Part V Discourse: language comprehension in context
Sample 3 Telling about a recent movie
Odessa! A swindler! down there . . . to study . . . the sea . . . (gesture of diving) . . . into . . . a diver! Armenia . . . a ship . . . went . . . oh! Batum!
a girl . . . ah! Policeman . . . ah . . . I know! . . . cashier . . . money . . . ah!
cigarettes . . . I know . . . this guy . . .
As many have noted before, though nowadays the comparison has less meaning, agrammatic speech has atelegraphicquality, as if motivated by the need to con- serve cost or effort. This observation, originally made by Pick (1931[translated 1973]), has spawned countless controversies over the nature of agrammatism:
does it arise from pressure to simplify linguistic expressions to their bare-bones information-bearing elements, to economize on articulatory effort or to circum- vent other performance restrictions (such as a limited sequential storage capacity for utterance planning)? Or does the absence of function words and grammati- cal inflections signify a selective impairment of grammatical or morphological competence? These are issues we shall explore later.
In 1874 another milestone in the history of aphasiology was laid by Karl Wernicke with the publication of a monograph that identified a second lan- guage area, damage to which produced symptoms that were complementary to those of Broca’s aphasia. The complementary nature of the language disorder in Wernicke’s aphasia is evident from their strikingly different language pro- ductions:
Speech sample: Wernicke’s aphasia What brings you to hospital?
Boy, I’m sweating, I’m awful nervous, you know, once in a while I get caught up, I can’t mention the tarripoi, a month ago, quite a little, I’ve done a lot well, I impose a lot, while, on the other hand, you know what I mean, I have to run around, look it over, trebbin and all that sort of stuff.
Thank you Mr X. I want to ask you a few –
Oh sure, go ahead, any old think you want. If I could I would. Oh, I’m taking the word the wrong way to say, all of the barbers here whenever they stop you its going around and around, if you know what I mean, that is tying and tying for repucer, repuceration, well, we were trying the best that we could while another time it was with the beds over there the same thing . . . The speech of a Wernicke’s patient is quite fluent: noumsandersor painful, groping and prolonged pauses. Speech rate and intonation sound normal. There are no obvious difficulties with articulation, unlike the Broca’s patient. But the Wernicke’s aphasic does have problems with the phonological form of some words, making numerous sound substitutions (paraphasias) and occasional neologisms(see Table3.1).
Table 3.1 Typical phonological errors in Wernicke’s aphasic speech
Spoken form Target word Error type Error label tarripoi, trebbin not known substitution(?) neologism
tying trying omission paraphasia
repuceration recuperation transposition paraphasia
Wernicke’s enduring contribution to the field was to draw some deceptively simple but quite powerful inferences about the functional significance of direct and indirect neural pathways connecting the two primary language areas. Wernicke’s theory is traditionally dubbed bothconnectionistandlocalizationist. It is not ‘con- nectionist’ in the contemporary computational sense, but in fact articulates the logic of thedouble dissociation,5 which underlies all subsequent proposals for modular neuropsychological theories of language. Nor is it particularly localiza- tionist, in that Wernicke’s model can accommodate the kinds of insights into apha- sic language performance that are usually attributed to such anti-localizationists as Hughlings Jackson (1866), Henry Head (1926) and Kurt Goldstein (1948).
The classical account: the Broca-Wernicke-Lichtheim (BWL) model
Wernicke’s language area is located on the left superior temporal gyrus, in the auditory association area surrounding the primary auditory cortex,
5 Double dissociation is a methodological requirement for localizing some particular mental function to a brain area. It is required to demonstrate not only that loss or damage to the brain area in question is associated with loss or impairment of the mental function in question, but also that preservation of the area in question, in the face of possibly extensive damage elsewhere in the brain, is associated with normal maintenance of the mental function in question. See discussion below on the role of the arcuate fasciculus in conduction and transcortical aphasias.
The classical account: the Broca-Wernicke-Lichtheim (BWL) model 51 Table 3.2 Complementary symptoms of Broca’s and Wernicke’s aphasia
Broca type Wernicke type
–dysfluent effortful speech – fluent but empty speech, normal prosody – absence of function words and
inflectional morphology
– function words and grammatical inflections present
– short utterances – utterances of normal length – relatively intact comprehension – poor comprehension – awareness of deficit – unaware of deficit
though it is sometimes taken, incorrectly, to extend to the posterior region of the supra-marginal gyrus of the temporal lobe and even to theangular gyrusat the junction of the parietal, temporal and occipital lobes (see Figure1.1, p. 11).
