The MIT Encyclopedia of
Communication Disorders
Edited by Raymond D. Kent
A Bradford Book
The MIT Press
Cambridge, Massachusetts
London, England
Aphasia: The Classical Svndromes
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and management of primary progressive aphasia. Neurophysiology and Neurogenic Speech and Language Disorders
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Sapin, L. R., Anderson, F. H., and Pulaski, P. D. (1989). Pro-
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(1997). The gradual deterioration of syntax and semantics
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Aphasia: The Classical Syndromes
Aphasia is an acquired disorder of language subsequent
to brain damage that affects auditory comprehension,
reading, oral-expressive language, and writing. Early
observations by Broca (1861a, 1861b) and Wernicke
(1874) suggested that aphasia might be classified into a
variety of syndromes, or types, based on differences in
auditory comprehension and oral-expressive language
behaviors. Moreover, different syndromes were believed
to result from different sites of brain damage. Revisions
of early classification systems yield a contemporary taxonomy that comprises seven syndromes: global, Broca's,
transcortical motor, Wernicke's, transcortical sensory,
conduction, and anomic (Benson, 1988; Kertesz, 1979).
Classification is based on the aphasic person's auditory
comprehension, oral-expressive fluency (phrase length
and syntax), spoken repetition, and naming abilities. The
seven syndromes can be divided into nonfluent, those
with short phrase length and impaired morphosyntax
(global, Broca's, and transcortical motor), and fluent,
those with longer phrase length and apparent preservation of syntactic structures (Wernicke's, transcortical
sensory, conduction, and anornic). An aphasic person's
syndrome may be determined by informal examination
249
or by administering a standardized test, for example, the
Western Aphasia Battery (WAB) (Kertesz, 1982) or
the Boston Diagnostic Aphasia Examination (BDAE)
(Goodglass and Kaplan, 1983). The following describes
each syndrome and the assumed site of lesion associated
with each.
Global Aphasia. This nonfluent syndrome is associated
with a large left hemisphere lesion that may involve the
frontal, temporal, and parietal lobes, insula, and underlying white matter, including the arcuate fasciculus
(Dronkers and Larsen, 2001). It is the most severe of
all of the syndromes. Auditory comprehension is
markedly reduced and may be limited to inconsistent
comprehension of single words. Oral-expressive language is sparse, often limited to a recurring intelligible"bees, bees, beesy'-or unintelligible-"doobe,
doobe,
doobe"-stereotype.
Other automatic expressions, including profanity and counting, may also be preserved.
Globally aphasic patients are unable to repeat words,
and no naming ability is present. Reading and writing
abilities are essentially absent.
Broca's Aphasia. This nonfluent syndrome receives its
name from the early reports by Paul Broca (1861a,
1861b). Classical localization of the lesion resulting in
Broca's aphasia is damage in the left, inferior frontal
gyrus-Broca's
area (Brodmann's areas 44 and 45)
(Damasio, 1992). However, both historical (Marie,
1906) and contemporary (Mohr, 1976; Dronkers et al.,
1992) reports question the classical lesion localization.
Patients have been described who have lesions in Broca's
area without Broca's aphasia, and other patients have
Broca's aphasia but their lesion does not involve Broca's
area. Auditory comprehension is relatively good for
single words and short sentences. However, comprehension of grammatically complex sentences is impaired.
Their phrase length is short, and they produce halting,
telegraphic, agrammatic speech that contains, primarily,
content words. For example, describing how he spent
the weekend, a patient with Broca's aphasia related,
"Ah, frat, no Saturday, ah, frisk, no, fishing, son."
Repetition of words and sentences is poor. Naming
ability is disrupted, and reading and writing show a
range of impairment.
Transcortical Motor Aphasia. Lichtheim (1 885) provided an early description of this noniluent syndrome,
and he observed that the site of lesion spared the perisylvian language region. Currently, it is believed that the
lesion resulting in transcortical motor aphasia is smaller
than that causing Broca's aphasia and is in the left
anterior-superior frontal lobe (Alexander, Benson, and
Stuss, 1989). With one exception, language behaviors are
similar to those in Broca's aphasia: good auditory cornprehension for short, noncomplex sentences; short, halting, agrammatic phrase production; disrupted naming
ability; and impaired reading and writing. The exception
is relatively preserved ability to repeat phrases and sentences. Essentially, patients with transcortical motor
250
Part 111: Language
aphasia repeat much better than would be predicted
from their disrupted, volitional productions.
