Cerebral Cortex Flashcards

1
Q

Cerebral Cortex (aka Neocortex)

A

Lobes/regions
-frontal, parietal, temporal, occipital, insular and limbic
Columnar arrangement
-specific input/output layers
-some differences in number of layers (e.g., paleocortex)
-subtle differences in appearance/thickness of layers
▪ Broadmann classification of anatomical/functional areas in cortex

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2
Q

Connections of the cerebral cortex
Commissural fibers

A

▪ cortical connection between right and left hemispheres
- corpus callosum
▪ primary pathway between hemispheres
▪ lesions = disconnection syndromes
➢ e.g., pure word blindness (alexia without agraphia)
▪ can write, but not read
▪ language areas of left cortex have no access to visual input
- anterior commissure (between right and left temporal lobes)

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3
Q

Connections of the cerebral cortex
Association fibers

A

▪ cortical connections within the same hemisphere
➢ e.g., superior longitudinal (arcuate) fasciculus connects Wernicke & Broca’s areas
▪ lesion = conduction aphasia

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4
Q

Functional areas

A

Three areas of different function
▪ as always, it is nowhere near this simple - lots of overlap

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5
Q

Primary areas

A

▪ ‘first in, last out’
- primary motor area
- primary sensory areas
▪ receive inputs from sensory thalamus

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6
Q

Association areas

A

Unimodal association areas
▪ e.g., visual or auditory association areas
Multimodal association area
▪ multiple types of stimuli represented

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7
Q

Occipital Lobe
Primary visual area (area 17)

A

Function
- receive visual input from retina
▪ retinotopy
➢ specific map of visual field
➢ large foveal representation
Lesion
- loss of specific region of visual field

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8
Q

Occipital Lobe
Visual association areas (area 18, 19)

A

Function
- beginning (continuation?) of dorsal & ventral visual processing streams
▪ ‘where” & ‘what’ pathways
➢ see visual system notes
Lesion
- visual agnosia (= ventral stream)
- prosopagnosia (= ventral stream)
- color agnosia (= ventral stream)
- alexia

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9
Q

Visual agnosia (= ventral stream)

A

▪ inability to recognize an object by sight

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10
Q

Prosopagnosia (= ventral stream)

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▪ difficulty recognizing familiar faces (even your own)

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11
Q

Color agnosia (= ventral stream)

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▪ inability to recognize colors

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12
Q

Alexia

A

▪ inability to ability to understand written/printed word (language)

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13
Q

Parietal lobe
Primary somatosensory area (area 3,1,2) (S1) in postcentral gyrus

A

Somatotopically organized = sensory homunculus
Function
- cutaneous and proprioceptive information
Lesion to S1
- anesthesia (hypesthesia)
▪ loss of sensation on contralateral side
➢ e.g., unable to accurately judge location or intensity of stimulus
➢ requires a fairly large lesion – much more impairment if both S1 & S2 are involved

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14
Q

Parietal Lobe
Somatosensory association area (area 5,7) (S2) in posterior parietal lobe

A

Function
- keep track of relationships between body and outside world
- multimodal cutaneous, proprioceptive, auditory, and visual inputs
▪ includes motivation, attention, and salience of stimuli
Lesion to S2
▪ many different (or combination of ) symptoms depending on location of damage
- Agnosia (“lack of knowledge”)

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15
Q

Agnosia

A

▪ loss of sensory interpretation
▪ many sub-types of agnosia
➢ damage to association area of a specific sensory input (visual, auditory,
somatosensory)
▪ loss of ability to recognize objects, persons, sounds, shapes, or smells with sensation
and memory still intact
➢ can often identify the separate parts, but not the whole

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16
Q

Prosopagnosia

A
  • can identify eye, lips, etc, but not recognize face
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17
Q

Agraphesthesia (cutaneous kinesthesia)

A
  • difficulty recognizing a familiar form (number/letter) traced on the area of
    skin (back, palm, etc….)
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18
Q

Astereoagnosia (stereoanesthesia

A
  • tactile amnesia (tactile agnosia)
  • inability to judge the form of an object by touch
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19
Q

Non-dominant hemisphere (right parietal lobe)

A

▪ large role in spatial attention
➢ lesions may cause contralateral neglect (hemispatial neglect)
▪ ignore stimuli on left side
* ignore left visual field or left side of objects
* may even claim left arm is not theirs
▪ motor neglect - does not use left limbs – although motor system is intact
▪ anosagnosia - ignorance of the presence of disease

