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Neuro Flashcards

1
Q

Frontal lobe function (5)

A
  1. regulate and initiate motor function
  2. language
  3. cognitive functions
  4. attention
  5. memory
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2
Q

Parietal lobe function (3)

A
  1. sensation – touch, pain
  2. sensory aspects of language
  3. spatial orientation and self perception
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3
Q

Occipital lobe function (1)

A

process visual info

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4
Q

Temporal lobe function (3)

A
  1. process auditory info
  2. emotions
  3. memories
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5
Q

limbic lobe parts (4)

A

amygdala, hippocampus, cingulate gyrus, mamillary body

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6
Q

limbic lobe functions (5)

A
  1. learning
  2. memories
  3. reward
  4. emotion
  5. motivation
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7
Q

Which are white matter tracts (3)

A
  1. Association fibres
  2. Commissural fibres
  3. Projection fibres
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8
Q

which association fibres connect which lobes (4 pairs)

A
  1. superior longitudinal fasciculus (frontal nad occipital)
  2. arcuate fasciculus (frontal and temporal)
  3. Inferior longitudinal fasciculus (temporal and occipital)
  4. Uncinate fasciculus (anterior frontal and temporal)
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9
Q

characteristics of localisation of function in primary cortices

A
  1. function predictable
  2. organised topographically
  3. left right symmetry
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10
Q

function of primary motor cortex

A
  1. controls fine, discrete precise voluntary movements
  2. provide descending signals to execute movements
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11
Q

function of premotor area

A

planning movements (externally cued)

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12
Q

function of supplementary area

A

planning complex movements (internally cued)

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13
Q

function of primary somatosensory area

A

process somatic sensations from receptors in body (eg fine touch, vibration, proprioception, 2-point discrimination, pain, temp)

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14
Q

function of somatosensory assocation

A

interpret significance of sensory info

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15
Q

difference between broca’s area and wernicke’s area

A

Broca: speak, production of language
wernicke’s understanding of language

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16
Q

what happens to frontal lobe lesions

A

change in personality and inappropriate behavior

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17
Q

what happens to parietal lobe lesions (eg right hemisphere lesion)

A

contralateral neglect
lack of awareness of self on left side
lack of awareness of left side of extrapersonal space

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18
Q

what happens to temporal lobe lesions

A

agnosia (inability to recognise), anterogade amnesia (cannot form new memories)

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19
Q

what happens to broca’s and wernicke’s area lesions

A

broca: expressive aphasia (poor production of speech)
wernicke’s: comprehensive aphasia (poor comprehension of speech, production is fine)

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20
Q

what happens to primary visual cortex lesion

A

blindness in corresponding part of visual field

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21
Q

what happens to visual association lesion

A

deficits in interpretation of visual info
prosopagnosia (inability to recognise familiar or learn new faces

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22
Q

what are some scans to assess cortical function

A

PET (positron emission tomography)
fMRI
EEG (electroencephalography)
MEG (magnetoencephalography)
TMS (transcranial magnetic stimulation)
tDCS (transcrania direct current stimulation)

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23
Q

what are some scans to assess structures

A

DTI (Diffusion tensor imaging) –> based on diffusion of water molecules

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24
Q

what is MS

A

autoimmune
loss of myelin from neurons of CNS

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25
Q

main symptoms of MS (5)

A

blurred vision
fatigue
difficulty walking
numbness and tingling
muscle stiffness

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26
Q

what are the blood supplies to brain

A

carotid artery and vertebral
artery

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27
Q

what are types of haemorrhage (4)

A

epidural, subdural, subarachnoid, intracerebral

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28
Q

what is extradural haemorrhage

A

trauma caused
immediate clinical effects (arterial, high pressure)

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29
Q

what is subdural haemorrhage

A

trauma caused
delayed presentation of clinical effects (venous, low pressure)

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30
Q

what is subarachnoid haemorrhage

A

ruptured anneurysm

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31
Q

what is intracererbral haemorrhage

A

spontaneous hypertensive

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32
Q

risk factors of stroke

A

age
hypertension
DM
smoking
cardiac disease

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33
Q

what are the cerebral artery perfusion for cerebrum

A

anterior, middle, posterior cerebral artery

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34
Q

what are anterior cerebral artery symptoms lesion

A

paralysis of contralateral structures (leg > arm) , loss of appropriate social behavior, disturbance of intellect, executive function &w judgement

