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Flashcards in Cortex 2b Deck (46):

where does striate cortex lie?

what Brodmann's area is it?

what does it constitute?

where does it receive input from?

striate cortex (area 17)

lies along the banks of the calcimine fissure medially and extends onto the occipital pole

constitutes the PRIMARY VISUAL CORTEX (V1)

receives visual input from the retina through the lateral geniculate nucleus


where are optic nerve tract fibers going?

what are other visual pathways?

what is the light reflex?

to the lateral geniculate to the visual cortex

other visual pathways:
- one to pons
-one to olive
-one to SC (visual reflexes)
-one to superior colliculus from cerebral cortex
-visual fibers going to suprachiasmatic nucleus to thalamus for circadian rhythms

light reflex: visual fibers to pretectum to CN 3--> constricted pupil


80% of fibers to optic nerve go to where?

20% go where?

80% to lateral geniculate to V1

20% for light reflex

some go to pulvinar and association cortex, superior colliculus


what effect does the SNS have on the pupil?

dilates pupil- active process of SNS


what is the macula?

a specialized region in the retina adapted for high visual acuity, contains only cones whereas the periphery of the retina contains primarily rods

cones- mediate color vision and provide high visual acuity

Rods- mediate light perception, provide low visual acuity with good perception of contrasts and function chiefly in nocturnal vision

rods:cones= 20:1

macula is curved- see opposite visual fields


what does the superior retina see?

what does the inferior retina see?

superior sees inferior visual fields

inferior sees superior visual fields


what does the nasal retina see?

what does the temporal retina see?

nasal sees temporal visual field

temporal sees nasal visual field


what is Meyer's Loop?

fibers of neurons from inferior that see superior lateral quadrant??


the L visual hemifield is seen by ?

nasal retina of the L eye and the temporal retina of the R eye because of curvatures of the retina

nasal crosses over in optic chiasm, temporal stays ipsilateral


the optic tract has fibers from ?

where does the optic tract project to?

fibers from BOTH eyes

projects to the lateral geniculate


what is outside of the binocular vision?

why does this occur?

monocular vision-- occurs because the nose blocks line of sight


what is the result of a transection of the L optic nerve?

monocular vision- R eye can still see-- can still see that side's visual field but peripheral vision becomes affected

lose ipsilateral peripheral vision


what is the result of a transection at the optic chiasma?

knocks out crossing nasal retina fibers only (corpus callosum lesion)- complete loss of peripheral vision - have tunnel vision; but still have binocular vision


what is the result of a transection of the L optic tract?

loss of R half of visual field; impairment is contralateral to lesion


what is the organization of V1?

Cortical modules
-each module represents a single point in visual space
-each module forms from 2 vertically oriented ocular dominance columns - each column receives info from one eye

subunits of cortical modules:
-blobs- color channel


what are the 2 parallel visual pathways? (Channels)

1- parvocellular pathway (P channel) (dorsal lateral geniculate)

2-Magnocellular pathway (M channel) (ventral lateral geniculate


what is the striate cortex?

visual cortex

6 layers- but layer 4 is subdivided-- receiving area

"striate cortex" because there are multiple lines


what is the M channel? what does it do?

comes from the magnocellular pathway in the ventral lamina of the lateral geniculate

projects to area 4 (4C alpha)

thought to be specialized for the analysis of object motion


what is the P-IB channel?

pavocellular interblob
comes from dorsal layers of the lateral geniculate
concerned with object orientation
thought to be devoted to the analysis of object shape


what is the blob channel?

3rd channel "coneocellular"

color vision-- neurons are wave length sensitive

from lateral geniculate, ascending up to layer 2-3 where blobs are (blobs have color pigments)

sensitivity isn't direction of light like the other channels. its ability to see color

usually you lose all 3 color channels in a brain lesion. if you do lose one but not the others its a problem with the eye itself


what is beyond V1?

primary 2 large scale cortical streams of visual processing


what are the 2 streams of visual processing?

1- Dorsal Stream= striate cortex to parietal lobe
"WHERE stream"
receives from magnocellular pathway

2- Ventral Stream= striate cortex to temporal lobe
"WHAT stream"
receives from parvocellular pathway


what is the dorsal stream?

"WHERE pathway" (Magnocellular pathway)
V5- multimodal

Medial Temporal- visual perception of motion-object MOTION
-neurons- large receptive fields that respond to stimulus movement in a narrow range of directions

Medial superior temporal-
-neurons response to complex motion-sensitive properties

MST roles:
-directing eye movements
-motion perception

projects to motor cortex for visual guided movements


what is the ventral stream?

"WHAT pathway" Parvocellular pathway

V4 (unimodal area)
-receives afferents from blob and interblob areas
-important for shape and color perception
-visual memory

IT (inferiotemporal)
-important in visual perception of visual memory
-response to pictures of faces


what is prosopagnosia?

difficulty in recognizing faces although vision is normal

problem with inferiotemporal -- ventral stream


describe the central connection for audition?

bilateral system- different fibers cross at different levels

bipolar cells in spiral ganglion, go into either cochlear nuclei- from here on= bilateral

major cross over occurs in trapezoid body then to dorsal or intermediate acoustic stria, superior olive in lower pons (subconscious picking out of location of sound, efferents to hairs to buffer sounds to up specific frequencies) --> up lateral lemniscus--> up to primary auditory cortex in superior temporal gyrus (areas 1, 41)


what is the primary auditory cortex?

area 41

tonotopically arranged
-anterior- lower sounds
-posterior- higher sounds

bilaterally innervated

columnar organization based on frequency- depth of column is sensitized to each frequency


what is the result of a lesion to the primary auditory cortex?

one side:
-loss of localization- of just that frequency


what are the 2 separate pathways to the primary auditory cortex?

