Jargonaphasia

SIGNORET

Chapter 1

Introduction

JASON W. BROWN

Publisher Summary

This chapter discusses the paraphasia and jargon theories. Historically, jargon was first defined as a series of speech sounds without meaning and later as a combination of verbal (lexical) and literal (sound) errors, either type alone giving rise to the pure form of the paraphasic defect. Wernicke argued that verbal paraphasia occurred with a lesion of left posterior Tl and T2 and was because of an interruption of a control system modulating Broca’s area. Presumably, paraphasia and jargon reflected the extent of interruption in this system. The idea that a left temporal lesion could de-afferent Broca’s area, allowing it to run on uninhibitedly, constitutes perhaps the first theory of jargon production. There have been several other theories of jargon advanced over the years. The classification of Alajouanine, Sabouraud, and DeRibaucourt was an important advance in that afterward it was no longer sufficient to speak of jargonaphasia as if it was a unitary deficit. The recognition of several different, perhaps independent, types of jargon invalidated much of the older literature in which the form of jargon was left unspecified. Moreover, with the identification of at least three forms of jargon—asemantic, neologistic, and undifferentiated—a heavy burden was placed on correlative anatomical studies to explain the qualitative differences. The explanation of symptom change and the diversity of symptom expression has never been the strong point of the Wernicke approach.

Historically, jargon was first defined as a series of speech sounds without meaning (Bastian, 1869), later as a combination of verbal (lexical) and literal (sound) errors, either type alone giving rise to the pure form of the paraphasic defect (Kussmaul, 1876; Mirallie, 1896; Niessl von Mayendorff, 1911). Wernicke (1874) argued that verbal paraphasia occurred with a lesion of left posterior T1 and T2, and was due to an interruption of a control system modulating Broca’s area. Presumably, paraphasia and jargon reflected the extent of interruption in this system. The idea that a left temporal lesion could de-afferent Broca’s area, allowing it to run on uninhibitedly, constitutes perhaps the first theory of jargon production.

However, there have been other views. Niessl von Mayendorff (1911) proposed that paraphasia and jargon resulted from the inferior language ability of the right hemisphere after lesion of the left temporal lobe, a view that predicted an abolition of pre-existing paraphasia by a second lesion in the right Wernicke area. Henschen (1920) gave a critical discussion of this theory. He reported a case with a bilateral lesion of T1 without paraphasia, and suggested that, if the right hemisphere did have a role in the residual jargon or paraphasic speech of an aphasic, this was not necessarily through the mediation of the right temporal lobe. Henschen also reviewed the anatomical cases of jargonaphasia to date (see Kertesz, this volume) and concluded that the disorder was due to a large lesion, generally softening, involving posterior T1 and T2. These were all unilateral lesions except for one bilateral case reported by Mingazzini (1913). Unfortunately, these cases were not sufficiently well documented to be certain of the clinical type of jargon, though it is likely that the majority were neologistic.

There have been several other theories of jargon advanced over the years, many of which are discussed in this volume. Goldstein (1948) wrote that paraphasia was due to impaired inner speech; but then, what is the cause of the impaired inner speech? Jargon has also been attributed to impaired auditory feedback, inattention, or hyperfluency. Luria wrote of paraphasia as due to an equalization of associative strengths, after Pavlov. In certain of these accounts we are left to wonder if the deficit that is invoked as anexplanation is not just another manifestation of the jargon state rather than its cause.

The classification of Alajouanine, Sabouraud, and DeRibaucourt (1952) was an important advance in that afterward it was no longer sufficient to speak of jargonaphasia as if it was a unitary deficit. The recognition of several different, perhaps independent, types of jargon invalidated much of the older literature in which the form of jargon was left unspecified. Moreover, with the identification of at least three forms of jargon—asemantic, neologistic, and undifferentiated a— heavy burden was placed on correlative anatomical studies to explain the qualitative differences. Of course, the explanation of symptom change and the diversity of symptom expression has never been the strong point of the Wernicke approach. Yet other theories of jargon are no less obligated to account for the heterogeneity of the clinical picture, as well as the links between jargon and other fluent aphasic disorders.

