Higher Order Function (Exam 2) Flashcards

1
Q

What are the main connections in layer 1 of the Neocortex?

A

Dendrites and axons from other layers

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2
Q

What are the main connections in layer 2 of the Neocortex?

A

Cortical to cortical connections

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3
Q

What are the main connections in layer 3 of the Neocortex?

A

Cortical to cortical connections

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4
Q

What are the main connections in layer 4 of the Neocortex?

A

Receive inputs from thalamus

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5
Q

What are the main connections in layer 5 of the Neocortex?

A

Sends outputs to subcortical structures (other than thalamus)

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6
Q

What are the main connections in layer 6 of the Neocortex?

A

Sends outputs to thalamus

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7
Q

In classifying neocortex what is the primary cortex?

A
  • Primary Sensory Cortex
  • Primary Motor Cortex
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8
Q

In classifying neocortex what are the types association cortices?

A
  • Unimodal Association Cortex
  • Heteromodal Association Cortex
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9
Q

Describe the Unimodal Association Cortex

A
  • Area adjacent to primary cortex involved in processing for a single sensory or motor modality
  • Somatosensory, visual or auditory association cortex, premotor cortex, supplementary motor area
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10
Q

Describe the Heteromodal Association Cortex

A
  • Integrating function from multiple sensory and/or motor modalities
  • Prefrontal cortex, parietal and temporal heteromodal association cortex
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11
Q

How does cortical sensory processing occur?

A
  • Sensory input travels to primary sensory cortex via thalamic relay
  • Primary cortices relay to unimodal and heteromodal association cortex
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12
Q

Where does the primary somatosensory cortex receive input from and how is it organized?

A
  • Received Input from: VPL and VPM
  • Organized: In somatotopic manner
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13
Q

Where is the secondary somatosensory cortex located and what does it respond to?

A

Located: operculum and dorsal insula
Responds: touch, pressure, limb position and pain from both sides of the body

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14
Q

The somatosensory perception of the SI is done through parallel processing of different sensory modulated by area. What does each area provide sensory from?

A
  • Area 3a: muscle spindle afferents
  • Area 1 and 3b: cutaneous afferents
  • Area 2: Joint receptors
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15
Q

A lesion to SI would impair what?

A
  • 2 point discrimination
  • Localization of stimuli
  • Position sense
  • May recognize primary modalities (pain, touch, temp) with poor localization
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16
Q

What Brodmann’s area is associated with Somatosensory Perception: Unimodal association cortex?

A

Area 5

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17
Q

Where does the Somatosensory Perception: Unimodal Association area receive input from and integrates what information?

A
  • Receive input from: SI
  • Integrates information between body segments and somatosensory modalities
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18
Q

What would a lesion to the Somatosensory: unimodal association cortex cause?

A
  • Astereognosis
  • Tactile agnosia
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19
Q

Somatosensory Perception: Heteromodal Association cortex is related to what Brodmann’s area?

A
  • Area 7
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20
Q

Where does Somatosensory Perception: heteromodal association area receive input from and what processing is done here?

A

Input from: Area 5 and visual information
- Eye limb processing for most visually triggered or guided movements

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21
Q

What Brodmann’s area is related to the visual cortex?

A

Area 17

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22
Q

Where does the primary visual cortex get input from and it integrates information from?

A

Input from: Lateral geniculate nucleus of the thalamus
Integrate information from both eyes about shape, color, size, location and direction of movement for contralateral hand of visual field

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23
Q

A lesion to unilateral visual cortex can result in?

A

Homonymous Hemianopia

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24
Q

A lesion to bilateral visual cortex can result in?

A

Cortical blindness - no useful vision
(pupillary light reflex intact)

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25
Q

Unimodal Visual Association Areas are associated with what Brodmann’s area?

A
  • Area 18 & 19
  • Parts of areas of 20, 21 & 37
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26
Q

Heteromodal Visual Association areas what are the dorsal and ventral pathways responsible for?

A

Dorsal: Where? (analysis of motion and spatial awareness)
Ventral: What? (analysis of form and color)

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27
Q

What cortex is associated with the dorsal pathway of visual perception?

A

Parieto-occipital association cortex

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28
Q

What is the blood supply to the parieto-occipital association cortex?

A

MCA-PCA watershed territory

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29
Q

What would a lesion in the MCA-PCA watershed territory cause?

A

Deficits in visual spatial analysis
(more common with non dominant hemisphere lesions)

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30
Q

What cortex is associated with the ventral pathway of visual perception?

A

Occipitotemporal association cortex

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31
Q

What is the clinical implication of the ventral pathway of visual perception?

A
  • Formed visual hallucinations arise from inferior occipitotemporal association cortex
  • Causes: toxic, withdrawal, focal seizure, complex migraine, midbrain ischemia, psychiatric disorder
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32
Q

What is the blood supply to the occipitotemporal association cortex?

A

PCA

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33
Q

What can occur if there is an issue with the blood supply to the occipitotemporal association cortex?