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35
Q

what is middle cerebral artery symptoms lesion

A

classic stroke
contralateral hemiplegia (arm > leg)
contralateral hemisensory deficits
hemianopia
aphasia

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36
Q

what is posterior cerebral artery symptoms lesion

A

visual deficits (homonymous hemianopia, visual agnosia)

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37
Q

what are the 2 major descending tracts

A

pyramidal(pass thru pyramids of medulla) and extrapyramidal (dont pass thru pyramids of medulla)

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38
Q

what are the 2 pyramidal tract pathway

A

corticospinal
corticobulbar

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39
Q

what are the 4 extrapyramidal tract pathway

A

tectospinal
vestibulospinal
rubrospinal
reticulospinal

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40
Q

function of pyramidal tracts

A

voluntary movements of body and face

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41
Q

where nerve pass from in pyramidal tracts

A

motor cortex to spinal cord or cranial nerve nuclei in brainstem

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42
Q

function of extrapyramidal tracts

A

involuntary movements for balance and posture and locomotion

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43
Q

where nerve pass from in extrapyramidal tracts

A

brainstem nuclei to spinal cord

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44
Q

function of primary motor cortex

A

controls fine, discrete voluntary movements
provide descending signals to execute movements

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45
Q

function of premotor area

A

plan movements
regulate externally cued movements

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46
Q

function of supplementary area

A

plan complex movements (internally cued, speech)

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47
Q

function of vestibulospinal

A

stabilise head during body &head movements
coordinate head movements with eye movemetns
mediate postural adjustments

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48
Q

function of tectospinal

A

orientation of head and neck during eye movements
from superior colliculus of midbrain

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49
Q

function of reticulospinal

A

from medulla n pons
change in muscle tone asociated with voluntary ovement
postural ability

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50
Q

upper motor neuron lesion negative signs (3)

A

loss of voluntary motor function
paresis (graded weakness of movements)
paralysis (complete loss of voluntary muscle activity)

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51
Q

upper motor neuron lesion positive signs (5)

A

increased abnormal motor function due to loss of inhibitory descending inputs
spasticity (increase muscle tone)
hyper-reflexia (exaggerated reflexes)
clonus (abnormal oscillatory muscle contraction)
babinski’s sign (abrnomal response in foot)

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52
Q

lower motor neuron lesion signs (6)

A

weakness
hypotonia
hyporeflexia
muscle atrophy
fasciculations (visible twitch)
fibrillations (twitching of individual muslce fibres, recorded in needle EMG)

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53
Q

what is motor neuron disease (MND)

A

neurodegenerative disorder of motor system

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54
Q

MND Upper Motor Neuron signs

A

spasticity (increased tone of limbs and tongue)
babinski’s sign
brisk limbs and jaw reflexes
loss of dexterity
dysarthria(difficulty speaking)
dysphagia (difficulty swallowing)`

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55
Q

MND lower motor neuron signs

A

weakness
muscle wasting
tongue fasciulations and wasting
nasal speech
dysphagias

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56
Q

structure of basal ganglia

A

caudate nucleus
lentiform nucleus (lentiform +caudate = putamen)
caudate +putamen = striatum
substantia nigra (midbrain)

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57
Q

function of basal ganglia

A

decision to move
perform associated movements (change facial expression)
perform movements in order
suppress unwanted movements

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58
Q

signs of parkinson’s disease

A

bradykinesia
hypomimic face
akinesia
rigidity
tremor at rest

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59
Q

what is parkinson’s disease

A

degeneration of dopaminergic neurons that originate in substantia nigra and project to striatum

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60
Q

what is huntington’s disease

A

degeneration of GABAergic neuron in striatium, caudate and then putamens

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61
Q

signs of huntington’s

A

choreic movements
rapid jerky involuntary mvoements (hand–> face –> legs –> rest of body)
speech impairment
difficulty swallowig
dementia
cognitive decline
unsteady gait