20
Q

Dominant hemisphere (left parietal lobe)

A

▪ helps assemble information to plan for movement
* many interconnections with premotor areas
➢ lesions may cause apraxia
▪ ideomotor apraxia
* deficit in ability to plan or execute complex motor action
* can still explain how to perform it & do it unconsciously
 e.g., cannot touch nose when asked (or shown), but can spontaneously scratch an itch on nose
 (similar symptoms can be seen in premotor damage)
▪ right side often takes over spatial processing after left side damage
* i.e., few cases of neglect from damage to dominant hemisphere
➢ lesions in this area often affect language strongly (see Wernicke’s aphasia below

21
Q

Parietal Lobe
Angular gyrus (area 39)

A

Function
▪ plays role in interpretation of language, mathematics and cognition
Lesion (Gerstmann’s syndrome)
▪ sensory aphasia
➢ see discussion of Wernicke’s area below
▪ dyslexia
➢ impairment or difficulty with fluency or comprehension accuracy in the ability to
read (also may impair writing, phonics)
▪ agraphia
➢ inability to write
▪ acalculia
➢ arithmetic deficits
▪ finger agnosia
➢ inability to distinguish between fingers
▪ right-left disorientation

22
Q

Parietal eye fields

A

scanning/smooth pursuit eye movements

23
Q

Parietal lobe
Supramarginal gyrus (Area 40)

A

Function
▪ language perception and processing
Lesion
➢ see Wernicke’s discussion below
▪ sensory aphasia
▪ sensory dysprosodia

24
Q

Temporal lobe
Primary auditory area (area 41)

A

Function
a receives auditory information from cochlea
▪ tonotopy = frequency map
Lesion
- rarely disabling, due to strong bilateral input (anterior commissure)
- may cause deafness if both sides are damaged (e.g. coup-counter-coup injury)

