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NBS3 quicknotes > NB3 EXAM 2 > Flashcards

NB3 EXAM 2 Flashcards

1
Q

The fibers of the lateral olfactory tract termine where

A

olfactory tubercle, anterior perforated substance, entorhinal cortex and pyriform cortex

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2
Q

what is the only system that projects directly to the cortex without going to thalamus first

A

olfactory

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3
Q

which system is responsible for the identification of odors

A

orbitofrontal cortex

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4
Q

which system is responsible for the emotional response to odors

A

hypothalamus, entorhinal cortex, hippocampus and hypothalmus

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5
Q

hyposomia is

A

rediced ability to detect odors

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6
Q

anosmia is

A

complete inability to detect odors

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7
Q

parosmia

A

change in normal perception of odors

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8
Q

phantosmia:

A

sensation of an odor that is not there

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9
Q

what taste buds are located on the front of the tongue, side of tongue and back of tongue

A

fungiform, foliate, and circumvallate

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10
Q

in taste, once VII, IX, and X neurons get to the NTS, where to they project?

A

to the VMP of the thalmus and then to the insular and frontal cortex

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11
Q

what higher brain centers project to the NTS for taste manipulation

A

amygdal and hypothalamus. the insular and frontal cortex indirectly

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12
Q

defect in LCA

A

the retinal pigment epithelium fails to phagocytose the shed outer segments of the photoreceptor cells.

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13
Q

papilladema

A

swelling of the optic nerve head, correlated with intracranial pressure increases

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14
Q

what causes retinitis pigmentosa

A

Loss of Rod photoreceptors; mutations in rhodopsin and other components of the g-protein cascade cause retinitis pigmentosa. You will see thin vessels, pale retina, and protrusion of RPE cells into the retina itself

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15
Q

what is usually the first complaint for people with retinitis pigmentosa?

A

loss of night vision

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16
Q

Macular Degeneration

A

loss of cone photoreceptors and loss of foveal vision since the fovea is made solely of cones

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17
Q

the Cone “on” pathway depends on

A

MGLUR6

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18
Q

the “off” cone pathway depends on

A

ionotropic glutamate receptor

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19
Q

why do people with metastatic melanoma become night blind?

A

because they are producing atibodies to the trp channel, so the channel cannot open and the cell cannot depolarize to sense light.

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20
Q

congenital stationary night blindness

A

mutations in MGLUR6

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21
Q

lesion in the left occipital lobe –>

A

a problem with the PCA. This leads to pure alexia (inability to read) without agraphia .

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22
Q

dyslexia is involved with what part of he brain

A

palum temporale

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23
Q

in terms of language what does the right hemisphere do

A

intonation and language used in social context, like sarcasm

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24
Q

sensory neglet or asomatognosia comes from

A

damage to the superior part of the parietal love

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25
Q

tectospinal tract does

A

originated in the superior collicuus and turns gaze to an area of interest. involves only muscles inntervated in the upper cord

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26
Q

damage to the medial pathways

A

causes changes in muscle tone and may include defecits in maintaing balance

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27
Q

4 projections of motor nucelu

A

red nucleus
reticular formation
superior colliculus
vestibular nuceli

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28
Q

horizantal eye movements are related to

A

PPRF (Pons)

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29
Q

Vertical eye movements are related to

A

Mesencephalic reticular formation, MRF (midbrain)

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30
Q

what 4 things project to the PPRF

A

cortical frontal eye fields, basal ganglia, cerebellum, superior colliculus

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31
Q

most important structure in initiating saccadic eye moveents?

A

superior colliculus

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32
Q

retinal input goes to the ___ layer of the superior colliculus

A

superior layer

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33
Q

the deep layer of the superior colloculus contins

A

motor innervtion

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34
Q

is the sensory map of the superficial layer of the superior colliculus in register with the motor map that generates the appropriate moveents?

A

yes

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35
Q

where do frontal eye fields project to initiate eye movement?

A

both to the brainstem directly to initiate movement and to the deep layers of the superior colliculus

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36
Q

a lesion to both the frontal eye fields and the superior colliculus results in

A

no saccades

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37
Q

a lesion to the frontal eye fields results in

A

the ability to make saccades to visual targets without the ability to to make saccades to remembered targets

