Exam 2 Flashcards

1
Q

What are neuromodulators?

A

alter neurotransmitter release/response of receptors to neurotransmitters

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2
Q

What bone does the brainstem sit on?

A

clivus

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3
Q

Which cut can you see the mickey mouse on? If mickey mouse right side up on a CT - which is patient’s right?

A

axial, patient’s right on your left

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4
Q

What area of brainstem does sensory info go through? Is it an ascending or descending tract?

A

posterior Tegementum brainstem; ascending tracts

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5
Q

What type of output information is sent to the brainstem from the cerebellum?

A

Vestibular information:
To vestibular nucleus through middle cerebellar peduncle and to red nucleus (then to vestibular nucleus) through superior cerebellar peduncle.

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6
Q

Which cranial nerves exit from the pons?

A

CNs V through VIII

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7
Q

What are the two areas of the Tectum and their functions?

A

pretectal area/pretectum (pupillary and accommodative reflexes) and colliculi (inferior - auditory, superior - visual)

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8
Q

What does the basilar/anterior brainstem contain? (which tracts, which nuclei and which axons)

A

Motor/descending tracts, motor nuclei (substantia nigra, pontine nuclei, inferior olive), pontocerebellar axons

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9
Q

Where is the medial longitudinal fasciculus located?

A

tegmentum

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10
Q

Which area of the brainstem does the cerebral/sylvian aqueduct run through?

A

midbrain

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11
Q

Which cranial nerve exits the midbrain dorsally?

A

CN IV trochlear

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12
Q

Where is the substantia nigra located? What disease process is it involved in?

A

upper midbrain (basilar?), Parkinson’s

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13
Q

Which area of the brainstem is anterior to the fourth ventricle?

A

pons

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14
Q

What cranial nerve is responsible for lateral movement of the eye and where does it exit the brainstem?

A

CN VI abducens; lower pons

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15
Q

What axons form the medulla pyramids? And where do these tracts cross?

A

coricospinal axons (descending, motor); pyramidal decussation

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16
Q

The olivary nuclei are lateral to the pyramids. Which cranial nerve is between them?

A

CN XII

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17
Q

What is the most important function of the reticular formation? How does it do this?

A

consciousness/arousal, ascending reticular activating system

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18
Q

What reticular nuclei produce Dopamine? Acetylcholine? Serotonin? Norepinephrine? Where are they located?

A

ventral tegmental area VTA (tegmentum of midbrain); pedunculopontine nuclei (caudal midbrain); raphe nuclei (midline brainstem); locus ceruleus and medial reticular area

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19
Q

What two diseases are involved with dopamine problems (both excessive and lack of)?

A

excess VTA activity - Schizo, decreased dopamine in parkinson’s

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20
Q

Which neurotransmitter do amphetamines and cocaine stimulate the release of?

A

dopamine

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21
Q

What type of drug inhibits the reuptake of serotonin? What are the two uses of these drugs?

A

SSRIs ex: prozac, celexa, zoloft; depression and pain control

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22
Q

What are the 4/5 Ds of brainstem disfunction?

A

Diplopia, Dysphagia, Dysarthria, Dysmetria and also Dizziness if vestibular affected

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23
Q

If there is high ICP and the brainstem slides down the clivus, where does it go?

A

foramen magnum

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24
Q

What is a rotary nystagmus?

A

from hemorrhage/brainstem prob affecting oculomotor control; circular eye movement

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25
Q

With corticobulbar lesions, what symptoms are associated with UMN lesions? LMN lesions?

A

UMN - muscle hypertonia; LMN - flaccid paralysis

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26
Q

Which type of ischemia can cause transient symptoms when neck is extended and rotated?

A

vertebrobasilar artery insufficiency

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27
Q

Which nuclei controls the pupil and accommodation?

A

Edinger-Westphal

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28
Q

Which colliculus controls reflex head and eye movements?

A

Superior

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29
Q

What is the difference between Benedikt’s and Weber’s syndrome? (hint: involve third nerve palsy)

A

Benedikt’s more associated with tremor, contralateral hyperkinesis; Weber’s more with contralateral hemiparesis

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30
Q

Which area of the brainstem when damaged causes loss of vital functions that ODs see little of?

A

medulla

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31
Q

What is the function of the red nucleus?

