Aphasias

24 important questions on Aphasias

What study shows the damage to patient Tan's brain structures (not just on the surface of the brain, and thus expanding from Broca's finding)?

Dronkers et al., 2007 - MRI

= found that Patient Tan's lesions extended into regions underlying the superficial cortical zone of Broca's area, and included the insular cortex and portions of the basil ganglia
---> suggests that damage to the classic regions of the frontal cortex (known as Broca's area) may not be solely responsible for the speech production deficits of Broca's aphasics

(p. 473 neuropsychology textbook)

How does Broca’s aphasia typically present?

Speech is typically:

---> Non-fluent
---> Effortful
---> Dysarthric - slurred, hollow, whispery
---> Dysprosodic - monotone, lack of intonation
---> Agrammatic - the primary feature in patients' speech

What is agrammatic speech?

  • Word order is impaired
  • Verbal economy: content words for intended meaning are favoured compared to grammatical words


e.g. omission of definite articles (‘the’, ‘a’) and function words such as prepositions (‘of’, ‘to, ‘in’)
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Do Broca's aphasia patients know they have a speech problem?

Yes - patients have good insight - they know what they are saying is not how they want to say it

In Broca's aphasia patients, where is the lesion?

Left inferior frontal gyrus
Brodmann’s areas: 44 & 45
---> called Broca's area

  • Damage to Broca’s area typically results in only transient deficits

  • Broca's aphasia usually only persists with additional damage to underlying white matter and basal ganglia (Mohr et al., 1978; Naeser et al., 1986) - remember the limitation with Broca's lateral level finding

What was the historical view of Broca's aphasia? What was the problem with this view?

Historical view of Broca’s aphasia: loss of motor forms of speech
BUT this fails to explain agrammaticism
---> impaired syntax

What have studies regarding articulatory deficits demonstrated? What does this suggest?

Studies have shown that articulatory deficits are caused by lesions outside of Broca’s area (Dronkers et al., 1996)


---> Role of Broca’s area may be more general cognitive functioning, for example response selection (Schnur et al., 2009)

How does Wernicke’s aphasia typically present?

  • Primarily a comprehension deficit:
e.g. "Pick up the red disk” & “Place the disk into the square hole” - they fail at this


  • Patients have impaired comprehension of all speech, including their own

= Are not aware of their impairments and do not attempt to correct

  • In practice, both speech comprehension and production are affected

In Wernicke's aphasia, what is speech typically like?

- Fluent
- Well articulated

- Syntactically and prosodically correct

- Loghorrea

- Preservation of social conventions

- Presence of neologisms (creation of new words) and paraphasias

What are additional problems seen in patients with Wernicke's aphasia?

- Speech repetition
- Naming (some anomia)
- Reading and writing

Regarding Wernicke's aphasia, where is the lesion?

Left posterior superior temporal gyrus
- Wernicke's aphasia


  • Posterior superior temporal lesion is obligatory for Wernicke’s aphasia (Kertesz, 1993)


  • Correlation between severity of comprehension loss and the amount of lesion in Wernicke’s area, but not overall temporoparietal lesion size (Naeser et al., 1987)

What is Conduction Aphasia?

- Intact speech comprehension
- Intact speech production

- Impaired naming (anomia)
(Wernicke, 1874)

  • Main deficit is the inability to repeat non-meaningful words and word sequences that are heard
  • Ability to repeat stock phrases may be preserved (Goodglass, 1993) 


EXP: McCarthy and Warrington (1984)
Patient ORF
Repetition of single words - 85%
Single non-words - 39%
(slide 4, p. 5 lecture notes)

Regarding conduction aphasia, where is the lesion?

Lesion to arcuate fasciculus
(white matter tract that connects Wernicke’s area and Broca’s area)

= Disconnection of auditory language comprehension centre from speech planning centre
i.e. Broca & Wernicke's area are intact but the connection between these 2 areas are impaired ---> they can't repeat things that don't make sense

(p. 474 neuropsychology textbook)

Who is a classic Conduction aphasia patient?

Patient JL

---> shows that route is for repetition of unfamiliar words (phonologically based) and learning new words
(see slide 6, p. 5 lecture notes)

How can patients with conduction aphasia repeat known words? What study shows this?

Geschwind (1965): Mental representation

Perception of non-words fails to produce an image meaning that this alternative route for production cannot be used

Is conduction aphasia really a disconnection syndrome?

  • Some patients with lesions to the arcuate fasciculus do not have conduction aphasia (Shuren et al., 1995; Kreisler et al., 2000)

  • Cortical lesions without subcortical extension may also produce conduction aphasia (Anderson et al., 1999; Quigg et al., 2006)

What are problems understanding anatomy?

It is difficult to associate symptoms with a particular locus of damage:

1) Few patients have been studied in detail

2) Lesions are rarely found in identical locations or restricted to discrete regions, and symptoms are heterogeneous

3) Immediately following onset symptoms are generally severe, but there is often considerable improvement with time.

4) The production and comprehension of language depends on complex and dynamic interaction between numerous regions, covering large amounts of cortex and subcortex

What are imaging studies that have demonstrated increased neural activity in the left hemisphere during linguistic tasks?

  • Listening to words, including passive listening (Lassen et al., 1978; Petersen et al., 1988)

  • Phonetic and semantic analysis (Binder et al., 1997)

  • Word recognition (Petersen et al., 1990)

  • Deciding if words end in a syllable/consonant (Zatorre et al., 1992)

  • Word association task (Markus & Boland, 1992)

  • Grammatical processing (Embick et al., 2000; Sahin, Pinker and Halgren, 2006)

  • Production of spoken and signed language (Horwitz et al., 2003)

What did Posner & Raichle (1994) study?

- Different language processing tasks
- Visual and auditory stimuli are processed in modality-specific areas

- Output task activates left motor areas
- Association task produces activity in left inferior frontal

(slide 1, p. 7 lecture notes)

What evidence shows that the left hemisphere is more important than the right hemisphere when it comes to language?

Split-brain patients

Sperry et al. (1969) & Gazzaniga (1970)---> The left hand projects to the sensory cortex in the right side of the brain, which can no longer communicate with the left hemisphere language areas
(see slide 2, p. 7 lecture notes)

There is variability is split-brain patients, how is this?

Some patients say nothing when items are presented to the right hemisphere (left hand/visual field)
Other patients may offer a rudimentary description

(Zaidel, 1994) 

In the majority of people the left hemisphere is specialised for...

Phonological and syntactic processing
BUT
Patients with right hemisphere damage do not perform as well as non-brain damaged controls on many language tasks (Gardner, 1994)

---> Is there any language in the right hemisphere? 

What are ways in which communication may be affected in patients with right hemisphere brain damage?

- Responsiveness
- Non-literal language i.e. they interpret everything literally, they don't understand figures of speech
- Inferences
- Narrative - they focus on fine detail rather than the bigger picture
- Pragmatics
- Prosody - monotone, lack of intonation
- Affect and humour - laugh at inappropriate things; they don't understand higher, more complex humour (e.g. sarcasm)

There is no obvious localisation of language processes within the right hemisphere, thus, what might communication difficulties in patients with right hemisphere brain damage be due to?

  • Studies using gross classification of lesion location
  • Right hemisphere has more white matter and less grey matter than the left hemisphere  (Gur et al., 1980)
---> Processing by large networks rather than discrete areas

(slide, 1, p. 8 notes)

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