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Review

Old and recent approaches to the problem of non-verbal conceptual disorders in aphasic patients

Guido Gainotti a,b,*aCenter for Neuropsychological Research and Institute of Neurology of the Catholic University of Rome, Italyb IRCCS Fondazione Santa Lucia, Department of Clinical and Behavioral Neurology, Rome, Italy

a r t i c l e i n f o

Article history:

Received 17 September 2013

Reviewed 11 November 2013

Revised 19 November 2013

Accepted 16 January 2014

Action editor Marjorie Lorch

Published online 28 January 2014

Keywords:

Aphasic non-verbal

cognitive disorders

Preverbal conceptual disturbances

Defective semantic

activation control

Verbal mediation hypothesis

* Center for Neuropsychological Research,00168 Roma, Italy.

E-mail addresses: gainotti@rm.unicatt.it,0010-9452/$ e see front matter ª 2014 Elsevhttp://dx.doi.org/10.1016/j.cortex.2014.01.009

a b s t r a c t

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

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

can actually be solvedwithout the use of language. In this survey, I will discuss in a historical

perspective the different interpretations provided by classical and contemporary authors to

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

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

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

systematic investigations using methods drawn from experimental psychology, to clarify

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

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

have tried to analyse andexplain thedifferences between thenon-verbal semantic defects of

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

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

preverbal conceptual disorder, which cannot be attributed to a loss of semantic represen-

tations but rather to a defect in their controlled retrieval, seems substantially confirmed.

Nevertheless, twomain issuesmust 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 dis-

turbances 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.

ª 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

Institute of Neurology, Po

g.gainotti@hsantalucia.itier Ltd. All rights reserve

of verbal communication disorders but often have great dif-

ficulty 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

liclinico Gemelli, Catholic University of Rome, Largo A. Gemelli, 8,

.d.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 9 79

(e.g., Finkelnburg, 1870) or conceptual (e.g., Bay, 1962) activ-

ities 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 pro-

ponents 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 task-

appropriate control of semantic retrieval/activation.

In the present review, I intend to survey this very complex

issue froma historical perspective. I will first take into account

the pioneers of modern neurolinguistics who, after Broca’s

(1861) discovery, proposed different explanations of the non-

verbal cognitive disturbances observed in patients with se-

vere 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 experi-

mental data relevant to this issue. Finally, in the last part of

the survey I will discuss how this problem has been consid-

ered by proponents of the ‘semantic hub hypothesis’, partic-

ularly 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 dis-

orders 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 be-

tween the points on which a wide consensus seems to have

been reached and those that are still open and require further

investigation.

2. Early proponents of a non-verbal cognitiveimpairment in aphasia

2.1. Trousseau and the ancillary use of words forcognitive 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 activ-

ities that can be performed without the ancillary use of words

and other (higher) cognitive activities that cannot be per-

formed without the thought formulae (“formules de la pen-

see”) that are represented by words. The former are usually

spared in aphasic patients, but the latter are often impaired.

2.2. 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 panto-

mime 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 impair-

ment 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 consid-

ered representatives of the ‘Noetic School’.

2.3. Marie and the impairment of ‘intelligence’ inaphasia

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 distur-

bances 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 ‘semanticmemory’.

This suggestion is supported by Marie’s definition of ‘intelli-

gence’, considered as a sphere “where are stored, among

others, various aspects of didactically acquired knowledge”.

2.4. 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 ‘intelli-

gence’. Pursuing Finkelnburg’s (l870) and Jackson’s (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 cogni-

tive tasks that can be performed with simple perceptual ac-

tivity, 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 ac-

tivity between the initial conception and the final execution of

the act.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 980

2.5. Goldstein and loss of the abstract attitude inaphasia

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 dis-

turbances in aphasia (Noppeney & Wallesch, 2000). Together

with Gelb, he studied the naming disorders of First WorldWar

brain-injured (Gelb & Goldstein, 1924). These authors

concluded that the naming impairment is only a manifesta-

tion of amore 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, in-

fluences 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 consid-

ered 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 distin-

guished from other forms of language. To be sure, these au-

thors 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

aphasiawas the frail body of data provided by these authors to

support their theories. Their arguments consisted of individ-

ual 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 van-

tage 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 non-

verbal aspects of processing in their patients using the rudi-

ments of formal testing. Head, in particular, used an impres-

sive systematic neuropsychological battery, and Goldstein

used a forerunner of Weigl’s 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 pre-

vious authors, in particular by Head.