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Temporal Lobe Auditory association area (area 42)
Function combines auditory inputs ▪ analogous to S2 ▪ distinguish harmony, melody, speech, noise 2 Lesion a total destruction of one side causes little noticeable effect ▪ auditory agnosia ➢ inability to interpret the significance of sound
26
Wernicke’s area –Area 22 in dominant hemisphere
➢ left side in 95% of right-handed people; 60% of left-handed ▪ includes surrounding regions of parietal lobe ➢ supramarginal gyrus & angular gyrus ➢ thus, common symptoms of damage listed here Function ▪ production and interpretation of both written and spoken language Lesion ▪ Fluent aphasia (aka- Wernicke’s, receptive or sensory aphasia) ➢ patients use inappropriate or nonsense words ▪ because motor speech pathways are intact, patients may talk more than usual (thus the ‘fluent’) ➢ difficulty/inability to interpret speech
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Area 22 non-dominant hemisphere
Function ▪ comprehension of non-verbal components of language (prosody) Lesion ▪ sensory dysprosodia (sensory aprosodia) ➢ difficulty of speech in interpreting the normal pitch, rhythm and variation of stress/tone in speech “musical aspects of speech”
28
Frontal lobe Primary motor area (area 4) (M1) in pre-central gyrus
Somatotopic organization referred to as motor homunculus Function - major skeletal muscle control site ▪ has lowest threshold to induce movement ➢ movements are specific – single joints/muscles - primary contributor to corticospinal (and corticopontine) tracts Lesion of area 4 - initial contralateral flaccid paralysis, that quickly becomes - hemiparesis with (mild) spasticity -more obvious deficits in distal limb regions and skilled movements
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Frontal lobe Pre-motor area & supplemental motor area (area 6) in precentral gyrus/sulcus and some of superior frontal gyrus
Function - stimulation requires more current, but induces movement in larger groups of muscles Lesion to pre-motor area or to supplemental motor area - very few symptoms if damage is small and limited to one of these regions - BUT.... ▪ lesions of these areas in combination with M1 damage results in serious impairment ➢ full hemiparesis with spasticity (spastic paralysis
30
Frontal eye field (area 8) = middle frontal gyrus
Function - initiation, guidance of saccades Lesion to area 8 - loss of conjugate gaze (coupled) ▪ eyes cannot move simultaneously in the same direction in order to visualize an object ▪ destructive lesion ➢ = conjugate gaze toward lesion ➢ inability to look to contralateral side ▪ irritative (stimulating) lesion (e.g., seizure activity) ➢ = conjugate gaze away from lesion ▪ inability to look toward ipsilateral side
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Frontal lobe Areas 44, 45 in inferior frontal gyrus
Function - motor production of language - different role if dominant or non-dominant hemisphere
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Broca’s speech area in dominant hemisphere
Function ▪ motor programs for generation of language ➢ premotor for speech (also affects written language)
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Lesion to Broca's area
▪ nonfluent aphasia (aka - Broca’s aphasia; expressive aphasia) ➢ speech is halting, lack function words (e.g., articles and pronouns) ➢ language comprehension is not affected (usually) ➢ often accompanied by right side weakness of arm and/or leg ▪ dysarthria ➢ difficulty of motor control of tongue/mouth to produce speech ▪ agraphia ➢ inability to write ▪ specific to speech ➢ i.e., not involved in dysphagia ▪ difficulty with motor function of swallowing
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Frontal lobe Area 44,45 in non-dominant hemisphere
Function ▪ prosody ➢ fluctuations in pitch, tone, loudness, melody, timing, pauses, stresses, intensity, vocal quality and accents of speech
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Lesion to area 44,45 in non-dominant hemisphere
motor aprosodia ▪ disruption of expression of non-verbal elements of speech ▪ e.g., tone, rhythm, even facial expressions
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Arcuate (superior longitudinal) fasciculus
▪ white matter (association) tract ▪ connects Wernicke’s area to Broca’s area ➢ parietal/temporal cortex to frontal lobe - damage to arcuate fasciculus may result in ▪ conduction aphasia ▪ damage is often posterior to Wernicke’s area ➢ spontaneous speech largely intact ➢ comprehension almost entirely intact ➢ difficulty in speech repetition
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Prefrontal area (areas 10-12)
Function ▪ executive functions ➢ planning, insight, foresight, decision making
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Two major areas of the prefrontal area
Dorsolateral prefrontal cortex ➢ function ▪ working memory (short-term memory) ➢ lesion ▪ problems with planning and attention Ventromedial prefrontal cortex ▪ includes orbitofrontal & some anterior cingulate cortex ▪ interconnected with limbic structures (esp. amygdala) ➢ function ▪ switching behaviors
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Lesions to Ventromedial prefrontal cortex
(e.g., Phineas Gage & prefrontal lobotomy) * impulsiveness, trouble suppressing emotions, poor decision making  e.g., poor bets as seen in Damasio studies ▪ perseveration - persist on single topic ▪ akinetic mutism - frontal lobe lesion * conscious alert patient who retains ability to move/speak but fails to do so * damaged pathways inhibit motivation/increase apathy cause passiveness to interact or respond ▪ akinesia: lack of movement ▪ mutism: lack of speech ▪ apathy: lack of interest, indifference
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Memory and learning
Temporal lobe and limbic lobes involved in complex aspects of learning and memory ▪ limbic lobe is “deep” to temporal lobe Inferior/medial temporal lobes - significant role in creating long-term memory/learning - transition short term to long term memory ▪ hippocampus & entorhinal cortex
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Lesion to memory
amnesia ▪ loss of memory - anterograde amnesia ▪ loss of ability to memorize new things after “injury” ▪ seen after bilateral damage to the hippocampus - retrograde amnesia ▪ loss of ability to recall information from before damage occurred ▪ if seen, usually psychological or the result of massive & widespread damage to many cortical areas (e.g., late-stage Alzheimer’s)
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Short-term memory ▪ Working memory
➢ few seconds to minute ▪ e.g., remember the beginning of a sentence while reading the end of the sentence ➢ requires dorsolateral prefrontal cortex
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Long term memory ▪ Explicit memory (declarative memory)
* episodic & semantic memory ▪ conscious and purposeful recall of previous experiences and information (dates, facts, times, places, etc...) ▪ consolidation requires intact hippocampus to preserve as long-term memory ▪ memory in distributed neural networks in cerebral cortex
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Episodic memory
▪ specific recall of the events in a person’s life ▪ evidence to suggest associated with non-dominant hemisphere
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Semantic memory
▪ recall of factual knowledge of historical events/people ▪ recognize people ▪ “academic” information ▪ evidence to suggest associated with dominant hemisphere
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Implicit memory
➢ memory/recall of previous experiences will unconsciously influence current task without conscious awareness ▪ e.g., amygdala
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Procedural learning (motor skills)
➢ complex motor tasks; skills & habits ▪ e.g., riding a bike, tying your shoes ➢ requires cerebellum