The proximity of Wernicke’s area to the primary auditory cortex is paralleled by the proximity of Broca’s area to that of the primary motor cortex, which directly controls the muscles of articulation and vocalization. The auditory/acoustic analy- sis routines for speech perception and the articulatory engrams (memory traces) for speech production are traditionally considered to be stored in these two anatomically separate regions,6 which are directly connected via a subcortical fibre tract known as thearcuate fasciculus.
The complementary symptom patterns of Broca’s and Wernicke’s aphasia are summarized in Table3.2. To a degree, this complementarity follows from the proximity of the respective language areas to their respective adjacent motor and sensory regions. But the contrasting pattern of deficits project from speech into language itself: Broca’s aphasia into the grammatical impairments of language production and perception; Wernicke’s aphasia into symptoms of lexical deficits.
As was appreciated in Wernicke’s time, everything in the cerebral cortex is interconnected. However, more complex mental tasks are likely to involve dis- tributed neural networks invoking transient connections between localized nuclei of cells which are functionally more specialized for particular components of the task at hand. Localized networks in close spatial proximity to primary sen- sory and motor projection areas of the cortex are more likely to be functionally specific, serving ‘simpler’ or more ‘basic’ operations on sensory input or motor output. From such considerations, it may be inferred what the consequences of a disconnection in the direct pathways between the anterior and the posterior lan- guage centres might be: a breakdown in those kinds of language processing tasks that require close co-operation between speech perception and production at a relatively elementary level. The ability to repeat or ‘parrot back’ a short phrase is an example of such a task, whereas to maintain an interlocutor role in a con- versational exchange of any substance would be an example of a complex verbal exchange, engaging the full cognitive resources of speaker and listener. Thus,
6 This is an oversimplification. See Blumstein, Burton et al.(1994) and chapter 8 for further discussion.
1 motor (Broca’s) aphasia 2 sensory (Wemicke’s) aphasia 3 conduction aphasia
4 transcortical sensory aphasia 5 transcortical motor aphasia 6 apraxia or dysarthria 7 hearing impairment
C conceptual
5
1
6 7
4
3 O
O O
2
motor M A auditory
Figure 3.4 The Wernicke-Lichtheim model
disconnection of the direct connections between the sensory and motor speech areas through a lesion of the arcuate fasciculus should impair simple repetition more than it should conversational language use. This is precisely the predicted symptom pattern ofconduction aphasia.
Lichtheim (1884), Wernicke’s disciple and the third contributor to the classi- cal BWL model, refined the ‘connectionist’ model further, expressing the indi- rect pathway between the sensory and motor language areas which is utilized in all ‘conceptual’ uses of language, as a link in a famous schematic diagram (Figure3.4).
The ‘C’ node in the diagram does not represent a neural ‘centre’ in the sense that the ‘M’and ‘A’ nodes in the diagram stand for the speech motor and auditory centres respectively, but rather, an abstract locus forafferentor incoming infor- mation from auditory perception to the conceptual level of speech processing, and a locus for conceptual formulation of speech acts that are ultimately assembled in the speech motor area as ‘instructions’ or motor commands to the articula- tors. The seven numerically labelled inequality signs stand for different types of disconnection between ‘centres’ that could arise from localized brain lesions.
For example,=3 represents disconnection of the arcuate fasciculus. Damage to the speech centres themselves (=1,=2) represent Broca’s and Wernicke’s apha- sia respectively. The ‘disconnections’=4 and=5 were labelled ‘transcortical sensory aphasia’ and ‘transcortical motor aphasia’.
It is hard to imagine what kind of brain lesion might selectively cut the flow of information from the speech perception system to the conceptual processor
The classical account: the Broca-Wernicke-Lichtheim (BWL) model 53 whilst preserving the information flow from the conceptualizer to the speech pro-
duction centre, to produce what is known astranscortical sensory aphasiain the BWL schema (and vice-versa in the case oftranscortical motor aphasia)7. This distinction was subsequently abandoned by many aphasiologists. However, it is possible to have widespread brain damage to peripheral regions of the cortex whilst preserving intact the more medial cortical tissue that encompasses the pri- mary language areas. Such a pattern of damage to cortical tissue can arise from anoxia due to carbon monoxide poisoning. Norman Geshwind described such a case of a woman who suffered massive cortical damage by carbon monoxide poi- soning (Geschwind, Quadfasel and Segarra,1968). Although blind and severely intellectually impaired, she was capable of primitive verbal interaction with her environment. She could repeat phrases and even complete stock, over-learned sayings, such as ‘Ask me no questions and I’ll . . . [tell you no lies].’ She learned to sing along with advertising jingles that she heard repeated over the radio that was constantly left playing by the bed. In short, thanks to the preservation of the sensory and motor speech centres and their direct interconnections, this patient was capable of the type of language performance which is disrupted in conduc- tion aphasia. Geschwind referred to this rare syndrome as ‘disconnection of the speech areas’. In the classical BWL model it would be a particularly severe case of
‘transcortical sensory-motor aphasia’. Notice the complementarity of the symp- toms of ‘conduction’ aphasia and ‘transcortical’ aphasia, linked to the disruption or preservation of the direct or indirect anatomical pathways between the recep- tive and motor language areas. This constitutes a ‘double dissociation’ between two distinct symptom patterns and two distinct sites of lesion.
