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Biomedical subjects

Mitsuru Kawamura

Publications and source records attributed to Mitsuru Kawamura.

43 records · Page 3Linked to original sources

Lewy body-free nigral degeneration--a case report.

A 70-year-old Japanese woman developed progressive, dopa-responsive parkinsonism consisting of akinesia, resting tremor, rigidity, and postural instability. Neuropathological examination revealed a marked loss of nigral neurons, but no Lewy bodies (LBs) were observed. Lewy bodies were also absent from their usual site, with the exception of a small number seen in the dorsal motor nucleus of the vagus nerve (DVN) and sympathetic ganglion. We propose that our case and several similar reported cases represent Lewy body-free nigral degeneration.

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Recognition of emotion from facial, prosodic and written verbal stimuli in Parkinson's disease.

Although the basal ganglia are thought to be important in recognizing emotion, there is contradictory evidence as to whether patients with Parkinson's disease (PD) have deficits in recognizing facial expressions. In addition, few studies have examined their ability to recognize emotion from non-visual stimuli, such as voices. We examined the ability of PD patients and age-matched controls to recognize emotion in three different modalities: facial, prosodic, and written verbal stimuli. Compared to controls, PD patients showed deficits in recognizing fear and disgust in facial expressions. These impairments were not seen in their recognition of prosodic or written verbal stimuli. This modality-specific deficit suggests that the neural substrates for recognizing emotion from different modalities are not fully identical.

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Pure topographical disorientation--the anatomical basis of landmark agnosia.

We used MRI studies of four patients to investigate the lesions responsible for landmark agnosia. A detailed investigation of the relationship between the symptoms and the lesions suggests that the right posterior part of the parahippocampal gyrus is critical for the acquisition of novel information about buildings and landscapes, and that the same region plus the anterior half of the lingual gyrus and the adjacent fusiform gyrus play an important role in the identification of familiar buildings and landscapes. Furthermore, the lesion responsible for prosopagnosia, which frequently occurs with landmark agnosia, seems to involve the posterior half of the lingual and fusiform gyri. This suggests that the lesions responsible for landmark agnosia and prosopagnosia are close to each other, but distinct.

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Utilization behavior as a white matter disconnection syndrome.

We report a case of utilization behavior that was examined neuropathologically. A 72-year-old right-handed male patient, who was admitted with a complaint of transient loss of consciousness, displayed utilization behavior several times. He used daily objects that were placed in front of him, such as a teacup and a toothbrush, without instructions to do so. If the examiner asked the patient not to use the objects, the patient did not use them. MRI revealed acute infarction of the left superior frontal gyrus, where decreased blood flow was revealed by SPECT. The patient died of an acute worsening of dilated cardiomyopathy. Neuropathological examination demonstrated an acute phase infarction of the subcortical white matter of the left superior frontal lobe, which correlated well with neuroradiological findings. Utilization behavior has been thought a "frontal lobe symptom". However, we propose that utilization behavior might be considered a white matter disconnection syndrome.

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Kinesthetic alexia due to left parietal lobe lesions.

To investigate the neuropsychological mechanisms of kinesthetic alexia, we asked 7 patients who showed kinesthetic alexia with preserved visual reading after damage to the left parietal region to perform tasks consisting of kinesthetic written reproduction (writing down the same letter as the kinesthetic stimulus), kinesthetic reading aloud, visual written reproduction (copying letters), and visual reading aloud of hiragana (Japanese phonograms). We compared the performance in these tasks and the lesion sites in each patient. The results suggested that deficits in any one of the following functions might cause kinesthetic alexia: (1) the retrieval of kinesthetic images (motor engrams) of characters from kinesthetic stimuli, (2) kinesthetic images themselves, (3) access to cross-modal association from kinesthetic images, and (4) cross-modal association itself (retrieval of auditory and visual images from kinesthetic images of characters). Each of these factors seemed to be related to different lesion sites in the left parietal lobe.

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[Longitudinal study of procedural memory in patients with Alzheimer-type dementia].

We never forget how to ride a bicycle, and it is thought that procedural memories are retained for a long time. Recently, it was reported that patients with dementia of the Alzheimer type(DAT) could not only acquire, but also retain, long-lasting procedural memories. Previous group studies had shown procedural memory retention times of only 1 month in DAT patients, while amnesic patients and healthy people could retain such memories for 12 months. The relationship between the ability to retain procedural memory and the stage of the disease is not clear, as to date there has been no longitudinal study of procedural memory retention in DAT patients. Thus, we examined DAT patients' ability to retain long-term procedural memories (after 1, 5 and 20 months), and analyzed the relationship between procedural memory ability and the progress of disease. Motor-type procedural memory was examined using the mirror tracing task and the bi-manual coordinated tracing task. All three of the DAT patients showed improvement in their performance. The time required for the tracing was reduced between trials, and the improvement did not disappear between sessions, or rather, their times further decreased in subsequent sessions. Even the most severe DAT patient (Mini Mental State Examination(MMSE) score of 4) was able to acquire the procedural memory and retain it for at least 3 months. Furthermore, one of the subjects showed retention of the procedural memory at 20 months. Our results suggest that DAT patients can retain procedural memories for extended periods, with no relationship between retention ability and disease progression. It is possible for even severely demented patients to acquire and retain motor-type procedural memories. Cognitive rehabilitation in DAT appears to be effective, and it is possible for DAT patients to learn new things. It may be that DAT patients can ameliorate their quality of life by using retained procedural memory.

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