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62
Q

what is ballism

A

from stroke affecting subthalamic nucelus
uncontrolled flinging
contralaterally

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63
Q

what is cerebellum separated from cerebrum by

A

tentorium cerebelli

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64
Q

signs of cerebella dysfunction

A

ataxia (impairment in movement coordination and accuracy)
dysmetria (inappropriate force and distance for target directed movement)
intention tremor
dysdiadochokinesian (inability to preform rapidly alternating movements)
scanning speech (staccato)

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65
Q

what is alpha motor neuron

A

LMN of brainstem and spinal cord
innervate extrafusal muscle fibres of skeletal muscles
activate muscle contraction

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66
Q

what are the 3 types of motor unit

A

S, type l
FR, type llA
FF, type llB

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67
Q

how do we regulate muscle force

A

recruitment and rate coding

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68
Q

motor unit type switching

A

llB to llA after training
l to ll in severe deconditioning or spinal cord injury
loss of l and ll but preferentially ll in ageing

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69
Q

what stimulates involuntary coordinated pattern

A

peripheral stimuli

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70
Q

example of descending control of reflexes

A

jendrassik manoeuvre

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71
Q

which dominates normal condition, inhibitory or excitatory control

A

inhibitory

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72
Q

which dominates decrebration condition, inhibitory or excitatory control

A

excitatory from suprasinal areas

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73
Q

what is order of descending control of reflexes

A

activate alpha motor neurons
activate inhibitory interneurons
activate propriospinal neurons
activate gamma motor neurons
activate terminals of afferent fibres

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74
Q

what motor neuron is hyper reflexia associated with

A

UMN lesion

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75
Q

what is clonus (abnormal, hyper reflexia) associated with

A

UMN lesion
involuntary and rhythmic muscle contractions
loss of descending inhibition

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76
Q

what is babinski’s sign associated with

A

UMN lesion
big toe curl upwards in adults when sole stimulated with blunt instrument (normally curl downwards) –> positive babinski’s sign

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77
Q

what is hypo-reflexia associated with

A

LMN disease

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78
Q

examples of primary headache

A

migraine
tension-type headache
cluster headache

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79
Q

what are secondary headache

A

spercipitated by other condition (eg tumor)

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80
Q

which is more long lasting – tension type or cluster headache

A

tension type , migraine
they can last long but usualy shorter (30mins-1hr)

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81
Q

which is more short lasting – tension type or cluster headache

A

cluster headche
but usually longer (45mins -3hrs)

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82
Q

key red flags of secondary headache

A

age, onset, systemic symptoms, neurological signs

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83
Q

migraine characteristics

A

unilateral
pulsating quality
moderate or severe pain intensity
aggravation by routine physical activity
last hrs or some days

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84
Q

does migraine associate with aura

A

can be with or without aura

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85
Q

symptoms associated with migraine

A

nausea and / or vomiting
photophobia and or phonophobia

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86
Q

what is visual aura in migraine

A

complex array of symptoms reflecting focal cortical or brainstem dysfunction

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87
Q

how long is the graded evolution of visual aura

A

5-20 mins (< 1hr)

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88
Q

describe aura in migraine

A

expanding C
elemental visual disturbance

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89
Q

4 phases of migraine

A

premonitory
aura
headache
recovery

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90
Q

acute treatment for migraine

A

paracetamol
NSAIDS
prokinetics
triptans

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91
Q

long term preventives of migraine

A

TCA (tricyclic antidepressants)
B-blockers
serotonin antagonists
ACEi
calcium channel blockers
anticonvulsants

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92
Q

is tension type headache episodic

A

yes

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93
Q

how will patients describe tension type headache

A

tight muscles ard head and neck

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94
Q

characteristics of tension type headache

A

bilateral
mild or moderate pain
not aggravated by any movements
no added features (eg N+V, photophobia phonophobia)

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95
Q

treatments for tension type headache

A

simple analgesics (paracetamol, aspirin)

96
Q

characteristics of cluster type headache

A

unilateral pain
at least one of the following ipsilateraly (conjnctival redness, lacrimation, nasal congestion and/or hinorrhoea, forehead and facial sweating, miosis, ptosis, restlessness or agitation, not associated with brain lesion on MRI)

