Chapter 13: Aphasia

Posted on Jun 12, 2025

Chapter 13 Aphasia

Key Focus: Types of Aphasia, Brain-Language Links, Parsing Deficits, & Treatment

Overview

This chapter explores aphasia—an acquired language disorder from brain damage (e.g., stroke)—to understand how the brain organizes language. It covers core topics: the left hemisphere’s role in language, classic aphasia syndromes (Broca’s, Wernicke’s, Conduction), why patients struggle with complex sentences, and evidence-based treatments. Real-world relevance: Explains why someone with Broca’s aphasia can understand simple sentences but not passives, and how therapies like singing (MIT) improve speech fluency.

1. Introduction (pp. 491-492)

1.1 What Is Aphasia?

  • Definition: Acquired language disorder from brain damage (stroke, tumor, TBI)—no loss of general intelligence (e.g., can solve math but can’t say “I want water”).
  • Core Goal: Use aphasia as a “window” to answer:
    1. Are specific brain regions for language tasks (speaking vs. understanding)?
    2. Which regions handle grammar vs. word meaning?
    3. How do regions communicate for fluent language?
    4. Do all brains organize language the same way?
MethodFocusExample
Neuroimaging (Intact Brains)Measure activity in healthy people.fMRI shows Broca’s Area activates when planning sentences; ERP N400 spikes for “The cat barked” (semantic oddity).
Lesion Studies (Damaged Brains)Link damage to deficits (tests if a region is necessary for a function).Damage to Wernicke’s Area → comprehension loss.

1.3 Left Hemisphere Dominance

Nearly all humans use the left hemisphere for core language functions:

A. The WADA Test (Wada & Rasmussen, 1960)

  • Procedure: Anesthetize one hemisphere (left/right) via artery injection; test language (name pictures, repeat phrases).
  • Result:
    • Left hemisphere anesthetized: ~96% right-handers / ~70% left-handers become mute and can’t understand.
    • Right hemisphere anesthetized: Speech/understanding intact (minor prosody/humor deficits).

B. Left Hemisphere Damage = Aphasia

  • Severe aphasia (no speech/understanding) almost always follows left hemisphere damage.
  • Right hemisphere damage: Subtle deficits (e.g., can’t understand sarcasm) but no core aphasia.

2. Aphasiology: Brain Damage & Language Loss (pp. 492-504)

2.1 Historical Debate: Localization vs. Equipotentiality

HypothesisCore ClaimEvidence For/Against
EquipotentialityLanguage needs “mass action” of the whole brain—no specific regions.❌ Disproven: Aubertin’s patient stopped speaking when left frontal lobe was pressed.
LocalizationSpecific regions for specific language functions.✅ Broca’s patients (Leborgne/Lelong) had left frontal damage and non-fluent speech.

2.2 Key Historical Discoveries

A. Paul Broca (1861): Broca’s Area

  • Patients: Leborgne (said only “tan”) and Lelong (said 5 words) → both understood language.
  • Autopsy: Both had lesions in the left inferior frontal lobe (later named Broca’s Area).
  • Conclusion: Broca’s Area is critical for fluent speech production.

B. Carl Wernicke (1870s): Wernicke’s Area

  • Patients: Susanne Adam/Rother → fluent but meaningless speech (“feffort,” “stam”) + severe comprehension loss.
  • Autopsy: Lesions in left posterior temporal lobe (later named Wernicke’s Area).
  • Theory:
    • Motor Aphasia (Broca’s): Frontal damage → non-fluent speech, intact comprehension.
    • Sensory Aphasia (Wernicke’s): Posterior damage → fluent nonsense, no comprehension.

2.3 Classic WLG Model (Wernicke-Lichtheim-Geschwind)

Integrates Broca’s/Wernicke’s work—3 core left-hemisphere structures:

StructureLocationFunction
Wernicke’s AreaTemporal/parietal junctionDecode sound → meaning (comprehension); retrieve sound codes (production).
Broca’s AreaLeft inferior frontal lobeBuild grammar; plan speech movements.
Arcuate FasciculusWhite matter tract (Wernicke’s → Broca’s)Relay sound/meaning info from Wernicke’s to Broca’s.

How It Works (Example: Saying “I ate breakfast”)

  1. Concept (“I ate breakfast”) → Wernicke’s Area.
  2. Wernicke’s retrieves words (“I,” “ate,” “breakfast”) + sound codes.
  3. Arcuate fasciculus sends info to Broca’s Area.
  4. Broca’s organizes grammar + plans speech movements.
  5. Motor cortex executes speech.

2.4 Three Aphasia Syndromes (WLG Predictions)

TypeLesion LocationKey SymptomsExample Speech
Wernicke’s (Fluent)Wernicke’s Area- Fluent but meaningless speech (neologisms: “feffort”).
- Severe comprehension loss.
- Preserved prosody.
“It had a feffort and the stam of foriment.”
Broca’s (Non-Fluent)Broca’s Area + subcortical structures- Halting, telegraphic speech (omits “the,” “-ed”).
- Intact comprehension for simple sentences.
- Apraxia (speech movement difficulty).
“Cinderella … ball … dance … shoe.”
ConductionArcuate fasciculus- Intact comprehension + fluent speech.
- Severe repetition deficit (can’t repeat phrases).
- Can paraphrase (e.g., “pastry cook tired” → “baker felt sleepy”).
“The quick brown… thing… jumps over sleepy dog.”

