Parkinson Disease: Kanazawa A

Miziuno Y, Okuma Y, Kikuchi S, Kuno S, Hashimoto T, Hasegawa K, Mano Y, Miwa H, Murata M, Yamamoto M, Yokochi F, Okiyama R, Kanazawa A, Shinpo K, Chuma T, Higashi T, Maruyama T, Mizuta E, Yamazaki S, Anonymous00188. · Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan · Rinsho Shinkeigaku. · Pubmed #12708433 No free full text.

This publication has no abstract.

Kanazawa A. · Department of Neurology, Juntendo Tokyo Koto Geriatric Medical Center. · Nippon Rinsho. · Pubmed #15462384 No free full text.

Abstract: Parkinson's disease (PD) is a slowly progressive disorder which begins with motor symptoms. Several cognitive deficits can be observed in nondemented patients with PD during their history. The core symptom in the cognitive deficits in PD is the executive dysfunction. Neuropsychological tests such as Wisconsin Card Sorting Test, Trail Making Test are used to measure the degree of this dysfunction. Executive dysfunction is thought related to abnormalities in the dorsolateral prefrontal circuit which largely passes through the caudate nucleus. The dysfunction emerges as the pathology spreads to the nigrocaudate project corresponding to Hoehn & Yahr stage II-III. Effective therapy for cognitive dysfunction in PD remains elusive, however donepezil, Attention Process Training, Music therapy and Transcranial magnetic stimulation have been reported to have partial efficacy.

Noda K, Kobayashi T, Matsuoka S, Takanashi M, Kanazawa A, Mizuno Y. · Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan. · No To Shinkei. · Pubmed #15782604 No free full text.

Abstract: We report a 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty in eye-lid opening, and marked pseudo-bulbar palsy. He felt difficulty of it, hand movement at 59 years old. When he was 60 years old, monotonous speech and slowness of movement appeared. He visited a neurologist who noted vertical gaze palsy, neck rigidity, and bradykinesia. He was diagnosed as progressive supranuclear palsy (PSP) and given 300 mg L-Dopa/Benserazide by the neurologist. This medication improved his rigidity and bradykinesia. At 62 years of the age, his eye-lids closed involuntary and it was difficult to open. In addition, he began to complain of wearing-off, autonomic symptoms, and dysphagia. Anti-parkinsonian drugs were increased, but his bradykinesia progressed. At 64 years of the age, he was admitted to the Neurology Service of Juntendo Hospital. On admission, he was alert and not demented. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, upward and downward gaze were markedly restricted. His face was hypomimic and seborrhoic. It was difficult to swallow liquid or solid for him. No weakness was noted, but he walked in small steps with freezing and falling tendency to backward. Rigidity was noted on his extremities and stronger on his left side than right. Tremor was absent. Bradykinesia of his body and extremities was marked. No cerebellar ataxia was noted. Deep tendon reflexes were within normal range. Planter response was flexor bilaterally. Myerson's sign was noted. Sensory and autonomic function were normal. He was treated with L-Dopa, Pergolide, and Bromocriptine. However, these medications improved his bradykinesia and gait disturbance only slightly, dysphagia became progressively worse. He developed aspiration pneumonia when he was 65 years old and admitted to Juntendo Hospital. A large amount of sputum was aspirated from his trachea. Two days after from admission, he was found dead on his bed. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had progressive supranuclear palsy (PSP). Other differential diagnoses included Parkinson's disease, pallido-nigroluysian atrophy (PNLA), multiple system atrophy (MSA), and corticobasal degeneration(CBD). Many participants considered that PSP or PNLA was most likely. Post-mortem exmination revealed marked nigral neuronal loss and gliosis. The globus pallidus and the luysian body changed mildly. However, the frontal cortex was relatively spared, there were many ballooned neurons in the cortical layer. Other parts were spared. With sliver (Bodian and Gallyas-Braak) and anti-phsphorylated tau stain, abundant astrocytic plaques, neurofibrillary tangles, and argyrophilic threads on the frontal cortex, striatum, and substantia nigra were seen. There was no tufted astrocyte which was hallmark of diagnosis of PSP. In addition, several Lewy bodies were seen in the brainstem. Because astrocyte plaque was considered specific for pathology of CBD, the pathologist revealed that the pathological diagnosis of this patient was CBD. Nevertheless, discussion was focused on the relatively mild degeneration of the frontal cortex for CBD.

Kanazawa A, Ikebe S, Komatsuzaki Y, Takanashi M, Mori H, Mochizuki H, Mizuno Y. · Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo 113-8421. · No To Shinkei. · Pubmed #11277107 No free full text.

