[Utilization of the prolonged nasotracheal intubation in a case of delayed decannulation].
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Biomedical subjects
Publications and source records attributed to H Nagara.
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Chronological morphological investigation was carried out in the spinal cord of quaking mice from day 3 to day 130. Numbers of myelinated fibres were far fewer in quaking mice at day 3 compared to controls. However, when the animals became older, myelination progressed and numbers of myelinated fibres increased although myelin sheaths remained far thinner than the size of axons. Many oligodendroglia during day 5 to 15 in quaking mice revealed prominent dilation and proliferation of smooth walled vesicles and cisterns but after 20 days, such changes were no longer observed. Tortuous bizarre oligodendroglial processes, aberrant myelination and myelin figures were very prominent around day 5--15, but such changes also gradually subsided. Density of glial cells during pre-myelination gliosis was similar in both quaking and control mice. However, glial cell population decreased far slower pace than controls when myelination progressed. Thus, glial cell density remained proportionally higher in quaking than controls although the density declined with age in both.
Radial component of myelin sheaths was investigated in C57BL and quaking mice. In immature myelinated fibres of C57BL mice, more than one group of radial component were observed in the several regions of myelin sheaths while in mature fibres, one group of radial component was localized between the internal mesaxon and outer tongue process which were situated within 90 degrees of each other. In thinly myelinated fibres of adult quaking mice, numerous groups of radial component were found at random distance and directions but they were always closely related to the cytoplasmic islands of oligodendroglia. Even in quaking mice, small well myelinated fibres showed normal mature pattern of radial component. Possible functional significance of radial component was briefly discussed.
Neurotoxic effects of adriamycin (ADM) were examined in rats. The drug was administered through retrograde axoplasmic transport from the transected sciatic nerve in very small amounts (0.05 mg of adriamycin). Using the autofluorescence specific to adriamycin as a histological tracer, alterations in primary sensory neurons in dorsal root ganglia (DRG) and in motor neurons in the spinal cord were observed chronologically by light and electron microscopy. In the DRG at the fifth and sixth lumbar levels, small neurons initially showed alterations in mitochondria, wavy nuclear membranes and enlarged cisternae of rough endoplasmic reticulum, and disappeared early in the experiments. Large neurons, which showed accumulation of neurofilaments, dense bodies and vacuoles in the perikarya in addition to nucleolar and nuclear chromatin alterations, degenerated slowly. In contrast, motor neurons in the anterior horn at the sixth lumbar level survived throughout the administration of adriamycin despite the presence of transient weak adriamycin autofluorescence and vacuoles in the cytoplasm. Thus, the susceptibility and vulnerability of motor neurons in spinal cord to adriamycin differed from that of primary sensory neurons; small neurons in the DRG were more susceptible than large sensory neurons. Administration through retrograde axoplasmic transport proved to be a useful technique for the evaluation of the neurotoxicity of adriamycin without the complications of systemic effects.
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Intracytoplasmic, rod-shaped and eosinophilic inclusions were recognized only in Purkinje cells in a case of Crow-Fukase syndrome. The ultrastructure of the inclusions was similar to that of the Hirano body and was suspected to have some relation to neurofilaments.
In order to evaluate the effects of lesions in the upper motor neuron on the lower one, a morphometric study of the 5th lumbar ventral roots was performed in 16 patients with cerebrovascular diseases (CVD) and 8 age-matched controls plus 7 patients with muscular disorders as pathological controls. As a lesion of the upper motor neuron, the degree of lateral corticospinal tract degeneration in the spinal cord were classified into 4 groups. Total fascicular area (TFA), total myelinated fibers (TF) and large fibers (LF) of the ventral roots were significantly (p less than 0.001) decreased in CVD patients who revealed severe degeneration in the lateral corticospinal tracts in affected sides compared with those of controls. The apparent unilateral fiber loss in the ventral root was also observed in some cases whose lateral corticospinal tracts were degenerated with ipsilateral predominance. Therefore, the degree of degeneration of the lateral corticospinal tracts seemed to parallel that of fiber loss of the ventral roots. On the other hand, there were no significant decreases of TFA and TF in the patients with muscular disorders, which makes less likely the possibility that fiber loss in the ventral roots of CVD cases is attributed to long-term bed rest or lack of muscle movements in extremities. These findings suggest a trans-synaptic effect of the degenerated upper motor neuron (lateral corticospinal tract) in CVD patients facilitating fiber loss in the ventral roots.
Morphometric studies of the 5th lumbar ventral spinal roots and hypoglossal nerves were made in twenty-one patients with motor neuron diseases and 12 age-matched controls. To evaluate the correlation between the numbers of the myelinated fibers and the patterns of white matter degeneration in spinal cords, the latter were classified into three groups: group A with selectively demarcated degeneration of lateral and anterior corticospinal tracts, group B with diffuse degeneration of antero-lateral spinal columns and group C with no degeneration of the spinal white matter. Although the numbers of large myelinated fibers of the 5th lumbar ventral roots were decreased in all three groups, the numbers in group C were significantly better preserved than those in group A. Even in the hypoglossal nerve, the numbers of total and large myelinated fibers were decreased and in addition, the longer the duration of bulbar signs and the more severe the pathological changes found in the hypoglossal nuclei, the fewer the number of myelinated fibers. Especially group A showed a significantly more severe decrease in the numbers of total and large myelinated fibers of the 5th lumbar ventral roots and hypoglossal nerves than group C. These findings suggest that the degeneration of the upper motor neuron accelerates that of the lower motor neuron system in motor neuron diseases.