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Acquired Phonological and Deep Dyslexia Matthew A This article was downloaded by: [The University of Manchester Library] On: 22 June 2012, At: 13:49 Publisher: Psychology Press Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK Neurocase: The Neural Basis of Cognition Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/nncs20 Acquired phonological and deep dyslexia Matthew A. Lambon Ralph a & Naida L. Graham a b a MRC Cognition and brain Sciences Unit, Cambridge, CB2 2EF b Department of Neurology, University of Cambridge, Cambridge, UK, CB2 2QQ Available online: 17 Jan 2008 To cite this article: Matthew A. Lambon Ralph & Naida L. Graham (2000): Acquired phonological and deep dyslexia, Neurocase: The Neural Basis of Cognition, 6:2, 141-178 To link to this article: http://dx.doi.org/10.1080/13554790008402767 PLEASE SCROLL DOWN FOR ARTICLE Full terms and conditions of use: http://www.tandfonline.com/page/terms-and-conditions This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. The publisher does not give any warranty express or implied or make any representation that the contents will be complete or accurate or up to date. The accuracy of any instructions, formulae, and drug doses should be independently verified with primary sources. The publisher shall not be liable for any loss, actions, claims, proceedings, demand, or costs or damages whatsoever or howsoever caused arising directly or indirectly in connection with or arising out of the use of this material. Neurocase (2000) Vol. 6, pp. 141-178 0 Oxford Universip Press 2000 PREVIOUS CASES Acquired Phonological and Deep Dyslexia Matthew A. Lambon Ralph’ and Naida L. Graham112 ’MRC Cognition and Brain Sciences Unit, Cambridge CB2 2EF and 2Departmentof Neurology, University of Cambridge, Cambridge CB2 2QQ, UK Aphasic patients with deep dyslexia present with a number The most common view of deep dyslexia is that there is no of generally co-occurring features or symptoms (Coltheart, sublexical computation of sound from print (i.e., non-word 1980a). Besides the principal characteristic - production of reading is impossible) and the limited reading that does occur semantic paralexia (e.g., producing ‘talk’ to the target speak)- is mediated via meaning (and most authors assume that there the features also include visual and derivational paralexia (e.g., must be some impairment to the semantic route as well, see deep + ‘deer’;depth + ‘deep’),function word substitutions below). The absolute character of this assumption is called into (e.g., her + ‘she’),an almost complete inability to derive question by some recent papers arguing for implicit activation phonology directly from print (i.e., read non-words), reading of non-word pronunciations (e.g., Buchanan etal., 1996, P629; accuracy is affected by imageabilitykoncreteness (highly Katz and Lanzoni, 1992, P650) and/or partial non-semantic imageablekoncrete better than low imageable/abstract words) reading to explain the different error patterns between naming and by the part of speech (typically, nouns > adjectives > and reading observed in patients with deep dyslexia (South- verbs > functors). Deep dyslexia has been described most often wood and Chatterjee, 1999, P687). We note, in this regard, that in patients with Broca’s aphasia who have a severe expressive for a considerable number of the cases summarized here, non- aphasia but relatively good comprehension, poor short-term word reading was very impaired but not completely abolished. memory and inability to manipulate phonological information. It would seem reasonable to conclude, therefore, that there is Writing is also impaired and some patients present with both some, albeit very limited, sublexical computation of sound deep dyslexia and dysgraphia (e.g., Nolan and Caramazza, from print in deep dyslexia. The same conclusion was reached 1983, P661). The critical feature of phonological dyslexia is by Patterson (1978, P667) after finding above-chance perform- the presence of a lexicality effect on reading accuracy (i.e., ance on a series of spoken-to-written non-word matching tests word > non-word reading). Many features listed above for in two deep dyslexic subjects. Limited non-word readinghub- deep dyslexia are found patients with phonological dyslexia in lexical processing would also seem to add support to the notion although this varies across individuals. In effect the presence of a continuum between phonological and deep dyslexia, of semantic paralexia is the differential diagnostic between assuming that this continuum is primarily governed by the phonological and deep dyslexia. Due to the potential overlap