97
Q

acute treatment for cluster headache

A

triptan (nasal or subcutaneous)
high flow O2

98
Q

preventive management for cluster headache

A

verapamil (calcium channel blcokers)

99
Q

what is the difference between vestibular and hearing organ

A

vestibular: capture low frequency (movement)
hearing: capture high frequency (sound)

100
Q

what is the function of outer ear

A

capture sound and focus it to tympanic membrane
amplify upper range of speech frequencies by resonance in canal
protect ear from external threats

101
Q

function of middle ear

A

mechanical amplification

102
Q

what is the hearing part of inner ear

103
Q

function of cochlea

A

transduce vibration into nerve impulses
captures the frequency and intensity of sound

104
Q

cochlea contain which 3 compartments

A
  1. scala vestibuli
  2. scala media
  3. scala tympanic
105
Q

function of scala vestibuli and scala tympanic

A

bone structure
contain perilymph
high in sodium

106
Q

function of scala media

A

membranous structure
contains endolymph
high in potassium
location of Organ of Corti

107
Q

where does organ of corti lie on

A

basilar membrane

108
Q

how is basilar membrane arranged

A

tonotopically, same principle of xylophone

109
Q

which 2 hair cells do organ of corti contain

A

inner hair cells (IHC)
outer hair cells (OHC)

110
Q

what is above the hair cells

A

tectorial membrane

111
Q

function of inner hair cells

A

carry 95% of affernet info of auditory nerve
transduction of sound into nerve impulse

112
Q

function of outer hair cells

A

carry 95% of efferent info of auditory nerve
modulate sensitivity of response

113
Q

name of hairs of hair cell

A

stereocilia

114
Q

longest cilia name

A

kinocilium

115
Q

what happens when deflection of stereocilia towards kinocilium

A

opens K+ channels
depolarise the cell releasing NT to afferent nerve which then depolarises

116
Q

how does stereocilia deflection change according to amplitudes

A

higher amptitudes, cause greater deflection of stereocilia and K+channel opening

117
Q

describe the auditory pathway

A
  1. spinal ganglions via CN8 (vestibulo-cochlear nerve) travels to ipsilateral cochlear nuclei in brainstem (pons)
  2. auditory info crosses at superior olivary complex , after that all connections are bilateral
  3. signals then travel to lateral lemnisicus, then to the inferior colliculus, then to the medial geniculate body at thalamus
  4. lastly to the auditory cortex
118
Q

what are the types of hearing loss (3)

A
  1. conductive hearing loss: problem in outer or middle ear
  2. sensorineural hearing loss: problem at cochlear (hearing organ) or auditory nerve (nerve) (90% of hearing loss)
  3. central hearing loss: problem at brain and brainstem (v. rare)
119
Q

conductive hearing loss causes

A

outer ear: wax, foreign body
middle ear: otitis (inflammation, build up of fluid behind eardrum)

120
Q

sensorineural hearing loss causes

A

cochlear: noise, presbycusis (age related), ototoxicity (drugs, chemotherapy)
auditory nerve: acoustic neuroma

121
Q

clinical assessments for hearing loss

A

weber test, rinne test, tuning fork

122
Q

what are otoacoustic emissions (OAEs)

A

normal cochlea produces low intensity sounds called (OAEs), these sound are produced by OHCs as they expand and contract
performed in newborn hearing screening and hearing loss monitoring

123
Q

where is the vestibular organ

A

in inner ear, contain hair cells for hearing and balance

124
Q

what are vestibular organs (4)

A

utricule, saccule, semicircular canals, cochlea

125
Q

what joims the utricule and saccule

A

conduit, saccule also joined to cochlea

126
Q

what are otolith organs

A

utricle and saccule

127
Q

where are utricle and saccule

A

on maculae, placed horizontally in utricle and vertically in saccule

128
Q

what are maculae

A

contain hair cells, a gelatinous matrix , with otoliths on top

129
Q

which otolith for which movement

A

utricule –> horizontal
saccule–> vertical

129
Q

what are functions of otholiths

A

they are carbonate crystals, help with deflection of hairs

130
Q

where are hair cells in canals located in

A

crista on ampulla

131
Q

what do the rest of the canal has

A

endolymph (high in potassium)

