Maximal recovery from acquired language impairment may require progression from one behavioural treatment protocol to the next in order to build upon residual and relearned cognitive-linguistic and sensory-motor processes. We present a five-stage treatment sequence that was initiated at one year post stroke in a woman with acquired impairments of spoken and written language. As is typical of individuals with left perisylvian damage, she demonstrated marked impairment of phonological retrieval and sublexical phonology, but she also faced additional challenges due to impaired letter shape knowledge and visual attention. The treatment sequence included (1) written spelling of targeted words, (2) retraining sublexical sound-to-letter correspondences and phonological manipulation skills, (3) training strategic approaches to maximise interactive use of lexical, phonological, and orthographic knowledge, (4) lexical retrieval of spoken words, and finally (5) sentence-level stimulation to improve grammatical form of written narratives. This Phase II clinical study documented positive direct treatment outcomes along with evidence of a significant reduction in the underlying deficits and generalisation to untrained items and language tasks. Improvements on a comprehensive assessment battery were realised as functional gains in everyday written and spoken communication, including improved lexical retrieval and grammatical complexity of written narratives. This case provides a valuable example of the cumulative therapeutic benefit of sequential application of theoretically motivated treatment protocols.
PMID: 18625494;PMCID: PMC2689874;Abstract:
To examine the validity of different theoretical assumptions about the neuropsychological mechanisms and lesion correlates of phonological dyslexia and dysgraphia, we studied written and spoken language performance in a large cohort of patients with focal damage to perisylvian cortical regions implicated in phonological processing. Despite considerable variation in accuracy for both words and non-words, the majority of participants demonstrated the increased lexicality effects in reading and spelling that are considered the hallmark features of phonological dyslexia and dysgraphia. Increased lexicality effects were also documented in spoken language tasks such as oral repetition, and patients performed poorly on a battery of phonological tests that did not involve an orthographic component. Furthermore, a composite measure of general phonological ability was strongly predictive of both reading and spelling accuracy, and we obtained evidence that the continuum of severity that characterized the written language disorder of our patients was attributable to an underlying continuum of phonological impairment. Although patients demonstrated qualitatively similar deficits across measures of written and spoken language processing, there were quantitative differences in levels of performance reflecting task difficulty effects. Spelling was more severely affected than reading by the reduction in phonological capacity and this differential vulnerability accounted for occasional disparities between patterns of impairment on the two written language tasks. Our findings suggest that phonological dyslexia and dysgraphia in patients with perisylvian lesions are manifestations of a central or modality-independent phonological deficit rather than the result of damage to cognitive components dedicated to reading or spelling. Our results also provide empirical support for shared-components models of written language processing, according to which the same central cognitive systems support both reading and spelling. Lesion-deficit correlations indicated that phonological dyslexia and dysgraphia may be produced by damage to a variety of perisylvian cortical regions, consistent with distributed network models of phonological processing.
Phonological deficits are common in aphasia after left-hemisphere stroke, and can have significant functional consequences for spoken and written language. While many individuals improve through treatment, the neural substrates supporting improvements are poorly understood. We measured brain activation during pseudoword reading in an individual through two treatment phases. Improvements were associated with greater activation in residual left dorsal language regions and bilateral regions supporting attention and effort. Gains were maintained, while activation returned to pre-treatment levels. This case demonstrates the neural support for improved phonology after damage to critical regions and that improvements may be maintained without markedly increased effort.
Objective: To determine whether damage to left posterior inferior temporal cortex (PITC) is associated with agraphia and to characterize the nature of the spelling impairment. Background: Left angular gyrus may play a critical role in spelling. However, this traditional view is challenged by reports of agraphia after left temporo-occipital lesions and by functional imaging studies demonstrating activation of left PITC during writing in normal individuals. Methods: Patients with focal damage to the left temporo-occipital cortex and normal control subjects were administered a comprehensive spelling battery that included regular words, irregular words, and nonwords as stimuli. Results: Although patients performed worse than control subjects in all experimental conditions, the spelling deficit was particularly severe for irregular words, whereas regular word and nonword spelling were less impaired. Additional analyses indicated that orthographic regularity and word frequency had a much more pronounced effect on spelling accuracy in patients compared with control subjects. Most errors on irregular words were phonologically plausible, consistent with reliance on a sublexical phonologic spelling strategy (i.e., phoneme-grapheme conversion). Overall, the spelling impairment of the patients showed the characteristic profile of lexical agraphia. Lesion analyses indicated that the damage in the majority of patients encompassed an area within the left PITC (BA 37/20) where the authors previously obtained evidence of activation in a functional imaging study of writing in normal participants. Conclusions: The behavioral and neuroanatomic observations in the patients are consistent with functional imaging studies of writing in neurologically intact individuals and provide converging evidence for the role of left PITC in spelling. Together, these findings implicate left PITC as a possible neural substrate of the putative orthographic lexicon that contains stored memory representations for the written forms of familiar words.