3. The application of methods drawn fromexperimental psychology to study non-verbalcognitive disorders in aphasia

3.1. The psychometric studies of Weisenburg andMcBride

Weisenburg and McBride (1935) were the first authors to

investigate the non-verbal cognitive disorders of aphasic pa-

tients using designs and procedures drawn from the field of

experimental psychology. However, the cognitive tasks they

usedwere 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 actualizationof 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 non-

verbal 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 antici-

pated 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 Bay’s observations was raised

by Zangwill (1969), who noted that Bay had provided no con-

trol data on the modelling capacities of brain-damaged

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 9 81

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 usedby 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

Raven’s Progressive Matrices (Raven, 1962), Elithorn’s

Perceptual Maze test (Elithorn, 1955), Gottschaldt’s

Hidden Figures test (1929) and Weigl’s 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 pa-

tients 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 Weigl’s 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

functionally independent, structures might subsume lan-

guage and non-verbal cognitive abilities.

3.4. Duffy and the construct of a central symbolic defectin 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

Finkelnburg’s (1870) concept of “asymbolia”. After prompting

the translation into English of Finkelnburg’s main article

(Duffy & Liles, 1979), Duffy provided the following experi-

mental evidence in support of his contention:

1. In aphasia, a strong relationship exists between scores

obtained on tests of pantomime expression and panto-

mime 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 re-

duces 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 Duffy’s

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 panto-

mime recognition defects are more strongly related to disor-

ders of reading comprehension than auditory comprehension.

It must be acknowledged, however, that both of these objec-

tions 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 recogni-

tion) 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 cognitiveimpairment and semantic disintegration in aphasia

Gainotti et al. (Gainotti, Carlomagno, Craca, & Silveri, 1986;

Gainotti, D’Erme, Villa, & Caltagirone, 1986; Gainotti &

Lemmo, 1976; Gainotti, Miceli, & Caltagirone, 1979; Gainotti,

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 982

Silveri, Villa, & Caltagirone, 1983) made the following as-

sumptions: (a) only some components of aphasia are inti-

mately 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 sub-

set 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 pa-

tients 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) Raven’s coloured matrices (Gainotti,

D’Erme, et al., 1986). The presence of a semantic-lexical

impairment at the receptive level was assessed by

measuring the number of semantic errorsmade 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 non-

verbal cognitive impairment and the presence of a semantic-

lexical 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 phe-

nomena. In fact, the presence of a semantic-lexical disorder

also had a strongly negative effect on results obtained with

Raven’s 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 ofconcepts’ 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 patientsmay be due to a ‘defective analytical isolation

of individual features of concepts’. This hypothesis can be

considered an updated and more precise reformulation of

Goldstein’s (1948) view, because it replaces the construct of

“loss of the abstract attitude” (which is too general and diffi-

cult 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 individ-

ual features of concepts accounted not only for results ob-

tained 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) substan-

tially 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 posi-

tions 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 pre-

verbal 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 co-

workers, it consists of disruption of the conceptual represen-

tations subsuming both semantic-lexical knowledge and non-

verbal 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 Weigl’s test of abstract thinking, by Gainotti, D’Erme,

et al. (1986) with Raven’s coloured matrices and by Cohen

and colleagues, who checked the ‘defective analytical isola-

tion of individual features of concepts’ hypothesis, show that

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 9 83

only some of the non-verbal cognitive disorders of aphasic

patients are due to an underlying basic (symbolic or concep-

tual) 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 mis-

naming 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 ob-

jects he recognized, as was suggested by his ability to mime

their use. Occasionally, however, he showed semantic “para-

praxias” (e.g., he used a toothbrush like a comb). Suspecting

that thesemiming errorsmight be due to an implicit semantic

paraphasia, Beauvois et al. (1978) inhibited verbal mediation

by giving special instructions and placing adhesive tape over

the patient’s mouth. In these conditions, semantic para-

phasias 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 cognitivedisorders 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 pa-

tients 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, short-

term memory or attentional resources, which make it diffi-

cult 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.,

Beeson, Bayles, Rubens, & Kaszniak, 1993; Purdy, 2002) indi-

cate 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 Kasniak’s (2002)

review documented that this can be a problem for in-

dividuals 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 non-

verbal 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 significantlymore 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