132
Q

what are hair cells surrounded by

A

cupula, which helps hair cell movement

133
Q

describe hair cells potentials

A

resting potential: basal discharge to nerve
depolarisation: move towards kinocilium
hyperpolarization: move away kinocilium , reduction in nerve discharge

134
Q

what are vestibular reflexes(2)

A

vestibulo-ocular reflex (VOR)
vestibulo-spinal reflec (VSR)

135
Q

what is vestibulo ocular reflex

A

keep images fixed in retina
connection between vestibular nuceli and oculomotor nuclei
eye movement in opposite direction to head movement but same velocity and amplitude

136
Q

how do we categorise vestibular disorders

A

timing
laterality

137
Q

in vestibular disorder, what complaints are in acute and unilateral

A

imbalance, dizziness, vertigo, nausea

138
Q

in vestibular disorder, what complaints are in slow, unilateral or any bilateral loss

A

imbalance and nausea, BUT no vertigo

139
Q

where are the problems for peripheral vestibular disorders

A

vestibular organ or CN VIII
BPPV (bnenign paroxysmal positional vertigo)
vestibular neuritis

140
Q

where are the problems for central vestibular disorders

A

CNS (brainstem or cerebellum)
stroke, MS, tumors

141
Q

core exams for vestibular disorders

A

eyes, ears, legs

142
Q

red flags for vestibular disorders

A

headache, gait problems, hearing loss, prolonged symptoms,hyper-acute onset

143
Q

timings for balance disorders:
vestibular neuritis and stroke?

144
Q

timings for balance disorders:
BPPV

A

intermittent

145
Q

timings for balance disorders:
migraine, meniere’s disease

146
Q

timings for balance disorders:
schwannoma vestibular, degenerative conditions (MS)

A

progressive

147
Q

what is HINTS exams for acute dizziness

A

Head Impulse test Nystagmus Test of Skew deviation

148
Q

what is BPPV

A

peripheral disorder
otoliths (crystals) from utricle detach from maculae and float around semi-circular canals
induce bigger endolymph flow when head moves

149
Q

what happens in alzheimers MRI

A

slightly large ventricle
narrowed gyri
widened sulci
atrophy
hippocampal atrophy (shrinkagemof hippocampus with space taken by CSF)

150
Q

what is lewy bodies dementia

A

caused by aggregation of alpha synuclein
lead to lewy bodies deposition and internal symptoms

151
Q

presentation of lew bodies dementia

A

preserved hippocampus volume
medial temporal lobe lower volume
reduced availability of dopamine transporter in caudate and putamen

152
Q

presentation of AD

A

hippocampus atrophy
medial temporal lobe atrophy

153
Q

what is meningitis and cause of it

A

inflammation of meninges caused by viral or bacterial infection

154
Q

what is encephalitis and cause of it (2)

A

inflammation of brain caused by infection or autoimmune mechanisms

155
Q

what is cerebral vasculitis

A

inflammation of blood vessel walls

156
Q

functions of BBB

A

solutes that can exchange across peripheral capillaries cannot cross BBB
allows BBB to control the exchange of these substances using specific membrane transporters in and out of CNS
reduce entry of infectious agents into CNS tissue

157
Q

what happens in BBB disruption (4steps)

A
  1. endothelial layer disruption, BBB gets compromised (eg stroke / physical trauma)
  2. blood component leas into brain including fibrinogen
  3. astrocytes react to fibrinogen leakage, withdraw astrocyte end feet from vessel walls, compromising BBB
  4. compromising BB leads to build up of collagen in basement membrane which narrows vessel walls leading to small vessel diseases
158
Q

symptoms of encephalitis

A
  • initially flu like symptoms (eg high temp and headache)
  • then, confusion, disorientation, seizures, change in personality and behavior, weakness, loss of movement, speaking difficulty, loss of consciousness
159
Q

encephalitis causes

A

viral infection (Herpes Simplex, Measles, varicella, rubella)
mosquito, tick, insect bites, bacterial and fungi infection, trauma, autoimmune

