Is facial nerve decompression surgery effective?
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Biomedical subjects
Publications and source records attributed to M Toshima.
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A 66-day-old female with infant botulism is reported. She was admitted to our hospital with respiratory failure. Laboratory examinations detected botulinal toxin type A in her feces. This was the first case with no history of honey ingestion among the 13 cases of infant botulism reported in Japan. It is possible that other cases, in which honey had not been consumed, remain undiagnosed. Further studies may be needed to clarify the factors necessary to cause infant botulism.
It is hypothesized that blockade of the tympanic isthmus causes isolation of the attic and the adjacent middle ear spaces and that subsequent building up of the negative pressure in these spaces results in retraction of the pars flaccida, leading to formation of attic retraction pockets and cholesteatomas. To examine this theory, computerized tomographic (CT) findings of these conditions were evaluated in a series of 53 ears with retractions of the pars flaccida (attic retractions of Tos type II or deeper), including both retraction pockets and cholesteatomas. In 26 of 28 ears with attic retraction pockets, at least a portion of attic was aerated, and in 22 of these 26 ears, the mastoid antrum was also aerated. In contrast, in the 25 cases with attic cholesteatomas, these numbers decreased to 10 and 5, respectively, and the lack of aeration of the attic was demonstrated in 15 of 25 (60%) of the cases. In three cases of cholesteatoma, follow-up CT revealed either growth of a cholesteatoma from a retraction pocket or development of a small cholesteatoma into a large one. In these ears it was seen that the well-pneumatized attic and mastoid antrum seen in the initial CT was depleted by the growth of cholesteatoma that took place over a period of 4 months to 2 years. These results, showing good patency of the aditus and a pneumatized antrum in early stages of most cases of retraction pockets and cholesteatomas, are not in agreement with the hypothesis that the blockade of the tympanic isthmus is responsible for the pathogenesis of retraction pockets and cholesteatomas originating in the pars flaccida.
A case of aortic valve replacement after 16 years from the repair of ruptured sinus valsalva aneurysm (RSVA) was reported. The patient has undergone direct closure of RSVA with VSD type I at 34 years old. At the operation, no attempt was made as to aortic valve regurgitation because of small regurgitation, Selloers 1 on aortography. At 50 years old, he developed dyspnea on exertion, to-and-fro murmur due to aortic valve regurgitation, Selloers 3. Aortic valve replacement, we confirmed the completely closure of right coronary sinus valsalva, and histopathologically observed the degenerative change of only right coronary cusp.
U88999E, 7-[4,(4, 4'-difluorobenzhydryl)piperazino-1-methyl]-4- isopropyl-2-methoxy-2,4,6-cycloheptatrien-1-one hydrochloride, is a recently developed tropolone derivative that inhibits lipid peroxidation and also acts as a calcium antagonist. The effects of U88999E on basilar artery tone were examined in two model systems: 1) an in vitro preparation of arterial rings that measures isometric tension, and 2) an in vivo model of cerebral vasospasm measuring arterial diameter. U88999E elicited dose-dependent relaxation of preconstricted arterial rings maintained in vitro. Ring preparations were preconstricted using elevated potassium (40 mmol/L), uridine triphosphate (10(-3) mol/L), or endothelin-1 (10(-8) mol/L); U88999E reversed these constrictions across a concentration range of 10(-8) to 10(-5) mol/L. The potency of U88999E for relaxing preconstricted vessels was slightly less than that observed for flunarizine or diltiazem. A dose-dependent, relaxing effect of U88999E on potassium-induced contractions was observed in the presence of calcium concentrations ranging from 0.03 to 20 mmol/L. Vasospasm of basilar arteries after subarachnoid hemorrhage was inhibited in a dose-dependent and significant manner by intravenous injections of U88999E. Animals receiving intraperitoneal injections of U88999E also exhibited a tendency for reduced vasospasm; however, this effect did not achieve statistical significance. These findings suggest that U88999E may be useful in the prevention of cerebral vasospasm after subarachnoid hemorrhage.
A randomized, double-blind controlled trial is reported comparing phenobarbital and clonazepam for the purpose of sedative-hypnotic taper in inpatients with chronic, nonmalignant pain. After receiving the Minnesota Multiphasic Personality Inventory (MMPI) and a standardized psychiatric diagnostic interview, patients' baseline sedative-hypnotic use was assessed over 48 hours. Baseline use was converted into phenobarbital or clonazepam equivalents and administered in four doses daily using a blinded liquid pain cocktail. Baseline dose was maintained for two days and then tapered by 10% per day. Over the first week of taper, differences in mean and maximum Beck Anxiety and Benzodiazepine Withdrawal scores were not significant. However, when scales 1, 3, or 8 of the MMPI were taken as covariates, differences on the Withdrawal Scale only increased to a trend level for mean scores and to a significant level for maximum scores. These findings support the superiority of benzodiazepines over barbiturates for sedative-hypnotic taper for symptoms of withdrawal but not of recurrent or rebound anxiety.
