“Because without our language, we have lost ourselves. Who are we without our words?” Melina Marchetta, Finnikin of the Rock
TABLE OF CONTENTS
Introduction 6
1. Single-patient studies 1.1 Cognitive neuropsychology...11
1.1.2 Single case studies...12
1.1.3 Modality-specific deficit...15
1.2 Aphasia...20
1.2.1 Aetiology...24
1.2.2 Brief history of aphasiology...25
1.2.3 Present-day classification...28
1.2.4 Fluent aphasias...29
1.2.5 Nonfluent aphasias...32
1.2.6 Primary progressive aphasia...34
1.2.7 Verb-selective deficit in nonfluent PPA...38
1.3 Nouns and verbs in the brain...40
1.3.1 Morphosyntax/semantics interface and patient MC...53
1.3.2 Patient HG...60
1.4 Conclusions...65
2. Methods...70
2.1 Case presentation: Patient ZS...70
2.3 Control group...73 2.4 Materials...74 2.5 Procedures...75 3. Results...79 3.1 B.A.D.A...79 3.1.1 B.A.D.A results...80
3.1.2 B.A.D.A results discussion...81
3.1.3 Summary of results...87
3.2 Spontaneous speech production...88
3.3 Interim discussion...90
3.4 Word production by phonetic cue...92
3.4.1 Word production by phonetic cue – results...92
3.4.2 Word production by phonetic cue – discussion...94
3.5 N/V homonymes...100
3.5.1 N/V homonyms – results...104
3.5.2 N/V homonyms – discussion...104
3.6 Naming by definition...106
3.6.1 Naming by definition – results...110
3.6.2 Naming by definition – discussion...112
3.7 Word definition...113
3.7.1 Word definition – results...114
3.7.2 Word definition–discussion...115
4. Conclusions...120
References 130
Appendix 156
List of tables
Table 1: Nouns and verbs...49
Table 2: B.A.D.A results...80
Table 3: Circumlocutions...83
Table 4: Word production by phonetic cue results...93
Table 5: N/V homonyms results...104
Table 6: Animacy hierarchy test...108
List of figures
Figure 1: Diagram elaborated by Wernicke...27
Figure 2: Wernicke and Broca's aphasias diagram...27
Figure 3: Lateral view of the left hemisphere of the human brain...34
Figure 4: Neuroanatomical correlates of different types of PPAs...38
Figure 5: Animacy hierarchy...67
Figure 6: Lemma interacting with other levels of the lexical system...68
Figure 7: ZS' brain CT scan: axial plane...70
Figure 8: ZS's brain CT scan II: axial plane...71
Figure 9: Lexical connections...96
Figure 10: Lexical connections based on shared semantic features...98
Figure 11: Lexical connections based on verbal inflection...99
Figure 12: ZS's FTL brain damage...128
Introduction
Language is a cognitive tool that allows us to communicate but, first of all, it reflects “the way in which we represent and categorize the world (e.g., events, objects, places, abstract notions, emotions, etc.)” (Romagno, 2012). It is clear, then, that “language does not function as a mirror of what we experience in everyday life, but as an autonomous system of classification and, therefore, of knowledge” (Romagno, 2012). Linguistics, being the main discipline to investigate language, needs to address issues that stray the mere structure of languages to look into what is universal about this mental activity. By merging with neuroscience, psychology and cognitive sciences, linguistics can answer questions that it could not obtain by itself. The main discipline that will constrain the following study is, thus, cognitive neuropsychology. The importance of merging linguistics with neuroscience relies on the fact that both can benefit from this alliance. Linguists can clarify aspects about language such as distinguishing “what is socioculturally determined and, therefore, dependent on historical accidents, from what is, instead, neurobiologically dependent and, therefore, universal” (Romagno, 2012b), while neuroscience can analyze the “principles underlying the organization and change of language systems [which] leads to exploring cognitive processes” (Romagno, 2012b).
Our ability to linguistically encode reality onto lexical-semantics grants us the opportunity to exchange messages and live in society. Human cognitive ability to achieve such a goal can also be lost; brain damage of diverse origins can impair more or less severely our language faculty. We can define the condition of a speaker who loses his or her capacity to produce or comprehend speech due to a brain injury as aphasia. Any mental activity involving memory, speech, face recognition or mathematical calculation relies on the normal functioning of certain brain areas that come into operation when we remember, speak, recognize someone or calculate; aphasia is, in this sense, a speech
disorder caused by brain damage affecting language areas.
For what concerns the aetiology, the brain damages causing aphasia, among other disorders, are cerebral vascular accidents (CVA; also know as stroke), head traumas (e.g. concussion), neuron atrophy, neurodegenerative diseases and also abscesses or tumors. The location of an injury causing language deficits is usually in the left hemisphere of the brain, and only occasionally a right hemisphere lesion causes aphasia.
Language is the most adaptable and refined communication system developed by homo sapiens; using a discrete number of sounds bound together by grammatical constraints it is possible to generate thousands of lexemes and sentences. The development of our culture made it possible for written language to arise alongside spoken language, which, allows us to represent linguistic signs graphically. Aphasia causes speakers to lose either of these modalities of speech, expanding to oral and written output (i.e. production) and/or to oral and written input (i.e. comprehension), depending on the size and the site of the brain lesion. Aphasic patients often display what is referred to as
modality-specific deficits, under which condition the individual is affected in
only one or more of these modalities of output/input but not in the other(s); however, it is also true, since language brain areas are close to each other and functionally related, that patients display an impairment of almost all linguistic capabilities.
For this thesis, an aphasic patient who will be referred to as ZS, was tested on different levels of linguistic processing; the modality of the experimental analysis is that of a single case study. Patient ZS was compared to five neurologically unimpaired individuals matched with sex, age and education. The patient in question suffers from a N/V dissociation and modality-specific deficits.
The purpose of the following study is to shed light on the underlying causes determining the patient's linguistic behavior. An investigation as such will allow to look at the relations that exist between semantics and grammar, the noun/verb distinction and lexical access.
Language processing in aphasia is of great interest for disciplines like linguistics and neuroscience; the former can grasp form it how language comprehension and production is achieved, which, can be applied to fields like that of philology, phonology, historical linguistics, language teaching, semantics and so on; the latter can design more efficient ways to diagnose and treat speech disorders, which would be of extreme importance for speech therapy and neuropsychological rehabilitation.
Ferroni & Favilla (2009) state: “in the same way as Moro (2006) wonders how the brain is able to produce solely the natural-historical languages that exist and had existed, neuroscientists that study consciousness, wonder why the world is perceived and categorized in the way it is, and not otherwise”. This also leads to support the idea that our cognitive structures are nothing but an external projection of the functional brain mechanisms that create them, and that some of them had arisen from a simultaneous crossing and sharing of differentiated synaptic pathways which developed during evolution to then assume different and autonomous forms (Grimaldi, 2006). “The natural (and neutral) conclusion seems to be that the world itself, as we know it, is a creation of the brain” (Ferroni & Favilla, 2009).
