The oculomotor nerve roots of 61 autopsy cases, aged between 25 and 96 years, were studied by a combined light and electron microscopy. Occasional myelinated fibers were present with “focal argyrophilic swelling” resembling axonal swelling in the aged, In longitudinal sections, these focal argyrophilic swelling of myelinated fibers were identified as round, oval or spindle shapes. In transverse sections, they had both 5-10μ and 10-20μ in diameter. Focal argyrophilic swellings with 10-20μ in diameter were observed frequently in the aged, especially over 80 years, Focal argyrophilic swellings with 5-10μ in diameter were seen frequently in the aged with carcinoma. Histochemically, it was confirmed that these focal argyrophilic swellings were lipid deposit. Electron microscopically, they were observed as the deposit of dense bodies, lipids, lysosomes and vesicles in the cytoplasm of Schwann cells bordered on the axolemma. It was commen ted that focal argyrophilic swellings of the oculomotor nerve roots in the aged might be caused by metabolic dysfunction in the Schwann cells.

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The cerebral circulation time was measured by serial carotid angiographies in 252 cases of cerebrovascular diseases and 12 cases of other diseases with normal angiograms. The cerebral circulation time (CCT) was the time from the maximum filling of the carotid syphon to appearance of the venous angle by serial cerbral angiography. One hundred and sixty cases of cerebral infarction with non-specific angiographical changes were classified into three groups according to grades of arteriosclerotic changes on arteriograms. Of these patients, cerebral hemodynamics was investigated by the N₂O method in 31 cases and relationships between cerebral blood flow and CCT were studied.
Results:
1) The mean value of CCT in the normal control group (mean age 40.1±15.3 year-old) was 4.17±1.03 seconds.
2) In cases of the acute stage of cerebral hemorrhage, CCT was markedly prolonged with a mean value of 6.33±0.99 seconds and that of CCT in the acute stage of subarachnoid hemorrhage was 5.43±1.05 seconds. In the chronic stage of cerbral hemorrhage and sub arachnoid hemorrhage, mean value of CCT was shortened as 5.86±0.92 and 4.64±1.03 seconds, respectively.
3) In cases of cerebral infarction, CCT was prolonged in accordance with severities of angiographical arteriosclerotic changes. The mean values of CCT were 4.94±0.95 seconds in grade 0-1 group, 5.43± 1.33 seconds in grade II group, 5.70±0.76 seconds in grade III group, respectively. A marked delay of CCT was shown in the cases of middle cerebral artery occlusion. (mean value, 6.18±1.04 seconds).
4) No significant relationship was recognized between CCT and duration of diseases from the onset or hypertension in cases with cerebral infarction.
5) Effects of age on CCT was recognized in those above 71-year-old, and CCT was significantly delayed in these cases,
6) Cerebral blood flow (CBF) measured by the N₂O method was decreased correspondingly with severity of angiographical arteriosclerotic changes, and cerebrovascular resistance (CVR) was also increased, as well.
7) There was a significant negative correlation between CCT and CBF in cases with cerebral infarction, and a significant positive relationship between CCT and CVR was observed.
In conclusion, CCT can be clinically utilized as an index of hemodynamic changes in cerebrovascular diseases, and its delay suggests impairment of cerebral circulation.

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The abnormality of serum electrolyte concentration in patients with cerebrovascular accident (CVA) of acute stage have been reported by several authors. Serum electrolyte disorder is deemed to be a factor to impede the recovery of motor or mental function in CVA patients, but it is little known in chronic stage. In this study, the values of serum sodim and potassium concentrations were estimated in CVA patients of chronic stage, in relation to the diet ingestion, the administration of diuretics, and the blood pressure, The subjects were 14 cases of cerebral hemorrhage and 86 cases of cerebral infarction.
The level of serum potassium in CVA patients (3.93± 0.44mEq/L, mean value±S.D.) was significantly lower than that in normal age-matched controls (4.07± 0.32), The serum potassium level was particularly lower in cerebral hemorrhage (3.63±0.46) than in cerebral infarction (3.94±0.41). The serum potassium concentration was investigated by means of classifying the CVA patients into the subgroups, with or without oral diet ingestion, with or without diuretic administration, and with or without hypertension, because these factors might influence serum electrolytes. It was found that these factors had no significant influence on the level of serum potassium.
The serum sodium concentration in the CVA patients who could not take oral diet (138.3±2.6mEq/L) was significantly lower than that in CVA patients who could eat (141.0±2.7). Hypertension and diuretics administration had little influence on serum sodium concentration.
In chronic stage of CVA, the significant low concentration of serum potassium found in cerebral hemorrhage in comparison with cerebral infarction might be attributed to the extent of organic brain damage, and the maintenance of serum sodium concentration might have a certain connection with oral diet ingestion.

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