dark adaptation Flashcards
what is the light levels the human visual system operates ?
- the human visual system operates over about 14 log units ( threshold is about 10^13 x diameter than the brightest light we can operate under )
- we can detect a few quanta of light against complete blackness
- we can see a white polar bear against dazzling white snow
what are the 4 mechanisms which allow the visual system to operate over this huge range ?
- duplex retina ( 2 photoreceptor sub-systems)
- changes in pupil size
- photochemical adaptation ( changes in concentration of bleached and unbleached photopigment )
- neural adaptation ( neural responsiveness e.g. changes in receptive field size, temporal summation, negative feedback loops)
what is the duplex retina mechanism ?
- two sub-systems of photoreceptors- rods and cones
- when fully dark adapted, rods are highly sensitive to dim light in low light levels ( scotopic conditions ) but saturate under higher light levels
- cones are used in high light levels ( photopic conditions), but are less sensitive than rods in low light levels
- in intermediate light levels both are active ( mesopic conditions )
- nearly doubles the range of light levels over which the visual system can operate
explain the mechanism of changes in pupil size ?
- pupil light reflex helps us deal with range of luminance experienced by visual system
- average min pupil = 2mm and average max pupil = 8mm
- area of biggest pupil is 16x bigger than area of smallest this means that retinal illuminance can be increased by 16x by dilating pupil
- this only accounts for 1.2 log units of 13 log unit range in intensity encountered by visual system
- therefore we cannot keep retinal illuminance constant
what do we need to function over different light levels ?
- we require photochemical and neural adaptation mechanism to allow us to function over different light levels
what is adaptation ?
- adaptation is an increase or decrease in retinal sensitivity with changing light levels
what is dark adaptation ?
- retinal adaptation to increase sensitivity in response to reduction in illuminance
- takes up to 50 minutes to be complete when moving from very bright to very dim light levels
what is light adaptation ?
- is reduction in sensitivity to light when we move to higher retinal illuminance level rapidly
- very fast ( seconds )
where does adaptation occur ?
- the fact that we can remain dark adapted in the covered eye, but light adapted in the uncovered eye
- this tells us that the mechanism for light and dark adaptation must take place in the retina this is before the optic chiasm
what does it mean that one part of the retina can be dark adapted and one part can be light adapted ?
- the fact that one part of the retina can be dark adapted and one part can be light adapted tells us that this is something that occurs on a very localised level
what is the importance of adaptation ?
. increasing light intensity increases retinal ganglion cell response ( action potentials/second)
. the response of retinal ganglion cells is limited ( maximum around 500 spikes/second )
. without adaption there would be saturation of the RGC response at 500 spikes/second
. adaptation allows the RGC to respond to a large range of intensities
how to record dark adapation function ?
- subject in bright light
- switch light off
- measure how their visual threshold changes over time in the dark
- we do this by increasing the intensity of target until subject sees it
- repeat at regular intervals , record time and ‘ threshold ‘ intensity
explain the assessment of dark adaptation graph ?
- after exposure to the brightest lights , the dark adaption function has two distinct curves
- first curve - describes cone adaption ( cone branch ) after 10 minutes we have kink in the curve called the rod cone break
- the rods take over as being the most sensitive photoreceptor
- we get a rod branch of the dark adaptation function
- where the graph levels off is known as absolute threshold when completely dark adapted
why does the dark adaption curve look this way ?
- cones dark-adapt faster than rods - cones determine threshold initially but cone absolute sensitivity is worse
- at rod-cone break rod sensitivity exceeds cone sensitivity
- after rod-cone break rod determine threshold
what are the two components of photopigment ?
- photopigments is protein ( opsin) + chromophore ( retinal )
what is the structure of photopigment in dark ?
- unbleached ( purple ) photopigment ( opsin + 11-cis retinal ) absorbs light to initiate phototransduction cascade
what happens in the phototransduction cascade?
- photopigment breaks down into components ( opsin + all trans retinal ) and loses colour ( is bleached ), cannot absorb light
how does photopigment regenerate ?
- all-trans retinal diffuses to RPE where its isomerised to 11-cis
- then diffuses back to photoreceptors , recombines with opsin , ready to absorb new photon
- regeneration of photopigment follows exponential function ( like radioactive decay )
- half time = time take for amount of bleached photopigment to be halved
what is the halftime of cones?
- 1.7 minutes
what is the halftime of rods ?
