c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

Available online at www.sciencedirect.com

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Review

Old and recent approaches to the problem of nonverbal conceptual disorders in aphasic patients
Guido Gainotti a,b,*
a
b

Center for Neuropsychological Research and Institute of Neurology of the Catholic University of Rome, Italy
IRCCS Fondazione Santa Lucia, Department of Clinical and Behavioral Neurology, Rome, Italy

article info

abstract

Article history:

From the first research on aphasia, it has been shown that, in addition to verbal communi-

Received 17 September 2013

cation disorders, aphasic patients often have difficulty on non-verbal cognitive tasks, which

Reviewed 11 November 2013

can actually be solved without the use of language. In this survey, I will discuss in a historical

Revised 19 November 2013

perspective the different interpretations provided by classical and contemporary authors to

Accepted 16 January 2014

explain this puzzling observation. First, I will take into account the different positions of

Action editor Marjorie Lorch

classical authorities on this topic, starting from the first debates (mainly based on anatomo-

Published online 28 January 2014

clinical observations) on the organisation of language in the brain. Then, I will attempt to
summarize the work of authors who have tackled this complex issue more recently, in

Keywords:

systematic investigations using methods drawn from experimental psychology, to clarify

Aphasic non-verbal

the meaning of non-verbal cognitive disorders in aphasia. Finally, in the last part of the

cognitive disorders

survey, I will discuss the interpretation of proponents of the semantic hub hypothesis who

Preverbal conceptual disturbances

have tried to analyse and explain the differences between the non-verbal semantic defects of

Defective semantic

patients with semantic dementia and aphasic stroke patients. The hypothesis which as-

activation control

sumes that most non-verbal cognitive disorders observed in aphasic patients are due to a

Verbal mediation hypothesis

preverbal conceptual disorder, which cannot be attributed to a loss of semantic representations but rather to a defect in their controlled retrieval, seems substantially confirmed.
Nevertheless, two main issues must still be clarified. The first is that some of the non-verbal
cognitive defects of aphasic patients seem due to the negative influence of language disturbances on abstract non-verbal cognitive activities, rather than to a preverbal conceptual
disorder. The second issue concerns the exact nature and the neuroanatomical correlates of
the defective controlled retrieval of unimpaired conceptual representations, which should
subsume most of the non-verbal cognitive disorders of aphasic patients.
2014 Elsevier Ltd. All rights reserved.

1.

Introduction

Since the earliest investigations of aphasia, it has been

stressed that aphasic patients not only exhibit different types

of verbal communication disorders but often have great difficulty on non-verbal cognitive tasks that apparently can be
solved without the use of language. Different interpretations
have been advanced to explain these unexpected findings.
Some authors assumed that disruption of preverbal symbolic

* Center for Neuropsychological Research, Institute of Neurology, Policlinico Gemelli, Catholic University of Rome, Largo A. Gemelli, 8,
00168 Roma, Italy.
E-mail addresses: gainotti@rm.unicatt.it, g.gainotti@hsantalucia.it.
0010-9452/$ e see front matter 2014 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.cortex.2014.01.009

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

(e.g., Finkelnburg, 1870) or conceptual (e.g., Bay, 1962) activities might subsume both the verbal and non-verbal cognitive
disorders of aphasic patients. Others (e.g., Head, 1926;
Trousseau, 1865) claimed that language is so important for
the development of thought that severe language disorders
lead to impairment of both verbal and non-verbal cognitive
activities. Still others (e.g., De Renzi, Faglioni, Savoiardo, &
Vignolo, 1966) stressed the significant, but not very high,
level of the relationships between verbal and non-verbal
cognitive disturbances and surmised that anatomically
contiguous, but functionally independent, cortical areas
might subsume language and non-verbal cognitive abilities. In
recent years, interest in this problem was renewed by proponents of the semantic hub hypothesis, in particular by
Jefferies and Lambon Ralph (2006), who proposed that the
non-verbal cognitive disturbances of patients with stroke
aphasia might be due to disorders affecting the taskappropriate control of semantic retrieval/activation.
In the present review, I intend to survey this very complex
issue from a historical perspective. I will first take into account
the pioneers of modern neurolinguistics who, after Brocas
(1861) discovery, proposed different explanations of the nonverbal cognitive disturbances observed in patients with severe forms of aphasia. Then I will summarize the work of
authors who, in a more recent era, tackled this question in a
series of systematic investigations aimed at determining
which interpretation best explains the clinical and experimental data relevant to this issue. Finally, in the last part of
the survey I will discuss how this problem has been considered by proponents of the semantic hub hypothesis, particularly Lambon Ralph, Jefferies and coworkers (e.g., Corbett,
Jefferies, Ehsan, & Lambon Ralph, 2009; Gardner et al., 2012;
Jefferies, Baker, Doran, & Lambon Ralph, 2007; Jefferies &
Lambon Ralph, 2006) who tried to analyse and explain the
differences existing between the non-verbal conceptual disorders observed in semantic dementia (SD) and patients with
stroke aphasia. The recurrence of certain interpretations in
the work of various authors, as well as the novelty of their
contributions, will be discussed by trying to distinguish between the points on which a wide consensus seems to have
been reached and those that are still open and require further
investigation.

2.2.

2.1.
Trousseau and the ancillary use of words for
cognitive activities
Trousseau (1865) was one of the first authors to question the
ability of some aphasic patients to express their thoughts
through gestures and drawings and to claim that cognitive
impairment is far from homogeneous in aphasia. Trousseau
made a distinction between certain types of cognitive activities that can be performed without the ancillary use of words
and other (higher) cognitive activities that cannot be performed without the thought formulae (formules de la pensee) that are represented by words. The former are usually
spared in aphasic patients, but the latter are often impaired.

Filkelnburg and the construct of asymbolia

Some years later, the existence of a cognitive impairment in

aphasia that largely exceeds the linguistic sphere was
confirmed by Finkelnburg (1870), who explained it from a
different theoretical point of view. He reported five patients
who, in addition to a language disorder, showed a number of
non-verbal receptive and expressive symbolic disturbances
(e.g., a violinist was unable to recognize musical notes, a
businessman was unable to recognize pieces of money and a
Prussian embassy official was unable to recognize insignia of
rank and social class) and were unable to acquire and retain
new signs or comprehend pantomimes. Finkelnburg (1870)
argued that the notion of aphasia as a purely verbal disorder
could not explain these findings and proposed that aphasia
should be considered as an aspect of asymbolia, defined as
partial or complete loss of the capacity to comprehend or
express concepts by means of acquired signs. The work of
Finkelnburg (1870) was so influential that Jackson (1878)
mentioned the frequency with which disorders in pantomime production and recognition are observed in aphasic
patients and acknowledged that in aphasia there is a loss or
defect in symbolizing relations of things in any way.
Some decades later the construct of a cognitive impairment in aphasia concomitant to (and possibly underlying) the
properly verbal disturbance was strongly argued by Goldstein
(1948), Head (1926) and Marie (1906), who are usually considered representatives of the Noetic School.

2.3.
Marie and the impairment of intelligence in
aphasia
Marie (1906) put the question in very sharp terms, claiming
that in aphasia there is a marked impairment of intelligence
in general, but the examples of non-verbal cognitive disturbances that he offered as proofs of his statement suggest that
Marie (1906) used the term intelligence in a sense loosely
corresponding to the present construct of semantic memory.
This suggestion is supported by Maries definition of intelligence, considered as a sphere where are stored, among
others, various aspects of didactically acquired knowledge.

2.4.

2.
Early proponents of a non-verbal cognitive
impairment in aphasia

79

Head and the purposeful use of symbols

Head (1926) also reported clinical observations showing that

the cognitive impairment of aphasic patients extended
beyond the purely linguistic domain. He did not, however,
presume that aphasia was due to a general loss of intelligence. Pursuing Finkelnburgs (l870) and Jacksons (l878) lines
of thought, Head considered these cognitive impairments as
the consequence of a defect in the purposeful use of symbols.
He claimed that aphasic patients are not impaired on cognitive tasks that can be performed with simple perceptual activity, but are usually defective when an intermediate (verbal
or non-verbal) symbolic activity is required by the task. Thus,
the greatest cognitive impairment of aphasic patients is
observed on tasks that require an intermediate symbolic activity between the initial conception and the final execution of
the act.

