C H A P T E R 6
The goal of this chapter is to give insights into the underlying sources of breakdown in object naming following brain damage. In particular, I will focus on the neurological disorders of different types of aphasia and, citing clinical literature as evidence, I will describe the nature of word finding difficulty in aphasic patients and normal subjects. I review modern models that address processing stages of picture naming. These include the component models, such as the perceptual model of Murphy & Smith, (1982) and parallel activation model such as the cascade model (Humphreys, Riddoch & Quinlan, 1989).
It was not until the early nineteenth century that the French neurologist Bouillaud (1825) recognised that the cerebral structures controlling the use of language were, at least in part, independent of those controlling the non‑speech movements of the articulator organs. In the second half of the century the generic term “aphasia” was applied to the group of difficulties in speech, auditory comprehension, reading and writing.
The symptoms of aphasia were first described by Imhotep, and can be found in the Edwin Smith Surgical Papyrus, noted to have been written about 3000 BC, “…one having a wound in his temple, perforating his temporal bone… and he is speechless. An ailment not to be treated.” An important concept is the recognition that aphasia is a language disorder and not a speech disorder. De Vito (1970) writes that,
“aphasia as viewed by most contemporary researchers, involves language disturbances in decoding, manipulating and / or encoding symbols whose etymology is to be found in brain damage.”
It was the famous Parisian clinician Trousseau who replaced Broca’s term “aphemia” for the disturbance of the “faculty of speech” and thus first used the term “aphasia” in 1864. ” Aphasia” was more popular and therefore remained.
6.1 Object naming disorders
Aphasia may be accompanied by such conditions as demonstrable paralysis or paresis of the speech mechanism but these conditions should be called dysarthrias, as distinct from aphasias, and will not be of concern in this thesis.
6.1.1. T O T phenomenon and name production
The naming of people, objects, colours, etc. is a very frequently occurring process which only really comes to attention when it fails.
On occasion everyone has “gaps” in memory when the name of a perhaps rare object simply will not come forward. It produces a “tip‑of‑the‑tongue” (TOT) experience during which one feels that the elusive word is only just out of reach and will perhaps come back later. Wlliam James (1893) described the ‘gap’ referred to above as containing “the wraith of the name”, and notes that it is specific and active as the person will quickly negate wrong names which are proposed. TOT is a phenomenon which most people experience from time to time with less common words. There are, however, a group of patients classed as “anomics” who, due to damage to certain areas of the left cerebral hemisphere, have lost the ability to produce the name of even common place objects, colours etc. Naming difficulty is common to virtually all aphasic patients irrespective of aphasia type (Goodglass and Kaplan, 1983). Such people have conversations which appear grammatically normal, well articulated and of normal intonation, but lack substantive content. For example, some patients may be able to show by gestures or by circumlocutions that they have grasped the meaning of a picture while others give an impression of impaired comprehension. The patient cannot supply the information carrying nouns, principle verbs and adjectives. Many aphasic patients show this kind of problem to some extent and might more accurately be referred to as disnomic rather than anomic, meaning a disruption but not a total failure in the ability to name. A common way to search for the underlying mechanisms of naming difficulty has been the analysis of naming errors in patients representing major clinical syndromes of aphasia. This is based on the widely held assumption that the distribution of naming error types differentiates the major aphasia syndromes of Broca’s, Wernicke’s, conduction and anomic aphasia (Benson, 1979; Goodglass and Geschwind, 1976). However, the results have not been clear‑cut.
One reason is that a naming error may have multiple underlying sources that remain unclear if the analysis is limited to error classification only (Willimas and Canter, 1982). Another reason may be that some patients have not always had those aphasic symptoms that their labels would imply. For instance, part of the patients labelled, for example, Broca’s or Wernicke’s aphasics could actually have partially recovered (e.g., Kohen and Goodglass, 1985).
Previous studies of anomia have focused on many different variables. Word finding has been analysed in relation to the frequency with which words appear in the language (Wepman, Bock, Jones and VanPelt, 1964) and in terms of broad semantic categories (Goodglass, Klein, Carey and Jones,1966). Frequency of use can serve as an index of word comprehension. Common words are more likely to be understood than rare words. Also factors such as the picturability of an object to be named (Goodglass, Hyde and Blumstein, 1969), and the motor schema involved in the knowledge of a word’s referent (Gardner, 1973) have been investigated.