- 5.2 minutes
how do we know about photopigment regeneration ?
- it is investigated using retinal densitometry
- light is shone through in the eye through a half silvered mirror
- some of the light is absorbed by photopigment as it hits the retina
- some of the light is absorbed by other structures such as the RPE
- some of the light reflects off the sclera at the back of the eye and bounces back through pupil
- when the retina is dark adapted there is more unbleached pigment available to absorb light
- when retina has more bleached photopigment in light adapted state , there is less light absorbed by the photoreceptor
- as the eye gradually dark adapts , the proportion of light reflected back out pupil gradually decreases
- by monitoring this using a photocell and galvanometer we are able to monitor the rate of dark adaptation
what is photochemical adaptation ?
- change in ratio of bleached: unbleached photopigment in retina
does the process of photopigment regeneration control rate of adaptation ?
- time course of rhodopsin regeneration ( measured by retinal densitometry ) mirrors time course of rod branch of dark adaptation function
- photopigment regeneration is at the bottom of the process of dark adaptation
why isn’t the concentration of unbleached pigment what limits threshold during dark adaptation ?
. bleached photopigment can’t absorb light, so require unbleached photopigment for vision
. if it’s a limitation in concentration of unbleached photopigment which limits sensitivity in dark - we would expect 50% regeneration of rhodopsin to cause 50% recovery of threshold
. yet when 90% of rhodopsin has regenerated, threshold is still elevated by 1000x
does the concentration of photoproducts of bleaching limit threshold during dark adaptation ?
. rhodopsin breaks down into other photoproducts e.g.opsin and metarhodopsin II , when it absorbs light and is bleached
. good correlation found between threshold and concentration of bleached photoproducts e.g. opsin
what actually limits threshold during dark adaptation?
- the presence of bleached photoproducts like opsin rather than the lack of unbleached photopigment
what is dowling-rushton relationship ?
- log sensitivity during dark adaptation is linearly related to concentration bleached photopigment
how does the concentration of photoproducts limit threshold ?
. bleached photoproducts (e.g.opsin) weakly activate further visual transduction
. has same effect on retina as adapting to real light, but stable on retina , son not seen as light ( troxler effect )
. retina responds to background light by reducing retinal gain ( amplification) resulting in low sensitivity
. retina therefore responds to photoproducts by having low sensitivity
. as photoproducts decay sensitivity recovers
what is the equivalent background theory ?
. at any time during dark adaptation, retinal sensitivity is equivalent to sensitivity caused by adaptation to a background light
. e.g. at 17 mins, 10% of rhodopsin is still bleached
. detecting light at this time, would be like detecting light against a background which bleached 10% of rhodopsin
why is it in the first 0.3 seconds during dark adaption threshold drops very steeply ?
. this is due to neural not photopigment changes
what is the Arden and weale theory ?
. post-receptoral factors
e.g. changes in receptive field size ( increase in size, loss of centre surround organisation ), also involved in dark adaptation
how does retinal location of target affect the dark adaption function ?
. sensitivity improves with eccentricity up to 15 degrees due to greater rod density
. at fovea - no rod cone break
. if we move target to 2.5 deg - rod-cone break and better absolute sensitivity
. if we move target to 5 deg- prominent rod-cone break, lower threshold
how does target size affect dark adaptation ?
. small test spot at fovea - cone branch only
. larger stimulus - rod branch present ( stimulus incorporates rods also)
. increase in stimulus size - lower absolute threshold ( lots of spatial summation makes us more sensitive )
how does target wavelength affect dark adaptation ?
. cone peak sensitivity is at longer wavelength than rod
. cones more sensitive than rods to long wavelength stimuli (>700nm) even in the dark adapted eye - no rod branch
. test flash - 507nm ( peak rod sensitivity ) gives prominent rod branch and low final threshold
how does adapting light wavelength affect the dark adaptation function ?
. red adapting light will not bleach much rhodopsin
. rods remain sensitive when light turned off
. red lights used in military ready rooms
. allows cones to function
. doesn’t bleach rods, so night vision remains good
how does adapting light intensity and duration affect the dark adaptation function ?
. higher initial threshold
. more prominent cone branch
. later rod-cone break
. longer time to reach final threshold
explain the process of light adaptation ?