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2.5.
Goldstein and loss of the abstract attitude in
aphasia
Goldstein (1948) was probably the representative of the Noetic
School who had the greatest influence on subsequent thought
about the relationships between linguistic and cognitive disturbances in aphasia (Noppeney & Wallesch, 2000). Together
with Gelb, he studied the naming disorders of First World War
brain-injured (Gelb & Goldstein, 1924). These authors
concluded that the naming impairment is only a manifestation of a more basic cognitive disorder, defined as a loss of the
abstract attitude, in which the subject detaches himself from
the immediate sensory components of a situation and relies
on abstract rules and general concepts. Thus, aphasia
(particularly amnestic aphasia) is the result of a basic deficit of
abstractive ability, and disruption of verbal behaviour is only
an effect of a more general disorder. On the other hand,
Goldstein (1948) acknowledged that language, in turn, influences thought formation, because language is not only a
means of communicating thinking, but also of developing and
supporting it. Thus, a language defect might impede the
development and achievement of thinking.
A comparative analysis of the fine-grained positions of
these classical authors reveals two different lines of thought.
On one hand, authors such as Finkelnburg (1870) and Marie
(1906) assumed that language disorders should be considered as only one aspect of a more basic preverbal cognitive
impairment. On the other hand, authors such as Trousseau
(1865) and, at least in part, Head (1926) and Goldstein (1948)
believed that non-verbal cognitive impairment could in part
be due to a defect of inner language, which they distinguished from other forms of language. To be sure, these authors maintained that the cognitive impairment of aphasic
patients is (at least in part) a by-product of their language
disorder and attributed this defect to the weakness of thought
processes, that did not have adequate verbal support for their
development. A weak aspect of the assumptions made by the
early proponents of a non-verbal cognitive impairment in
aphasia was the frail body of data provided by these authors to
support their theories. Their arguments consisted of individual case studies that showed an association between aphasia
and non-verbal symbolic disturbances (Finkelnburg, 1870),
loss of previously acquired knowledge and skills (Marie, 1906)
or loss of the abstract attitude (Goldstein, 1948). They did not,
however, demonstrate that a necessary relationship exists
between language and cognitive disturbances.
Two more general points should be stressed at the end of
this section dealing with the work of early proponents of a
non-verbal cognitive impairment in aphasia. The first is that
most of these authors distinguished between aphasia in
general and a subset of patients. Goldstein (1936), for instance,
was very explicit that semantic aphasia (SA) and the loss of
controlled use of meaning/abstract thought, were not true of
aphasia in general (e.g., not for those with a core phonological
or motor language disorder) but rather of a specific subset of
patients. Head (1926) was equally clear on this point. From the
neuroanatomical perspective, he associated SA specifically
with parietal lesions and, from the neuropsychological vantage point, noted the overlap within the parietal region of a

shared symbolic processing deficit for numbers, space, and

other kinds of symbols.
The second point that should be explicitly acknowledged is
that Head and Goldstein were already attempting to test nonverbal aspects of processing in their patients using the rudiments of formal testing. Head, in particular, used an impressive systematic neuropsychological battery, and Goldstein
used a forerunner of Weigls colour sorting test (skeens of
wool dyed to different colours and shades), free sorting (items
on his desk) and category fluency. Thus, even if modern, more
detailed neuropsychological testing arrived later (e.g., De
Renzi onwards) formal testing had already been used by previous authors, in particular by Head.

3.
The application of methods drawn from
experimental psychology to study non-verbal
cognitive disorders in aphasia
3.1.
The psychometric studies of Weisenburg and
McBride
Weisenburg and McBride (1935) were the first authors to
investigate the non-verbal cognitive disorders of aphasic patients using designs and procedures drawn from the field of
experimental psychology. However, the cognitive tasks they
used were not those best suited to control for the assumptions
of the noetic school, because most of these tests involved
executive functions or perceptual-motor and visual-spatial
abilities, not the symbolic or categorical activities that the
noetic authors considered typically impaired in aphasic
patients.

3.2.
Bay and the poor differentiation and actualization
of concepts
Bay (1962, 1964) used much more appropriate methods to test
the assumptions of the noetic authors. In support of his
claim that aphasia should be considered as a loss of concepts
that can be expressed in words, Bay showed that aphasic
patients often perform poorly on modelling tasks because
they fail to reproduce the typical features of the targets.
Furthermore, to stress the analogy between verbal and nonverbal aphasic disturbances, Bay claimed that patients who
are unable to name a missing feature in an incomplete
drawing are also unable to complete it. He also made a
distinction between poor differentiation and actualization of
concepts subsuming both verbal and non-verbal symbolic
disabilities. This interesting difference seems to have anticipated the distinction, proposed by Darley (1982) and McNeil
(1982, 1988) between disorders of access and disorders of
knowledge (see McNeil & Pratt, 2001, for review). A similar
distinction between semantic representation and semantic
retrieval disorders has recently been developed and supported
in well-controlled experiments by Jefferies and Lambon Ralph
(2006) and will be discussed in Section 4 of the present review.
A methodological objection to Bays observations was raised
by Zangwill (1969), who noted that Bay had provided no control data on the modelling capacities of brain-damaged

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

patients without aphasia. It is, therefore, impossible to say

whether the poor modelling performances of aphasic patients
are due to poor differentiation and actualization of concepts
or to the influence of constructional apraxia, which is often
observed in aphasic patients with lesions located in the
temporo-parietal areas of the left hemisphere.

3.3.
The problem-solving and associative tasks used
by De Renzi
Much less questionable from a methodological point of view
are the results obtained by De Renzi and colleagues in a series
of well-controlled neuropsychological investigations (Basso,
De Renzi, Faglioni, Scotti, & Spinnler, 1973; Basso, Faglioni, &
Spinnler, 1976; De Renzi et al., 1966; De Renzi, Faglioni,
Scotti, & Spinnler, 1972; De Renzi, Pieczuro, & Vignolo, 1968;
De Renzi & Spinnler, 1967; Faglioni, Spinnler, & Vignolo,
1969; Spinnler & Vignolo, 1966).
These authors utilized two partly separable subgroups of
cognitive tasks:
(a) the first consisted of problem-solving tasks, such as
Ravens Progressive Matrices (Raven, 1962), Elithorns
Perceptual Maze test (Elithorn, 1955), Gottschaldts
Hidden Figures test (1929) and Weigls Sorting test
(Weigl, 1941) that used non-verbal abstract material as
stimuli and required patients to analyse or organise
these stimuli to solve a visual-spatial or logical problem.
(b) the second group consisted of associative tests (such
as the Coloring Drawings of Objects, Meaningful
Sound Recognition or Use of Objects tests) that used
concrete pictorial material as stimuli and required patients to match two different features belonging to the
conceptual representation of the same object.
Results obtained in this complex and articulated series of
investigations can be summarized as follows:
1. Aphasic patients showed consistent impairment in both
subgroups of cognitive tasks.
2. Only part of this impairment concerned aphasic patients
specifically; as the rest of the impairment could be
observed in both aphasic and non-aphasic brain-damaged
patients, it seemed generally due to the effects of brain
injury.
3. The specific cognitive defects of aphasic patients seemed
linked to the abilities tapped by the associative tests and
by Weigls test of abstract thinking; in fact, no difference
could be found between patients with aphasia and those
with right-brain damage on tests that loaded more highly
on executive functions or visual-spatial factors.
4. The correlations between severity of language impairment
and results obtained on non-verbal problem-solving and
associative tasks were rather variable as a function of both
the parameters chosen to evaluate the severity of aphasia
and the type of cognitive task. Stressing the significant but
not absolute value of these relationships, De Renzi and
associates did not hold that a functional relationship exists
between linguistic and non-verbal cognitive disturbances.
Rather, they surmised that anatomically contiguous, but

81

functionally independent, structures might subsume language and non-verbal cognitive abilities.

