[Copying impairment in alexia without agraphia--comparison of the right with the left hand (author's transl)].
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[Anatomo-clinical observations in a case of alexia without agraphia].
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["Sub-angular" alexis and associated neuropsychologic signs: clinical and tomodensitometric study].
A clinical case of alexia without agraphia is reported. The computerized tomography (CT) showed a left sub-cortical parieto-occipital hemorrhage. The cortical lesion probably involved the posterior part of the angular gyrus but spared the medial occipital cortex. There was no evidence of a corpus callosum lesion. The clinical findings associated with the alexia and the localisation of the haematoma could be compared to the case reported by Greenblatt as a "subangular alexia" and considered as a disconnection of the left angular gyrus from right angular gyrus and both left and right occipital areas. The semiological aspects of the present case have been found to consistently differ from the classical forms of alexia usually described. Some common features with phonological alexia have been observed.
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Impaired activation of the phonological lexicon: effects upon oral reading.
The role of the phonological lexicon in oral reading is examined in a patient with a small focal left hemisphere lesion. Impaired access to the patient's phonological lexicon is suggested by a number of findings, including the production of phonemic errors across a variety of tasks; increasing difficulty in word production with increasing word length; and difficulty on tests of homophone and rhyme judgments. Two competing models of reading are tested: the nonlexical ("rules") and the lexical ("no-rules") models. The rules model predicts that a disturbance in the phonological lexicon will result in surface alexia; the no-rules model predicts phonological alexia. Results indicate that the patient's reading is most similar to phonological alexia, providing support for the no-rules model. The applicability of the no-rules model to other forms of acquired alexia is explored.
Anomia↗
Occipital lobe infarction and positron emission tomography.
Even though the PET study revealed a total infarct in the territory of the left PCA in our 3 cases of pure alexia, it is still obscure which part of the left occipital lobe is most closely associated with the occurrence of the pure alexia. In order to elucidate the intralobar localization of the pure alexia, it is needed to have an ideal case who shows an pure alexia due to the localized lesion within the left occipital lobe. Furthermore, high-resolution PET scanner will circumvent the problem in detecting the metabolism and blood flow in the corpus callosum which plays an important role in the pathogenesis. We have shown that the occlusion of the right PCA also produced a left unilateral agnosia which is one of the common neurological signs in the right MCA infarction. To tell whether the responsible lesion for the unilateral spatial agnosia differs between the PCA occlusion and the MCA occlusion, the correlation study should be carried out in a greater number of the subjects. Two distinctive neuropsychological manifestations, cerebral color blindness and prosopagnosia, have been considered to be produced by the bilateral occipital lesion. The PET studies disclosed reduction of blood flow and oxygen metabolism in both occipital lobes in our particular patient who exhibited cerebral color blindness and prosopagnosia.
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Auditory repetition priming is impaired in pure alexic patients.
Alexia without agraphia, or "pure" alexia, is an acquired impairment in reading that leaves writing skills intact. Repetition priming for visually presented words is diminished in pure alexia. However, it is not possible to verify whether this priming deficit is modality-specific or modality independent because reading abilities are compromised. Hence, auditory repetition priming was assessed with lexical decision and word stem completion tasks in pure alexic patients with lesions in left inferior temporal-occipital cortex and the splenium. Perceptually based, modality-specific priming models predict intact auditory priming, since auditory association cortex is spared in the patients. Alternatively, modality-independent models, which suggest that priming reflects the temporary modification of an amodal system, might predict impairments. Baseline performance was matched in the patients and controls, although lexical decision priming measures showed an interaction between group and repetition lag. The patients showed intact immediate priming but significantly less priming than controls at longer delays. Furthermore, word stem completion priming was abolished in the patients. One explanation for the deficit is that left inferior temporal-occipital cortex supports amodal aspects of priming, as suggested by recent neuroimaging results. Another possibility is that long-term auditory priming relies on covert orthographic representations which were unavailable in the patients. The results provide support for interactive models of word identification.
