PSYC 301 MT2 - Perception

sensation

detection of internal/external stimuli

raw info about environment is made available to brain through senses

perception

awareness and interpetation of sensory info by brain

sensation vs. perception

perceptual deficits can exist without sensory loss

primary visual cortex (V1)

visual info travels from retina → subcortical relays → V1, first cortical stage

V1 damage

some patients with V1 lesions show blindsight:

e.g. can guess visual stimuli (forced-choice discrimination) or navigate obstacles above chance, despite reporting blindness

higher visual cortices I: secondary visual cortices (~24)

get visual input from V1 → analyze form, motion, shape, colour

secondary visual cortices V5 damage

akinetopsia: bilateral damage can cause selective loss of visual motion perception (i.e motion blindness)

higher visual cortices II

1. visual association cortices (~7): integrate input from visual cortex with other sensory systems (auditory, proprioceptive) for multisensory perception

2. dorsal stream: V1 → dorsal prestriate cortex → posterior parietal association cortex

3. ventral stream: V1 → ventral prestriate cortex → inferotemporal

functions of two streams - theory 1: what vs. where

monkey studies:

posterior parietal lesion (dorsal) → poor spatial/location discrimination → "where" pathway

inferotemporal cortex lesion (ventral) → poor object discrimination → "what" pathway

human support:

dorsal damage → can describe objects but can't reach accurately

ventral damage → can reach for objects but can't identify them

functions of two streams - theory 2: action vs. perception

patient DF: carbon-monoxide poisoning → bilateral ventral-stream lesions

ventral lesion → visual form agnosia (cannot identify shapes but dorsal, visuomotor abilities spared (can grasp objects correctly)

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streams differ not from the type of information carried but the use of that information

dorsal: direct behavioural interaction with objects

ventral: conscious perception

functions of two streams - theory 2: action vs. perception - opposite pattern

dorsal damage → action → optic ataxia (poor visually guided reaching)

agnosia

inability to recognize objects/shapes (with no evidence of significant memory loss) → perceptual loss (not sensory)

agnosia - types - apperceptive agnosia

apperceptive agnosia: recognition failure due to impaired perceptual processing

agnosia - types - apperceptive agnosia - features

can't recognize objects from unusual views or degraded images

often rely on local features instead of holistic form

severe cases: difficulty copying shapes or matching objects

agnosia - types - associative agnosia

normal perception but can’t link perception to meaning

ventral not dorsal stream (e.g. hands know what to do with the object but can’t only use the visual information from photo of lock to determine what it is)

agnosia - types - associative agnosia - features

can copy drawings but can't name or recognize them visually

when told the name of objects, can describe it accurately → stored knowledge intact

agnosia - types - prosopagnosia

failure to recognize faces, with intact object recognition

agnosia - types - prosopagnosia - features

can describe features (eyes, hair, etc.) but can't identify the person

affects both familiar (retrograde) and new (anterograde) faces

can still recognize people by voice, clothing, or gait

agnosia - types - prosopagnosia - treatment

training programs and coping strategies (e.g. using other features)

agnosia - types - prosopagnosia - structures affected

bilateral occipito-temporal damage

face processing - structures

network of occipito-temporal areas:

1. occipital face area (OFA)

2. fusiform face area (FFA)

3. anterior temporal cortex (AT)

is FFA purely for faces?

FFA also active for visual expertise (any category you’ve become an expert at recognizing visually)

e.g. bird or car experts

prosopometamorphopsia

disorder where faces appear distorted (e.g. warped, drooping, stretched)

prosopometamorphopsia - features

only affects faces, not other objects

can involve one or both sides of the face

prosopometamorphopsia - structures affected

linked to abnormal activation in face-processing network (not absence of it)

can be experimentally induced via stimulation through intracranial electrodes in right inferior temporal lobe