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ANAT 323 > lecture 11: basal nuclei > Flashcards

lecture 11: basal nuclei Flashcards

1
Q

which of the following locations for an UMN lesion would result in symptoms that are ipsilateral to the lesion

1) ventral horn
b) medullary pyramid
c) lateral corticospinal tract
d) decussation of the pyramids

A

lateral cortcospinal tract

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2
Q

which of the symptoms is/are not associated with a lower motor neuron lesion

a) muscle fascicualtors
b) spastic paralysis/paresis
c) postive babinski
d) decreased or absent deep tendon

A

c and d

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3
Q

lateral moot pathways are for what movement

A

appendicular (skilled and voluntary )

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4
Q

medial motor pathways are for what

A

posture, balance, stance (axial m)

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5
Q

what structure forms are upstream loop with motor cortex

A

basal nuclei

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6
Q

what is the function of the basal nuclei

A

responsible for iniating and terminating voluntary motor movement (and making it smooth)

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7
Q

decision to move, the direction and the amplitude is controlled by basal nuclei or cerebellum

A

basal nuclei

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8
Q

the coordination of movements is basal nuclei or cerebullum

A

cerebllim

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9
Q

extrapyramidal pathways get cortical input via what fibers

A

corticofugal fibersw

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10
Q

what are the 4 extrapyramidal pathways

A

rubro spinal (red nuc)
tectospinal (sup collic)
reticulospinal (reticular formation)
vestibulospinal (vestibular n)

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11
Q

extrapyramidal pathways originate and synapse where

A

brainstem

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12
Q

the motor pathways cannot start movement without upstream motor loop from where

A

basal nuclei

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13
Q

basal nuclei communicates with cortex and what other subcortical structure

A

thalamus

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14
Q

are basal nuclei cortical or subcortical

A

subcortical

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15
Q

what forms the basal nuclei

A

caudate nucleus
lentiform nucleus (putamun, GB)
sub thalamic nuclei
substantia nigra

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16
Q

what other subcortical structures are not basal nuclei but have important connections to it

A

thalamus
nucleus accumenbens
amygdaloid body

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17
Q

what are the two divisions of the globes pallid us

A

interna and externa

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18
Q

is the head of the caudate located rostral or caudal

A

rostral

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19
Q

what is the lentiform nucleus

A

putamen
globus pallidus interna and externa

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20
Q

what forms the most lateral part of the Lentiforn nucleuis

A

putamen

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21
Q

what forms the inner part of the LN

A

globus pallisud

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22
Q

what is the black substance in the midbrain called

A

substantia nigra

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23
Q

what forms the emotion connections for the basal nucleis

A

amygdaloid body

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24
Q

amygdaloid body is at the head or tail of the caudate

A

tail

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25
Q

be able to visualize the basal nuclei

A
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26
Q

the CN follows the curvature of what

A

the lateral ventricles

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27
Q

is the caudate nucleus a key input or output nuclei of the basal gang and explain

A

input
(info coming from outside basal nuclei comes to the caudate nucleus first)

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28
Q

what is the function of the caudate nuc

A

involved in cognitive processes controlled y the basal nuclei

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29
Q

true or false: caudate nucleus is a key output nucleus of the basal nuc

A

false, input

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30
Q

what forms the dorsal striatum

A

caudate nucleus and putamen

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31
Q

true or false:> the dorsall striatum is an input nucleus

A

true

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32
Q

the LN is composed of…

A

GB and putamen

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33
Q

true or false: putamen is an output nucleus

A

false, input

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34
Q

true or false: globes pallid us is an input nucleus

A

false, output

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35
Q

what is the function of the putamen

A

input nucleus of basal nuc involved in motor function

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36
Q

what is th function of the GP

A

output nucleus, relate information to the cortex via the thalamus (always happens indirection since it =must pass thru thalamus first)

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37
Q

the GP relays information directly or indirectly to the cortex and explain

A

always happens indirection since it =must pass thru thalamus first)

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38
Q

true or false: GP is more medial aspect of the LN

A

true

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39
Q

where is the sub thalamic nuclei located

A

inferior to the thalamus
superior to the midbrain
caudal to the hypothalamus

(edge of diencephalon, rostral edge of midbrain)