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The pattern of neuropsychological impairment associated with left posterior cerebral artery infarcts.
We investigated the neuropsychological correlates of left posterior cerebral artery (LPCA) infarcts with a quantitative systematic approach and found a pattern of impairment extending well beyond the classical syndrome of alexia without agraphia. Sixteen consecutive patients with CT scan evidence of an infarct confined to the territory of LPCA were given a battery of tests assessing the following abilities. (1) Reading and writing; (2) naming and pointing to colours; (3) naming the same 30 objects on visual (objects and coloured photographs), tactile and verbal presentation; and (4) verbal memory. These tests were administered to large control samples and the performance of LPCA patients was considered pathological if it fell below the score of the last or second to last control patient. Seventy five per cent of PCA patients had alexia without agraphia. Although a lesion of the CT scan slice where the pineal is represented appeared to be crucially associated with alexia, the severity of the disorder increased when contiguous upper or lower slices were also involved. Not only colour anomia, but also object and especially photograph anomia could almost always be shown in alexics and were highly correlated with the degree of the reading impairment. The naming deficit was also present when items were presented in the tactile and verbal modality, in spite of the integrity of the oral language areas. Every right-handed patient, alexic as well as nonalexic, was impaired on at least two of the three verbal memory tests and most on all of them. The findings are discussed in terms of the anatomofunctional mechanisms subserving verbal memory and the transmission of visual information to the speech areas.
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A critical appraisal of neuropsychological correlates of Japanese ideogram (kanji) and phonogram (kana) reading.
Owing to the Japanese language's unique writing system, which consists of phonograms and ideograms, reading impairments of Japanese brain-damaged patients have attracted the interest of many researchers. Past case reports as well as some widely accepted handbooks and textbooks have concluded that a specific aphasia type or lesion site is associated with a particular impairment pattern of phonograms and ideograms in reading. However, the methodology and analytical procedures in previous studies were inadequate for reliable generalizations to be made. First, the test materials were unspecified or inappropriate, or the number of test items was small. Secondly, the conclusions were presented without providing individual performance data to support them. Thirdly, in associating patterns of reading impairment with lesion sites, only single cases were reported. The present investigation was designed to overcome the omissions of previous studies, and examined the ability to read 46 single phonograms and 46 single ideograms aloud in four groups of sufficiently large numbers of patients; namely, seven pure alexics, 23 Broca aphasics, 13 Wernicke aphasics, and seven patients with alexia and agraphia. Ours are the first data to demonstrate unequivocally no consistent linkage between aphasia type and the patterns of impairment of phonogram and ideogram reading. The impairment patterns were not uniform across patients even in the same aphasia group. A majority of the cases in each group showed that phonograms and ideograms were unselectively impaired. However, ideogram reading was more difficult in three cases in the pure alexia and Broca aphasia groups, respectively, and in one case in the Wernicke aphasia group. Phonogram reading was more severely disturbed in four cases among the Broca aphasics and in one case among the patients with alexia with agraphia. An apparent variability of impairment patterns characterized the Broca aphasic group. These dyslexic patterns did not appear to correlate with the site and extent of lesions identified by computerized tomography scans. Past reports linking a particular impairment pattern of phonogram and ideogram reading and a specific lesion site were studies of single cases, and their conclusions seem oversimplified. While sensory and motor dysfunctions can usually be neuroanatomically localized in individuals, impairments of certain high cortical functions, such as the reading of phonograms and ideograms, may not be correlated with damage to definite neuroanatomical structures.
Adult↗
Unidirectional dyslexia in a polyglot.
Alexia is usually seen after ischaemic insults to the dominant parietal lobe. A patient is described with a particular alexia to reading Hebrew (right to left), whereas no alexia was noted when reading in English. This deficit evolved after a hypertensive right occipitoparietal intracerebral haemorrhage, and resolved gradually over the ensuing year as the haematoma was resorbed. The deficit suggests the existence of a separate, language associated, neuronal network within the right hemisphere important to different language reading modes.