3.4.
Duffy and the construct of a central symbolic defect
in aphasia
The line of research followed by Duffy and colleagues (Duffy &
Duffy, 1981; Duffy, Duffy, & Mercaitis, 1984; Duffy & McEwen,
1978; Duffy & Watkins, 1984) was much more related to
Finkelnburgs (1870) concept of asymbolia. After prompting
the translation into English of Finkelnburgs main article
(Duffy & Liles, 1979), Duffy provided the following experimental evidence in support of his contention:
1. In aphasia, a strong relationship exists between scores
obtained on tests of pantomime expression and pantomime recognition. Furthermore, both of these measures
are highly correlated with scores of verbal expression and
verbal comprehension (Duffy & Duffy, 1981).
2. There are strong similarities between gestural and speech
characteristics of fluent and non-fluent aphasic patients
(Duffy et al., 1984).
3. Manipulating variables that affect performance on verbal
comprehension tasks has similar effects on performance
of pantomime recognition tests. In particular, the presence
of semantically related response choices significantly reduces scores obtained on both verbal recognition and
pantomime recognition tests (Duffy & Watkins, 1984).
According to Duffy and Duffy (1981), the occurrence of
verbal and non-verbal deficits can be explained as either a
consequence of a central symbolic deficit or a problem of
verbal mediation of non-verbal behaviour. Nevertheless,
Varney (1978, 1982) raised two main objections to Duffys
claim that a central symbolic defect might subsume both the
gestural and verbal disturbances of aphasic patients. The first
was that only about 50e60% of aphasic patients show defects
in pantomime comprehension. The second was that pantomime recognition defects are more strongly related to disorders of reading comprehension than auditory comprehension.
It must be acknowledged, however, that both of these objections challenge a strong version of the central symbolic
deficit theory (which considers each component of the
aphasic symptom-complex in terms of symbolic disruption),
but neither is necessarily at variance with a theory which
simply states that a functional relationship exists between
some aspects of verbal and non-verbal (pantomime recognition) disorders in aphasia. Gainotti and associates constructed
their model of the relationships between non-verbal cognitive
impairment and semantic-lexical disintegration in aphasia by
drawing on this distinction between central (semantic) and
more peripheral aspects of language disintegration.

3.5.
The relationships between non-verbal cognitive
impairment and semantic disintegration in aphasia
Gainotti et al. (Gainotti, Carlomagno, Craca, & Silveri, 1986;
Gainotti, DErme, Villa, & Caltagirone, 1986; Gainotti &
Lemmo, 1976; Gainotti, Miceli, & Caltagirone, 1979; Gainotti,

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Silveri, Villa, & Caltagirone, 1983) made the following assumptions: (a) only some components of aphasia are intimately linked with the non-verbal cognitive impairment; (b)
these components should be related to the comprehension
and expression of concepts through language; (c) a selective
relationship should, therefore, exist between non-verbal
cognitive impairment and disruption of the semantic-lexical
level of language, whereas phonology and syntax should be
less relevant to non-verbal cognitive functions. This model,
which is consistent with the distinction made by Head (1926)
and Goldstein (1936) between aphasia in general and a subset of patients, was tested in a series of neuropsychological
investigations conducted in large groups of unselected
aphasic and non-aphasic right and left brain-damaged patients and normal controls by means of the following tests: (1)
comprehension of symbolic gestures (Gainotti & Lemmo,
1976); (2) conceptual relationships, in which subjects had to
select the picture conceptually related to the target (Gainotti
et al., 1979); (3) drawing simple objects from memory, in
which the influence of constructional apraxia was controlled
by having patients copy simple geometric figures (Gainotti
et al., 1983); (4) classificatory activity (Gainotti, Carlomagno,
et al., 1986); and (5) Ravens coloured matrices (Gainotti,
DErme, et al., 1986). The presence of a semantic-lexical
impairment at the receptive level was assessed by
measuring the number of semantic errors made on the Verbal
Sound and Meaning Discrimination test (Gainotti,
Caltagirone, & Ibba, 1975; Gainotti, 1982). Aphasic patients
scored significantly worse than non-aphasic (right and left)
brain-damaged patients on the tests of comprehension of
symbolic gestures, conceptual relationships, drawing from
memory and classificatory activity. Furthermore, a strong
relationship was found in aphasic patients between nonverbal cognitive impairment and the presence of a semanticlexical disorder, because in all cognitive tests considered the
worst results were obtained by aphasic patients with
semantic-lexical disturbances.
These results confirm the existence of an intimate link in
aphasia between disruption of the semantic-lexical level of
language and impairment on non-verbal conceptual tasks, but
do not support a strict causal link between these two phenomena. In fact, the presence of a semantic-lexical disorder
also had a strongly negative effect on results obtained with
Ravens coloured matrices, which is a problem-solving test
that requires relational reasoning (Baldo, Bunge, Wilson, &
Dronders, 2010) and that is based on abstract material,
rather than on stored representations. This suggests that only
part of the non-verbal cognitive disorders of aphasic patients
are due to an underlying conceptual disorder, which is
expressed in both the verbal and the non-verbal modality and
that another part is probably due to the negative impact of
disrupted language on the cognitive processing of non-verbal
material.

3.6.
The defective isolation of individual features of
concepts hypothesis
One of the main cognitive functions of language in analysing
external stimuli consists of the ability to focus attention on
specific features of concepts. Drawing on this assumption,

Cohen and associates (Cohen, Engel, Kelter, List, & Strohner,

1976; Cohen, Glockner, Lutz, Maier, & Meier, 1983; Cohen,
Glockner-Rist, Lutz, Maier, & Meier, 1982; Cohen & Kelter,
1979; Cohen, Kelter, & Woll, 1980; Cohen & Woll, 1981; Kelter,
Cohen, Engel, List, & Strohner, 1976; Koemeda-Lutz, Cohen, &
Meier, 1987) proposed that the non-verbal cognitive defects of
aphasic patients may be due to a defective analytical isolation
of individual features of concepts. This hypothesis can be
considered an updated and more precise reformulation of
Goldsteins (1948) view, because it replaces the construct of
loss of the abstract attitude (which is too general and difficult to define operationally), with the more specific and
operationally well-defined notion of a defect in the isolation
of individual features of concepts. Cohen and others based
their hypothesis on the contrasting results obtained on two
non-verbal matching tasks (Cohen et al., 1980; Kelter et al.,
1976) in which subjects had to decide which of two pictures
was more closely related to a third target picture. In one
condition the decision had to be based on the existence of a
common situational context, whereas in the other condition
the decision had to be based on the isolation and appreciation
of critical features of the depicted objects. Aphasic patients
did not score worse than control subjects on the first type of
task, but scored significantly worse than any other control
group on the second task, which required comparing different
concepts with respect to individual features. The researchers
assumed that this basic defect in the appreciation of individual features of concepts accounted not only for results obtained on non-verbal cognitive tasks but also for those
obtained on verbal tasks. Nevertheless, the validity of this
model remains controversial because results of a series of
other experimental investigations, reported by Cohen et al.
(1983), failed to substantiate the hypothesis, whereas results
of more recent research (Lupyan & Mirman, 2013) substantially confirmed it.
If we try to summarize results obtained in these different
and well-controlled research directions, we obtain the same
diverging lines of thought that we found surveying the positions of the early proponents of a non-verbal cognitive
impairment in aphasia.
On one hand, we find results, such as those of Bay, of Duffy
and coworkers, and (in part) of Gainotti and associates, which
stress the existence in some aphasic patients of a basic preverbal defect, that has a negative impact on both verbal and
non-verbal cognitive abilities. According to Bay, this basic
defect consists of a poor differentiation and actualization of
concepts; according to Duffy and associates, it consists of a
central symbolic defect; and according to Gainotti and coworkers, it consists of disruption of the conceptual representations subsuming both semantic-lexical knowledge and nonverbal conceptual activities. In partial agreement with these
positions are the results obtained by De Renzi and colleagues
on the associative tests, in which patients had to match two
different features belonging to the conceptual representation
of the same object.
On the other hand, results obtained by De Renzi et al. (1966)
with Weigls test of abstract thinking, by Gainotti, DErme,
et al. (1986) with Ravens coloured matrices and by Cohen
and colleagues, who checked the defective analytical isolation of individual features of concepts hypothesis, show that

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

only some of the non-verbal cognitive disorders of aphasic

patients are due to an underlying basic (symbolic or conceptual) disorder; and, as language strongly affects cognition,
others occur because language disorders can hamper every
type of thought process (Carruthers, 2002; Clark, 1998;
Vigotsky, 1962).

3.7.