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38
Q

a lesion to the superior coliculus results in

A

ability to make saccades to remembered targets but not to visual targets

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39
Q

what area is involved in controlling smooth pursuits

A

middle temporal area

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40
Q

if you see nystagmus think

A

lesion to the vestibular nerve

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41
Q

striatum =

A

caudate and putamen

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42
Q

Lentiform =

A

putamen and the globus pallidus

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43
Q

hemiballismus is ___ and results from ___

A

It is increase in movement due to damage of the subthalamic nucleus

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44
Q

huntington’s is a problem of the

A

striatal neurons of the indirect pathway

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45
Q

dopamine is ____ to striatal neurons of the indirect pathway

A

inhibitory to

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46
Q

dopamine is _____ to the striatal neurons of the direct pathway

A

excitatory

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47
Q

indicrect pathway will ___ movement

A

decrease

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48
Q

direct pathway will ___movement

A

increase

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49
Q

major function of vestibulocerebellar pthway

A

balance and eye movements

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50
Q

major function of spinocerebellar pthway

A

motor execution, regulate tone, posture and locomotion

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51
Q

major function of cerebrocerbellum pthway

A

coordination and planning of voluntary movement

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52
Q

inputs to the vestibulocerebellar pathway

A

vestibular nerve, vestibular nucelei, inferior olive

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53
Q

sources of the outputs of the vestibulocerebellar pathway

A

perkinje cells and fastigial nucleus

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54
Q

targets of outputs of the vestibulocerebellar pathway

A

vestibular nuceli, reticular formation, VL of the thalamus

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55
Q

what part of the motor system does the vestibulocerebellar target?

A

UMN of medial pathways

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56
Q

Major signs of damage to the vestibulocerebellar pathway

A

stagering gait or nystagmus

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57
Q

inputs of the spinocerebellar pathway

A

all 4 of the spinocerebellar tracts and the inferior olive

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58
Q

sources of outputs of the spinocerebellar pathway

A

fastigial nucleus and interposed nucleus

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59
Q

targets of outputs of the spinocerebellar pathway

A

vestibular nuceli, reticular formation, VL of thalamus, red nucelus

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60
Q

part of motor system targeted by the spinocerebellar pathway

A

UMN of medial and lateral pathways

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61
Q

signs of damage to the spinocerebellar pathway

A

intention tremor

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62
Q

inputs of the cerebrocerebellar pathway

A

pontine nuclei (relaying info from the sensory and motor cerebral cortex) and inferior olive

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63
Q

sources of outputs of the cerebrocerebellar pathway

A

dentate nucleus

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64
Q

targets of outputs of the cerebrocerebellar pathway

A

VL of the thalamus and the red nucleus

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65
Q

part of motor system targeted by the cerebrocerebellar pathway

A

motor cortex

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66
Q

if you see gait ataxia and nystagmus and decide tht you have a problem with the verims and flocculonodular lobe aka vestibulocerebellar, what arteries may be involved

A

AICA - flocculus
PICA - vermis
SCA - rostral vermis

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67
Q

If you see a patient with incoordination of the limbs with decomposition of movement and you believe tht the paravermal and lateral hemispheres may be damaged, what arteres do youthink?

A

PICA - caudal portions of lateral hemispheres

SCA - rostral portions of lateral hemispheres

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68
Q

patellar reflex level

A

L4

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69
Q

achilles reflex level

A

S1

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70
Q

what are the locations and relevant pathways ofthe five UMN

A

1- reticular formation: medial and lateral reticulospinal
2-vestibular nuceli - medial and lateral vestibulospinal tracts
3-superior colliculus- tectospinal
4- rednucleus -rubrospinal
5-motor cortex - corticospinal and corticobulbar tracts

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71
Q

describe the pathway of the medial vestibulospinal pathway

A

utricle and saccule –> medial vestibular nucelus –> descending MLF -> cervical spinal cord for neck movements and postural movements to stabalize head

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72
Q

describe the pathway of the lateral vestibulospinal pathway

A

utricle, saccule and cerebellumm –> lateral vestibular nucelus –> ipsilateral projections to the spinal cord

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73
Q

what are the lateal pathways used for?

A

to control the limbs

74
Q

which pthways are consdered lateral pathways

A

corticospinal and rubrospinal

75
Q

path of rubrospinal tract?

A

originates in the red nucleus, crossesmidline and descends laterally

76
Q

the medial pathways are the ___ and are important for maintaing posture and balance

A

vestibulospinal, tectospinal and reticulopsinal

77
Q

tectospinal originates

A

originates in the superior colliculus

78
Q

the tectospinal is responsible for

A

turning gaze to an area of interst

79
Q

where do the medial and lateral reticulospinal trct originate

A

medial in the pons

lateral in the medulla

80
Q

what are the reticulospinal trats important for

A

influence on muscle tone

81
Q

what is in the inferior cerebellar peduncle?

A

spinal cerebellar tracts heading to cerebelum

82
Q

what is in the middle cerebellar peduncle?

A

neurons from the cortex that travel via the pontine nuclei

83
Q

what is in the superior cerebellar peduncle?

A

mostly outputs from the deep nuclei of the cerebellum to the thalamus

84
Q

wernike and broca are located on which side of the brain?

