Agraphia For Kanji Research Articles

Strategic Use of Kana Dictation for Auditory Comprehension : A Study of a Case with Word-Meaning Deafness and Kanji Agraphia

Strategic Use of Kana Dictation for Auditory Comprehension : A Study of a Case with Word-Meaning Deafness and Kanji Agraphia

Alexia and agraphia in Japanese

AbstractDissociated performance in the reading/writing of kanji (morphogram) and kana (phonogram) in alexia and agraphia in Japanese has attracted attention because kanji and kana differently convey semantics, orthography, and phonology. Although the dissociation between kanji and kana is relative, but not absolute, detailed case studies, in addition to recent neuroimaging and neurophysiological studies, have revealed the partially separable mechanisms of the kanji and kana writing systems. Kanji words are processed mainly, not exclusively, via the orthographic–semantic route, and kana words are processed via both orthographic–semantic and phonological routes. Pure alexia with lesions in the left medial occipital lobe and splenium shows alexia for both kanji and kana, but at the chronic stage, alexia for either kanji or kana may remain depending on the compensatory mechanism. The left occipitotemporal area is important for reading/writing. The slightly different location and extent of lesions are associated with distinct symptoms: kanji alexia with the lesion in the mid‐fusiform gyrus (visual word form area; VWFA), kana alexia with lesions posterior to VWFA, and kanji alexia with kanji agraphia with lesions lateral to VWFA. The left angular gyrus has traditionally been considered important for writing. However, it is unclear whether the crucial site is the angular gyrus or the cortical and subcortical regions adjacent to it. In neurodegenerative diseases, reading/writing abilities are differentially impaired depending on the specific distribution of neuronal degeneration in each disease. Examining the reading/writing abilities of kanji and kana can facilitate understanding of the writing system and related disorders.

Erratum for Dementia with Lewy Bodies with Pure Agraphia for Kanji (Japanese Morphograms).

Erratum for Dementia with Lewy Bodies with Pure Agraphia for Kanji (Japanese Morphograms).

Asymmetric Bálint’s syndrome with multimodal agnosia, bilateral agraphesthesia, and ineffective kinesthetic reading due to subcortical hemorrhage in the left parieto-occipito-temporal area

ABSTRACT We report a patient with asymmetric Bálint’s syndrome (predominantly right-sided oculomotor apraxia and simultanagnosia and optic ataxia for the right hemispace), and multimodal agnosia (apperceptive visual agnosia and bilateral associative tactile agnosia) with accompanying right hemianopia, bilateral agraphesthesia, hemispatial neglect, global alexia with unavailable kinesthetic reading, and lexical agraphia for kanji (Japanese morphograms), after hemorrhage in the left parieto-occipito-temporal area. The coexistence of tactile agnosia, bilateral agraphesthesia, and ineffective kinesthetic reading suggests that tactile-kinesthetic information can be interrupted because of damage to the fiber connection from the parietal lobe to the occipito-temporal area, leading to these tactually related cognitive impairments.

Selective impairment of On-reading (Chinese-style pronunciation) in alexia with agraphia for kanji due to subcortical hemorrhage in the left posterior middle temporal gyrus

ABSTRACT We report a patient with alexia with agraphia for kanji after hemorrhage in the left posterior middle temporal gyrus. The results of single-character kanji reading and two-character on- (Chinese-style pronunciation), kun- (native Japanese pronunciation), and Jukujikun (irregular kun-) reading word tests revealed that the patient could not read kanji characters with on-reading but read the characters with kun-reading. We consider that this on-reading alexia was caused by disconnection between the posterior inferior temporal cortex (orthographic lexicon) and the posterior superior temporal gyrus (phonological lexicon), and preserved kun- and Jukujikun-reading was realized by bypassing the orthography-to-phonology route by the semantic route.

Kanji (Morphogram) and Kana (Phonogram) Problem in Japanese Alexia and Agraphia.

The kanji and kana (or kanji vs. kana) problem in the Japanese language denotes the dissociation between kanji (morphograms) and kana (phonograms) in reading/comprehension and writing. Since paragraphia of kana in a patient with amyotrophic lateral sclerosis was first reported in 1893, kanji-kana dissociation has been the central topic in Japanese aphasiology. Recent advancements in lesion-to-symptom analyses and functional imaging studies have identified some areas whose damage causes dissociative disturbances of reading or writing between kanji and kana. That is, (1) angular alexia with agraphia causes kanji agraphia; alexia of kana with an angular gyrus lesion is the result of a damage to the middle occipital gyrus; (2) alexia with agraphia for kanji is caused by a posterior inferior temporal cortex (mid-fusiform/inferior temporal gyri; visual word form area) lesion, whereas pure agraphia for kanji is caused by a posterior middle temporal gyrus lesion; and (3) pure alexia, particularly for kanji, results from a mid-fusiform gyrus lesion (Brodmann's Area [BA] 37), whereas pure alexia for kana results from a posterior fusiform/inferior occipital gyri lesion (BA 18/19).