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40
Q

is subthalamic nuclei receiving input or giving output

A

receiving input

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41
Q

what is the function of the sub thalamic nuclei

A

receives input from the cortex and other basal nuclei (not a main input nuclei)

described at the clock of the basal nuclei as it regulates the output rhythm

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42
Q

what BN structure regulates the output rhythm

A

substhalmic nuc

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43
Q

true or false: the sub thalamic nucleus is a main input nuclei

A

false, not a main

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44
Q

where is the substantial nigra located

A

rostral midbrain in cerebral peduncle

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45
Q

the substantia nigra is located in rostral midbrain in BLNAK

A

cerebral peduncle

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46
Q

what are the 2 divisions of the substantia nigra

A

pars compact and pars reticula

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47
Q

what is the function of the pars compacta (what does it contain)

A

contains primarily dopaminergic neurons that project to other basal nuclei_

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48
Q

what its he name of the grey matter connection between head of caudate and putamen

A

nucleus accumens

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49
Q

what is the function of nucleus accumebsn

A

involved in reward behaviour, addiction, emotions

pleasure cetner

input nucleus of BN

receives limbic input entire the basal nuclei

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50
Q

true or false, the substantia nigra is involved in reward behaviour, addiction, emotions

A

false, thats nucleus accumebs

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51
Q

what is the pleasure centre of the brain

A

nucleus accumebns

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52
Q

what is the ventral striatum

A

nucleus accumbers and olfactory tubercle

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53
Q

what are the input nuclei of the basal

A

caudate (key)
putamen (key)

sub thalamic (not main)
nucleus accumebns (mostly limbic)

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54
Q

what is the output nuclei of the BG

A

globes pallidus

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55
Q

what are the 4 main blood supply of the BN

A

anterior cerebral a (lenticulostriate)
middle cerebral artery (lenticulostriate)
anterior choroidal
posterior cerebral a (deep)

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56
Q

what blood supply supplies the most rostral end of the basal nuc

A

anterior cerebral a (lenticulostraite)

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57
Q

what does the anterior cerebral a (lenticulostriate) supply

A

anterior (rostral) putamen and globes pallodus, head of caudate nuc

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58
Q

what does the middle cerebral a (lenticulostriate)

A

muddle of putamen and GP and body of the caudate

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59
Q

muddle of putamen and GP and body of the caudate
what blood supply

A

middle cerebral a (lenticulostraite)

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60
Q

anterior (rostral) putamen and globes pallodus, head of caudate nuc
what blood supply

A

anterior cerebral a (lenticulostraite_

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61
Q

what does the anterior choroidal a supply in BN

A

posterior (caudal) putamen and GP< and tail of caudate nucleus

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62
Q

posterior (caudal) putamen and GP< and tail of caudate nucleus

what blood s

A

anterior choroidal

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63
Q

what does posterior cerebral a (deep) supply of Bn

A

substantia nigra, subthalamic n and thalamus

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64
Q

substantia nigra, subthalamic n and thalamus

what blood supply

A

posterior cerebral (deep)

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65
Q

be able to locate blood supply on BN

A
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66
Q

BN form an upstream motor loop with circuit of connections with motor and premotor cortices in IPSILATERAL OR CONTRALATERAL HEMISTEPHRE

A

IPSILATERAL

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67
Q

true or false, BN forms a circuit of connections with motor and premotor cortices in contralateral hemisphers

A

false, ipsilateral

68
Q

what are the main inputs to the basal nucelsu

A

cortex to dorsal striatum (via corticostriatal fibers)

substantial nigra to dorsal striature (via nigrostriatal gibers)

69
Q

input to BN from cortex to dorsal striatum is via what fibers

A

corticostriateal

70
Q

input to BN fromsubstantial nigra to dorsal striature is via what fibers

A

(via nigrostriatal fibers)

71
Q

output from BN is what structure

A

globes pallidus interna to thalamus (via thalamic fasciculus)