Chapter 1 – Single-patient studies
1.1 Cognitive neuropsychologyFollowing Goodglass et al. (1966), Caramazza & Zurif (1976), Marin et al. (1976), Caramazza (1986, 1997), Caramazza & Coltheart (2006), Vallar & Papagno (2007) and also Mazzucchi (2012) among many others, it is necessary to introduce what cognitive neuropsychology is. This discipline started in the second half of nineteenth century with neurologists such as Carl Wernicke (1848-1905) and Ludwig Lichteim (1845-1928), but also with Henry Charlton Bastian (1837-1915); the aim was that of building inferences about the cognitive architecture of the intact language-processing system after studying patients with brain lesions. Their results merged into a language processing
diagram elaborated by Wernicke in 1874, and later modified in collaboration
with Lichtheim in 1885. At the beginning, they were not very successful among the scientific community for their neuroscientific methods and were labeled as diagram-makers, even though their cognitive neuropsychology ended up being successful and it enjoys contemporary appreciation and support.
The patients studied at the time offered the opportunity to draw on the conclusion that aphasic syndromes are not, even if labeled under fixed diagnosis, homogeneous and theoretically founded, but vary under functional, anatomical and neuropathological circumstances; only a detailed psycholinguistic description of spared and impaired linguistic capacities could render a precise taxonomy of aphasias. For instance, Wernicke's diagram did not account for pseudowords processing, which need a non-lexical computation at a neural level. Pseudowords are not processed in the mental lexicon as they are phonological or orthographical sound sequences with no meaning at all.
Revolution” new types of research began about memory and reading (Marshall
and Newcombe (1966, 1973), Shallice and Warrington (1970). Importantly, many advancements in the description of aphasia symptoms were made with psycholinguistic means (Caramazza & Zurif, 1976; Marin, Saffran, & Schwartz, 1976). Finally, cognitive neuropsychology started publishing in 1984 in its own journal.
Cognitive neuropsychology aims to unveil what are the cognitive mechanisms that generate human thinking, as Caramazza & Sloan (1978) postulated, “knowing that damage to a particular area of the brain affects a specific language component can lead to the formulation of testable hypotheses about the structure of that component and the interaction of that component with other cognitive processes”. Moreover, Caramazza (1986) maintains: “our objective is to specify functional architectures which permit computationally explicit accounts of the input/output relationship for specific cognitive systems”, or, more broadly, that “these are questions concerning how we perform such tasks as understanding sentences, adding numbers, writing words, drawing pictures, and so forth. I shall assume, without supporting argument, that the kind of answers we are to consider appropriate consist of computationally explicit, information-processing accounts of cognitive performance”. In our case, the cognitive mechanisms taken into account are the ones that generate language, and, the evidence that is considered comes from patients' impairments: “the degree of detail of a proposed functional architecture is determined by the range of input/output pairs we take into consideration, or, more generally, by the range of evidence we deem relevant to the formulation of our explanatory account” (Caramazza, 1986).
The most important distinction and definition to bare in mind is between
cognitive neuroscience and cognitive neuropsychology: “Cognitive
cognition, and so it is a branch of neuroscience. Cognitive neuropsychology is the use of investigations of people with impairments of cognition (acquired or developmental) to learn more about normal cognitive processes, and so it is a branch of cognitive psychology, just as Rapp and Goldrick (2006) say” (Caramazza & Coltheart, 2006). Nevertheless, criticisms has been made for whay concerns “the term cognitive neuropsychology [which] often connotes a purely functional approach to patients with cognitive deficits that does not make use of, or encourage interest in, evidence and ideas about brain systems and processes” (Schacter, 1992, p. 560). Still, as Caramazza (1992) says, cognitive neuropsychology can often be seen as overlapping with, interrelating with or it can be mistaken for cognitive neuroscience as the functioning of cognitive processes can be brought back to neural systems or the contrary; this is also because the main source of data is biological manipulation (e.g. the brain damage) which is then interfaced with patient's pattern of performance. Caramazza (1986) observes that “valid inferences about the structure of cognitive systems from the analysis of the performance of brain-damaged patients are only possible for observations of individual patients’ performances”. Further, “it is equally clear that neuropsychological data are by their very nature function–brain pairings, and therefore they offer a potential window into the neural organization of cognitive systems” (Caramazza, 1992), thus resulting in a controversy that is still on today.
Following Goodglass et al. (1966), Caramazza & Zurif (1976), Caramazza (1986, 1987), Marin et al. (1976), Caramazza (1986, 1997) and also Mazzucchi (2012), cognitive neuropsychologists study the functional architecture of cognitive processes, building it up from pathological data. In other words, they infer, on the basis of experimental and pathological data, functioning models of various cognitive processes (e.g. word retrieval). The main principles upon which cognitive neuropsychology is based are those of modularity, universality and transparency. Modularity supports the idea that a complex cognitive
function is the result of a series of functionally-independent sub-components that form operations, which can undergo isolated impairment as a result of brain damage; universality affirms that the structure of cognitive functions is universal, as otherwise it would not be possible to draw any inferences from different individuals if there were subjective variations in the functional brain and cognitive structures; finally, transparency argues that when one or more cognitive-processes components are impaired, other components can continue to operate normally even if they would still suffer disturbances from the the malfunctioning input deriving from the impaired component.
A functional diagnosis of the cognitive flaw aims thus at the establishment
of the functional locus of the impairment. Two patients displaying the same
functional locus of the impairment will consequently also display the same symptoms. It follows that, being able to know the normal functioning and structural arrangement of the mind/brain will allow to identify the consequences of a certain impairment in a determined area.
When investigating such phenomena it is very important for the methods to joint theory and evidence, as Caramazza (1986) specifies: “by method, I mean, broadly, the criteria of adequacy for relating data to theory, that is, the rational basis for supposing that an explanatory account can validly be applied to the phenomena of interest”. It is in fact true that, as Caramazza (1986) acknowledges, “there is a complex, mutual interdependence between theory and evidence”.
1.1.2 Single case studies
Cognitive neuropsychology studies rather the symptoms than syndromes, and thus single case studies are usually taken into account (Goodglass et al., 1966); Caramazza & Zurif (1976); Caramazza (1986, 1987); Caramazza & Coltheart,
2006). As stated by Buxbaum (2006), who was studying a case of neglect1:
“nearly every possible fractionation of the disorder has been reported, raising the possibility that each patient may be as unique as a snowflake”.
