[A case of left atrial myxoma associated with the pigmentation of the lips, palms and soles and the chordal rupture].
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Biomedical subjects
Publications and source records attributed to H Kanaya.
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We describe a patient with established systemic lupus erythematosus (SLE) in whom an intracerebral hemorrhage developed secondary to a ruptured aneurysm of the lenticulostriate artery (LSA). A 24-year-old woman with a four-year history of SLE was admitted to the department of internal medicine of Iwate Medical University for the treatment of lupus nephritis in 1985. She suddenly complained of severe headache and nausea, and soon lost consciousness. The computed tomographic scan revealed intracerebral hemorrhage in the left front-temporal region and subarachnoid hemorrhage. Left common carotid angiography demonstrated a 3 X 3 mm aneurysm of the LSA and displacement of other LSAs and anterior cerebral artery. The incidence of intracerebral hemorrhage in SLE was about ten percent in the reported central nervous system SLE, and it seemed that the prognosis of SLE with intracerebral hemorrhage was poor. The mechanisms of the intracerebral hemorrhage and the aneurysmal formation in SLE seemed to be due to lupus angiitis, but without clinical, radiologic and pathologic correlation. In operation, a ruptured aneurysm without neck was found in LSA and extirpated. In the pathological study, there was transmural angiitis, which fibrinoid necrosis, elastic tissue disruption and infiltration of inflammatory cells were found. Inflammatory cells were chiefly lymphohistiocytic with some polymorphonuclear leukocytes. It seemed that pathologic studies confirmed transmural angiitis with secondary aneurysm formation.
A 43-year-old female was admitted showing abnormal feeling in the left eye region. Left facial hypesthesia and quadrantic hemianopsia of left eye were the detectable neurological findings. A plain skull x-ray film revealed a double floor and dilatation of the sella turcica. The tomogram of the sella turcica demonstrated a dilatation of superior orbital fissure. Caudocranial projection revealed a dilatation of foramen ovale. A computerized tomography scan revealed a slightly high density tumor which was enhanced slightly with a contrast medium in the parasellar region and left middle fossa. Carotid angiogram demonstrated the displacement of the left carotid fork to the upper and lateral direction. However, no other sign was found. The sinogram of cavernous sinus clearly demonstrated an indentation in the left cavernous sinus. The endocrinological tests were almost normal except for hyperprolactinemia. A trigeminal neurinoma and a pituitary tumor were suspected. The tumor was totally removed and was histologically diagnosed as a cavernous angioma. At operation it seems to be extracerebral in the middle fossa and originate in the cavernous sinus. Diagnostic problems endocrine findings and the origin are discussed.
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We present a case of isolated fourth ventricle which developed after massive ventricular hemorrhage, due to a ruptured cerebral aneurysm. In an adult an isolated fourth ventricle seems to be very rare, also the symptom of unconsciousness and respiratory arrest and the rapid development in this case seemed very unusual. The aqueductal occlusion was considered to be related to the intraventricular hematoma which remained as clots over a 2-month-period of time. This case was a 57-year-old woman admitted to our hospital in a state of coma. CT showed a massive ventricular hematoma and right carotid angiogram showed an aneurysm of the anterior communicating artery. Bilateral ventricular drainage was performed because of progressive decerebrate rigidity. Since consciousness gradually arose to the Japan Coma Scale 3, clipping of the neck of the aneurysm was performed 25 days after onset. Premature rupture occurred during the operation. After surgery, CT Showed ring-like high densities due to the premature rupture of aneurysm in both lateral ventricles, and also in the fourth ventricle as well. Although the lateral ventricles drainage functioned effectively, the fourth ventricle showed remarkable gradual dilatation. The patient was stuporous, but respiratory arrest occurred suddenly 43 days after onset. Since it was considered that the intraventricular hematoma blocked the aqueduct, the same as in the outlet of the fourth ventricle and that the dilated fourth ventricle compressed the brain stem, the ventriculostomy was performed through suboccipital craniectomy. The cerebellar hemispheres showed remarkable swelling bilaterally, and no cerebrospinal fluid was found in the cisterna magna.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a patient suffering from persistent myoclonic jerks in the right forearm without any definite EEG abnormality under routine recording conditions. By computer summation, using the jerk-locked averaging technique, a sharp spike was recognized as a precisely time-locked event in relation to myoclonic twitches. A cranial CT scan revealed a small cortical lesion, which was found very close to the sensorimotor cortex of the right arm. Cerebral blood flow study using the xenon inhalation method revealed a discrete focus of high flow, which corresponded well with the CT lesion. On electrical stimulation of the right median nerve, a large somatosensory evoked potential and an enhanced transcortical long loop reflex were observed. Electrocorticogram showed active focal spike discharges localized at the left precentral gyrus. We postulate that an epileptogenic focus in the motor cortex and an enhanced transcortical long loop reflex appear to be important for the occurrence of epilepsia partialis continua in this patient.
