Week 5: Visual Pathways, Vision Loss Flashcards

1
Q

Trace the visual pathway from the retina to the brain.

A
  1. Bipolar cells (Neuron 1) - rod/cone cells synapse at dendrites, axons contact retinal ganglion cells
  2. retinal ganglion cells (neuron 2) - dendrites synapse at bipolar cells, axons collect at optic disc and form optic nerve.
  3. optic chiasm: nasal retinal fibers cross, temporal retinal fibers remain uncrossed
  4. Lateral geniculate nucleus (neuron 3)-in thalamus, receive most fibers from optic tract of same side. Some axons go to brain stem for visual reflexes.
    - lateral: fibers from lower retinal quadrants
    - medial: upper retinal quadrants
    - axons project to cortex as geniculocalcarine tract or optic radiations
  5. optic radiations: axons from LGM pass through posterior limb of internal capsule (most posterior=retrolentiform part)
    • Axons from lower retinal quads: fibers that travel through temporal lobe form loop of Meyer, anterior toward tip of inferior horn of lateral ventricle, then turn to reach occipital lobe (
    • axons from upper retinal quads: travel directly posteriorly to occipital lobe through parietal lobe
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2
Q

Where is the primary visual cortex located?

A

-gyri within and next to calcarin sulcus on the medial surface of the occipital lobe

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3
Q

Axons that terminate in the upper calcimine sulcus are derived from which retinal quadrants?

A

upper retinal quadrants=lower quadrants of contralateral half of binocular visual field

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4
Q

Where is the macula and peripheral fields represented on the primary visual cortex?

A
  • macula is most posterior

- peripheral fields are more anterior

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5
Q

Where is the visual association cortex? What is its function?

A
  • partly medial and largely lateral surface of occipital lobe adjoining primary visual cortex
  • receive afferents from primary visual cortex
  • interpretation of form, color, depth, location ,motion
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6
Q

What is the “what” pathway for vision?

A
  • ventral pathway from occipital association areas that goes down to temporal lobes
  • perception of shape and color used for objective identification, e.g. face recognition
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7
Q

What is the “where” pathway for vision?

A

-dorsal pathway from occipital association area to multimodal association cortex to analyze motion and location of objects in the visual field

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8
Q

What is papilledema? How does it look clinically?

A
  • edema of the optic disc resulting form an increase in intracranial pressure
  • mild: seen as blurring of the edges of the disc
  • severe: mushrooming of the disc and retina around it, obliteration of the vessels at the disc margin and hemorrhages
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9
Q

What do lesions in the the optic nerve result in?

A
  • impaired vision in the corresponding eye

- horizontal meridian is respcted

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10
Q

What does a lesion of the optic chiasm result in?

A
  • affects nasal retinal fibers because they cross=temporal visual fields of both eyes
  • bitemporal hemianopsia-loss of vision in temporal visual fields of both eyes
  • can occur due to pituitary adenoma that grows upward and compresses the chasm from below
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11
Q

What does a lesion of the optic tract result in?

A
  • contralateral homonymous hemianopsia: field deficits in both eyes representing corresponding halves of two visual fields
  • causes: tumor, infarct, demyelinating disease
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12
Q

What does a lesion of the optic radiations result in?

A
  • contralateral homonymous hemianopsia
  • associated with motor and sensory losses because of fibers running in posterior limb of internal capsule
  • usually vascular lesions
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13
Q

Describe the visual loss from a lesion of the temporal lobe

A
  • affects fibers that course from internal capsule to visual cortex through temporal lobe
  • loss of vision in upper quadrants of the contralateral visual field
  • superior quadrantanopsia: spares fixation and termed pie in the sky
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14
Q

Describe the visual loss from a lesion of the parietal lobe

A
  • contralateral inferior quadrantanopsia

- causes: tumors, infarcts, occlusion of MCA

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15
Q

Describe the visual loss from a lesion of the cortical/subcortical lesions in the occipital lobe

A
  • homonymous hemianopsia with macular sparing in the contralateral halves of the visual fields
  • cause: vascular lesions of PCA
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16
Q

Trace the pathway of the visual reflex.

A

AFFERENT limb
-fibers in optic tract go through brachium of superior colliculus to enter pretectal area
-terminate in pretectal nuclei in midbrain
-project bilaterally through posterior commissure and periaqueductal gray to Edinger Westphal nucleus
EFFERENT Limb
-EW Nucleus to ciliary ganglion to constrictor of the pupil

17
Q

What are the three reflex responses that take place upon focusing on a near object after looking far away?

A
  1. Convergence of both eyes via medial rectus
  2. pupillary constriction
  3. rounding of the lens due to contraction of the smooth muscle of ciliary body
    Pathway: normal light afferent–>Visual cortex–>center for accommodation–>EW nuc. and III motor–>medial rectus and ciliary ganglion (sphincter pupillae)
18
Q

What are the 4 major causes of vision loss?

