岡山医学会雑誌

The first case is 28 years old femal who admitted with porphyrin-uria and left sided visual disturbance which was occured suddenly with vomitting. The carotid cerebral angiography demonstrated the occulsion of left side int. carotid artery at the point of C₂ and the primitive trigeminal artery the same side.
The anastomosis to the anterior cerebral artery and the middle cerebral artery are made through this anomalous artery and Willis circle.
The second case is 20 years old female who admitted with Jacksonian type seizures and no neurological signs. The cerebral carotid angiography demonstrated the primitive trigeminal artery in right side.

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The author devised on pparatus for continuous monitoring of acid base balance of CSF without any CSF exposure to the atomosphere. The apparatus is an extracorporeal “ventriculo-cisternal circulation system” which is consisted of pressure pump, glass capillary electrode, Clark PO₂ electrode and Severinghaus Pco₂ electrode, all-lined up on a stainless steal conduit betweeen lateral ventricle and cisterna magna.
In the experimental cases of 5 dogs, the ventriculo-cisternal circulation system was used for monitoring acid base balanec of the CSF under acute intracranial hypertension produced by extradural balloon inflation. The blood Pco₂ was constantly watched during experiment to be kept in the normal range by means of a respirator. Pco₂ in the CSF began to increase in early stage above the pressure of CSF of 300 mmH₂O and incseased more and more in parallel with raised pressure. HCO₃^- in the CSF was decreased when acute and more severe intracranial hypertension was maintained for hours. Hypercapnic acidosis and metabolic acidosis occured in the CSF specifically when the intracranial pressure was raised acutely.
Clinically, acid base balance of the CSF was studied on acute intracranial hypertension of three patients who suffered from brain tumor. Intracranial pressure was monitored continuously by pressure gauge transducer connected to the ventricular drainage. In this clinical research, CSF, arterial blood and jugular blood were sampled for measurement. Pco₂ in the CSF was increased when the intracranial pressure was elevated above 500 mmH₂O and metabolic acidosis was added when the pressure was more elevated continued. That is to say, CSF became acidosis as same as experimental results. On the contrary, arterial blood became respiratory alkalosis when the intracranial pressure was elevated to 500-1000 mmH₂O. This phenomenon suggest that increse of hydrogenic ions induced by intracranial hypertension stimulates respiratory center.
Hypercapnic acidosis and metabolic acidosis occur specifically in the CSF independently from the change in the blood when the intracranial pressure rises. Namely, the acid base balance of the CSF can not evaluated from that of the blood.
The author adovocates this state is hidden acidosis.

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