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Neuroanatomy > Bridges Basal Ganglia > Flashcards

Bridges Basal Ganglia Flashcards

1
Q

two parts of substantia nigra

A

pars compacta and pars reticulata

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2
Q

part of substantia nigra…sends dopaminergic fibers to neostriatum (this part damaged in Parkinson’s disease)

A

pars compacta

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3
Q

area that sends dopaminergic input to neostriatum (in addition to pars compacta of substantia nigra)

A

ventral tegmental

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4
Q

area of neostriatum that receives dopaminergic projections from the ventral tegmental area

A

ventral striatum/nucleus accumbens

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5
Q

pars reticulata (part of SN) resembles what structure cytologically?

A

globus pallidus

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6
Q

when we are faced with many alternative actions…basal ganglia do not trigger movement but release the chosen action and reject the other unwanted possibilities

A

action selection hypothesis

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7
Q

basal ganglia receive input from this structure…why it is suggested involved in habit formation and motor activity

A

posterior parietal cortex

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8
Q

input to basal ganglia

A

cerebral cortex

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9
Q

output of BG to cerebral cortex; this output is via what?

A

prefrontal, orbitofrontal, cingulate, premotor, supplementary motor, primary motor; thalamus

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10
Q

does the BG or cerebellum have projections to brainstem nuclei?

A

cerebellum

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11
Q

does the BG or cerebellum receive direct information from the spinal cord?

A

cerebellum

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12
Q

NT for inhibitory input from ventral striatum to output nuclei

A

GABA

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13
Q

NT for cortex to neostriatum

A

glutamate

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14
Q

NT for input from subthalamic nucleus to output nuclei

A

glutamate

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15
Q

NT used in input from neostriatum to GP externa, and from GP externa to subthalamic nucleus

A

GABA

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16
Q

NT for SN (pars compacta) and ventral tegmentum to input nuclei

A

dopamine

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17
Q

dopamine receptor that is inhibitory…acts in indirect pathways (inhibits the indirect pathway…why dopamine always enhances facilitation of cerebral cortex)

A

D2

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18
Q

dopamine receptor that is excitatory

A

D1

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19
Q

NT from output nuclei to thalamus

A

GABA

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20
Q

NT from thalamus to cortex

A

glutamate

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21
Q

activation of direct or indirect pathway will increase the facilitation of cortical neurons concerned with motor function (more input from thalamus helping neurons in motor cortex)?

A

direct

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22
Q

activation of direct or indirect will decrease thalamus facilitation of motor cortical neurons?

A

indirect

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23
Q

abnormal involuntary movements

A

dyskinesia

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24
Q

slow writhing movements of extremities or head and trunk (dystonia)

A

athetosis

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25
Q

random controlled movement patterns that occur continuously (sometimes flicking mvmnts involving extremities and facial muscles)

A

chorea

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26
Q

type of chorea…normal progression of movements cannot occur; person performs one movement pattern for few seconds, switch suddenly to another movement pattern (typically involved with childhood)

A

St Vitus’ Dance

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27
Q

chorea occurs from widespread damage to what structures? what neurons seem to be affected more?

A

caudate nucleus and putamen; Gaba-ergic

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28
Q

uncontrollable succession of violent, flailing, movements of large areas of body; what structure is normally damaged?

A

hemiballismus; subthalamic nucleus

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29
Q

more commonly involved in cognitive deficits/dementia with movement disorders; what specific structures are most likely?

A

limbic loop; ventral pallidum, ventral striatum, dopaminergic ventral tegmentum

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30
Q

typical presentation of a patient with Parkinson’s disease

A

unilateral resting tremor, reduced arm swing, slowed hand movement, change in gait/dexterity/energy level

31
Q

surviving neurons from Parkinson’s disease contain these eosinophilic structures; what do these contain?

A

Lewy bodies; alpha-synuclein

32
Q

what is major pathological finding in Parkinson’s disease? where does this occur?

A

dopaminergic neurons; SNc

33
Q

this drug binds dopamine receptors…can cause similar Parkinson-like disorder

A

antischizophrenic

34
Q

the tremor of Parkinson’s disease may involve this; oscillating state of activity of neurons that control extensor and flexor muscles (normally damped by basal ganglia)

A

subthalamic nucleus

35
Q

deep brain electrical stimulation is designed to treat Parkinson’s by stimulating this area, and decreasing activity of this area

A

thalamus, subthalamic nucleus

36
Q

possible treatment for Parkinson’s…based on the increased activity of GP interna

A

pallidotomy

37
Q

another surgical intervention for Parkinson’s disease that has a good effect on the tremor (but not on any of the other symptoms)

A

thalamotomy

38
Q

Syndenham’s chorea/St Vitus’ Dance can follow these childhood diseases

A

streptococcal infection or acute rheumatic fever

39
Q

option for symptomatic treatment for Huntington’s disease (but there is no treatment)

A

haloperidol

40
Q

gene for Huntington’s Disease located on what chromosome? what protein does this encode for?

