Perception, Agnosia and related disorders Flashcards
3 Types of Retinal Ganglia cells
- M-cells:
10% of ganglia. Large, well-myelinated cells that process motion and contrast but NOT color - P-cells:
80% of ganglia. Smaller, and therefore have higher resolution, and color-activated cells - Gamma-cells:
10% of ganglia. heterogenous properties
Retina to Visual cortex
- Lateral geniculate nucleus:
Magno cells, Parvo cells, Interlaminar.
Reorganization in: origin, retinotopy, function - Retino-geniculo-striate pathways:
- N. Suprachiasmaticus: sensitive to dark/light, related to sleep procedure;
- Colliculus superior: in brainstem, programming the eye movement which is so fast and reflexive ;
- Corpus geniculatum lateral: 90% of fibers going back of the brain.
Retinotopy
in primary visual cortex (V1, BA 17) in calcarine fissure,
high degree of specialization (like the sensory-motor homunculus):
up/down, right/left, polar/rostral
Lesions in Optic Nerve
(EXAM)
- monocular blindness: lesion in one eye or optic nerve > total blindness in one eye.
- bitemporal hemianopia: lesions of the optic chiasm, the area where the optic nerves from the right and left eyes cross near the pituitary gland > visual defect in temporal areas in both eyes.
- right-sided nasal hemianopia: lesion in right optic nerve at chiasm (the part which does NOT cross at the chiasm i.e. the nasal part) > visual defect in right nasal visual field.
- homonymous hemianopia: lesion in one-side optic TRACT after chiasm > visual field defect involving either the two right or the two left halves of the visual fields of both eyes
- quadrantanopia : lesions to the contralateral inferior parts of the posterior visual pathway > visual defect in one quarter of field, involving either the two right or the two left halves of the visual fields of both eyes
- macular sparing: unilateral visual cortex lesions > partial loss of vision in the same half of both eyes with the center, the macula, spared
[pic]
V1 to higher Visual cortex
the higher data go in visual processing:
the more complex processing,
the less retinotopy
V1 (contrast & orientation)
> V2 (figure-ground separation):
> > Ventral path [what, object recognition => through the memory area]:
V4 (color, form) > IT
> > Dorsal path [where, how => through the motor area]:
V3 (disparity) > V5/MT (movement) > MST ( moving stimuli with directional selectivity) > PPC
- dMST: object motion
- lMST: retinal slip by self or eye motion
Achromatopsia (color perception disorder)
- a condition characterized by a partial or total absence of color vision, disability to perceive any colors; seeing only black, white, and shades of gray.
- usually deficit in V4, which contains high % of neurons responding to color
- combined with:
- upper visual field defect
- other agnosia
Agnosia
inability to recognize or identify objects, persons, or sounds using one or more of their senses despite otherwise normally functioning senses.
- Apperceptive agnosia : Impairment of high level percepts.
Retained semantic knowledge accessible through other modalities such as auditory, which is not the case for associative visual agnosia.
Lesions: toxic or anoxic brain damage
bilaterally - Associative agnosia: Inability to activate semantic identifying information. More general loss of semantic knowledge, with no ability to access this via any sensory modality.
+ no difficulties in perception, only in naming and semantic knowledge.
Lesions: bilateral temporal lesions
HSV
Alexia without Agraphia
sees letters but difficulties to comprehend,
difficulties in spatial orientation,
intact writing undisturbed
Lesions: visual-verbal disconnection
Prosopagnosia (Face recognition defect)
Inability to recognize people by looking at their face.
Ventral occipitotemporal pathology (especially right side) is observed.
combined with:
* upper visual field defect
* other agnosias
* achromatopsia
Lesions: gyri lingualis & fusiformis
Prosopagnosia Assessments:
- Mooney closure test (faces with/without proper orders)
- Benton-Van Allen face recognition test (defining age/sex/characteristics in silhouettes)
- Benton-Test
Akinetopsia (Motion recognition defect)
lesion in V5 or around it. Deficit with motion recognition. They recognize the objects but can not process data about their motions (fast objects like jump instead of moving)
combined with:
* lower quadrant field
defects
* optic ataxia
* neglect
Lesion: bilateral medial temporal gyrus
> good remission
Pathology of neglect
mostly right hemisphere in inferior parietal lobe
» If we had a lesion in left hemisphere, the right part can compensate for the left side, so we wont have the neglect
Neglect
contralateral neglect of sensory stimuli or motor function, usually specialized to right parietal cortex (why? the right side processes both hemifields while the left parietal process only the right visual fields)
extent correlates with size and
location but not with gender or
age
combined with:
* hemianopia
* neglect in further modality
* anosognosia
Lesion:
mostly right parietal lesions
but also cingulum, prefrontal cortex,
thalamus, striatum
Three Visual Pathways (from ganglia cells)
1.) Suprachiasmatic Nucleus (N. Suprachiasmaticus): sensitive to changes in light/dark, therefore modulates circadian rhythm
2.) Colliculus superior: very primitive part of brain (located in the midbrain), sensitive to visual movement, controls REMs that move toward a visual target (saccades)
3.) Lateral Geniculate Nucleus (LGN): MOST other visual information goes here that goes on to striate cortex
Trade-offs in the visual cortices
The higher up in the visual cortices you go (V1 to V4/V5), the less precise the retinotopy is, because there is a trade-off between precision and specialization
