SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
We present a case of eclampsia complicated by alexia without agraphia. To our knowledge, this syndrome has never before been described in the literature.
We describe a 65-year-old male who presented with acute onset inability to read, without any difficulty in writing. A clinical diagnosis of alexia without agraphia was made and the patient was subjected to routine investigations including contrast MRI. MRI showed a ring-enhancing lesion in left occipital area, suggestive of neurocysticercosis supported by quantitative enzyme-linked immunosorbant assay from purified cell fraction of taenia solium cysticerci (PCF-ELISA). Patient was treated with albendazole and prednisolone for one week. The clinical manifestation as well as the radiological finding resolved after treatment.
A proficient stenographer who had had cerebral metastases suffered from pure alexia for normal print but could still read stenography with ease. It is suggested that especially the visuospatial properties of stenography made possible "alternative" reading, most likely via the right hemisphere.
OBJECTIVES: To report and discuss the neuropsychological deficits and neuroimaging findings in a patient with probable Marchiafava-Bignami disease. DESIGN AND METHOD: A right-handed woman with chronic alcoholism demonstrated mutism, impaired comprehension of spoken language, alexia, and right-handed agraphia. The syndrome of interhemispheric disconnection was manifested by left-handed deficit of constructional ability and agraphia. The patient underwent brain computed tomographic scans, technetium 99 hexylmethylpropylene amineoxime-single photon emission computed tomography, and magnetic resonance imaging (MRI) that also included fluid attenuated inversion recovery images. SETTING: Clinical neurology department. RESULTS: The patient's symptoms were related to scattered lesions of the corpus callosum and to extensive symmetrical lesions of the centrum semiovale. Only the latter were detected by computed tomographic scans. Results of single photon emission computed tomography did not show areas of focal hypoperfusion. Results of fast spinecho MRI showed all lesions were hyperintense in T1-weighted images and hypointense in T2-weighted images. Fluid attenuated inversion recovery images revealed that periventricular lesions had a hypointense core surrounded by a hyperintense rim; callosal lesions were still hyperintense. CONCLUSIONS: We believe that our patient's symptoms are due to the discontinuous affection of the corpus callosum and to the bilateral cutting of the outflow from the cortex. The MRI findings may be interpreted as indicating central necrosis and peripheral demyelination of periventricular lesions and demyelination of the corpus callosum. The combined use of fast spin echo and fluid attenuated inversion recovery MRI reproduced with more accuracy than fast spin echo MRI alone some features of Marchiafava-Bignami disease known from observations at autopsy.
Alexia without agraphia occurred in a 41-year-old man suffering from a left occipital brain tumor. The syndrome disappeared following excision of the neoplasm.
Two cases, one with probable Pick's disease and one with herpes simplex encephalitis, are presented, focusing on Gogi (word-meaning) aphasia-like syndrome as their salient clinical feature. Their aphasic symptoms were characterized by impaired kanji processing and preserved kana processing in writing and oral reading known as a defining feature of Gogi aphasia, but little evidence of so-called "phonetic use of kanji in writing" and "confusion between on- and kun-readings of kanji in oral reading" often observed in Gogi aphasia. Systematic neuropsychological test batteries administered to them showed that the selective impairment of kanji processing did not always arise from a disturbance of a specific ability known to be essential to Gogi aphasia (i.e., failure in comprehending the semantic content of spoken and written language), but rather from an amnestic disruption in the ability to access the correct orthographic and phonological forms of kanji words. This selective impairment of kanji processing may be compatible with "alexia with agraphia of kanji," recently known to be attributable to left posterotemporal lesions. These results suggest that Gogi aphasia (or similar syndromes) is not necessarily a real syndrome but a polytypic constellation of symptoms.
On the basis of data indicating the failure to encode letters as abstract orthographic identities in a pure alexic patient (D.M.) coupled with hypotheses about the effect of such a failure on word reading, an attempt at changing the nature of letter processing in D.M. was conducted. The training procedures failed to produce any fundamental change in the operations used by D.M. to encode isolated letters or words. However, rapid and massive benefits occurred in the overall speed of reading as a result of the training program. These appear to result from an increased rate of letter identification and the faster integration of individual letters into letter combinations. The observations gathered throughout this rehabilitation attempt provided evidence which constrains the range of possible explanations for the characteristic features of pure alexia. It is proposed that the letter-by-letter reading procedure which is the hallmark of the disorder may follow from an incapacity to directly encode visual letters as abstract orthographic types.
An experimental treatment study designed to improve both the accuracy and the speed of reading was administered to a patient with pure alexia and impaired letter naming. The study focused on the use of letter-by-letter reading. A two-stage approach was employed. The first stage implemented a tactile-kinesthetic strategy to improve accuracy. The second stage concentrated on speed. At the end of the treatment, patient DL was reading both trained and untrained words more accurately and with considerably greater speed than prior to treatment. Accuracy and speed of reading at the sentence level improved as well.
Four patients with alexia without agraphia had CT lesions which correlated with the clinical findings. All lesions were vascular; two were spontaneous intracerebral hematomas and two were ischemic infarctions in the posterior cerebral artery distribution. The lesions were located in the posterior portion of the dominant hemisphere. The location of the lesion correlated with the presence or absence of visual field abnormalities.