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Orthography influences the perception of speech in alexic patients.
Interactive models of reading propose that phonological representations directly activate and/or constrain orthographic representations through feedback. These models also predict that spoken words should activate their orthographic forms. The effect of word orthography on auditory lexical access was investigated in two patients with alexia without agraphia. Several theories of alexia suggest that letter-by-letter reading results from impaired access to orthographic representations. Although alexics can often correctly identify orally spelled words and spell to dictation, it is unknown whether they can access the whole orthographic "word-form" as a unit via auditory presentation. The nonobligatory activation of orthography was examined in an auditory lexical decision task, in which the orthographic and phonological similarity between prime and target was manipulated. In controls, the combined effect of phonological and orthographic relatedness (OP) produced greater facilitation than phonological relatedness alone, indicating that orthography can influence auditory lexical decisions. The alexics displayed patterns of facilitation comparable to controls, suggesting they can quickly access whole-word orthographic information via the auditory modality. An alternate account posits that the OP advantage does not require on-line access of orthography, but instead is a developmental by-product of learning to read an orthographically inconsistent language. The results have implications for cognitive theories of alexia and provide support for interactive models of word recognition.
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Neurosurgery and the anatomy of reading: a practical review.
Tumors and vascular malformations in the posterior parts of the dominant hemisphere are frequently associated with preoperative alexias, and surgical maneuvers in these areas may cause the appearance of this neurobehavioral deficit as an operative complication. Lesions of the dominant (left) angular gyrus are associated with the syndromes of alexia with agraphia. Alexia without agraphia results from lesions of the pathways which conduct visual information from the calcarine areas to the left angular gyrus (splenium of the corpus callosum, left lingual and fusiform gyri, left transverse and vertical occipital fasciculi). A brief bedside examination (outlined in the text) provides useful pre- and postoperative localizing information. Fresh cadaver studies of the brain in situ have shown that the approximate center of the left angular gyrus area is found by first locating a point 9 cm forward along the midline from the inion and then moving 4 1/4 cm laterally. These measurements define a point which is a few centimeters medial and posterior to the center of the parietal eminence.
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Impaired reading in patients with right hemianopia.
A left occipital stroke may result in alexia for two reasons, which may coexist depending on the distribution of the lesion. A lesion of the left lateroventral prestriate cortex or its afferents impairs word recognition ("pure" alexia). If the left primary visual cortex or its afferents are destroyed, resulting in a complete right homonymous hemianopia, rightward saccades during text reading are disrupted ("hemianopic" alexia). By using functional imaging, we showed two separate but interdependent systems involved in reading. The first, subserving word recognition, involved the representation of foveal vision in the left and right primary visual cortex and the ventral prestriate cortex. The second system, responsible for the planning and execution of reading saccades, consisted of the representation of right parafoveal vision in the left visual cortex, the bilateral posterior parietal cortex (left > right), and the frontal eye fields (right > left). Disruption of this distributed neural system was demonstrated in patients with severe right homonymous hemianopia, commensurate with their inability to perform normal reading eye movements. Text reading, before processes involved in comprehension, requires the integration of perceptual and motor processes. We have demonstrated these distributed neural systems in normal readers and have shown how a right homonymous hemianopia disrupts the motor preparation of reading saccades during text reading.
Adult↗
[Dyslexia of digits and numbers in multiple sclerosis].
In a 32-year-old man with remitting-progressive multiple sclerosis a right-side hemiparesis and alexia of digits of numbers developed during an exacerbation. While reading aloud the patient changed digits, left them out or transposed. No changes were observed in reading of letters, words and no agraphia was present. Alexia persisted for about one month. The location of alexia in the occipital lobe and its association pathways with the left parietal lobe are discussed.
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Unilateral right cerebral representation of reading in a familial left-hander.