Lichtheim also elaborated the classical model further to provide a disconnec- tion account of acquired reading and writing disorders. Reading and writing may be described as secondary or derived language competencies. Writing systems (orthographies) are parasitic upon, or iconic representations of, spoken language.
Thus, it is only possible to decipher ancient scripts if one knows or simultaneously reconstructs the spoken language in which the text was written. Also, reading and writing can only be taught to children who have substantially completed primary language acquisition. In a literate individual, reading and writing skills provide alternative sensory and motor access channels (other than listening and speak- ing) to acquired linguistic competencies. Thus, auditory perceptual impairments which may disrupt spoken language comprehension do not necessarily mean that the individual concerned will be reading-impaired. Similarly, the cortical speech area which controls articulation and vocalization is distinct from that which inner- vates the muscles of the dominant hand, so a patient may be quite dysfluent yet be able to communicate through writing. Reading and writing are to a degree functionally independent of speaking and listening – precisely to what degree, and exactly how literacy skills interact with primary linguistic competencies,
7 This criticism was originally made by Freud (1891[English translation1953]) in a brilliant but overlooked monograph, and later more influentially by Goldstein (1948).
is of course a matter of ongoing research and debate. Lichtheim’s proposal for the neuroanatomical basis of reading and writing skills and how they connect to the neuroanatomy of language has been largely adopted with refinements by contemporary neuropsychology.
Lichtheim proposed that decoding of written symbols took place in the left angular gyrus at the junction of the occipital, temporal and parietal lobes, also adding a visual input pathway to Wernicke’s language flow diagram. He also proposed a motor-control centre to support writing, similar to Broca’s area for speech, connected through both direct and indirect pathways to the other language centres and the (somewhat mysterious) ‘C node’ or conceptual centre. Without going into details, you can appreciate how the addition of these secondary nodes and pathways resulted in a range of possible new symptom patterns of differen- tial receptive or productive, speech or language, reading or writing impairments, depending upon what ‘centres’ sustained damage or what connecting ‘pathways’
between centres were disrupted. You can appreciate also that one could take the BWL model and weaken its anatomical claims by denying the strict localization of ‘centres’ to specific brain regions. One would then have a ‘functional’ neu- ropsychological model, the empirical validity of which would rest entirely upon observed patterns of language performance deficit. This is why it was argued previously that the BWL model, although localizationist, can accommodate non- localizationist theories, if it is interpreted as a modular functionalism, essentially the theoretical position espoused by contemporary cognitive neuropsychologists such as Coltheart (2002).
Norman Geschwind (1974) gives one of the most compelling defences of the classical BWL model in the modern era. His account of anomia is an appropriate way to conclude this brief description of the traditional neuroanatomical model of language organization. Pure cases of naming disorder (anomia), uncontaminated by any other signs of language disorder, are rare. However, naming difficulties are present, to some degree, in most forms of aphasia and can be traced to a host of possible causes: semantic memory loss, sensory perceptual disorder, failures of phonological retrieval, etc., which are variously expressed in ‘naming’ tasks: con- frontation naming (object or picture naming), word-finding in connected speech, or greeting an acquaintance.
As Geschwind (1974) observes, the anatomical basis of anomic disorder has been a traditional battleground between localizationists who implicate the left parieto-temporal region and those who assert no specific site of lesion but a correlation with overall cortical damage affecting processes critical to various aspects of naming behaviour. Geschwind argues, as much on grounds of com- parative neuroanatomy as regional brain–symptom correlations, for the special status of the parietal-occipital-temporal junction (POT), an area encompassing the supra-marginal angular gyrus. This was one of the cortical regions identi- fied as having undergone most rapid expansion in the recent evolution of the human brain (referred to in chapter1). The POT, centred as it is at the junction of three lobes and the secondary association areas of the somaesthetic (tactile and
Non-localizationist views 55 body orientation), the visual and the auditory senses, is strategically located for
the formation ofcross-modalsensory connections. Geschwind points out that a large proportion of words8or the concepts that they denote may be thought of as complexes of cross-modal associations. There are problems with the notion that lexical items are literally stored in the POT (see the ‘postscript’ to this chapter) and Geschwind did not formulate his theory in these terms. As David Caplan (1987) points out, Geschwind’s analysis of the neuroanatomical basis of naming and anomia is clearly in the spirit of classical localizationism. But it is also consistent with the non-localizationist emphasis on phylogenetically and ontogenetically late-developing cortical structures in the service of language and symbolic rep- resentation.