1- Dorsal "where & how" stream
~3 pathways
-localizing sound sources
-using sounds to guide movements
-projects to frontal and parietal

2- Ventral pathways
-linguistic function
-identifying the source of speech (who is speaking or what is emitting sounds); learning voices
-Uncinate fasciculus
-Arcuate fasciculus


what are the 2 language centers?

1- Broca's (44,45)

2- Wenicke's (22)


what is Wernicke's language center?

Brodmann's area 22

acts to decode the sounds of language so that spoken as well as written words and sentences can be understood and comprehended

this is where sounds that you are hearing get interpreted as language. also determines what you are saying


what is Broca's language center?

Brodmann's area 44,45)

final sequential (syntactical, grammical) inprint so as to become organized and expressed as temporally ordered motoric linguistic articulations (speech)

receives the command to say something from Wernicke's. Allows you to say something, line up works in a way that makes sense. Then sends info to motor strip to physically say the words.


what is aphasia?

partial or complete loss of language abilities following brain damage, often without the loss of cognitive faculties or the ability to move the muscles used in speech


what is anomia?

=inability to find words


what is alexia?

=inability to read


what is agraphia?

=inability to write


what is Wenicke- Geschwind model?

repeating a spoken word:
auditory cortex-->


what is pure work deafness?

=bilateral destruction of A1

individual becomes cortically deaf

although able to hear they cannot perceive or comprehend non-verbal sounds or understand spoken language

Wernicke's area in the L hemisphere are disconnected from all sources of auditory input and thus cannot extract meaning from the auditory environment= AUDITORY AGNOSIA

these patients are NOT deaf, no permanent loss of acoustic sensitivity
-this is bc sounds continue to be received in thalamic and subcortical centers including the amygdala. Hence, the patients can still detect sounds. However, they are unable to identify them and cannot recognize the sounds of speech, including spoken language
-never the less, these patient can still speak. unfortunately, they are unable to perceive the words that they are saying as that info can no longer to received within the neocortex and can't be transferred to Wernicke's area which is responsible for comprehending the sounds of speech


what is Broca's aphasia?

=non-fluent speech

few words, short sentences, any many pauses

the words that can be produced come with great effort and often distorted

the melodic intonation is flat and mono pitched. this gives the speech the general appearance of a telegraphic nature, because of the deletion of function words and disturbances in word order.

the repetition of words and phrases is impaired

aural comprehension for conversational speech is relatively intact. there is often an accompanying R hemiparesis involved the face, arm and leg


what is Wernicke's aphasia?

patient does not appear to have any difficulty articulating speech, but may be paraphasic

comprehension of speech is impaired and sometimes as much as single words are not comprehended

speaks in meaningless jargon, "neoligistic jargon" devoid of any content but free use of verb tenses, clauses and subordinates


what is conduction aphasia?

fluent paraphasic expression that is characterized by numerous phonetic substitutions ("fetter" for "better")

comprehension is intact

severe impairment of repetition

reading aloud is characterized by paraphasic output but comprehension is good

writing impairment is mild

frequent self corrections

patient would know what he wanted to say but can't say it

could not repeat simple statements, read out loud or write

sentences are usually short and often unrelated to each other

arcuate fasciculus is knocked out but wernicke's is knocked out (similar to wenicke's aphasia- difference is they understand!!)


what is transcortical aphasia?

the cortical border zones surrounding the language axis have been destroyed

the language axis of the L hemisphere becomes completely disconnected from surrounding cortical tissue but presumably remains an intact functional unit

the cerebrum is unable to communicate with the language zones. as such, an individual in unable to verbally describe what they see, feel, touch, or desire. moreover, because the language axis can't communicate with the rest of the brain, linguistic comprehension is largely abolished

communication b/w wernicke's, broca's and the inferior parietal lobule is maintained, associations from other brain regions can't reach the speech center
-although able to talk, the pt has nothing to say. moreover, although able to see and hear, the patient is unable to linguistically understand what they perceive. however, they are capable of generating automatic-like responses to well known phrases, prayers or songs


how does alexia without agaphia work?

splenium of CC

disconnection of the language centers from visual perceptual areas

patient can't read but other language functions are intact

pt must have a lesion of the L occipital lobe that also includes the pathways connecting the visual perceptual areas. these pathways make up the splenium of CC

this produces a visual field cut on the R side and visual info can only be perceived by the R hemisphere. since the connections b/w the R hemisphere visual perception areas the L hemisphere language centers are lesioned, the pt can't decode the language related visual info and can't read. Howevere, the pt comprehends auditory info and can write and speak normally. this results in the paradoxical symptoms of a pt who can write spontaneously but can't read their own writing


what is agraphia?

can't write

presumably the parietal lobe contracts the written-word images (probably via interaction with Wernicke's area) which assists in converting these into graphemes

these motor-graphemes (or written word/letter images) are then transmitted to the L frontal convexity (broca's and exner's area) for grapheme conversion and motoric expression


what are the 2 stages involved in the act of writing?

1-linguistic stage
-involves the encoding of auditory and visual info into syntactical-lexical unites- the symbols for letters and written words
-this is mediated through the angular gyrus which thus provides the linguistic rules which subserve writing

2-motor-expressive-praxic stage
-this stage is mediated presumably by Exner's writing area (premotor area)


what are subtypes of agraphia?

b/c different regions of the brain contribute to the ability to write, damage to these differ areas, therefore, affect different aspects of the ability to write. thus, there are different subtypes of agaphia, depending on which areas of the brain have been damaged

frontal agraphia
pure agraphia
alexic agraphia
apraxic agraphia
spatial agraphia