Two new cases of alexia without agraphia are presented. Pertinent clinical findings, anatomy, pathophysiology and differential diagnoses are reviewed. The importance of carefully examining the inferior portion of the left side of the splenium of the corpus callosum on CT and/or MR scans in patients who present with this clinical syndrome is stressed.
A 10-year-old boy with a functional reading deficit (i.e. functional alexia) was successfully treated with hospital based escape/avoidance procedures. A multiple baseline design was used to evaluate the effectiveness of treatment. Generalization of treatment effects across individuals, settings and time was demonstrated. Extension of these procedures to other functional deficits is discussed.
Alexia with agraphia has not been reported in multiple sclerosis (MS), while aphasia is rare. This report documents these findings in a woman with relapsing MS. Associated features included dysmnesia, achromatopsia and elements of Gerstmann's syndrome. Cranial CT showed a large contrast-enhancing area of demyelination in the left temporo-parietal region.
The case is reported of a patient who, after a left occipital infarction, presented a deficit in naming visually presented objects with neither aphasia, nor perturbation in the perceptive and associative processing of visual informations. This visuo-verbal disconnection was accompanied by disturbance of the semantic function when this was explored via the visual channel. In addition the patient showed an alexia which could be described as an abstraction defect. Finally, the patient showed a deficit in naming colors and faces, without evidence for agnosia. This observation argues in favor of maintaining a distinction between visual associative agnosia and optic aphasia. It also demonstrates that the naming deficit implies a deficit in extracting semantic values from visual informations such as objects or graphic symbols.
A case of pure alexia due to an ischemic lesion of the occipital temporal region is described. Written words could be matched but not read. Immediate memory span for graphemes was defective. The reading defect probably depends on the inability to modify the written word "globally"; the phonological process was intact, but the memory disturbance impeded reading. The dissociation is explained by the preservation of word forms, which are linked to the semantic stage. Non-written stimuli trigger a "meaning" which evokes the word form and so the written word is recognized even though it cannot be read.
We describe a patient with literal alexia, agraphia, and only minimal aphasia, resulting from a left occipito-parietal ischemic infarction. Neither impaired visual processing nor impaired oral output could explain the patient's letter reading deficit, since he retained the ability to match letters of mixed case, and remained able to spell aloud and to pronounce and comprehend orally spelled words. His residual word reading was characterized by better performance for nouns and highly imageable words than for functors , poorly imageable words, and nonwords. We propose that this patient's letter reading deficit was due to a partial disconnection of his visual from his linguistic systems, with residual word reading accomplished by a semantically mediated compensatory mechanism. We suggest, further, that the dissociations between word and letter reading observed in some alexic individuals may be attributed, in part, to a difference in the relative contributions of dorsal and ventral occipital structures to the reading process.
We describe a patient with phonological alexia caused by a small hemorrhage in the posterior-inferior portion of the left temporal lobe. The lesion induced a highly selective impairment of phonological reading without concomitant oral language deficits other than anomia for objects presented in the visual and tactile modalities. We propose that an intact dorsal pathway from inferior visual association areas to Wernicke's area via the angular gyrus could mediate reading by the lexical route, while damage to a ventral pathway disrupted the patient's ability to read nonwords. We suggest further that although visually and tactually presented objects could be recognized and both verbally and nonverbally identified, they could not be named because of a disconnection from the area of word representations.
This case report documents the partial recovery, over a 12-month period, of pure alexia in an adult female following a left occipital infarction. Measures of speed and accuracy were obtained on an oral reading and a lexical decision task immediately postonset and then on 10 subsequent occasions. Explicit letter-by-letter reading was observed only during the first week poststroke but a significant effect of word length was seen in all testing sessions. Reading accuracy was relatively good at all stages and reading latency showed a remarkable decrease over time but did not reach normal reading rates. The inability to use higher-order orthographic knowledge, as manifest in the absence of a word superiority effect, was still noted at one year postonset. We therefore concluded that the change in behavior was attributable to increased proficiency in the use of the adaptive letter-by-letter procedure rather than to the resolution of the underlying deficit. It is suggested that longitudinal neurobehavioral studies add to our understanding of the alexic deficit and provide insight into the recovery process.
We report a patient (MT) with a highly specific alexia affecting the identification of letters and words but not numbers. He shows a corresponding deficit in writing: his letter writing is impaired while number writing and written calculation is spared. He has no aphasia, no visuo-perceptual or -constructional difficulties, or other cognitive deficits. A similar pattern of performance has to our knowledge only been reported once before [Anderson, S. W., Damasio, A. R., & Damasio, H. (1990). Troubled letters but not numbers. Domain specific cognitive impairments following focal damage in frontal cortex. Brain, 113, 749-766]. This study shows that letter and number reading are dependent on dissociable processes. More interestingly, it points to a common mechanism subserving the perception and production of letters. We suggest that a deficit in a visuo-motor network containing knowledge of the physical shape of letters might explain the pattern of performance displayed by MT.