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Reversible posterior leucoencephalopathy during oral treatment with methotrexate.
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Alexia without agraphia following cerebral venous thrombosis associated with protein C and protein S deficiency.
A 26-year-old right handed female was admitted to hospital with right homonymous hemianopia associated with alexia without agraphia. Her cranial magnetic resonance imaging and magnetic resonance angiography revealed a left occipital venous infarction due to thrombosis of the left transverse, sigmoid sinuses and the left internal jugulary vein. The underlying conditions were protein C and protein S deficiency associated with the use of oral contraceptives. To our knowledge, alexia without agraphia has never been described due to a venous infarction associated with hereditary thrombophilia in the literature.
Alexia without agraphia following biopsy of a left thalamic tumor.
Alexia without agraphia is a rare disconnection syndrome characterized by the loss of reading ability with retention of writing and verbal comprehension. We report a patient who developed alexia without agraphia after undergoing a biopsy for a malignant glioma involving the left thalamus. A 15-year-old right-handed male presented with 3 days of severe headache, and vomiting, and 1 month of blurry vision in his right visual field. Magnetic resonance imaging of the brain disclosed a large exophytic mass originating in the left thalamus, with mass effect and hydrocephalus. The patient underwent biopsy of the left thalamic mass via a transcallosal approach. Postoperatively, the patient complained of inability to read or identify letters. Examination revealed alexia without agraphia. The syndrome of alexia without agraphia can be rarely caused after surgery. A transcallosal procedure through the splenium of the corpus callosum may disrupt the visual association fibers traveling from the right occipital cortex to the left angular gyrus. In our case the syndrome occurred because of a preexisting right homonymous hemianopia resulting from a left thalamic tumor.
Temporal processing deficits in letter-by-letter reading.
Theories of the cognitive impairment underlying letter-by-letter reading vary widely, including prelexical and lexical level deficits. One prominent prelexical account proposes that the disorder results from difficulty in processing multiple letters simultaneously. We investigated whether this deficit extends to letters presented in rapid temporal succession. A letter-by-letter reader, G.M., was administered a rapid serial visual presentation task that has been used widely to study the temporal processing characteristics of the normal visual system. Comparisons were made to a control group of 6 brain-damaged individuals without reading deficits. Two target letters were embedded at varying temporal positions in a stream of rapidly presented single digits. After each stream, the identities of the two letters were reported. G.M. required an extended period of time after he had processed one letter before he was able to reliably identify a second letter, relative to the controls. In addition, G.M.'s report of the second letter was most impaired when it immediately followed the first letter, a pattern not seen in the controls, indicating that G.M. had difficulty processing the two items together. These data suggest that a letter-by-letter reading strategy may be adopted to help compensate for a deficit in the temporal processing of letters.
Alexia without agraphia in multiple sclerosis: case report with magnetic resonance imaging localization.
The syndrome of alexia without agraphia occurs rarely in multiple sclerosis (MS). We report a patient with right homonymous hemianopsia and alexia without agraphia as his initial manifestations of relapsing-remitting MS. Magnetic resonance imaging (MRI) demonstrated a hyperintense lesion in the left occipital subcortical white matter (WM) and an enhancing lesion in the splenium of the corpus callosum. The clinical presentation and MRI findings were consistent with disconnection of the functional right occipital visual cortex from structures responsible for language comprehension in the left hemisphere. The diagnosis of MS was confirmed by subsequent development of additional periventricular WM lesions.
Alexia without agraphia in a child with acute disseminated encephalomyelitis.
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Alexia without agraphia in a postpartum eclamptic patient with factor V Leiden deficiency.
We present a case of eclampsia complicated by alexia without agraphia. To our knowledge, this syndrome has never before been described in the literature.
Transitory alexia without agraphia: a disconnection syndrome due to neurocysticercosis.
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.
Alexia with agraphia.
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.
[Auditory agnosia, pure word deafness, Wernicke's aphasia without alexia: clinical and conceptual aspects].
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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.
Word and letter reading and the mechanism of the third alexia.
Four patients, two with global aphasia and two with Broca's aphasia, demonstrated the seemingly paradoxical ability to read words but not their component letters. Picture naming was only moderately impaired, and repetition of word and letter names was intact, excluding both a generalized dysnomia and an articulatory disturbance as the cause of the literal alexia. Matching tests revealed processing deficits in three of the patients, more severe for letters than for words. Oral reading of word lists showed that short, high-frequency, and picturable words were read best, whereas nonsense trigrams, which require phonetic processing, were the most difficult. The residual reading of patients with severe Broca's or global aphasia and the "third alexia" appears to involve purely visual, nonphonetic mechanisms for word recognition, using posterior left hemisphere or even minor hemisphere centers. Letter reading, by contrast, along with phonetic reading of syllables, appears to be a more specialized, anterior left hemisphere process.
