Biomedical subjects

K Muneda

Publications and source records attributed to K Muneda.

4 recordsLinked to original sources

PubMed2001

[True posterior communicating artery aneurysm].

We report a case of a true posterior communicating artery aneurysm. A 51-year-old male suffered a subarachnoid hemorrhage with severe headache and vomiting. A true posterior communicating artery aneurysm was recognized after repeated angiography on the seventh day. Right frontotemporal craniotomy was performed and the aneurysm was successfully clipped. The incidence of true posterior communicating artery aneurysms ranges from 0.1-2.8%, and 21 cases including our case have been reported in detail. There are no reported cases in which the aneurysm arises from the branching site of perforating arteries. In almost all cases the dome of the aneurysm projects inferiorly or posteriorly or laterally, so perforating arteries from the posterior communicating artery rarely interfere with dissection of the aneurysm or neck clipping. In a few cases, true posterior communicating artery aneurysms had been diagnosed as IC-PC aneurysms preoperatively, leading to intraoperative aneurysmal rupture or postoperative neurological deficit or death. In the cases of a fusiform aneurysm or an aneurysm of wide-based neck, there may be no other choice than trapping of the aneurysm. It is difficult to predict whether trapping causes postoperative ischemic complications.

Cerebral Angiography↗

PubMed1989

[A case of posttraumatic cerebral air embolism].

We report a case of cerebral air embolism that occurred after chest trauma. The diagnosis was confirmed by CT and skull roentgenogram which demonstrated air bubbles in intracranial arteries. It is well recognized that cerebral air embolism is caused by various diagnostic and therapeutic procedures, and trauma. But it may often be overlooked because it is diagnosed clinically and there are no characteristic symptoms nor signs. Although various ways of treatment have been reported, prevention and early diagnosis are the most important. It is very rare that air bubbles are detected in skull roentgenograms in cases of cerebral air embolism. Only three other cases have been reported. One of these cases reported by Westcott awakens our interest because the patient died within only several minutes after the onset and underwent cardiac massage before the roentgenogram was taken, in the same way as our case. We think some artificial force is necessary to push air into intracranial arteries to the extent that it is detected on a skull roentgenogram. Little has been reported on CT findings in cerebral air embolism. Roughly speaking, three kinds of abnormal findings have been reported. They are air, edema, and infarction. In only nine cases including ours, air bubbles were detected on CT. In those cases CT scans were performed soon after the onset, twelve hours at the latest. Abnormal findings were detected in either bilateral hemispheres or in the right hemisphere only. Almost all lesions are located in the territory of the cortical branches, but in one case bilateral, thalamic infarction was noted, which is thought to be caused by embolism of thalamoperforators.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

[A case of pseudohypoparathyroidism with intracerebral calcification].

Intracerebral calcifications, especially in the basal ganglia, are observed in many kinds of diseases. A 41-year-old man is reported, who suffered from an acute epidural hematoma and underwent surgery to remove the hematoma. We detected very extensive intracerebral calcification on CT. Laboratory findings revealed hypocalcemia and hyperphosphatemia. General physical examination revealed characteristics typical of pseudohypoparathyroidism. The patient was diagnosed as having pseudohypoparathyroidism type I by the Ellsworth-Howard test. Since the advent of CT, the incidence of basal ganglia calcification has increased. CT is 5 to 15 times more sensitive than skull radiography in the detection of intracerebral calcification. Although many pathological states can cause basal ganglia calcification, most of the calcifications which are recognized on CT scans are physiological. But in cases in which basal ganglia calcifications are recognized also on plain radiographs, various kinds of symptoms including ones of basal ganglia origin are often recognized, and calcifications often extend to regions other than basal ganglia, eg. cerebellum, thalamus, etc. Pseudohypoparathyroidism is a rare disease which presents hypocalcemia, some characteristic physical appearances, and dementia. It is important to decide whether further examinations are necessary or not, when basal ganglia calcification is recognized incidentally on CT scan.

Acute Disease↗

PubMed1987

[Two cases of percutaneous transluminal angioplasty (PTA) for the treatment of subclavian steal syndrome].

Recently percutaneous transluminal angioplasty (PTA) has been used to treat atherosclerotic lesion of the brachiocephalic arteries. We treated two patients with subclavian steal syndrome successfully by PTA. The first patient was a 52-year-old man complaining of vertigo and ischemic symptoms of the left arm. Blood pressure was 110/90 mmHg in the left arm and 140/92 mmHg in the right. On the angiogram, about 80% stenosis was found in the proximal portion of the left subclavian artery, and retrograde filling of the left vertebral artery was observed. At first, a carotid-subclavian bypass surgery was performed, but unfortunately failed because of obstruction of the artificial arterial graft. Then we performed PTA using Grüntzig balloon dilatation catheter. The dilatation was carried out successfully. Immediately after PTA, to-and-fro and antegrade flow of the vertebral artery was observed, and one month later it became normal flow. Neurological symptoms gradually disappeared within two months. The second patient was a 57-year-old man suffering from vertigo on effort and TIA. Blood pressure was 130/78 mmHg in the left arm, and 152/82 mmHg in the right. Angiogram showed more than 95% stenosis of the left subclavian artery, and retrograde filling of the left vertebral artery. We also observed bilateral severe stenosis of the MCA. Carotid-subclavian bypass was dangerous because of the low perfusion of the ipsilateral MCA area. PTA was performed as the first choice, and the dilatation of the stenosis was sufficient. In two months natural antegrade filling of the left vertebral artery was obtained. We followed these patients for 12 months and no restenosis was observed neurologically and radiologically. We performed PTA with the Grüntzig balloon catheter using the Seldinger's method through the right femoral artery. Diameter of the balloon was 6 mm and its length was 4 cm. After setting the balloon to the stenotic lesion, we inflated the balloon with 5atm (75 psi) pressure for 30 minutes. Monitoring the blood pressure and arterial pressure wave at the tip of the catheter, we repeated inflation of the balloon 4 times. We used continuous venous infusion of low molecular dextran and heparin during PTA procedures. No complication occurred and neurological symptoms disappeared gradually. PTA is a safe and effective method, so it should be the first choice in the treatment of subclavian steal syndrome caused by severe stenosis of the subclavian artery.

Angiography↗