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The case of a right-handed man with pure alexia without hemianopia due to intraparenchymal haematoma is reported. Ct scan and nuclear magnetic resonance showed a lesion in the lateral temporo-occipital area confirming the assumption that the anatomic pathways responsible for reading run close to the lateral temporo-occipital or inferior temporal gyrus.
An HIV-positive patient presented the classical syndrome of pure alexia. Neuroradiologic investigation by computed tomography showed a ring-like lesion in the left posterior white matter. The clinical manifestations as well as the radiologic findings resolved after antiprotozoal treatment.
A patient who developed pure alexia without agraphia following a stroke is described. An infarction of the left occipital pole was demonstrated by Magnetic Resonance Imaging (MRI). The literature on this rare syndrome is reviewed, and the localisation of damage in relation to the clinical findings discussed.
Unusual findings at autopsy prompted this case report of a patient with the syndrome of alexia without agraphia. The expected disconnection of the left angular gyrus from both visual cortices was not found at postmortem examination. Multiple cerebral metastases were identified, but none were present in the presumed pathways connecting the left occipital lobe and the left angular gyrus.
A left-handed patient was studied who had the acute onset of alexia without agraphia, a left homonymous hemianopia, and prosopagnosia. Neurodiagnostic tests including computerized axial tomography and angiography disclosed bilateral lesions in the posterior cerebral hemispheres involving the splenium of the corpus callosum. Neuropsychologic examination indicated marked impairment of facial discrimination, deficient naming and memory of presented visual material, and mild visual agnosia with relative preservation of other cognitive functions. These findings are consistent with a double disconnection syndrome involving disconnection of the dominant angular gyrus and right inferotemporal cortex from their bilateral visual inputs.
A patient who had alexia without agraphia, right homonymous hemianopia, and intact color-naming was studied anatomically. Pathologic involvement of the splenium and related forceps was restricted to the inferior third, supporting published suggestions that inferior elements of this commissure and left peristriate cortex may be essential to the decoding to the written word, while color-naming may be functionally aligned to more dorsal elements.
A patient with alexia without agraphia, hemianopia, or color-naming defect was found at operation to have a meningioma arising from the tentorium cerebelli that compressed the inferior aspect of the left temporal-occipital junction. It is presumed to have involved only the left ventral visual association cortex and its inferior outflow tracts to the angular gyrus. The input from the right occipital area also was disconnected from the visual language verbal association area by involvement of the ventral outflow of the splenium of the corpus callosum. Preservation of color naming and matching suggests that these functions are dependent on the integrity of more dorsal occipital association systems.
The authors report a patient with pure alexia (letter-by-letter reading) selectively impaired for kana (Japanese phonograms), cerebral achromatopsia, and right lower quadrantanopsia after hemorrhage in the left posterior occipital lobe, mainly under the lateral occipital gyri. The patient also could not recognize some single-character kana, nor could he discriminate between two shapes of a similar size. The authors believe that the posterior occipital lobe, including the lateral occipital gyri, is specialized to recognize kana characters in this patient.
Twenty-one patients with right hemisphere damage were studied (11 men, 10 women; average age = 41.33; range = 19-65). Patients were divided in two groups: pre-Rolandic (six patients) and retro-Rolandic (15 patients) right hemisphere damage. A special reading test was given to each patient. The observed errors included: literal errors (substitutions, additions, and omissions of letters), substitutions of syllables and pseudowords for meaningful words, left hemispatial neglect, confabulation, splitting of words, verbal errors (substitutions, additions, and omission of words), grouping of letters belonging to two different words, misuse of punctuation marks, and errors in following lines. It was proposed that spatial alexia is characterized by: (1) some difficulties in the recognition of the spatial orientation in letters; (2) left hemispatial neglect; (3) tendency to "complete" the sense of words and sentences; (4) inability to follow lines when reading texts, and sequentially explore the spatial distribution of the written material; and (5) grouping and fragmentation of words, most likely as a consequence of the inability to interpret the relative value of spaces between letters correctly.
Following a left temporoparietal-occipital haemorrhage and surgery, a 43-year-old, right-handed male exhibited alexia without agraphia. A remediation programme consisted of training in head turning to compensate for a right visual field defect, letter-by-letter reading aloud and covertly, drill with flash-cards to improve word recognition and practice in naming objects to improve dysnomia. The patient's reading improved markedly over a 6-week period and he was able to resume work as a respiratory therapy supervisor. A post-morbid depression resolved concomitantly with the patient's return to work. The training programme and the patient's post-training approach to reading are discussed in terms of hemispheric functioning as well as 'direct path' and 'indirect path' reading. The effectiveness of training is considered in the context of spontaneous recovery.
A case of alexia without agraphia is presented. It is a rare but classic disconnection syndrome, first described by Dejerine in 1892. Recent advances in modern neuroimaging techniques such as FLAIR MRI can now localise in vivo the site of origin of the syndrome, especially when computerised axial tomogram of the brain is normal.