Wernicke's Aphasia. This fluent syndrome received its
name from the early report by Carl Wernicke (1874).
The traditional belief is that Wernicke's aphasia results
from a lesion in Wernicke's area (posterior Brodmann's
area 22) in the left hemisphere auditory-association cortex (Damasio, 1992), with extension into Brodmann's
areas 37, 39, and 40. However, Basso et al. (1985) have
reported cases of Wernicke's aphasia resulting from
exclusively anterior lesions, and Dronkers, Redfern, and
Ludy (1995) have found Wernicke's aphasia in patients
whose lesions also spared Wernicke's area. Spoken
phrase length averages six or more words, and a semblance of syntax is present. However, the oral-expressive
behavior includes phonological errors and jargon. One
patient with Wernicke's aphasia described where he went
to college, Washington and Lee University, by relating,
"There was the old one, ah Frulich, and the young one,
young hunter, ah, Frulich and young hunter or Brulan."
A salient sign in Wernicke's aphasia is impaired auditory
comprehension. These patients understand little of what
is said to them, and the deficit cannot be explained by
reduced auditory acuity. In addition, verbal repetition
and naming abilities are impaired, and there is a range of
reading and writing deficits.
Transcortical Sensory Aphasia. This fluent syndrome
may result from lesions surrounding Wernicke's
area, posteriorly or inferiorly (Damasio, 1992). Oralexpressive language is similar to that seen in Wernicke's
aphasia: longer phrase length and relatively good syntax.
Auditory comprehension is impaired, similar to that in
Wernicke's aphasia, and naming, reading, and writing
deficits are present. The salient sign in transcortical sensory aphasia is preserved verbal repetition ability for
words and, frequently, long and complex sentences. Essentially, transcortical sensory aphasia patients repeat
better than one would predict based on their impaired
auditory comprehension.
'
Conduction Aphasia. Wernicke (1874) described this
fluent syndrome. Lesion localization has been controversial. Geschwind (1965) proposed that conduction
aphasia results from a lesion in the arcuate fasciculus
that disrupts connections between the posterior language
comprehension area and the anterior motor speech area.
Damasio (1992) suggested that conduction aphasia results from damage in the left hemisphere supramarginal
gyms (Brodmann's area 40), with or without extension
to the white matter beneath the insula, or damage in
the left primary auditory cortices (Brodmann's areas 41
and 42), the insula, and the underlying white matter.
Dronkers et al. (1998) reported that all of their patients
with conduction aphasia had a lesion that involved the
posterior-superior temporal gyms, often extending into
the inferior parietal lobule. The salient sign in conduction aphasia is impaired ability to repeat phrases and
sentences in the presence of relatively good auditory
comprehension and oral-expressive abilities. Although
auditory comprehension is relatively good, it is not
perfect. And, while oral-expressive language is fluent
(longer phrase length and a semblance of syntax), patients with conduction aphasia make numerous phonological errors and replace intended words with words
that sound similar. Naming, reading, and writing abilities are disrupted to some extent.
'
i
'
I
Anornic Aphasia. This fluent syndrome is the least severe. Anomia-word-finding difficulty-is present in all
aphasic syndromes; thus, localization of the lesion that
results in anomic aphasia is not precise. It can be found
subsequent to anterior or posterior lesions (Dronkers
and Larsen, 2001), and Kreisler et al. (2000) report
anomic aphasia resulting from a lesion in the thalamus;
medial temporal area; or frontal cortex, insula, and anterior part of the temporal gyri. Patients with anomic
aphasia display longerphrase length and preserved syntax; mild, if any, auditory comprehension deficits; good
repetition ability; and mild reading and writing impairment. Frequently, the anomic patient will substitute
synonyms for the intended words or replace the desired
word with a generalization, for example, "thing" or
"stuff."
