PY2507.5 2.0 ~ {Impairments of obj manipulation&recognition: Apraxia & V agnosia
pathways to the brain for visual processing
dorsal + ventral [there are 3 in tota from v1 and v2l]
dorsal pathway
where/how - process spatial info, guiding actions & understanding object actions - from primary visual cortex [v1] to posterior parietal cortex - involved in spatia awareness and coordination
ventral stream
what pathway - responsible for object identification & recognition - from visual cortex [v1] to inferior temporal cprtex - involved in recognizing faces, objects and scenes
impairments of early visual processing
lesions that affect one eye only in will only affect peripheral [so retina or optic nerve] + lesions after optic chiasm always involve damage to both eyes
occipital lobe and its specialization
OL is made of diff areas with diff neuronal composition + visual info reaches V1 first, then it passes to V2 and then to other visual areas
v1 - area 17
primary visual coortex aka striate cortex for its characteristic apperance - much of it is contained in the calacrine sulcus -
v2
secondary visual cortex - adjacent to v1 - when stained with special enzyme you can see blob like structures which are involved in colour perception while cells surrounding blobs are involved in seeing form & motion perception
damage to occipital areas
since v1 receives input from both eyes disturbance restricted to 1 eye means damage is outside the brain [retina or optic nerve] - depending on extent of which part of v1 is affected + extent of lesion then diff parts of visual fields are lost
different types of lesions
extensive lesions produce loss of half vf - hemianopia + partial lesions produce deficit to only a quadrant of visual field - quandrantopia + small lesions produce small blind spots - scotomas
what region of visual field is spared
generally central [macular] region - because the foveaa projects to both hemispheres
v1 - blind sight
people with damage to v1 report blindness in part of vf - however formal tests reveal that they are geenrally aware if something [e.g. light] has entered their blind region - visual input is processed in subcortical areas [thalamus] but not to the point to allow conscious perception let alone recognition
v4 - deficits in colour perceeption
area v4 recieves input from the blobs of v1 [specialized in detection of colour] lesions. produce loss of colour perception + failure to recall or imagine colour [colour cognition]
v5 - deficits of movement perception
specialized for detection of movement - LM (Zihl et al.,1983) reported that he couldn't see people moving, they suddenly appear & disappear
what did we learn / infer from patient LM (Zihl et al.,1983)
brain must analyse form separately for recognition & motion detection
2 purposes of visual processing
to construct tri-dimensional objects from 2D pattern of light on our retina so that objects can be later recognized from diff perspectives + to construct visual objects to guide our actions
challenge with the retina
captures a flat 2D image of the world, but we perceive objects in 3D so our brains must reconstruct ddepth, shape, size & relative position of objects in enviro allowing us to perceive the world in 3D
binoculur vision + stereopsis
our 2 eyes provide slightly diff perspectives - so our brains use disparity [diff] between images from each eye to compute depth [stereopsis]
after constructing depth then what
object recognition - brain groups pixels into shapes, sizes and textures that identify familiar objects - ventral stream plays sig role in recognizing and categorizing these objects
key brain regions involved in visual processing
primary visual cortex [v1] - processes basic features like edges and motion & higher-order areas + v4 for color + v5 for motion + IT cortex for object recognition
embodied cognition
our cognition is deeply rooted in the body's interactions with the world. - shaped & influenced by physical body and its movements, sensory experiences & enviro interactions
from v1 qnd v2 which 3 pathways emerge
dorsal stream [to parietal cortex] ~ optic apraxia + dorso-ventral (intermediary)[to superior temporal sulcus] ~ ideo-motor apraxia + ventral stream [to inferior temporal cortex] ~ visual agnosia + ideational apraxia
(Ungerleider. and Mishkin, 1982) - diff roles atributed to pathways
dorsal - for localizing objects - WHERE stream
ventral - for recognition of objects - WHAT stream
what did Goodale & Milner 1992; Goodale, 2011: structural and spatial attribute processing of objects by both streams, for different purposes
d - vision for ACTION [viewer centered]
v - vision for PERCEPTION [object centered]
optic ataxia
first desccribed by balint (1909) and Holmes (1918) - deficit in reaching/grasping under visual guidance + difficullty forming appropriate hand postre for diff objects as well as directing movement to right location in space