Turning to the individual chapters, Buckingham (Chapter 3) raises several points to which I would like to respond. The observation that anomia deteriorates to phonemic (conduction) aphasia, or that phonemic aphasia recovers to anomia, is taken to disconfirm the microgenetic account of these disorders. The reasoning is unclear to me. The deterioration refers to a progressive lesion, not a worsening of the aphasia. Indeed, I wonder if severity is a concept of any meaning whatsoever in language pathology. It is simply a question of the disturbance moving from one state (level) to another. Buckingham implies that I disavow multiple level deficits, but the notion of a combined semantic and phonological disturbance is central to my account of neologistic jargon. Personally, I have no problem with the idea of an anomia submerged in phonemic aphasia or in neologistic jargon. The fact that a patient is one moment anomic, the next paraphasic, is precisely the sort of dynamic change that is captured by the microgenetic model. What would bother me is the idea that anomia can occur SIMULTANEOUSLY with phonemic or semantic paraphasia.

The anomic deficit—inability to evoke a word, not paraphasia—seems one that is positioned just at the point of lexical selection, displaying that moment where an abstract semantic representation is first isolated out of a background field prior to achieving lexical form. The phonological representation is not evoked and the background semantic content does not achieve full lexical differentiation. This is why the anomic has more diffuse—or less stable—semantic categories than the phonemic aphasic; witness the poor performance of anomics on TOT studies. In a way, the deficit in anomia is comparable to that in amnestic states. In the latter (e.g., Korsakoff syndrome), the failure in evocation is at the semantic level, involving temporally linked experiential events. In my view, this is the same deficit but at a different stage in retrieval.

Butterworth, Swallow, and Grimston (Chapter 5) also claim that there is an anomia in jargon, on the finding of hesitations (lexical search) before neologisms. It is of interest that the hesitations are longest for neologisms, less for phonemic paraphasias, and least for verbal paraphasias. Might this be consistent with the idea that the neologism involves a two-level deficit, semantic plus phonemic, and therefore the latency is greatest before the neologism? In this chapter, the authors find evidence from a study of the gestures of their patient to support the concept of an anomia submerged in the jargonaphasia. However, many neologisms do not show exceptional hesitation, suggesting that anomia may not be an intrinsic aspect of neology.

Probably the anomia, if present at all DURING the paraphasic error, occurs only with device-generated neologisms. This would account for their aberrant phoneme frequency. In other words, neologisms with normal phoneme frequencies represent phonemic paraphasias superimposed on lexical targets, whether correct or not, as the underlying (?paraphasic) lexical item, being a real word of the language, will, by virtue of WORD frequency effects, constrain the PHONEME frequency of the neologism in the direction of a normal distribution. On the other hand, neologisms that are not determined by semantic intentions (i.e., where there is no underlying lexical frame), will have a phoneme frequency distribution that reflects intrinsic relationships within the sound system itself. Here the neologism, and thus its phoneme frequency distribution, is no longer constrained by the need to realize possible lexical targets. These neologisms might be associated with an anomia, in that they reflect an output of phoneme strings when lexical search has been unsuccessful. This is a possible explanation of the frequency data in our case of phonemic jargon. Of course, why some patients are simply anomic and others fill the anomic spaces with device-generated phoneme strings, is another problem entirely. No doubt it has something to do with the pathological locus, to involvement of regions, for example Wernicke’s area proper, which mediate phonological realization.

With regard to pathological correlation, few will disagree with Kertesz (Chapter 4) that neologistic jargon is associated with large lesions of left posterior T1 and T2. The localization of semantic jargon, however, is another matter. There are too few cases with pathology to be certain on this point, but such evidence as does exist points to bilateral (basal) temporal lesions. This was present in Green’s case, and has been inferred in the majority of clinical reports (Brown, 1979). Several personal cases, all with bilateral pathology, are reported in this collection just to provide some perspective on Kertesz’s conclusions.

