[Role of the cervical sympathetic ganglia on neurogenic control and autoregulation of basilar arterial flow (authors transl)].
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Biomedical subjects
Publications and source records attributed to T Shima.
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Severe epistaxis following head injury occur from damage to the anterior ethmoidal or sphenopalatine arteries. However, the more massive, life-threatening posttraumatic epistaxis is that arising from ruptured aneurysm, arteriovenous fistula, or tear of the intracranial extradural portion of the internal carotid artery. The authors had opportunities to treat successfully 3 cases of massive delayed epistaxis from the aneurysm of this site following closed head injury. Case 1. A 23-year-old man was injured in a motorcycle accident on April 19, 1968 and taken to an emergency hospital, where the findings were semicomatose state, profuse bleeding from the left nostril and oral cavity, and laceration above the left eye associated with fracture of the left sphenoid. Since regaining consciousness he was blind in the left. Slight localized protrusion of the cavernous portion of the left internal carotid was shown by angiography, which was performed on the next day (Fig. 1). Three days later, he was transfered to Toyokogyo Hospital. On April 29, he had sudden severe epistaxis. The nasal bleeding recurred massively 6 times over 2 months, requiring the replacement of more than 8000 cc of blood. Sixty days after the trauma, carotid angiography demonstrated an large aneurysm arising from the left internal carotid (Fig. 2). The authors were consulted on this occasion. Intra- and extracranial trapping of the internal carotid artery associated with muscle embolization (Jaeger's operation) was performed (Fig. 3). Postoperative course was uneventful except occurrence of temporary diabetes insipidus. Case 2. This 59-year-old man was admitted to our clinic on November 7, 1970, Because of posttraumatic recurrent massive epistaxis. Thirty-seven days before admisstion, he was hitted by a car and lost consciousness. Profuse nasal bleeding occurred immediately after the accident. Despite skin lacereation above the right eye, visual acuity was not distrubed and no fracture line was found. Two weeks after the injury, he had sudden massive bleeding from the right nostril. The epistaxis recurred 5 times over 3 weeks. Carotid angiography revealed an aneurysm arising from the right internal carotid (Fig. 4). The internal carotid was gradually occluded at the cervical level without any neurological complication. Case 3. A 33-year-old man was referred to our department on October 7, 1974, complaining of recurrent profuse bleeding from the oral cavity. About 2 months prior to admission, he fell from the fourth floor on the street and became comatose. Several fracture lines of the frontal bones were found on skull film. Thirty-six days after the accident, sudden severe epistaxis occurred. Massive bleeding from the oral cavity repeated every 7 to 10 days. Visual acuity was lost within 10 weeks. III and VI cranial nerves palsy was found on the both sides. Carotid angiography demonstrated a small aneurysm of the left internal carotid (Fig. 5). Occlusion of the internal carotid at the cervical level stopped bleeding without further neurological deficit...
Recent advances in microneurosurgery have markedly improved the result of surgical treatment of aneurysm and arteriovenous malformation in the posterior cranial fossa. However, more precise study on hemodynamics of the vertebro-basilar system may be necessary for further progress in treatment of the vascular lesions. From this point of view, the authors studied the basilar arterial flow of the dog by means of an electromagnetic flow-meter and the flow probe which was specially devised by the authors. (1) The ratio of absolute value of the mean basilar flow to the total brain weight was calculated, and the flow rate was expressed in ml/100 g brain/min. Mean value was 7.1 ml/100 g brain/min under normocapnea. (2) The effect of occlusion of the common carotid, of the external carotid, of the intracranial internal carotid, and of the extracranial internal carotid on the basilar flow was less remarkable in this order. (3) Under normocapnea, occlusion of the unilateral common carotid artery produced 115% increase in the basilar arterial flow. Bilateral common carotid occlusion resulted in 312% increase of the flow, demonstrating a remarkable ability of compensation of the basilar artery through the circle of Willis and leptomeningeal anastomoses. Under hypercapnea, unilateral common carotid occlusion was followed by 81% increase in the basillar flow. Occlusion of both common carotids caused 230% increase in the basilar flow. Percent increase in the basilar flow after unilateral or bilateral common carotid occlusion under normocapnea was significantly larger than under hypercapnea (p less than 0.05 and p less than 0.01 respectively). It may be supposed that under normacapnea the increased basilar flow following bilateral common carotid occlusion may compensate the decrease in total cerebral blood flow due to carotid occlusion. However, the compensatory rise in the basilar flow under hypercapnea may be not enough to supply the dilated vascular bed in the carotid and basilar territories. There might be even a risk of deficiency of blood supply in the territory of the basilar artery, if the vascular resistance in the carotid area could become less than that in the basilar. The significance of CO2 inhalation therapy for ischemic cerebral lesion was discussed. (4) After the both common carotid arteries were occluded, the basilar aretry was clamped temporarily. Following release of basilar occlusion, reactive hyperemia was observed in the basilar flow. Magnitude and duration of the reactive hyperemia increased progressively depending on duration of the basilar occlusion to some extent. The phenomenon may be best explained by a progressive accumulation of vasodilating metabolities in the ischemic area. (5) Unilateral vertebral occlusion caused 37% decrease in the basilar flow. Bilateral vertebral occlusion resulted in reverse of the basilar flow, averaging 61% of the original value in flow rate. (6) Occlusion of the unilateral subclavian artery produced "subclavian steal phenomenon"...
