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PubMed1998

Treatment of a case of phonological alexia with agraphia using the Auditory Discrimination in Depth (ADD) program.

Phonological alexia and agraphia are acquired disorders characterized by an impaired ability to convert graphemes to phonemes (alexia) or phonemes to graphemes (agraphia). These disorders result in phonological errors typified by adding, omitting, shifting, or repeating phonemes in words during reading or graphemes when spelling. In developmental dyslexia, similar phonological errors are believed to result from deficient phonological awareness, an oral language skill that manifests itself in the ability to notice, think about, or manipulate the individual sounds in words. The Auditory Discrimination in Depth (ADD) program has been reported to train phonological awareness in developmental dyslexia and dysgraphia. We used a multiple-probe design to evaluate the ADD program's effectiveness with a patient with a mild phonological alexia and mixed agraphia following a left hemisphere infarction. Large gains in phonological awareness, reading and spelling nonwords, and reading and spelling real words were demonstrated. A follow-up reassessment, 2 months posttreatment, found the patient had maintained treatment gains in phonological awareness and reading, and attained additional improvement in real word reading.

Agraphia↗
PubMed2003

Agraphia with abnormal writing stroke sequences due to cerebral infarction.

A 65-year-old, right-handed man presented with speech and gait disturbances. He was alert and cooperative, showing mild right hemiparesis and sensory disturbance. Spontaneous speech was fluent; object naming, word fluency and reading were fully preserved. Sentence repetition and verbal comprehension were mildly impaired. Writing was slow, hesitant and difficult for both spontaneous writing and dictation. Copying was better, although he had some difficulty in copying letters and also complex figures. Sequences of strokes in forming written characters were abnormal; strokes were formed by piecing together several fragments. Computed tomography and magnetic resonance imaging showed a subcortical infarct in the left frontoparietal region. Characteristics of agraphia resembled 'apractic agraphia' and agraphia may have resulted largely from loss or unavailability of the memory of motor patterns necessary for writing letters.

Aged↗
PubMed1990

Pure agraphia of kanji due to thrombosis of the Labbé vein.

A case is described of a 56 year old Japanese male with pure agraphia of kanji (the Japanese morphograms) due to haemorrhagic infarction of the left temporal lobe caused by the rare condition of cortical vein thrombosis of Labbé. Writing kanji was severely impaired without disturbed consciousness, aphasia or apraxia. On the other hand, writing kana (the Japanese syllabograms), and reading kanji and kana were almost intact. This suggests that the process of writing kanji involves a different pathway from that of reading kanji in the left temporal lobe. Pure agraphia of kanji is considered to be similar to lexical agraphia in Indo-European languages, in that the writing system with a poor or irregular phoneme-grapheme transformation is impaired by the left temporal lesion. This case indicates the necessity for considering thrombosis of the Labbé vein when a subcortical haematoma is detected in a temporal lobe on computed tomography of the brain.

Agraphia↗
PubMedDate not supplied

Transtentorial herniation with posterior cerebral artery territory infarction. A new mechanism of the syndrome of alexia without agraphia.

A 39-year-old male developed a right homonymous hemianopsia and alexia without agraphia following emergency surgery for hemorrhage into a left frontal tumor. A computerized tomographic (CT) scan demonstrated low density areas in the left frontal region and in the territory of the left posterior cerebral artery. The alexia without agraphia syndrome appeared to result from compression of the left posterior cerebral artery by a transtentorial pressure cone, a mechanism not previously reported in this syndrome. The behavioral investigation confirmed the diagnosis and replicated recent findings related to the syndrome of alexia without agraphia.

Adult↗
PubMed1997

Frontal pure agraphia for kanji or kana: dissociation between morphology and phonology.

We present two patients with frontal pure agraphia more impaired for either kanji or kana (two separate writing systems for the Japanese language). The lesion of patient 1 (preferentially disturbed for kanji) was restricted to the foot of the middle frontal gyrus and the adjacent anterior precentral gyrus, whereas the lesion of patient 2 (preferentially disturbed for kana) included the posterior two thirds of the middle frontal gyrus. Both patients made agraphic errors (impaired recall) for kanji and agraphic or paragraphic errors (changing into other symbols) for kana. The double dissociation and the difference in types of errors between kanji writing and kana writing suggests that there are two pathways involved in writing, i.e., a morphologic route and a phonologic route. We concluded that damage to the morphologic route may yield agraphia for kanji and that damage to the phonologic route may yield agraphia for kana.

Aged↗
PubMed1986

[Alexia without agraphia: a clinico-tomographic study].