The verbal mediation hypothesis

Data in favour of a negative influence of language disorders on

non-verbal cognitive activities (namely of the so-called verbal
mediation hypothesis), have been repeatedly found in studies
conducted in patients suffering from a visual-verbal or from a
tactual-verbal disconnection syndrome (e.g., Beauvois,
Saillant, Meininger, & Lhermitte, 1978; Geschwind & Fusillo,
1966; Lhermitte & Beauvois, 1973) because a rebound of misnaming in non-verbal task performance has often been
observed in these conditions. For example, Lhermitte and
Beauvois (1973) showed that in visual-verbal disconnection
misnaming can influence results obtained in a drawing from
memory task. Thus, in one case of misnaming their patient
drew what he had said (a bird), instead of what he had seen
(a mouse) and in other instances he included details in his
drawings that belonged in part to the stimulus and in part to
the misnamed response. On the other hand, Beauvois et al.
(1978) described a patient with tactual-verbal disconnection
who was selectively unable to name tactually presented objects he recognized, as was suggested by his ability to mime
their use. Occasionally, however, he showed semantic parapraxias (e.g., he used a toothbrush like a comb). Suspecting
that these miming errors might be due to an implicit semantic
paraphasia, Beauvois et al. (1978) inhibited verbal mediation
by giving special instructions and placing adhesive tape over
the patients mouth. In these conditions, semantic paraphasias no longer appeared and the patient flawlessly mimed
the use of tactually presented objects. It can, therefore, be
concluded that the intermediate use of language generally
helps solve apparently non-verbal tasks and that, accordingly,
language disorders also impair performance on these tasks.

3.8.
The relationship between non-verbal cognitive
disorders and executive defects in aphasia
In previous sections of this review, we have seen that even if
most non-verbal cognitive disorders observed in aphasic patients seem due to a preverbal conceptual disorder, other
disturbances cannot be explained on these grounds and seem
due either to the negative influence of language disorders on
non-verbal cognitive activities or to the repercussion of other
kinds of cognitive disturbances. In particular, some authors
wondered whether non-verbal disorders of aphasic patients
could be due to a number of what could be called supporting
non-linguistic processes, such as executive functions, shortterm memory or attentional resources, which make it difficult to be precise about the nature of the non-verbal processes
that are impaired in these patients. Keil and Kasniak (2002),
for instance, focused on the complexity of the relationships
between language and executive functions, because, although
an executive deficit can exacerbate the language defect, the
reverse can also be true. Results of several studies (e.g.,

83

Beeson, Bayles, Rubens, & Kaszniak, 1993; Purdy, 2002) indicate that aphasic patients could have co-occurring executive
defects, but testing these deficits is confounded by language
difficulties. One technique used to overcome this source of
confound is the adoption of non-verbal tasks; but, even in this
case, patients still need to use language skills to understand
the task instructions and demands. Keil and Kasniaks (2002)
review documented that this can be a problem for individuals with aphasia. Furthermore, the relatively few
studies that have directly examined executive functions in
aphasic patients have shown that these defects are highly
variable, depending on the lesion site and the severity of
aphasia. Glosser and Goodglass (1990), for instance, used nonverbal tasks to assess disorders of executive control in aphasic
patients, right-brain-damaged patients, and healthy controls.
They showed that aphasic patients with frontal-lobe lesions
were significantly more impaired on these tasks than aphasics
with retro-rolandic or mixed lesions in the left hemisphere.
They concluded that aphasics impairments in executive
control are independent of their linguistic and visuospatial
deficits and are specific to lesions in left frontal and prefrontal
regions. Purdy (2002), on the other hand, compared aphasic
patients with a control group and showed that patients with
Wernickes aphasia had difficulty on the Wisconsin Card
Sorting test (WCST) (Milner, 1963) and on the Tower of Hanoi
(Shallice, 1982); the latter tests planning and requires
attending to specific rules, whose understanding can be
hampered by severe comprehension disorders. The relationships between linguistic and non-linguistic skills supporting
communication processes, were also thoroughly investigated
in rehabilitation studies by Johnsen (1992) and HelmEstabrooks (2002). The former used computerized pictorial
communication as an aid for aphasic patients and found no
systematic relationships between linguistic and non-linguistic skills; indeed, in some patients communication disturbances were, to some extent, compensated for by pictorial
communication, but in other patients the disorder was
deeper, leading to an inability to fully use alternatives for
spoken or written language. Consistent with these data,
Helm-Estabrooks (2002) found no significant relationship between linguistic and non-linguistic skills of attention, memory, executive function and visuospatial abilities, but observed
individual profiles of strengths and weaknesses in these nonlinguistic skills. Taken together, these studies suggest that
aphasia and defects of executive and other cognitive functions
are frequently concomitant conditions, but that the influence
of these cognitive disorders on non-verbal processes still
needs clarification.

3.9.
The distinction between permanent loss and
difficulty of access to the semantic representation in aphasia
In Section 3.2 of the present survey, we saw that Bay (1962,
1964) had suggested a distinction be made between poor differentiation and poor actualization of concepts and that a
similar distinction between disorders of access and disorders
of knowledge had been proposed by Darley (1982) and McNeil
(1982, 1988). Empirical support for these distinctions was
provided by Butterworth, Howard, and McLoughlin (1984),
who tried to control the relations between semantic errors in

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c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

expression and comprehension by administering two lexical

comprehension tasks and a picture naming task to patients
with various aphasic syndromes. As no correlation was found
between pictures that had elicited semantic errors in
comprehension and in naming tasks, Butterworth et al. (1984),
concluded that the multimodal semantic disorder of their
aphasic patients was not due to a permanent loss of information stored in the semantic representation, but rather to an
inability to intentionally access structurally intact semantic
information. This distinction between loss of information and
difficulty of access to the semantic representation has raised
considerable interest and a number of criteria aiming at distinguishing between loss of information (storage deficit) and
difficulty of access have been proposed over the years by
Warrington, Shallice and coworkers (e.g., Shallice, 1988;
Warrington, 1975; Warrington & McCarthy, 1983; Warrington
& Shallice, 1979). The first and the most widely accepted criterion is the consistency of errors on the same items across
successive administrations of the same test or across different
tasks using the same stimuli. The second criterion is the
presence of discrepancies between results obtained on tasks
requiring a propositional access to the semantic knowledge
(such as lexical comprehension tasks or semantic probing
tasks) and results obtained on tasks based on a more automatic access to the same information (such as the semantic
priming effect). The last criterion, stressed by Warrington and
coworkers as a marker of access disorders (Crutch &
Warrington, 2001, 2004, 2005; Warrington & Cipolotti, 1996;
Warrington & McCarthy, 1983, 1987) was refractoriness,
operationally defined as reduced ability to utilize the system
for a period of time after activation. According to this criterion, increasing the inter-trial interval should not improve
performance in semantic defects resulting from a loss of information, but should be highly beneficial in access deficits.
According to Warrington and coworkers, refractoriness could
account not only for rate of presentation effects, but also for
the lack of consistency and of sensitivity to the frequency
effects that should be typical of access deficits. The validity of
the distinction between storage and access deficits, based on
these criteria has been criticized from the theoretical point of
view by several authors (e.g., Caplan, 1987; Hagoort, 1998;
Rapp & Caramazza, 1993). Furthermore inconsistent results
were obtained in studies aiming to empirically check the
validity of these criteria in aphasic patients, as we will see in
the concluding part of this survey. In spite of this, the merit of
a set of explicit criteria, potentially useful to distinguish between two different types of semantic disorders, must
certainly be acknowledged. This is clearly shown by the data
reported in the next section of this review.