Kertesz also raises the related issue of the evolution of neologistic jargon. The majority of cases seem to resolve toward semantic jargon. This would argue that the lesion of semantic jargon, is, if anything, smaller than that of neologistic jargon, certainly left-sided. Yet I wonder about this. In my experience, neologistic jargon tends to recover into a state of fluent empty speech with skewed meaning content and occasional paraphasia rather than the semantic anomaly of the typical jargon case. This is not to say that semantic jargon does not occur with a unilateral left lesion, but rather that in true (unintelligible) semantic jargon a bilateral lesion is often present.

Again, with regard to recovery, it is argued that the tendency for neologistic jargon to evolve toward semantic jargon rather than phonemic aphasia disconfirms the concept of a two-level deficit in neologistic jargon. In other words, if neologistic jargon represents a combined semantic and phonological disturbance, why does it recover only to the semantic deficit? The fact is that neologistic jargon evolves in both directions, though admittedly the recovery to phonemic aphasia is less frequent. Why should this be? Presumably, if right hemisphere compensation is involved, this should, because of its presumably better semantic ability, bias recovery toward a residual phonological deficit. A possible explanation is that semantic recovery leads to anomia in most cases, and that it is not possible to have a phonemic paraphasia, as distinct from device-generated jargon, superimposed on an empty anomic segment. That is, semantic recovery occurs from incorrect selection (semantic paraphasia) toward correct but incomplete selection (anomia). The deficit in anomia is just prior to full lexical differentiation. How could one have a deficit of phoneme sequencing or selection on empty word frames? This predicts that phonemic (conduction) aphasia would occur ONLY with complete recovery of semantic-lexical intentions. The fact that such recovery is usually incomplete (e.g., anomic) explains the recovery bias. In contrast, recovery of the phonemic disturbance exposes underlying semantic errors. In such cases, lexical realization is adequate from the phonological, but not the semantic, standpoint.

The cases of phonemic (undifferentiated) jargon described by Peuser and Temp (Chapter 11), and by Perecman and myself (Chapter 10), are the first thorough reports of this disorder in the literature. The chapter by Anderson (Chapter 13) which describes the prosodic contours in our case is a valuable addition. There are, however, important differences between these cases which need to be emphasized. The first case produced simple but variegated CV strings in relation to a type of mumbling behavior. This patient had a large central lesion, and seems closer to Alajouanine’s case of undifferentiated jargon. Our case had a richer phoneme inventory with more complex clusters, and was more clearly situated among the fluent aphasias, both clinically and anatomically. Conceivably, these cases represent a dissolution within the phonetic and phonemic systems respectively. Alternatively, there could be a continuum between them, leading from mumbling to simplified Honolulu utterances as in Pueser’s case, to well-articulated complex jargon as in our case. Anatomically, the situation is no less uncertain. I have described a mumbler with a large left central lesion (Brown, 1979), yet there is a case— the only other of which I am aware— reported by Kähler and Pick (1879) of mumbling in association with bilateral temporal lesions, as were present in our case of complex jargon.

Zaimov (Chapter 8) provides a somewhat different approach to paraphasia and possible links to schizophrenia. Lecours, Osborn, Travis, and Rouillon (Chapter 2) also discuss structural similarities between schizophrenic and aphasic language. Such similarities are not wholly unexpected, in view of the fact that normal speech errors, and sleep speech and transitional speech, resemble certain types of aphasic utterances. The problem with most studies of schizophrenic speech is that they tend to focus on mild cases, or patients under treatment, where the regression does not penetrate too far into intrasentential material. Like the confabulating Korsakoff patient, the schizophrenic gives the impression of a thought disorder, or a paramnesia. When such cases are then juxtaposed to aphasic disorders such as Broca’s aphasia, obviously the similarities are not very striking. However, careful investigations carried out years ago by Kleist and others— and for that matter my own experience with regressed psychotics— point to close relationships between schizophasic and aphasic jargon. These findings are, it seems to me, buttressed by recent work on hemispheric asymmetries in schizophrenia, evidence for limbic-temporal dysfunction, and preliminary PET studies which suggest temporal lobe dysfunction in schizophrenics (Farkas et al.,