Semantic errors in a deep dyslexic

A case of a Swedish-speaking deep dyslexic is reported whose semantic paralexias appeared to result mainly from a lexical retrieval failure in oral reading. He was able to draw correct pictures of the written words for which he had simultaneously produced a semantically erroneous oral reading response. Repeated attempts to correct paralexic responses were common, indicating that the patient was often aware of the errors. His lexical retrieval problems and semantic errors extended to naming as well, and the results support Nolan and Caramazza's (1982, Brain and Language, 16, 237-264), dual-deficit model of deep dyslexia.     

Phonological and semantic information in word and nonword reading in a deep dyslexic patient

Deep dyslexia is diagnosed when brain-injured, previously literate adults make reading errors that include hallmark semantic paralexias (e.g., reading HEART as BLOOD) and are also impaired at reading nonwords (e.g., FRIP). The diversity of these symptoms have led most researchers to conclude that there are multiple sources of impairment in this syndrome and that one of the most critical is a failure to process phonological information at a sublexical level. The patient (SD) reported in this study fits the deep dyslexia profile to the extent that she makes several semantically related reading errors. She also shows the classic frequency and image ability effects of the syndrome. However, as we report, she does read some nonwords correctly and she shows a strong advantage for naming when phonemic cues are presented. We discuss the performance of SD, on these preliminary tasks, in terms of a phonological selection impairment.     

Acquired dyslexia in three writing systems: study of a Portuguese-Japanese bilingual aphasic patient

The Japanese language is represented by two different codes: syllabic and logographic while Portuguese employs an alphabetic writing system. Studies on bilingual Portuguese-Japanese individuals with acquired dyslexia therefore allow an investigation of the interaction between reading strategies and characteristics of three different writing codes. The aim of this study was to examine the differential impact of an acquired brain lesion on the reading of the logographic, syllabic and alphabetic writing systems of a bilingual Portuguese-Japanese aphasic patient (PF). Results showed impaired reading in the logographic system and when reading irregularly spelled Portuguese words but no effects on reading regular words and nonwords in syllabic and alphabetic writing systems. These dissociations are interpreted according to a multi-route cognitive model of reading assuming selective damage in the lexical route can result in acquired dyslexia across at least three different writing codes.     

The interaction of multiple routes in oral reading: evidence from dissociations in naming and oral reading in phonological dyslexia

During oral reading we hypothesized that lexical representations are activated and selected for output by the simultaneous activation of the semantic, the direct lexical orthography to phonology, and the sublexical grapheme-to-phoneme conversion (GPC) routes (Southwood & Chatterjee, 1999). Serial models of reading argue that the semantic route governs oral reading with minimal influence from the nonlexical direct route and the sublexical GPC route. These models predict that semantic errors should occur in reading when the semantic route and GPC are both impaired. The Simultaneous Activation Hypothesis predicts few semantic errors in oral reading but many during picture naming. Semantic errors are infrequent in reading because information from all three reading routes constrains activation of a phonological entry. By contrast phonological selection in picture naming is constrained primarily by the semantic route and if damaged additional information is unavailable to select the appropriate phonological code. In agreement with the Simultaneous Activation Hypothesis five phonological dyslexics produced semantic errors during picture naming but not when reading aloud. Phonological errors were present during oral reading and minimal during picture naming.     

Mimicking aphasic semantic errors in normal speech production: evidence from a novel experimental paradigm

Semantic errors are commonly found in semantic dementia (SD) and some forms of stroke aphasia and provide insights into semantic processing and speech production. Low error rates are found in standard picture naming tasks in normal controls. In order to increase error rates and thus provide an experimental model of aphasic performance, this study utilised a novel method- tempo picture naming. Experiment 1 showed that, compared to standard deadline naming tasks, participants made more errors on the tempo picture naming tasks. Further, RTs were longer and more errors were produced to living items than non-living items a pattern seen in both semantic dementia and semantically-impaired stroke aphasic patients. Experiment 2 showed that providing the initial phoneme as a cue enhanced performance whereas providing an incorrect phonemic cue further reduced performance. These results support the contention that the tempo picture naming paradigm reduces the time allowed for controlled semantic processing causing increased error rates. This experimental procedure would, therefore, appear to mimic the performance of aphasic patients with multi-modal semantic impairment that results from poor semantic control rather than the degradation of semantic representations observed in semantic dementia [Jefferies, E. A., & Lambon Ralph, M. A. (2006). Semantic impairment in stoke aphasia vs. semantic dementia: A case-series comparison. Brain, 129, 2132-2147]. Further implications for theories of semantic cognition and models of speech processing are discussed.     