The authors report the clinical findings and CT-scanning results in two cases of alexia without agraphia and review the literature on this subject. Both patients had extensive infarction in the territory supplied by the left posterior cerebral artery and developed severe alexia without agraphia, right hemianopia without color-anomia and one of them presented with transient verbal memory difficulties. In both cases the evolution was very good, with total regression of the alexia after 17 months in the first patient and almost complete recovery after there months in the second one. The authors comment on the causes and possible mechanisms of the alexias, especially of the alexia without agraphia, and suggest that every patient with right hemianopic disturbances due to occlusion of the left posterior cerebral artery be thoroughly studied from a neurological point of view, so that this syndrome can be detected since, notwithstanding its recognized rarity, it seems highly probable that many cases have been overlooked as a result of incomplete examination of the patients.

Adult↗
PubMed2004

[A case of dementia with motor neuron disease associated with agraphia--the omission of kana letters].

We report a 55-year-old right-handed Japanese man with motor neuron disease and dysgraphia of kana letters. He was admitted to our hospital because of dysarthria and dysphasia. On admission, the results of general physical examination were within normal limits. Neurological examination revealed severe dysarthria, dysphasia, impaired movement of the tongue without fasciculation and slight distal muscle weakness in the bilateral upper limbs. There were no fasciculation of the muscle. Deep tendon reflexes were hyperactive without Babinski's signs. Sensation, coordination, and gait were normal. Neurophysiological studies demonstrated normal motor nerve conduction velocities and sensory action potential. The results of needle electromyography of the upper limbs were compatible with motor neuron disease (MND). Magnetic resonance imaging (MRI) showed atrophy of the bilateral temporal region of the brain. 99mTc-HMPAO SPECT (Single Photon Emission Computed Tomography) showed reduced uptake of tracer in the bilateral temporal region. On neuropsychological examination, his behavior was normal, and orientation and intelligence were also preserved, but his speech was severely impaired. Reading comprehension was slightly impaired. In regard to writing comprehension, he had no difficulty in copying of words though dictation was found to be impaired. He omitted one kana letter in a word. Agraphia is accompanied by various factors such as aphasia, dementia, agnosia, alexia. But in this case at least for early stage, agraphia existed without other higher cortical dysfunction. He did not show severe dementia in his early stage of his disease, but developed it later in the disease's progression. In this case, agraphia might be due to the atrophic changes in the temporal lobe.

Agraphia↗
PubMed2006

[A case of alexia with agraphia caused by the re-infarct in left lateral occipital gyrus].

The angular gyrus has been proposed as the key area of reading and writing function. In recent PET (positron emission topography) activation studies, role of angular gyrus in the reading and writing has been reestimated. Whether the angular gyrus is necessary for reading and writing or not is now under discussion and should be clinically revised. We experienced a case that presented classical alexia with agraphia of kana (Japanese syllabogram) caused by the re-infarct in left lateral occipital gyrus. This case showed the alexia with agraphia more apparent in Japanese kana than in kanji characters. Interestingly, no higher cortical dysfunction was revealed at the first cerebral infarction in left angular gyrus which was assumed as the key area for alexia with agraphia. This case supported the opinion which pointed out the importance of left occipital gyrus on Japanese kana reading.

Aged↗
PubMed1991

[Two cases of pure agraphia developed after thalamic hemorrhage].

We have observed two cases suffered from left thalamic hemorrhage, that showed pure agraphia. The first case was a 49 year-old, right handed male, who was educated through 11th grade. The CT scan revealed left thalamic hemorrhage with ventricular casting. The second case was a 48 year- old, right handed male, who was educated through 9th grade. The CT scan revealed left thalamic hemorrhage which is smaller than that of the first case, without intraventricular rupture. With a standard neuropsychological evaluation performed at chronic stage, neither cases showed oral language disorder, apraxia and agnosia. On the Wechsler Adult Intelligence Scale, total IQ of the first and second case were 71 and 80 respectively. Each case developed severe writing disorder. The first case showed severe neographism and scrawl, mild literal paragraphia, which were frequently accompanied with perseveration. The second case showed literal paragraphia and no response, but neographism was not detected. The common characteristics of both cases were; 1) intact copy writing. 2) discrepancy between difficulty in writing "Kana" and that in "Kanji". 3) anosognosia of agraphia. The cerebral blood flow study by 123I-IMP Single photon emission computed tomography revealed low perfusion of the left cerebral hemisphere in both cases. From these findings, we concluded that dysfunction of the left cerebral cortex is responsible for producing agraphia in these cases.