Cautions
The classification of aphasia into the classical syndromes
is not exempt from controversy. Some (Caramazza,
1984; Caplan, 1987) have challenged its validity. Darley
(1982) suggested that aphasic people differ on the basis
of severity or the presence of a coexisting communication disorder, frequently apraxia of speech. He advocated viewing aphasia unmodified by adjectives. The
relationship between the site of lesion and the corresponding syndrome is also controversial. The classical
sites of lesion for most aphasic syndromes are challenged by exceptions (Basso et al., 1985; Murdoch, 1988;
Pronkers and' Larsen, 2001). Some of the inconsistency
may result from the time post onset when behavioral
observations are made. Improvement in aphasia over
time results in approximately 50% of aphasic patients
changing from one syndrome to another (Kertesz and
McCabe, 1977).Thus, an acutely aphasic patient with an
inferior left frontal gyms lesion may display the expected
Broca's aphasia; however, at 6 months after onset, the
same patient's language characteristics may resemble
anomic aphasia. Confusion may also result from the
methods employed to classify the aphasias. For example,
classifications made with the WAB do not always agree
with those made with the BDAE (Wertz, Deal, and
Robinson, 1984). Finally, controversy and confusion
may result from misuse of the term syndrome (Benson
and Ardila, 1996). The behavioral profile that constitutes
a specific aphasic "syndrome" is characterized by a
range of impairment and not by identical performance
among all individuals within a specific syndrome. In
many, certainly not all, aphasic people, impaired behavioral features-fluency, auditory comprehension, verbal
I
Aphasia: The Classical Syndromes
naming-tend
to result in different clusters
that represent different profiles. These have led to the
development and use of the classical syndromes in
aphasia.
-Robert
Ogar
T. Wertz, Nina
Ij:
Dronkers, and Jennifer
References
*lexander, M. P., Benson, D. F., and Stuss, D. T. (1989).
Frontal lobes and language. Brain and Language, 37,
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Basso, A,, Lecours, A. R., Moraschini, S., and Vanier, M.
(1985). Anatomical correlations of the aphasias as defined
through computerized tomography: Exceptions. Brain and
Language, 26,201-229.
Benson, D. F. (1988). Classical syndromes of aphasia. In
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Broca, P. (1861a). Remarques sur le siege de la faculti du langage articulk, suivies d'une observation d'aphemie (perte de
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Broca, P. (1861b). Nouvelle observation d'aphkmie produite
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Caplan, D. (1987). Neurolinguistics and linguistic aphasiology.
Cambridge, U.K.: Cambridge University Press.
Caramazza, A. (1984). The logic of neuropsychological research and the problem of patient classification in aphasia.
Brain and Language, 21, 9-20.
Darnasio, A. R. (1992). Aphasia. New England Journal of
Medicine, 326, 53 1-539.
Darley, F. L. (1982). Aphasia. Philadelphia: Saunders.
Dronkers, N. F., and Larsen, J. (2001). Neuroanatomy of the
classical syndromes of aphasia. In R. S. Berndt (Ed.),
Handbook of neuropsychology (2nd ed., vol. 3). Amsterdam:
Elsevier.
Dronkers, N. F., Redfern, B. B., and Ludy, C. A. (1995). Lesion localization in chronic Wernicke's aphasia. Brain and
, Language, 51,62-65.
Dronkers, N. F., Redfern, B. B., Ludy, C., and Baldo, J.
(1998). Brain regions associated with conduction aphasia
and echoic rehearsal. Journal of the International Neuro~s~chological
Society, 4, 23-24.
Dronkers, N. F., Shapiro, J. K., Redfern, B., and Knight,
R. T. (1992). The role of Broca's area in Broca's aphasia.
Journal of Clinical and Experimental Neuropsychology, 14,
52-53
Geschwind, N. (1965). Disconnection syndromes in animals
and man. Brain, 88, 237-294.
Goodglass, H., and Kaplan, E. (1983). The Boston Diagnostic
Aphasia Examination. Philadelphia: Lea and Febiger.
KerteSz, A. (1979). Aphasia and associated disorders: Taxonomy, localization, and recovery. New York: Grune and
Stratton.
Kenesz, A. (1982). The Western Aphasia Battery. New York:
Grune and Stratton.
Kenesz, A., and McCabe, P. (1977). Recovery patterns and
Prognosis in aphasia. Brain, 100, 1-18.
Kreisler, A., Godefroy, O,, Dalmaire, C., Debachy, B.,
Leclercq, M., Pruvo, J.-P., et al. (2000). The anatomy of
$
revisited. Neurology, 54, 1117-1 122.
g
25 1
Lichtheim, L. (1885). On aphasia. Brain, 7,433484.
Marie, P. (1906). Revision de la question de l'aphasie: La troisieme circonvolution frontale gauche ne joue aucun role
special dans la fonction du langage. Semaine Medicale, 26,
241-247.
Mohr, J. P. (1976). Broca's area and Broca's aphasia. In
H. Whitaker and H. Whitaker (Eds.), Studies in neurolinguistics (vol. 1, pp. 201-233). New York: Academic
Press.