A

the left

85
Q

the sensory/ expressive language area is

A

Wernicke, posterior

86
Q

the motor/ expressive languge area is

A

Broca, anterior

87
Q

what connects the wernicke and broca areas

A

arcuate fasciculus

88
Q

pathway of repeating a spoken word

A

primary auditory cortex –> wernicke –> Broca –> motor primary cortex –> corticobulbar

89
Q

repeating a written word

A

eyes –> primrary visual cortex –> wernicke –> broca –> motor cortex

90
Q

WADA test

A

uses a barbituate to determine dominant side.

91
Q

brocas aphasia is

A

nonfluent, very simple sentences, comprehesion is preserved. right hemiparesis in the arm
(MCA)

92
Q

wernicke’s aphasia

A

speech is fluent but they arent making any sense.No motor signs

93
Q

conduction aphasia

A

arcuate fasciculus impaired so fluent and comprehesion is preserved but cannot repeat

94
Q

a lesion of the left occipital lobe and in the splenium of the corpus callosum would be caused by _____ and would lead to _____

A

PCA
the connections between the unilateral language areas are severed. So you get pure alexia (inability to read) without agraphia (inaibility to write)

95
Q

a lesion of the dominant angular gyrus would cause

A

alexia and agraphia

96
Q

dyslexia is believed to be due to

A

a lack of assymmetry in the planum temporale

97
Q

the right hemisphere contributes to language in what way?

A

stress, timing and intonation –> monotone and dont understand jokes

98
Q

the loss of musical skills results from

A

infarction of the posterior part of the right superior temporal gyrus

99
Q

spacial perception is processed by the

A

superior parietal lobule

100
Q

asomatognosia is the

A

neglect of personal space

101
Q

damage to the right (nondominant) superior parietal lobe results in

A

asomatognosia on the left side

102
Q

prosopagnosia

A

inability to recognize faces

103
Q

which lobe is responsible for personality

A

frontal lobe

104
Q

two areas involved in consciousness?

A

1) The reticular formation: responsible for wakefulness

2) The cerebral cortex: responsible for state of awareness

105
Q

type of waves when alert and awake and in REM

A

beta waves, 14-30 hz, high frequency, low amplitude

106
Q

typeof waves when quiet waking / eyes closed

A

alpha waves, 8-14

107
Q

type of waves in sleep stage 1 and 2

A

theta waves, 4-8 hz

108
Q

type of waves in sleep stage 3 and 4

A

delta waves, .5-4 hz

109
Q

what keeps the thalamus in transmission mode?

A

cholinergic inputs from the rostral pons and basal forbrain. pedunculopontine and laterodorsal tegmental nuclei

110
Q

what keeps the thalamus in burst mode?

A

the reticular nucelus releasing GABA and hyperpolarizing the thalamus

111
Q

charactersitics of REM sleep

A

loss of muscle tone, eye movements, high frequency and low amplitude waves. No regulation od body temperature, sympathetics lost,

112
Q

PGO spikes are

A

ponto-geniculo occipital spikes, correlated with eye movements in REM sleep

113
Q

PGO ON SPIKES are regulated by

A

nucleus reticularis pontis oralis

114
Q

PGO OFF spikes are rgulated by the

A

serotonergic cell in the raphe nuclei of the brainstem which regulate the nucleus reticularis pontis oralis

115
Q

what regulates circadian rythms

A

suprachiastmatic nucleus

116
Q

narcoslepy is

A

onset of REM sleep

117
Q

cataplexy is

A

abrupt loss of muscle tone without loss of consciousness

118
Q

sleepwalking occurs during

A

the 1st stage 4 non-REM period

119
Q

caffeine is an antagonist to

A

adenosine receptors (adenosine is sleep promotine)

120
Q

auras preceed the onset of

A

focal seizures

121
Q

petit mal siezures are

A

absence siezures which are non convulsive and found in children

122
Q

Grand mal seizures

A

tonic - clonic -patient falls to the ground rigid followed by jerking

123
Q

myoclonic siezures

A

brief jerking movement with both sides of body

124
Q

most frequent site of epileptic focus

A

medial surface of the temporal lobe

125
Q

smells, deja vu, fear and anxiety auras are due to

A

amygdala being involved in the damaged area

126
Q

the two forms of memory are

A

declarative and nondeclrative. declarative pertains to dates and facts, non-declarative pertains to habits.