A 41-year-old man suffered from traffic accident was referred to us because of chest and back pain. The CT examination showed periaortic hematoma and aortography revealed aneurysmal formation at the distal site to the left subclavian artery. We repaired the aortic injury with prosthetic graft at the acute phase successfully. As the results of the conservative treatment of the traumatic aortic injury are poor, we recommend operation at the acute phase.
A floating ball thrombus after mitral valve replacement is very rare. A 48-year-old female with a left atrial floating ball thrombus after mitral valve replacement is presented. She had headache and dizziness on the 16th post-operative day. Echocardiography revealed a floating ball thrombus in the left atrium. The ball thrombus was removed successfully on the 5th day after detecting that. The principle of the treatment of the floating ball thrombus is to remove that promptly after the diagnosis is established. But in the case of complicating with fresh cerebral or cerebellar infarction, the timing of the surgery is controversial.
We tested susceptibilities of 46 strains of clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) to arbekacin (ABK), tobramycin (TOB), ticarcillin (TIPC), clavulanic acid/ticarcillin (CVA/TIPC) and fosfomycin (FOM). Twelve strains had penicillinase activity. Most strains were resistant to TOB, TIPC, FOM and CVA/TIPC, but ABK inhibited 80% of the 46 MRSA strains at a concentration of 1.56 microgram/ml. The combination of ABK and FOM was indifferent. Synergism was observed, however, between FOM and TIPC against 79% of penicillinase non-producing MRSA. This synergism may mean that FOM inhibits the production of penicillin-binding protein 2' in some strains of penicillinase non-producing MRSA.
A fifty-five-year-old man revealed abnormal shadow on chest X-P. Congenital Bronchial Cyst (CBC) is believed to be caused by the abnormal budding process during the early development of the foregut and after born result in formation of noninfected cysts in the lung. In this case, CBC was lined by columnarciliated epithelium and contained cartilages and bronchial mucous glands in their wall. They were located along the tracheobronchial tree and cystgraphy presented dumbbell-like change of cysts that were seen during the development stage. These findings support the past reports radiographically that CBC may result from occlusion of the proximal side of bronchus during the early development by unknown mechanism.
We investigated the vasodilatory effect of intracisternal (i.c.) and intravenous (i.v.) administration of calcitonin gene-related peptide (CGRP) on arterial narrowing after experimental subarachnoid hemorrhage (SAH). Forty-one rabbits were divided into five groups: control (normal animals); SAH plus i.c. infusion of vehicle; SAH plus i.c. infusion of CGRP; SAH plus i.v. infusion of vehicle; SAH plus i.v. infusion of CGRP. In all but the control group, either CGRP (100 ng/kg/min) or vehicle solution was infused for two hours immediately prior to sacrifice by perfusion-fixation. A morphometric technique was employed to measure the luminal diameter of rabbit basilar arteries two days after SAH. The diameter of the basilar arteries in either the i.c. or i.v. CGRP groups was significantly greater than that of the respective vehicle group (i.c., p < 0.001; i.v., p < 0.01). Although there was no significant difference in systemic arterial blood pressure after infusion between the i.c. vehicle and i.c. CGRP groups, i.v. CGRP caused significant hypotension. Our results suggest that exogenous CGRP has some therapeutic potential for arterial narrowing after SAH not only by intrathecal application, but also by systemic use.
The effect of bilirubin on vasoreactivity was examined in the exposed rabbit basilar artery (diameter, 1045 +/- 17 microns; n = 18) and its cortical branches (diameter, 265 +/- 11 microns; n = 43) in vivo. Vasoconstriction induced by uridine triphosphate (UTP; 10(-5) to 10(-3) mol/L) was observed in vivo before and after a 60-minute application of supersaturated bilirubin (10(-4) mol/L). Bilirubin was dissolved in modified artificial cerebrospinal fluid (pH 7.4) or in physiological salt solution (pH 7.6). The latter was spectrophotometrically estimated to contain a higher concentration of free bilirubin because of the formation of less colloid. After treatment with bilirubin in artificial cerebrospinal fluid, the effect was minimal in the basilar arteries (n = 7), whereas the diameter of the branches was reduced by 9.6 +/- 1.5% (n = 23) and UTP-induced vasoconstriction was potentiated. After application of bilirubin in physiological salt solution, the basilar arteries contracted slightly (-2.1 +/- 0.9%; n = 6) and the UTP-induced vasoconstriction in the branches was attenuated (n = 12). After a 60-minute incubation of basilar artery with bilirubin in physiological salt solution in vitro, isometric tension recordings showed a diminution in KCl- and UTP-induced vasoconstrictions. Acetylcholine- and sodium nitroprusside-induced relaxations were also attenuated. It is suggested that bilirubin may exert different effects depending on the size of arteries and the concentration of free bilirubin. The constrictor and potentiating effects of bilirubin could be caused by the impairment of the relaxation mechanism. When the toxic effect of bilirubin becomes severe, the constrictor mechanism is also damaged.