Murdoch, B. E. (1988). Computerized tomographic scanning: Its contributions to the understanding of the neuroanatomical basis of aphasia. Aphasiology, 2,437-462.
Wernicke, C. (1874). Der aphasische Symptomencomplex. Breslau, Poland: Kohn and Weigert.
Wertz, R. T., Deal, J. L., and Robinson, A. J. (1984). Classifying the aphasias: A comparison of the Boston Diagnostic
Aphasia Examination and the Western Aphasia Battery. In
R. H. Brookshire (Ed.), Clinical Aphasiology Conference
proceedings (pp. 40-47). Minneapolis: BRK.
Further Readings
Alexander, M. P. (1997). Aphasia: Clinical and anatomic
aspects. In T. E. Feinberg and M. J. Farah (Eds.), Behavioral neurology and neuropsychology (pp. 133-149). New
York: McGraw-Hill.
Bogen, J. E., and Bogen, G. M. (1976). Wernicke's region:
Where is it? Annals of the New York Academy of Sciences,
280, 834-843.
Caplan, D., Hildebrandt, N., and Marlies, N. (1996). Location of lesions in stroke patients with deficits in syntactic
processing in sentence comprehension. Brain, 119, 933949.
Damasio, H., and Damasio, A. R. (1989). Lesion analysis in
neuropsychology. New York: Oxford University Press.
Dronkers, N. F. (1996). A new brain region for coordinating
speech articulation. Nature, 384, 159-161.
Freedman, M., Alexander, M. P., and Naeser, M. A. (1984).
Anatomic basis of transcortical motor aphasia. Neurology,
34,409417.
Geschwind, N. (1972). Language and the brain. Scientific
American, 226, 76-83.
Godefroy, O., Duhamel, A., Leclerc, X., Saint Michel, T.,
Henon, H., and Leys, D. (1998). Brain-behavior relationships: Models for the study of brain damaged patients.
Brain, 121, 1545-1 556.
Goodglass, H. (1993). Understanding aphasia. San Diego, CA.
Academic Press.
Kertesz, A., Sheppard, A., and MacKenzie, R. (1982). Localization in transcortical sensory aphasia. Archives of NeurolOD, 39,475-478.
Kirshner, H. S., Alexander, M., Lorch, M. P., and Wertz,
R. T. (1999). Disorders of speech and language. Continuum:
Lifelong Learning in Neurology, 5, 1-237.
Naeser, M. A., and Hayward, R. W. (1978). Lesion localization in aphasia with computed tomography and the Boston
Diagnostic Aphasia Exam. Neurology, 28, 545-55 1.
Palumbo, C. L., Alexander, M. P., and Naeser, M. A. (1992).
CT scan lesion sites associated with conduction aphasia. In
K. Se (Ed.), Conduction aphasia (pp. 51-75). Hillsdale, NJ:
Erlbaum.
Sarno, M. E. (Ed.). (1998). Acquired aphasia (3rd ed.). San
Diego, CA: Academic Press.
Sternmer, B., and Whitaker, H. A. (Eds.). (1998). Handbook of
neurolinguistics. San Diego, CA: Academic Press.
252
Part 111: Language
Vignolo, L. A., Boccardi, E., and Caverni, L. (1986). Unexpected CT-scan findings in global aphasia. Cortex, 22,
55-69.
Wertz, R.T. (1983). Classifying the aphasias: Commodious or
chimerical? In R. H. Brookshire (Ed.), Clinical Aphasiology
Conference proceedings (pp. 296-303). Minneapolis: BRK.
Willmes, K., and Poeck, K. (1998).To what extent can aphasic
syndromes be localized?Brain, 116, 1527-1 540.
Aphasia, Wernicke's
A new concept in aphasiology was created when Wernicke (187411977) described ten patients with different
forms of aphasia, and showed that two of the patients
had fluent but paraphasic speech with poor comprehension (i.e., sensory aphasia). At autopsy of another patient, a lesion was found in the left posterior temporal
lobe. This type of aphasia has been called by many
names, including receptive, impressive, sensory, or more
generally fluent aphasia. In most of the current classification systems, this type of syndrome is called Wernicke's aphasia. It affects 15%-25% of all patients with
aphasia (Laska et al., 2001).
Although the exact boundaries of Wernicke's area are
controversial, the typical lesion associated with Wernicke's aphasia is most often located in the posterior
temporal area. The middle and superior temporal lobe
posterior to the primary auditory cortex are affected in
almost all cases. The primary auditory cortex is also
often affected, as are the white matter subjacent to the
posterior temporal lobe, the angular gyms, and the
supramarginal gyms. In rare cases, restricted subcortical
lesions may resul't in Wernicke's aphasia and hemiplegia,
the latter being uncommon in cases with cortical lesions.