A case of multiple meningiomas in the posterior fossa is reported. Computed tomography scans clearly demonstrated the tumors. They were removed completely and the patient was discharged without any neurological deficits. The clinical features are discussed and the pertinent literature is reviewed.
The inactivation of potassium (K) contractures induced by prolonged conditioning depolarization and repriming after 190 mM K+ contractures were studied at both room and low temperatures using frog single twitch muscle fibers. Effects of conditioning K+ depolarization and external Ca2+ reduction on the biphasic K contractures were also studied. When the conditioning depolarization with 15-30 mM K+ was prolonged, the peak tension of test 190 mM K+ contractures was inhibited in parallel with the shortening of plateau duration at both room and low temperatures. Such parallel changes were also observed during the early stage of repriming after 190 mM K+ contracture at both temperatures. On the other hand, the peak tension of the secondary component of the test 80 mM K+ contractures was rather potentiated by the conditioning depolarization, even though the time course of the component was markedly shortened. The foregoing changes were also illustrated in a diagramatic way. These results suggested that the peak tension and the time course of the test K contractures after conditioning depolarization and during repriming may be determined by a balance between the activation and the inactivation processes of the contractures. This view is supported by the results obtained under conditions in which the concentration of external Ca2+ was reduced. Furthermore, based on additional experimental results, it was suggested that the initial component is not accompanied by an inactivation process and that Ca uptake by sarcoplasmic reticulum may partially contribute to determining the spontaneous relaxation phase of the secondary component, at least at room temperature.
Fine structural changes in the sarcoplasmic reticulum (SR) in myocardial ischemia, induced by occlusion of the anterior descending branch of the left coronary artery in the canine heart, were studied by the freeze-fracture technique in situ and in vitro and compared to the alterations in Ca2+-stimulated ATPase activity and sodium dodecyl sulfate gel electrophoresis of the isolated SR. Both SR in situ and the isolated SR exhibited the typical intramembranous particles of 70-90 A in freeze-fracture replicas, and the numbers of particles were more numerous in the concave face (PF) than in the convex face (EF). The numbers of particles in the PF were 2748/micron 2 on the average. In ischemia for 1-2 hr, a significant decrease in the numbers of the particles was found in SR in situ, and corresponding changes were noted in the isolated SR. Decreases in Ca2+-stimulated ATPase activity and in the major protein band of ATPase were recognized simultaneously. The close correlation of the changing patterns between the reduction in Ca2+-ATPase and that in the intramembranous particle density during ischemia supports the suggestion that a large part of the intramembranous particles represents ATPase protein itself. The decrease in the particles of SR membrane indicates the degradation of ATPase in the process of ischemic myocardial necrosis.
