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3.6 Neuropsychology > Week 2: Chapter 19 - Language > Flashcards

Week 2: Chapter 19 - Language Flashcards

1
Q

What has research shown about language localization in the brain?

A

Language is distributed across a broad neural network, not localized to a single area.

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2
Q

What did Nina Dronkers’ 2007 study reveal about Broca’s area?

A

Aphasia in Broca’s patients involved regions beyond Broca’s area, challenging the classic localization model.

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3
Q

What does the Wernicke-Geschwind model propose?

A
  1. Wernicke’s area for comprehension
  2. Info passed via arcuate fasciculus
  3. Broca’s area for articulation
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4
Q

What areas are part of the core language network?

A

Inferior frontal gyrus (Broca), superior temporal gyrus (Wernicke), supramarginal gyrus, angular gyrus, medial temporal gyrus, and more.

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5
Q

What deeper structures within the lateral fissure are important for language?

A

Insula, Heschl’s gyrus, and the superior temporal plane.

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6
Q

What subcortical regions contribute to language?

A

Thalamus, caudate nucleus, and cerebellum.

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7
Q

What roles does the right hemisphere play in language?

A

Interpreting prosody, emotional tone, and contextual meaning.

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8
Q

What are the two major language pathways in the brain?

A

Dorsal and ventral pathways.

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9
Q

What is the function of the dorsal language pathway?

A

Converts sound to motor representations (speech production, repetition).

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10
Q

What is the function of the ventral pathway?

A

Converts sound to meaning using top-down semantic processing.

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11
Q

What happens when the ventral pathway is damaged?

A

Ability to read aloud is preserved, but comprehension is impaired.

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12
Q

What happens when the dorsal pathway is damaged?

A

Impaired speech/repetition, but comprehension remains intact.

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13
Q

What did Penfield’s cortical stimulation studies reveal?

A

Mapped speech zones, revealing positive and negative speech effects.

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14
Q

What are examples of positive effects from stimulation?

A

Involuntary vocalizations (e.g., “Oh”).

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15
Q

What are common negative effects of stimulation?

A

Speech arrest, slurred speech, anomia, misnaming, number confusion.

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16
Q

What did Ojemann find about Broca’s area stimulation?

A

Disrupted speech, facial movement, phoneme discrimination, and gesture coordination.

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17
Q

What does TMS allow researchers to do?

A

Temporarily disrupt or enhance brain activity in healthy individuals (a “virtual lesion”).

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18
Q

What are TMS limitations?

A

Auditory distraction, discomfort, limited reach to deep brain areas.

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19
Q

What did TMS studies reveal about Broca’s area?

A

Anterior region → semantic processing

Posterior region → phonological processing

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20
Q

What did reaction time studies show using TMS?

A

Region-specific delays in semantic vs. phonological tasks confirmed functional subdivisions.

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21
Q

What did Binder et al. (1997) find using fMRI?

A

Word processing activated widespread areas across temporal, frontal, parietal, and occipital lobes, plus thalamus and cerebellum.

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22
Q

What did Petersen et al. (1988) discover about language tasks?

A
  • Word processing → sensory areas
  • Speech → bilateral motor areas, supplementary speech area
  • Verb generation → Broca, posterior temporal, cingulate, cerebellum
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23
Q

What does this imaging evidence suggest about language?

A

Language is supported by a distributed and flexible neural network.

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24
Q

What does the Core Language Network model propose?

A

Five functional modules, each with specialized nodes for specific language tasks.