4.
Distinction between the non-verbal
conceptual disorders observed in SD and
semantic stroke patients
Recently, the debate over the qualitative aspects and the
mechanisms underlying the non-verbal cognitive disorders of
aphasic patients was strongly influenced by the discovery that
in SD bilateral atrophy of the anterior temporal lobes (ATLs)
provokes a selective semantic impairment that affects more

or less equally all verbal and non-verbal reception and

expression of all kinds of concepts (Lambon Ralph &
Patterson, 2008; Patterson, Nestor, & Rogers, 2007). Therefore, it became necessary to reconsider the problem of the
non-verbal cognitive disorders of aphasic patients by keeping
in mind the following questions: (a) Are there qualitative differences between the multimodal semantic disorder of SD and
the non-verbal cognitive disorders of patients with stroke
aphasia? (b) Which mechanisms underlie the non-verbal
cognitive disorders of patients with stroke aphasia? To
answer these questions, Jefferies and Lambon Ralph (2006)
employed a case-series design to compare SD and
comprehension-impaired aphasic stroke patients directly on
the same battery of semantic tests. Although the two groups
obtained broadly equivalent scores, they showed qualitatively
different semantic deficits. The SD group showed strong correlations between different semantic tasks and substantial
item consistency when the same items were assessed across
different verbal and non-verbal tasks; by contrast, the aphasic
stroke patients showed consistency across different input
modalities but performed inconsistently on tasks requiring
different types of semantic processing. The SD patients were
also highly sensitive to frequency/familiarity factors and
made coordinate and superordinate semantic errors in picture
naming ; by contrast, the aphasic stroke patients were insensitive to familiarity/frequency, made associative semantic
errors in picture naming and improved considerably when
phonemic cues were provided. Furthermore, the aphasic
stroke patients were influenced by the ease with which relevant semantic relationships could be identified and distracters rejected. From the anatomical point of view, aphasic
patients semantic disorders could result from both prefrontal
and temporo-parietal lesions. The authors proposed that the
semantic disorders of SD patients might be due to disruption
of amodal representations and that the semantic disorders of
aphasic stroke patients might result from a defect in the executive processes that help direct and control semantic activation in a task-appropriate fashion. Both the qualitative
differences between SD patients and aphasic stroke patients
and the neuroanatomical lesions subsuming the SA of stroke
patients were confirmed and refined in a number of lather
studies (Corbett et al., 2009; Corbett, Jefferies, & Lambon
Ralph, 2011; Gardner et al., 2012; Jefferies et al., 2007;
Noonan, Jefferies, Corbett, & Lambon Ralph, 2010). Results of
these studies further supported the hypothesis that semantic
disturbances of SD patients and of subjects with stroke
aphasia might be due to disorders affecting semantic representations in a different manner (i.e., a loss of these representations in SD and a defect in the executive processes
controlling their activation in a task-appropriate fashion in
aphasic stroke patients). The model of Jefferies and Lambon
Ralph (2006) is very appealing, well constructed and based
on systematically controlled empirical data. In fact, no previous research on the non-verbal cognitive disorders of
aphasic patients had investigated (with the same set of items)
both verbal and non-verbal cognitive disturbances of aphasic
patients, controlling for the consistency of errors across tasks
and the influence of frequency/familiarity factors. Nevertheless, an interpretation of the non-verbal cognitive disorders of
aphasic patients based simply on a defective controlled

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

activation of semantic representations seems to contrast with

the complexity of the phenomena reported by previous investigations and the mechanisms proposed to account for
them. Furthermore, some of the data reported by Jefferies and
Lambon Ralph (2006), and confirmed in other investigations,
created some difficulty for the model. One of these findings
was that (similar to results of previous investigations) the
cognitive impairment of aphasic stroke patients was not
limited to tasks based on conceptual representations but also
affected performance on tasks based on more abstract material, such as Ravens coloured matrices, on which SD patients
performed rather well but aphasic stroke patients performed
very poorly. We have seen in Section 3.5 of this review that
very low scores on Ravens test had already been observed by
Gainotti, DErme, et al. (1986) in aphasic patients with
semantic-lexical disorders. This observation was considered
inconsistent with the view of a strict causal link between
preverbal conceptual disorders and every form of non-verbal
cognitive disturbance because Ravens Matrices are based on
abstract material and not on stored representations. Thus,
performance on them should not be affected by a disorder
selectively affecting these representations. The observation of
Jefferies and Lambon Ralph (2006) that the performance of
their SD patients on Ravens matrices was largely intact
strongly supports this interpretation. To circumvent this
possible objection, Jefferies and Lambon Ralph (2006) considered Ravens matrices, the WCST, the Brixton Spatial Rule
Attainment task (Burgess & Shallice, 1997) and the Elevator
Counting subtests (Roberson, Ward, Ridgeway, & NimmoSmith, 1994) as executive tests. Poor scores on these tests
were, therefore, taken as confirmation that aphasic patients
pathological performance on non-verbal semantic tests was
due to a defect in executive functions, which allowed controlling the semantic activation of aphasic stroke patients in a
task-appropriate fashion. At this point, it must be noted that
two possible (non-exclusive) models can be considered here
as consistent with the general model proposed by Jefferies and
Lambon Ralph (2006): (a) the first model assumes that there is
a domain-general executive system which interacts with
preverbal semantic cognition in any task that requires
controlled semantic selection, whereas (b) the second model
hypothesizes the existence of domain-specific semantic control mechanisms that dissociate from other executive skills.
These two hypotheses mirror the broader debate about
domain-general (e.g., Duncan, 2005) versus domain-specific
(e.g., Shallice, Stuss, Picton, Alexander, & Gillingham, 2008)
cognitive control/executive systems. In the current context,
the dual impairments of semantic control and non-semantic
executive tasks fit with the domain-general hypothesis,
because the authors found a correlation in the performance of
the SA patients on both types of tasks, which suggests that
domain-general mechanisms may have a role in semantic
cognition. This interpretation contrasts, however, with the
fact that Ravens matrices have usually been considered as a
visual-spatial task or as a problem-solving task (Baldo et al.,
2010; Raven, 1962), but never as an executive test. Considerations similar to those concerning Ravens matrices could be
(more debatably) made with respect to the WCST, because this
test, which is rightly considered an executive test in nonaphasic patients, is based on classification/categorization

85

activities, which have frequently been found impaired in

aphasic patients (De Renzi et al., 1966; Gainotti, Carlomagno,
et al., 1986; Gelb & Goldstein, 1924; Lupyan & Mirman, 2013;
Noppeney & Wallesch, 2000). Furthermore, Baldo et al. (2005)
administered the WCST to stroke patients with and without
aphasia and to normal participants under conditions of
articulatory suppression and showed that language plays a
role in this problem-solving task, possibly through covert
language processes. An objection that could be raised to this
hypothesis is that, according to Baddeleys dual task logic (e.g.,
Baddeley, Baddeley, Bucks, & Wilcock, 2001), the fact that
articulatory suppression affects WCST performance might
reflect a language component in the WCST or might just be a
generic second task effect. Therefore, the meaning of the
pathological results obtained by aphasic stroke patients on
non-verbal cognitive tests based on abstract material (and not
on stored representations) is still controversial, as is the
neuroanatomical substrate of the lesions that should affect
the task-appropriate control of semantic activation in these
patients. Jefferies and Lambon Ralph (2006) claimed and
confirmed in further studies (Corbett et al., 2009, 2011;
Gardner et al., 2012; Jefferies et al., 2007; Noonan et al., 2010)
that the defect in the executive processes that direct and
control semantic activation in a task-appropriate fashion results from both prefrontal and temporo-parietal lesions.
Nevertheless, although the role of the left inferior frontal
cortex in cognitive control mechanisms is generally
acknowledged (e.g., Badre, Hoffman, Cooney, & DEsposito,
2009; Bedny, McGill, & Thompson-Schill, 2008; ThompsonSchill, Bedny, & Goldberg, 2005), the role of the temporoparietal cortex in the control of semantic activation is less
clear. According to Badre, Poldrack, Pare-Blagoev, Insler, and
Wagner (2005), a qualitative difference exists between the
left inferior frontal and middle temporal cortex in semantic
control processes; by contrast, according to Gardner et al.
(2012), the deficit in semantic control is greater in patients
with left prefrontal damage than in those with lesions
affecting the temporo-parietal cortex.
Furthermore, Robinson, Shallice, Bozzali, and Cipolotti
(2010) and Schnur et al. (2009) showed that in aphasic patients poor cognitive control in naming and sentence generation is related to damage in the left inferior frontal cortex, not
the temporo-parietal cortex. On the other hand, a role of
posterior temporal-inferior parietal regions in semantic control is suggested by two recent transcranial magnetic stimulation (TMS) studies by Whitney, Kirk, OSullivan, Lambon
Ralph, and Jefferies (2011, 2012), by a large-scale functional
Magnetic Resonance Imaging (fMRI) meta-analysis by
Noonan, Jefferies, Visser, and Lambon Ralph (2013) and, more
in general by the literature on cognitive control (e.g., Duncan,
2010) and attention (Astafiev et al., 2003), where it is generally
agreed that both parietal and prefrontal regions contribute to
executive processing/topedown attention. Assuming that
white matter pathways interconnecting the frontal (and the
temporo-parietal) regions with the anterior temporal cortices
should be critical for semantic control processes, Harvey, Wei,
Ellmore, Hamilton, and Schnur (2013) examined the role of the
uncinate fasciculus (UF), the inferior longitudinal fasciculus
(ILF) and the inferior fronto-occipital fasciculus (IFOF) in the
control of word comprehension in aphasic patients. They

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c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

showed that only the structural integrity of the UF and the

functional connectivity strength of the regions it connects
(i.e., the left inferior frontal and the anterior temporal cortices)
predicted patients performance, whereas the structural
integrity of the ILF and the IFOF did not predict performance
on semantic control tasks. However, at variance with these
conclusions, Duffau, Herbet, and Moritz-Gasser (2013) have
shown that there is a parietal branch of IFOF that allows direct
connection between parietal regions, posterior temporal and
inferior frontal areas, thus allowing a control network to
emerge. The same authors, used direct electrical stimulation
to compare UF versus IFOF in picture naming and found semantic naming errors only after IFOF stimulation. This contrasts with the claims that UF is the key pathway for semantic
control. It can be concluded that the current literature contains inconsistent findings with regard to the roles of UF and
IFOF (and more in general of the frontal and temporo-parietal
regions) in semantic control.