2.5 Limitations of the WLG Model

  • Lesion Location ≠ Symptom: Broca’s aphasia can occur without Broca’s Area damage (basal ganglia lesions); small Broca’s lesions cause only short-term deficits.
  • Insula Is Critical: All patients with speech apraxia have insula damage (WLG ignores this region).
  • VLSM Challenges: Sentence comprehension depends on wide-ranging regions (not just Wernicke’s); lesion size matters more than location.

3. Broca’s/Wernicke’s Aphasia & Parsing Deficits (pp. 504-516)

3.1 Broca’s Aphasia: Hidden Comprehension Problems

Early researchers thought Broca’s patients had intact comprehension—not true: they struggle with syntactically complex sentences.

Reversible vs. Non-Reversible Sentences

Sentence TypeExamplePatient Performance
Non-Reversible“The cheese was eaten by the mouse.”Good (~85% correct) → semantics clarify roles (cheese = eaten).
Reversible“The girl was kissed by the boy.”Poor (~50% correct) → need syntax to know who kissed whom.

3.2 Why Broca’s Patients Struggle with Parsing: 4 Hypotheses

HypothesisCore ClaimStrength/Weakness
Global Parsing FailureCan’t build syntactic structures—rely on semantics.❌ Weakness: Can judge grammaticality (e.g., reject “Was the girl enjoy the show?”) 85% correct.
Trace DeletionCan’t link “fillers” (displaced words) to “gaps” (original positions) → guess roles.✅ Explains 50% correct on reversibles; ❌ Weakness: Struggle with simple actives (“The dancer applauds the actor” = 75% correct).
Mapping HypothesisCan build structures but can’t assign semantic roles (who did what).✅ Explains grammaticality judgment skills; ❌ Weakness: Doesn’t explain why mapping fails.
Slowed SyntaxParse sentences too slow—info decays before linking to meaning.✅ Cross-modal priming: Activate fillers 0.5s late (normal = at gap); explains preserved grammar knowledge.

3.3 Wernicke’s Aphasia: Comprehension Loss from Lexical Access Failure

  • Core Deficit: Can’t link speech sounds to word meanings (e.g., hear /kæt/ but can’t retrieve “cat”).
  • Key Symptoms:
    • Lexical substitutions (e.g., “boat” for “coat”).
    • Can’t detect own errors (say “feffort” and not realize it’s meaningless).
    • Better reading than listening (visual input lasts longer).

3.4 Broca’s vs. Wernicke’s: Side-by-Side

FeatureBroca’s AphasiaWernicke’s Aphasia
Speech FluencyNon-fluent, telegraphicFluent (but meaningless)
ComprehensionGood (simple sentences)Severe loss
Key DeficitGrammar/speech planningSound-meaning linking
Error TypeOmit function words (-ed, the)Neologisms (feffort)

4. Treatment & Recovery from Aphasia (pp. 516-520)

4.1 Spontaneous Recovery

  • Definition: Improvements without treatment—starts days after damage.
  • Key Factors:
    • Small lesions → full recovery; large lesions → permanent deficits.
    • Most recovery in 3–6 months (minor gains for years).
    • Younger/healthier patients recover faster.
  • Case Example: Wernicke’s patient Susanne Adam went from no comprehension to understanding most speech in 3 weeks.

4.2 Neural Mechanisms of Recovery

  1. Restoration: Swollen neurons regain function.
  2. Reorganization: Right hemisphere homologs (similar regions) take over (e.g., right Broca’s Area plans speech).
  3. Plasticity: New connections form (e.g., Wernicke’s → Broca’s via right hemisphere).

4.3 Evidence-Based Treatments

TreatmentTarget DeficitMethodEvidence
Melodic Intonation Therapy (MIT)Non-fluent speech (Broca’s)Sing phrases → fade melody to speech (recruits right hemisphere).PET shows more left Broca’s activation; 30–40% fluency gain.
Intensive Semantic Training (IST)Word finding (Wernicke’s)Practice word properties (syllables, first sound) without speaking → name pictures.Naming accuracy up from 30% to 70%; generalizes to untrained words.
Phonological Components Analysis (PCA)Word finding (all aphasias)Identify 5 phonological features (syllables, rhymes) → name pictures.7/10 patients improved; gains last 6 months.
tDCS/TMSAll typesNon-invasive brain stimulation (boosts plasticity).tDCS improves naming by 20–30%; TMS suppresses overactive right hemisphere.
AmphetaminesAll typesStimulants boost plasticity; paired with speech therapy.50% more fluency gain than therapy + placebo.

4.4 Treatment Principles

  1. Early Intervention: Start 2–7 days post-stroke (heightened plasticity).
  2. Intensity: 3–5 sessions/week (45–60 mins).
  3. Task Specificity: Match therapy to deficit (MIT for fluency, PCA for word finding).

Quick Review Questions

  1. What is the key difference between Broca’s and Wernicke’s aphasia?
  2. Why does the WLG model fail to explain modern aphasia data?
  3. What is the slowed syntax hypothesis, and how does it explain Broca’s parsing deficits?
  4. What is spontaneous recovery, and what factors influence it?
  5. How does Melodic Intonation Therapy (MIT) work to improve speech fluency?