. this is when we are going from lower to higher light levels
. increment threshold , that is the amount by which the target needs to be brighter than its background to be seen increases
. our visual system becomes less sensitive to light as background light levels increase
. at low levels of background light this is determined by neural factors such as changes in receptive field size
. at higher light levels its determined by the amount of bleach pigment present in the retina
. reduction in sensitivity as we move to conditions of high illuminance is very important in stopping the response of our retinal ganglion cells from becoming saturated at high light levels
. this process happens rapidly
what are the factors that affect the rate of dark adaptation ?
. age
. retinal disease e.g. AMD, retinitis pigmentosa, CSNB
. systemic conditions e.g. vitamin A deficiency
how do we investigate and diagnose different causes of poor night vision ?
. psychophysical techniques
. fundus and anterior eye examination
. electrophysiology
how is the goldmann adaptometer used in the clinical measurement of dark adaptation ?
. adapting light in hemispherical bowl
. all light extinguishes
. threshold measured at intervals post bleach
. takes more than 30 mins for full dark adaptation curve
. uses method of ascending limits ( yes/no paradigm )
how does the goldmann adaptometer show retinal disease ?
. thresholds are either very elevated or dark dark adaptation is very delayed ( fundus albipunctatus )
what happens in fundus albipunctatus ?
- this is where the process of dark adaptation takes up to four hours to complete
what are computer based systems used in measurement of dark adaptation ?
. AdaptDx- presents a brief flash of light which bleaches the central part of the retina and then measures the time taken for retinal sensitivity to recover to a criterion value
. its measuring how long it takes for threshold to drop to a certain point
. the test takes 20 minutes
how does the photostress test used in the clinical measurement of dark adaptation ?
. measure best VA
. bleach with ophthalmoscope
. time taken to return to within 1 line of best VA
. >60 sec pathological
. can be completed readily in practice by Optom
what are some non-retinal causes of not seeing well in the dark ?
1- age related problems
. Miosis
. lens opacities
. both these things mean that retinal illuminance is reduced and absolute threshold elevated
2- eye myopia
. eye focuses at about 1m in dark
. usually only when no visual stimulus, but possible when stimulus is degraded e.g. driving at night
. may benefit from -0.50 over-correction
what are the retinal causes of not seeing well in the dark ?
- age
- reduced rate of photopigment regeneration causes slowed dark adaptation. photoreceptor death ( particularly of rods ) elevates absolute threshold - age related macular degeneration (AMD)
- pathological worsening of normal ageing changes
- photoreceptor death raises absolute threshold
- thickening of Bruch’s membrane , RPE and photoreceptor damage and reduced choroidal circulation slow photopigment regeneration
how does chronic open angle glaucoma reduce the ability to see in the dark ?
. ganglion cell loss coincides with area of max rod density ( 15 degrees) which is reduced scotopic sensitivity
how does vitamin A deficiency reduce the ability to see in the dark ?
. vitamin A important part of rhodopsin
. deficiency reduces rhodopsin concentration slows photopigment regeneration
. results in raised absolute threshold and prolonged dark adaptation
what inherited night blindness ?
. inherited conditions giving symptoms of night-blindness
what are progressive conditions that cause gradual degeneration ?
. retinitis pigmentosa - condition where vision get worse over time
what are the stationary conditions of inherited night blindness ?
. theses conditions do not change over time
. congenital stationary night blindness (CSNB)
. ( types I, II and III)
how do differentially diagnose inherited night blindness ?
. dark adaptometry
what is Type II CSNB fundus albipunctatus ?
. autosomal recessive
. affects rod and cone photopigment kinetics
. grossly extended adaptation times
. eventually normal thresholds
what is retinitis pigmentosa ?
. autosomal recessive, autosomal dominat or X-linked recessive
. progressive photoreceptor degeneration
. caused by progressive shortening of rod and cone outer segment due to abnormal disc shedding
. first symptoms is ‘night blindness’ ( aged 20 )
. central vision initially good, later affected
. fundus shows pigment clumping in mid-periphery ( bone-spicule appearance ) and attenuated blood vessels
. grossly elevated rod and cone threshold
how is the visual system able to function ?
. the visual system is able to function over a wide range of retinal illuminance levels as a result of the duplex retina , pupil diameter changes, and retinal adaptation ( photochemical and neural )
what is the limiting factor in photochemical adaptation ?
. the limiting factor in photochemical adaptation is the rate of removal of photoproducts of bleaching
what is the benefit of the assessment of dark adaptation ?
. assessment of dark adaptation can help with the diagnosis of congenital and acquired retinal disease