The only way to address these issues, considered the vastness of symptoms that brain injury manifests, seems to be the single case; as stated by Caramazza (1986): “the single-case approach in the analysis of cognitive impairments allows valid inferences about the structure of normal cognitive systems”.
For instance, Broca's aphasia was thought to be due to a single cause that brought about both agrammatic comprehension and production. But, “agrammatic comprehension and agrammatic production do not always co-occur; indeed, they doubly dissociate” (Caramazza & Berndt, 1985).
Under this assumption, what can be said about normal cognitive functioning? Caramazza (1986) stands out with what he calls “universality
assumption”, that is, “there is no qualitative variation across neurologically
intact people in the architecture of the cognitive system that these people use to perform in a certain cognitive domain”, and from the basis of this we can draw universal observations about a general way of working of the brain. It is true, in fact, that neuroanatomy is the same across individuals, and even though it may vary in the way each brain develops, it would still have the same basic components; we could then say that there are indeed some types of constraints governing brain morphology and processing even if each brain is unique in development and functioning. Again, Caramazza (1986) argues that “the justification for using the performance of groups of subjects in our experimental investigations is based on the assumption that the averaged performance of the group essentially reflects the performance of any individual
1 Hemispatial neglect is a condition in which neurologically impaired patients suffer from a loss of attention or awareness to one side of the visual field as the brain is unable to process and perceive stimuli; a unilateral visual neglect can be a symptom of lesions to the
in the reference population from which the group was drawn. Thus, any conclusions arrived at for the group of subjects tested will be assumed to be true of all individuals in the reference population. This argument is only valid if the assumption of universality is true”. This is not to say that group analysis has no use and that syndromes cannot be grouped together, but then, every type of disorder would have a subtype, and each subtype will be found to have another subtype inwardly. All of these sub-groups lead to the “expectation that individual differences will tend to cancel each other out in group performance” (Caramazza, 1986). Cognitive neuropsychology is not to answer question like: “Is it the case that patients of type R also manifest property y?” (Caramazza, 1986), being R a clinical category and y some pattern of performance, which would serve to group together different types of syndromes using statistical methods; rather, cognitive neuropsychology looks at the uniqueness of a patient performance, and thus asks the question “Is it the case that patients of type R also necessarily manifest property y?” (Caramazza, 1986).
Of course, every patient does not entail the formulation of a different model, but rather, “what is being claimed is that the performance of each patient potentially provides relevant evidence for a model. Therefore, the performance of all individual patients (as well as the performance of normal subjects) must be considered in the evaluation of a proposed model of a cognitive system. The pattern of performance of a single patient can be used to propose a specific hypothesis, but ultimately, the evaluation of a model is based on the full range of available relevant evidence, including the performance of other patients and normal subjects” (Caramazza, 1996).
Furthermore, it is not only the impairment that guides research towards single cases but also the different populations taken into account: “not only is the question of what observations constitute relevant evidence theory-dependent, but also, the definition of a reference population is theory
dependent” (Caramazza, 1986).
Finally, it is assumed by Caramazza (1992) that “theories about the architecture of a cognitive system are postulated in which that system is considered to be composed of information-processing components each responsible for one of the information processing jobs that need doing if cognition is to run smoothly. It is this property of cognitive systems that makes them amenable to neuropsychological investigation. In other words, it is because cognitive systems are composed of relatively autonomous processing components that “local” brain damage can result in dissociation of functions”. This contrasts with the Fodorian (Fodor, 1983) view of modularity in favor of a more componentially-structured mind.
Unfortunately, as Fodor, Bever, and Garrett (1974) stated: “[it is] the sad truth that remarkably little has been learned about the psychology of language processes in normals from over one hundred years of aphasia study”, as studies of this kind were conducted by neurologists, whose main concern was not to unfold the normal functioning of language processing.
Importantly, these theories brought about the box-and-arrows models which are still very useful today; these theories helped formulation a representation of general cognitive architecture of cognitive systems (see Coltheart et al., 2001).
1.1.3 Modality-specific deficits
Of fundamental importance for this type of discipline is to consider data coming from patients that present with grammatical and semantic category-specific deficits that are restricted to one modality of output (Caramazza & Hills 1991; Hillis et al. 2003; Rapp & Caramazza 2002). Goodglass, Klein, Carey & Jones (1966) were the first to investigate the incidence of
category-specific disorders across different patients with a mixed range of language impairments; during their experiment they noticed that patients presented with selective comprehension difficulties with any of the categories assigned for the tasks (namely letters, numbers, concrete nouns, action words and colors). On the other hand, there were cases in which portions of knowledge were preserved. They came to the conclusion that category-specific comprehension disorders might be the rule, rather than the exception. Pavio (1971) and Goldstein (1948), showed that, for instance, concrete and abstract vocabulary can represent an important variable in language processing, both with normal subjects and with aphasic patients.
Modality-specific impairments do not solely encompass the so-called single
dissociation across modalities, but they can also happen to extend to two
modalities of input/output (i.e. oral and written production, auditive and written comprehension). Single dissociation is, in fact, only one manifestation of an impairment, but then we can also encounter what is defined as double
dissociation; Caramazza (1986) clearly specifies the distinction between single
and double dissociations as follows: “[single dissociation] refers to a differential pattern of spared and impaired performance; “double dissociation” refers to the occurrence of both a particular pattern of spared and impaired performance and the reverse pattern in which the previously impaired performance is now intact and the previously spared performance is now impaired”.
Moreover, patients present with double dissociations that are opposite to each other with nouns and verbs across modalities; spared comprehension and production of nouns in the presence of impaired comprehension and production of verbs can also follow the precise opposite pattern. The latter would indicate that the lexical system is organized in grammatical classes (Miceli et al., 1984). Also worth-noting is the fact that even within the class of verbs and nouns we
can observe a dissociation, which can be caused by the so-called concreteness
effect (Warrington, 1981) or its reverse as well (Papagno et al., 2009).
On a sub-lexical level, Hillis & Caramazza (1991) found that “performance by patients who are unable to produce orally the names of objects in response to pictures, despite preserved ability to write their names and preserved motor processes for producing speech, provide evidence for the functional and neural independence of mechanisms for accessing phonological representations of words from those mechanisms used for accessing the orthographic representations of the same words (Caramazza and Hillis, 1990)”.
Double dissociation affect both grammatical and semantic categories. Specifically, to give an example, grammatical categories might be those of nouns and verbs while semantic categories could feasibly refer to animate and inanimate referents. For instance, patient EBA., reported by Hillis & Caramazza (1995) “makes far more errors on nouns than on verbs in spoken output tasks, but makes far more errors on verbs than on nouns in written input tasks”; Caramazza & Hillis (1991) had also previously reported the opposite dissociation between nouns and verbs in all speech tasks in patient HW. Patients RC and JR (Shapiro & Caramazza, 2003; Shapiro, Shelton & Caramazza, 2000), brought forth further evidence by displaying mirror dissociations; they presented with double dissociations with nouns and verbs which were opposite from one another. Patient KSR (Rapp & Caramazza 2002) represents another case: this patient was able to process verbs in oral production but not in written production when the opposite pattern is displayed with nouns; in other words, the patient was able to process nouns in oral production but not in written production.