72
Q

output from BN is from GPi or GPe

A

GPi

73
Q

what are the two important thalamic nuclei for the BN pathways

A

ventral anterior and ventral lateral

74
Q

what are the 3 NT of the basal nuclei pathway

A

inhibitory: gaba
excitatory: glutamate

inhib/excite: dopamine

75
Q

dopamine can be both inhibitory or excitatory, true or false

A

true, depending on what receptor

76
Q

know the general basal nuclei pathway

A
77
Q

the direct pathway is aka the blank pathways

A

go pathway

78
Q

explain the direct pathways

A

1) excitatory projections: cortex to striate (asking to initiate movement)

2) inhibitory projections: striatum to GPI

3) inhibitory projections: GPi to thalamus

4) inhibition releases tonic inhibition (ie. disinhibition of the thalamus)

5) increase excitatory output from thalamus to the cortex

(dopamine from the Sec enhances excitation of the dorsal striatum though D1 receptions
=pathway will be upreglation, dopamine says more go)

79
Q

GPi is an inhibitor or excitatory of the thalamus

A

inhibitor

80
Q

dorsal striatum is an inhibitor or excitatory of the thalamus

A

excitator

81
Q

the cortex sends glutamate or gaba to striatum in the direct pathway

A

glutamate

82
Q

the striatum sends gaba or glutameate to the GPI

A

gaba

83
Q

GPI sends gaba or glutamate to thalamus

A

gaba

84
Q

the thalamus tries to send GABA or glutament back up to cortex

A

glutameate

85
Q

the substance nigra sends glutament or gaba in the direct pathway

A

glutameate

86
Q

in the direct pathway, dopamine from the Sec enhances excitation or inhibition of the dorsal striatum though D1 receptions

A

enhances excitation
(=pathway will be upreglation, dopamine says more go))

87
Q

in the direct or indirect pathway do we get disinhibition of the thalamus

A

direct pathway

88
Q

does disinhibition of the thalamus mean more or less excitatory signals to the cortex

A

more

89
Q

inhibition of the GPi inhibits or disinhibits the thalamus in direct pathway

A

disinhibits

90
Q

know the direct pathway (via the ninja nerd)

A

1) cortex sends excitation (via glutamate) to the striatum

2) striatum (which is excited) sending a lot of inhibition signals to GPi via gaba

3) GPi is inhibited therefore there a decrease of gaba release from GPi to Thalamus (therefore thalamus is excited )

4) increase in excitation (glutamate) from thalamus to the cortex

5) increase in motor activity

=substantion nigra will act on d1 receptors on striatum to further enhance activity and excite them

91
Q

explain the pathway of the indirect/stop pathway

A

1) excitatory projections from cortex to striatum

2) inhibitory projection from striatum to GPE

3) inhibitory projections fro mGPe to STn

4) excitatory projections from Stn to GPI (excitation of the GPI increases inhibition of the thalamus)

5) inhibitory projections from GPI to thalamus (a lot of them)

6) decrease excitatory output from the thalamus to the cortex

=dopamine from Sac inhibits excitatory interneurons in striatum (d2 receptors)
=downregulates the patwath/inhibts

92
Q

in the indirect pathway, the cortex sends excite or inhibit to striatum

A

excite (Glut)

93
Q

in the indirect pathway, the striatum sends excite or inhibit to GPi

A

does not communicate directly with GPI

94
Q

in the indirect pathway, the striatum sends excite or inhibit to GPe

A

inhibitory (GABA)

95
Q

in the indirect pathway, the SNc sends excite or inhibit to striatum

A

inhibitory (GABA)

96
Q

in the indirect pathway, the GPe sends excite or inhibit to STn

A

inhibitory (GABA)

97
Q

in the indirect pathway, the STn sends excite or inhibit to GPi

A

excitatory (GLUT)

98
Q

in the indirect pathway, the GPi sends excite or inhibit to thalamus

A

inhibit

99
Q

true or false, in both pathways, the cortex is always sending inhibitory signals to the striatum

A

false, always excitatory

100
Q

true or false, in both pathways, the striatum is always sending inhibitory signals to the GPi

A

false, always inhibits the GP (but not directly interna in the indirect)

