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Which four nuclei of the brain does the retina project to, and what are their functions?
LGN: Perception of objects
Superior colliculus: Control of eye movements
Pretectum: Control of the pupil
Suprachiasmatic nucleus: Control of diurnal rhythms and hormonal changes
How is the LGN structured?
The Lateral Geniculate Nucleus functions to gate signals from the retina to the brain, and is organized into 6 layers: 2 magnocellular and 4 parvocellular layers. There are different lamninae for the separate eyes, organized in a retinotopic fashion.
What are magnocellular layers, and what is their function?
In the LGN, there are magnocellular layers and they synapse to layer IV of the visual cortex -> V1 -> V2 -> V5. Encode MOVEMENT and DEPTH, and are considered the "WHERE" pathway.
What are parvocellular layers, and what is their function?
In the LGN, there are parvocellular layers and they synapse to layer IV of the visual cortex -> V2 -> V4. Encode COLOR and DETAIL, and are considered the "WHAT" pathway.
Characteristics of LGN development in a newborn?
-Input from OD and OS are segregated
-6 layers, 2 magno, 2 parvo
-Parvocellular: rapid growth from birth to 6 months, slow growth to adult size by 1 year old
-Magnocellular: slow growth to adult size by 2 years old
-Maximum dendritic spines by 4mo, declines to adult levels by 9mo.
What anatomical changes take place in the striate cortex?
-First neurons to differentiate take positions in the deeper cortical layers (inside out process) -> neurons that differentiate later migrate past older neurons to take their place in more superficial layers.
-Radial migration
-Development of orientation columns and ocular dominance columns
-overabundance of dendritic spines, then pruned back to adult levels
Lissencephaly type I
complete arrest of cortical neuronal migration from 12 to 16 weeks gestation -> smooth brain!
May occur as:
-isolated lissencephaly
-Miller-Dieker syndrome (specific dysmorphic characteristics, and deletion of part of chromosome 17)
-Norman-Robert syndrome (dysmorphic characteristics, no deletion of part of chromosome 17)
Miller-Dieker syndrome characteristics
-microcephaly, with bitemporal narrowing
-small nose
-upslanted eyes
-protruding upper lip
-micrognathia (undersized jaw)
Ocular dominance columns (development)
Prenatal: no ocular dominance columns in the LGN, input from both eyes overlaps
3 wks before birth: Segregation into ocular dominance columns begins
6 weeks after birth: segregation of ocular dominance columns is completed
If one eye is deprived, it will be underrepresented in the ocular dominance columns
Effect of visual deprivation on ocular dominance columns?
In a monkey study: monocular deprivation led to a loss of response from the deprived eye and an increased response from the seeing eye. There were very few binocularly driven cells. The effect was reduced with late deprivation.
In a related experiment, surgically induced strabismus or prism led to a massive loss of binocular neurons. These monkeys had poor binocular disparity.
Orientation deprivation
Cats reared in an environment with overwhelming horizontal stimuli led to more cortical neurons with "preference" for horizontally oriented lines. Opposite occurred for cat raised with vertical lines.
Causes of amblyopia in children?
-strabismus
-media opacities
-ptosis
-occlusion
-astigmatism
Critical period of visual development
is 2-14 weeks in cats/monkeys, but is significantly longer in humans. Tied to periods of dendritic growth and synaptogenesis.
What affects the severity of amblyopia?
-degree of imbalance between the eyes
-age of onset of the amblyopic condition
When does amblyopia occur?
-Amblyopia does not occur before 2 months of age (since binocular interaction at the striate cortex is not yet established)
-does not develop after 6 to 8 years of age
What are the developmental stages of amblyopia?
Critical period: from birth to 6 months, aggressive treatment to avoid legal blindness
Sensitive period: 6 months to 8 years (upper age limit for development of amblyopia), aggressive treatment to avoid vision impairment
Susceptible period: 8 years to 18 years, aggressive treatment, amblyopia can reoccur if amblyotic factor is still present
Residual plasticity period: 18yrs to adulthood, success if patient is compliant, if amblyotic risk factor is still present amblyopia not likely to occur
What are the effects of parvo maldevelopment?
-aniso amblyopia
-strabismic amblyopia
-fine stereopsis deficit
-contrast sensitivity deficit (high spatial frequency)
What are the effects of magno maldevelopment?
-esotropia
-congentital nystagmus
-coarse stereopsis deficit
-contrast sensitivity deficit (low spatial frequency)
-motion VEP (visual evoked potentials) deficit
Cortical Visual Impairment
Can be caused by insult to the occipital lobe or geniculostriate pathway due to: hypoxia/ischemia, hydrocephalus, hemorrhages, cerebral malformations, head trauma, or infections.
Associated with: cerebral palsy, seizures, microcephaly, cognitive impairment.
Dorsal Stream
The "WHERE" pathway: Occipital lobes process visual data -> Posterior parietal lobes process whole visual scene, attend to component parts -> Motor cortex facilitates movement throughout visual scene -> Frontal cortex directs attention to chosen part of visual scene through head and eye movements.
Ventral Stream
The "WHAT" pathway: Occipital lobes process visual data -> Temporal lobes enable recognition of people/objects, routes, visual memory
Effect of dorsal stream dysfunction
difficulty with complex visual scenes, moving accurately through space, making judgements of obstacles
Effect of ventral stream dysfunction
difficulty recognizing faces, difficulty recognizing shapes and forms, difficulty with visual memory, remembering where things are
Periventricular Leukomalacia
PVL: caused by ischemia in the brain to the white matter adjacent to lateral ventricles, occurs between 23-24 weeks gestation. Can also be caused by maternal infection, fetal infection, high metabolism, or circulatory issues.
Only 1.1% incidence if born after 29 weeks, may lead to cerebral palsy.
Effects of PVL and CVI on vision?
-loss of vision
-normal pupil responses
-strabismus
-nystagmus
-visually inattentive
-attraction to movement
-look and touch occur as separate functions
-delayed visual response
-single symbol acuity 20/40
-crowded symbol acuity 20/200