Goodglass and Geschwind (1976) define anomia as a selective loss of lexical repertoire, primarily nouns and verbs, but adjectives and adverbs as well. There is usually the feeling that the individual once had the capacity to produce the word that now she/he cannot. The inability to express the required word is one of the more frequent sources of anomia (Benson, 1979). Prompting usually successfully produces the word, as in the TOT state observed in normal subjects. This state, according to Brown and McNeill (1966) is when the individual is absolutely certain of “knowing” a word he/she wants to say, but still cannot immediately produce. Left alone she/he may well recall part of the word such as the initial letter. However, like anomic patients, the individual with the TOT phenomenon responds to minimal cues such as the invisible letter and is able to produce the correct word.
I will define Anomia as a difficulty in finding or producing the correct word. A patient with object anomia can pick up and use a knife and a cup, for example, but be unable to name them. This syndrome indicates that recognition of objects for manipulation and for use require different underlying processes than for naming.
For many clinicians, anomic aphasia is the equivalent of anomia but this is not true, strictly speaking.
Major confusion still abounds concerning the characteristics of anomic behaviour in different types of aphasia. More attention seems to have been paid to properties of the words themselves and their inter‑relations, than to the actual process of naming.
Williams (1968) claims that four variables influence the naming performance of aphasics. These are “the characteristics of the referent, its name, the type of stimulus presentation and the situation”. It has been found that, variability in the language performance of aphasics is dependent to some extent on a variety of internal and external variables; Diamond, Epstein and Bender, 1969). This variability in language performance may be taken as evidence against the notion of aphasia as a “loss of words” and interpreted as a deficiency in a retrieval processes which leads to naming errors and paraphasias.
Most aphasic patients who suffer from anomia do so independent of the modality in which the stimulus is presented (Goodglass, 1968). Naming is nearly always successful if phonetic prompting of the initial syllable is given. The patient can usually, in a roundabout way, describe the function of the object so that the problem is seen as one of word‑finding. All the processes concerned with object recognition are intact. More specific Anomia also exists, in the form of category and modality‑specific anomia.
The presence of anomia by itself fails to indicate an aphasic condition. However anomia is probably the most common finding in aphasia such that it is unwise to consider a diagnosis of aphasia in a patient without anomia (Brown, 1972).
Brown, (1972) suggests that anomia underlies all other language disorders, being the key disturbance. Word production anomia occurs in patients who cannot produce the correct word even when appearing to know what is wanted.
On confrontation‑naming the patient fails to produce words unless aided by prompting. The main defect appears to be initiating articulation, although defective articulation and inability to name are often intermixed. Sometimes the patient’s output is so “contaminated” by paraphasias that the required word is not presented. Due to phoneme substitution (despite the number of syllables and the infliction being correct) the name produced is totally incorrect. Thus we see the inability to produce the correct word rather than lack of knowledge of it. As regards the pathology, the areas usually involved are anterior, damage to the motor speech area of the left frontal lobe causing articulation problems (such as Broca’s aphasia) or to the pathways leading to Broca’s area ( such as conduction aphasia ) producing excessive literal paraphasia Cohen (1970); Bub and Kertez (1982).
Some aphasic individuals have more of a problem finding the appropriate word when asked to name an object than in spontaneous speech. Although the patient cannot comply, he can give a functional description. Phonemic prompting is seldom of any benefit. The disability appears to be a one way process since on being given the correct name, the patient is able to choose the correct item from a selection of items. Katz and Foder (1964) suggest the cause as being a difficulty in entry to, or use of, the so called word dictionary or “lexicon”.
Pathology in such “pure” anomia is usually located in the posterior portion of the second temporal gyrus or in Brodmann’s area 37, the temporal‑occipital junction area of the dominant hemisphere. To illustrate the wide variety of anomic conditions two more distinct types can be mentioned.
(i) Semantic anomia: In semantic anomia, the patient, as well as not producing the words nor accepting prompts, also can not select the correct item when the correct name is given. Such a patient seems to have lost or forgotten the symbolic meaning of the word. Semantic representations do not include the spoken names of concepts which must be retrieved separately. If an object or picture is to be named successfully, it must first endure perceptual analysis to create an internal representation of the object’s visual features and their relations to one another.
