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An 84-year-old woman with a history of dry age-related macular degeneration presented with an acute inability to read, but intact writing ability (pure alexia or alexia without agraphia). She denied any difficulty speaking, paresthesias, or hemiparesis. Her visual acuity was 20/20 in each eye. Macular examination, optical coherence tomography, and fluorescein angiography demonstrated the previously diagnosed macular drusen and geographic atrophy of the retinal pigment epithelium consistent with the dry form of age-related macular degeneration both eyes. Automated perimetry revealed a right homonymous hemianopsia. Neuroimaging confirmed a left occipital ischemic infarction with involvement of the splenium of the corpus callosum producing the classic disconnection syndrome of alexia without agraphia.

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After a stroke involving the left occipitotemporal cortex our patient shows a word-length effect and has problems to identify letters or numbers in strings of symbols. But he is normal in identifying isolated letters and in non-verbally categorizing even complex images such as faces or natural scenes. His cortical lesion is stretching from the visual word form area (VWFA) anteriorly causing additional problems to name visual stimuli and to match acoustic stimuli with images. We conclude that our patient suffers from pure alexia without deficits to identify even complex visual stimuli. Our results directly contradict several explanations for letter-by-letter reading.

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We present a patient with reading inexpertise and right hemianopia following left posterior cerebral artery (PCA) stroke. We examine the extent of disruption to reading performance and the extent of white matter tract damage relative to a patient with more limited PCA infarction and isolated right hemianopia. We show white matter disconnection of the temporal occipital fusiform cortex in our pure alexia patient. Connectivity-based laterality indices revealed right hemisphere laterality in the alexia patient; this was not associated with improved reading function. We speculate that the degree of premorbid laterality may be a critical factor affecting the extent of reading dysfunction in alexia.

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Pure alexia is an acquired reading disorder, typically due to a left occipito-temporal lesion affecting the Visual Word Form Area (VWFA). It is unclear whether the VWFA acts as a unique bottleneck for reading, or whether alternative routes are available for recovery. Here, we address this issue through the single-case longitudinal study of a neuroscientist who experienced pure alexia and participated in 17 behavioral, 9 anatomical, and 9 fMRI assessment sessions over a period of two years. The origin of the impairment was assigned to a small left fusiform lesion, accompanied by a loss of VWFA responsivity and by the degeneracy of the associated white matter pathways. fMRI experiments allowed us to image longitudinally the visual perception of words, as compared to other classes of stimuli, as well as the mechanisms of letter-by-letter reading. The progressive improvement of reading was not associated with the re-emergence of a new area selective to words, but with increasing responses in spared occipital cortex posterior to the lesion and in contralateral right occipital cortex. Those regions showed a non-specific increase of activations over time and an increase in functional correlation with distant language areas. Those results confirm the existence of an alternative occipital route for reading, bypassing the VWFA, but they also point to its key limitation: the patient remained a slow letter-by-letter reader, thus supporting the critical importance of the VWFA for the efficient parallel recognition of written words.

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Impaired visual attention is common following strokes in the territory of the middle cerebral artery, particularly in the right hemisphere, while attentional effects of more posterior lesions are less clear. Commonly, such deficits are investigated in relation to specific syndromes like visual agnosia or pure alexia. The aim of this study was to characterize visual processing speed and apprehension span following posterior cerebral artery (PCA) stroke. In addition, the relationship between these attentional parameters and single word reading is investigated, as previous studies have suggested that reduced visual speed and span may explain pure alexia. Eight patients with unilateral PCA strokes (four left hemisphere, four right hemisphere) were selected on the basis of lesion location, rather than the presence of any visual symptoms. Visual attention was characterized by a whole report paradigm allowing for hemifield-specific measurements of processing speed and apprehension span. All patients showed reductions in visual span contralateral to the lesion site, and four patients showed bilateral reductions in visual span despite unilateral lesions (2L; 2R). Six patients showed selective deficits in visual span, though processing speed was unaffected in the same field (ipsi- or contralesionally). Only patients with right hemifield reductions in visual span were impaired in reading, and this could follow either right or left lateralized stroke and was irrespective of visual field impairments. In conclusion, visual span may be affected bilaterally by unilateral PCA-lesions. Reductions in visual span may also be confined to one hemifield, and may be affected in spite of preserved visual processing speed. Furthermore, reduced span in the right visual field seems to be related to reading impairment in this group, regardless of lesion lateralization.

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PURPOSE: Damage to left ventral occipito-temporal cortex can give rise to written language impairment characterized by pure alexia/letter-by-letter (LBL) reading, as well as surface alexia and agraphia. The purpose of this study was to examine the therapeutic effects of a combined treatment approach to address concurrent LBL reading with surface alexia/agraphia. METHOD: Simultaneous treatment to address slow reading and errorful spelling was administered to 3 individuals with reading and spelling impairments after left ventral occipito-temporal damage due to posterior cerebral artery stroke. Single-word reading/spelling accuracy, reading latencies, and text reading were monitored as outcome measures for the combined effects of multiple oral re-reading treatment and interactive spelling treatment. RESULTS: After treatment, participants demonstrated faster and more accurate single-word reading and improved text-reading rates. Spelling accuracy also improved, particularly for untrained irregular words, demonstrating generalization of the trained interactive spelling strategy. CONCLUSION: This case series characterizes concomitant LBL with surface alexia/agraphia and demonstrates a successful treatment approach to address both the reading and spelling impairment.