A

upper limb flexion

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32
Q

What are the functions of the corticospinal tract? Medial lemiscus? Spinothalamic? Spinocerebellar?

A

motor, conscious proprioception, pain and temperature, unconscious proprioception

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33
Q

Brainstem gray matter becomes less organized and segmeneted into nuclei as it rises up? T?F

A

False, becomes more segmented

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34
Q

If pupil is spared, what is a possible cause of CN III palsy?

A

microvacular problem ex: diabetes

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35
Q

Which CN III muscles will be spared with a inferior divisional palsy?

A

levator and superior rectus, won’t have ptosis

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36
Q

What are the causes of aberrant regeneration? What is the most common kind in cranial nerve III?

A

congenital, trauma, neoplasm, aneurysm (last two for recent onset); bilateral lid-gaze dyskinesis (upper lid elevates on downgaze)

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37
Q

What are the two most common causes of trochlear nerve palsy? What kind of surgery can cause it?

A

head trauma and congenital; ear nose throat surgery can affect trochlear pulley

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38
Q

What type of head tilt to patients present with a SO palsy?

A

head tilt away from side of lesion to correct extorsion, may tilt head down/chin tilt to correct hypertropia

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39
Q

What level of the midbrain is the CN IV nucleus?

A

inferior colliculus

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40
Q

Name the three branches of the trigeminal. Anatomy bonus review: What foramen do they go through?

A

Ophthalmic, Maxillary, Mandibular (superior orbital fissure, foramen rotundum, foramen ovale)

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41
Q

Which nerves of the ophthalmic innervate the eyelid?

A

frontal - medial upper inner eyelid, lacrimal - lateral upper outside eyelid, nasociliary - medial eyelid

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42
Q

Which nerve may be infected if have Hutchinson sign? What else would you test?

A

nasociliary; corneal reflex

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43
Q

Which nerve is involved in chewing?

A

mandibular

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44
Q

What nerve problem do people describe as being the worst possible pain?

A

trigeminal neuralgia aka TIC douloureux

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45
Q

Which nucleus/receptors to CN V info of propioception, light touch/discrimination and pain and temp go to?

A

Rostral to caudal: Mesencephalic; chief senosry (or pontine); spinal trigeminal

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46
Q

The trigeminal nerve is involved in the efferent portion of the corneal blink reflex. T/F

A

false, it is involved in the afferent portion

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47
Q

What is the pathway of the abducens fascicle? (from nucleus until it exits brainstem)

A

from abducens nucleus at posterior pons, goes through tegmentum to pontomedullary junction, nerve then crosses over petrous bone

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48
Q

Do all esotropes have CN VI palsies?

A

no

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49
Q

What is otitis media? Gradenigo syndrome?

A

Otitis media is inflammation of the middle ear. Inflammation can affect CN VI as it passes over petrous apex of temporal bone and cause Gradenigo syndrome. Signs include periorbital unilateral pain (CN V compression), diplopia (CN VI palsy due to compression), and otorrhea (drainage from ear).

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50
Q

What is the most common cause of CN VI palsy?

A

Kids: neoplasm/trauma
Adults: neoplasm/trauma/vascular

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51
Q

What percentage of CN VI palsies resolve on their own after trauma?

A

half

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52
Q

Which of the peripheral CN is most frequently damaged? What is the name for its palsy?

A

CN VII; Bell’s palsy

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53
Q

What are the five functions the PNS?

A

SLUDS: salivate, lacrimate, urinate, defecate and sweat

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54
Q

What is the function of the nucleus solitarius; what is the function of the nucleus ambiguus?

A

Solitarius (S for sensory; located in the medulla) receives sensory input from CN VII, IX, and X.

aMbigus (M for motor, located in the medulla just posterior to the inferior olivary nucleus) receives motor input from CN IX and X.

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55
Q

What are symptoms of Bell’s palsy?

A

Unable to wrinkle brow, weak lid closure, flattened nasolabial fold, difficulty puffing cheeks and saying m/p, crocodile tears due to aberrant regeneration

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56
Q

When there are multiple CN palsies, where is a very likely area that could be damaged?

A

cavernous sinus

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57
Q

The facial nerve is involved in the efferent portion of the corneal blink reflex. T/F

A

true, and the trigeminal is the afferent

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58
Q

What type of vestibulocohlear damage has more severe symptoms? Which is usually more severe damage?