160
Q

encephalitis treatment

A

antivirals (acyclovir)
steroids
antibiotics/antifungi
ventilation
analgesics
anti-convulsants

161
Q

what is the cellular pathology of MS (4 steps)

A

inflammation
demyelination
axonal loss
neurodegeneration

162
Q

what are some bacterial causes of meningitis

A

meningococcal
pneumococcal
haemophilus influenzae type B (Hib)
Streptococcal (esp in new borns)

163
Q

what is myelitis

A

infection of spinal cord

164
Q

what is encephalomyelitis

A

when both brain and spinal cord are involved in infection

165
Q

hallmarks of encephalitis

A

fever
seizures
behvaioural changes
confusion and disorientation

166
Q

hallmarks of meningitis

A

sudden fever
severe headache
n+v
double vision
drowsiness
sensitivity to bright light
stiff neck
rash

167
Q

what are tests to diagnose meningitis / encephalitis

A

neurological exam
CT, MRI
lumbar puncture (CSF usually clear & colorless, low glucose in bacterial meningitis, increase WBC =infection)
blood and urine tests

168
Q

what are common treatments for meningitis and encephalitis

A

AB, antivirals, corticosteroids, immune suppressors

169
Q

what are the 3 layers of coat of eye

A

sclera – hard and opaque
choroid – pigmented and vascular
retina – neurosensory tissue

170
Q

what is characteristic of sclera

A

white of eye
high water content
protective outer coat layer

171
Q

what is uvea

A

vascular coat of eyeball

172
Q

where is uvea located

A

between sclera and retina

173
Q

what does uvea consist of (3 parts from front to bk)

A

iris
ciliary body
choroid
(intimately connected and a disease of one part can affect the other portions but not necessarily the same degree)

174
Q

function of retina

A

capture light rays that enter eyes
these light impulses are then sent to brain for processing via optic nerve

175
Q

what does optic nerve connect to

A

connects to back of eye near the macula

176
Q

what is the visible portion of optic nerve

A

optic disc

177
Q

where is macula located

A

centre of retina, temporal to optic nerve

178
Q

what is macula responsible for

A

detailed central vision eg reading

179
Q

where is fovea

A

centre of macula (for detail central vision, contains only cones) so for sharper visions

180
Q

what is blind spot

A

where the optic nerve meets retina and no light sensitive cells

181
Q

which part has the highest cone photoreceptors

182
Q

what is central vision responsible for

A

detail day vision
color vision
reading
facial regonsition

183
Q

how to assess central vision

A

visual acuity assessment

184
Q

what is peripheral vision responsible for

A

shape
movement
night vision
navigation vision

185
Q

how to assess peripheral vision

A

visual field assessment

186
Q

what happens when there is loss of visual field

A

unable to navigate in environment
pt need white stick

187
Q

how many layers for retina

A

3
outer, middle, inner

188
Q

function of retina outer layer

A

contains photoreceptors (1st order neuron)
for light detection

189
Q

function of retina middle layer

A

bpolar cells (2nd order neuron)
for local signal processing to improve contrast sensitivity

190
Q

function of retina inner layer

A

retinal ganglion cells (3rd order neuron)
for transmission of signal from eye to brain

191
Q

2 main classes of photoreceptors

A

rods and cones

192
Q

compare rods and cone photoreceptors

A

rod: x100 more sensitive to light , slow response to light , responsible for night vision , more rods than cones
cone: less sensitive to light, faster response, resposnsible for day light, fine vision and color vision

193
Q

what lens in convex lens

A

converging lens

194
Q

what lens in concave lens

A

diverging lens

195
Q

what is emmetropia

A

perfect vision, parallel light rays fall on retina

196
Q

what is ametropia

A

msimatch between axial length anad refractive power
parallel light rays don’t fall on retina

197
Q

what is near sightedness

198
Q

what is far sightedness

199
Q

what is myopia

A

parallel rays converge at a focal point anterior to retina
vision: not clear, genetic factor
need concave lens

200
Q

causes of myopia

A

excessive long globe (long eye)
lens thinner in middle and thicker at edges
excessive refractive power