Abstract: We report an 84-year-old woman with progressive mental deterioration. She was well until January 1994, when she was 80 years of the age. At that time she developed a delusional ideation, in that she stated that she would be killed by her fellow members of the society for elderly, in which she was belonging. At times, she closed the shutter of her house saying that a stranger was wandering outside of her house. In 1995, she could not identify the face of her son's wife. When she went out for shopping, she lost her way to the home. She prowled about in and out of her home. In 1996, she had to be admitted to a nursing home, where quarrelled with other patients and behaved violently. She was admitted to the neurology service of Hatsuishi Hospital on November 20th, 1997. Family history revealed that her mother was said to be demented. On admission, she was alert and behaved in a good manner. She was disoriented to the time and unable to do serial 7. Her memory was very poor. She did not show aphasia or apraxia. Cranial nerves appeared to be intact. She showed no weakness or muscle atrophy. Gait was normal for her age. Plastic rigidity was noted in four limbs more on the right side. No ataxia was noted. Deep tendon reflexes were exaggerated, however, no Babinski sign was noted. Sensory examination was intact. Her hospital course was characterized by the development of progressive gait disturbance, violent behaviour, and prowling around. On November 30th, 1998, she fell down and suffered from a fracture in the neck of her femur. Although replacement of the femur head was performed, she became unable to walk after this episode. Her mental functions deteriorated further. She developed pneumonia and expired on February 2, 1999. She was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient probably had diffuse Lewy body disease, because of the combination of dementia and parkinsonism. Other possibilities discussed in the CPC included Pick's disease, frontotemporal dementia and parkinsonism, and Alzheimer's disease. Post-mortem examination revealed moderate atrophy in the frontal and temporal cortices. Microscopic examination showed atrophy and gliosis in the hippocampus. Many diffuse plaque and neuritic plaques were seen in the frontal cortex by methenamine silver staining. Neurofibrillary tangles were also found. The Meynert nucleus was preserved. The putamen and the substantia nigra were also intact. Pathologic diagnosis was consistent with Alzheimer's disease.

Kanazawa A, Mizuno Y, Narabayashi H. · Department of Neurology, Juntendo University School of Medicine. · Rinsho Shinkeigaku. · Pubmed #11676156 No free full text.

Abstract: Executive function declines in Parkinson's disease (PD). However, it has not been clearly shown at what stage in PD, this decline starts to occur. We here report a study aiming to answer this question. We conducted Wisconsin Card Sorting Test (WCST) and Trail Making Test A and B (TMT A, B) in three normal control groups (young, adult, and aged) and three PD patients groups (Hoehn & Yahr stage I, II, and III). We intend to analyze at what age or stage the decline in executive function would take place. The score of all the normal subjects and PD patients were 25 points or above by Mini-Mental State Examination. WCST in stage I PD patients (mean age 60.8, n = 9) was essentially same as those of young normal (mean age 23.1, n = 9) and adult normal (mean age 61.5, n = 10) subjects. Elderly normal subjects (mean age 75.8, n = 4) showed a significantly lower mean category achievement score (3.0 as the mean score) and higher numbers of errors and perseverations compared with those of young and adult normal subjects. Stage II (mean age 62.6, n = 8) and III PD (mean age 62.9, n = 8) patients showed significantly lower mean category achievement scores (2.4 and 2.1, respectively as the mean scores) and higher numbers of errors and perseverations compared with those of adult control subjects (5.4 as a mean score). TMT (B-A) in elderly normal subjects revealed significantly longer score (209 seconds as the mean score) compared with those of young and adult normal subjects (20 and 45 seconds, respectively as the mean scores). TMT (B-A) in stage III PD patients was significantly longer (219 seconds) compared with that of adult normal subjects (45 seconds as the mean), however TMT (B-A) in stage II PD patients (102 seconds as the mean) did not show prolongation. TMT (B/A) showed essentially similar results as TMT (B-A), however, stage II PD patients showed significant prolongation compared with that of normal adult subjects. Therefore, TMT (B/A) appears to be a more sensitive indicator of decline in executive function in PD. Between WCST and TMT, the former appeared to be a more sensitive indicator. Our results indicate that the decline in executive function takes place in normal ageing. In PD, this decline starts much earlier than the normal subjects. The onset in this decline coincides with the stage of PD, in which bilateral symptoms start to present. Anatomo-chemical subsrate of cognitive decline in PD is still to be debated, however, we believe that involvement of nigro-caudatal projection is at least in part responsible, as nigroputaminal pathway is mainly involved in motor functions. We also point out the importance of age factor in the evaluation of cognitive-executive function in PD, as this function is age-dependent in normal subjects.