A

peripheral; central

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59
Q

What is a vestibular schwannoma?

A

benign intracranial tumor of scwann cells of the vestibulocochlear nerve

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60
Q

What does the Hallpike maneuver test for? What type of damage is it indicative of?

A

Hallpike maneuver tests for BPPV by provoking maximal movement of otoconia. Nystagmus and vergtigo are elicited when moved from sitting to supine with head at 45 degrees; peripheral CN VIII damage/BPPV

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61
Q

Which peripheral diagnoses involve positional true vertigo? Sudden onset of true vertigo? Episodic vertigo?

A

BPPV benign paroxysmal positional vertigo; labyrinthitis; Meniere’s disease

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62
Q

Which of these are not associated with hearing loss: BPPV, labrynthitis, Meniere’s disease

A

BPPV and labyrinthitis have no associated hearing loss.

Meniere’s is associated with tinnitis, aural fullness (stuffy feeling in ear), and hearing loss.

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63
Q

What gives a positive Romberg test?

A

Being unable to stand still with eyes closed. This indicates an issue with equilibrium. The entire test is based on the premise that your equilibrium depends on inputs from at least two of the following: visual info, vestibular info, and proprioceptive info.

64
Q

What is oscillopsia?

A

when your visual field shakes

65
Q

Where would the uvula be positioned in a right glossopharyngeal nerve palsy?

A

to the left

66
Q

What controls the afferent gag reflex? Efferent gag reflex?

A

CN IX controls the afferent, CN X controls the efferent.

9 before 10, A before E

67
Q

What is the vaso-vagal response?

A

patient faints from certain triggers ex: eye being touched

68
Q

What are the vagus visceral actions of CN X?

A

decrease heart rate, constrict bronchi, affect speech, increase digestive activity

69
Q

What muscles are innvervated by CN XI? What are their actions?

A

Trapezius and sternocleido-mastoid. Yes, no, I don’t know. (moves head and shoulders)

70
Q

How could you cause a lesion in CN XI?

A

Neck surgery, damage to neck

71
Q

What sounds are hard to make with the tongue with CN XII damage? X damage?

A

CN XII: “la” from ipsilateral tongue damage

CN X: “kuh” from soft palate damage (layrnx, pharynx, trachea, etc.)

72
Q

What are the three cerebellar peduncles and where do they attach?

A

superior (cerebrum/midbrain?), middle (pons) and inferior (medulla)

73
Q

Is the gray matter on the inside or outside of the cerebellum? What does the white matter contain?

A

outside; deep cerebellar nuclei

74
Q

What are the two main functions of the cerebellum?

A

Compare actual movement to intended movement

Make adjustments to movements

75
Q

Cerebellar damage results in a muscle palsy of all voluntary muscles. T/F

A

false, not a palsy/loss of sensation/muscle strength, simply a lack of coordination

76
Q

What are the three cortical layers?

A

outer interneurons, Purkinje cells, inner interneurons

77
Q

Which cells are the cerebellar cortex output cells and what do they inhibit?

A

Purkinje cells; inhibit deep cerebellar and vestibular nuclei

78
Q

What do the mossy fibers do? Are they afferent or efferent to the cerebellum?

A

synapse with interneurons that carry info to purkinje cells, they come from the spinal cord, reticular formation, vestibular system and pontine nuclei; afferent

79
Q

Which cerebellar cells send out tonic excitary signals?

A

deep nuclei

80
Q

What arteries supply the cerebellum and what arteries do they come from?

A

superior cerebellar and anterior inferior cerebellar (from the basilar artery), posterior inferior cerebellar (from the vertebral)

81
Q

What are the functions of the anterior, posterior and flocculonodular lobes of the cerebellum?

A

Anterior: Analyzes ongoing movements, especially of lower limbs
Posterior: Plans voluntary movements
Flocculonodular: Eye movements and postural adjustments

82
Q

What is the spinocerebellum? What is its function and to which deep nucleus does it send output?

A

Vermis and paravermis; gross limb movements and speech control; outputs to the fastigial nucleus.

83
Q

What is the cerebrocerebellum? What is its function and to which deep nucleus does it send output?