Double dissociations affecting grammatical category within a single patient suggest that “phonological and orthographical representations of nouns and
verbs are processed by independent neural mechanisms” (Hillis & Caramazza, 1995) and that specific brain regions that are damaged provide processing for the two distinct modalities (Hillis et al. 2003).
Caramazza & Hillis (1991) discussed the general organization of the lexical system and the internal structure of its processing components in the light of the evidence brought about by double dissociations. They argued, by analyzing the cases of patients SJD and HW, that either grammatical class (i.e. nouns vs. verbs) or that semantic categories such as abstract/concrete, living things/inanimate objects, animals/fruit/vegetables and so forth establish a dimension of lexical organization of words. HW presented with a dissociation between oral and written production of words: “she produced semantic paraphasias (see section about 1.2.4) in oral but not in written production while her ability to to comprehend the very same words was entirely normal in both modalities” (Caramazza & Hillis, 1991), and she made semantically related errors in reading as well; SJD made semantically related errors in written but not in oral production and she did not made those errors in reading either. The two patients also displayed a grammatical class dissociation between nouns and verbs, even though their difficulties in written and oral production were not uniformly distributed across verbs and nouns. To verify whether it was due to grammatical or semantic class, the patients were also tested with oral and written naming of pictured objects and actions which are semantic prototypes2
of nouns and verbs, respectively; SJD and HW displayed once again the same dissociations despite of this. Allport & Funnell (1981) proposed that verb processing impairments could result from a damage to abstract words processing, but this hypothesis does not agree with all forms of grammatical-class effects; accordingly, “there are reports of greater difficulty in naming objects than actions, ruling out the possibility that grammatical-class effects are always merely the consequence of greater difficulty on processing abstract
words” (Caramazza & Hillis, 1991). Neither SJD nor HW showed greater difficulty with abstractness or concreteness, representing thus true cases of grammatical-class impairments. Also, the two patient were tested with a noun/verb homonyms task; in this way, the researchers could rule out the possibility that the patients' impairment were simply dependent on phonological or orthographical forms of words. Both SJD and HW confirmed once more their modality-specific deficit, which was restricted to either nouns or verbs as grammatical classes.
As Romagno (2012) suggests, the fact “that either noun or verb processing is spared in one modality rules out a breakdown in access to referential semantic knowledge as the cause of the deficits”, indicating, contrarily, that “the locus of functional deficit is at a level where lexical phonological representations (for HW) and lexical orthographical representations (for SJD) are specified for output, either because of damage directly to modality-specific lexical representations or because of damage to access of those representations. This conclusion implies that seemingly counterintuitive possibility that semantic errors can arise from damage to processes at the level of phonological or orthographical output representations” (Caramazza & Hillis, 1991). Moreover, the two patient are then impaired with “the activation of the category verb in modality-specific lexical components” (Caramazza & Hillis, 1991) either because of a damage to the lexical system of because of lexical retrieval. This last fact would also entail that phonological and orthographical output representations are organized by grammatical class; in conclusion, it seems that “grammatical category information is represented separately and redundantly in each modality-specific lexical system”.
Rapp et al. (1997) also suggested that graphic output can be accomplished
independently from phonological mediation; the patient from the study could in
lexical-phonological and lexical-orthographical forms of words are separate but activated and processed in parallel; inner speech (i.e. hearing one's voice while reading mentally or writing), for instance, would be just an on-line two-parallel processes that take place simultaneously, and not causally related. Another explanation provided by Romagno (2012) is that these phenomena might be “manifestations of disconnections between morphosyntactic processors, segregated by grammatical category, and morphophonological processors segregated by modality”.
Other patients, described in the literature (Hillis & Caramazza, 1991), show double dissociation even throughout single semantic categories such as animals and vegetables; such data indicate that the semantic system is organized categorically. Furthermore, not only were the deficits in one semantic category, but also dissociated though different modalities of input, namely that production and comprehension can be impaired in selective semantic categories (Goodglass et al., 1966).
To better understand these issues it necessary to describe what speech disorders are, and what form they can take.
1.2 Aphasia
Aphasiology has been a long debated field of study within the scientific community (Goldstein, (1948); Goodglass et al. (1966, 1976); Zurif et al. (1972, 1974, 1976), among many others); its importance relies on the fact that aphasia can bring to the surface many of the unsolved issues about language processing and its pathologies.
Following Goldstein, (1948), Goodglass et al. (1966, 1976), Zurif et al. (1972, 1974, 1976), Breedin & Saffran (1979), Baxter & Warrington (1985),
Caramazza & Hillis (1991) and Vallar & Papagno (2007), and Làdavas (2012) aphasia is an acquired disorder pertaining to the formulation/encoding and comprehension/decoding of linguistic messages and linguistic information. This type of disorder is the consequence of a focal lesion to the brain that hits individuals that previously had a normal use of language. Aphasia is a consequence of injuries such as vascular focal damage, trauma, infection or degeneration of tissues. Aphasia is, then, a behavioral manifestation of a neurological impairment which can be brought back to different diseases.
A main distinction is provided by medical studies (Vallar & Papagno, 2007); Aphasia can affect language in every possible way: from oral/written production to oral/written comprehension. Aphasic patients often display such behavioral manifestations in parallel or in an isolated fashion; regardless of the locus of the impairment along the anteroposterior left hemisphere, in fact, the majority of the aphasic patients suffers from a disturbance of almost all linguistic units. Furthermore, we must think of language as a whole system that can be damaged at different levels and sub-levels; also to be remembered is the fact that deficits can affect not only a particular grammatical class (e.g., function words, nouns, verbs, affixes and more) but even a particular semantic group of elements (e.g., artificial and natural objects). Moreover, patients are now seen as unique and different from one another; there is thus an infinity of variables to be considered, and it is rather complex to be able to group each aphasic disorder as precisely as we would like to.
Nevertheless, the comprehension and production failures exhibited by patients remain amenable to further analysis, since the lexical disruption experienced is rarely total (Goodglass & Geschwind, 1976). As Caramazza & Sloan (1978) argue: “most often, some element of a word's meaning is retained, so a patient knows the class to which a word belongs (e.g. color terms, body parts) without grasping its full meaning. Thus, the meaning components that
are spared can be examined and compared with those that are lost in an attempt to identify the elements involved in comprehension failure”.
