[The Life of Mokichi Saito].

Mokichi Saito (1882-1953) was born in Yagamata in 1882. After he graduated from junior high school, he was adopted by the Saito family. He started writing songs from the time he was in school. He eventually became a doctor, and soon after that, he published his first work, "Red Light." While studying in Europe, he wrote "The Brain Map in Progressive Dementia." After returning to Japan, he composed several songs. She was a best mother for her children. I have written his story because he had a peculiar character, even according to his wife.

[From "Shaking Palsy" to "Parkinson's Disease": Was Charcot Correct?]

In light of contemporary knowledge, we review a classic case of "Parkinson's disease" presented by Charcot. The patient, Bachère, provided an opportunity to change the name of the disease from "Shaking palsy" to "Parkinson's disease". We also explore a total of 4 cases of "Parkinson's disease in extension", especially that of Rab. Léon, described in 2 articles (1889 and 1892) in Nouvelle Iconographie de la Salpêtrière. Although diagnosed by Charcot as a type of Parkinson's disease, and historically accepted as such, he may have been misled. English text is available

[An Autopsy Case of Amiotrophic Lateral Sclerosis Characterized by Upper Motor Neuron Degeneration and Progressive Pseudobulbar Palsy].

This is a case report of autopsy findings for a male Japanese patient who presented with progressive gait disturbance and dysarthria. Neurological examination at the age of 61 years revealed pseudobulbar palsy and upper motor neuron disorder. The patient appeared unaware of his illness. Electrophysiological examination showed lower neuron damage. The patient was diagnosed with amyotrophic lateral sclerosis characterized by lower motor neuron damage. He died of pneumonia 2 years and 3 months after diagnosis. Neuropathological examination demonstrated severe degeneration of the upper neurons and mild degeneration of the lower neurons. Immunohistological examination indicated transactivation-responsive DNA-binding protein-43-positive pathology in the frontal and temporal lobes, amygdala, corpus striatum, and spinal cord. We believe the neuropathological findings correlate well with the clinical features. Furthermore, we also discuss the lesions involved in the patient's dementia. (Received March 28, 2017; Accepted September 19, 2018; Published November 1, 2018).

[Prosopometamorphopsia].

Facial perception relies on both configural processing and analytical processing. Seventeen years ago, Haxby and colleagues proposed an influential neural model in which a core system and an extended system were involved in facial processing. Herein, first analyze configural processing on the basis of the Haxby model. We review previous findings from published electrophysiological and neuroimaging studies, and describe previously reported clinical cases, and finally we discuss our own clinical cases an findings. Based on this work we have sketched out a new framework for facial perception suggesting that suggests that the extended system includes more widely distributed regions than originally expected.

[Samuel Alexander Kinnier Wilson].

Samuel Alexander Kinnier Wilson is considered a pioneer in extrapyramidal system research largely due to his dissertation on progressive lenticular degeneration, later known as "Wilson's Disease". His concept of neurological symptomatology was based on the clinical observations of Pierre Marie, Joseph Babinski and John Hughlings Jackson, who he observed when he was young. To keep focusing on the nature of actual symptoms while performing medical examinations is the essence of neurological symptomatology, which in turn form the spirit of neurology. This paper will discuss major events in Wilson's later life that would explain how his basic idea for neurological symptomatology was eventually formed.

[The cause of failure of eradication treatment of Helicobacter pylori].

The drug treatment, the combination of lansoprazole + amoxicillin + clarithromycin, for Helicobacter pylori infection with gastroduodenal ulcer was approved for the national heath insurance November 2000 in JAPAN, and has been widely applied. However, failures of eradication have been counted in 10-20% of the cases. The major reason of the failure has been reported as the drug resistance of the H. pylori. Here, we surveyed the antimicrobial resistance of 70 clinical isolates in a Showa University Hospital 2001, 1 to 2002, 1. As a result, the ratio of primary resistance to amoxicillin was about 1.4%, and clarithromycin was about 11.4%. Among 70 H. pylori positive cases, 14 cases were treated with eradication 3 drug combination therapy. In 5 cases, H. pylori were detected after eradication treatment and these five strains acquired the second resistance to neither amoxicillin nor clarithromycin. To distinguish the cause of H. pylori culture-positive after eradication treatment is whether the failure of eradication itself or re-infection, we attempted the analysis of the restriction pattern of H. pylori genome (genome type) using pulsed-field gel electrophoresis. In all 5 cases, genome types of before and after treatment were identical, suggesting the failure of eradication treatment. Three of 5 cases, isolates before and after treatment were susceptible to both of amoxicillin and clarithromycin. Thus, the reason of failure of eradication is considered to ingestion compliance, not antimicrobial agent resistance nor reinfection. The rest of 2 cases, the primary resistance to clarithromycin may result the failure of eradication. Test for drug susceptibility and genome type analysis of H. pylori are significant in certification of an authenticity of an eradication treatment.