Wernicke’s 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 relation-

ships between linguistic and non-linguistic skills supporting

communication processes, were also thoroughly investigated

in rehabilitation studies by Johnsen (1992) and Helm-

Estabrooks (2002). The former used computerized pictorial

communication as an aid for aphasic patients and found no

systematic relationships between linguistic and non-linguis-

tic skills; indeed, in some patients communication distur-

bances 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 be-

tween linguistic and non-linguistic skills of attention, mem-

ory, executive function and visuospatial abilities, but observed

individual profiles of strengths and weaknesses in these non-

linguistic 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 anddifficulty 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 dif-

ferentiation 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

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 984

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 infor-

mation 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 dis-

tinguishing 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 cri-

terion 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 auto-

matic access to the same information (such as the ‘semantic

priming’ effect). The last criterion, stressed byWarrington 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 crite-

rion, increasing the inter-trial interval should not improve

performance in semantic defects resulting from a loss of in-

formation, 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 be-

tween 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-verbalconceptual disorders observed in SD andsemantic 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). There-

fore, 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 dif-

ferences between themultimodal 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 cor-

relations 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 insen-

sitive 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 rele-

vant semantic relationships could be identified and dis-

tracters 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 ex-

ecutive processes that help direct and control semantic acti-

vation 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 repre-

sentations in a different manner (i.e., a loss of these repre-

sentations 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 pre-

vious 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. Neverthe-

less, 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 8e8 9 85

activation of semantic representations seems to contrast with

the complexity of the phenomena reported by previous in-

vestigations 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 mate-

rial, such as Raven’s 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 Raven’s test had already been observed by

Gainotti, D’Erme, 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 Raven’s 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 Raven’s matrices was largely intact

strongly supports this interpretation. To circumvent this

possible objection, Jefferies and Lambon Ralph (2006) consid-

ered Raven’s matrices, the WCST, the Brixton Spatial Rule

Attainment task (Burgess & Shallice, 1997) and the Elevator

Counting subtests (Roberson, Ward, Ridgeway, & Nimmo-

Smith, 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 con-

trolling 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 consistentwith the generalmodel 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 con-

trol 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 Raven’s 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. Consider-

ations similar to those concerning Raven’s matrices could be

(more debatably)madewith respect to theWCST, because this

test, which is rightly considered an executive test in non-

aphasic patients, is based on classification/categorization

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 Baddeley’s 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 re-

sults 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, & D’Esposito,

2009; Bedny, McGill, & Thompson-Schill, 2008; Thompson-

Schill, Bedny, & Goldberg, 2005), the role of the temporo-

parietal 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 pa-

tients poor cognitive control in naming and sentence gener-

ation 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 con-

trol is suggested by two recent transcranial magnetic stimu-

lation (TMS) studies by Whitney, Kirk, O’Sullivan, 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

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 986

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 se-

mantic naming errors only after IFOF stimulation. This con-

trasts with the claims that UF is the key pathway for semantic

control. It can be concluded that the current literature con-

tains 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. 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 dif-

ferences 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, scat-

tered 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 consis-

tency 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 associa-

tive 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 consis-

tency 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

in aphasic patients are probably due to a multimodal control

deficit that is not ascribable to loss of semantic representa-

tions, leaves open a number of questions, tackled in the pre-

vious section of the present review. These questions concern:

(a) the extent to which some of the non-verbal cognitive dis-

orders of aphasic patients are not due to amultimodal control

deficit, but to the negative influence of a severe language

disorder on non-verbal cognitive activities; (b) the exact na-

ture 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 contro-

versial issue of the non-verbal cognitive disorders of aphasic

patients.

r e f e r e n c e s

Astafiev, S. V., Shulman, G. L., Stanley, C. M., Snyder, A. Z., VanEssen, D. C., & Corbetta, M. (2003). Functional organizationof 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 Alzheimer’s disease. Brain,124(8), 1492e1508.

Badre, D., Hoffman, J., Cooney, J. W., & D’Esposito, M. (2009).Hierarchical cognitive control deficits following damage to thehuman 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 andgeneralized selection mechanisms in ventrolateral prefrontalcortex. Neuron, 47(6), 907e918.