Aphasia generally affects all the different modules of language (phonological and articulatory, morphosyntactic, lexical or even semantic), and it can strike either at comprehension or production through both orality or written form. This creates a vast variety of symptoms depending on the different kinds of impairment of each patient and on the linguistic unit compromised. Aphasiology research have “established that although no two aphasics are exactly alike either in the nature of the disorder or in the consequent language performance, it is the case that there are discernible patterns of dissolution” (Caramazza & Sloan, 1978).
As different linguistic functions are impaired and some are spared, it is important to disentangle diverse cognitive capabilities from others; for instance, “the class of patients usually said to have relatively intact comprehension (those with anterior damage) [which] is now believed to be deficient in the ability to integrate correctly understood lexical items into certain types of syntactic frames” (Caramazza & Zurif, 1976) has to be distinguished from “the class of patients who exhibit poor comprehension (those with posterior damage)”. In fact, the last-mentioned population is “said to lack an understanding of individual lexical items but to have retained an implicit understanding of the syntactic rules for combining words into grammatical sentences” (Caramazza & Sloan, 1978).
A main distinction can be made, accordingly, between anterior and posterior damages. Following Vallar & Papagno (2007), such a distinction does not grant a precise diagnosis or dichotomy but rather a qualitative description of the impairments. Speech characteristics are then gathered as follows:
strenuous articulation.
• Posterior: fluent and abundant but with phoneme, free/bound morphemes and content word choice difficulties.
Fronto-temporal lobe (FTL) impairments constitute a unique population of
patients as they allow for significant comparison between them and
anterior-temporal lobe (ATL) impairments. As we will see in section 1.2.4 and 1.2.5,
FTL damages are usually associated with output impairments, whereas ATL damages are usually associated with input impaiments.
The brain damage is located in the left hemisphere, in right-handed individuals for the majority of patients3; the focal damage is indeed located
across brain areas that surround the left-hemisphere lateral sulcus (also called lateral fissure or Sylvian fissure). It is important though, to bare in mind that “focal brain damage to the dominant hemisphere (left hemisphere in most right-handed individuals) does not simply result in an overall undifferentiated reduction of language capacity or a random constellation of symptoms” (Geschwind, 1970, 1972; Luria, 1970). Accordingly, different parts of the brain process different language functions.
Worth-noting is the fact that extralinguistic psychological variables might be present in such a deficit: attention, short-term memory and behavior (e.g. inertia, disinhibition, self-awareness4) can play a role in the linguistic difficulty.
Aphasia arises from biological and organic causes, being it caused by a brain damage. Its aetiology is not restricted to few phenomena, but is rather due to diverse accidents.
3 This is in fact true for the 95% of documented cases. If aphasia is caused by a right lesion, we talk about crusade aphasia. Language is lateralized in the left hemisphere of left-handed individuals as well (60%), and the remaining 40% shows lateralization of language either in the right hemisphere or in both hemispheres.
4 Post-stroke patients often suffer from anosognosia, namely, a deficit affecting self-awareness and the realization of having a disorder.
1.2.1 Aetiology
Stroke, or cerebral vascular accidents (CVA) is one of the organic causes that motive aphasia incursion. Strokes present themselves as a chronic or isolated vascular damage; its aetiology comprise high pressure levels, hypertension, high cholesterol levels, diabetes, cigarettes consumption and more. When strokes hit the brain chronically they generate damages during time and worsen the condition continuously; this last type is called multi-infarctual stroke, and just like the isolated type can cause death. Among other consequences of this disease it is common to come upon dysarthria, motor difficulties, dysphagia and, of course, many other cognitive and psychological impairments such as damage to sight, hearing and behavioral anomalies.
From a biological standpoint, stoke is an arteriosclerosis of blood vessels brought about by a clot that blocks blood flow in the brain; strokes can also occur because of an internal bleeding in or around the brain that creates swelling and pressure, compressing and damaging brain tissues. Without the correct blood flow, brain cells stop receiving oxygen and fundamental nutrients for their sustenance, and start to decease. Strokes often result in permanent impairements such as paralysis, loss of sensory function, problems thinking and speaking, or even regulating emotions. Stokes represent a leading cause of long term disability; besides muscle weakness and trouble walking, talking and understanding speech, symptoms can include loss of balance, disorientation and difficulty seeing out of one or both eyes.
Dementia diseases can also be caused by a vascular problem, as blood vessels stop working properly, and brain cells irreversibly decease. Dementia, as well as Alzheimer’s neurodegenerative disease, can also be caused toxic “amyloid plaques” (i.e. proteins). Patternson et al. (2007) describe different
types of aphasia and dementia caused by left-hemisphere stroke such as
transcortical sensory aphasia (TSA) and semantic dementia (SD); these types
of diseases not only cause language impairment in general (i.e. word-finding difficulties, phonetic production anomalies, syntactic disorders and so on), but they hit at the core of conceptual knowledge.
As already mentioned in the Introduction, other diseases that can bring about aphasia are head traumas (e.g. concussion), neurodegenerative diseases and also abscesses or tumors.
Another cause of aphasia is cerebral atrophy; the patient observed in this study, ZS, suffers precisely from this type of aetiology. Atrophy is a loss of neurons and the connections between them; this decreasement of nervous cells can be caused by a progressive loss of cytoplasmic proteins. Atrophy can be generalized (i.e. affecting the whole brain) or it can be focal (i.e. limited to one specific area); focal atrophy results in a decrease of the functions of the damaged brain area (e.g. language), precisely like the patient discussed in this study. ZS suffers from a brain atrophy that impaired her language faculty, sparing many other cognitive skills. Atrophy often occurs naturally because of age advancement.
Now, having presented aphasia and its main causes, we need to look at the principal branching and at the many forms that this disease can take.
1.2.2 Brief history of aphasiology
Following Vallar & Papagno (2007), we can draw a traditional view of what aphasia was in the past and how its description changed over time.
between comprehension deficit (i.e. receptive or sensory aphasia) and production deficit (i.e. expressive or motor aphasia). This type of view originates from the language processing diagram elaborated by the German neurologist Carl Wernicke (1874), and later modified in collaboration with Ludwig Lichtheim (1885).
Of fundamental importance is also Paul Broca (1824-1880), a French doctor who owned two great discoveries in this field. In 1861, he studied the well-known patient Monsieur Leborgne, later called “Tan-tan” because of his linguistic output which was limited to this syllable; this patient allowed doctor Broca to assign to the frontal lobe the role of regulating articulated language production, specifically at the foot of the third frontal convolution. Later on, in 1865, on the basis of a functional-anatomical analysis, doctor Broca found language to be lateralizated in the frontal lobe of the left hemisphere.