Kana and Kanji Agraphia in Patients with Amyotrophic Lateral Sclerosis: Characteristics and Responsible Brain Regions.

Kana and Kanji Agraphia in Patients with Amyotrophic Lateral Sclerosis: Characteristics and Responsible Brain Regions.

Brodmann Areas 39 and 40: Human Parietal Association Area and Higher Cortical Function

The anatomy and function of the angular gyrus (Brodmann Area 39) and supramarginal gyrus (Brodmann Area 40) are described here. Both gyri constitute the inferior part of the parietal lobe. Association fibers from the angular gyrus project to the dorsolateral prefrontal cortex via the superior longitudinal fasciculus (SLF) II/arcuate fasciculus (AF), whereas those from the supramarginal gyrus project to the ventrolateral prefrontal cortex via SLF III/AF. Damage to the left angular gyrus causes kanji agraphia (lexical agraphia) and mild anomia, whereas damage to the left supramarginal gyrus causes kana alexia (phonological dyslexia) and kana agraphia (phonological agraphia). Damage to either gyrus causes Gerstmann's syndrome (finger agnosia, left-right disorientation, agraphia and acalculia) and verbal short-term memory impairment. "Angular alexia with agraphia" results from damage to the middle occipital gyrus posterior to the angular gyrus. Alexia and agraphia, with lesions in the angular or supramarginal gyrus, are characterized by kana transposition errors in reading words, which suggests the impairment of sequential phonological processing.

Investigation of a Case of Semantic Category-specific Deficits Accompanied by Alexia and Agraphia of Kanji after Herpes Simplex Encephalitis:

Investigation of a Case of Semantic Category-specific Deficits Accompanied by Alexia and Agraphia of Kanji after Herpes Simplex Encephalitis:

左角回から側頭葉にかけての深部白質の脳梗塞で漢字の純粋失書を呈した1例

左角回から側頭葉にかけての深部白質の脳梗塞で漢字の純粋失書を呈した1例

Temporal lobe epilepsy manifesting as alexia with agraphia for kanji

Alexia with agraphia results from lesions of the left angular gyrus or the left posteroinferior temporal lobe. In Japanese or Korean persons, lesions of the latter cause alexia with agraphia for ideograms. We describe a case of alexia with agraphia for kanji (Japanese ideograms) caused by temporal lobe epilepsy. After generalized convulsions, a 32-year-old man noticed that he had difficulty in reading and writing kanji, although he could read and write kana (Japanese syllabograms). His EEG showed frequent sharp waves on the left occipitotemporal region. MRI of the brain revealed a hyperintense lesion on the left hippocampus. Single-photon-emission computed tomography revealed marked hyperperfusion at the left hippocampus and the left posteroinferior temporal cortex. Antiepileptic drugs improved his alexia with agraphia for kanji. This is the first report describing alexia with agraphia for kanji caused by temporal lobe epilepsy.

Functional dissociation between Kana and Kanji: agraphia following a thalamic hemorrhage

We report the case of a 61-year-old woman with a left thalamic hemorrhage causing agraphia of Kanji (morphograms). Single-photon emission computed tomography (SPECT) showed a decrease in the blood flow in the left thalamus from the superior temporal convolution to the parietal lobe, as well as in the frontal lobe while computed tomography showed no remarkable lesions in the cortex. The agraphia in this case may be due to the thalamic lesion itself, but the SPECT findings strongly suggest that a secondary cortical lesion may be involved in producing the higher cognitive disorder.