A

Lateral hemispheres; fine, voluntary movement; ouputs to dentate nucleus.

84
Q

Wha is the functional name for the Flocculonodular lobe?

A

vestibulocerebellum

85
Q

Which nucleus in the cerebellum is most lateral? (hint: most of its fibers go through superior peduncle)

A

dentate nucleus

86
Q

What three types of information are sent from the cerebellum to the UMN system to then go through the corticospinal tract?

A

Proprioception, vestibular information, environmental cues.

87
Q

What three systems are needed for postural control? Where do these inputs come from?

A

Vision (from cortex, thalamus, basal ganglia); vestibular (brainstem, cerebellum); somatosensation (spinal cord)

88
Q

What is the difference between cerebellar ataxia and sensory ataxia?

A

Cerebellar: unable to stand with feet together, but vibratory sense, proprioception, and ankle reflexes work.
Sensory: can stand together, but vibratory sense, proprioception and ankle reflexes are dysfunctional

89
Q

Cerebellar lesions affect the ipsilateral side of the body. T/F

A

true, efferents go to contralateral cortex and red nucleus but then those cross again in their descending tracts

90
Q

Which functional division of the cerebellum is damaged in ataxic gait?

A

spinocerebellar

91
Q

Which functional division projects to the dentate nucleus? Fastigial nuclei?

A

cerebrocerebellum; spinocerebellum

92
Q

What is dysdiadochokinesia? What division is usuallly damaged?

A

can’t rapidly alternate movement; cerebrocerebellar

93
Q

What part of brain involved in helping adapt to yoked prisms in prism adaptation experiments?

A

olivary nucleus

94
Q

Hypermetric saccade is an initial overshoot or undershoot?

A

overshoot

95
Q

What type of saccadic disfunction is horizontal around fixation but has no quick phase?

A

ocular flutter

96
Q

What causes downbeat nystagmus?

A

Arnold-chiari malformation (tonsils protruding into foramen magnum)

97
Q

What is the name for the series of very debilitating cerebellar ataxias?

A

spinocerebellar ataxia

98
Q

What separates the posterior lobe (inferior portion called cerebellar tonsils) and flocculonodular lobe?

A

posterolateral fissure

99
Q

What are the output motor areas of the basal ganglia?

A

motor areas of cortex via the thalamus, pedunculopontine nucleus

100
Q

What is the main function of the basal ganglia? What does it work with to do this?

A

inhibit unwanted mov’t; cerebellum

101
Q

What is the striatum composed of? What does it initiate?

A

caudate and putamen; automatic overlearned processes ex: playing piano

102
Q

What separates the thalamus and caudate nucleus from the globus pallidus and putamen?

A

internal capsule

103
Q

What is this structure mainly composed of? What is it called above the basal ganglia?

A

fibers of the corticospinal ascending and descending?; corona radiata

104
Q

The basal ganglia has several direct connections to lower motor neurons to influence movement. T/F

A

false, indirect and direct connections to thalamus

105
Q

Which neurotransmitter is sent from cortex to the putamen? Is it excitatory or inhibitory?

A

glutamate; excitatory

106
Q

What two ways does the putamen inhibit output nuclei?

A

GABA, substance P

107
Q

What is pill rolling an example of?

A

resting temor in Parkinson’s

108
Q

What types of visual symptoms do Parkinson’s patients exhibit?

A

CI, difficulty in upgaze, slow saccades

109
Q

What happens when you tap between eyebrows of a Parkinson’s patient?

A

can’t suppress blink, have difficult reopening lids (apraxia)

110
Q

What is another Parkinson-like disease that results in difficulty with downgaze as opposed to upgaze?

A

PSP progressive supranuclear palsy

111
Q

Is Hungtington’s a hyperkinetic or hypokinetic disease?

A

hyperkinetic

112
Q

What happens to the caudate nucleus and ventricles in Huntington’s?

A

atrophy; enlarge

113
Q

What is chorea? Dystonia?

A

involuntary movement disorders; part of dystonias nonprogressive genetic mov’t disorders

114
Q

What type of dystonia is a hand dystonia?

A

focal dystonia

115
Q

What type of damage leads to ballism?

A

subthalamic nucelus stroke contralaterally

116
Q

What is the function of the substantia nigra? What substance does it contain?