The effect of hemoglobin on the vasodilatory effect of calcium antagonists was studied in isolated rabbit basilar arteries using an isometric tension measurement method. The ability of nimodipine to relax or inhibit contractions elicited by high K+ depolarization or serotonin (5-hydroxytryptamine, 5-HT) was investigated in control arterial rings and rings pretreated by hemoglobin. Hemoglobin (10(-6) and 10(-5) M) reduced the relaxation induced by nimodipine (10(-10) to 10(-8) M) in the rings contracted by 40 mM KCl. This reduction in relaxation was also observed with 3 x 10(-10) to 3 x 10(-9) M nicardipine, 3 x 10(-8) to 3 x 10(-7) M verapamil, and 10(-7) to 10(-6) M diltiazem. On the other hand, the effect of nimodipine was not influenced by endothelial removal or by pretreatment with 10(-5) M albumin or 10(-6) M prostaglandin F2 alpha. Hemoglobin restored the 10(-10) and 10(-9) M nimodipine-induced inhibition of the contraction elicited by CaCl2 (0.3 to 20 mM) in a K(+)-rich, Ca(++)-free solution. This restoration was greater at higher concentrations of CaCl2. Hemoglobin enhanced both the nimodipine-sensitive tonic phase and the less sensitive phasic phase of contractions produced by 10(-6) M of 5-HT. It abolished the inhibitory effect of 10(-8) and 10(-7) M nimodipine on the phasic contraction. Endothelial removal also enhanced both phases of the contraction, but did not abolish the effect of nimodipine. This study showed that the vasodilatory effect of calcium antagonists, especially nimodipine, on the vasoconstriction induced by other vasoactive substances decreased in the presence of hemoglobin.
To clarify specific mechanisms underlying cholesteatoma-induced bone destruction, surgical specimens of middle ear inflammatory granulation tissue with or without cholesteatoma were maintained in vitro and the bone-resorbing activity in their culture supernatants was analyzed by means of calcium release from mouse calvaria. Almost the same levels of bone-resorbing activity and prostaglandin (PG) E2 were found in the supernatants of both types of tissue. By contrast, aural polyp tissue yielded hardly any such activity or PGE2. Under the influence of indomethacin, however, only tissue with cholesteatoma produced considerable bone resorption activity, whereas PGE2 production was suppressed completely. Such activity in the cholesteatoma culture supernatant was not due to contamination of endotoxin and proved to be blocked by the introduction of anti-interleukin (IL)-1 alpha antibody into the calvarial assay system. Anti-IL-1 beta antibody had no effect on such activity. Interleukin-1 alpha was detected only in cholesteatoma tissue culture supernatants by means of enzyme-linked immunosorbent assay and by bioassay. These data suggest that the bone destruction in otitis media with cholesteatoma may be attributed to IL-1 alpha in addition to PGE2.
The sera from patients with various liver diseases were investigated for the antibody against calmodulin (CaM) extracted from bovine brain by the enzyme linked immunosorbent assay. The specificity and purity of CaM were confirmed by the Western blot technique using anti-CaM antibody (anti-CaM) positive sera. IgA class antibody was frequently detected in patients with hepatocellular carcinoma (HCC), autoimmune hepatitis (AIH) and chronic active hepatitis (CAH). On the other hand, IgG class antibody was very often present in patients liver cirrhosis, AIH and acute viral hepatitis (AVH). Sixty seven percent of patients with AVH in the acute phase were positive for IgM class anti-CaM and 33% of patients with AVH in the convalescent phase positive respectively. In AVH, the titer of anti-CaM reached its peak on 26.3 days after the onset. The titer of anti-CaM in fulminant hepatitis was higher than that in AVH. Seventy percent of type A hepatitis patients were positive for IgM class anti-CaM, 33% of type B and 33% of type non-A non-B. These results suggest that the frequency and titer of anti-CaM may depend upon the type of hepatitis and the degree of liver cell injury.
The number and distribution of valves were examined in 26 great saphenous veins. The number of valves per vein ranged from 3 to 11 with an average of 6.7. The valves tended to be concentrated in two segments; one within 10 cm from the sapheno-femoral junction, and the other between 35 cm and 45 cm from the sapheno-femoral junction. More than 55% of the valves were located in these two segments. This fact should be taken into account when obtaining vein segments in graft operations.
The relative position of the sapheno-femoral junction (SFJ) with respect to the origin of the arterial trunk from which the deep femoral artery arises was examined. Among 47 SFJ's, 9 (19%) were located at a proximal level to the arterial trunk, another 9 (19%) were located at an equal level to the trunk, and the remaining 29 (62%) were located at a distal level to the trunk. "In situ" saphenous vein graft for occlusion of the femoral artery is best indicated when the SFJ is located proximal to the arterial trunk. Our results suggested that such cases are encountered in as few as 19% of patients.