Aphasia

 
Def of Aphasia:
A disorder of language that is neurogenic
(caused by brain disease or injury), which
involves the symbolic use of sound (i.e.
Language in the meaningful sense of the
word). Is not due to deafness or motor-
paralysis, mental retardation etc.
Differential diagnosis and disorders
which make it hard to identify aphasia
 Dysathria – poor articulation of speech due to
slurring or fragmentation of the sound structure
of speech. Is a motor problem due to poor
coordination of breathing and speech muscles.
Cause slurred speech and staccato speech.  
 Apraxia – disorders of skilled movements. Can
include symbolic movements. Cause by left
parietal lesions. Some apraxias particularly
affect the ability to speak, e.g Buco-facial
apraxia.
Language is assessed in terms of:

 Language comprehension: understanding

language as opposed to hearing or seeing it
 Language production: speech output, not
just the utterance of noise, but the
utterance of meaningful noise, and also the
spontaneous production of language
 Repetition: copying of language.
Other important terms
 Anomia: ability to name things, tested on
confrontation
 Word-finding difficulties: difficulty finding the
particular word you are looking for, seen in the
patient’s spontaneous speech.
 Paraphasia (next to speech) – distortions in
speech output
 Semantic paraphasias: say a word that is
meaningfully related to the word you want to say.
E.g. “whiskey” when you want to say “wine”.
 Literal paraphasias: is phonologically different
from the word you want to say. E.g. “broddel”
instead of “bottle”.
 Alexia –aphasia for written language
(can’t comprehend)
 Dyslexia – milder form of the above
 Agraphia – disorder of writing, can’t
produce (write) language.

You can have an Alexia/agraphia without

aphasia
But you should not find an aphasia without
an alexia/agraphia
Fig 1: Connectionist model of language
Fig 2: Lichtheim & Wernicke’s nosological scheme
Wernicke’s aphasia
 Can’t comprehend, can’t repeat, can speak spontaneously
 Spontaneous speech is however not normal
 Is fluent, but is paraphasic, semantically paraphasic in
particular. In extreme cases, word salad.
 Make a particular type of literal paraphasic errors
(neologism – make up new words, predominantly by
putting old words together - Jargon aphasia.
 Not always entirely aware that they are not making sense,
because their comprehension is impaired.
 Lesion site: left primary projection cortex (Wernicke’s
area)
 Broca’s aphasia
 Speech out-put problems
 Output is non-fluent, not only i.t.o. few words per minute
(i.e. less than 60), but also in terms of short phrase length
which leaves out connecting words and overemphasises
of nouns. This leads to telegramatism.
 Effortful and halting speech.
 Lesion site: Just in front of motor area – Broca’s area: i.e.
Posterior part of the inferior frontal convulsion
 Same difficulties usually extend to written language
 Conduction Aphasia
 Comprehension and Production is still relatively intact
 Repetition is impaired – sound images received by
Wernicke’s area can not be transmitted forward to
Broca’s area to be produced
 However, spontaneous output is also not normal
 Is paraphasic, but predominantly of literal type. This
takes a particular form in that they will approximate the
word closer and closer and sometimes they will get there
 Lesion site: Posterior temporal lobe or insular cortex
(track of fibres (white matter) that connects Broca’s &
Wernicke’s area (arcuate fasciculus)
 Transcortical sensory aphasia (TCSA)
 Disruption to links between Wernicke’s area and the
concept centre
 Unable to comprehend, but still able to produce and to
repeat
 Circumlocutory – go around words. Leave out concrete
words, but full of connectives
 Speech is fluent, but empty of meaning
 Severe word-finding difficulties, specifically for concrete
words and nouns - Use phrases like “thing a ma jig” and
“you know what”
 Pathology: Alzheimer’s patients in the 2nd stage of
disease.
 Lesion: From Wernicke’s upwards towards parietal lobe.
Transcortical motor aphasia (TCMA)
 Due to damage to fibres linking the concept centre with
Broca’s area
 Non-fluent speech output
 Tend to say very little, lack of initiation of speech
 Paucity of spontaneous output
 Can repeat
 Often has a compulsion to repeat back what is heard –
echolalia
 Lesion: Damage is to fibres that lead to Broca’s area. Is
not always in transcortical area, lesion may also be in
supplementary motor area.
Other types not included in
Lichtheim’s model
Global aphasia
  Poor production and comprehension
 Damage to both Wernicke’s and Broca’s
area
 Often a stroke may initially be cause a
global aphasia and then recover to a
Broca’s or Wernicke’s aphasia.
Mixed transcortical aphasia

 Affect both transcortical motor and

transcortical sensory fibres.
 Caused by watershed infractions of middle
cerebral area (thus speech area is isolated)
 Can repeat, but can’t understand or produce.