Isolated thalamic agraphia with impaired grapheme formation and micrographia

Two patients with isolated thalamic agraphia are described. Both showed kanji (Japanese morphograms) agraphia due to impaired character recall, grapheme deformity and micrographia (progressive reduction in character size during writing) after a lesion that involved the ventral lateral and ventroposterolateral nuclei. Single photon emission computed tomography with a (99m)Tc-ethylcysteinate dimer revealed hypoperfusion in the left precentral gyrus (Brodmann Area 6) and anterior supramarginal gyrus in both. Six months later, the extent of blood flow reduction decreased in the supramarginal gyrus in both patients and the precentral gyrus in patient 1. By this time, the writing impairment improved to nearly the normal range. Our study suggests that kanji agraphia (corresponding to lexical agraphia in Western countries) with poor grapheme formation and micrographia arises from a lesion in the ventral lateral and ventroposterolateral nuclei in the left thalamus. The accompaniment of poor grapheme formation and micrographia may reflect disruption of the cortico-subcortical motor circuit involving the putamen, thalamus, premotor cortex and sensorimotor cortex. It is also suggested that multiple cortical sites can be a target for secondary dysfunction that yields agraphia in a thalamic lesion, and that the recovery of reduced cortical blood flow does not always proceed in parallel with that of agraphia.

Lesion localization of non-aphasic alexia and agraphia

The author reviews the lesion localization of non-aphasic alexia and agraphia and proposes a new classification of alexia and agraphia on this basis. The newly proposed alexia and agraphia are pure alexia for kana (Japanese phonograms), or more generally pure alexia for letters, caused by a lesion in the posterior occipital area (posterior fusiform/inferior occipital gyri), and pure agraphia for kanji (Japanese morphograms) caused by a lesion in the posterior middle temporal gyrus and also a lesion restricted to the angular gyrus. In addition, the anatomical lesions presumably responsible for the parietal apraxic agraphia, frontal pure agraphia and thalamic agraphia are discussed.

Pure alexia caused by separate lesions of the splenium and optic radiation

Pure alexia is severe difficulty in reading and understanding written language but with normal oral language and writing abilities. We report a patient with pure alexia caused by two different infarct lesions in the left lateral thalamus and the left splenium of the corpus callosum. A 56-year-old right-handed man was admitted to hospital with right homonymous hemianopia associated with pure alexia. He could write kana characters but not kanji. His cranial magnetic resonance imaging revealed two different infarct lesions in the left optic radiation and the left splenium of the corpus callosum. Magnetic resonance angiography showed mild stenosis at the origin of the right vertebral artery and stenosis of the left distal posterior cerebral artery. The mechanism of developing pure alexia can be simply explained by disconnection. We assumed that agraphia of kanji was caused by the effect of ischemia and edema following transient obstruction in branches from the distal posterior cerebral artery.

Alexia and agraphia with lesions of the angular and supramarginal gyri: Evidence for the disruption of sequential processing

Objective To determine the features of alexia or agraphia with a left angular or supramarginal gyrus lesion. Methods We assessed the reading and writing abilities of three patients using kanji (Japanese morphograms) and kana (Japanese syllabograms). Results Patient 1 showed kana alexia and kanji agraphia following a hemorrhage in the left angular gyrus and the adjacent lateral occipital gyri. Patient 2 presented with minimal pure agraphia for both kanji and kana after an infarction in the left angular gyrus involving part of the supramarginal gyrus. Patient 3 also showed moderate pure agraphia for both kanji and kana after an infarction in the left supramarginal and postcentral gyri. All three patients made transposition errors (changing of sequential order of kana characters) in reading. Patient 1 showed letter-by-letter reading and a word-length effect and made substitution errors (changing hiragana [one form of kana] characters in a word to katakana [another form of kana] characters and vice versa) in writing. Conclusion Alexia occurs as “angular” alexia only when the lesion involves the adjacent lateral occipital gyri. Transposition errors suggest disrupted sequential phonological processing from the angular and lateral occipital gyri to the supramarginal gyrus. Substitution errors suggest impaired allographic conversion between hiragana and katakana attributable to a dysfunction in the angular/lateral occipital gyri.

Pure agraphia for Kanji (logogram) characters and visual images deficits in Alzheimer’s disease

漢字に選択的な失書を呈したアルツハイマー病と思われる症例を報告した。症例は51 歳右利きの男性で，漢字が思い出せずまた書けないことが主訴であった。本症例の特徴は，軽度の記憶障害および構成障害を認めるが，全般的知的機能障害が軽度であり，また失行，失認は認められず，さらに言語症状としては失語が存在せず，文字の読みにも問題がなく，仮名書字の障害が極めて軽度であるのに対して，漢字書字の障害が重度であったことである。漢字構造の結合・分解課題や漢字の正誤弁別課題の結果から，本症例における漢字失書は，漢字の視覚的イメージ (字形) の想起困難，および書字行為の間，そのイメージを保持することの障害により生じた可能性が高いと考えられた。またこの背景には，漢字の視覚的イメージの細部の想起障害と書字運動覚の障害の存在が示唆された。MRI および脳血流画像所見から，本症例の漢字失書の出現には，両側頭頂葉および左側頭葉後下部の障害が関与していると想定された。