Wernicke's model draws on the assumption of a principal dichotomy between two centers of language processing and elaboration: auditive and
motor images of words; these two centers are located at the level of motor and
auditive associative areas which are connected by a bundle of fibers hypothesized by the doctor to be the arcuate fasciculus (external capsule).
The two types of word representation are independent but they work in combination to realize a word image (i.e. lexical-phonological representation).
In the upstream of the diagram are located the auditive analysis and the
Figure 1: Diagram elaborated by Wernicke (Vallar and Papagno, 2007)
Anticipating some of the most modern theories, including the antithesis between signified and signifier, Wernicke incorporated conceptual
representations (meanings of words) to the diagram. The doctor underlined this
type of knowledge to be distributed across the cortex of both hemispheres, not being, thus, a localized center. As already mentioned, the module was created with the collaboration of doctor Lichtheim, and it is consequently called the
Wernicke-Lichtheim model.
Figure 2: Wernicke and Broca's aphasias diagram (Vallar & Papagno, 2007)
As Figure 1 and 2 show, damage to one or more of the parts of the model entail different types of aphasia, including sensory aphasia (Wernicke's aphasia), motor aphasia (Broca's aphasia), pure verbal deafness, pure anarthria, conduction aphasia and transcortical motor and sensory aphasia (see section 1.2.4 and 1.2.5).
More specifically, an impairment to the connection between A and B will cause a repetition deficit while sparing comprehension, whereas an impairment to the connection between A and C will cause the oppose effect; an impairment to C-B will induce a production deficit while sparing repetition.
The clinical reality and the evidence that is present nowadays contrasts with some of these principles (e.g. almost all of the aphasic patients show deficits in written language).
At last, around the sixties, neurologist Norman Geschwind (1926-1984) and psychologist Harold Goodglass (1920-2002) brought about more modern neurolinguistic and psychometric methods of diagnosis and investigation. The most characteristic trait about the methods used by cognitive neuropsychology is the usage of diagrams made with boxes and arrows (the so-called
“box-and-arrows” models).
Today's models include a non-lexical part of language processing; in these kind of units, the information bypasses other systems such as auditive-lexical conversion and semantics to be transferred directly from acoustic analysis to the phonemic buffer; the same is valid for graphemic-phonemic conversion.
1.2.3 Present-day classification
Even though symptoms come first than syndromes, it is important to group a main list of aphasia typologies.
It is now a fact that, independently of the location of the brain damage (as long as it is placed in the anteroposterior area of the left hemisphere), the majority of aphasic patients display a parallel impairment in both production
and comprehension, written and oral language. In other words, aphasia affects language as an entire system of which the different parts are involved in a homogeneous way.
From a ontogenetic and phylogenetic perspective, in fact, there are secondary centers of elaboration for auditory and motor images, but they are super-modal and not modality-specific as Wernicke thought; these centers lose their specificity along with development of the brain.
Language impairments can undergo what is called dissociation, but usually the different components of the linguistic system are impaired in a disproportionate fashion (as already mentioned in section 1.1.3). Dissociation proves, though, that linguistic modules are indeed independent at a mental level, and this is in line with many contemporary discoveries in the fields of theoretical linguistics and psycholinguistics.
Another type of dichotomy is the fluent/nonfluent one, which correlates with frontal and temporal lesions; This type of contrast does not correspond to a precise separation of the two but rather to different qualitative characteristics of the language disorder. It has been observed that, production and comprehension are usually impaired in parallel, and, anterior and posterior lesions are different in the sense that the former causes nonfluent deficits while the latter causes fluent deficits. Nonfluent aphasia presents itself as a slow, strenuous and laborious articulatory emission in which syntactic structures are simplified; fluent aphasia exhibits, on the contrary, an abundant production which is associated with phonological, morphological (e.g. free and bound morphemes) and content words choice confusion.
Following Vallar & Papagno (2007), fluent aphasic patients' speech is abundant but presents with prosodic or articulatory difficulties; their sentences are rather long and syntactically complex. Morphosyntax is usually impaired as well as function words and affixes. These patients also present with anomias (e.g. incapacity of naming objects, actions and more; namely, lexical-retrieval difficulties), semantic paraphasias (i.e. the replacement of an element with another which pertains to the same semantic category; e.g. naming tiger a cat),
phonemic paraphasias and neologisms / new-formations (i.e. the substitution
of phomenes into an existing word and the creation of non-existing words, respectively). In the case of a severe impairment, patients' linguistic production is reduced to a series of non-existing words (neologistic jargon) due to the high amount of paraphasias; new-formations can also be combined with existing ones, creating, thus, non-sense sentences (semantic jargon).
Fluent aphasias are classified as follows:
• Wernicke's aphasia: this type of aphasia affects different components
of the language system such as the lexicon, phonology and morphosyntax; repetition, naming and comprehension are all impaired depending on the severeness of the damage.
The brain damage involves the 22th Brodmann's area (see Fig. 3), namely
the medium-posterior circuit of the first temporal circumvolution (also called Wernicke's area).
• Conduction aphasia: this type of aphasia usually presents with spared
oral comprehension and impaired repetition; it can be brought back to a phonological disorder that affects naming and spontaneous speech while sparing lexical-semantic and syntactic operation abilities. The repetition deficit can be caused by a phonological short-term memory loss as the auditive-verbal
memory span undergoes reduction (it is, in fact, also referred to as repetition aphasia).
The brain damage is normally located in the 40th Brodmann's area (see Fig.
3), namely the arcuate fasciculus.
• Trans-cortical sensory aphasia: the main observable symptoms are
impaired comprehension and spared repetition, yet another interpretation can be inferred. Trans-cortical aphasia can also be the result of a severe lexical-semantic disorder both in the input and/or in the output processing modality; the patient would be then impaired with both spontaneous speech production and comprehension while retaining morphosyntactic and phonological abilities. The deficit is often associated with echolalia (i.e. uncontrolled and continuous repetition of what is being said by the interlocutor).
Patients affected by this type of aphasia generally exhibit an extended lesion located in the left temporo-parietal region, which is also referred to as 45th Brodmann's area (see Fig. 3).
• Amnestic aphasia: the main impairment brought about by amnestic
aphasia is represented by a lexical-retrieval deficit both in naming and in spontaneous speech, as well as in comprehension; patients can also be affected by a slight phonological and morphosyntactic deficit. Contrary to other types of aphasia, this disorder aggravates progressively.
Lesions causing amnestic aphasia are usually located in the left
temporo-parietal areas. The damage preserves Wernicke's area, affecting the 37th and 39th Brodmann's areas (see Fig. 3).
1.2.5 Nonfluent aphasias
Nonfluent aphasic patients produce short sentences and also lack a correct prosodic pitch production; their speech behavior results in a tiresome and rather slow production. Ordinarily, nonfluent aphasias are characterized by an incorrect syntactic structure and by articulatory difficulties.