(ii) Colour Anomia: Colour anomia is the best example of category specific anomia. Googlass et al. (1966) isolated colour anomia as one of the more common forms of the rare category‑specific naming disturbances.
Colour anomia (Geschwind and Fusillo, 1966) is frequently associated with alexia and some degree of impairment of object naming (De Renzi, Zambolin and Crisi, 1987) and the disorder affects naming as well as comprehension of colour names.
Pathology is usually in a primary sensory area or the pathways connecting such as area to the language area. Although prediction from the site of pathology of the different types of anomic disorders is low, improved testing techniques promise better predictions in the future.
Geschwind and Fusillo (1966) defined colour anomia as disconection (access disorder). Destruction of the left calcarine area, when coupled with a lesion to the splenium, disconnected the intact right calcarine area from the intact left hemisphere angular gyrus, where visual and verbal information are combined.
Thus, preserved colour information in the right hemisphere cannot be transmitted to the intact language areas of the left hemisphere.
When we look at an object various mental activities occur so that a name or description can be given. Often, reports Benson, 1979, the word given is the most common name that can identify the figure. However, with so many associations available the process is undoubtedly very complex. The word chosen depends to some extent upon the strength of these associations. Even if the stimulus had been received through a different sense modality the same name would eventually have been produced. Therefore Benson says that naming is one of many activities in a complex function, often called concept formation, that is relatively independent of the sensory modality. Upon sight of an object initial cortical stimulation occurs in the visual cortex, area 17. The impulse is then conveyed to the surrounding visual association cortex, areas 18 and 19. One major pathway connects the corpus callosum to the analogous association cortex in the opposite hemisphere. This connection integrates stimuli activating the two hemispheres. This allows a single image to be formed from stimuli activating the visual areas of the two hemispheres. A direct link from the sensory association cortices to the angular gyrus also exists.
It is probable that association between the different sensory stimuli (cross‑modal association) occurs in the angular gurus.
Such activities seem essential for the production of a name. Whether there is only an entry into the lexical store via the angular gyrus or whether it is possible from either hemisphere remains unknown. There could be two separate functions of cross‑modal association and word selection. In “pure” anomia, patients readily describe the object they cannot name indicating the good working order of cross‑modal associations.
6.2 Object knowledge organization
There have been several proposals to explain the organization of object knowledge (Collins & Loftus, 1975, Rosch, 1975). These proposals are based on hierarchical structures which have been found useful in understanding the impairments of knowledge from neurological damage (Warrington, 1975; Diesfelt 1985). The organization of knowledge may also reflect “Fields” of knowledge (Konorski, 1967) such as animate versus man‑made objects (Warrington & MaCarthy, 1983, 1987; Warrington & Shallice, 1984); knowledge may even be normally organised into more specific categories which are selectively impaired with brain damage (Nelson, 1946; Mckenna & Warrington, 1979). For some as yet unknown reason, selective impairments of knowledge are more likely to occur from diffuse than from focal brain damage.
Naming can be disrupted, according to Whitehouse, Caramazza and Zurif (1978) by malfunction in any one of a series of stages along the information‑processing chain which generates the resulting name. The problem may concern disruption at the level of organization or at the level of retrieval. It is possible that conceptual elements, although controlled at a non‑linguistic level, are insufficiently structured for adequate lexical organization.
Whitehouse et al (1978) suggest that one factor leading to the difficulty in naming is a disturbance of the conceptual representation associated with a label. Of course this conclusion does not necessarily exclude the possibility that some anomic disorders may result from difficulties purely at the retrieval level (Kay & Ellis, 1987).
For speech to occur the selection made must reach the speech area of the frontal cortex and the articulation centres must be activated. Prior to speech one is allowed to “hear” the name; part of a feedback system provides for any necessary alterations.
Brown and Mcneill (1966) found that when subjects were unable to produce the required word in response to hearing its definition, they could often write the initial letter, and 57% of the time they correctly gave the number of syllables of the missing word, even though they could not produce the word. Moreover, 60% of subjects distinguished between associates which resembled the target word in sound from those which were related by meaning. The important implications of this classic study is that a word contains both semantic and acoustic representations.
Barton (1971) extended and adapted Brown and McNeil’s study to demonstrate the tip‑of‑the‑tongue (TOT) phenomenon in aphasics.
