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PubMedDate not supplied

[Clinical picture of left posterior cerebral artery occlusion. Alexia syndrome without agraphia].

The authors present a clinical description of three cases of occlusion of the left posterior cerebral artery. The pathogenesis of the syndrome of alexia without agraphia is discussed, together with other coexistent symptoms and signs such as hemianopsia, colour anomia, disturbances of recent memory. The discussion is based on own observations and a review of the pertinent literature.

Brain Ischemia↗
PubMed1981

[Alexia without agraphia, right homonymous hemianopsia, and color anomia. Report of four cases with location of the lesion by computerized axial tomography of the brain (author's transl)].

Two patients with left occipitotemporal hematomas and another two with ischemic lesions in the territory of the left posterior cerebral artery presented alexia without agraphia, right homonymous hemianopsia, and a disturbance in the naming of colors. The etiology and the location of the lesion was demonstrated by computerized axial tomography in all four cases. After a period of follow-up of more than one year a good evolution was substantiated in the patients with hematoma. The mechanisms underlying the appearance of symptoms are discussed, and a comment is made on the importance of the splenium of the corpus callosum in the transfer of visual impulses, with the dissociations appearing in the disconnection syndromes due to lesions at this level.

Anomia↗
PubMed1994

[Alexia without agraphia in the Arabic language. Neurolinguistic and and MRI study].

A 33 year-old woman developed an alexia without agraphia, a color anomia, a right hemianopia, an aphasic amnesia and a verbal amnesia. The brain MRI showed the lesions in the left splenium of corpus callosum, forceps major, optic radiations and anterieur temporal lobe. The fact that she measured writing comprehension and had complete recovery of reading impairment despite the persistence of anatomic lesions plead in favour of an active participation of the right hemisphere (RH) on reading; this capacity of the RH may be due to the linguistic particularities of arabic writing.

Adult↗
PubMed1997

Alexia and agraphia in posterior cortical atrophy.

A 65-year-old woman with progressive visuospatial dysfunction for 2 years complained of later-onset associated memory impairment. MRI revealed diffuse cerebrocortical atrophy, which was especially severe in both parieto-occipital regions but spared the calcarine and pericalcarine cortices. Examination 5 years after onset revealed left visual hemi-neglect, oculomotor apraxia, optic ataxia, simultanagnosia, verbal alexia, lexical and spatial agraphia, and anterograde amnesia. This patient's disorder is considered in the context of previous reports on the array of cognitive disturbances associated with posterior cortical atrophy (pCA). Special emphasis is made on her reading and writing disturbances, because their prevalence and range of individual variability have not been established in pCA. This array of neuropsychological manifestations may help to distinguish among different clinical and etiological types of pCA, and to elucidate the pathophysiology of a syndrome that has been associated with conditions as diverse as Alzheimer's disease, subcortical gliosis, and prion diseases. The parameters described in our case may thus help to address these issues in clinico-pathological studies with large numbers of patients with pCA.

Aged↗
PubMed1997

[Pure alexia: presentation of three cases and review of the literature].

INTRODUCTION: Pure alexia is a syndrome characterized by the inability to read aloud in the absence of agraphia or apnasia. CLINICAL CASES: Three clinical cases showing this syndrome are presented. Case I had a left occipital lesion compatible with a subacute haematoma. He had problems with reading, visuo-spatial recognition, digital gnosia and memorizing texts. One year later there was considerable improvement in most of the sub-tests evaluated. There was still deficient colour naming right/left orientation and understanding of letters and words. Case 2 presented with a right homonymous hemianopia and slight left paresis. He had a small left occipital ischaemic infarct. One year later there was improvement on testing, with some deficit still in visual recognition, naming colours and memory. Case 3 presented with right homonymous hemianopia, slight right paresis and a left occipito-parietal expansive lesion. He had defective reading, choosing and naming of colours, right/left orientation and memory. On later evaluation, considerable improvement was seen. There was still colour agnosia, although less severe and mild 'laziness' of the right side. CONCLUSIONS: In the review of the literature, the disorder and the contributions of various authors, from Déperine in 1892 to the present day, are considered in detail.

Aged↗
PubMedDate not supplied

Pure alexia: clinical-pathologic evidence for a lateralized visual language association cortex.

Traditional views of pure alexia have held that the disorder results from a disconnection between the secondary visual cortices of both hemispheres and the angular gyrus of the dominant hemisphere. Evidence has accumulated, however, suggesting the importance of the posterior inferior temporal area in visual language processing. We describe clinical-pathological support for the presence of a lateralized visual language association area residing in the dominant posterior inferior temporal lobe.

