Visual Pathway Flashcards

1
Q

what converts light into action potentials?

A

retinal rod, cone and ganglion cells

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2
Q

the lens is under what control and what does it do?

A

the ciliary muscle
- and it produced the image onto the retina

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3
Q

axons in the optic nerve decussate where?

A

at the optic chiasm

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4
Q

fibres from the nasal retina cross and join with the uncrossed fibres in the ……… retina to form the ……. …….

A

fibres from the nasal retina cross and join with the uncrossed fibres in the temporal retina to form the optic tract

-> thus each optic tract carries info from the contralateral visual hemifield

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5
Q

what is the LGN (lateral geniculate nucleus)?

A

connection of the optic nerve with the thalamus. it is a thalamic nucleus which provides a relay station for all axons of the retinal ganglion cells subserving vision.

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6
Q

fibres pass in the optic radiation from the LGN to reach visual cortex of the occipital lobe (6 and 7) through what lobes of the brain?

A

parietal and temporal lobes

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7
Q

visual information is further processed by neighbouring visual association areas which detect what?

A

they detect lines, orientation, shapes, movement, colour and depth: their is also a distinct area responsible for face recognition.

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8
Q

lesions posterior to the optic chiasm produce …… field defects

A

homonymous
-> indicating involvement of the same past of the visual field in both eyes. as info from 2 visual fields is seperated beyond this point

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9
Q

unilateral visual loss with a central or paracentral scotoma is hallmark of what kind of lesion?

A

an optic nerve lesion

  • as most fibres in the optic nerve subserve macular vision.
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10
Q

describe some examination findings in optic neuropathy?

A
  • reduced acuity in the affected eye
  • a scotoma (central)
  • impaired coloured vision
  • afferent pupillary defect
  • optic atrophy - pale disc
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11
Q

what is papilloedema?

A

swelling of the optic disc, shows as disc pinkness, blurring and heaping up of disc margins. nasal first.

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12
Q

what is optic neuritis?

A

one of the most common causes of subacute visual loss. symptoms may vary from a mild fogging of central vision w colour desaturation to dense central scotoma and complete blindness
- pain on eye movement
- confers a higher risk to developing MS
- recovering involves high dose IV steroids or oral
- can also be caused by infection or inflam disorders e.g. sarcoidosis or vasculitis

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13
Q

what is ant ischaemic optic neuropathy?

A

the ant part of optic nerve is supplied by post ciliary arteries, occlusion or hypoperfusion leads to infarction to optic nerve head
- results in sudden or stuttering visual loss (lower half of visual field)

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14
Q

bitemporal heminiopia or quadrantopia occurs with compression of the chiasm from above or below. name some common causes of compression?

A
  • pituitary tumours
  • meningioma
  • craniopharyngioma
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15
Q

optic tract lesions cause a … ……

A

homonymous hemianopia (loss of contralateral visual field in both eyes)

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16
Q

optic radiation lesions cause ….. …… ….

A

homonymous contralateral quadrantopic defects

-> temporal lobe lesions (ie tumour, infarction) cause upper quadrantic defects (‘pie in the sky’)
-> parietal lobe lesions cause lower quadrantic defects (‘pie on the floor’)

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17
Q

for a left afferent pupillary defect what happens in the eye?

A
  • the left pupil is unreactive to light (direct reflex)
  • the consensual reflex is also absent
  • however when left is shone in right intact eye, consensual reflex of the right eye remains intact
18
Q

how does RAPD occur?

A

incomplete damage to one optic nerve relative to the other

19
Q

what is Horners syndrome?

A

damage to the sympathetic nervous supply to the eye (hypothalamus -> down brainstem to cervical cord of T1 nerve root -> paravertebral sympathetic chain, on via carotid artery wall -> to the eye

20
Q

what are the symptoms of Horner’s syndrome?

A

unilateral miosis (constricted pupil)
partial ptosis
loss of sweating on the same side

21
Q

what causes Horners syndrome?

A

hypothalmic, brainstem lesions -> cerebral infarction, brainstem demyleniation
cervical cord -> syringomelia, and cord tumours
t1 root - alpical lung tumour, TB, cervical rib, brachial plexus trauma
sympatheyic chain and carotid artery in neck
miscellaneous -> congential, cluster headache, transient and idopathic

22
Q

lesions affecting the calcarine sulcus of the occipital lobe tend to cause a?

A

homonymous hemianopia with sparing of the macula. macular vision is spared given the dual blood supply to ant portion of the visual centre (PCA, MCA)

23
Q

optic nerve damage causes what kind of field defect?

A

ipsilateral monocular blindness

24
Q

name 2 types of photoreceptors in retina?

A

rods and cones
- contain light-sensitive surface membrane proteins called rhodopsin
- rhodopsin in these cells are stimulated to propagate second messenger responses which convert light energy into electrical signals
- photoreceptors synapse with retinal bipolar cells which in turn transmit these signals to retinal ganglion cells.

25
Q

what kind of cells converge at the optic disc forming the optic nerve?

A

the retinal ganglion cells

26
Q

rods are used for?

A

seeing in dim light

27
Q

cones are used for?

A

seeing in normal daylight

28
Q

do rods or cones have higher convergence?

A

rods have more convergence, increasing sensitivity, while decreasing acuity. (more rods are required to stimulate ganglion cell)

29
Q

where are cones found?

A

central retina (fovea)

30
Q

where are rods found?

A

peripheral retina

31
Q

what are the 3 basic types of retinal ganglion cells?

A

M - movement
P - form and colour
nonM-nonP cells - colour

32
Q

long wavelength cones (L-cones) are sensitive to mostly light within what spectrum?

A

red spectrum

33
Q

the medium wavelength cones (m-cones) are responsive to light in what spectrum?

A

green spectrum

34
Q

the short wavelength cones (s-cones) primarily detects light in what spectrum?

A

blue spectrum

35
Q

what photoreceptor cells are responsible for colour vision?

A

cones
-> they detect light within a particular spectrum

36
Q

axons arising for the nasal retina eventually terminate on what layers of the contralateral geniculate nucleus?

A

layers 1, 4 and 6

37
Q

axons of ganglion fibres from temporal retina will terminate on what layers of the ipsilateral geniculate nucleus?

A

2, 3 and 5

38
Q

what broadman area is the primary visual cortex found?

A

broadmann area 17

39
Q

photo transduction cascade of rod cells in response to light

A
  • when light activates the rod cells. 11-cis is converted to trans-retinal releasing opsonin.
  • opsonin activates transducin and activates PDE which breaks down C.GMP so Ca and Na influx cannot occur. thus cell becomes less pos = hyperpolarized. IPSP.
  • less glutamate being released from rods
  • as little glutamate is being released this stimulates the bipolar neurone
  • bipolar cells become depolarized and produce EPSP. glutamate released stimulating ganglion cells
  • ganglion cells produce A.P’s

opposite response in dim light
- all trans -> 11 cis
- more glutamate being released which inhibits bipolar = IPSP
- less glutamate moving down ganglion and optic nerve

40
Q

the primary visual cortex is divided into …. functionally distinct layers. which layer recieves most visual input from the LGN?

A

6 layers
Layer 4 received most visual input. 4ca recieves mostly magnocellular input from LGN, while 4cb recieves input from parvocellular pathways.