Visual processing

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Visual

Normal visual processing

Visual cortex

 

Striate cortex

• Visual processing involves signal relay from the retina via the lateral geniculate nucleus to the striate cortex (area V1/primary visual cortex/calcarine cortex/Brodmann area 17).

• Has strong retinotopic localisation, such that striate occipital lesions cause deficits restricted to segments of the visual field.

• Primary visual cortex (V1/Area 17)
• Sup: Cuneus gyrus
• Calcarine fissure
• Inf: lingual gyrus

• The band/line of Gennari
• Myelinated fibres of optic radiation that enter the visual cortex on the layer 4
• Gives the striated appearance of the visual cortex on myelin staining

• Occipital (striate) cortex has dominance columns, except in
• The region where the blind spot is located.
• The cortical region representing the monocular temporal crescent of both eyes
 

 

 

Extra-striate cortex (Association cortexes)

• Located in Brodmann areas 18/19 at occipital lobe

• Organised more by process than by visual field location
• Different areas of extrastriate cortex are involved in colour, motion perception, etc:

• Defects
• Deficits in certain aspects of vision:
• Perception of motion, affecting the entire visual field.

• Comprised of
• V2
• V3
• Selective for orientation.
• V4
• V5 (MT: Middle temporal)

• Function
• Integrating visual information

Dorsal and ventral processing stream (Sheth 2016)

• Dorsal stream
• Aka
• Dorsal (Parietal lobe/magnocellular) visual pathway
• 'Where' pathway/stream:
• Location of object in space.
• Spatial processing
• Visual-motor control over objects by processing their "extrinsic" properties—the ones that are critical for handling them, such as their size or their position and orientation in space.
• Within retina
• A more complete coverage of space including the visual periphery, with larger receptive fields, and foveal sparing in some instances.
• Occipitoparietal
• Runs superolaterally from the striate cortex into occipitoparietal and temporoparieto-occipital areas
• Connection:
• Occipital → parietal lobe
• Navigation centre of the cerebrum
• White matter tracks
• Occipital short association fibres
• Superior longitudinal fasciculus (SLF) I and III

• Ventral stream:
• Aka
• Temporal lobe/Parvocellular visual pathway/stream
• "What" pathway/stream
• Object recognition
• Consciously perceive, recognise, and identify objects by processing their "intrinsic" visual properties, such as shape and colour.
• Within retina
• show greater focus or coverage of visual space in close proximity to the fovea
• Occipitotemporal
• Runs below the calcarine fissure into the medial temporal lobe
• White matter tracts
• Inferior Longitudinal fasciculus (ILF)
• Visual information:
• Occipital cortex → ILF → temporo-occipital regions with the lateral and medial part of the temporal pole
• Broadcasts critical information for visual cognition in general, and for object recognition in particular
• Right ILF
• Connections between both the occipital and fusiform faces areas (FUSA) in the fusiform gyrus (occipitotemporal gyrus) (face selective regions) → anterior temporal structures
• Function
• Face processing network
• Deficit
• Prosopagnosia (i.e. an inability to recognise familiar faces)
• Congenital or Progressive
• Left ILF
• Inferolateral occipito-temporal pathway
• Fusiform area
• Where the Visual word form area, (word specific selective area) is located
• If damaged causes pure alexia
• Function
• Reading, lexical retrieval and semantic processes
• Lt hemispheric dominance for language processing

Deficits of visual processing

Disorders of ventral stream: what stream

• Visual agnosia

• Prosopagnosia

• Alexa

• Achromatopsia

Disorders of dorsal stream: where stream

Disorders of motion perception (Akinetopsia: A, Kine (motion) Opsia (See) )

• Patients may have no impression of motion in depth or of rapid motion.

• Selective impairment of motion perception is rare

• Tends to be associated with damage to areas of extrastriate visual cortex analogous to V5 (bilateral lesions of the lateral occipitotemporal area)

• Fast targets appear to jump rather than move.

