Biomedical subjects
Publications and source records attributed to H Oki.
An 8-year-old girl experienced five repeated hemorrhagic episodes around the cerebellar vermis. Surgical specimens histologically showed abnormal vascular components invaded by tumor cells. Autopsy disclosed medulloblastoma disseminating in the subependymal zone of the ventricles. An atypical clinical course is reported with special attention to the cause of hemorrhage.
We have recorded movement-related cortical potentials (MRCPs) preceding voluntary finger extension in patients with Parkinson's disease and in patients with brain tumors that may involve the motor system. Three components of potential shifts preceding the voluntary movement were identified in all subjects. There were no differences between the healthy subjects and those with Parkinson's disease, or between pre- and postoperative recordings from the same parkinsonian patients in terms of onset latencies and gradients of these potential shifts. There was no evidence of MRCPs from the depth electroencephalogram recorded from the thalamic ventrolateral (VL) nucleus. After removal of the cerebellar dentate nucleus along with a tumor, MRCPs were still identified. After removal of tumors from the supplementary motor cortex and frontal association cortex, a part of the MRCPs preceding the voluntary movement was absent. The generation of MRCPs was considered not to be greatly affected by the cerebellar system because: (1) no MRCPs were detected from the thalamic VL nucleus, which is the relay nucleus of the dentato-rubro-thalamic pathway, believed to be related to voluntary movement; (2) destruction of the VL nucleus did not cause any changes in the MRCPs recorded at other sites, and (3) the MRCPs did not disappear when the dentate nucleus, an output system, was excised.
We report a case of Locked-in syndrome caused by thrombus in basilar artery resulting in a brainstem infarction in the ventral pons, magnetic resonance imaging (MRI) shows abnormal signal intensity regions in the ventral pons and basilar artery clearly.
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A 32-year-old female was admitted complaining of pain over the whole body and dysesthesia in all extremities. On admission, physical examination revealed hypertension, tachycardia, abdominal distension and urinary retention. Neurological examination revealed sensory impairment over the whole body and mild muscular weakness with absent deep tendon reflexes. Abdominal roentgenogram showed gaseous distension of the bowels. CT scans showed low density areas on the bilateral parieto-occipital lobes. CAG showed diffuse narrowing of the cerebral arteries. Laboratory examinations showed an albumino-cytologic dissociation (cells; 21/3mm, prot.; 78 mg/dl) of the cerebrospinal fluid and increased levels of norepinephrine (214 micrograms/day) and epinephrine (16.1 micrograms/day) in the urine. Motor nerve conduction velocities of the median nerves was 42.8 m/sec in the right and 50.0 m/sec in the left. The autonomic function tests revealed hyper-responsiveness to 10 mg of phentolamine and low baroreflex sensitivity. Within 2 months, most symptoms improved. Repeated CT scans showed no abnormality, while CAG showed only mild arterial narrowing. This case was diagnosed as having acute autonomic and sensory neuropathy which was a subtype of acute polyradiculoneuritis. Occult encephalitis or autonomic dysfunction was considered to contribute to the peculiar findings on CT and CAG.
A 58-year-old female was admitted to our hospital because of weakness of the right lower extremity and dysesthesia of the right upper extremity. From her clinical symptoms the patient was tentatively diagnosed as having a sort of cerebral infarction and treated with administration of urokinase and antiplatelet agents. However, angiographical examination revealed a unruptured aneurysm of the A1 portion of the left anterior cerebral artery. Preoperative angiogram showed that the dome of the aneurysm compressed one of the neighboring perforating artery which arose from adjacent to the neck of the aneurysm. The patient underwent neck clipping of aneurysm successfully. During the operation, the perforator was hardly adhered to the dome of the aneurysm. So, careful dissection was made only around the neck and the perforator was spared. Her symptoms were disappeared immediately after surgery. The perforator was demonstrated with better filling in the postoperative angiogram than that in the preoperative angiogram. The pathomechanisms of cerebral ischemia caused by unruptured aneurysm were reviewed on the literature. Most of the cases were caused by release of fragmental thrombi from a large aneurysm. There was a very exceptional case whose symptoms had seemed to be related to the direct compression of the neighboring perforator by the aneurysm. The compressed perforator in this case was seemed to be corresponded with the medial proximal striate artery stated by Yaşargil.
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Adult identical twins with Moyamoya disease are reported. Laboratory examinations such as blood types, AB, Rh(+), HLA (human leucocytic antigen) analysis [AW26(9), A26(10), BW62(15), BW61(40), CW3], and finger prints, and hairs confirmed that two patients were identical twins. Both had normal serum immunoglobulin levels and no anti-DNA antibodies. Patient No. 1, a 39-year-old female, was admitted to our service with chief complaints of nausea, vomiting and left hemiparesis with sudden onset on Oct 31, 1981. The patient had an episode of tetraplegia that occurred suddenly at 4 years of her age and lasted about a week. Motor weakness had completely disappeared but moderate mental retardation remained. She had been employed just prior to this attack. CT and angiographic examinations revealed ventricular hemorrhage with Moyamoya disease, which had miliary aneurysm in the branch of the right posterior choroidal artery. The operation of encephalomyosynangiosis was performed on her left hemisphere. The postoperative course was uneventful. Patient No. 2, the twin sister of patient No. 1, was in good health and mental state until 19 years of her age, when she suddenly lost consciousness and developed hemiparesis. After this attack, her motor function had recovered well. However, mental ability gradually deteriorated and she was admitted to a psychiatric ward. CT examination and angiographic studies were performed on Oct 12, 1982, and she was diagnosed as having Moyamoya disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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