A

4; huntingtin

41
Q

Huntington’s Disease is example of this mutation, who’s length directly correlates to age of onset; what codon is involved?

A

trinucleotide repeat; CAG

42
Q

repetitively tapping forehead around eyebrow causes uncontrollable blinking of the eye

A

glabellar reflex/Myerson’s sign

43
Q

ventral fusion of caudate and putamen that merges into nucleus accumbens and striatal portions of olfactory tubercle

A

ventral striatum

44
Q

caudate + putamen + globus pallidus

A

corpus striatum

45
Q

caudate + putamen

A

neostriatum (dorsal striatum)

46
Q

putamen + globus pallidus

A

lenticular (lentiform) nucleus

47
Q

region of neostriatum that receives dopaminergic neurons from ventral tegmental area

A

nucleus accumbens (of ventral striatum)

48
Q

input nuclei of basal ganglia

A

caudate nucleus and putamen (neostriatum), ventral striatum (nucleus accumbens)

49
Q

output nuclei of basal ganglia

A

SNr and GP internal, ventral pallidum (extension of GP below anterior commissure)

50
Q

intrinsic nuclei of basal ganglia

A

SNc, GP external, subthalamic nucleus

51
Q

NT from thalamus, cortex, and subthalamic nucleus that is excitatory

A

glutamate

52
Q

major input to basal ganglia (excitatory)

A

corticostriatal projection

53
Q

skeletomotor loop mainly concerns this basal ganglia…used in control of musculature, acquisition of motor skills

A

putamen

54
Q

where is output of skeletomotor loop (putamen) directed back to (via GP and thalamus)?

A

supplementary motor, premotor, motor cortex

55
Q

nucleus involved in oculomotor and spatial memory loop…receives input from remainder of frontal and parietal lobes (*controls extraocular muscles and aspects of orientation memory*)

A

caudate

56
Q

this may be involved in action selection

A

prefrontal/executive loop

57
Q

where do hippocampal formation, amygdala, and anterior cingulate gyrus project in limbic loop?

A

ventral striatum

58
Q

OCD and schizophrenia have been associated with this basal ganglia loop

A

limbic

59
Q

this may involved hyperactivity in cognitive circuitry regulating prefrontal speech areas

A

Tourette’s syndrome

60
Q

striosomes (patch of neurons in neostriatum) have this kind of receptors

A

opiate

61
Q

what is input to striosomes? where do they project?

A

limbic cortical area; SNc

62
Q

what is most common presenting sign of Parkinson’s?

A

rhythmical tremor (that disappears during voluntary activity)

63
Q

gene for familial Parkinson’s that is located on chromosome 4 encodes for this…necessary for ER to Golgi trafficking (concentrated in presynaptic terminals)

A

a-synuclein

64
Q

symptoms of Parkinson’s appear after this percentage of dopaminergic innervation of neostriatum has been lost

A

85%

65
Q

precursor for dopamine that can cross BBB…given as treatment for Parkinson’s (w/ peripheral DOPA decarboxylase)

A

L-DOPA

66
Q

fetal dopaminergic cells can be taken from this area as possible treatment for Parkinson’s

A

mesencephalon

67
Q

growth factors that could be injected to save/rescue patient’s own dopaminergic neurons

A

GDNF and PDGF

68
Q

abnormal posture held for a long time (terminal stage of Huntington’s disease)

A

dystonia

69
Q

earliest Huntington’s effects stem from loss here

A

striatal neurons of indirect pathway (GABA projecting to external GP, also cholinergic within)

70
Q

loss of GABA neurons in Huntinton’s disease early on is similar to lesion of this

A

subthalamic nucleus

71
Q

changes in personality/non-motor aspects in Huntington’s disease is associated with this

A

caudate nucleus

72
Q

in Parkinson’s….lack of dopaminergic input causes reduced activity of neurons with these receptors; and increased activity of neostriatal neurons with these receptors

A

D1; D2 (overall enhanced inhibition of thalamus)

73
Q

blood supply to head of caudate

A

medial striate

74
Q

blood supply to posterior limb IC

A

anterior choroidal

Neuroanatomy (10 decks)

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