Word-finding abilities of three types of aphasic subjects

Word-finding difficulties are often observed among different types of aphasic patients. This investigation analyzed the word-finding abilities of 30 aphasic subjects (10 Broca's, 10 Wernicke's, and 10 anomic). Forty nouns counterbalanced according to word length and frequency of occurrence in English language usage were used as stimuli and presented through four modalities (oral expression, writing, auditory comprehension, and reading comprehension). It was expected that patterns of word finding abilities would help in the classification of the different types of aphasia. In addition, long words and less frequently occurring words in English language usage should prove more difficult in word-finding ability, regardless of modality. The results of this study found long words and less frequent words were more difficult for aphasic subjects. Among the modalities, long words were significantly harder than short words for the writing modality only. It was also found that semantic errors were the most common errors for all types of aphasic subjects. Broca's subjects produced significantly moreno response errors in oral expression; Wernicke's subjects produced significantly more semantic and phonemic errors in reading comprehension; and, Wernicke's subjects produced significantly more unrelated errors in both oral expression and reading comprehension. Clinical implications were also discussed.The present study was based on a doctoral dissertation completed at the City University of New York in partial fulfillment of the requirements of the doctoral degree in Speech and Hearing Sciences by the first author under the direction of the second author. The authors wish to thank Dr. Louis J. Gerstman for his assistance with the statistical analysis of this research and Dr. Robert Goldfarb for all his helpful suggestions and editorial comments.     

Crossed Aphasia in a Dextral: A Test of the Alexander–Annett Theory of Anomalous Organization of Brain Function

A case of crossed aphasia is presented in a strongly right-handed 77-year-old white female without history of familial sinistrality or prior neurological illness. She developed a right middle cerebral artery infarction documented by CT and accompanied by obvious clinical signs of a conduction aphasia with some resolution but continuing obvious language defect after 9 weeks in rehabilitation. Comprehensive neuropsychological and aphasia testing suggested anomalous lateralization of phonologic-output aspects of language, emotional prosody, motor planning and body schema modules with usual lateralization of lexical–semantic aspects of language and visuo-spatial functions. Experimental validation of the uncrossed lexical–semantic aspects of language using tachistoscope methods found support for the Alexander–Annett theory that different aspects of language can be dissociated in their lateralization. The subject had difficulty identifying a semantic associate of a picture presented to the left visual field (7 errors out of 10) relative to right visual field presentation (2 errors out of 10). Bilateral free naming errors (6 and 5 errors in the left and right visual fields, respectively) occurred consistent with the aphasic presentation, suggesting phonologic-output dysfunction from the right cerebral vascular accident. Implications of the results for aphasia classification are discussed.     

Picture-naming in aphasia

The distribution of picture-naming errors for Broca's aphasics (n = 9), Wernicke's aphasics (n = 9), conduction aphasics (n = 9), frontal anomics (n = 7), and posterior anomics (n = 9) was examined to determine the diagnostic power of error types in picture-naming. Negated responses were associated with Broca's aphasia, whole-part errors ("hose" for nozzle) were associated with frontal anomia, and poor phonemic cuing was associated with Wernicke's aphasia. In addition, the relative distribution of the three most prominent naming errors-phonemic errors, semantic errors, and multiword circumlocutions-tended to distinguish the two anomic subgroups from the other aphasia subgroups. Anomic aphasics produced the fewest phonemic errors and the most multiword circumlocutions; this pattern suggests minimal word-production difficulty in anomic aphasia relative to the other aphasia syndromes. Despite such group differences, the overall picture indicates that there is considerable similarity among aphasia syndromes in terms of picture-naming behavior.     

Self-monitoring behavior in a case of severe auditory agnosia with aphasia

This case report describes an unusual combination of speech and language deficits secondary to bilateral infarctions in a 62-year-old woman. The patient was administered an extensive series of speech, language, and audiologic tests and was found to exhibit a fluent aphasia in which reading and writing were extremely well preserved in comparison to auditory comprehension and oral expression, and a severe auditory agnosia. In spite of her auditory processing deficits, the patient exhibited unexpected self-monitoring ability and the capacity to form acoustic images on visual tasks. The manner in which she corrected and attempted to correct her phonemic errors, while ignoring semantic errors, suggests that different mechanisms may underlie the monitoring of these errors.     