Baldo, J. V., Bunge, S. A., Wilson, S. M., & Dronkers, N. F. (2010). Isrelational reasoning dependent on language? A voxel-basedlesion 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 cerebralareas critical to the performance of intelligence tasks. Brain,96(4), 715e728.

Basso, A., Faglioni, P., & Spinnler, H. (1976). Non-verbal colourimpairment 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 onour concepts of aphasia. In A. V. S. Reuck, & M. O’Connor(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). Semanticadaptation 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 withstroke-induced aphasia. Brain and Language, 45(2), 253e275.

Broca, P. (1861). Perte de la parole, ramollissement chronique etdestruction partielle du lobe anterieur gauche. Bulletin de laSociete d’Anthropologie, 2, 235e238.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 9 87

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). Thesemantic deficit in aphasia: the relationship betweensemantic errors in auditory comprehension and picturenaming. 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. discussion674e725.

Chertkow, H., Bub, D., Deaudon, C., & Whitehead, V. (1997). Onthe status of object concepts in aphasia. Brain and Language,58(2), 203e232.

Clark, A. (1998). Magic words: how language augments humancomputation. In P. Carruthers, & J. Boucher (Eds.), Languageand 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. Archivfur Psychiatrie und Nervenkrankheiten, 222(4), 325e338.

Cohen, R., Glockner, A., Lutz, M., Maier, T., & Meier, E. (1983).Cognitive impairments in aphasia: new results and newproblems. 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 andmatching tasks. Archiv fur Psychiatrie und Nervenkrankheiten,232(3), 223e234.

Cohen, R., & Kelter, S. (1979). Cognitive impairment of aphasics ina colour-to-picture matching task. Cortex, 15(2), 235e245.

Cohen, R., Kelter, S., & Woll, G. (1980). Analytical competence andlanguage impairment in aphasia. Brain and Language, 10(2),331e347.

Cohen, R., & Woll, G. (1981). Facets of analytical processing inaphasia: 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 semanticdementia and semantic aphasia: evidence from the non-verbal domain. Brain, 132(9), 2593e2608.

Corbett, F., Jefferies, E., & Ralph, M. A. (2011). Deregulatedsemantic cognition follows prefrontal and temporo-parietaldamage: evidence from the impact of task constraint onnonverbal 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 organisationof proper nouns: the case of people and brand names.Neuropsychologia, 42, 589e596.

Crutch, S. J., & Warrington, E. K. (2005). Abstract and concreteconcepts have structurally different representationalframeworks. 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 thecerebral lesion on abstract thinking. Cortex, 2, 399e420.

De Renzi, E., Faglioni, P., Scotti, G., & Spinnler, H. (1972).Impairment in associating colour to form, concomitant withaphasia. Brain, 95(2), 293e304.

De Renzi, E., Pieczuro, A., & Vignolo, L. A. (1968). Ideationalapraxia. A quantitative study. Neuropsychologia, 6, 41e52.

De Renzi, E., & Spinnler, H. (1967). Impaired performance on colortasks in patients with hemispheric damage. Cortex, 3,194e217.

Duffau, H., Herbet, G., & Moritz-Gasser, S. (2013). Toward apluri-component, multimodal, and dynamic organization ofthe ventral semantic stream in humans: lessons fromstimulation mapping in awake patients. Frontiers in SystemsNeuroscience, 7, 44.

Duffy, R. J., & Duffy, J. R. (1981). Three studies of deficits inpantomimic expression and pantomimic recognition inaphasia. Journal of Speech and Hearing Research, 24(1),70e84.

Duffy, R. J., Duffy, J. R., & Mercaitis, P. A. (1984). Comparison of theperformances of a fluent and a nonfluent aphasic on apantomimic referential task. Brain and Language, 21(2),260e273.

Duffy, R. J., & Liles, B. Z. (1979). A translation of Finkelnburg’s(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 relationshipbetween pantomime symbolism and pantomime recognitionin aphasics. Folia Phoniatrica (Basel), 30(4), 286e292.

Duffy, J. R., & Watkins, L. B. (1984). The effect of response choicerelatedness on pantomime and verbal recognition ability inaphasic 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 theprimate brain: mental programs for intelligent behaviour.Trends in Cognitive Science, 14(4), 172e179.