5.

in aphasic patients are probably due to a multimodal control

deficit that is not ascribable to loss of semantic representations, leaves open a number of questions, tackled in the previous section of the present review. These questions concern:
(a) the extent to which some of the non-verbal cognitive disorders of aphasic patients are not due to a multimodal control
deficit, but to the negative influence of a severe language
disorder on non-verbal cognitive activities; (b) the exact nature of the disturbances affecting the selection and activation
of the structurally unimpaired conceptual representations
and the neuroanatomical correlates of these disorders.. In
spite of these open questions, it must be acknowledged that
the work of Jefferies and Lambon Ralph (2006) has led to a
remarkable breakthrough in explaining the old and controversial issue of the non-verbal cognitive disorders of aphasic
patients.

references

Concluding remarks

The main conclusion that can be drawn from this survey of

the distinction proposed by Jefferies and Lambon Ralph (2006)
between the non-verbal conceptual disorders observed in SD
and in semantic stroke patients is that most of the non-verbal
cognitive disorders observed in aphasic patients are probably
due to a multimodal control deficit that affects the selection
and activation of conceptual representations. The strongest
support for this claim is represented by the qualitative differences observed between SD and aphasic stroke patients.
Indeed, unlike SD patients, aphasic stroke patients perform
inconsistently on tasks requiring different types of semantic
processing. This statement is in keeping with the few, scattered observations made on this subject by previous authors
who checked the correlations between results obtained on
verbal and non-verbal cognitive tasks or the item consistency
of semantic errors made across different tasks by aphasic
patients. As to the first point, the correlation between results
obtained on semantic-lexical and non-verbal cognitive tasks
is far from impressive and rarely exceeds the .50 level
(Chertkow, Bub, Deaudon, & Whitehead, 1997; Gainotti &
Lemmo, 1976). As to the second point, I have already noted
in Section 3.9 that Butterworth et al. (1984) found no consistency between pictures that elicited semantic errors in
comprehension and naming tasks. Furthermore, Silveri,
Carlomagno, Nocentini, Chieffi, and Gainotti (1989) studied
the semantic field integrity of anomic patients with and
without semantic comprehension disorders and found that
the mean number of errors obtained on the various associative categories did not vary as a function of the capacity to
name the corresponding item. On the other hand, Hillis, Rapp,
Romani, and Caramazza (1990) described a patient with a left
fronto-parietal lesion who showed an item-specific selective
semantic-lexical impairment across tasks of oral and written
picture naming, oral reading, writing-to-dictation and tactile
naming. Furthermore, a very similar pattern of item consistency in the verbal modality was reported by Miceli, Capasso,
and Caramazza (1994) in a patient with a left temporal lesion.
Recognizing that most non-verbal cognitive defects observed

Astafiev, S. V., Shulman, G. L., Stanley, C. M., Snyder, A. Z., Van

Essen, D. C., & Corbetta, M. (2003). Functional organization
of human intraparietal and frontal cortex for attending,
looking, and pointing. Journal of Neuroscience, 23(11),
4689e4699.
Baddeley, A. D., Baddeley, H. A., Bucks, R. S., & Wilcock, G. K.
(2001). Attentional control in Alzheimers disease. Brain,
124(8), 1492e1508.
Badre, D., Hoffman, J., Cooney, J. W., & DEsposito, M. (2009).
Hierarchical cognitive control deficits following damage to the
human frontal lobe. Nature Neurosciences, 12(4), 515e522.
Badre, D., Poldrack, R. A., Pare-Blagoev, E. J., Insler, R. Z., &
Wagner, A. D. (2005). Dissociable controlled retrieval and
generalized selection mechanisms in ventrolateral prefrontal
cortex. Neuron, 47(6), 907e918.
Baldo, J. V., Bunge, S. A., Wilson, S. M., & Dronkers, N. F. (2010). Is
relational reasoning dependent on language? A voxel-based
lesion symptom mapping study. Brain and Language, 113(2),
59e64.
Baldo, J. V., Dronkers, N. F., Wilkins, D., Ludy, C., Raskin, P., &
Kim, J. (2005). Is problem solving dependent on language?
Brain and Language, 92(3), 240e250.
Basso, A., De Renzi, E., Faglioni, P., Scotti, G., & Spinnler, H. (1973).
Neuropsychological evidence for the existence of cerebral
areas critical to the performance of intelligence tasks. Brain,
96(4), 715e728.
Basso, A., Faglioni, P., & Spinnler, H. (1976). Non-verbal colour
impairment of aphasics. Neuropsychologia, 14(2), 183e193.
Bay, E. (1962). Aphasia and non-verbal disorders of language.
Brain, 85, 411e426.
Bay, E. (1964). Principles of classification and their influence on
our concepts of aphasia. In A. V. S. Reuck, & M. OConnor
(Eds.), Disorders of language (pp. 122e142). London: Churchill.
Beauvois, M. F., Saillant, B., Meininger, V., & Lhermitte, F. (1978).
Bilateral tactile aphasia: a tacto-verbal dysfunction. Brain,
101(3), 381e401.
Bedny, M., McGill, M., & Thompson-Schill, S. L. (2008). Semantic
adaptation and competition during word comprehension.
Cerebral Cortex, 18(11), 2574e2585.
Beeson, P. M., Bayles, K. A., Rubens, A. B., & Kaszniak, A. W. (1993).
Memory impairment and executive control in individuals with
stroke-induced aphasia. Brain and Language, 45(2), 253e275.
Broca, P. (1861). Perte de la parole, ramollissement chronique et
destruction partielle du lobe anterieur gauche. Bulletin de la
Societe dAnthropologie, 2, 235e238.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

