vision lecture-sl-new.pptx

Module 202 –Theme 2 – 2022 Visual System Snezana Levic [email protected] OUTLINE Anatomy of the eye and the retina • Image formation and focusing problems • Phototransduction • Colour vision and colour blindness Central visual pathways and the visual cortex Medical conditions of central origin •...

Module 202 –Theme 2 – 2022 Visual System Snezana Levic [email protected] OUTLINE Anatomy of the eye and the retina • Image formation and focusing problems • Phototransduction • Colour vision and colour blindness Central visual pathways and the visual cortex Medical conditions of central origin • Optic nerve and optic tract; scotomas • Agnosia, prosopagnosia and blindsight Visual Reflexes (and their use in medicine) • Vestibulo-ocular and optokinetic reflexes • Pupillary response Eye and Retina Optically, the eye is quite like a camera Cornea and lens produce a focused image on the retina Focus is varied by changing the shape (and power) of the lens The iris acts as a diaphragm, varying its diameter by 4x, and thus retinal intensity by 16x Behind the retina is a pigment layer which absorbs unwanted light View of the retina through an ophthalmoscope In outside space, fovea covers a thumb nail at arm’s length (1-2 degrees). Optic disk- where the optic nerve leaves the eye, and blood vessels enter and leave the retina The cornea does 2/3 of the ray bending. The lens does the other 1/3, but also allows the focus to vary (accommodation) Common focusing problems (Refractive errors) Hypermetropia (long sightedness): eyeball too short or lens system too weak. Myopia (short sightedness): eyeball too long or lens system too strong. From Pocock & Richards Correction is usually via spectacle or contact lenses. The refractive power of a lens is measured in diopters (D). This is the reciprocal of focal length in metres: a 2D spectacle lens has a focal length of 0.5 m. Structure of the retina Light •Vertebrate retina evolved back to front: ganglion cells and blood vessels are in the light path to the photoreceptors (except in the fovea). •Receptors • 120 million rods (dim light) • 5 million cones (3 types – bright light and colour) •Processing layers • 3 direct vertical layers (receptors, bipolars and ganglion cells) • 2 transverse layers (horizontal and amacrine cells): signal processing including lateral inhibition (sharpens the edges and contrast) •Only 1 million retinal ganglion cells per eye: 125:1 convergence into optic Distribution of Rod and Cones in the Retina Rhodopsin and its chromophore - retinal Photosensitive pigment is a membrane- bound subunit called an opsin and a second small light- absorbing component called a chromophore. The chromophore of rods is a vitamin A–derived carotenoid called retinal. Rhodopsin is the photosensitive pigment in the rods. When hit by a photon the retinal in the rhodopsin molecule flips from 11cis to all-trans. Nonselective cation channels open Nonselective cation channels closed This sets off a series of biochemical events which results in closure of cGMP-gated nonselective cation channels that are open in the dark, leading - to An adequate intake of vitamin A is essential for normal vision. - Prolonged dietary deficiency of vitamin A leads to the inability to see in dim light (night blin hyperpolarization of the photoreceptor and a reduction in The ganglion cell response – the output Unlike the receptors, ganglion cells respond very weakly to changes in overall light intensity. Instead ofrespond the retina they to local contrast: light on a dark background or dark on a light background. Ganglion cell responses are of many kinds, but the basic pattern is either on-centre (left) or off-centre (right). This is due to lateral inhibition. Fields tend to be circular. Ganglion cells send action potentials down the optic nerve: receptors and bipolars have only graded electrical potentials. Colour vision: trichromacy •Approximate peak spectral sensitivities of human cones and rods Wavelength (nm) Living cone mosaic near the edge of the fovea There are typically more red cones than green cones, and far fewer blue cones than either of the other two. [Getting pictures like this involves impressive optical engineering. The colours are false.] The spacing of the cones is about 2 micrometres, and corresponds to an angle of 0.40 minutes of arc (1 degree = 60 minutes) Colour blindness Colour blindness results from a loss or modification of one or more of the three cone visual pigments (cone opsins). The genes for the red and green pigments are on the X chromosome and damage to one of these genes results in red/green colour blindness. Males have only one X chromosome, but females have two (i.e. an intact spare) which is why red/green colour blindness is much more common in males (7%, versus 0.5% in females). The blue pigment gene is on chromosome 7, which is paired in both sexes. Blue colour blindness is consequently much rarer than red/green. There is another, much rarer kind of colour blindness, which has nothing to do with the pigments, but is caused by damage to the cortical colour processing areas (V4). This is known as central achromatopsia. Central visual pathways and the visual cortex • Optic nerve from each retina divides into L & R halves. Central visual pathways • In the optic chiasm L halves from both eyes combine. Similarly R halves • Optic tracts relay in the lateral geniculate nuclei of the thalamus • Part of each optic tract goes to the superior colliculus in the mid-brain • The output of each lateral geniculate goes almost exclusively to the striate cortex in the occipital lobe (V1). • Here the image of one half of each combined visual field is represented in one half of V1. • The representation of the foveal region is hugely exaggerated • Thereafter the cortical input passes on to areas that process depth, motion, colour etc. Responses of cells in the primary visual cortex (V1) V1 begins processing in terms of orientation, edges, etc Simple cell responses are constructed from rows of ganglion cell (or LGN) on and off-centre fields. The visual cortex – columnar organization The primary visual cortex (v1, or Brodmann area 17) is organized in three overlapping patterns. 