Elithorn, A. (1955). A preliminary report on a perceptual maze testsensitive to brain damage. Journal of Neurology, Neurosurgery,and Psychiatry, 18(4), 287e292.

Faglioni, P., Spinnler, H., & Vignolo, L. A. (1969). Contrastingbehavior of right and left hemisphere-damaged patients on adiscriminative and a semantic task of auditory recognition.Cortex, 5(4), 366e389.

Finkelnburg, D. C. (1870). Niederrhenische Gesellschaft, Sitzungvom 21. Marz 1870 in Bonn. Berliner Klinische Wochenschrift, 7.pp. 448e450, 460e462.

Gainotti, G. (1982). Some aspects of semantic-lexical impairmentin aphasia. Applied Psycholinguistics, 3, 279e294.

Gainotti, G., Caltagirone, C., & Ibba, A. (1975). Semantic andphonemic aspects of auditory language comprehension inaphasia. Linguistics, 154e155, 15e29.

Gainotti, G., Carlomagno, S., Craca, A., & Silveri, M. C. (1986).Disorders of classificatory activity in aphasia. Brain andLanguage, 28(2), 181e195.

Gainotti, G., D’Erme, P., Villa, G., & Caltagirone, C. (1986). Focalbrain lesions and intelligence: a study with a new version ofRaven’s colored matrices. Journal of Clinical and ExperimentalNeuropsychology, 8(1), 37e50.

Gainotti, G., & Lemmo, M. S. (1976). Comprehension of symbolicgestures in aphasia. Brain and Language, 3(3), 451e460.

Gainotti, G., Miceli, G., & Caltagirone, C. (1979). Therelationships between conceptual and semantic-lexicaldisorders 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 contributionsof pFC and temporo-parietal cortex to multimodal semanticcontrol: exploring refractory effects in semantic aphasia.Journal of Cognitive Neuroscience, 24(4), 778e793.

Gelb, A., & Goldstein, K. (1924). Psychologische AnalysenHirnpathologischer Falle. Leipzig: Barth.

Geschwind, N., & Fusillo, M. (1966). Color-naming defects inassociation with alexia. Archives of Neurology, 15(2), 137e146.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 988

Glosser, G., & Goodglass, H. (1990). Disorders in executive controlfunctions 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. Journalof Psychology, 2.

Goldstein, K. (1948). Language and language disturbances. New York:Grune & Stratton.

Gottschaldt, K. (1929). On the effect of experience on figureperception. Psychologische Forschung, 12, 1e87.

Hagoort, P. (1998). The shadows of lexical meaning in patientswith 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 thefunctional 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 discussionand 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 thebrain. Brain, 1, 304e330.

Jefferies, E., Baker, S. S., Doran, M., & Lambon Ralph, M. A. (2007).Refractory effects in stroke aphasia: a consequence of poorsemantic control. Neuropsychologia, 45(5), 1065e1079.

Jefferies, E., & Lambon Ralph, M. A. (2006). Semantic impairmentin stroke aphasia versus semantic dementia: a case-seriescomparison. Brain, 129(8), 2132e2147.

Johnsen, B. (1992). Aphasia and its relation to language andthinking. Finding alternative ways for communication.Scandinavian Journal of Rehabilitation Medicine, 26, 70e78.

Keil, K., & Kasniak, A. W. (2002). Examining executive function inindividuals 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 conceptualanalysis and covert naming. Cortex, 12(4), 383e394.

Koemeda-Lutz, M., Cohen, R., & Meier, E. (1987). Organization ofand access to semantic memory in aphasia. Brain andLanguage, 30(2), 321e337.

Lambon Ralph, M. A., & Patterson, K. (2008). Generalization anddifferentiation in semantic memory insights from semanticdementia. Annals of the New York Academy of Sciences, 1124,61e76.

Lhermitte, F., & Beauvois, M. F. (1973). A visual-speechdisconnexion syndrome. Report of a case with optic aphasia,agnosic alexia and colour agnosia. Brain, 96(4), 695e714.

Lupyan, G., & Mirman, D. (2013). Linking language andcategorization: evidence from aphasia. Cortex, 49(5),1187e1194.

