PSYC 169 - Midterm 2

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64 Terms

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Primary areas

Neocortical regions that receive sensory signal or send motor commands

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Secondary areas

Areas that elaborate sensory information received from primary areas

  • Located adjacent to primary areas and are interconnected with them

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Association areas

All cortex not directly responsible for sensory input or motor output

  • Mediate complex activities such as language, planning, memory & attention

  • Located between the various secondary areas

  • Can receive signal from or send signal to secondary areas

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The lateralized forebrain

  • Most sensory and motor neurons cross after entering the brain

  • One side of the forebrain is responsible for the opposite side of body

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Primary visual cortex “V1” (striate cortex)

Large strip of cortex in the occipital lobe

  • Responsibilities: process basic visual information & sends info to secondary visual areas

  • V1 must function so that secondary visual areas can carry out their processing

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Sensation

The effects of a stimulus on the sensory organs

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Perception

The elaboration & interpretation of a sensory stimulus based on, for example, knowledge of how objects are structured

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Visual Processing

1) From eye to V1

2) From V1 to rest of the brain

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Retina

The internal surface of the eyes that contains specialized cells

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Photoreceptors

  • Located in the retina

  • Convert (or transduce) light into neural signals

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Geniculostriate pathway

  1. Light from each visual field hits both eyes

  2. Information from the nasal portion of the retina (traveling through the optic nerve) crosses at the optic chiasm

  3. Information from the temporal portion of the retina (traveling through the optic nerve) remains ipsilateral

  4. Information from both eyes is processed in the LGN

  5. The information travels from the LGN through the optic radiations to V1

  6. Basic visual information, such as orientation, is processed in V1

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Blindsight happens because perception is impaired

Physical damage to V1 in one hemisphere causes ‘cortical blindness’ in the contralateral visual field

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Retinotopic map of V1

Neurons that are ‘close’ together process information that is ‘close’ together in the visual fields

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Hemianopia

A type of blindness that occurs on half of the visual field

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Describe the two general ways hemianopia can occur

  • Can occur in the early visual pathway before V1

  • Can occur when there’s damage to V1

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Damage to V1 & the retinotopic map

  • The amount of damage in V1 is proportional to loss of information within the retinotopic map

  • “Cortical blindness” is caused by damage to V1 and not the eye or early visual pathways

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Patient D.B.

  • A portion of the right V1 was lesioned during surgical removal of an angioma

  • He couldn’t consciously “see” but sometimes “felt” something was moving

  • He could still accurately point to light shining in his left visual field despite no conscious awareness!

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Angioma

Collection of blood vessels that cause abnormal blood flow

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Blindsight “cortical blindness”

The conscious awareness of “seeing” is missing even though visual information is not reaching V1

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Tectopulvinar pathway

Evolutionarily ‘old’ compared to geniculostriate

<p><span>Evolutionarily ‘old’ compared to geniculostriate</span></p>
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Transcranial magnetic stimulation (TMS)

  • Uses electrical pulses to inhibit or activate areas of the brain

  • Evidence for blindsight

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Secondary visual areas

  • V2: assists V1 to integrate basic visual information & sends information to the other secondary visual areas

  • V3-V5: all do some form of color, form, or motion processing

    • V4 is more functionally specialized for color

    • V5 is more functionally specialized for motion

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Color vision deficiency (CVD)

  •  The decreased ability to see color as most people do

    • CVD can impair seeing:

      • The difference between color

      • How bright colors are

      • Different shades of colors

    • Typically CVD is inherited due to genetic mutations that caused missing cones

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Describe the three patients with damage to secondary visual areas & their symptoms & deficits

  • Patient J.I - Had achromatopsia

  • Patient P.B - color perception in a blindsight patient

  • Patient L.M - Had akinetopsia

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Patient J.I

  • Before his accident, he was an accomplished painter

    • He had no missing or damaged cones and saw color “normally” his whole life

  • He suffered a severe concussion (TBI) after a car accident

    • He could no longer distinguish any color whatsoever

      • His physical world, dreams and memory appeared in black and white

  • His diagnosis was achromatopsia

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Achromatopsia ‘cortical color blindness’

  • Failure to perceive color causing the world (or even dreams!) to appear in grayscale

    • Caused by damage only to area V4

    • Not the ‘typical’ color blindness (color vision deficiency)

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Patient P.B

  • Patient P.B was electrocuted, resulting in cardiac and respiratory arrest resulting in damage to V1 and V2

  • He had blindsight but could still perceive light…even colored light!

  • Conclusion: it’s likely some visual information reached area V4 even though his V1 and V2 were damaged

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Akinetopsia “motion-blindness”

  • Inability to perceive motion

  • Occurs when there’s damage to V5/MT

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Patient L.M

  • Was an 43-year-old woman whose area V5/MT was damaged after a stroke

  • She had difficulty pouring tea into a cup because the fluid appeared to be frozen

  • L.M found being in a room with other people disturbing because she could not see them moving

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Two streams of hypothesis of object recognition

A model of how visual information travels through association areas to support higher-level cognitive functions

  • It proposes there are two anatomically distinct processing streams that originate from the occipital lobe

    • Dorsal stream

    • Ventral stream

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Dorsal stream

The “how/where” pathway because it’s responsible for processing where objects are in space and their function

  • Leads to the parietal lobe

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Ventral stream

The “what” pathway because it’s responsible for recognizing “what” something is

  • Leads to the temporal lobe

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Recognition

The experience of “knowing”

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Agnosia

  • “Without knowledge”

  • A rare disorder whereby a patient is unable to recognize & identify objects, persons or sounds using one or more of their senses despite otherwise normally functioning senses

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Visual agnosia

  • A result of brain damage to the association areas within the ventral “what” pathway

  • Causes a selective impairment

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Patient Gottlieb L.