2. 3. Ocular dominance columns, driven by the left or right eye, but not both. Hypercolumn ce an in m Do ar ul ns Oc lum co 1. Colour Blobs Smaller orientational columns in which the orientation of optimal stimuli varies systematically across the surface. Colour ‘blobs’. Colour information is kept separate from orientation, and passed on to other regions such as V4 ta n e i Or c n tio ns m olu A hypercolumn contains one complete set of everything From Carpenter Medical conditions involving the visual pathways in the brain Causes of partial loss of vision From Pocock & Richards Scotomas Scotomas come in many kinds: they may be caused by retinal damage, lesions in the visual cortex, or by pressure from tumours restricting the optic nerve, chiasm, optic tract or optic radiation. Dorsal and ventral streams in the cortex The dorsal stream, from occipital to parietal cortex, is concerned with location, motion and action. The ventral stream, from occipital to temporal cortex, is concerned with object (and face) identity, and with conscious perception. Visual agnosia Patient DF The converse condition, in which a patient can describe but not act, is known as optic ataxia. Site of DF’s lesion in the ventral stream Prosopagnosia Is a special case of agnosia, and is the inability to recognise familiar faces. Oliver Sacks was a sufferer, and made the condition famous in 1985 in his book “The man who mistook his wife for a hat”. It is associated with damage to specific parts of the temporal lobe. The area most associated with prosopagnosia is the fusiform gyrus, on the underside of the temporal lobe. Blindsight Destruction of the striate cortex (V1) leads to blindness in the the part of the visual field that corresponds to the damaged area. The area of blindness (scotoma) may be small, or an entire hemifield. In the early 1970s Weiskrantz and his colleagues showed that, although individuals are not aware of stimuli within their blind field, if forced to guess they can perform some discrimination tasks (e.g. X vs O), and point accurately to the locations of stimuli, whilst still denying that they can see anything. Weiskrantz called this phenomenon “blindsight”. Although the route from the retina through V1 is by far the largest pathway to the cortex, it seems that it is not the only one. Some projections from both the LGN and the superior colliculus reach cortical areas involved especially in movement perception, without passing through V1. What is strange is that it is only the V1 input that is available to conscious scrutiny. Possible blindsight pathways (red) Visual Reflexes (and their use in medicine) Vestibulo-ocular reflex (VOR) Optokinetic reflex stabilizes gaze by stabilizes the image of a (OKR) countering movement of the head moving object on the retina Oculomotor nuclei Vestibular nucleus Semi-circular canals Nucleus of the optic tract Oculomotor nuclei Optokinetic nystagmus stimulus https://youtu.be/kAPtu1WTHYc Pupillary Reflex Normally, if one eye is illuminated both pupils will contract, because both the pretectal nuclei and the Edinger Westphal nuclei receive signals from both eyes. Pupillary Reflex Normally, if one eye is illuminated both pupils will contract, because both the pretectal nuclei and the Edinger Westphal nuclei receive signals from both eyes. Damage to one optic nerve will prevent light in that eye from closing the pupil (direct response), but light in the other eye will still do so (the consensual response). Pupillary Reflex Normally, if one eye is illuminated both pupils will contract, because both the pretectal nuclei and the Edinger Westphal nuclei receive signals from both eyes. Damage to one optic nerve will prevent light in that eye from closing the pupil (direct response), but light in the other eye will still do so (the consensual response). Damage to one oculomotor nerve will prevent pupil contraction in that eye, but stimulation of either eye will cause contraction in the pupil in the second eye. Summary of key content:  Image formation on the retina.  Structure of the retina: rods and cones, retinal ganglion cells.  Signal processing in the retina: lateral inhibition.  Central visual pathways and the visual cortex.  Visual reflexes. Learning outcomes: At the end of this lecture students should be able to:  Describe the structure and functions of the different parts of the visual system.  Reason how defects along the visual pathways affect function. Recommended readings •The Eye. A very short introduction. MF Land. Oxford Univ. Press, 2014 •Human Physiology - The Basis of Medicine. G Pocock and CD Richards. Oxford University Press. 4th edition, 2013. Chapter 12. •Neurophysiology. RHS Carpenter & B Reddi. Hodder Arnold. 5th edition, 2012. Chapter 7.