Marie, P. (1906). La troisieme circonvolution frontale gauche nejoue aucun role special dans la fonction du langage. SemaineMedicale, 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.), Handbookof speech-language pathology and audiology (pp. 738e786).Philadelphia, PA: WB Sanders.

McNeil, M. R., & Pratt, S. R. (2001). Defining aphasia: sometheoretical and clinical implications of operating from aformal definition. Aphasiology, 15, 901e911.

Miceli, G., Capasso, R., & Caramazza, A. (1994). The interaction oflexical and sublexical processes in reading, writing andrepetition. 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 semanticcognition in semantic aphasia: evidence for the roles ofprefrontal and temporo-parietal cortices. Journal of CognitiveNeuroscience, 22(7), 1597e1613.

Noonan, K. A., Jefferies, E., Visser, M., & Lambon Ralph, M. A.(2013). Going beyond inferior prefrontal involvement insemantic control: evidence for the additional contribution ofdorsal angular gyrus and posterior middle temporal cortex.Journal of Cognitive Neuroscience, 25(11), 1824e1850.

Noppeney, U., & Wallesch, C. W. (2000). Language and cognition -Kurt Goldstein’s theory of semantics. Brain and Cognition, 44(3),367e386.

Patterson, K., Nestor, P. J., & Rogers, T. T. (2007). Where do youknow what you know? The representation of semanticknowledge in the human brain. Nature Reviews Neuroscience,8(12), 976e987.

Purdy, M. (2002). Executive function ability in persons withaphasia. Aphasiology, 16, 549e557.

Rapp, B. C., & Caramazza, A. (1993). On the distinction betweendeficits of access and deficits of storage: a question of theory.Cognitive Neuropsychology, 10, 113e141.

Raven, J. (1962). Coloured progressive matrices. New York: ThePsychological Corporation.

Roberson, I. H., Ward, T., Ridgeway, V., & Nimmo-Smith, I. (1994).The test of everyday attention. Bury St Edmunds: Thames ValleyTest 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). Localizinginterference during naming: convergent neuroimaging andneuropsychological evidence for the function of Broca’s area.Proceedings of the National Academy of Sciences USA, 106(1),322e327.

Shallice, T. (1982). Specific impairments of planning. PhilosophicalTransactions of the Royal Society of London. Series B, BiologicalSciences, 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 prefrontallesions 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 abilityin anomic patients. Aphasiology, 3, 423e434.

Spinnler, H., & Vignolo, L. A. (1966). Impaired recognition ofmeaningful sounds. Cortex, 2, 337e348.

Thompson-Schill, S. L., Bedny, M., & Goldberg, R. F. (2005). Thefrontal lobes and the regulation of mental activity. CurrentOpinion in Neurobiology, 15(2), 219e224.

Trousseau, A. (1865). Clinique Medicale de l’Hotel Dieu de Paris. Paris:Bailliere.

Varney, N. R. (1978). Linguistic correlates of pantomimerecognition 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.), Thoughtand language. Cambridge, MA: MIT Press.

c o r t e x 5 3 ( 2 0 1 4 ) 7 8e8 9 89

Warrington, E. K. (1975). The selective impairment of semanticmemory.Quarterly Journal of ExperimentalPsychology, 27, 635e657.

Warrington, E. K., & Cipolotti, L. (1996). Word comprehension: thedistinction between refractory and storage impairment. Brain,119, 611e625.

Warrington, E. K., & McCarthy, R. (1983). Category-specific accessdysphasia. 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 ofabstraction. Journal ofAbnormal and Social Psychology, 36(1), 3e33.

Weisenburg, T. H., & McBride, K. E. (1935). Aphasia: A clinical andpsychological study. New York: Commonwealth Fund Hildredand Co.

Whitney, C., Kirk, M., O’Sullivan, J., Lambon Ralph, M. A., &Jefferies, E. (2011). The neural organization of semanticcontrol: TMS evidence for a distributed network in left inferiorfrontal and posterior middle temporal gyrus. Cerebral Cortex,21(5), 1066e1075.

Whitney, C., Kirk, M., O’Sullivan, J., Lambon Ralph, M. A., &Jefferies, E. (2012). Executive semantic processing isunderpinned by a large-scale neural network: revealing thecontribution of left prefrontal, posterior temporal, and parietalcortex to controlled retrieval and selection using TMS. Journalof 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.