101
Q

true or false, in both pathways, the GPi is always sending inhibitory signals to the thalamus

A

true

102
Q

true or false, in both pathways, the thalamus is always sending excite signals to the cortex

A

true

103
Q

by exciting the GPi, do we get increases or decreases in motor activity in the cortex

A

decreases (we are increasing the inhibition to the thalamus)

104
Q

by inhibiting the GPi, do we get increases or decreases in motor activity in the cortex

A

increases (we are decreasing the inhibition to the thalamus)

105
Q

in what pathway is the sub thalamic nucleus invovled

A

indirect

106
Q

understand the indirect pathway (ninja nerd)

A

1) cortex sends excitatory to the striatum

2) striatum sends inhibit (a lot of it) to the GPe

3) GPe is severely inhibited, but sends inhibitory signals to the Stn (technically activating STN)

4) STN (activated) sends excitatory signals to the GPi

5) Gpi (activtiated) sends inhibitory signals to the thalamus

6) thalamus (inhibited) decreases signals being send to the cortex

7) decreased motor activity

=substainta nigra will act on d2 receptors of striation to decrease inhibition and downregualte pathways

107
Q

what are the two relay nuclei in the thalamus involved in both pathways

A

ventral anterior
ventral lateral

108
Q

true or false: the basal nuclei circuit is purely a motor ciruit

A

false, also associative and limbic

109
Q

explain the motor circuit for the BN

A

motor performance

=inputs from motor and somatosensory cortices are integrated in the putamen

=seperate pathway for oculomotor pathway (input from frontal eye fields pass through caudate nucleus)

110
Q

in the motor circuit, we get inputs from where and where are they integrates

A

=inputs from motor and somatosensory cortices are integrated in the putamen

111
Q

explain the assocaitive circuit of the BN

A

cognition

inputs from frontal, parietal and temporal association cortices travel to caudate nucleus

involved in complex motor planning, cognitive processes and learning

112
Q

where do the inputs come from and go to in the associative circuit of the Bn

A

inputs from frontal, parietal and temporal association cortices travel to caudate nucleus

113
Q

what is the function of the associative circuit of the BN

A

involved in complex motor planning, cognitive processes and learning

114
Q

explain the limbic circuit of the BN

A

emotion

inputs from frontal assocaition areas and limbic lobe project to nucleus accumebns and ventral striatum

115
Q

where do inputs from limbic circuit come from and project to

A

inputs from frontal assocaition areas and limbic lobe project to nucleus accumebns and ventral striatum

116
Q

motor performance is associated with what circuit

A

motor cuirucit

117
Q

cognition is associated with what circuit

A

associative circuit

118
Q

emotion is associated with what circuit

A

limbic circuit

119
Q

lesions to basal nuclei will result in contralateral or ipsilateral motor deficits

A

contralateral

120
Q

true or false: lesions to basal nuclei will result in contralateral motor deficits

A

true

121
Q

lesions to the cerebellum will cause ipsilateral or contralateral motor deficits

A

upsulateral

122
Q

true or false: basal nuclei lesions and cerebellum lesions will cause opposite motor deficits

A

true
cerebellum (ipsilat)
basal nuc (contralat)

123
Q

explain why despite the BN having projections to ipsilateral motor coritices, that a lesion to it will cause contralateral deficits

A

because downstream corticospinal pathways project primarily to the contralateral side of the body

(ie: right basal nuc = right motor cortex = left side of the body)what

124
Q

what is the general effect of a lesion to the go pathway/direct

A

difficulty initiating movement = hypokinesia

125
Q

difficulty initiating movement = hypokinesia is from a lesion to what pathway

A

direct

126
Q

difficulty initiating movement = is known as…

A

hypokinesia

127
Q

what is hypokinesia

A

difficulty initiating movement = is known as…

128
Q

what is the general effect of a lesion to the stop pathway/indirect

A

excessive, uncontrollable movement = hyperkinesia

129
Q

excessive, uncontrollable movement = hyperkinesia is lesion to what pathway

A

indirect

130
Q

excessive, uncontrollable movement aka what

A

= hyperkinesia

131
Q

what is hyperkinesia

A

excessive, uncontrollable movement

132
Q

parkinson’s disease is caused by what

A

degeneration of substantia nigra, pars compacta

133
Q

degeneration of substantia nigra, pars compacta assocaited with what condition

A

parkinsonstr

134
Q

true or false: degeneration of substantia nigra, pars compacta is associated with hubtingon disease