Dissociated disorders of speaking and writing in aphasia.
Of 500 left brain-damaged patients with educational level above elementary school investigated with a standard quantitative battery for dissociation between oral and written expression, speech was found to be selectively impaired in seven (three with "pure anarthria," two with anarthria in the context of Broca's aphasia, and two with fluent aphasia with remarkable sparing of writing), and writing in another seven (two with "pure" agraphia, two with "agraphia with mild alexia," and three with "agraphia with mild fluent aphasia.") The nature of three conditions (pure anarthria, fluent aphasia with sparing of writing, and pure agraphia) is discussed, with evidence of a selective association between pure agraphia and lesions of the upper left parietal lobule.
[Alexia due to visual-verbal disconnection (Geschwind). Apropos of a case of pure verbal blindness without agraphia but with disorders of designation of colors, of names and of images].
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Troubled letters but not numbers. Domain specific cognitive impairments following focal damage in frontal cortex.
A well educated right-handed woman developed severe and stable alexia and agraphia following a circumscribed surgical lesion in the left premotor cortex. The lesion was located in Brodmann's field 6, above Broca's area, in the region traditionally referred to as Exner's area. The alexia and agraphia occurred in a pure form, that is, in the setting of otherwise normal cognitive and neurological function. She was not aphasic or hemiparetic and her visual perception, intellect, memory, oral spelling and drawing were normal. The patterns of impairment of reading and writing closely paralleled one another. Reading of single words and letters was severely impaired, and she was entirely unable to read sentences. She was virtually unable to write recognizable letters, could write no words, and her writing attempts were severely distorted spatially. By contrast, she could easily read all numbers and nonverbal symbols, and she was equally able to write numbers and perform written calculations without difficulty. These striking dissociations provide further evidence of the domain specificity of cognitive/neural representations. They also point to the possible role of premotor cortices in the coactivation of precise sequences of motor and sensory activity patterns involved in reading and writing.
Alexia without agraphia and associated disorders: importance of recognition in the rehabilitation setting.
Alexia without agraphia is readily recognized in its pure (without other neurologic findings) but rare form. However, this deficit is more common when associated with other behavioral disturbances that result from trauma or cerebral infarction to the posterior cerebral hemispheres. Two cases presented with alexia without agraphia following infarction within the posterior cerebral artery territory. Because of initial confusion and disorientation the patients were diagnosed as demented and unsuitable for rehabilitation. Both subjects had a visual field deficit and color agnosia. Prosopagnosia, simultanagnosia, and ataxia of visual-motor control were also present. The second case was unusual because of pure word blindness associated with a right occipital lobe lesion. Only a few such cases have been reported in the literature worldwide. This paper demonstrates that careful delineation of cognitive deficits permits greater understanding of functional disorders with improved rehabilitation outcome.
[Cerebrovascular disorder and the language areas].
Recent progress of imaging techniques has achieved precise descriptions of aphasic syndromes associated with cerebrovascular disorders. Infarction of the left anterior cerebral artery brings about transcortical motor aphasia. Occlusion of each branches of the left middle cerebral artery produces characteristic language symptoms. Recently, cases with infarction of the areas of prefrontal and precentral arteries were reported to manifest fluent aphasia indistinguishable from the classical transcortical sensory aphasia. Rare cases with lesions restricted to the Broca's area (territory of the precentral artery) produces aphasia with normal fluency, word finding difficulty and deficit in sentence comprehension. Classical non-fluent Broca's aphasia is caused by infarctions which at least involves the areas of precentral and central arteries. Aphemia or pure word dumbness results from damages which involves territory of the central artery. Conduction aphasia is most often associated with lesions of the posterior parietal artery territory. As in the case of Broca's aphasia, Wernicke's aphasia is a composite of conduction aphasia, pure word deafness, transcortical sensory aphasia, and alexia with agraphia. The lesion of Wernicke's aphasia naturally involves the areas of all of these aphasic symptoms. Transcortical sensory aphasia is associated with lesions in the posteroinferior temporal region, and is often associated with watershed infarctions of the middle and posterior cerebral arteries. Aphasia which results from putaminal hemorrhage has ambiguous manifestation, and is difficult to be classified into Wernicke-Lichtheim's model. Assessment of its fluency is notoriously difficult. Thalamic aphasia is similar to either anomic aphasia or transcortical sensory aphasia. It was pointed out that classical aphasic syndromes are still valid as cerebral arterial occlusion syndromes, but are insufficient for the purpose of more precise anatomo-clinical correlation.