Recent studies have not changed these classical views of
the clinico-anatomical relations of initial aphasia.
Patients with Wernicke's aphasia are usually older
than patients with Broca's aphasia. However, some rare
cases of children with acquired fluent aphasia and a
posterior temporal lesion have been described (Paquier
and Van Dongen, 1991). Ferro and Madureira (1997)
have attributed the age difference between patients ,with
fluent aphasia and those with nonfluent aphasia to the
higher prevalence of posterior infarcts in older patients.
The most common etiological factor in vascular Wernicke's aphasia is cardiac embolus, which more often
affects the temporal area, whereas carotid atherosclerotic
infarctions are in most cases located in the frontoparietal
area (Harrison and Marshall, 1987; Knepper et al.,
1989). Coppens (1991), however, points to a higher
mortality rate in older patients with stroke, which might
cause a selection bias in studies showing a relationship
between age and type of aphasia.
The typical clinical signs of ~ernicke's aphasia
include poor comprehension of spoken and written language and fluent but paraphasic (phonemic and semantic) speech. In some cases, neologistic jargon may occur.
Naming is also severely affected, and phonemic or semantic prompting is of no help. Poor repetition dis-
tinguishes Wernicke's aphasia from transcortical sensory
aphasia. Writing mirrors the speech output. Handwriting is usually well formed, but the text is without
content, and jargonagraphia may occur. Because of
posterior lesions, hemiparesis is present in rare cases, but
visual field defects are more common. Many patients
also show signs of anosognosia, especially during the
acute stage of the illness. In most cases, the use of gestural communication or pantomime is affected as well.
Patients not traditionally classified as having aphasia
may also show language disturbances resembling Wernicke's aphasia, such as patients with schizophrenia, dementia, or semantic dementia, a fluent form of primary
progressive aphasia.
Some authors suggest that Wernicke's aphasia is not a
uniform entity but includes many variants. Forms of
neologistic, semantic, and phonemic jargon and pure
word deafness may all be grouped under Wernicke's
aphasia. Pure word deafness is a rare disorder characterized by severe difficulties in speech comprehension
and repetition with preservation of other language functions, including the comprehension of nonverbal sounds
and music (Kirshner, Webb, and Duncan, 1981). However, when Buchman et al. (1986) reviewed 34 published
cases, they were unable to find any really pure casesthat is, cases without any other more generalized perceptual disorders that could be classified as acoustic
agnosia or mild language disorders such as paraphasia,
naming difficulties, and reading and writing disorders.
Most of the patients with "pure" word deafness have
had bilateral temporal lesions, but some patients with
unilateral left hemisphere lesions have been described
(Takahashi et al., 1992).
Personality factors may play a role in the clinical expression of aphasia. In some views, jargon aphasia is not
solely a linguistic deficit. Rochford (1974) suggested that
a pathological arousal mechanism and lack of control
were crucial to jargon aphasia. Weinstein and Lyerly
(1976) suggested that jargon aphasia could emanate
from abnormal adaptation to the aphasic speech disorder. They found a significant difference in premorbid
personality between patients with jargon aphasia and
those without jargon aphasia. Most of their patients with
jargon aphasia had a strong premorbid tendency to deny
illness or openly expressed fear of illness, indicating the
importance of anosognosic features in jargon aphasia.
Linguistically, patients with Wernicke's aphasia speak
with normal fluency and prosody without articulatory
distortions. They often provide long and fluent answers
(logorrhoea) to simple questions. In fact, patients with
Wemicke's aphasia produce an equal number of words
as persons without aphasia in spontaneous speech.
However, they show less lexical variety, a high proportion of repetitions, and empty speech (Bates et al., 2001).
This may give an impression of grammatically correct
speech, but the meaning of the utterances is lost because
of a high proportion of paraphasias and neologisms
(Lecours and Lhermitte, 1983). This type of speech error
is called paragrammatism. Patients with ~ernicke's
aphasia show morphological errors, but less so than
Aphasia, Wernicke's
,
patients with Broca's aphasia (Bates et al., 2001). However, there is some evidence that in highly inflected languages such as Finnish, the number of errors is higher
on inflected words than on the lexical stems (Niemi,
Koivuselka-Sallinen, and Laine, 1987). At least in spontaneous speech, distorted sentence structure in utterances
of patients with Wernicke's aphasia is related to the
lexical-semantic difficulties rather than to morphosyntactic problems (Helasvuo, Klippi, and Laakso, 2001).