Nonfluent aphasias are gathered as follows:
• Broca's aphasia: this type of aphasia represents the prototype of all
nonfluent forms of aphasia; the main manifestation of this disorder is what is referred to as telegraphic speech (i.e. the patient's production lacks function words and thus s/he will output only main discourse lexemes, like nouns and verbs). Naturally, morphosyntax and sentence subordination are also hindered, creating the so-called agrammatic speech; Broca's aphasia is indeed considered the morphosyntactic disorder par excellence. Usually, but not necessarily, this deficit moves along with thematic-role assignment difficulties. Moreover, this disorder is likely to be associated with dysarthria and its more severe form,
anarthria (i.e. the loss of neuromuscular control of the speech muscles), but
also with what is called phonetic disintegration (all deficits relating to articulation of phonemes).
This type of aphasia is generally differentiated from global aphasia as the former presents with spared comprehension whilst the latter does not. Also phonological and lexical-semantic abilities are spared in these patients.
Lesions causing this type of aphasia are located in the foot of the third left
frontal circumlocution, also referred to as 44th Brodmann's area or Broca's area (see Fig. 3). If dysarthria is included in the impairment, then the lesion
the patient is agrammatic, the damaged areas include the left perisylvian.
• Trans-cortical motor aphasia: this aphasia results from an
impairment to spontaneous speech and written language production while sparing naming, repetition, reading aloud and writing under dictation.
Trans-cortical aphasia is also called dynamic aphasia, and it shows a lesion in the 45th Brodmann's area (see Fig. 3).
• Trans-cortical mixed aphasia: the symptoms that characterize this
disorder are spared repetition and impaired comprehension/production. It is a severe type of nonfluent aphasias which can also impaire the lexical system (both in output that in input), while phonology and articulation are spared; the fact that repetition is spared entails, in many cases, the presence of echolalia. Lesions spare the arcuate fasciculus and Broca / Wernicke's areas while damaging wide regions of the left cortex and sub-cortex in
front-parietal-temporal areas.
• Global aphasia: this is the most severe amongst all types of aphasia;
patients' output is limited to some fractions of words and stereotypical forms (e.g. days of the week) accompanied by articulatory difficulties as well. All language processing components are critically compromised. High-frequency concrete words presented in written form are accessible to some degree to patients affected by this type of aphasia.
Lesions extend to the entire left cerebral artery zone.
A mapping of the brain elaborated by the American physiological society is presented below, in Fig. 3. It represents the main brain regions involved in
language processing.
Figure 3: lateral view of the left hemisphere of the human brain (Démonet et al., 2005).
1.2.6 Primary progressive aphasia
An important type of aphasia that has not been mentioned yet, but which is related to this thesis, is the so-called primary progressive aphasia. Patient ZS, who has been tested for this single case study, was diagnosed with this type of disorder approximately three years ago.
Following Vallar & Papagno (2007) again, we can describe primary progressive aphasia (PPA, hereinafter) as a syndrome that is subdivided in at least three different varieties; this disorder is characterized by a fronto-temporal lobe degeneration (FTLD) delimited to the prefrontal lobes and
anterior-temporal lobes.
PPA is a non-Alzheimer disease (AD, hereinafter). Mainly, the difference between the two is the change of personality noticeable in non-AD patients.
A typical grouping that includes the different branching of this disorder goes under the name of Pick's disease. The psychiatry professor Arnold Pick named this pathology in 1982 after having conduced a post-mortem on dementia patients. The main characteristic of these diseases is the neurodegenerative condition that leads to the death of nerve cells.
Symptoms depend on whether the atrophy is located (i.e. left vs. right; temporal vs. frontal); naturally, the atrophic areas can add up to cause simultaneous symptoms. As Wilson et al. (2012) maintained, “patients with primary progressive aphasia vary considerably in terms of which brain region is impacted” and this also implies different kinds of impairment.
Many aspects of this disease remain unknown but it seems to occur in the 8% of dementia patients; it shows up more often amongst individual under 65 years of age, being as common or even more than AD; the onset of the degeneration is, in fact, around the age of 50 and 60 years.
The first type of this disorder, and the most common, is characterized by severe personality and social conduit alterations; the patient presents with disinhibition and inertia as well as with initiative and concentration loss. Another typical difficulty concerns memory, which is impaired as a consequence of the fronto-temporal lobe degeneration.
Two further types are the progressive nonfluent aphasia (PNFA) and the
semantic dementia (SD); the former is characterized by a nonfluent,
agrammatic speech, while the latter by a loss of conceptual knowledge and semantic content of words.
symptoms include slow and pauseful spontaneous speech output with spared morphosyntax and phonology; patients have a good comprehension of single words but not of sentences. This kind of aphasia affects patients with atrophy located in the left posterior perisylvian and inferior parietal regions.
Gorno-Tempini et al. (2004, 2011) list yet another variant called semantic
PPA. Patients display spared syntax and impaired lexical-semantics, thus
overlapping considerably with SD (Neary et al., 1998). As it can be observed in Fig. 4 (below), each variant has a different pattern of atrophy.
The history behind this disorder goes back to Mesulam in 1982, in the U.S; the researcher introduced PPA to label patients who presented with isolated impairment of language output and input without any other cognitive deficit. To definitely be diagnosed with PPA, a patient must meet the criteria of having a deterioration of speech and language skills for more than 2 years without any other non-linguistic cognitive deficit (Mesulam, 2001).
It is now known, also, that PPA, FTLD, PNFA and SD can overlap in many ways. Moreover, another syndrome called progressive sopranuclear palsy (PSP) and also the cortical-basal syndrome have many parallelisms with FTLD; also articulatory apraxia (i.e. incapability of executing speech articulation motion) and motor neuron disease (i.e. progressive degeneration of motor neurons) are concomitant with the other symptoms mentioned. Finally, for this final reason, Andrew Kertesz came forward with the proposal of grouping all these syndromes under the name of Pick's disease.
As already stated (see section 1.2.1), degenerative neurological diseases seem to be connected to the excessive production of a toxic protein in the brain, but the aetiology is still unknown as many researchers propose that it might be liked to genetic causes.
Going into more detail, PPA is classified as such when the language component is impaired in an isolated fashion, namely, without other cognitive malfunctions, for the first two years (Mesulam, 1982). Typical of its beginning is the lexical-retrieval difficulty in spontaneous speech; later, other symptoms such as phonetic paraphasias, agrammatism and anomias will appear, resulting in a nonfluent aphasia. At this point, fluency and naming also aggravate, while comprehension is spared for a period of time; even though the last-mentioned is true, syntactically complex sentences might not be processed smoothly by the individual. At last, the disorder would evolve into a global aphasia.