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Pure alexia (PA) has been associated with visual deficits or a failure to activate the visual word form area (VWFA). We report a patient with pure alexia due to posterior cortical atrophy, in whom event-related potentials revealed a delay in the P100 component and an absent N170 compared with controls. Furthermore, there was a tendency for a larger delay in P100 latencies associated with incorrectly read words. This suggests that some cases of PA might result from deficits in visual perception, signaled by the P100 early potential which could lead to an inability to consistently activate the VWFA, marked by the absent N170.

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Pure alexia is characterized by an increased word-length effect in reading. However, this disorder is usually accompanied by right homonymous hemianopia, which itself can cause a mildly increased word-length effect. Some alexic studies have used hemianopic patients with modest word-length effects: it is not clear (a) whether they had pure alexia and (b) if not, whether their results could be explained by the field defect. Our goal was to determine if impairments in visual processing claimed to be related to alexia could be replicated in homonymous hemianopia alone. Twelve healthy subjects performed five experiments used in two prior studies of alexia, under both normal and simulated hemianopic conditions, using a gaze-contingent display generated by an eye-tracker. We replicated the increased word-length effect for reading time with right homonymous hemianopia, and showed a similar effect for a lexical decision task. Simulated hemianopia impaired scanning accuracy for letter or number strings, and slowed object part processing, though the effect of configuration was not greater under hemianopic viewing. Hemianopia impaired the identification of words whose letters appeared and disappeared sequentially on the screen, with better performance on a cumulative presentation in which the letters remained on the screen. The reporting of trigrams was less accurate with hemianopia, though syllabic structure did not influence the results. We conclude that some impairments that have been attributed to the processing defects underlying alexia may actually be due to right homonymous hemianopia. Our results underline the importance of considering the contribution of accompanying low-level visual impairments when studying high-level processes.

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Alexia without agraphia (pure alexia) was the first of the disconnection syndromes to be described by Dejerine who reported a patient of alexia without agraphia secondary to an embolic occipital lobe infarct. We herein report a 55-year-old man who presented with alexia without agraphia with magnetic resonance imaging suggestive of left posterior cerebral artery infarct involving left occipital lobe and splenium of corpus callosum. Alexia without agraphia is a relatively uncommon clinical condition, which should always be thought in a patient presenting with difficulty in reading with normal visual acuity. Ophthalmologists should also be aware of this disconnection syndrome as many patients initially take their advice due to predominant visual complaints. Early diagnosis and treatment of this condition help in ensuring the patient and attendants about nonprogressive nature of the disease and may prevent further episodes of stroke.

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Pure alexia is a selective deficit in reading, following lesions to the posterior left hemisphere. Writing and other language functions remain intact in these patients. Whether pure alexia is caused by a primary problem in visual perception is highly debated. A recent hypothesis suggests that a low level deficit - reduced sensitivity to particular spatial frequencies - is the underlying cause. We tested this hypothesis in a pure alexic patient (LK), using a sensitive psychophysical paradigm to examine her performance with simple patterns of different spatial frequency. We find that both in a detection and a classification task, LK's contrast sensitivity is comparable to normal controls for all spatial frequencies. Thus, reduced spatial frequency sensitivity does not constitute a general explanation for pure alexia, suggesting that the core deficit in this disorder is at a higher level in the visual processing stream.

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BACKGROUND: Alexia without agraphia is a neurological syndrome that is caused by a specific lesion in the left (or the dominant) cerebral hemisphere. It is characterised by a severe reading disorder with writing ability intact. CASE DESCRIPTION: We describe a patient who, after a fall from a staircase, could no longer read, even that which he had written shortly before. Initially, he also had problems with orientation and facial recognition. Two months after the accident, alexia without agraphia was still manifest while the other symptoms had disappeared. His ability to read showed a slow improvement; complete recovery occurred after two years. The absence of concomitant disorders was exceptional. CONCLUSION: The disorder alexia without agraphia seems improbable, but deserves serious attention to prevent diagnostic delay.

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We report for the first time a patient with childhood-onset Tourette's syndrome (TS) who developed alexia without agraphia, acalculia, visual agnosia for objects and faces, and preserved mnesic functions in older age. Neuroimaging studies demonstrated temporo-parieto-occipital cortical atrophy and fronto-temporo-parieto-occipital hypometabolism, both more prominent on the left side. This case fulfils the diagnostic criteria of posterior cortical atrophy (PCA). The possible link between TS and PCA is discussed.

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Alexia without agraphia (also called pure alexia or word blindness) was the first of the disconnection syndromes (syndromes caused by disconnection of the right from the left cerebral hemisphere through interruption of the communication pathways between them) to be described. Déjerine in 1892 reported a patient who developed this syndrome after an infarct of the left occipital lobe and splenium of the corpus callosum. We describe a patient who developed alexia without agraphia due to an embolic left occipital lobe infarct extending to the posterior commissure and splenium of the corpus callosum.

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