Non-localizationist views
The British neurologist Hughlings Jackson is usually credited with elaborating a key distinction between impairments of automatic and volitional behaviour, and linking it to brain evolution and the hierarchy of mental functions:
from simple reflexes to logical reasoning, and the kind of language use which sup- ports inference, plans, and the evaluation of options for action and communication about such things. He observed that ‘propositional speech’ is often impaired while the more automatic uses of language, such as expletives, emotional expressions, greetings or conversational routines, may be preserved intact. The notion that linguistic expressions serve a range of communicative functions linked to mental processes that may be arranged on a hierarchy of increasing evolutionary sophisti- cation may be found in nineteenth-century Darwinian psychology (Spencer, 1867 [reprinted1977]). However, it is a theme which is elaborated in the writings of subsequent non-localizationist theorists of aphasia such as Henry Head and Kurt Goldstein. And, as we shall see, the distinction betweenstrategic, consciously mediated language processing andautomatic, sub-conscious processing has been a critical consideration in experimental psycholinguistic investigations of apha- sia dating from the early 1980s (Milberg and Blumstein, 1981) to the present day.
Roman Jakobson (1941 [English translation 1968]) revived the idea that
‘ontogeny recapitulates phylogeny’ with his notion that in the course of lan- guage acquisition, the child retraces the evolution of language in the species, drawing the additional inference that language breakdown in aphasia represents a retreat to a more primitive or infantile level of language function. Jakobson’s notion that aphasics retreat to immature strategies in language processing has influenced psycholinguistic investigations of aphasia, through the application of heuristicsor processing strategies used by less than fully competent language users (young children, aphasics, second language learners) when presented with
8 With the notable exclusion of function words and connectives.
complex constructions, beyond the structures of simple sentences, issues that we shall take up in chapter12.
Site of lesion studies
World Wars I and II were a boon to the study of aphasia, providing neurologists with thousands of opportunities to observe the effects upon language of traumatic brain lesions of all shapes, sizes and locations. A. R. Luria was the most energetic collector of these ‘experiments of nature’ and one of the most skilful pioneers and practitioners of the art of overlaying sites of lesions and correlating them with acutely observed behavioural and subjective descriptions of language and cognitive impairment (e.g. Luria,1947[English translation 1970]).
Clinical correlations of this kind are fraught with methodological difficulties, and while many detailed and fascinating case studies can be found in the literature, only a very coarse-grained resolution on the question of localization of language functions can be expected when groups of patients with similar lesion sites are compared.
An example from Luria (1973) (Figure3.5), showing the relationship between the incidence of disorders of phonemic identification (the primary symptom of what he calledacoustic aphasia) and different lesion sites, serves to illustrate the kind of correlation that can be expected between a narrowly defined perceptual deficit and the focal point of a localized cortical lesion, typically produced by bul- let or shrapnel wound to the head. Patients with phoneme identification disorder have difficulty discriminating words likepat,bat,bet,bad,bird, . . . etc.
As you see, when the lesion is centred in the auditory association cortex or Wernicke’s area, the incidence of phonemic perception disorder is high (94.7 per cent – but, significantly perhaps, not 100 per cent, as strict localization would require). As the primary lesion site is located further away from the auditory association zone, the incidence of phonemic perception disorder declines, but it still remains a detectable symptom in a significant minority of patients whose pri- mary site of lesion may be at some distance removed from the auditory association cortex. Does this sort of data argue for or against the localization hypothesis? We leave you to ponder this question.
The association of damage to the anterior language areas with the symptom pattern of Broca’s aphasia and damage to the posterior language areas with those of Wernicke’s aphasia has been well established in carefully conducted surveys of the literature (Benson and Ardila,1996). But beyond this gross statistical correlation, the resolving power of these kinds of studies is inherently low. No two brain lesions are likely to be precisely identical and small differences observable at a gross neuroanatomical level may be crucially significant. Furthermore, individuals may differ significantly in how they accommodate to brain injury, depending on the configuration of the original impairments they experience, and the compensatory strategies that they adopt for circumventing their difficulties. It needs to be borne