17 Visual Pathways

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17 Visual pathways (Dr Merrick Moseley) Describe the basis of physiological optics and of the common defects of refraction Draw the binocular visual pathways, from retina to lateral geniculate nucleus to primary visual (striate) cortex, with special regard to the partial decussation at the optic chiasm and its consequences for the visual field representation at higher levels of the pathway Explain how specific visual field defects can arise from lesions at different sites, including the optic nerve, chiasm and radiation, and at different locations within striate cortex. Give examples of how some of these defects may arise Outline briefly the basic processes of visual integration occurring at different levels of the visual pathway, and how these relate to interpretation of the retinal image Explain briefly the concept of functional specialization and the clinical effects of focal extrastriate lesions, especially in relation to the visual perception of colour and motion Describe the afferent and efferent pathways underlying the pupillary light reflexes (direct and consensual) and the near reflex Outline briefly the circadian visual system and indicate its significance Physiological optics Image formation by the eye = refraction (bending of light) Amount of refraction depends on: radius of curvature and refractive index Measured as dioptric power (Dioptre = 1/f, where f= the focal length of the lens in metres) Structures involved: principally the cornea, aqueous humour, lens, vitreous humour Emmetropia = ideal focal state of the eye, optical optimum - Refraction at the cornea and lens produces point focus of light on the fovea Ametropia = error of refraction resulting in visual defects a) Myopia = short sight, light is brought to a focus before the retina typically because the eye is too long - Treat with concave lenses – need to lessen the refractive power of the eye b) Hypermetropia = long sight, typically because the eye is too short and point of focus is beyond the retina - Optical power needs to be increased therefore treat with positive convex lenses that will increase refraction c) Astigmatism = different focal points of different planes of light due to non-spherical shape of cornea - Different curvatures results in different refractive power in different directions - Correct with cylindrical lenses Presbyopia Natural occurring loss of accommodation (focus for near objects) Onset from 40 years Distance vision remains intact Corrected by reading glasses (converging lenses) to increase optical power of eye and view near objects satisfactorily

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visual pathway

Transcript of 17 Visual Pathways

Page 1: 17 Visual Pathways

17 Visual pathways (Dr Merrick Moseley) Describe the basis of physiological optics and of the common defects of refraction Draw the binocular visual pathways, from retina to lateral geniculate nucleus to primary visual (striate) cortex,

with special regard to the partial decussation at the optic chiasm and its consequences for the visual field representation at higher levels of the pathway

Explain how specific visual field defects can arise from lesions at different sites, including the optic nerve, chiasm and radiation, and at different locations within striate cortex. Give examples of how some of these defects may arise

Outline briefly the basic processes of visual integration occurring at different levels of the visual pathway, and how these relate to interpretation of the retinal image

Explain briefly the concept of functional specialization and the clinical effects of focal extrastriate lesions, especially in relation to the visual perception of colour and motion

Describe the afferent and efferent pathways underlying the pupillary light reflexes (direct and consensual) and the near reflex

Outline briefly the circadian visual system and indicate its significance

Physiological optics Image formation by the eye = refraction (bending of light) Amount of refraction depends on: radius of curvature and refractive index Measured as dioptric power (Dioptre = 1/f, where f= the focal length of the lens in metres) Structures involved: principally the cornea, aqueous humour, lens, vitreous humour

Emmetropia = ideal focal state of the eye, optical optimum- Refraction at the cornea and lens produces point focus of light on the fovea

Ametropia = error of refraction resulting in visual defects

a) Myopia = short sight, light is brought to a focus before the retina typically because the eye is too long

- Treat with concave lenses – need to lessen the refractive power of the eye

b) Hypermetropia = long sight, typically because the eye is too short and point of focus is beyond the retina

- Optical power needs to be increased therefore treat with positive convex lenses that will increase refraction

c) Astigmatism = different focal points of different planes of light due to non-spherical shape of cornea

- Different curvatures results in different refractive power in different directions- Correct with cylindrical lenses