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Colloid cyst is a relatively rare benign tumor which is usually found in the third ventricle. A patient who had a "colloid cyst" in his right lateral ventricle was experienced. A 33-year-old man had suffered from intermittent attacks of headache and vomiting for five months. On July 22, 1974, he was hospitalized to our clinic because of headache, memory and gait disturbance. At the time of admission his consciousness was clear but he had slight memory disturbance and urinary incontinence. Incipient papilledma was noted and the deep tendon reflexes of the lower extrimities were slightly accentuated. Lumbar puncture revealed a clear CSF and its pressure was within normal limit and the protein was 59 mg/dl. The plain skull films showed no abnormal findings. EEG showed an asymmetry of alpha-wave, and paroxysmal high voltage of slow wave was found in the right frontal area. Right cerebral angiography demonstrated an unrolling of the pericallosal arteries suggesting dilatation of the lateral ventricles. On the 9th hospital day, he suddenly began to complain of severe headache and became drowsy. Mannitol and hydrocortisone were injected intravenously without producing any remarkable effects. A ventricular drainage was done, and the patient recovered rapidly. A conray ventriculography revealed a round filling defect in the right lateral ventricle. A transventricular approach through a short linear incision in the right frontal cortex was preformed on the 25th hospital day. A cyst containing colloid substance, about 5x4 cm in size, was found to be attached to the medial wall of the right lateral ventricle anterior to the foramen of Monro. This cyst was almost completely removed. Histological findings revealed inner lining of epithelial cells, He died on the 25th postoperative day from bacterial meningitis. Autopsy confirmed the cyst to have originated from the right lateral ventricle. A review of the literature was made and the pathogenesis and diagnosis of this disease and the mechanism of development of the symptoms were discussed.
The depigmented lesion in a case of piebaldism (partial albinism) was examined by electron microscopy. In the epidermis melanocytes were absent and the number of Langerhans cells was increased. In addition several mast cells were found in the epidermis.
Neuromuscular blocking properties of ribostamycin (1 gm), dibecacin (100 mg) and tobramycin (60 mg) were studied in a man during anesthesia and surgery by observing the effects of these antibiotics on muscle twitch tension. These drugs alone did not show any neuromuscular blocking action in those therapeutic doses. However, during the recovery phase of d-tubocurarine block the intravenous administration of 1 gm of ribostamycin caused a fairly rapid decrease in twitch tension. Tobramycin 60 mg did not show any remarkable effect, but dibecacin 100 mg produced a slight potentiating effect on the action of d-tubocurarine. The enhancement of the action of d-tubocurarine was antagonized promptly by edrophonium and more slowly by calcium.