  • Suffered a head injury after a wooden fence was blown into his head during a storm

  • Ended up getting visual agnosia

    • Symptoms: when shown a pair of glasses, he named them as ‘a lamp’, yet he could recognize them by touch

  • He could perceive the object but he couldn’t associate them with a meaning

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Lissauer’s classic model of object recognition

  • Heinrich Lissauer examined Gottlieb L. in 1888 & proposed there were two major stages in object recognition

    • 1) Create a coherent percept of the object as a single entity

    • 2) Attach meaning to the percept

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What was Lissauer’s classic model of object recognition and what were the two agnosias derived from it?

Lissauer’s classic model of object recognition is that a person creates a coherent percept of the object as a single entity & attaches meaning to the percept. The agnosias derived from it are visual form agnosia & associative agnosia.

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Agnosias derived from Lissauer’s “classic” model of object recognition

  • Visual form agnosia (VFA)

  • Associative agnosia

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Visual form agnosia

The inability to group visual information together to create a coherent perceptual image of what one is seeing

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Associative agnosia

The inability to attach meaning to the perceptual image of an object

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Patient Mr. S - visual form agnosia

  • Clinical presentation: 25 year old male veteran with carbon monoxide poisoning

  • Behavioral performance:

    • Could follow moving visual stimuli

    • Could hardly recognize and name objects based vision alone

    • Could recognize objects by touch

    • Appeared “blind” for object recognition

  • He could not 1) copy or 2) match simple letter, shapes or objects

    • His deficits were due to the inability to group information into one visual image within his own mind

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Patient D.F - visual form agnosia

  • She was unable to copy the model drawings…but when asked to draw the model objects from her own memory she could!

  • This demonstrates visual form agnosia:

    • Is an impairment in grouping visual information into a coherent mental image

    • Is not an impairment in memory

  • She was unable to visually identify or copy a list of letters or numbers but she could identify 3D shapes of letters and numbers by touch and write them by memory

    • More evidence that VFA is a deficit in perception

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Perceptual tests of VFA: Incomplete Pictures Test

  • Predicted Performance

    • Healthy controls can recognize the object by the second drawing

    • VFA patients need more visual information or are completely unable to recognize the object

    • Healthy controls can pick which individual objects are in the overlap picture whereas VFA patients are impaired

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Perceptual tests of VFA: Unusual Views Test

  • Everyday common objects are shown from two angles

  • Normal performance requires the visual information to be grouped into one object and rotated in the mind’s eye

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What are some examples of test performance that would indicate a patient has visual form agnosia?

  • Unable to visually recognize objects

  • Can recognize objects by touch

  • Unable to copy, match or identify drawings of objects

  • Able to draw objects from memory

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Patient F.L - associative agnosia

  • Patient FL had brain damage from alcoholism

  • Symptoms:

    • Could copy line drawing copies very well but could not name to objects he was drawing

    • Could not “understand” objects because he couldn’t recognize them

      • He didn’t know how to use a key or to open an umbrella when it was raining because he couldn’t understand “what” the object was

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What are some examples of test performance that would indicate a patient has associative agnosia?

  • Success on perceptual tests

  • Impairment on tests assigning meaning to a visual mental image

    • Matching by function tests

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Challenge to Lissauer’s model: patient HJA’s performance on copying

  • HJA could copy all the drawings very well but couldn’t name/recognize what he drew

    • St. Paul’s cathedral

    • Everyday objects

  • Expected diagnosis?

    • Associative agnosia

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Patient HJA’s performance on copying

  • End result looks great! But what about the strategy?

    • Copied one small section in great detail & then moved on to the next small section

    • Most people copy by drawing the outline & then fill in the details

  • HJA was perceiving the world abnormally due to deficits in featural binding

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Featural binding

Combining different characteristics, such as color, shape, size, orientation and location to perceive objects

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Patient HJA

  • Had symptoms of both visual form and associative agnosia

    • Had integrative agnosia

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Integrative agnosia

A form of visual agnosia in which individuals are able to perceive the elements of an object but find it difficult to combine them into an integrated whole

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Prosopagnosia

Neurological disorder characterized by the inability to recognize familiar faces

  • Patients with prosopagnosia cannot visually recognize any previously known faces, including their own as seen in a mirror or photograph

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Specific brain regions involved with face processing

  • Occipital face area

  • Fusiform face area

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Occipital face area

Responsible for structural processing of faces

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Fusiform face area

Higher-order face processing such as identity

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Cause of prosopagnosia

  • Developmental prosopagnosia

  • Acquired prosopagnosia

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Developmental prosopagnosia

Alterations in the face processing areas are present from birth and are likely caused by genetic mutations or deletions that are inherited

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Acquired prosopagnosia

Strokes, head trauma, inflammation, infection, oxygen deprivation, etc. which damage the face processing areas

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Three basic stages of face processing

  1. Visual analysis

  2. Perceptual analysis

  3. Identity analysis

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Visual analysis

Decoding the visual information from a visual scene

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Perceptual analysis

Grouping the information together to “know” that it is a human face

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Identity analysis

“Knowing” that this face is one that you have encountered before