Agraphia↗
PubMed1986

[Alexia with agraphia produced by localized infarction in the inferior posterior region of the left temporal lobe].

There have been several reports on alexia with agraphia due to hemorrhage or trauma in the inferior posterior region of the left temporal lobe since Yamadori (1982) first reported a case of cerebral hemorrhage. We presented the first case of alexia with agraphia due to a circumscribed infarct in the inferior posterior region of the left temporal lobe. A 65-year-old right-handed man had an acute onset of inability to read Japanese "kana" letters and to write any letters. He had no difficulty in speaking or understanding. Neurological examination on admission was normal except for homonymous quadrantanopia in the right upper field. Neuropsychological findings: Spontaneous speech was fluent without dysprosody. There were no disturbances in auditory understanding or in repetition. He could read Japanese "kanji" characters correctly, however, he could not read any "kana" letters. Writing was also disturbed severely even as to his address, name or telephone number. Calculation was also difficult. There were no disturbances in naming colors, no ideomotor or constructional apraxia nor visual agnosia. X-ray computed tomography (CT) scan showed a faint low density area with ring enhancement suggesting a cerebral infarct in the inferior posterior region of the left temporal lobe. Patient's hospital course was characterized by a marked improvement of alexia, especially of "kana" letters as compared with that of "kanji" characters. Dissociative improvement of alexia compared with agraphia in this case could be explained by the fact that the lesion was in close contact with the occipital lobe and that he also had pure alexia in the early stage.

Agraphia↗
PubMedDate not supplied

[Pure bilateral agraphia, right astereognosia and arithmetic defects associated with a left parietal tumor (author's transl)].

A case of bilateral agraphia produced by a left parietal glioma is described in a 49 year-old right-handed woman. Hypothesis of a pure agraphia, etiology and non-frontal localisation of tumor are discussed. This agraphia is associated to a right astereognosia; neither functional nor behavioral relationships are found between these two defects, and it appears that their are probably associated according to the parietal locus of lesions.

Agraphia↗
PubMed1995

[Alexia-agraphia of kanji (Japanese morphogram) after left posterior-inferior temporal lesion].

Several cases of selective alexia with agraphia of kanji have been reported in Japan in this decade. It is well known that the lesion in the posterior inferior temporal lobe of the dominant hemisphere is responsible for this cognitive syndrome. Neuropsychological data in our patient suggest that the postero-inferior region of the temporal lobe of the dominant hemisphere may be the visuo-verbal association area for the analysis of the complex visuo-verbal information. The symptoms caused by the same lesion in western patients might be subangular alexia (alexia without agraphia). Alexia with agraphia of kanji and subangular alexia would appear to be distinct entities, but a dual processing hypothesis of visuo-verbal information and the concept of the visuo-verbal association area might well explain both syndromes.

Agraphia↗
PubMed1997

[Jargon agraphia in a case with Broca aphasia: dissociation between language and writing dominancy].

A 69-year-old left-handed man developed Broca aphasia and jargon agraphia following a right cerebral infarction. He learned to write with his right hand. There is no family history of left-handedness. Neurological examination revealed hemiparesis, sensory impairment, and hyperreflexia with pathological reflexes on the left side. An MRI demonstrated lesions in the area including the pre- and post-central gyri, the posterior part of the middle and inferior frontal gyri, and inferior parietal lobule on the right side. Neuropsychologically he was alert and cooperative. He demonstrated severe Broca aphasia and his verbal output was limited to a few residual words. On the other hand, he could communicate through writing Kanji words. Writing words was relatively preserved with Kanji but not with Kana characters. Asked to write a Japanese folk tale, he showed jargon agraphia mixed with some correct Kanji words. His comprehension of spoken and written sentences was well preserved. He showed mild ideomotor and buccofacial apraxia, left unilateral spatial neglect, and constructional impairment. Dissociation between spoken and written language is a prominent feature of this patient's language output. In this patient, right hemisphere seems to be dominant for language and praxis, and left hemisphere for motor engram of writing. Learning to write with the right hand may have enhanced the establishment and maintenance of motor engram for writing in the left hemisphere. The intact motor engram of characters in the left hemisphere could be retrieved by the right hand without control from the language area in the diseased right hemisphere, resulting in jargon agraphia especially with Kana characters. In left handed people, the hand with which they learn to write may effect interhemisphere lateralization of language functions.

Aged↗
PubMed1984

Alexia without agraphia: a study of a case of verbal alexia without accompanying colour-naming defect.