Dissociation of semantic and phonological errors in naming

We report the naming performance of a fluent aphasic, DP, who shows a striking dissociation between semantic and phonological (nonword) errors: he produced numerous semantic errors but virtually no phonological errors. DP's pattern of performance is the reverse of that reported for patient DM (Caramazza, Papagno, & Ruml, 2000), who only made phonological errors in a naming task. These patterns of performance are inconsistent with the proposal by Dell, Schwartz, Martin, Saffran, and Gagnon (1997) that the naming deficit in fluent aphasia is the result of global damage to all levels of the lexical access system and support instead the hypothesis that brain damage can selectively disrupt distinct subcomponents of the lexical processing system.     

The selective impairment of phonological processing in speech production

We report the naming performance of a patient (DM) with a fluent progressive aphasia who made phonological errors in all language production tasks. The pattern of errors in naming was strikingly clear: DM made very many phonological errors that resulted almost always in nonword responses. The complete absence of semantic errors and the very low ratio of formal errors relative to nonword errors (1.6:30.3) in DM's performance are discussed in the context of recent claims about the nature of naming deficits in fluent aphasics. We argue that DM's performance makes highly improbable the claim that fluent aphasia results from global lesions affecting all levels of the lexical access system equally.     

Effects of near and distant semantic neighbors on word production

One way to examine the dynamics of word processing is to investigate how processing is affected by the co-activation of similar words (“neighbors”). A unique prediction of attractor dynamical models is that near neighbors should exert inhibitory effects and distant neighbors should exert facilitative effects. In study 1, data from 62 unselected chronic aphasia patients revealed a higher rate of semantic errors for words with many near semantic neighbors and fewer semantic errors for words with many distant semantic neighbors. In study 2, this basic result was replicated in controls using a speeded picture-naming paradigm. Together, these two studies provide strong new evidence consistent with the attractor dynamics view of neighborhood effects. In addition, analyses of correlations between effect sizes and lesion locations, and comparisons with the existing literature on semantic deficits in aphasia and the speeded picture-naming paradigm, all provide converging evidence that the semantic error patterns found in the present studies were due to disruptions of cognitive control mechanisms.     

When does a deep dyslexic make a semantic error? The roles of age-of-acquisition, concreteness, and frequency

Semantic reading errors are the central and defining feature of deep dyslexia. This study compared the words the deep dyslexic patient LW read correctly with those she omitted and those to which she produced semantic errors in terms of their concreteness, age-of-acquisition, frequency, and length. Semantic errors were made to less concrete, later-acquired, and shorter words than were read correctly; there was no reliable effect of word frequency. More importantly, the actual semantic errors produced were later-acquired than the stimulus words, but they were not more concrete or reliably more frequent. These results implicate age-of-acquisition in the process that produces semantic errors. It is proposed that concreteness determines the specificity of the semantic system to activate a set of candidate responses and that age-of-acquisition biases the ease with which certain words can be selected from this set to be produced as reading responses.     

Deep dyslexia and semantic errors: a test of the failure of inhibition hypothesis using a semantic blocking paradigm

Deep dyslexia is an acquired reading disorder that involves the production of semantic errors and the inability to read aloud nonwords successfully. Several explanations for this reading impairment posit multiple loci of damage to account for the various error types produced in deep dyslexia. In contrast, the failure of inhibition hypothesis suggests that damage in the phonological output lexicon alone can explain these errors. Specifically, this hypothesis proposes normal processing via orthographic and phonological reading routes, as well as an intact semantic system. However, slowed or reduced inhibitory connections result in the failure to suppress spuriously activated neighbours in the phonological output lexicon, where neighbourhood can be defined in terms of phonology, orthography, or semantics. Given a failure to inhibit semantically related candidates, semantic reading errors occur. Important to the test of this hypothesis is that it evolves several predictions that are contrary to performance observed in the normal population. In particular, semantic errors are predicted to be greater in conditions where words are blocked according to semantic category than in random presentations. In addition, a semantic interference effect is expected. The results of semantic blocking were consistent with these predictions and lend support to the failure of inhibition hypothesis.     