• Particular difficulties are encountered judging the speed and direction of cars

Disorders of spatial perception

• Balint syndrome: Video
• A disorder of spatial perception comprising three aspects:
• Simultanagnosia
• Inability to comprehend a complex scene in its entirety—that is, only one component of the scene is perceived at a time
• Optic ataxia:
• Inability to reach by hand for targets presented visually
• Ocular motor apraxia
• Inability to direct gaze to a visual target
• Patients complain of visual difficulties, and may appear functionally blind.
• They exhibit a curious searching head thrust, by which they aim to search their environment item by item (sometimes unfortunately but accurately compared to the head thrusts of a hen searching for food).
• Damage
• Bilateral superior parieto-occipital.
• Strokes: ‘‘watershed’’ infarction, or
• Neurodegenerative as in the posterior cortical atrophy variant of Alzheimer’s disease.

• Dressing apraxia and constructional ‘‘apraxia’’
• Confusingly, these are not apraxias as such, but are rather visuospatial deficits resulting in difficulty dressing and drawing.
• Dressing apraxia: Video
• Test
• Asking the patient to don a jacket which has had the sleeves deliberately turned inside out.
• Constructional apraxia
• Test
• Drawing overlapping pentagons, the Neckar cube, or a clock face.
• Damage
• Left hemisphere: simplified drawings
• Right hemisphere: ‘‘explosion’’ of the constituent parts of the drawing

Other higher order deficits of vision

• Topographagnosia
• Getting lost in familiar surroundings can be due to deficits in either ventral or dorsal visual association cortices.

• Anton’s syndrome
• A form of anosognosia restricted to vision
• Preservation of the pupillary reaction to light
• Patient denies there is any visual disturbance despite being functionally blind.
• Patient will confabulate
• Damage:
• Primary visual cortex.

• Blindsight
• The existence of this condition is disputed
• It is claimed that in the context of blindness caused by primary visual cortex damage, residual unconscious visual function may occur, subserved by subcortical structures such as the lateral geniculate nucleus.

Pseudo-agnosia

• Optic aphasia
• Patient cannot name a visually presented object but can name when the object is heard in use-action or when placed in the hand (i.e., naming deficit is modality specific to vision).
• Patient can demonstrate its use by gesture or can point to it when named.
• Not a true agnosia
• May represent a visual verbal disconnection

Gain in visual processing (hallucinations)

• Visual gain (hallucinations)
• Charles Bonnet syndrome
• A form of release hallucinations
• This comprises positive visual phenomena occurring in areas of visual field deficit, whether this be total or partial.
• It often arises in the elderly as a result of ocular pathology—for example, age related macular degeneration causing vision loss/field
• The images tend to be complex (for example. animals, people) and insight to the disease is usually retained.
• Hallucinations
• Vivid
• Realistic
• Not familiar
• Formed
• Theory
• Reticular activating system in brain stem sends an ascending pathway to the accessory visual pathway to suppress it
• Accessory visual pathway sends signal down to the RAS to activate it: if there is light → RAS is activated to keep consciousness.
• Decreasing vision → dec. Accessory visual pathway signal to the reticular activating system → RAS activation reduces → the accessory visual pathway is not inhibited by the RAS → hallucinations
• Peduncular hallucinosis
• A form of release hallucinations
• Following midbrain stroke, vivid hallucinations may arise, which tend to occur in the evenings, and have a tendency to disappear over weeks.
• Has insight
• No auditory component
• Hallucinosis (odd hallucination)
• Vivid
• Realistic
• Familiar
• Formed
• Theory
• Reticular activating system in brain stem sends an ascending pathway to the accessory visual pathway to suppress it
• Accessory visual pathway sends signal down to the RAS to activate it if there is light during awake phase
• Midbrain stroke causes the RAS not able to inhibit accessory visual pathway → hallucination