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25
What determines complexity in the Core Language Network?
Number and interaction of modules (e.g., conversation > word recognition).
26
How are words represented in the Neural Webs model?
By distributed activation patterns across nodes and connections.
27
Give examples of modality-specific activation in the Neural Webs model.
* “Sunset” → visual cortex * “Run” → motor areas * All language → auditory & motor regions
28
What does the Neural Webs model suggest about language?
Language is context-sensitive, multimodal, and dynamically networked.
29
What are language disorders (aphasias)?
Disruptions in language due to brain injury, affecting speech, writing (agraphia), or reading (alexia).
30
What distinguishes aphasia from non-aphasic conditions?
Aphasia is not caused by general intellectual decline, sensory loss, or motor impairment (e.g., anarthria), though these may co-occur.
31
What is paraphasia?
Substitution of incorrect words or syllables (e.g., “pike” instead of “pipe”), despite correct articulation.
32
Who categorized 10 types of aphasia into comprehension and production disorders?
Howard Goodglass and Edith Kaplan (1972).
33
What are the three major aphasia categories?
1. Fluent Aphasias 2. Nonfluent Aphasias 3. Pure Aphasias
34
What characterizes Wernicke’s Aphasia?
Fluent but nonsensical speech (“word salad”), poor comprehension, impaired writing.
35
What is Transcortical Sensory Aphasia?
Preserved repetition and naming, but impaired spontaneous speech and comprehension.
36
What is Conduction Aphasia?
Fluent speech and comprehension, but inability to repeat words due to a disconnection between comprehension and production areas.
37
What defines Anomic Aphasia?
Fluent speech, good comprehension and repetition, but difficulty naming objects, especially nouns.
38
Which brain regions are associated with Anomic Aphasia?
Temporal cortex (nouns), left frontal cortex (verbs).
39
What defines Broca’s Aphasia?
Effortful, halting, grammatically poor speech, with preserved comprehension.
40
What is Transcortical Motor Aphasia?
Good repetition, but labored, limited spontaneous speech.
41
What is Global Aphasia?
Severe impairment of both speech production and comprehension.
42
What is Alexia?
Inability to read.
43
What is Agraphia?
Inability to write.
44
What is Word Deafness (auditory verbal agnosia)?
Inability to comprehend or repeat spoken words, despite normal hearing and speech.
45
What do language disorders reflect about brain function?
The distributed and modular nature of language, with most areas localized in the left hemisphere.
46
How does damage location influence aphasia type?
Specific language impairments depend on which cortical or subcortical region is damaged.
47
Why is language localization more complex than the Wernicke-Geschwind model suggests?
Language involves widespread brain regions, and symptoms vary by stroke patterns, time, and symptom combinations.
48
What is a key limitation of stroke-based aphasia research?
Strokes affect different parts of the middle cerebral artery (MCA), which supplies many cortical and subcortical areas, complicating localization.
49
Why is aphasia classification not always anatomically precise?
Each aphasia type involves multiple symptoms, each linked to different brain areas.
50
What are some symptoms of nonfluent aphasia?
Speech apraxia, sentence comprehension issues, repetitive speech, articulation difficulty, and working memory impairment.
51
What brain area is linked to apraxia of speech?
Insula.
52
What area is responsible for sentence comprehension problems?
Superior and middle temporal gyri.
53
What causes repetitive utterances in aphasia?
Damage to the arcuate fasciculus.
54
What is associated with articulation and working memory problems?
Ventral frontal cortex.
55
What causes comprehension loss in fluent aphasia?
Damage to the medial temporal lobe and underlying white matter, disrupting language network connectivity.
56
What type of memory is impaired in these cases?
Iconic (short-term auditory) memory for holding sentences.
57
What role does the basal ganglia play in language?
Some deficits from basal ganglia strokes may actually stem from subtle neocortical damage.
58
What thalamic nuclei influence language?
Pulvinar nucleus and ventrolateral thalamus.
59
What effects can thalamic stimulation have?
Speech arrest, naming difficulty, slowed speech, memory enhancement.
60
What symptoms can follow thalamic damage?
Word-finding problems, reduced fluency, and temporary dysphasia.
61
What language abilities can the right hemisphere show (based on split-brain studies)?
Limited speech production, good comprehension (especially nouns/verbs), basic reading, but poor writing.
62
Do right-hemisphere lesions cause classic aphasia?
No, but they result in subtle deficits, especially with abstract or emotional language.
63
What are common right-hemisphere language deficits?
• Difficulty following conversation • Missing the point or responding inappropriately • Impaired prosody and emotional expression
64
What is the functional specialization of the right hemisphere in language?
Semantic and emotional comprehension.
65
What is the specialization of the left hemisphere?
Syntax, grammar, speech planning, and language production.
66
What are the two main types of aphasia assessment tools?
• Comprehensive test batteries • Brief screening tests
67
What do comprehensive aphasia batteries assess?
• Auditory & visual comprehension • Oral & written expression (naming, reading, fluency, repetition) • Conversational speech
68
What are the downsides of comprehensive aphasia assessments?
Time-consuming and require specialized training.
69
What are the advantages of screening tests?
Quick to administer; effective at identifying presence of language disorders.
70
Name two common aphasia screening tests.
• Token Test • Halstead–Wepman Aphasia Screening Test
71
What did John Marshall (1986) observe about aphasia classification?
Only about 60% of patients fit into classic aphasia categories.
72
What is a common but highly variable symptom in aphasia?
Naming deficits—ranging from broad impairment to selective difficulty (e.g., naming colors or people).
73
What approach emphasizes individual language profiles over categories?
The psychobiological approach, which reconstructs language function based on unique patient data.
74
What distinguishes developmental dyslexia from acquired dyslexia?
It emerges during learning, not from brain injury.
75
Why is reading a focus in developmental language assessment?
It is more objectively measurable than speaking or writing.
76
Who advocated a model-based approach to reading assessment?
Max Coltheart (2005).
77
What does Coltheart’s model-based approach do?
Breaks reading into discrete subsystems (e.g., phonological decoding, visual word recognition).
78
What are two goals of model-based reading assessment?
1. Diagnose specific impairments 2. Test reading model validity
79
How does this differ from traditional neurology?
Neurology links dyslexia to comorbid symptoms and lesion sites, not reading process models.

3.6 Neuropsychology (20 decks)

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