Biomedical subjects
Publications and source records attributed to F Udaka.
Syringobulbia with a large syrinx was revealed by MR imaging. The syrinx extended from the medulla to vertebral level T10. We suspect that this giant syrinx may be produced by a congenital meningioma at C7, generating pulsatile flow in the original syrinx and causing a giant syrinx.
We report a Garcin syndrome due to nasopharyngeal carcinoma invading the skull base. MR Imaging of this patient shows the position of the tumour and reveals how the tumor invaded the skull and the effect of treatment.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Among 39 cases with acute-onset amnestic syndrome having unilateral localized infarct, 8 cases with anteromedial thalamic infarct ("thalamic" amnesia), and 18 cases with medial temporal lobe infarct including hippocampus in the posterior cerebral artery territory ("PCA" amnesia) were studied in terms of X-CT and MRI findings and neuropsychological examinations. Results were as follows: 7 out of 8 cases with thalamic amnesia (88%), and 15 of 19 cases with PCA amnesia (78%) showed left side lesions on CT scan. All groups showed a prolonged recent memory loss with little loss of immediate recall and remote memory, and disorientation and dyscalculia. In both types of amnesia, patients having a left sided lesion showed recent memory loss with new learning disabilities of verbal materials. Patients having a right sided lesion showed recent memory loss with new learning disabilities of both verbal and visuospatial materials. Judging from the X-CT and MRI findings, the lesions most probably causing amnesia in these cases seemed to be the anterior and dorsomedial nuclei of the thalamus in thalamic amnesia and hippocampus in PCA amnesia. Differential diagnosis in amnestic syndrome with localized infarct is also discussed.
A morphological study using a modified Golgi impregnation technique was carried out on Betz cells in the motor area of eight patients with motor neuron disease (MND) and age-matched controls without abnormal neuropathological findings during routine examination. Betz cells were categorized as normal (type I), or those with moderate (type II) or marked (type III) degeneration of dendrites. Types II and III Betz cells tended to be dominant in the cases of MND, whereas type I Betz cells constituted the highest percentage in most of the control cases. The frequently observed morphological alterations of Betz cells in MND were accumulation of lipofuscin, degeneration or loss of dendrites, and reactive astrocytic gliosis around the Betz cell soma. It was suggested that Betz cell changes in MND are not only due to aging but also to evident pathological processes, since the above-mentioned findings were more extensive in the MND cases than in the control cases. Also, the so-called lower motor neuron disease belongs to one basic disease termed "motor neuron disease", because the pathological changes of Betz cells were observed even in cases of spinal progressive muscular atrophy alone or associated with progressive bulbar palsy, which are devoid of pyramidal tract degeneration and signs of upper motor neuron lesion.
Levodopa or amantadine hydrochloride was administered to 25 patients with pathologic laughing and/or crying. This symptom was markedly improved in ten cases, most of which were devoid of a cortical atrophy or a periventricular lucency in computed tomographic scan and also devoid of a severe dementia or a disturbance in activity of daily living. The concentration of homovanillic acid in the CSF of the patients was significantly decreased, whereas the concentration of 5-hydroxyindoleacetic acid remained within the normal limit. Because part of pathologic laughing and crying seems to be caused by the decreased function of the dopaminergic neuron, levodopa or amantadine is worth trying.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To examine the metabolic products of thyroid hormones in the central nervous system, total and free rT3 as well as T4 in human cerebrospinal fluid (CSF) were determined in 41 patients. Total T4, T3, and rT3 concentrations in CSF were determined by RIA, and free T4, T3, and rT3 fractions were analyzed by the magnesium precipitation method. The mean (+/- SE) total T4 and T3 concentrations in CSF were 166 +/- 24 and 2.6 +/- 1.5 ng/dl, respectively; the values were approximatey 2% of those in normal control pooled sera. Total rT3 concentrations in CSF from 29 clinically euthyroid patients who were apparently in a normal nutritional state ranged from 5.2-23 ng/dl (mean +/- SE, 11.2 +/- 0.9 ng/dl); the value was approximately 40% of that in sera. A patient with primary hypothyroidism had a markedly diminished CSF rT3 concentration (1.1 ng/dl), and the remaining 11 patients, suffering from severe diseases such as meningitis and cerebrovascular accident, had significantly higher CSF rT3 concentrations (37.5 +/- 6.6 ng/dl) than the clinically euthyroid patients. Although free T4 and T3 concentrations in CSF (5.9 +/- 1.1 and 0.16 +/- 0.05 ng/dl, respectively) were similar to those in serum (2.1 +/- 0.2 and 0.22 +/- 0.01 ng/dl, respectively), the free rT3 concentration in CSF (0.70 +/- 0.12 ng/dl) was approximately 20 times higher than that (0.044 +/- 0.016 ng/dl) in serum. Furthermore, the reciprocal relationship was observed between CSF total rT3 concentrations and free rT3 percentages in CSF. These data suggest the possibility that rT3 may be produced from T4 in human brain and that there may be a transport mechanism regulating free rT3 in CSF.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study evaluated efficacy and safety of donepezil hydrochloride (donepezil) at 5 mg/day in patients with mild to moderately severe Alzheimer's disease for 24 weeks in a double-blind, placebo-controlled comparative trial. In this study, 268 patients were enrolled and 39 of these (15%) were withdrawn. In the evaluable population of efficacy, Protocol-Compatible (PC) analyzed patients (n = 228), better effects than that of placebo were confirmed using two primary efficacy measures: a cognitive performance test, the Japanese version of the Alzheimer's Disease Assessment Scale - cognitive subscale (ADAS-J cog, p = 0.003) and a clinical global assessment, the Japanese version of the Clinical Global Impression of Change (J-CGIC, p = 0.000). The superiority of donepezil was also shown by secondary measures: the Sum of the Boxes of the Clinical Dementia Rating (CDR-SB), the Mental Function Impairment Scale (MENFIS) and the caregiver-rated modified Crichton scale (CMCS). The same results were obtained in the intention-to-treat (ITT) analysis (n = 263). The incidence of drug-related adverse events was 10% (14/136) in the donepezil and 8% (10/131) in the placebo group; no significant difference was seen between the two groups. The main adverse events were gastrointestinal symptoms, and these were almost all mild, and they all disappeared with continued administration or temporary discontinuation of donepezil. These results indicate that the donepezil appears to be effective and well tolerated in patients with mild to moderately severe Alzheimer's disease.