psyc30018 exam (wk 6-12)

blindsight

to have unconscious vision for objects in our environment that we cannot perceive in a conscious manner

hemianopia

partial or total cortical blindness caused by destruction of primary visual cortex (V1)

clinical signs of blindness

1. no visual response to threat

2. optokinetic reflect may be absent (movement pursuit)

3. no alpha rhythm (EEG) on posterior regions

4. absence of visual evoked potentials (ERP)

Poppel et al., (1973)

observed that war veterans could orient gaze toward (unseen) stimuli in blind field

Humphery (1974)

showed that a blind monkey retains spatial navigation skills (e.g. Helen, the blind monkey)

blindsight in humans

1. orient gaze toward a stimulus in their blind field

2. point to the location of a stimulus

3. guess above chance when asked to judge object orientation (yet no awareness)

e.g. for letters, movement & shapes

geniculostriate pathway

links neurons from retina through subcortical areas all the way to V1

colliculus pathway

retina → superior colliculus (SC) → pulvinar → V2

pulvinar pathway

retina → superior colliculus (SC) → pulvinar → MT/V5 (brain area that supports movement and perception)

LGN pathway

retina → LGN (lateral geniculate nucleus) → MT/V5 (brain area that support movement and perception)

blindsight through the colliculus pathway

• monkeys lose blindsight after destruction of super colliculus

• fMRI casts doubt: activation in MT/V5 in response to moving stimuli - but no collicular response

• SC may be involved, but not significantly so

blindsight through the LGN pathway

1. blindsight dependent on the integrity of this pathway

• good integrity for people who have unconscious vision (blindsight positive) seen in regard to fractional anisotropy and mean diffusivity

• even more so in the damaged hemisphere

• (Ajina et al., 2015)

2. blindsight disappears with a reversible lesion & so does activity in higher visual regions

• (Schmid et al., 2010)

blindsight through the pulvinar pathway

• stronger connectivity in left side (damaged side) in this pathway suggested as a means to compensate for lack of V1 connectivity

• taken in individuals who experience early onset blindness

pulvinar v. LGN

• LGN = onset during adulthood

• P = onset at birth (connection between P & MT may be pruned during adulthood)

hypothesis for blindsight

1. colliculus pathway

2. LGN pathway

3. pulvinar pathway

4. residual vision mediated by islands of spared visual field? (Gazzaniga, 1994)

affective blindsight (evidence from TN)

• performed at chance in discriminating basic shapes (e.g. square v. circle)

• performed above chance in discriminating between facial expressions

affective blindsight (evidence from GY: blind to right hemifield)

• visual areas only respond to consciously seen stimuli

• amygdala responds to both seen and unseen fearful faces

(compensates for what the visual cortex can’t see?)

de Gelder & Nouchine (2006)

unseen body images selectively activate MT/V5 & pulvinar without V1

Hamm et al., 2003

• fear conditioning to unseen visual neutral cue in a patient w/ complete cortical blindness

• seen in patient K.H.J, who was observed to blink a lot more when there was a visual cue predicting an aversive stimuli (startle probe matches that of health participants)

• fear learning does not require visual awareness and cortical representation / subcortical pathways (the bypass V1) are sufficient to activate fear to unseen threats

evidence for SC-PUL-AMG

1. anatomical evidence (tracing) in macaques

2. DTI (diffusion imaging) shows connectivity in both humans and macaques

3. GY shows an increase in connectivity (DTI) on lesioned side of V1 compared to intact size (compensatory mechanism? - subcortical pathway used to strengthen residual vision)

4. reproducible on the large sample (622)

5. greater white matter connectivity correlated w/ stronger functional connectivity (specifically for fear recognition)

hypothesis for how the brain generates affective blindsight

1. pulvinar to amygdala pathway

2. degraded vision mediated by islands of spared visual field

3. other extrastriate (not V1) projections to the amygdala