Agraphia for Kanji Resulting From a Left Posterior Middle Temporal Gyrus Lesion

Objective: To clarify whether agraphia or alexia occurs in lesions of the left posterior middle temporal gyrus. Methods: We assessed the reading and writing abilities of two patients with this lesion using kanji (Japanese morphograms) and kana (Japanese syllabograms). Results: Patient 1 first presented with pure alexia more impaired for kana after an infarction in the left middle and inferior occipital gyri and right basal occipital cortex, and after a second infarction in the left posterior middle temporal gyrus adjoining the first lesion he showed alexia with agraphia for kanji and worsened alexia for kana; kanji alexia recovered over the following six to 10 months. Patient 2 presented with alexia with agraphia for kanji following a hemorrhage in the left posterior middle and inferior temporal gyri, which resolved to agraphia for kanji at two months after onset. Kana nonword reading was also slightly impaired, but became normal by six months post-onset. In both patients, kanji agraphia was mostly due to impaired character recall. Conclusion: The present patients demonstrate that damage to the left posterior middle temporal gyrus alone can cause agraphia for kanji. If the adjacent mid fusiform/inferior temporal gyri (Area 37) are spared, the kanji alexia is transient.

Pure alexia for kana. Characterization of alexia with lesions of the inferior occipital cortex

To characterize reading impairments caused by lesions in the posterior occipital cortices. We gave six patients with these lesions reading and writing tests and located a critical site for alexia using MRI and SPECT. The patients read three-character kana (Japanese syllabograms) nonwords, and five-character kana nonwords significantly or at a near significant level more poorly and slowly than normal subjects, whereas they read kanji (Japanese morphograms) almost correctly but more slowly. Letter-by-letter reading with a single-kana character identification impairment (in five patients), a word-length effect, kinesthetic facilitation, a lexicality effect, and minor to mild agraphia for kanji (in three patients) were observed. These deficits were characteristic of pure alexia. Alexia disappeared within a few months except in one patient who had extensive hypoperfusion in the left occipital lobe. A shared lesion was located in the left posterior fusiform/inferior occipital gyri (Area 18/19) on MRI, and there was blood flow reduction around this area on SPECT. This area coincided with the activation site for kana word covert reading in our previous study. These results suggest that pure alexia particularly for kana, or more generally pure alexia for letters, is caused by a lesion in the posterior inferior occipital cortex, characterized primarily by impaired kana character or letter identification, with relatively preserved kanji or word recognition.

Ubiquitin-positive frontotemporal lobar degeneration presenting with progressive Gogi (word-meaning) aphasia. A neuropsychological, radiological and pathological evaluation of a Japanese semantic dementia patient

A patient with progressive anomia and alexia with agraphia for kanji (Japanese morphograms) is described. The patient showed a deficit in single-word comprehension and on-reading (a type of reading that conveys phonetic value) dominance in kanji reading, i.e. on-preceding (pronouncing first with on-reading, irrespective of its preferred reading) and kun-deletion (inability to recall and recognize kun-reading [another type of reading that conveys meaning]) when reading a single-character kanji. These features were due to loss of lexico-semantic information and thus the patient was regarded as having progressive Gogi (word-meaning) aphasia by Imura, a Japanese manifestation of semantic dementia. Macroscopically, neuropathological examination disclosed atrophy of the left frontotemporal lobe with accentuation in the anterior portion of the temporal lobe. Histologically, there was neuronal loss in the cerebral cortex, hippocampus, parahippocampal gyrus, amygdala, caudate nucleus, and putamen. Ubiquitin-immunoreactive neuronal inclusions were present in the hippocampal dentate granular cells. This case demonstrates that progressive Gogi aphasia is semiologically identical to semantic dementia, and our patient clinicopathologically resembled those of Rossor et al. [Rossor, M.N., Revesz, T., Lantos, P.L., Warrington, E.K. Semantic dementia with ubiquitin-positive tau-negative inclusion bodies. Brain 2000; 123: 267–76.] and Hodges et al. [Hodges, J.R., Davies, R.R., Xuereb, J.H., Casey, B., Broe, M., Bak, T.H., et al. Clinicopathological correlates in frontotemporal dementia. Ann Neurol 2004; 56: 399–406.].