A 67 year old Japanese male patient had pure agraphia after a haemorrhage in the left superior parietal lobule. He developed diYculty in letter formation but showed no linguistic errors, consistent with the criteria of apraxic agraphia. He manifested a selective disorder of sequencing writing strokes, although he was able to orally state the correct sequences. The patient's complete recovery after 1 month, without new learning, showed that he had manifested a selective disorder of writing stroke sequences. These findings indicate that the final stage of the execution of writing according to acquired sequential memory shown as a stroke sequence can be selectively disturbed, and should be considered to be distinct from the ability of character imagery and the knowledge of the writing stroke sequence itself. This case also indicates that the left superior parietal lobule plays an important part in the execution of writing. (J Neurol Neurosurg Psychiatry 1999;66:233-237) Keywords: pure apraxic agraphia; left superior parietal lobule; writing stroke sequences Pure agraphia is an impairment in writing unaccompanied by any other relevant language disorder, 1 which occurs in association with lesions in the frontal lobe, 2 superior parietal lobule, 3-5 temporal lobe, 6 left caudate nucleus and internal capsule, 7 and left thalamus. Regarding the type of pure agraphia and the lesions, the parietal lobe is considered a candidate site of the causative lesion for disorders of spatial and kinesthetic movements of writing 3 4 ; however, the relation between the type of agraphia and other lesions remains uncertain. We herein report a case of pure agraphia after a haemorrhage in the left superior parietal lobule in a Japanese patient, who showed a characteristic impairment of writing, and we discuss the symptoms and the mechanism of pure agraphia after a left parietal lesion. Case descriptionA 67 year old, right handed, university educated Japanese male bank clerk was admitted to Takeda General Hospital on 12 October 1993. He had been in good health without any relevant history of disease, but was subsequently found to have hypertension. On the evening of 12 October he noted sudden weakness in his right arm while he was at his oYce. His colleagues noted at that time that he answered their questions irrelevantly and they brought him to the hospital. A neurological examination showed him to be alert, but disoriented as to time and place. The cranial nerves were all intact, and he showed no paresis in the limbs, and no pathological reflexes or sensory deficits. By the next day he had become well oriented, but he became aware of an impairment in his writing. Brain MRI performed 22 days after onset (fig 1) disclosed a circumscribed haemorrhage in the left superior parietal lobule. Seventeen days after onset, N-isopropyl-( 123 I)-p-iodoamphetamine single photon emission computed tomography (SPECT) disclosed decreased blood flow corresponding to the region showing a haemorrhage, as disclosed by MRI. Neuropsychological assess...

Among the reports of primary progressive aphasia, there are few about patients who exhibited progressive pure word deafness with detailed auditory and radiological examination as well as neuropsychological assessment. We describe a 67-year-old right-handed man who exhibited slowly progressive pure word deafness over a period of 9 years without exhibiting any other cognitive or mental deterioration. Magnetic resonance imaging of his brain revealed generalized cortical atrophy, particularly in the left superior temporal region. Auditory examination revealed severe disability in discriminating each syllable or mora of Japanese words despite adequate auditory acuity. He also showed impairment in temporal auditory discrimination assessed by the click fusion test and the click counting test. His ability to discriminate meaningful environmental sounds was mildly impaired. We discuss the pathophysiology of slowly progressive pure word deafness over a period of many years which was not complicated by other language or cognitive dysfunctions.

Our results indicated that the major neural network from occipital lobe to frontal cortex, which is mainly involved in the ventral visual pathway, demonstrated activation in these tasks. Result of this study will serve as base line data for analyzing the findings in patients with impaired visual perception.

We report a 60-year-old right-handed Japanese man who showed an isolated persistent typing impairment without aphasia, agraphia, apraxia or any other neuropsychological deficit. We coined the term ‘dystypia’ for this peculiar neuropsychological manifestation. The symptom was caused by an infarction in the left frontal lobe involving the foot of the second frontal convolution and the frontal operculum. The patient’s typing impairment was not attributable to a disturbance of the linguistic process, since he had no aphasia or agraphia. The impairment was not attributable to the impairment of the motor execution process either, since he had no apraxia. Thus, his typing impairment was deduced to be based on a disturbance of the intermediate process where the linguistic phonological information is converted into the corresponding performance. We hypothesized that there is a specific process for typing which branches from the motor programming process presented in neurolinguistic models. The foot of the left second frontal convolution and the operculum may play an important role in the manifestation of ‘dystypia’.