非交通性水頭症における水頭症性浮腫の発生機序に関する研究
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概要
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The hydrocephalic edema is defined as an increase of water content and volume in periventricular white matter. The pathophysiology of hydrocephalic edema was evaluated in experimental and clinical cases. The experiment revealed that dilatation of the olfactory ventricles and the hydrocephalic edema in the olfactory bulb occurring during the first week in the hydrocephalic cat. Hydrocephalic edema in the periventricular white matter developed three weeks or later, when intraventricular pressure became low. MR images following intraventricular injection of the EDTA-2Na-Mn salt (Mn) revealed that Mn diffusely migrated into the periventricular structures. The migration and absorption of Mn were confirmed by sequential changes of the longitudinal (T1) and transverse (T2) relaxation times in the periventricular white matter and basal ganglia. Mn-migration into periventricular structures was more rapid and remarkable in twenty first day-hydrocephalic cats than in seventh day-hydrocephalic cats. On the other hand, Mn collection was the most remarkable in the olfactory bulb in the acute and chronic stages. A dynamic change of the drainage system in noncommunicating hydrocephalus could be divided into three stages on the basis of the compensative drainage system into olfactory bulb and cerebral periventricular white matter. The hydrocephalic edema in an acute stage of the clinical noncommunicating hydrocephalus was confirmed in a white matter around lateral ventricles, which never extended into the rectal gyrus and olfactory bulb like as in cats. T1 and T2 values suggested an increse of water content, which returned to a normal range postoperatively, in clinical cases of acute hydrocephalus. On the other hand, chronic noncommunicating hydrocephalic cases did not have hydrocephalic edema in spite of a marked ventriculomegaly. Intraventricular pressure monitoring revealed an increase of the pressure beyond a normal range in some chronic cases which did not have an abnormal filignal in periventricular white matter. It is speculated that hydrocephalic edema easily occurs in clinical cases because the compensative olfactory CSF drainage system does not develop in clinical cases. On the basis of these findings, the mechanism on occurrence of hydrocephalic edema is not only CSF leakage but also compensative absorption into a white matter around lateral ventricles. However it is likely that secondary cerebrovascular disorder and cerebral metabolic disturbance operate to hydrocephalic edema in experimental and clinical cases because cerebral blood flow and metabolism show an decrease due to an elevation of intracranial pressure in acute stage of hydrocephalus.
- 神戸大学の論文