Presbyopia Natural occurring loss of accommodation (focus for near objects) Onset from 40 years Distance vision remains intact Corrected by reading glasses (converging lenses) to increase optical power of eye and view near objects satisfactorily

Primary visual pathwayOptic nerve carries innervation from retina Optic chiasm – nasal fibres cross-over but temporal do not[Pressure on chiasm causes loss of temporal fields due to damage to nasal fibres] Optic tract – projections to other visual pathways leave tract here:

- Hypothalamic tract: regulation of circadian rhythms- Pretectum: reflex control of pupil and lens- Superior colliculus: orienting movements of head

and eyes Lateral geniculate nucleus Optic radiations Terminate in primary visual cortex (V1) V1 cells respond and analyse edges, bars and slits

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Extrastriate areas – analyse colour and motion

Retinal projections of the visual fields Left field: maps to nasal retina of left eye and temporal retina of right eye Right field: maps to temporal retina of left eye and nasal retina of right eye Visual fields of both eyes overlap Nasal fibres temporal visual field Temporal fibres nasal visual field

Lesions of visual pathway

Extrastriate areas Concentric arrangement around V1 Visual processing continues beyond the striate visual cortex into extrastriate regions

(V2, V3, V4, V5/MT, V6, V7, V8) Involved in colour and motor processing

- Colour V4- Motion V5 (only true motion)- Both activate V1 + V2

Evidence: clinical conditions (e.g. cerebral achromatopsia – CO poisoning) and imaging (e.g. PET, fMRI)

Circadian visual pathway Retinohypothalamic tract projects from the optic tract to the suprachiasmatic nucleus of the hypothalamus – centre of

biological clock Light-dark cycle major zeitgeber – entrains biological clock from 24hrs20mins to 24hrs (without slip slowly out of sync –

jet lag) Intrinsically photoreceptive ganglion cells containing melanopsin Lesions of RHT = circadian blindness Also cosmetic glass eyes – loss of receptive cells causing jet lag symptoms. Now try to keep eye in order to preserve

pathway

Reflex pathways Retino-pretectal pathway mediating the pupil light reflex = direct light reflex + consensual light reflex Pretectum – located on roof of midbrainAfferent pathway: Rod and cone photoceptors detect light and send action potentials to brain along the optic nerve to pupil specific

ganglion cells Optic chiasm – cross over of fibres sends innervation to both sides of brain Exit at posterior third of optic tract Project to the pretectal nucleus (PTN) – ipsilateral and contralateral connection to the opposite side

A: loss of vision in right eyeUncommon – whiplash before seat belts

B: Bitemporal hemianopiaE.g. pituitary tumour compressing optic chiasm, temporal fibres unaffected but damage to nasal fibres causes loss of temporal fields

C: Homonomous hemianopia Affects right temporal fibres loss of right nasal fieldAnd left nasal fibres loss of left temporal field

D: Left superior quandrantanopiaAffects Meyer’s roots – inferior retinal fibres

E: Left homomonous hemianopia with macular sparingLoss of right nasal and left temporal fields but not loss of foveal innervation. Retained due to dual blood supply of calcarine sulcus

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Crossings enable consensual reflexEfferent pathway: Projections from PTN to Edinger-Westphal nucleus specific to sphincter Synapse at ciliary ganglion and exit midbrain at interpeduncular fossa Causes contraction of pupillary sphincters and constriction of both pupils Defects Unilateral afferent defect: reduced response in affected eye when directly stimulated; normal response in affected eye

when stimulated consensually Unilateral efferent defect: unequal pupil size (anisocoria)

The near response/Complex/Triad Pupillary miosis (sphincter pupillae) Convergence (medial rectus) Accommodation (ciliary muscle)

Common efferent pathway – III nerve Disassociation from light reflex = Argyll-Robertson pupil: light does not cause constriction but movement will e.g. due to

neurosyphyllis

Retino-tectal pathway Projection to superior colliculi – either side of midbrain Generation of saccadic eye movements – flicking movements Eye – head coordination of movement Also receives inputs from auditory system – startle reflex in response to sound More prominent role in non-humans