Week 5: Visual Pathways, Vision Loss Flashcards
Trace the visual pathway from the retina to the brain.
- Bipolar cells (Neuron 1) - rod/cone cells synapse at dendrites, axons contact retinal ganglion cells
- retinal ganglion cells (neuron 2) - dendrites synapse at bipolar cells, axons collect at optic disc and form optic nerve.
- optic chiasm: nasal retinal fibers cross, temporal retinal fibers remain uncrossed
- 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 - 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
Where is the primary visual cortex located?
-gyri within and next to calcarin sulcus on the medial surface of the occipital lobe
Axons that terminate in the upper calcimine sulcus are derived from which retinal quadrants?
upper retinal quadrants=lower quadrants of contralateral half of binocular visual field
Where is the macula and peripheral fields represented on the primary visual cortex?
- macula is most posterior
- peripheral fields are more anterior
Where is the visual association cortex? What is its function?
- 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
What is the “what” pathway for vision?
- 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
What is the “where” pathway for vision?
-dorsal pathway from occipital association area to multimodal association cortex to analyze motion and location of objects in the visual field
What is papilledema? How does it look clinically?
- 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
What do lesions in the the optic nerve result in?
- impaired vision in the corresponding eye
- horizontal meridian is respcted
What does a lesion of the optic chiasm result in?
- 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
What does a lesion of the optic tract result in?
- contralateral homonymous hemianopsia: field deficits in both eyes representing corresponding halves of two visual fields
- causes: tumor, infarct, demyelinating disease
What does a lesion of the optic radiations result in?
- contralateral homonymous hemianopsia
- associated with motor and sensory losses because of fibers running in posterior limb of internal capsule
- usually vascular lesions
Describe the visual loss from a lesion of the temporal lobe
- 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
Describe the visual loss from a lesion of the parietal lobe
- contralateral inferior quadrantanopsia
- causes: tumors, infarcts, occlusion of MCA
Describe the visual loss from a lesion of the cortical/subcortical lesions in the occipital lobe
- homonymous hemianopsia with macular sparing in the contralateral halves of the visual fields
- cause: vascular lesions of PCA
Trace the pathway of the visual reflex.
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
What are the three reflex responses that take place upon focusing on a near object after looking far away?
- Convergence of both eyes via medial rectus
- pupillary constriction
- 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)
What are the 4 major causes of vision loss?
- age-related macular degeneration (AMD)
- Glaucoma
- Cataracts
- Diabetic retinopathy
What is the pathophysiology of nonexudative (dry) AMD?
- 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
What is the pathophysiology of exudative (wet) AMD?
- 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
What are the signs and symptoms of AMD?
dry AMD more common -blurry vision image distortion due to elevated retina -central scotoma -difficulty reading, may need magnifying glass -difficulty driving
What is the etiology of AMD?
- age 75 and older
- family history of AMD
- smoking
- oxidative damage
- genetic polymorphisms aroud CFH gene
How is dry and wet AMD managed/treated?
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
What is the pathophysiology of open angle glaucoma?
- 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
What is the pathophysiology of closed angle glaucoma?
- 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
What are the signs and symptoms of glaucoma?
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
How is open angle glaucoma managed?
- 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
How is closed angle glaucoma managed?
- eyedrops to constrict pupils (cholinergics)
- oral glycerol or IV mannitol to decrease intraocular pressure
- laser iridectomy to increase outflow
What is the pathophysiology of cataract?
- 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
What is the etiology of cataracts?
- 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
What are the signs and symptoms of cataracts?
- blurry vision
- glare
- monocular diplopia (double vision)
- increasing myopia
- second sight (patients becoming more myopic need their reading glasses less)
How are cataracts treated and managed?
-cataract extraction and insertion of an intraocular lens when visual symptoms interfere with living functions
What is the pathophysiology of diabetes retinopathy?
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
What are the presenting signs and symptoms of diabetic retinopathy?
- many have no symptoms
- floaters (dark=hemorrhagic, light=as vitreous detaches from surface of retina)
- visual field loss
- poor night vision
How is diabetic retinopathy managed/treated?
- intense blood glucose control
- intense monitoring of coexisting HTN, renal conditions
- annual retinal exam
- laser photocoagulation
- pars plana vitrectomy
What is Argyl Robertson pupil (ARP) that occurs in tertiary syphilis?
ARP-normal accommodation reflex
- PRA-pupillary reflex absent
- lesion belived to be in the pretectal area