201
Q

symptoms of myopia

A

blurred distance vision
headache
squint to try to improve vision

202
Q

what is hyperopia

A

parallel rays converge at a focal point posterior to retina
need convex lens

203
Q

causes of hyperopia

A

excessive short globe
insufficient refractive power

204
Q

symptoms of hyperopia

A

visual acuity at near tends to blur relatively early
eyepain
headache in frontal region
burning sensation in eye

205
Q

what is presbyopia

A

loss of accommodation for near objects naturally
start at 40yo
corrected b reading glasses to increase refractive power

206
Q

what is near response triad

A

adaptations for near vision

207
Q

steps for near response triad

A

pupillary miosis (reduce size of pupil) to increase depth of field (done by sphincter pupillae) thickening of lens
convergence to align both eyes towards near object (medial recti from both eyes)
accommodation to increase refractive power of lens for near vision (contraction of circular ciliary muscle)

208
Q

visual pathway from eye to visual cortex

A

eye
optic nerve
optic chiasm
optic tract
lateral geniculate nucelus
optic radiation
primary visual cortex / Striate cortex

209
Q

visual pathway of retina

A

first order neurons (rod and cone)
second order neurons( retinal bipolar cells)
third order neurons (retinal ganglion cells)
optic nerve (CN ll)
partial decussation at optic chiasm
optic tract
lateral geniculate nucleus in thalamus

210
Q

how many ganglion fibres cross at optic chiasm

211
Q

what happens to crossed fibres at optic chiasm and where do they originate

A

originate from nasal retina
responsible for temporal visual field

212
Q

what happens to uncrossed fibres at optic chiasm and where do they originate

A

originate from temporal retina
responsible nasal visual field

213
Q

what happens to lesions anterior to optic chiasm

A

affect visual field in one eye only

214
Q

what happens to lesions posterior to optic chiasm

A

affect visual field in both eyes

215
Q

what happens to lesions at optic chiasm

A

damages crossed ganglion fibres from nasal retina in both eyes
bitemporal hemianopia (temporal field deficit in both eyes)

216
Q

what happens to lesions posterior to optic chiasm

A

right side lesion– left homonymous hemianopia in both eyes
left side lesion – right homonymous hemianopia in both eyes

217
Q

main cause of bitemporal hemianopia

A

pituitary gland tumor enlargemen

218
Q

main cause of homonymous hemianopia

219
Q

what is homonymous hemianopia with macular sparing

A

damage to primary visual cortex
often due to stroke

220
Q

what happens to pupil in light

A

pupil constriction
increase depth of field
mediated by PNS in CN lll
cause circular muscle to contract

221
Q

what happens to pupil in dark

A

pupil dilation
mediated by SNS
cause radial muscle contract

222
Q

what is direct pupillary reflex

A

constriction of pupil of light stimulated eye

223
Q

what is consensual pupillary reflex

A

constrcition of pupil of other eye

224
Q

what is neurological basis of pupillary reflex

A

afferent pathway on either side alone will stimulate efferent pathway on both sides

225
Q

what are afferent pathway of eye

A

sends messages from the pupil to the brain along the optic nerve to the optic tracts

226
Q

what are efferent pathway of eye

A

sends the message back from the brain to the pupil via nerves, resulting in pupil constriction and dilation

227
Q

what happens to right afferent defect

A

no pupil constriction in both eyes when right eye stimulated with light
normal constriction in both eyes when left eye stimulated with light

228
Q

what happens to right efferent defect

A

pupil constriction
no right pupil constriction when right or left eye stimulated with light
left pupil constricts whether right or left eye stimulated with light

229
Q

function of superior rectus

A

move eye up
CN lll

230
Q

function of inferior rectus

A

move eye down
CN lll

231
Q

function of lateral rectus

A

move eye towards outside (abduct)
CN Vl

232
Q

function of medial rectus

A

move eye towards nose (adduction)
CN lll

233
Q

function of superior oblique

A

move eye down and out in a diagonal pattern
CN lV

234
Q

function of inferior oblique

A

move eye up and out in diagonal pattern
CN lll

BRS Y2 (10 decks)

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