Furthermore, Goodglass et al (1976) showed differences in the TOT state between different types of anomics. More importantly, the latter authors demonstrated that groups of anomics were all similar in their rate of failure in naming the stimulus pictures, and implied that the differences found could not be attributed to the degree of impaired word finding. Goodglass et al. (1976),therefore concluded that a patient’s tacit knowledge of a target word depends on the type of aphasia suffered rather than overall naming ability.
Butterworth (1980b) argues that semantic errors of naming occur when conceptual knowledge activates the wrong lexical semantic representation because of overlap between the conceptual description of the object and the lexical‑semantic characterisation of the error word. This is a phenomenon which most people experience from time to time with less common words.
6.3. Modality‑Specific Aphasia
There are three types of confrontation naming impairment in which naming is impaired only from single a modality. Naming from verbal descriptions are intact.
First, there is impairment through vision called optic aphasia. This disorder is distinct from disorders of identification (agnosias) and from more general disorders of language (aphasias).
6.4.1. Optic aphasia
Optic aphasia is a neurological disorder in which patients are unable to name visually presented objects, but the knowledge about the object is still intact. The optic aphasic patient can answer questions about the seen object. This disorder was first described by Freund in 1889, but since then its existence has been continually questioned. It is a problematic matter and there is no obvious reason why naming, and naming alone, should be impaired with respect to a particular modality of presentation. The common interpretation of it is in terms of an anatomical visuo‑verbal disconection. However, the exact level of the psychological process impaired remains unspecified.
Riddoch and Humphreys (1987b) claim that optic aphasia arises from an inability to sort out visually similar structural descriptions. They deny the implication from optic aphasia that object knowledge has dual representations ( i.e., verbal versus visual).
Recently, Farah (1990) has suggested an explanation in terms not of a single defect, but of the superadditive effects of two individually mild disconection‑type deficits. Farah’s account suggests it might be two routes, first, semantic access from vision and second, phonological access from semantics. Only when these co‑occur may Optic aphasia ensue. More recently, Manning and Campbell (1992) investigated an optic aphasic patient, A.G., who shows a pure and isolated deficit in naming visually presented objects on confrontation, but with sparing of visual action names. An object on sight (in addition to a recognition defect) hence the term “modality“.
6.4.2. Lexical retrieveal
The process by which we remember the names has its theories. Norman and Bobrow (1979), suggested how name retrieval may involve three stages: one, the initial specification; two, matching the retrieved name to the initial specification and three, evaluating the match. This is assumed because people tend to retrieve names only after retrieval of contextual and personal information.
Presumably we do manage to retrieve that name from some form of memory store in function to provide a word appropriate to the meanings we need to express in words. The speech output lexicon, (Ellis & Young, 1988), speech output logogen system (Morton, 1980a; Morton & Patterson, 1980), the phonological lexicon (Allport & Funnell, 1981), or the phonemic word production system (Ellis, 1984 b)”.
It has been found that, variability in the language performance of aphasics is dependent to some extent on a variety of internal and external variables; Diamond, Epstein and Bender, 1969; Wigl and Bierwisch, 1970).
It is also possible that such organisation is sufficient, but that mechanisms responsible from these structures is disrupted. Results showed that Broca’s aphasias demonstrated a relatively intact underlying lexical structure. Such a result was supported in the research literature by Kok (1964) who reported several cases of anomia associated with left temporal‑occipital lesions where visual recognition is intact when assessed clinically but impaired when assessed tachistoscopically.
There are, however, a group of patients classed as “anomics” who, due to damage to certain areas of the left cerebral hemisphere have lost the ability to produce the name of even commonplace objects, colours etc. Such people have conversations which appears grammatically normal, well articulated and of normal intonation, but lacks substantive content. The patient cannot supply the information carrying nouns, principle verbs and adjectives. Many aphasic patients show this kind of problem to some extent and might more accurately be referred to as disanomic rather than anomic, meaning a disruption but not a total failure in the ability to name.
The cause of a patient’s failure to name an object could be related to the malfunction of any of the processes previously referred to, but for him to be diagnosed as suffering from anomic aphasia, vision, recognition, and articulation remain unaffected.
It is not normally difficult to determine whether or not an object is recognised as the patient can make use of descriptions of its function, where it is usually found etc. to demonstrate recognition.