A

false, parkinsons

135
Q

a degeneration of substantia nigra, pars compacta causes what

A

loss of dopiminergic neurons projection to the basal nuclei

136
Q

what are the characteric symptoms of parkinsons

A

akinesia (instability to initiate movement)
bradykinesia (slow execution of movements)
rigidity (esp in flexors)
involuntary tremor (persists as rest)

137
Q

what is akinesia

A

nstability to initiate movement)

138
Q

what is bradykinesia

A

(slow execution of movements)

139
Q

in parkinsons, rigidity is most common where

A

in flexors

140
Q

loss of dopaminergic neurons projection to basal nuclei causes problems with what pathway

A

direct pathway (difficukting initiating movement)

141
Q

be able to udnerstand the effect of parkinsons on BN pathways

A
142
Q

what are the treatments for parkinsons

A

L dopa therapy (precursor of dopamine)
=able to cross the blood brain barrier and be converted to dopamine centrally

deep stimulation of Stn

143
Q

what treatment can you do to supplement the lack of endogenous dopamine in parkinsons

A

L dopa therapy since its a precursor of dopamine

144
Q

Huntington diesease symptoms are usually bilateral or unilateral

A

bilateral

145
Q

Huntington disease is usually problems with stop or go pathway

A

stop

146
Q

is Huntington hereditary

A

yes, gets worse over time

147
Q

huntington diease is caused by degeneration of what

A

dorsal striatum

148
Q

degeneration of dorsal striatum is associated with what condition

A

huntington

149
Q

true or false: Huntington is a progressive, hereditary disorder that typically manifests later in life

A

true

150
Q

true or false: Huntington disease is only degeneration of the dorsal striatum and explain

A

false, also involves cortical degeneration (ex: frontal and temporal associateion cortices)

151
Q

what are the characteristic symptoms of Huntington disease

A

chorea (jerky movements)
cognitive and memory deficits (caudate circuits)
enlargement of ventricles (nuclear degeneration)

152
Q

true or false: Huntington starts to degenerate the go pathway first

A

false, stop pathway first

153
Q

what is chorea

A

jerky, random and uncontrollable movements

154
Q

chorea (jerky movements)
cognitive and memory deficits (caudate circuits)
enlargement of ventricles (nuclear degeneration)

associated with what condition

A

huntington

155
Q

akinesia (instability to initiate movement)
bradykinesia (slow execution of movements)
rigidity (esp in flexors)
involuntary tremor (persists as rest)

associated with what condition

A

parkinsons

156
Q

ballism is usually unilateral or bilateral

A

unilateral

157
Q

what part of the BN is affected in ballism

A

lesion (ex: due to a stroke) affecting the sub thalamic nucleus

158
Q

what blood vessel rupture could cause ballism

A

posterior cerebral (since ballism is lesions to the sub thalamic n)

159
Q

lesions affected the sub thalamic nucleus is associated with what condition

A

ballism

160
Q

ballism causes problems with the stop or go pathway first

A

stop

161
Q

explain the issue with a lesion to the sub thalamic nucleus

A

loss of excitatory projections to the GPI (decrease in active thalamic inhibition = a lot of uncontrollable movements)

162
Q

what are the characters symptoms of ballism

A

involuntary and uncontrolled flinging/flailing movements of the extremities
typically symptoms are unilateral

163
Q

involuntary and uncontrolled flinging/flailing movements of the extremities
typically symptoms are unilateral

what condition

A

ballism

164
Q

what is the treatment for ballism

A

dopamine antagonists
surgical interventions
deep brain stimulation of the GPi

165
Q

what are the treatments for Huntington

A

dopaminergic antagonists
nutrition (require increase caloric intake)

ANAT 323 (25 decks)

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