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Biomedical subjects

Mitsuru Doi

Publications and source records attributed to Mitsuru Doi.

4 recordsLinked to original sources

Anterior and posterior inferior cerebellar artery infarction with sudden deafness and vertigo.

We report a patient with anterior and posterior inferior cerebellar artery infarction, which manifested as profound deafness, transient vertigo, and minimal cerebellar signs. We suspect that ischaemia of the left internal auditory artery, which originates from the anterior inferior cerebellar artery, caused the deafness and transient vertigo. A small lesion in the middle cerebellar peduncle in the anterior inferior cerebellar artery territory and no lesion in the dentate nucleus in the posterior inferior cerebellar artery territory are thought to explain the minimal cerebellar signs despite the relatively large size of the infarction. Thus a relatively large infarction of the vertebral-basilar territory can manifest as sudden deafness with vertigo. Neuroimaging, including magnetic resonance imaging, is strongly recommended for patients with sudden deafness and vertigo to exclude infarction of the vertebral-basilar artery territory.

Acute Disease↗

Spontaneous haemophilus influenzae type B meningoventriculitis with intraventricular debris.

Here we report the first case of spontaneous occurrence of Haemophilus influenzae type B meningoventriculitis. A 47-year-old man suffered from fever and headache. He had neck stiffness, and his cerebrospinal fluid (CSF) was turbid and yellowish. Gram staining and latex agglutination test of his CSF indicated that Haemophilus influenzae type B was the causative organism. Cranial CT and MRI revealed right ventricular debris accumulation, periventricular hyperintense signal, and periventricular ependymal enhancement. He was treated with intravenous administration of antibiotics, and his clinical condition and MRI findings gradually improved. Six weeks after onset, he was discharged without sequelae.

Anti-Bacterial Agents↗

Brainstem infarction presenting with neurogenic stuttering.

We reported a sixty-year-old man who developed acquired stuttering after a brainstem infarction. Infarctions were detected in the midbrain and upper pons. Neurogenic stuttering of this patients indicated that the midbrain and upper pons could be lesion sites responsible for acquired stuttering. We speculated that the reticular network extending from the brainstem to the frontal cortices, and the periaqueductal gray matter could be closely related regions generating neurogenic stuttering.

Brain Stem Infarctions↗

Changes of intracranial pressure during head-down tilt in anesthetized and conscious rabbits.

Effects of head-down tilt on intracranial pressure were studied in anesthetized and conscious rabbits. Adult Japanese white rabbits of both sexes, weighing 2.5-3.5 kg, were used in the experiments. Experiment 1. Animals were anesthetized with pentobarbital, and ICP was monitored through a catheter inserted into the subarachnoid space. ICP elevated immediately after the onset of 45 degrees HDT and gradually reduced toward the baseline level in the next 8 hours. Experiment 2. Each rabbit was exposed to 45 degrees HDT for 24 hours and the ICP was measured through a catheter which had been implanted 7 days before. In the conscious rabbits, ICP increased about 4 mmHg after the onset of 45 degrees HDT, further increased gradually to the peak at 11 hours of HDT, and then started to return to the baseline. These results suggest that the time course of the change in ICP during HDT is considerably different between anesthetized and conscious rabbits.

Comparative Study↗