Several recent hypotheses of cerebral functional organization in natural left-handers hold that language, including reading, is localized either unilaterally in the left hemisphere or bilaterally, but not unilaterally in the right hemisphere. A case of alexia without agraphia in a left-hander with an infarct in the right occipital lobe and splenium of the corpus callosum is reported. That a permanent and complete alexia resulted from a single, right hemisphere lesion indicated that reading was completely lateralized to that hemisphere. The case demonstrates that in some natural left-handers language functions can be unilaterally represented in the right hemisphere.
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Seeing but not recognizing.
Visual recognition disturbances are caused by lesions that affect visual cortex as well as white matter connections between visual cortex and temporal and parietal cortex. Homonymous visual field defects are often present but do not explain the recognition difficulty. In "alexia without agraphia" (pure alexia), the intact right visual cortex is disconnected from the left parietal language center by a lesion in the splenium. In "prosopagnosia," visual cortex is disconnected bilaterally from temporal cortex. In simultanagnosia, visual association cortex is damaged. The first condition is most commonly caused by left posterior cerebral artery occlusion, the second by bilateral posterior cerebral artery occlusion or head trauma, and the third by watershed infarction, tumors, abscesses, head trauma, leukoencephalopathies and Alzheimer's disease. When such disorders are suspected, the examiner should supplement the routine visual examination with suggested screening maneuvers.
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The pathophysiology of letter-by-letter reading.
Pure alexia is a frequent and incapacitating consequence of left occipitotemporal lesions. It is thought to result from the disruption or the disconnection of the visual word form area (VWFA), a region reproducibly located within the left occipito-temporal sulcus, and encoding the abstract identity of strings of visual letters. Alexic patients often retain effective single letter recognition abilities, and develop an effortful letter-by-letter reading strategy which is the basis of most rehabilitation techniques. We study a patient who developed letter-by-letter reading following the surgical removal of left occipito-temporal regions. Using anatomical and functional MRI in the patient and in normal controls, we show that alexia resulted from the deafferentation of left fusiform cortex, and we analyze the network of brain regions subtending letter-by-letter reading. We propose that during letter-by-letter reading (1) letters are identified in the intact right-hemispheric visual system, with a central role for the region symetrical to the VWFA; (2) letters are serially transferred to the left hemisphere through the intact segment of the corpus callosum; (3) word identity is eventually recovered in the left hemisphere through verbal working memory processes involving inferior frontal and supramarginal cortex.
Adult↗
Acquired dyslexia.
Disorders of reading are frequently encountered in patients with acquired cerebral lesions. Investigations in the past few decades have improved our understanding of these disorders. In this article we review the peripheral dyslexias, including neglect dyslexia, attentional dyslexia, and pure alexia (or alexia without agraphia), as well as the "central" dyslexias, including deep, surface, and phonological dyslexia. Current accounts of acquired dyslexia are also discussed. Finally, we briefly describe the reading tasks that serve to differentiate the different reading disorders.
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Functional connectivity of the angular gyrus in normal reading and dyslexia.
The classic neurologic model for reading, based on studies of patients with acquired alexia, hypothesizes functional linkages between the angular gyrus in the left hemisphere and visual association areas in the occipital and temporal lobes. The angular gyrus also is thought to have functional links with posterior language areas (e.g., Wernicke's area), because it is presumed to be involved in mapping visually presented inputs onto linguistic representations. Using positron emission tomography , we demonstrate in normal men that regional cerebral blood flow in the left angular gyrus shows strong within-task, across-subjects correlations (i.e., functional connectivity) with regional cerebral blood flow in extrastriate occipital and temporal lobe regions during single word reading. In contrast, the left angular gyrus is functionally disconnected from these regions in men with persistent developmental dyslexia, suggesting that the anatomical disconnection of the left angular gyrus from other brain regions that are part of the "normal" brain reading network in many cases of acquired alexia is mirrored by its functional disconnection in developmental dyslexia.
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