127
Q

the aquisition of declarative memories is due to the

A

medial temporal lobe

128
Q

classical conditioning is

A

an innate reflex assocaited with an unrelated stimulus

129
Q

operant conditioning is

A

the probabilty of an altered behavioral response by association with reward

130
Q

retrograde amnesia

A

loss of memory for events prior to the trauma

131
Q

anterograde amnesia

A

inability to form new memories following brain trauma

132
Q

the cell affected in Alzheimer’s disease are

A

Hippocampal pyramidal cells

133
Q

bilateral lesions of the mammillary bodies leads to

A

Korsakoff syndrome

134
Q

what is the structure most involved with nondeclarative memories

A

the striatum

135
Q

what is working emory

A

retention od information needed to guide ingoing learning and behaviours

136
Q

what structure seems to be responsible for working memory

A

the hippocampus

137
Q

what area is responsible for problem solving using recent information to change behavior?

A

the prefrontal cortex

138
Q

senile plaques and neurofibrillary tangles are often seen in

A

Alzheimer’s disease

139
Q

a hall mark of alzheimer’s disease is ____ plaques

A

amyloid

140
Q

limbic system most involved with emotion is

A

amygdala

141
Q

what are the three nuceli of the amygdala

A

basolateral nuclei
corticomedial nuclei
central nucleus

142
Q

wht is the fx of the basolateral nuclei

A

visual, auditory, gustatory and tactile afferents

143
Q

fx of the corticomedial nuclei

A

receive olfactory afferents

144
Q

fx of the central nucleus

A

out put of the amygldala

145
Q

electrical stimulation of the amygdala priduces

A

fear

146
Q

urbache wiethe disease

A

is degenerative condition assciated with calcium deposit on the amygdala. Results in inaibility to discern fear.

147
Q

neuropathic pains results from a

A

direct injury to nerves in the PNS –> burning sensation

148
Q

scale of choice?

A

visual analogue scale

149
Q

children use what type of scale?

A

category scale

150
Q

thermoreceptive specific cell types in the dorsal horn respond to

A

innicuous cooling

151
Q

sensory-discriminative type of pain is

A

sense of the intensity, location, quality and duration of the pain

152
Q

the sensory-discriminative type of pain is sensed where

A

in the lateral system

153
Q

motivational-affective component of pain is

A

unpleasantness and urge to escape the unpleasantness

154
Q

The motivational-affective component of pain is sensed in the

A

medial system

155
Q

main player in initiation and modulation of descending controls of nociceptive information

A

Periaqueductal grey

156
Q

examples of acidic antipyretics are ___ and they can be used in treating ___

A

apririn and NSAIDs = ibuprofen

use to treat acute and chronic pain, inflammation

157
Q

examples of non-acidic antipyretics are ___ and they can be used to treat ___

A

acetaminophen,

used to treat acute pain and fever

158
Q

naloxone is an

A

opioid antagonist that has a high affinity for morphine receptor sites. It reverses the effect of opioid analgesics by displacement

159
Q

the reticular formation

A

modulates pain, muscle tone and reflexes and wakefulness

160
Q

midline raphe nucelus

A

produces seratonin, and regulates pain, arousal, and sleep

161
Q

locus cerelius are

A

NE projecting cells - only sourceof NE in the brain

162
Q

parasaggital lateral nuceli are the only source of

A

ACH in the brain

163
Q

anterior hypothalamus influenes

A

PNS

164
Q

posterior hypothalamus influences

A

SNS

165
Q

the magnocellular region of the supraoptic and paraventricular nuclei make

A

ADH and Oxytocin

166
Q

tubuloinfundibular region of the hypothaamus

A

brings hormones to the posterior pituitary

167
Q

the posterior nucleus of the hypothalamus ______ heat

A

generates

168
Q

the anterior nucleus of the hypothalamus _____ heat

A

dissipates

169
Q

the lateral nuclei of the hypothalamus generates

A

eating

170
Q

the ventromedial nucleus of the hypothalamus ___ eating

A

decreases

171
Q

damage to the lateral nuclei of the hypothalamus would lead to the

A

body wasting away

172
Q

the anterolateral and the DC project to the ___ of the thalamus

A

VPL

173
Q

the trigeminal system projects to the ___ of the thalamus

A

VPM

174
Q

the inferior colliculus projects to the ____ for ______

A

inferior colliculus projects to the MGB for hearing

175
Q

the superior colliculus projects to the ____ for ______

A

LGB for vision

176
Q

VL of the thalamus

A

cerebellum projects to the VL then goes to the precentral gyrus and frontal cortex for motor and movement planning

177
Q

the thalamus is fed by what artery

A

PCA

178
Q

infarction of the inferolateral artery does what

A

thalamic syndrone, with sensory loss, ataxia and paralysis t the contralateral side

179
Q

posterior commisure coordiantes

A

eye movements

180
Q

association fibers

A

connect adjacent gyri

181
Q

conductive aphasia

A

can produce speech and can follow commands but cannot repeat

182
Q

the projections of corticospinals through the internal capsule, the face is anterior or posterior

A

anterior

NBS3 quicknotes (4 decks)

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