degree of phonological impairment. between these conditions, this brief overview encompasses the In recent years, a number of authors have begun to explore past cases of both deep and phonological dyslexia summarized Downloaded by [The University of Manchester Library] at 13:49 22 June 2012 in this issue, as well as the phonological dyslexic past cases the possibility that reading is based upon primary, general that appeared previously (Neurocase 1995; 1 : 25 1-7). processing systems and that the different types of acquired The first descriptions of phonological dyslexia argued that dyslexia reflect damage to one or more of these (for an over- it should be considered as a separate type of dyslexia on the view, see Patterson and Lambon Ralph, 1999). Under this basis that a number of patients failed to show many of the approach pure alexia reflects a visual impairment (Behrmann symptoms of deep dyslexia (Beauvois and DCrouesnt, 1979, et al., 1998), surface dyslexia follows a major reduction in the P110). By studying the pattern of recovery in deep dyslexia influence of semantic memory on phonology (Patterson and and the pattern of symptoms across a series of phonological Hodges, 1992), and phonological dyslexia is due to a more dyslexics, Friedman (1996, P641) has argued, however, that generalized phonological impairment (Farah et al., 1996 P639; the two types of dyslexia reflect points along a continuum. At Patterson and Marcel, 1992, P120). This hypothesis is strongly one end sits deep dyslexia with all its co-occurring symptoms. supported by the extremely high association between poor At the other, there is ‘pure’ phonological dyslexia with phonological awareness skills and phonological dyslexia (with impoverished performance for non-words as the only reading the only exception seeming to be patient LB, DCrouesnt and deficit. In between are patients for whom the exact features of Beauvois, 1985, PI 13 -although we note, in turn, that this is their phonological dyslexia are predictable on the basis of one of only two cases with a right hemisphere lesion, see severity alone. below). Can the same argument be extended to deep dyslexia, 142 Previous cases: Phonological and deep dyslexia or even perhaps, the phonological-deep continuum? Most Should such cases be identified, it would be interesting to know explanations of deep dyslexia involve at least two functional how closely the longitudinal decline mirrored the pattern of impairments: (a) severely impaired direct activation of phono- recovery seen in some deep dyslexic patients folllowing acute logy from orthography (perhaps reflective of very impaired brain injury (Friedman, 1996, P643). general phonological processing), and (b) disrupted activation The large lesions typically found in deep dyslexia provide of sound from print via meaning (Morton and Patterson, 1980) one of the motivations behind the ‘right hemisphere hypo- due to either impaired semantic memory or access to/egress thesis’ which assumes that the residual reading abilities from it (reflected in anomia andor comprehension observed in deep dyslexia are underpinned by processes in the impairment). right hemisphere (Coltheart, 1980b, Saffran et al., 1980). The The lesion sites and aetiologies associated with phonological literature provides neuropsychological and neuro,imagingdata dyslexia can be summarized as follows. Setting aside the hemi- both for and against this hypothesis. One of the most highly spherectomy cases reported by Ogden (1996: P664), all cited papers reports the case of a 13 year old patient, N1. who patients had damage focused on the anterior perisylvian areas following a complete left hemispherectomy presented with a ranging from relatively circumscribed lesions typically of the pattern of dyslexia very similar to adult deep dyslexics left inferior, posterior frontal lobe to those patients with more (Patterson et al., 1989). Given that the left hemispherectomy extensive damage involving fronto-temporo-parietal areas. In was complete, and assuming that after 13 years the neural- the 37 papers on phonological dyslexia included in this review, functional components of the reading architecture closely seven exceptions to this pattern, with posterior left hemisphere resemble those found in adulthood, this evidence clearly sup- lesions in and around the occipito-temporo-parietal junction, ports the right hemisphere hypothesis. Similar su.pport can be were identified (Beauvois and DCrouesnC, 1979, P110, see also found in a patient following posterior callosal lesion who read DCrouesnC and Beauvois, 1979, P114; Caramazza et al., 1985, normally
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