A
  1. age-related macular degeneration (AMD)
  2. Glaucoma
  3. Cataracts
  4. Diabetic retinopathy
19
Q

What is the pathophysiology of nonexudative (dry) AMD?

A
  • drusen: deposits of extraceullar material that accumulate between the RPE Bruch’s membrane in the region of the macula
  • geographic atrophy: areas of atrophy of the RPE and pigment clumping the coalesce into bigger areas
  • damage to RPE leads to loss of photoreceptors
20
Q

What is the pathophysiology of exudative (wet) AMD?

A
  • new abnormal vessels grow from choroidal circulation into sub retinal space and form choroidal neovascular membranes (CNVM)
  • may have sub retinal hemorrhage and sub retinal fluid
  • more acute presentation
21
Q

What are the signs and symptoms of AMD?

A
dry AMD more common
-blurry vision
image distortion due to elevated retina
-central scotoma
-difficulty reading, may need magnifying glass
-difficulty driving
22
Q

What is the etiology of AMD?

A
  • age 75 and older
  • family history of AMD
  • smoking
  • oxidative damage
  • genetic polymorphisms aroud CFH gene
23
Q

How is dry and wet AMD managed/treated?

A

DRY AMD

  • follow with Amsler grid and get ophthal exam every 6 months
  • antioxidant vitamins
  • no current therapy for geographic atrophy…..transplantation of stem cell derived RPE in future

WET AMD

  • photodynamid therapy
  • anti- VEGF drugs
24
Q

What is the pathophysiology of open angle glaucoma?

A
  • chronic, slow progression
  • asymptomatic until late in disease course
  • due to blockage of Schelemm’s canal or adjacent tissue, trabecular meshwork
  • decreased aqueous outflow, chronic increased intraocular pressure damages retinal ganglion cells and their vascular supply
  • usually bilateral
  • 95% of all glaucomas
25
Q

What is the pathophysiology of closed angle glaucoma?

A
  • acute, abrupt blockage of aqueous outflow
  • shallow anterior chamber predisposed
  • pupillary dilatation can precipitate acute attack by increasing tightness of contact between iris and lens
26
Q

What are the signs and symptoms of glaucoma?

A
most common cause of blindness in african americans
OPEN ANGLE
-visual field loss
-blurry vision
-halos around lights due to corneal edema
CLOSED angle
-nausea
-vomiting
-intense pain
27
Q

How is open angle glaucoma managed?

A
  • observation every 3-6 months
  • Visual field exam every 6-12 mos.
  • gonioscopy and optic nerve exam yearly
  • beta blockers, carbonic anhydrase inhibitors, alpha adrenergic agonists: decrease aqueous fluid
  • increase outflow of aqueous fluid with cholinergics, prostaglandins
  • laser treatment
  • surgical treatments
28
Q

How is closed angle glaucoma managed?

A
  • eyedrops to constrict pupils (cholinergics)
  • oral glycerol or IV mannitol to decrease intraocular pressure
  • laser iridectomy to increase outflow
29
Q

What is the pathophysiology of cataract?

A
  • cortical degeneration: opacities that radiate from the periphery of the lens to lens poles caused by swelling and liquefaction of younger cortical fiber cells
  • nuclear sclerosis: opacity of centrally located lens often with lens discoloration, caused by deterioration of older cortical fiber cells
30
Q

What is the etiology of cataracts?

A
  • usually age related
  • may result from systemic diseases: diabetes, hypocalcemia, myotonic, atopic dermatitis, wilson’s
  • senile cataracts are associated with UVB exposure
  • 50% of those greater than 75 of age are affected
31
Q

What are the signs and symptoms of cataracts?

A
  • blurry vision
  • glare
  • monocular diplopia (double vision)
  • increasing myopia
  • second sight (patients becoming more myopic need their reading glasses less)
32
Q

How are cataracts treated and managed?

A

-cataract extraction and insertion of an intraocular lens when visual symptoms interfere with living functions

33
Q

What is the pathophysiology of diabetes retinopathy?

A

NON PROLIFERATIVE
-venous dilation
-A/V nicking
-microaneurysms in venous capillary bed–>result in dot-blot appearance of retina as veins are deep in the retina
-macular edema
PROLIFERATIVE
-areas of retinal neovacularization which extend into the vitreous and bleed
-vitreous scaffolds areas of neovascularization
-exudates
-retinal detachment may result from scarring
-recurrent vitreous hemorrhage may result

34
Q

What are the presenting signs and symptoms of diabetic retinopathy?

A
  • many have no symptoms
  • floaters (dark=hemorrhagic, light=as vitreous detaches from surface of retina)
  • visual field loss
  • poor night vision
35
Q

How is diabetic retinopathy managed/treated?

A
  • intense blood glucose control
  • intense monitoring of coexisting HTN, renal conditions
  • annual retinal exam
  • laser photocoagulation
  • pars plana vitrectomy
36
Q

What is Argyl Robertson pupil (ARP) that occurs in tertiary syphilis?

A

ARP-normal accommodation reflex

  • PRA-pupillary reflex absent
  • lesion belived to be in the pretectal area