A
  • Bilateral deficit
  • Prosopagnosia (inability to recognize people by looking at their face- despite being able to describe features)
  • Achromatopsia (central disorder of color perception)
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34
Q

What areas are located in the transverse temporal gyri and what are their Broadmann’s area?

A
  • Primary auditory area (AI) (Area 41)
  • Secondary Auditory Area (AII) - (Area 42)
  • Auditory Unimodal Association Area (Area 22)
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35
Q

Where does the primary auditory area receive input from and what is that input?

A
  • Input from medial geniculate nucleus of thalamus
  • Sound frequency and location from both ears
36
Q

When can a lesion to the primary auditory area be detected?

A

Can not be detected clinically unless bilateral

37
Q

Where does the secondary auditory area receive input from?

A

Medial geniculate nucleus of thalamus

38
Q

What does the auditory unimodal association area interconnect with, what is it function and where does it project to?

A
  • Interconnects: medial geniculate nucleus
  • Function: Discriminates auditory frequencies, sequence or pattern
  • Projects: Heteromodal association areas in prefrontal and tempoparietal areas
39
Q

T/F: There is symmetrical anatomy between left & right hemispheres
- Most functions are distributed symmetrically
- Homologous regions from each side connected through association fibers of corpus callosum

A

True

40
Q

What is the dominant hemisphere for most people?

A
  • Left hemisphere is dominant for language
41
Q

What are the functions of the dominant hemisphere?

A
  • Language
  • Skilled motor formulation
  • Arithmetic (sequential & analytical calculating skills)
  • Musical ability (sequential and analytical skills in trained musicians)
  • Sense of direction: (Following a set of written directions in sequence)
42
Q

What are the functions of the non dominant hemisphere?

A
  • Prosody (emotion conveyed by tone of voice)
  • Visual spatial analysis and spatial attention
  • Arithmetic (ability to estimate quantity and to correctly line up columns of number on the page)
  • Musical ability (in untrained musicians and for complex musical pieces in trained musicians)
  • Sense of direction (finding one’s way by overall sense of spatial awareness)
43
Q

What makes up the core language circuit and what are their Broadmann’s area?

A

Core language circuit: Wernicke’s area (22), Broca’s area (44 & 45) and arcuate fasciculus

44
Q

Where is Wernicke’s area located?

A
  • Posterior 2/3 of superior temporal gyrus in dominant hemisphere
  • Adjacent to primary auditory cortex
45
Q

What occurs in Wernicke’s area?

A

Language processing to enable sequences of sounds to identified and comprehended as meaningful words

46
Q

What is Brodmann’s number and function of wernicke’s adjacent association cortex?

A
  • Brodmann’s: 37, 39 & 40
  • Assists in language processing
47
Q

Where is Broca’s area located?

A

Opercular and triangular portion of the inferior frontal gyrus

48
Q

What is the function of Broca’s area?

A

Motor program to activate sequences of sounds to produce words and sentences are formulated here and communicated to face region of the primary motor cortex

49
Q

What are the Brodmann’s number and function of the adjacent Broca’s area?

A

Brodmann’s Area: 6,8,9,10,46 and 47
- Assist with production of speech

50
Q

How do we repeat a word that we hear?

A
  • Sound goes to Primary Auditory cortex then to Wernicke’s area
  • Sound is converted to a neural representation of the word then Wernicke’s area communicated via arcuate fasciculus (subcortical white matter pathway) with Broca’s area
  • Broca’s area converts neural representation of words back into sounds then to primary motor cortex then to corticobulbar tract
51
Q

What are some aspects of Broca’s aphasia?

A
  • Decreased fluency
  • Shorter phrase length (<5 words)
  • Effortful & telegraphic speech that is monotonous and lacks grammatical structure
  • Some preservation of over learned tasks
  • Comprehension intact except for syntax
  • Reading comprehension (except syntax) preserved
  • Writing and reading aloud are both slow, effortful and grammatical
  • Impaired reptition
52
Q

What are some aspects of Wernicke’s Aphasia?

A
  • Impaired comprehension
  • Speech has normal fluency, prosody & grammatical structure but lacks meaning
  • Paraphasic errors (insert inappropriate word with similar meaning or sound)
  • Reading comprehension impaired
  • Writing is fluent, but meaningless
  • Unaware of deficit
  • Impaired repetition
53
Q

A MCA superior division infarct can cause what?

A
  • Broca’s aphasia
  • Dysarthria
  • R hemiparesis (UE/face > LE)
  • Frustration
  • Apraxia
54
Q

A MCA Inferior division infarct can cause what?

A
  • Wernicke’s aphasia
  • Contralateral visual field cut
  • Apraxia (hard to demonstrate due to comprehension)
55
Q

A lesion where would cause Global aphasia?

A
  • Both Broca’s and Wernicke’s area
56
Q

A lesion where would cause conduction aphasia?

A
  • Connection between Broca’s and Wernicke’s area but area themselves are intact
57
Q

A lesion where would cause transcortical aphasia?