damage in what areas of brain result in optic ataxia
bilateral damage to dorsal stream esp posterior parietal lobes [can also stem from unilateral damage to either LH/RH] in the last case deficits are more pronouned with contra-lateral hand
what was original interpretation of optic ataxia
deificit in spatial vision - but patients were able to describe orientation, shape, size and relative location of objects which they fail to grasp (Perenin & Vighetto, 1988) - so its more a deficit at the interface between vision and action
visual agnosia
inability to recognize objects visually, despite having intact vision due to damage to ventral streams especially in inferotemporal cortex so a patient can see shapes & movement but can't identify what the object is
subtypes of visual agnosia [Heinrich Lissauer end of 19th century]
apperceptive agnosia - can't form a coherent visual perception of objects + associative agnosia - can describe or copy an object's shape but can't name or recognize [patient sees key but cant identify it until they touch it]
contrast between 2 patients reviewed in Goodale, 2011 - visual agnosia vs optic ataxia [patient DF]
va from carbon monoxide poisoning, prominent bilateral lesions in lateral OC, unable to recognize faces, objects or simple geometric shapes BUT no problem with grasping and grip scaling
contrast between 2 patients reviewed in Goodale, 2011 - visual agnosia vs optic ataxia [patient RV]
oa - lesion to posterior parietal lobe, no problem in recognizing objects & discriminating shapes, including no problem in judging size & orientation BUT serious difficulties in grasping
apraxia
first identified by Carl Liepmann (1905,1908) - associated with LH damage esp Linferior parietal lobulee - inability to carry out complex motor actions - difficulty in demonstrating object use following a verbal command or picture than in manipulation of real object
2 types of apraxia according to Liepmann
ideomotore apraxia - problem with spatio-temporal realization of gestures + odeational/conceptual apraxia - conceptual problems with functional knowledge about objects
ideo-motor apraxia 1
damage to computation of gestures - difficulties in computing the right spatio-temporal framework for gestures [both familiar and novel] & imitation in pantomime - errors in spatial & temporal paramters of actions - no diificuties with gesture coomprehension
ideo-motor apraxia 1 - lesions
to frontal supplemntary motor areas, superior parietal lobe, parietal-fronta connections as well as subcortical lesions involving basal ganglia
ideomotor apraxia 2
damage to manipulation knowledge - disrupted stored represenations of gestures so patientss have prob in both recognizing & producing familiar gestures [and pantomiming function of objects
ideational apraxia
disrupted functional knowledge [conceptual/ventral apraxia] - errors associating a function with the proper object, lesions in TL [part of ventral stream or TPjunction] + deficits in sequencing actions to reach a goal [making a cup of tea] linked to FL lesions
schematic model of visual processing - damage to areas for diff types of agnosias
apperceptive - visual object analysis to visual structural descriptions
associative - visual structural descriptions to semantic system
apperceptive agnosia
prob deriving a complete representation from a visual input, prob is in visual recognition so difficulty in copying or drawing objects due to gross bilateral damage to lateral parts of OL
Marr's stages of visual processing
proposed by David Marr - 3 key stages
2D representation (primal sketch)
the 2½D Sketch [viewpoint-dependent] based on stereopsis + motion parallax [effect of mvnt on perception]
3D representation (true 3D model) - object-centered representation
simultagnosia
affects ability to perceive more than one object or feature at a time, typically dissociation between ability to perceive individual objects + ability to perceive a scene or multiple objects simultaneously - due to damage of posterior parietal cortex or parieto-occipital junction
the case of HJA (Riddoch and Humphreys, 1987)
suffered bilateral infraction affecting both OL - severe prob recognising objects and faces, he was better at recognizing object silhouettes than regular line drawings and better at gglobal letters than small [so authors suggested he has a prob in intergrating visual features into a whole percept.
associative agnosia
prob with associating visual representation with a meaning so an object can be readily copied but not recognized - due to lesions of the anterior temporal lobels [generally on the left]
2 types of deficits in associative agnosias
deficit in accessing stored represntations of objects [patients can't distinguish between real and made up objects]
deficit in linking structural descriptions to corresponding meanings