR: Disinhibition of VA/VL: INCREASE ACTIVITY OF CORTICAL CELLS

62
Q

Indirect pathway

A

Striatum to GPPEx - inhibitory: GPPEx to subthalamic nucleus - inhibitory: Subthalamic to GPPIn/SNPR - excitatory: GPPIn/SNPR to VA/VL - inhibitory: VA/VL to cortex - excitatory

63
Q

Indirect pathway

A

Increase activity in striatum of neurons which project through the indirect pathway: Increase inhibition of GPPEx: Disinhibition of subthalamic nucleus: Increase activity of GPPin/SNPR: Increase inhibition of VA/VL: DECREASE ACTIVITY IN CORTICAL CELLS

64
Q

Indirect pathway Mnemonic

A

INDIRECT INHIBITS

65
Q

Dopamine there has a net ___________ effect on VA/VL.

A

DISINHIBITORY (Indirect pathway is inhibited, and direct pathway is excited.)

66
Q

When dopaminergic neurons are lost, the net effect is an ____________ in tonic inhibition of VA/VL.

67
Q

Why are anti-cholinergic agents somewhat useful in treating Parkinson’s disease?

A

Removal of cholinergic excitation of the indirect pathway produces a net decrease in inhibition of the thalamus,which may account for the beneficial effects of anticholinergic agents in parkinsonism.

68
Q

Independent BG-cortex circuitry

A
  1. motor circuit 2. prefrontal circuit 3. oculomotor circuit 4. limbic circuit
69
Q

Motor circuit

A

VA/VL, Putamen -> motor/sensory cortex

70
Q

Prefrontal circuit

A

VA/MD, Head of caudate -> prefrontal cortex

71
Q

Oculomotor circuit

A

VA/MD, Caudate -> frontal eye fields

72
Q

Limbic circuit

A

VA/MD, Nucleus accumbens, ventral caudate and ventral putamen -> anterior cingulate cortex

73
Q

Parkinson’s

A

Net disinhibition of GPPIn/SNPR, increased tonic inhibition of VA/VL.

74
Q

BG injury can lead to which cortical symptoms?

A
  1. release phenomena 2. positive sings - involuntary movements 3. loss of function - inability to initiate motor acts, akinesia
75
Q

Resting tremor

A

not an intentional tremor, occurs after cerebellar damage

76
Q

akinesia

A

lack of movement

77
Q

bradykinesia

A

slowness of movement

78
Q

athetosis

A

slow writhing movement of hands

79
Q

chorea

A

sudden movements of the limbs and facial movements

80
Q

ballismus

A

sudden ballistic movements

81
Q

dystonia

A

persistent distorted postures or movements

82
Q

What are the hallmarks of PD (paralysis agitans)?

A
  1. progressive 2. neurodegenration of dopamine cells from SNPC 3. Middle/old age 4. symptoms: resting tremor, akinesia, bradykinesia, dystonia, rigiditiy, cogwheel rigidity
83
Q

What are common treatments for PD?

A

L-DOPA (precursor to dopamine) - eventually looses its efficacy. New potential fetal transplants of dopaminergic cells. Surgical ablation of GP (pallidotomy) and/or subthalamus.

84
Q

MPTP (synthetic heronin) causes what kind of symptoms?

A

PD disease by destroying dopamine cells in SNPC

85
Q

What are the hallmarks of HD (H’s chorea)

A
  1. degeneration of GABAergic striatal neurons from D2 inhibitory pathway 2. middle age 3. symptoms: chorea, dementia, and eventual death 4. no effective therapy 5. AD mutation 6. genetic screening of markers
86
Q

Lenticulostriate arteries

A

Small vessels from the initial portion of MCA which supply large parts of the basal ganglia

87
Q

Anterior choroidal artery

A

From the internal carotid and supplies portion of the anterior GP and putamen

88
Q

Recurrent artery of Heubner

A

From the initial portion of ACA and supplies part of the head of the caudate and putamen

89
Q

What are symptoms of stokes that damage subthalamic nucleus?

A

hemiballism

90
Q

Tarditive dyskinesia

A

After prolonged treatment with many antipsychotic drugs (haloperidol - antagonists of dopamine), induce supersensitivity which can cause involuntary movements of face and tongue.

Neuro 3 (5 decks)

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