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A case of giant aneurysm arising from the anterior communicating artery, 24 X 28 X 30 mm in diameter was found in a 30 year old man. About ten years ago he became blind and recently developed right anosmia and diencephalic seizures. No subarachnoid hemorrhage, however, was found. Radiograms and tomograms of the cranium showed a ring-like calcification, but by angiography it couldn't be recognized as a giant aneurysm. The right frontal craniotomy and partial resection, therefore, was performed. A histological study of the resected material revealed that it was a spontaneously thrombosed giant aneurysm. The inner layer of its wall had neither endothelium nor elastic lamina, but had deposits of calcium salt. The outer layer was composed of collagen fibers without cell infiltration. The aneurysm was thrombosed except for its neck but its organization occurred incompletely. We want to emphasize the importance of a correct preoperative diagnosis, as an erroneous operative procedure can result in disaster. Volume, viscosity and tension of flowing blood into the aneurysm as well as the size of its neck and dome regulate dynamic properties. These properties may determine the enlargement rate or growth of the aneurysm. The dynamic characteristics and features of the inner surface of the aneurysmal wall may regulate the formation of thrombosis in the aneurysm. The intraluminal thrombosis and strength of aneurysmal wall, for example, calcium deposits, may prohibit aneurysm from its rupture.
Electric thrombosis may be one of useful method to provide protection against re-bleeding from the intracranial aneurysm which cannot be obliterated by clipping or ligation of its neck without disturbing arterial circulation. However, a better method is required to make the aneurysm to be almost completely thrombosed within one or two hours and to avoide marked damage of its wall, dislodging of the formed thrombus and excessive thrombosis. In this report a method of electric thrombosis of the experimental aneurysm was studied, and effects of hematocrit value and alteration in intraaneurysmal hemodynamics on thrombus formation and progression of thrombosis were investigated. An aneurysm-like vein pouch of 6 to 9 mm in diameter and of 5 to 8 mm in height was made on the common carotid artery of the dog. One week later, patency of the "aneurysm" was confirmed on angiogram. An anodal electrode of a platinum needle of 0.2 mm in diameter was inserted into the "aneurysm" to place the tip of the needle approximately at the center of the sack. Two platinum plates of 3 mm in diameter and of 0.1 mm in thickness were used as the cathodes and were placed externnally on the aneurysm wall. Direct current of 3 mA was applied for 5 or 10 minutes, or current of 5 mA for 5 minutes. Intraaneurysmal pulsating jet and turbulent flows were reduced by occlusion or stenosis of the common carotid. Size of the thrombus immediately after passing current and further progress of thrombosis were evaluated on angiogram and also on plethysmogram of the "aneurysm". Hematocrit value of 45% or more was favorable in producing a thrombus. Although direct current of 3 or 5 mA was desirable to avoid injury of the "aneurysm" wall and to inhibit dislodging of the formed thrombus, only a small thrombus was produced around the anode. Simultaneous occlusion or stenosis of the carotid artery proximally to the "aneurysm" during application of the current markedly promoted thrombus formation. With current application for 5 minutes, 30 to 40% or more of "aneurysm" lumen was occupied by the thrombus in a half of the cases. When the thrombus had reached to approximately 40% of aneurysm "sack" 5 minutes after passing DC current, it progressed to 80% within the following one hour. The most favorable site of the anode for progression of thrombosis was the proximal wall (cardiac side) of "aneurysm". Proximal occlusion or stenosis of the carotid artery promoted remarkably also progress of thrombosis. Excessive thrombosis, dislodging or spontaneous resolution of the formed thrombus was not found throughout one month follow-up. Histologically, the thrombus was organized within one month and covered with the endothel extending from the parent artery.
This is a case report involving a 9 year old girl with a teratoma that infaced mainly the bilateral hypothalamus. The girl was observed for 14 months after partial surgical removal. During that time she showed aphagia, adipsia, hypopituitarism, and visual and psychiatric disturbances. Severe hypernatremia also was present, even though large amounts of 5% glucose solution without salt were given I.V. Food and water were given by nasal gastric gavage and later gavage via gastric fistula, but the hypernatremia remained unchanged. When pitressin or spironolacton (anti-aldosterone) were administered, remarkable effect on the hypernatremia couldn't be found. Upon autopsy it was discovered that the bilateral hypothalamus, left subthalamus and ventral part of the thalamus were invaded by teratoma. Comparing many similar clinical reports and manifestations of hypothalamic lesions in experimental animals, it is reasonable to assume that the mechanisms of hypernatremia were caused by the disturbances of ADH secretion, thirst centre and osmoreceptor in the hypothalamus.
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