A 57 year-old woman developed a slowly progressive environmental agnosia and dressing apraxia without disturbances of language, memory, orientation and social activities. Two years later, alexia, agraphia, visual agnosia, constructional apraxia, simultagnosia and imitation apraxia of nonsymbolic gestures were also noted. Ophthalmic examination demonstrated a left inferior quadranopsia. Oral comprehension was normal. There was no loss of insight, and behavioral response was appropriately concerned. Computed tomography and magnetic resonance imaging revealed bilateral cortical atrophy in parieto-occipital areas, most pronounced on the right side, with enlargement of the ventricles. Positron emission tomography demonstrated low flow and metabolism values in the right parietal, temporal and occipital regions. This case is very similar to those of posterior cortical atrophy recently reported by Benson et al. (1988). It suggests a selectively degenerative dysfunction of posterior association cortex, sparing oral language and verbal memory.
We report here a case of multiple sclerosis (MS) showing pure alexia. The patient was a 28 year-old, right-handed male student of medicine. He had been healthy prior to college, but when he tried to read the newspaper one morning in January of 1983, he suddenly became aware that he could not. He could speak fluently and had no disturbances of auditory comprehension. No signs of abnormality were noted in his writing ability. Thereafter, the patient occasionally experienced difficulty in reading, together with right homonymous hemianopsia. These symptoms, however, usually vanished following sleep. In April, 1984, the patient experienced headache and ataxia when walking, followed by repeated remission and exacerbation of the symptoms. Corticosteroid therapy produced complete disappearance of the headache and ataxia. In September of 1985, he was hospitalized at our department due to the clouding of consciousness accompanied by convulsions. Neurologically, no abnormalities of the ocular fundus were noted and Babinski's sign was negative, but left hemiplegia was observed. Neuropsychologically, his intelligence was normal and he had no difficulty in writing, but paralexia was noted. There were no disorders of spontaneous speech or auditory comprehension. Examination by CT scan and magnetic resonance imaging revealed a number of lesions in the white substance of the cerebrum, including the left occipital lobe. The abnormal signs seen radiographically vanished when cortical hormones were administered. It has been thought that the symptoms of multiple sclerosis are due mainly to disorders of the white substance, and that MS seldom produces symptoms of aphasia, due to the fact that the lesions in this disease are generally small.(ABSTRACT TRUNCATED AT 250 WORDS)
The authors presented a case of relatively pure syndrome of alexia with agraphia in a patient speaking Serbo-Croatian language. Reading disturbances showed some characteristics of a deep dyslexia. Besides severely impaired reading and writing abilities, some components of Gerstamnn's syndrome were also present. Infarction in the posterior half of the left supramarginal and in the anterior half of the left angular gyrus was accurately located by the graphic reconstruction of CT scans.
A right-handed man, born of a right-handed family, presented an infarct in the territory of the right middle cerebral artery, with a left hemiplegia, a left lateral homonymous hemianopsia and an expression aphasia. The oral trouble disappeared in some weeks, but later a permanent linguistic deficit persisted, affecting mainly the written language and realizing a clinical picture of alexia-agraphia with Gerstmann's syndrome. The neurolinguistic study showed a preferential alteration of the phonologic system in the written language, and at a lesser degree in the oral modality. The extent of the lesion and the relative integrity of oral expression and comprehension, suggested that these functions were localized in the left hemisphere, whereas lecture, writing, calculation, body-parts notion, laterality notion, had been simultaneously implanted during the ontogenesis in the right hemisphere. The latter was probably also responsible for phonological aspects of written and spoken language, according to a scheme opposite to that of usual right-handers.
Oral and written speech centers are commonly attributed to the dominant hemisphere, while body, spatial and facial recognition to the non-dominant. This paper examines the case of a 63 year old entirely right-handed male who presents alexia, agraphia, difficulties in spelling and word-finding together with left spatial and body agnosia, musical, letter and face agnosia, constructional apraxia and left hemianopsia. Computerized axial tomography confirms a right occipital tumor identified as an adeno-carcinoma probably of digestive origin. The role of right hemisphere as a spatial prerequisite to final elaborate speech is discussed.
The authors report the anatomical and clinical findings observed in a case of alexia iwthout agraphia due to left posterior cerebral artery infarction, in which there were lesions of the occipital and thalamic regions, the splenium of the corpus callosum, and the hippocampus. They discuss, more particularly, the memory difficulties, and the objects naming trouble.
An adult patient with literal alexia, agraphia, slight anomia, and dyscalculia due to a left hemisphere infarct showed lack of sequential skills while pattern recognition remained intact. Some words were recognized as patterns, but could not be read phonetically. Therapy concentrated on forming an association of the visual pattern of the complete word with the retained auditory pattern. In this way the patient learned to read several hundred words and short phrases, even as anomia worsened. The patterns learned could not be generalized to noun declension or verb conjugation, or broken into smaller words. This learning process is characteristic of right hemispheric skills which were utilized as left hemispheric functions deteriorated.