A
  • Other language areas in frontal, temporoparietal or subcortical structures
  • But Broca’s, Wenicke’s and connection between them are intact
58
Q

Deficits where cause Alexia and what function is impaired?

A
  • Deficits in central language processing
  • Impair the ability to read
59
Q

Deficits where cause Agraphia and what function is impaired?

A
  • Deficits in central language processing
  • Impair the ability to write
60
Q

What is apraxia?

A
  • Inability to carry out an action in response to verbal command that is not directly caused by the absence of comprehension, motor function or coordination
  • Inability to formulate the correct motor sequence
61
Q

Both hemispheres are involved in attention what is the asymmetry?

A
  • Left hemisphere attends mainly to the right
  • Right hemisphere attends strongly to the left and less strongly to the right
62
Q

What is a right hemisphere lesion going to cause?

A

Profound deficit in attention to the left side

63
Q

What is a left hemisphere lesion going to cause?

A

Mild to no deficits in attention to the right side

64
Q

How is visual spatial analysis performed?

A

Distributed network involving bilateral frontal and parietal association cortex

65
Q

Where is the parietal association cortex located?

A

Junction of parietal, temporal and occipital lobes

66
Q

What information is given to us by the parietal association cortex?

A
  • Spatial analysis including visual, proprioceptive, vestibular, auditory and surrounding cortical inputs
  • Information about surrounding environment and the relative position of the body in space
67
Q

Which hemisphere is more important for spatial analysis and integration?

A

Non- dominant (usually right) hemisphere is more important than the dominant

68
Q

Describe Hemineglect Syndrome

A
  • Profound neglect of the contralateral half of the external world and their own bodies
  • Unaware of deficits (anosognosia)
  • May fail to recognize or deny that left side of body belongs to them
69
Q

Lesions where can cause hemineglect syndrome?

A

Right parietal or frontal cortex

70
Q

What is sensory neglect?

A

Patient ignores visual, tactile, or auditory stimuli from contralateral hemispace

71
Q

What is motor-intentional neglect?

A

Patient performs fewer movements in contralateral hemispace

72
Q

What is conceptual neglect?

A

Patient internal representation of their own bodies or the external world exhibit contralateral neglect

73
Q

Lesions to non dominant hemispheres may cause what?

A
  • Receptive aprosody (difficulty judging meaning imparted by tone)
  • Expressive aprosody (difficulty producing emotionally appropriate expressions with voice)
74
Q

What are the types of MCA infarcts?

A
  • Superior division infarct
  • Inferior division infarct
  • Deep territory infarct
  • Proximal stem infarct
75
Q

What deficits can be seen with left MCA superior division infarct?

A
  • R face & arm weakness (UMN)
  • Broca’s aphasia
  • May be some R loss & arm cortical sensory loss
76
Q

What deficits can be seen with right MCA superior division infarct?

A
  • L face & arm weakness (UMN)
  • L hemineglect
  • May be some L face and arm cortical sensory loss
77
Q

What deficits can be seen with a left MCA inferior division infarct?

A
  • Wernicke’s aphasia
  • R visual field deficit
  • R face and arm cortical sensory loss
  • Mild R sided weakness
78
Q

What deficits can be seen with a right MCA inferior division infarct?

A
  • Profound L hemineglect
  • L visual field deficit
  • L face and arm cortical sensory loss
  • Mild L sided weakness
79
Q

What deficits can be seen with a left MCA deep territory stroke?

A
  • R pure motor hemiparesis (UMN)
  • Larger lesions may produce cortical deficits such as aphasia
80
Q

What deficits can be seen with a right MCA deep territory stroke?

A
  • L pure motor hemiparesis (UMN)
  • Larger lesions may produce cortical deficits such as L hemineglect
81
Q

What deficits can be seen with a left MCA Stem infarct?

A
  • R hemiplegia
  • R hemianesthesia
  • R homonymous hemianopia
  • Global aphasia
  • L gaze preference
82
Q

What deficits can be seen with a right MCA stem infarct?

A
  • L hemiplegia
  • L hemianesthesia
  • L homonymous hemianopia
  • Profound L hemineglect
  • R gaze preference
83
Q

What deficits can be seen with a left ACA infarct?

A
  • R leg weakness (UMN) –> larger infarcts may cause hemiparesis
  • R leg cortical sensory loss
  • Frontal lobe behavioral abnormalities
  • Transcortical aphasia
84
Q

What deficits can be seen with a right ACA infarct?

A
  • L leg weakness (UMN) –> larger infarcts may cause hemiparesis
  • L leg cortical sensory loss
  • Frontal lobe behavior abnormalities
  • L hemineglect
85
Q

What deficits can be seen with a left PCA infarct?

A
  • R homonymous hemianopia
  • May cause Alexia without agraphia (corpus callosum)
  • Aphasia, R hemisensory loss, R hemiparesis (thalamus and internal capsule)
86
Q

What deficits can be seen with a right PCA infarct?

A
  • L homonymous hemianopia
  • L hemisensory loss and L hemiparesis (thalamus and internal capsule)