Dyslexia, Acquired↗
PubMed1998

The evolution of alexia and simultanagnosia in posterior cortical atrophy.

Early alexia and higher visual impairments characterize Posterior cortical atrophy (PCA), a progressive dementing syndrome most often caused by Alzheimer disease. Posterior cortical atrophy is rare, and the nature of the visual impairments in PCA are unclear. The authors observed two patients who had an insidiously progressive reading difficulty characterized by letter-by-letter reading and otherwise intact cognitive functions. Over time, these patients developed "ventral simultanagnosia" with preserved detection of multiple stimuli but inability to interpret whole scenes. Subsequently, they progressed to Balint syndrome with "dorsal simultanagnosia," optic ataxia, and oculomotor apraxia. Structural imaging was normal, but functional imaging revealed posterior cortical dysfunction. On a letter reading task, both patients had a word superiority effect, and on a whole word reading task, they could not read most words with missing or crosshatched letters. An inability to assess whole scenes progressed to an inability to detect more than one stimulus in an array. These findings suggest an evolution of PCA with progressive difficulty in visual integration beginning with letters, progressing to whole scenes, and culminating in Balint syndrome. These changes may reflect an extension of the pathophysiology of PCA from the extrastriate visual cortex to its occipitotemporal and occipitoparietal connections.

Aged↗
PubMed1997

[Cerebral achromatopsia without prosopagnosia, alexia, object agnosia].

A 62-year-old woman was admitted for a disorder of color vision. This cerebral achromatopsia was isolated, without prosopagnosia, alexia, object agnosia. MRI showed bilateral temporo-occipital infarcts, including lingual and fusiform gyrus. Neuropsychological examination and topographic hypotheses are discussed.

Color Perception↗
PubMed1997

[Letter-by-letter alexia after left hemispheral lesion without hemianopsia nor callosal involvement. 2 cases].

We describe two patients suffering from a letter-by-letter reading following an infarct in the left posterior cerebral artery's territory. Unlike most of the verbal alexics, this strategy was particularly fast and effective. Two other features distinguished these patients from verbal alexics: the absence of hemianopia and the sparing of the corpus callosum. A study of the reading of letters and words by each hemisphere was performed. In the first case, the left hemisphere was unable to identify any letter or word. The visual stimuli did not activate the visual word form, not the system which normally recognize letters. However, this latter could be activated by the information transmitted by the right hemisphere via the corpus callosum. In the second case, the left hemisphere could, as well as the right one, identify all the letters. On the other hand, identification of words was impaired, and did not improve when the duration of the visual presentation increased. The left hemisphere, unable to access to the visual word form, could not decipher letter-by-letter. One hypothesis is that the left visual working memory was reduced, and could not store more than one letter. The right hemisphere deciphered the words sequentially, and transmitted the information to the left systems which recognize the letter. These two observations confirm that letter-by-letter alexia could result exclusively from the destruction, of the inaccessibility of the visual word-form. A lesion of the left ventral occipito-temporal structures is sufficient, and a left hemianopia, or a splenial lesion is not absolutely necessary. The sparing of the corpus callosum allows a fast transmission to the left phonological processing, if the left systems recognizing letters are efficient.

Aged↗
PubMed2003

Mechanisms of pure alexia: spatially based impairment, letter identification deficit, or both?

We studied reading performance for words and for isolated letters in a pure alexic patient. She performed reasonably well when naming isolated letters but was slower in reading letters than a control subject when reaction times (RTs) were recorded. When the patient read isolated letters, RTs were slower for a subset of letters that cannot be recognized from their left part alone (e.g. "b", an ambiguous letter, could be read "b" "h" "l" or "k" whereas "a" has no predictable confounders). We observed a significant positive correlation between the RTs for reading a word and the mean RTs for reading each of its composing letters before its uniqueness point (i.e. the point, when reading from the left to the right, where a word cannot be a word other than the one it is). This result suggests that, in our patient, the letter identification deficit can account for the slow, letter-by-letter reading behaviour, insofar as each letter represents a perceptual problem. Our findings can be accounted for by a deficit in the parallel processing of the left and right parts of each letter, compounded with a bias to process first the left part of the letter, and may thus reconcile the hypotheses of spatially-based deficit (Rapp and Caramazza, 1991) and of a perceptual deficit occurring at the letter identification level (Behrmann and Shallice, 1995; Perri et al., 1996).

Aged↗