A

sends dopamine to striatum and subthalamus; melanin

117
Q

Which basal ganglia nuclei has a cognitive but not motor function?

A

caudate

118
Q

Where is the LGN relative to the thalamus?

A

lateral

119
Q

Which thalamic nuclei relays info from inferior colliculus to the auditory cortex?

A

MGN

120
Q

What small part of the basal ganglia is involved with the subthalamus?

A

substantia nigra, and red nucleus

121
Q

What is located in the epithalamus?

A

pineal body, habenular nuclei

122
Q

What calcifies in the diencephalon and serves as a landmark on a CT scan?

A

pineal body

123
Q

What is the function of the habenular nucelI?

A

olfactory/emotional response to odor

124
Q

What connects the pituitary to the hypothalamus?

A

infandibulum

125
Q

What lies behind chiasm on the hypothalamus?

A

mammillary bodies

126
Q

What is another name for the posterior pituitary? Anterior pituitary?

A

neurohypophysis; adenohypophysis

127
Q

Where is oxytocin released?

A

released from posterior pituitary; come from hypothalamus

128
Q

What hormone can lead to hyperplasia of the thyroid gland? What is this called?

A

TSH; goiter

129
Q

What would happen with a lack of antidiretic hormone?

A

dehydration, decrease in blood pressure

130
Q

What hormone is released from the anterior pituitary in response to somatostatin?

A

trick question - somatostatin aka GHIH inhibits release of growth hormone

131
Q

What causes the release of growth hormone? What is its function?

A

GHRH; increase glucose synthesis in liver, increased tissue growth

132
Q

What would cause sexual disfunction and bitemporal visual field loss?

A

pituitary tumor

133
Q

What inhibits the release of CRH in the hypothalamus? ACTH in the anterior pituitary?

A

excess cortisold/steroids in circulation for both (negative feedback)

134
Q

Where are corticosteroids released from? What do they do?

A

adrenal cortex in the kidneys; decrease inflammation, increase glucose production, breakdown fat/muscle, decrease immune response

135
Q

What are the three parts of the limbic lobe?

A

cingulate gyrus, parahippocampal gyrus and subcallosal gyrus

136
Q

What hormone is released in response to stress/high emotion?

A

cortisol

137
Q

What type of memory is involved in forming long term memories?

A

declarative

138
Q

What type of memory does not go through the limbic system? What are the three stages of it?

A

procedural; cognitive, associative, autonomous

139
Q

The nasal and temporal nerve fibers separate at the optic disc. T/F

A

false, separate at macula

140
Q

What type of visual field defect would see with a coloboma?

A

superior field defect because of incomplete fetal fissure closure inferior to amcula

141
Q

What section of the optic nerve is longest?

A

intraorbital

142
Q

What are the signs of optic neuropathy?

A

reduced VA, decreased colour vision, RAPD, VF defect, disc swelling/edema, pallor, cupping (not pink and distinct)

143
Q

Why do you see superior temporal defection in junction scotoma?

A

nasal fibers of contralateral eye loop into optic nerve

144
Q

What four areas do extrageniculate projections go to?

A

hypothalamus, pretectal area, superior colliculus, pulvinar nucleus

145
Q

What layers are from the ipsilateral eye AND contain magnocellular cells in the LGN?

A

layer 2

146
Q

What is the function of the konio cells?

A

not too sure, but involved in blue and yellow colour perception

147
Q

Where are the Meyer’s loops located?

A

temporal lobe

148
Q

What type of field defect do you see with temporal lobe damage?

A

superior field defect (Meyer’s loops involved)

149
Q

What type of damage can result in hemispatial neglect and an inferior field defect?

A

parietal lobe damage

150
Q

What layer of cortex do most LGN fibers go to?

A

four

151
Q

What neurological visual condition can halt the formation of ocular dominance columns?

A

ambylopia

152
Q

Which visual cortex layers provide feedback to LGN?

A

layers 5 and 6

153
Q

What symptoms do you have with ventral pathway damage?

A

visual agnosia, prosopagnosia

154
Q

Where is the dorsal pathway located? What symptoms do you have when it’s damaged?

A

parietal lobe; where/how pathway so optic ataxia

155
Q

What kind of CN palsy is the most common form of ophthalmoplegia?

A

CN VI