Burgess, P. W., & Shallice, T. (1997). The Hayling and Brixton tests.
Bury St Edmunds: Thames Valley Test Company.
Butterworth, B., Howard, D., & McLoughlin, P. (1984). The
semantic deficit in aphasia: the relationship between
semantic errors in auditory comprehension and picture
naming. Neuropsychologia, 22(4), 409e426.
Caplan, D. (1987). Neurolinguistics and linguistic aphasiology.
Cambridge, UK: Cambridge University Press.
Carruthers, P. (2002). The cognitive functions of language.
Behavioural and Brain Sciences, 25(6), 657e674. discussion
674e725.
Chertkow, H., Bub, D., Deaudon, C., & Whitehead, V. (1997). On
the status of object concepts in aphasia. Brain and Language,
58(2), 203e232.
Clark, A. (1998). Magic words: how language augments human
computation. In P. Carruthers, & J. Boucher (Eds.), Language
and thought: Interdisciplinary themes (pp. 162e183). New York,
NY: Cambridge University Press.
Cohen, R., Engel, D., Kelter, S., List, G., & Strohner, H. (1976).
Restricted associations of aphasics and schizophrenics. Archiv
fur Psychiatrie und Nervenkrankheiten, 222(4), 325e338.
Cohen, R., Glockner, A., Lutz, M., Maier, T., & Meier, E. (1983).
Cognitive impairments in aphasia: new results and new
problems. In R. Bauerle, C. Scwarze, & A. von Stechov (Eds.),
Meaning, use and interpretation of language (pp. 30e45). Berlin:
Walter de Gruyter.
Cohen, R., Glockner-Rist, A., Lutz, M., Maier, T., & Meier, E. (1982).
Cognitive impairments of aphasics in picture sorting and
matching tasks. Archiv fur Psychiatrie und Nervenkrankheiten,
232(3), 223e234.
Cohen, R., & Kelter, S. (1979). Cognitive impairment of aphasics in
a colour-to-picture matching task. Cortex, 15(2), 235e245.
Cohen, R., Kelter, S., & Woll, G. (1980). Analytical competence and
language impairment in aphasia. Brain and Language, 10(2),
331e347.
Cohen, R., & Woll, G. (1981). Facets of analytical processing in
aphasia: a picture ordering task. Cortex, 17(4), 557e569.
Corbett, F., Jefferies, E., Ehsan, S., & Lambon Ralph, M. A. (2009).
Different impairments of semantic cognition in semantic
dementia and semantic aphasia: evidence from the nonverbal domain. Brain, 132(9), 2593e2608.
Corbett, F., Jefferies, E., & Ralph, M. A. (2011). Deregulated
semantic cognition follows prefrontal and temporo-parietal
damage: evidence from the impact of task constraint on
nonverbal object use. Journal of Cognitive Neuroscience, 23(5),
1125e1135.
Crutch, S. J., & Warrington, E. K. (2001). Refractory dyslexia:
evidence of multiple task-specific phonological output stores.
Brain, 124, 1533e1543.
Crutch, S. J., & Warrington, E. K. (2004). The semantic organisation
of proper nouns: the case of people and brand names.
Neuropsychologia, 42, 589e596.
Crutch, S. J., & Warrington, E. K. (2005). Abstract and concrete
concepts have structurally different representational
frameworks. Brain, 128, 615e627.
Darley, F. L. (1982). Aphasia. Philadelphia, PA: WB Sanders.
De Renzi, E., Faglioni, P., Savoiardo, M., & Vignolo, L. A. (1966). The
influence of aphasia and of the hemispheric side of the
cerebral lesion on abstract thinking. Cortex, 2, 399e420.
De Renzi, E., Faglioni, P., Scotti, G., & Spinnler, H. (1972).
Impairment in associating colour to form, concomitant with
aphasia. Brain, 95(2), 293e304.
De Renzi, E., Pieczuro, A., & Vignolo, L. A. (1968). Ideational
apraxia. A quantitative study. Neuropsychologia, 6, 41e52.
De Renzi, E., & Spinnler, H. (1967). Impaired performance on color
tasks in patients with hemispheric damage. Cortex, 3,
194e217.

87

Duffau, H., Herbet, G., & Moritz-Gasser, S. (2013). Toward a

pluri-component, multimodal, and dynamic organization of
the ventral semantic stream in humans: lessons from
stimulation mapping in awake patients. Frontiers in Systems
Neuroscience, 7, 44.
Duffy, R. J., & Duffy, J. R. (1981). Three studies of deficits in
pantomimic expression and pantomimic recognition in
aphasia. Journal of Speech and Hearing Research, 24(1),
70e84.
Duffy, R. J., Duffy, J. R., & Mercaitis, P. A. (1984). Comparison of the
performances of a fluent and a nonfluent aphasic on a
pantomimic referential task. Brain and Language, 21(2),
260e273.
Duffy, R. J., & Liles, B. Z. (1979). A translation of Finkelnburgs
(1870) lecture on aphasia as asymbolia with commentary.
Journal of Speech and Hearing Disorders, 44(2), 156e168.
Duffy, R. J., & McEwen, W. J. (1978). A study of the relationship
between pantomime symbolism and pantomime recognition
in aphasics. Folia Phoniatrica (Basel), 30(4), 286e292.
Duffy, J. R., & Watkins, L. B. (1984). The effect of response choice
relatedness on pantomime and verbal recognition ability in
aphasic patients. Brain and Language, 21(2), 291e306.
Duncan, J. (2005). Frontal lobe function and general intelligence:
why it matters. Cortex, 41(2), 215e217.
Duncan, J. (2010). The multiple-demand (MD) system of the
primate brain: mental programs for intelligent behaviour.
Trends in Cognitive Science, 14(4), 172e179.
Elithorn, A. (1955). A preliminary report on a perceptual maze test
sensitive to brain damage. Journal of Neurology, Neurosurgery,
and Psychiatry, 18(4), 287e292.
Faglioni, P., Spinnler, H., & Vignolo, L. A. (1969). Contrasting
behavior of right and left hemisphere-damaged patients on a
discriminative and a semantic task of auditory recognition.
Cortex, 5(4), 366e389.
Finkelnburg, D. C. (1870). Niederrhenische Gesellschaft, Sitzung
vom 21. Marz 1870 in Bonn. Berliner Klinische Wochenschrift, 7.
pp. 448e450, 460e462.
Gainotti, G. (1982). Some aspects of semantic-lexical impairment
in aphasia. Applied Psycholinguistics, 3, 279e294.
Gainotti, G., Caltagirone, C., & Ibba, A. (1975). Semantic and
phonemic aspects of auditory language comprehension in
aphasia. Linguistics, 154e155, 15e29.
Gainotti, G., Carlomagno, S., Craca, A., & Silveri, M. C. (1986).
Disorders of classificatory activity in aphasia. Brain and
Language, 28(2), 181e195.
Gainotti, G., DErme, P., Villa, G., & Caltagirone, C. (1986). Focal
brain lesions and intelligence: a study with a new version of
Ravens colored matrices. Journal of Clinical and Experimental
Neuropsychology, 8(1), 37e50.
Gainotti, G., & Lemmo, M. S. (1976). Comprehension of symbolic
gestures in aphasia. Brain and Language, 3(3), 451e460.
Gainotti, G., Miceli, G., & Caltagirone, C. (1979). The
relationships between conceptual and semantic-lexical
disorders in aphasia. International Journal of Neuroscience, 10(1),
45e50.
Gainotti, G., Silveri, M. C., Villa, G., & Caltagirone, C. (1983).
Drawing objects from memory in aphasia. Brain, 106(3),
613e622.
Gardner, H. E., Lambon Ralph, M. A., Dodds, N., Jones, T.,
Ehsan, S., & Jefferies, E. (2012). The differential contributions
of pFC and temporo-parietal cortex to multimodal semantic
control: exploring refractory effects in semantic aphasia.
Journal of Cognitive Neuroscience, 24(4), 778e793.
Gelb, A., & Goldstein, K. (1924). Psychologische Analysen
Hirnpathologischer Falle. Leipzig: Barth.
Geschwind, N., & Fusillo, M. (1966). Color-naming defects in
association with alexia. Archives of Neurology, 15(2), 137e146.