 Repeat quite a lot – echolalia

 
 A cognitive neuropsychological framework for
understanding language disorders

Figure 3 shows a
modular system or
‘functional
architecture’ for
identifying and
producing spoken
words
 Acoustic/auditory
analysis module:
responsible for converting
the speech signal of a word
into a phonemic code
 The Phonemic code can
then access that word’s
entry in the auditory input
lexicon
 The auditory input
lexicon is a store of
information about the
sound of each word that we
know
 The meaning of the
activated word can
become available within
the semantic system
 Semantic context can
also aid word
identification
 Both the auditory input
lexicon and the semantic
system have links with
the phonological output
lexicon
 The phonological output
lexicon comprises of info
about how to say all the
words that we know.
 Its output goes to a
phonemic response buffer
where the info about how to
say the word is held until we
are ready to say it.
 There is also a two-way link
between the phonological
output lexicon and the
phonemic response buffer
- allows the two modules to
become interactive in the
generation of speech.
 The direct link from the
acoustic analysis system to
the phonemic response
buffer via the acoustic to
phonological conversion
system. Allows us to repeat
nonsense words such as
BLIG and SPONE.
 Info can also flow from the
phonemic response buffer
back to the acoustic analysis
module – this allows
phonemic info to be
recycled in the system and
provides the basis for ‘inner
speech’.
Disorders of Language (a
psycholinguistic approach)
Pure word deafness

 This disorder provides evidence for the

existence of a separable acoustic/auditory
analysis module
 Disorder is characterized by an inability to
understand spoken words despite being
able to read, write and speak normally
 Can recognize music and
environmental sounds,
BUT has a specific
problem in perceiving
speech-like sounds.
 The perceptual deficit
responsible for pure
word deafness involves a
deficit in phonemic
processing
 I.e. the patient is unable
to segment a string of
speech sounds into its
constituent phonemes
Pure word meaning
 Patient is unable to understand
deafness what a word means even though
he/she is able to repeat and write
words to dictation accurately
 Auditory lexicon is intact – can
distinguish between real words
and non-words (i.e. still has a
internal representation of each
known word).
 Semantic system is also intact,
given that he/she is able to
comprehend written material
 Deficit lies in the connection
between the auditory input
lexicon and the semantic system.
Auditory phonological agnosia
 This disorder provides
neuropsychological support for
the existence of a direct rout
between the acoustic analysis
module and the phonemic
output buffer, i.e. that part of the
system that allows us to repeat
unfamiliar and non-words.
 Patients loose the ability to
translate acoustic inputs into
speech – the only way in which
we can repeat non-words. The
only route for repetition becomes
via the auditory input lexicon
Anomia
 Is a condition in which the patient has problems
finding the right word
 Patients often resort to elaborate
circumlocutions
 E.g. for “doll” – they may say “solid
representation of a baby”
 Analysis of this disorder has been the primary
basis for proposing an auditory output lexicon
 Distinction between semantic anomia and word
selection anomia
 Semantic anomia: Patient
has problems finding words
because of a semantic
disturbance – make
semantic errors
 In word selection anomia
the semantic input appears
intact (since these patients
can understand what people
are saying to them) and the
defect lies within the
phonological output lexicon
itself.
Neologistic Jargonaphasia
(Wernicke’s aphasia revisited)
 These patients may suffer from a form of word
selection anomia (which would explain the
neologisms they make)
 Is exacerbated by a failure to monitor the lexical
status of words they produced – something
termed ‘phonological derailment’
 It may be that attention may play a significant
role in the fact that these patients are unable to
monitor the errors they make when speaking