A 47-year-old man developed a persistent form of alexia without agraphia as the result of a haemorrhagic intracerebral lesion in the left inferior temporo-occipital region, due to the rupture of an arteriovenous malformation. Surgical evacuation of the haematoma and excision of the malformation did not produce any modification of the reading deficit, which remained unchanged during a 4-year follow-up. The reading deficit was restricted to words and the patient was able to read only letter-by-letter, so that the whole words were reconstructed from the auditory names of the letters. So far, the disconnection explanation is the standard explanation of alexia without agraphia and the present case of verbal alexia may be regarded as being within this overall category. However, this explanation meets with unanswered questions that suggest more flexible interpretations. Neurolinguistic studies have questioned the unique character of alexia without agraphia as a clinical entity and, in contrast to the disconnection hypothesis, support the notion that the different varieties of alexia that are traditionally described represent distinctive syndromes, each with its own clinical features and pathophysiological basis. In this context, the reading properties in this case seem fully compatible with a deficit of the visual word-form system postulated by Warrington and Shallice, that is, the relatively early stage of the reading process through which a word-form or equivalent unit is attained. This system might be lateralized to the left hemisphere, as suggested by the fact that this case, like other cases of verbal alexia, had sustained damage to the left hemisphere and did not show any differential preservation of the reading of concrete words.

Brain↗
PubMed1988

Lexical agraphia from focal lesion of the left precentral gyrus.

Lexical agraphia reflects a dysfunction of the lexical spelling system and is characterized by better spelling of nonwords and regular words than irregular words. All previously reported cases with documented focal lesions had involvement of temporo-parieto-occipital regions. We now report a case of lexical agraphia following a discrete lesion of the left precentral gyrus. Our case complements previous neuroanatomical accounts of agraphia and provides further support for the independence of neuronal systems that mediate spelling from those involved in spoken language and reading.

Aged↗
PubMed2000

[A case of callosal apraxia without agraphia and acquired stuttering associated with callosal infarction].

We report a 52-year-old right-handed man with cerebral infarction of the right anterior cerebral artery area. The MRI findings showed cerebral infarction in the trunk of the right corpus callosum, although some part of the posterior half of the trunk was spared. Some part of right precuneal gyrus, cingulate gyrus were also involved. The clinical feature of this case is characterized by following two points. First, although callosal apraxia is usually accompanied by agraphia, he showed apraxia with the left hand, but showed no agraphia. Secondary, he showed speech dysfluency mainly characterized by initial syllable repetitions. The nature of this speech dysfluency was determined as acquired stuttering. This case suggests that the pathway for praxis locates distinct portion from that for writing on corpus callosum. We analyzed callosal lesions of previous studies reporting callosal apraxia without agraphia, then compared to that of this case. And we also reviewed acquired stuttering report caused by callosal lesions. Consequently, we suggest that apraxia and stuttering were caused by damage of the trunk of the corpus callosum. While writing was preserved by the intact fibers in the posterior half of the trunk.

Apraxias↗
PubMedDate not supplied

[Alexia without agraphia, colour "agnosia" and right visual field defect: a syndrome of the posterior cerebral artery (author's transl)].

Two cases of alexia without agraphia are reported, with differences in the characters of the alexia and in the accompanying signs. The visual field defect was limited to quadranopia in both cases which was upper quadrantic and mild in one, lower quadrantic and severe in the other. These differences make it unlikely that a similar anatomical location of the lesion and a unique mechanism are responsible of all cases of alexia without agraphia. Persistance of visual inputs in the right visual field is partial in our cases, but alexia without hemianopsia does exist. These facts are against the mechanism of "splenio-cortical" disconnection proposed by Geschwind as the only explanation. A "cortical", or agnosic mechanism has been also claimed, with lesions of the lingual and fusiform gyri on the dominant side, as well as "subangular", mechanism, with intrahemispheric disconnection by a lesion located between the visual associative areas and the angular gyrus: in these last two situations an hemianopsia is not necessarily associated to the alexia without agraphia.

Agnosia↗
PubMed1979

Apraxic agraphia with neglect-induced paragraphia.

Agraphia may result from the loss or unavailability of the memory of movements necessary to form written letters. For this mechanism to be invoked, it must first be demonstrated that there is no language deficit and that there is no disconnection between language and motor areas. A left-handed patient demonstrated bilateral agraphia and apraxia, but not aphasia, following a right parietal infarction. Preservation of the ability to type with the left hand demonstrated that the right hemisphere was not disconnected from language input. In addition, paragraphic errors while typing were shown to be secondary to left hemispatial neglect.

Aged↗