88

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

Glosser, G., & Goodglass, H. (1990). Disorders in executive control

functions among aphasic and other brain-damaged patients.
Journal of Clinical and Experimental Neuropsychology, 12, 485e501.
Goldstein, K. (1936). The problem of the meaning of words. Journal
of Psychology, 2.
Goldstein, K. (1948). Language and language disturbances. New York:
Grune & Stratton.
Gottschaldt, K. (1929). On the effect of experience on figure
perception. Psychologische Forschung, 12, 1e87.
Hagoort, P. (1998). The shadows of lexical meaning in patients
with semantic impairment. In B. Stemmer, & H. Whitaker
(Eds.), Handbook of neurolinguistics (pp. 235e248). New York:
Academic Press.
Harvey, D. Y., Wei, T., Ellmore, T. M., Hamilton, A. C., &
Schnur, T. T. (2013). Neuropsychological evidence for the
functional role of the uncinate fasciculus in semantic control.
Neuropsychologia, 51(5), 789e801.
Head, H. (1926). Aphasia and kindred disorders of speech. New York:
Macmillan.
Helm-Estabrooks, N. (2002). Cognition and aphasia: a discussion
and a study. Journal of Communication Disorders, 35(2), 171e186.
Hillis, A. E., Rapp, B. C., Romani, C., & Caramazza, A. (1990).
Selective impairment of semantics in lexical processing.
Cognitive Neuropsychology, 7, 191e243.
Jackson, J. H. (1878). On affections of speech from disease of the
brain. Brain, 1, 304e330.
Jefferies, E., Baker, S. S., Doran, M., & Lambon Ralph, M. A. (2007).
Refractory effects in stroke aphasia: a consequence of poor
semantic control. Neuropsychologia, 45(5), 1065e1079.
Jefferies, E., & Lambon Ralph, M. A. (2006). Semantic impairment
in stroke aphasia versus semantic dementia: a case-series
comparison. Brain, 129(8), 2132e2147.
Johnsen, B. (1992). Aphasia and its relation to language and
thinking. Finding alternative ways for communication.
Scandinavian Journal of Rehabilitation Medicine, 26, 70e78.
Keil, K., & Kasniak, A. W. (2002). Examining executive function in
individuals with brain injury: a review. Aphasiology, 16,
305e335.
Kelter, S., Cohen, R., Engel, D., List, G., & Strohner, H. (1976).
Aphasic disorders in matching tasks involving conceptual
analysis and covert naming. Cortex, 12(4), 383e394.
Koemeda-Lutz, M., Cohen, R., & Meier, E. (1987). Organization of
and access to semantic memory in aphasia. Brain and
Language, 30(2), 321e337.
Lambon Ralph, M. A., & Patterson, K. (2008). Generalization and
differentiation in semantic memory insights from semantic
dementia. Annals of the New York Academy of Sciences, 1124,
61e76.
Lhermitte, F., & Beauvois, M. F. (1973). A visual-speech
disconnexion syndrome. Report of a case with optic aphasia,
agnosic alexia and colour agnosia. Brain, 96(4), 695e714.
Lupyan, G., & Mirman, D. (2013). Linking language and
categorization: evidence from aphasia. Cortex, 49(5),
1187e1194.
Marie, P. (1906). La troisie`me circonvolution frontale gauche ne
joue aucun role special dans la fonction du langage. Semaine
Medicale, 26, 241e247.
McNeil, M. R. (1982). The nature of aphasia in adults. In N. J. Lass,
L. V. McReynolds, J. L. Northern, & D. E. Yoder (Eds.), Speech,
language and hearing: Vol. III. Pathologies of speech and language
(pp. 692e740). Philadelphia, PA: WB Sanders.
McNeil, M. R. (1988). Aphasia in the adults. In N. J. Lass,
L. V. McReynolds, J. L. Northern, & D. E. Yoder (Eds.), Handbook
of speech-language pathology and audiology (pp. 738e786).
Philadelphia, PA: WB Sanders.
McNeil, M. R., & Pratt, S. R. (2001). Defining aphasia: some
theoretical and clinical implications of operating from a
formal definition. Aphasiology, 15, 901e911.

Miceli, G., Capasso, R., & Caramazza, A. (1994). The interaction of

lexical and sublexical processes in reading, writing and
repetition. Neuropsychologia, 32, 317e333.
Milner, B. (1963). Effects of different brain lesions on card sorting.
Archives of Neurology, 9, 100e110.
Noonan, K. A., Jefferies, E., Corbett, F., & Lambon Ralph, M. A.
(2010). Elucidating the nature of deregulated semantic
cognition in semantic aphasia: evidence for the roles of
prefrontal and temporo-parietal cortices. Journal of Cognitive
Neuroscience, 22(7), 1597e1613.
Noonan, K. A., Jefferies, E., Visser, M., & Lambon Ralph, M. A.
(2013). Going beyond inferior prefrontal involvement in
semantic control: evidence for the additional contribution of
dorsal angular gyrus and posterior middle temporal cortex.
Journal of Cognitive Neuroscience, 25(11), 1824e1850.
Noppeney, U., & Wallesch, C. W. (2000). Language and cognition Kurt Goldsteins theory of semantics. Brain and Cognition, 44(3),
367e386.
Patterson, K., Nestor, P. J., & Rogers, T. T. (2007). Where do you
know what you know? The representation of semantic
knowledge in the human brain. Nature Reviews Neuroscience,
8(12), 976e987.
Purdy, M. (2002). Executive function ability in persons with
aphasia. Aphasiology, 16, 549e557.
Rapp, B. C., & Caramazza, A. (1993). On the distinction between
deficits of access and deficits of storage: a question of theory.
Cognitive Neuropsychology, 10, 113e141.
Raven, J. (1962). Coloured progressive matrices. New York: The
Psychological Corporation.
Roberson, I. H., Ward, T., Ridgeway, V., & Nimmo-Smith, I. (1994).
The test of everyday attention. Bury St Edmunds: Thames Valley
Test Company.
Robinson, G., Shallice, T., Bozzali, M., & Cipolotti, L. (2010).
Conceptual proposition selection and the LIFG:
neuropsychological evidence from a focal frontal group.
Neuropsychologia, 48(6), 1652e1663.
Schnur, T. T., Schwartz, M. F., Kimberg, D. Y., Hirshorn, E.,
Coslett, H. B., & Thompson-Schill, S. L. (2009). Localizing
interference during naming: convergent neuroimaging and
neuropsychological evidence for the function of Brocas area.
Proceedings of the National Academy of Sciences USA, 106(1),
322e327.
Shallice, T. (1982). Specific impairments of planning. Philosophical
Transactions of the Royal Society of London. Series B, Biological
Sciences, 298(1089), 199e209.
Shallice, T. (1988). From neuropsychology to mental structure.
Cambridge, UK: Cambridge University Press.
Shallice, T., Stuss, D. T., Picton, T. W., Alexander, M. P., &
Gillingham, S. (2008 Mar 28). Multiple effects of prefrontal
lesions on task-switching. Frontiers Human Neuroscience, 1, 2.
Silveri, M. C., Carlomagno, S., Nocentini, U., Chieffi, S., &
Gainotti, G. (1989). Semantic field integrity and naming ability
in anomic patients. Aphasiology, 3, 423e434.
Spinnler, H., & Vignolo, L. A. (1966). Impaired recognition of
meaningful sounds. Cortex, 2, 337e348.
Thompson-Schill, S. L., Bedny, M., & Goldberg, R. F. (2005). The
frontal lobes and the regulation of mental activity. Current
Opinion in Neurobiology, 15(2), 219e224.
Trousseau, A. (1865). Clinique Medicale de lHotel Dieu de Paris. Paris:
Baillie`re.
Varney, N. R. (1978). Linguistic correlates of pantomime
recognition in aphasic patients. Journal of Neurology,
Neurosurgery, and Psychiatry, 41(6), 564e568.
Varney, N. R. (1982). Pantomime recognition defect in aphasia:
implications for the concept of asymbolia. Brain and Language,
15(1), 32e39.
Vigotsky, L. S. (1962). In E. Haufmann, & G. Valker (Eds.), Thought
and language. Cambridge, MA: MIT Press.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8 e8 9

Warrington, E. K. (1975). The selective impairment of semantic

memory. Quarterly Journal of Experimental Psychology, 27, 635e657.
Warrington, E. K., & Cipolotti, L. (1996). Word comprehension: the
distinction between refractory and storage impairment. Brain,
119, 611e625.
Warrington, E. K., & McCarthy, R. (1983). Category-specific access
dysphasia. Brain, 106, 859e878.
Warrington, E. K., & McCarthy, R. (1987). Categories of knowledge:
further fractionations and an attempted integration. Brain,
110, 1465e1473.
Warrington, E. K., & Shallice, T. (1979). Semantic access dyslexia.
Brain, 102, 43e63.
Weigl, E. (1941). On the psychology of so-called processes of
abstraction. Journal of Abnormal and Social Psychology, 36(1), 3e33.
Weisenburg, T. H., & McBride, K. E. (1935). Aphasia: A clinical and
psychological study. New York: Commonwealth Fund Hildred
and Co.

89

Whitney, C., Kirk, M., OSullivan, J., Lambon Ralph, M. A., &
Jefferies, E. (2011). The neural organization of semantic
control: TMS evidence for a distributed network in left inferior
frontal and posterior middle temporal gyrus. Cerebral Cortex,
21(5), 1066e1075.
Whitney, C., Kirk, M., OSullivan, J., Lambon Ralph, M. A., &
Jefferies, E. (2012). Executive semantic processing is
underpinned by a large-scale neural network: revealing the
contribution of left prefrontal, posterior temporal, and parietal
cortex to controlled retrieval and selection using TMS. Journal
of Cognitive Neuroscience, 24(1), 133e147.
Zangwill, O. L. (1969). Intellectual status in aphasia. In P. J. Vinken, &
G. W. Bruyn (Eds.), Handbook of clinical neurology (Vol. 4); (pp.
105e111). Amsterdam: North-Holland Publishing.