The same has been found in sentence comprehension.
Patients with Wernicke's aphasia performed correctly
only on sentences that did not require semantic operations (Pinango and Zurif, 2001). According to these
findings, the deficit in phonemic hearing does not explain
the nature of comprehension problems in patients with
Wernicke's aphasia.
Most patients show skill in pragmatic abilities, such
as using gaze direction and other nonverbal actions in
conversation. Unawareness of one's own speech errors
usually occurs initially in Wernicke's aphasia, but some
degree of auditory self-monitoring develops after onset,
and patients then begin to use various self-repair strategies to manage conversation (Laakso, 1997). In contrast to self-repair sequences in nonaphasic speakers,
these sequences are very lengthy and often unsuccessful.
The initial severity of the aphasia is considered the
most important single factor in predicting recovery from
aphasia. Wemicke's aphasia is usually tantamount to
severe aphasia. In a study by Ross and Wertz (2001), of
all patients with aphasia, those with Wernicke's aphasia
and global aphasia showed the most severe impairment
in language functions and communication. These
patients showed only limited recovery when measured
at the impairment level by the Boston Diagnostic Aphasia Examination (BDAE) and at the disability level by
CADL. In addition to initial severity of aphasia, supramarginal and angular gyri involvements seem to relate to
poor recovery in comparison with cases without extension to the posterior superior temporal gyms (Kertesz,
Lau, and Polk, 1993).
Patients who have recovered from Wernicke's aphasia
have shown a clear increase in activation in the right
perisylvian area, suggesting a functional reorganization
of the language with the help of the right hemisphere
(Weiller et al., 1995). However, Karbe et al. (1998)
reported that increased activity in the right hemisphere
was present in patients with poor recovery and reflected
the large lesions in the left hemisphere. Patients with
good recovery showed increased activation in the left
hemisphere surrounding the damaged area.
The classification of aphasia depends strongly on the
methods used in the assessment. The major diagnostic
tests, such as the BDAE, the Western Aphasia Battery
(WAB), or the Aachener Aphasie Test (AAT), have
slightly different criteria for classification. For example,
whereas the WAB assigns all patients to some aphasia
classification, up to 70% of patients examined with the
BDAE might be designated as having unclassified aphasia. Another issue that confuses classification is the time
after onset at which the evaluation is done. Depending
253
on the sample studied, more than half of patients with
aphasia will show evolution to another type of aphasia
during the first year after the onset of illness (Ross and
Wertz, 2001). Patients with initial Wernicke's aphasia.
will usually evolve to have a conduction or transcortical
type of aphasia, and may evolve further to have anomic
aphasia (Pashek and Holland, 1988). On the other hand,
the condition of elderly patients with initial global
aphasia tends to evolve to Wernicke's aphasia during
the recovery period, and the condition of younger
patients evolves to Broca's aphasia. This could explain
why only one-third of patients with fluent aphasia and
lesions in Wernicke's area have a persisting aphasia, and
only slightly more than half of patients with chronic
Wemicke's aphasia have lesions in Wemicke's area
(Dronkers, 2000).
-Matti Lehtihalmes
References
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Further Readings
Aphasia Treatment: Computer-Aided
Rehabilitation
Best, W., and Howard, D. (1994). Word sound deafness
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The role of technology in treating clinical aphasiology
has been evolving since studies f i s t demonstrated the
feasibility of using computers in the treatment of aphasic
adults. This journey began with remote access to treatment in rural settings using large computer systems
over the telephone. There followed the introduction and
widespread use of personal computers and portable
computers, with the subsequent development of complex software and multimedia programs. This changing
course is not simply the result of technological progress
but represents greater understanding by clinicians and
researchers of the strengths and limitations of computeraided treatment for aphasia and related disorders.
Four common types of treatment activities are appropriate for presentation on a computer: stimulation,
drill and practice, simulations, and tutorials. Stimulation
activities offer the participant numerous opportunities to
respond quickly and usually correctly over a relatively
long period of time for the purpose of maintaining and
stabilizing the underlying processes or skills, rather than
simply learning a new set of responses. It is easy to design computer programs that contain a large database of
stimuli, and then to control variables (e.g., word length)
as a function of the participant's response accuracy. Drill
and practice exercises teach specific information so that