The simultaneous activation hypothesis: explaining recovery from deep to phonological dyslexia

Deep dyslexia evolved into phonological dyslexia in one patient. Semantic errors resolved while phonological and derivational errors persisted in reading. Nonword reading improved but remained inferior to word reading. Despite a residual semantic deficit naming improved. The Simultaneous Activation Hypothesis explains recovery from deep to phonological dyslexia and the continued dissociation between reading and naming errors. Partial recovery to all three reading routes increased constraints for word selection at the phonological output lexicon (POL) improving word reading. With recovery, the POL receives additional supportive information from the partially recovered direct oral reading route and grapheme-to-phoneme conversion (GPC) eliminating semantic errors in oral reading. Nonword reading also improved because of partial recovery to all three routes. Semantic errors in naming persisted because additional constraints were unavailable at the POL to activate a phonological entry. Phonological and derivational errors were more frequent in reading than in naming the result of incomplete GPC recovery. Residual nonword reading deficits resulted from incomplete GPC recovery, indicated by the persistence of neologisms in nonwords. The Simultaneous Activation Hypothesis readily accounts for the evolution from deep to phonological dyslexia.     

Simultaneous activation of reading mechanisms: evidence from a case of deep dyslexia

We report the performance of LC, a deep dyslexic. We investigated extensively her errors according to serial cognitive neuropsychological models of oral reading. Initial evaluation of her reading suggested impaired access to the phonological output lexicon (POL). Impaired grapheme-to-phoneme conversion (GPC) and semantic errors in reading suggested that LC read via an impoverished semantic route. However, a serial model of oral reading could not explain error differences in reading, picture naming, spontaneous speech, and repetition. Neologisms occurred in oral reading but not in spontaneous speech and repetition. Semantic errors in naming exceeded those in oral reading. To account for these different error patterns we propose that the semantic route, the direct route from the orthographic input lexicon to the POL, and GPC activate simultaneously during reading, converging at the POL to constrain phonological selection. These routes are modular but not functionally encapsulated. For LC, the POL receives ambiguous information due to degradation of all routes, causing reading errors.     

Support for anterior temporal involvement in semantic error production in aphasia: new evidence from VLSM

Semantic errors in aphasia (e.g., naming a horse as “dog”) frequently arise from faulty mapping of concepts onto lexical items. A recent study by our group used voxel-based lesion-symptom mapping (VLSM) methods with 64 patients with chronic aphasia to identify voxels that carry an association with semantic errors. The strongest associations were found in the left anterior temporal lobe (L-ATL), in the mid- to anterior MTG region. The absence of findings in Wernicke’s area was surprising, as were indications that ATL voxels made an essential contribution to the post-semantic stage of lexical access. In this follow-up study, we sought to validate these results by re-defining semantic errors in a manner that was less theory dependent and more consistent with prior lesion studies. As this change also increased the robustness of the dependent variable, it made it possible to perform additional statistical analyses that further refined the interpretation. The results strengthen the evidence for a causal relationship between ATL damage and lexically-based semantic errors in naming and lend confidence to the conclusion that chronic lesions in Wernicke’s area are not causally implicated in semantic error production.     

Words fail: Lesion-symptom mapping of errors of omission in post-stroke aphasia

Impaired object naming is a core deficit in post-stroke aphasia, which can manifest as errors of commission – producing an incorrect word or a non-word – or as errors of omission – failing to attempt to name the object. Detailed behavioural, computational, and neurological investigations of errors of commission have played a key role in the development of neurocognitive models of word production. In contrast, the neurocognitive basis of omission errors is radically underspecified despite being a prevalent phenomenon in aphasia and other populations. The prevalence of omission errors makes their neurocognitive basis important for characterizing an individual's deficits and, ideally, for personalizing treatment and evaluating treatment outcomes. This study leveraged established relationships between lesion location and errors of commission to investigate omission errors in picture naming. Omission error rates from the Philadelphia Naming Test for 123 individuals with post-stroke aphasia were analysed using support vector regression lesion-symptom mapping. Omission errors were most strongly associated with left frontal and mid-anterior temporal lobe lesions. Computational model analysis further showed that omission errors were positively associated with impaired semantically driven lexical retrieval rather than phonological retrieval. These results suggest that errors of omission in aphasia predominantly arise from lexical–semantic deficits in word retrieval and selection from a competitor set.