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No detailed reports on pneumocephalus caused by any factors other than head trauma, and their courses accompanied with this disease have been so far available. We recently experienced a case of pneumocephalus complicated with severe clouding of consciousness, ocular deviation, and unilateral spatial neglect with the results being reported hereinafter. A 54-year-old man had often received ear douche therapy due to chronic sinusitis and tubal obstruction about 3 years before without any history of head trauma. On Jan. 6, 1984, sudden clouding of consciousness accompanying stiffness of the left arm occurred immediately after ear douche, and then he was transferred to our center. At admission, semicomatose, bilateral ocular deviation to the right, and left hemiparesis were observed. Plain skull X-ray films showed a retention of air in the frontal and temporal regions, while CT scan revealed air retention on the bilateral frontal region, bilateral temporal tip and suprasellar cistern. However, no abnormal findings were detected in the brain. Consciousness and hemiparesis recovered on the next day of hospitalization, however, the left hemispatial neglect still remained. This symptom was still observed on the 3rd day but disappeared by the 4th day of hospitalization. For clarifying its cause, cerebral angiography, CT scan and electroencephalography were then performed. CT scan revealed no anomalies in the brain, while cerebral angiography showed a cerebral circulation pattern in favor of the right internal carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)
There are 5 reported cases of meningioma complicated by chronic subdural hematoma so far as we reviewed. Considering frequency of occurrence, association of meningioma and chronic subdural hematoma is very rare. Recently, we experienced with a case of convexity menigioma complicated by chronic subdural hematoma. The patient was a 61-year-old woman who complained of headache and numbness of the left hand. She received hysteromyomectomy 28 years before but had no past history of trauma of the head. She suffered from frequent profound pain in both orbits for one year, and she consulted a neighboring practitioner due to occurrence of numbness of the left hand and malaise. Then, CT scan revealed abnormalities, so that she was referred to our center. On admission, neurological oxamination revealed no abnormalities but plain X-ray film of the skull showed a round destruction in the right parieral bone. CT scan showed a round high density area of 3 cm in diameter in the right parietal region, this is markedly enhanced with contrast media. There is a crescent-shaped low density area extending forward from the high density area. The body of the right lateral ventricle is totally collapsed. Selective arteriography of the right external carotid revealed tumor stain in the parietal region. Therefore, under the diagnosis of association of chronic subdural hematoma and convexity meningioma, craniotomy of the right frontal, parietal and temporal regions was carried out and a meningioma of 10 g, and a subdural hematoma with its capsule touching the maningioma were entirely extirpated.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the role of glucagon in the development of diabetes mellitus, spontaneously diabetic non-obese mice were studied before (group 1) and after the onset of diabetes mellitus (group 2). In group 1, fasting blood glucose and insulin in plasma and pancreas did not differ significantly, while plasma glucagon was elevated (48.9 +/- 10.4 versus control 18.6 +/- 6.0 pmol/l). In group 2, the insulin content of plasma and the pancreas were markedly reduced, whereas plasma glucagon was elevated (180.9 +/- 59.1 pmol/l). When diabetic mice were treated with insulin for 4 weeks (group 3), plasma glucagon was markedly reduced compared with that of group 2 (30.3 +/- 9.0 pmol/l). In group 1, glucagon and glucagon-like immunoreactivity of the intestine were reduced. The glucagon content of the intestine was elevated in group 2. Group 3 elicited increased contents of gastric glucagon as well as intestinal glucagon-like immunoreactivity. We conclude that, in addition to insulin deficiency, hypersecretion of glucagon might contribute to the development and clinical course of diabetes mellitus in the non-obese diabetic mouse.
When the concentration of external Ca2+ was reduced for 30 sec in a single twitch muscle fiber of a frog, the peak tension of the initial component of biphasic 80 mM K+ contractures was potentiated, whereas that of the secondary component was markedly inhibited, despite the fact that in the early stage it was potentiated usually in case of contractures in 60 and 40 nM K+ but rarely in 80 mM K+. These changes were not observed, however, in the presence of 0.5-1 nM Mn2+, i.e., Mn2+ having been substituted for Ca2+. The foregoing result and the authors' previously reported data indicated the following. First, the concentrations of divalent cations having an equal effect in bringing about the peak tensions of both components are 3 mM Mg2+, 0.7 mM Mn2+, 0.5 mM Ni2+, and 1.8 mM Ca2+. Secondly, this sequence constitutes their increasing order of effectiveness on the time course of the secondary component. Meanwhile, a similar order was found to exist in another experiment concerning the effectiveness in inhibiting the inactivation of K contractures facilitated by lowering the concentration of external Ca2+. All these findings indicated that the divalent cations act on the activation processes of both components in a stabilizing manner, differing from the way in which they act on the inactivation process of the secondary component. The mechanisms in which the peak tensions of the initial and secondary components are inhibited in a low Ca2+ solution and the divalent cations act on both components are discussed. Finally, another experiment made in the absence and presence of Ca2+ revealed that the effect of high concentrations of Mn2+ in the initial component is different from that on the secondary component.
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