At first, the disease will not be severe, for a period of time that extends from 2 to 14 years; the final result will be a dementia. Before finally becoming a dementia, other cognitive functions, such as memory and non-verbal intelligence together with visual-spatial perception, will be spared. It is also common that behavioral and dis-executive impairments will appear later in the progression of the disease. The disorder can also be accompaigned by pure anarthria and pure motor aphasia converging into a disprosodic, trammeled and slow speech that leads to articulatory problems and even mutism. FMRI scans reveal a hypoperfusion or a selective left hemispheric atrophy located in the frontal lobe (nonfluent types) and in the temporal lobe (fluent types); the second-mentioned are typically set to evolve towards a SD.
Findings from Wilson et al. (2012) suggest that syntactic impairment depends more on damage in the left frontal and posterior perisylvian regions and also in their connection. On the other hand, anterior temporal regions and the ventral tracts that link frontal and temporal language regions have been observed to be less important for syntax. Anterior temporal regions are said to be linked to SD and semantic PPA (Hodges et al., 1992) and, analogously to patient ZS, the damage is usually bilateral even if more extensive in the left
hemisphere.
Figure 4: Neuroanatomical correlates of different types of PPAs
(Gorno-Tempini et al., 2004).
Nonfluent PPA is of extreme importance for this thesis as patient ZS presents precisely with this type of aphasia; moreover, ZS, who was previously administered with linguistic testing by the hospital personnel, displayed a verb-selective impairment.
1.2.7 Verb-selective deficit in nonfluent PPA
Of fundamental importance for this thesis is the fact that the nonfluent variant of PPA associates with verbselective deficit; patient ZS, in fact, presents precisely with both a nonfluent PPA and verb-selective deficit.
Stroke and focal degeneration disease of neurons can both cause dissociation of grammatical classes (i.e. nouns and verbs), which leads to suppose that their neuroanatomical organization must be separated in one way or another.
Hillis et al. (2002) state that “disproportionate impairment in naming verbs has generally been observed in patients with frontal lesions and non-fluent
aphasia, whereas selective impairment in naming nouns has generally been observed in patients with posterior temporal lesions and fluent aphasia (Tranel
et al., 2001; Damasio & Tranel, 1993; Zingeser & Berndt, 1990; Miceli et al.,
1984)”. Bak (2000; 2001) provided evidence for a selective deficit for verb processing in focal dementia such as the frontal variant of fronto-temporal dementia (FTD).
As it will be argued in the next section, the noun/verb (N/V) dissociation is thought to be rather based on semantics (or maybe, lexical semantic features5)
than grammar; this suggestion arises from the observation that, prototypical verbs relate to actions and more abstract concepts which makes them less
imageable, whereas prototypical nouns relate to objects and more concrete reasoning (i.e. relying on sensory features) being thus more imageable. This
last observations would lead to the conclusion that it may rather be a semantic phenomenon and not a grammatical one; nevertheless, things get more complex when considering that nouns and verbs lay on a graded multifactorial scale (Romagno, 2012). This type of dissociation is not only spread in a cross-modal fashion but it is also argued that it could even be given by a disruption at a presemantic level of processing where picture stimuli are recognized as actions versus objects (Druks, 2002).
It is still not very clearly understood whether verb-selective deficit is caused by a grammatical class effect or if it is due to a more general semantic impairment, as it could be, for instance, a damage to the semantics of actions. It may also be that both semantics and grammatical classes are affected; take, for example, patient EBA (Hillis & Caramazza, 1995) cited above: his dissociations might be the manifestation of a disruption of the semantic system organization as well as of the grammatical processes organization, at the level
5 Lexical semantics refers to those features of semantics that affect the lexicon such as dinamicity, telicity and agentivity; it further relates to antonyms, synonyms, homonyms and so on.
of modality-specific lexical forms. This means that there should be separate neural mechanisms underlying semantics and grammatical class processing. Moreover, dissociations between morphosyntax and semantics have been reported in FTD patients (Breedin & Saffran, 1999; Schwartz et al. 1979; Hodges & Patternson, 1996), supporting this hypothesis.
Hillis et al. (2002) investigated verb-selective deficit in patient MML who showed deterioration of verb oral naming relative to nouns, while presenting with spared repetition and writing production (of verbs) after 10 years of onset of the disease; at 10.5 years of onset she began having difficulties also with verb writing. Her FTD (frontal variant) matches with what was predicted by Bak (2000; 2001) and it “indicates that the neural mechanisms subserving the lexical–phonological processing of verbs for output are sufficiently distinct from those involved in processing the lexical–orthographic representation of verbs and the lexical–phonological and lexical–orthographic representations of nouns, such that only the first can be initially impaired in focal degeneration” (Hillis et al., 2002). The fact that written forms of verbs (with oral naming first, also) deteriorated before those of nouns could indicate that the neural mechanisms that are vulnerable to spread of the disease are those of lexical-orthography and lexical-phonology and that these mechanisms are adjacent (even if independent, as already mentioned). It might be then, that deterioration could first hit lexical-orthographical and lexical-phonological levels of processing before affecting action semantics of verbs.
1.3 Nouns and verbs in the brain
Now that the main topics about aphasia, cognitive neuropsychology and language processing have been introduced, we can move forward into linguistics issues. Many aphasic patients including ZS display what is referred to as noun/verb (N/V) dissociation, and thus it will be of fundamental
importance to discuss this topic with some examples of various patients that have been documented in the literature.
The noun/verb dissociation has long baffled scientists from different disciplines (linguistics, psychology, cognitive science and neuroscience).
The main questions to be asked in this field are: What kind of patterns can account for lexical/morphosyntactic processes in the brain? How are linguistic distinctions captured in the brain? How does the architecture of grammar mirror the organization of concepts?
The source of data and information comes from aphasic patients. These display many different patterns of performance and behavior, ranging from general and not very serious deficits to severe impairments. Some patients do indeed have a deficit just at the phonetic level, while others are hit at the core of conceptual knowledge. The noun/verb dissociation represents one of the most prominent symptoms that is encountered in speech disorders. Understanding how word classes can be distinctly processed into the brain, and how each part of our biology serves a precise purpose is of great importance for scientific research.
Aphasic deficits also differ on a sub-level of psycholinguistic processing of words such as frequency of use, categories differences (e.g. natural vs. artificial objects) and grammatical class (e.g. nouns, verbs and function words). Imageability , first discussed by Paivio et al. (1967, 1968), has a strong relevance for what concerns nouns and verbs; imageability is the ease with which a word evokes a sensory mental image. On the other hand, concreteness usually refers to whether the concept itself, or the object is situated in time and space (Paivio, 1967). Prototypical nouns, for instance, bear sensory features as they are concrete and can thus interface with touch, smell, sight and so on;
