Shifting of dural arteriovenous malformation from the cavernous sinus to the sigmoid sinus to the transverse sinus after transvenous embolization. A case of left spontaneous carotid-cavernous sinus fistula.

The angiographic features of left spontaneous carotid-cavernous sinus fistula and multiple dural arteriovenous malformations that developed after transvenous embolization are described. A dural arteriovenous malformation involving the left sigmoid sinus was demonstrated, along with a marked decrease in size of the left carotid-cavernous sinus fistula and the disappearance of venous drainage from the left cavernous to the right cavernous sinus after embolization with spring coils via the left superior ophthalmic vein. The dural arteriovenous malformation of the left sigmoid sinus subsequently extended to the transverse sinus after partial embolization of the sigmoid sinus. Finally, a dural arteriovenous malformation involving the left transverse sinus developed, with the disappearance of the arteriovenous malformation affecting the sigmoid sinus and left carotid-cavernous sinus fistula following complete embolization of the sigmoid sinus via the left transverse sinus.     

Peritumoral brain edema associated with meningioma--histological study of the tumor margin and surrounding brain.

Thirty-nine cases of intracranial meningiomas were analyzed to identify factors causing brain edema. Edema was significantly correlated with tumor size and the destruction of the leptomeninges and cortex. Meningotheliomatous meningioma tended to have more peritumoral edema. There was no correlation between the presence of edema and location of the tumor or histological features including lymphocytic infiltration and the presence of glial fibrillary acidic protein-positive cells in the tumor tissue. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of humoral edema-promoting factor or edema fluid into the white matter, resulting in vasogenic edema.     

Non-prostanoid thromboxane A2 receptor antagonists with a dibenzoxepin ring system. 2.

A series of 11-[2-(1-benzimidazolyl)ethylidene]-6,11-dihydrodibenz[b,e]oxep in-2- carboxylic acid derivatives and related compounds were synthesized and found to be potent TXA2/PGH2 receptor antagonists. Each compound synthesized was tested for its ability to displace [3H]U-46619 binding from guinea pig platelet TXA2/PGH2 receptors. Structure-activity relationship studies revealed that the following key elements were required for enhanced activities: (1) an (E)-2-(1-benzimidazolyl)ethylidene side chain in the 11-position of the dibenzoxepin ring system and (2) a carboxyl group in the 2-position of the dibenzoxepin ring system. The studies also indicated that the TXA2/PGH2 receptor binding affinities of this series of compounds in guinea pig platelet were poorly correlated with those in human platelet. Introduction of substituent(s) to the benzimidazole moiety was effective and sodium (E)-11-[2-(5,6-dimethyl-1-benzimidazolyl)ethylidene]- 6,11-dihydrodibenz[b,e]oxepin-2-carboxylate monohydrate (57) recorded the highest affinity for human platelet TXA2/PGH2 receptor with a K(i) value of 1.2 +/- 0.14 nM. It demonstrated potent inhibitory effects on U-46619-induced guinea pig platelet aggregation (in vitro and ex vivo) and human platelet aggregation (in vitro). Compound 57, now designated as KW-3635, is a novel, orally active, and specific TXA2/PGH2 receptor antagonist with neither TXA2/PGH2 receptor agonistic nor TXA2 synthase inhibitory effects. It is now under clinical evaluation.     

Surgical repair of discrete subaortic stenosis complicated with prosthetic valve endocarditis--a case report]

A 46-year-old man was referred to our hospital because of prosthetic valve regurgitation. Eight years previously he had undergone aortic valve replacement because of aortic regurgitation due to infective endocarditis. At reoperation, we found prosthetic valve endocarditis and discrete subaortic stenosis. The obstructing fibrous tissue was resected and the aortic valve was replaced. Because discrete subaortic stenosis is usually located just below the aortic valve, the aortic valve cusps are liable to become thickened by the jet through the discrete stenosis and thus are vulnerable to infective endocarditis. It is pointed out that care must be taken not to overlook discrete subaortic stenosis in the presence of other associated cardiac disorders.     

Effect of denopamine on residual left ventricular dysfunction after complete revascularization]

Denopamine (15 mg/day) was administered to 20 patients with residual left ventricular dysfunction after successful percutaneous transluminal coronary angioplasty (75% or more diameter stenosis). Echocardiography was performed before and 6 months after denopamine administration to analyze the left ventricular function. There were significant decreases in both end-diastolic and end-systolic dimensions from 58 +/- 8.3 to 54 +/- 8.4 mm (p = 0.001), and from 44 +/- 10.1 to 40 +/- 10.3 mm (p = 0.005)), respectively, while % fractional shortening remained nearly constant (from 25 +/- 8.3 to 27 +/- 9.6%). Thus, denopamine improved the left ventricular function by decreasing left ventricular size while maintaining wall contractility.     

Quadro-pulse stimulation is more effective than paired-pulse stimulation for plasticity induction of the human motor cortex

OBJECTIVE: Repetitive paired-pulse transcranial magnetic stimulation (TMS) at I-wave periodicity has been shown to induce a motor-evoked potential (MEP) facilitation. We hypothesized that a greater enhancement of motor cortical excitability is provoked by increasing the number of pulses per train beyond those by paired-pulse stimulation (PPS). METHODS: We explored motor cortical excitability changes induced by repetitive application of trains of four monophasic magnetic pulses (quadro-pulse stimulation: QPS) at 1.5-ms intervals, repeated every 5s over the motor cortex projecting to the hand muscles. The aftereffects of QPS were evaluated with MEPs to a single-pulse TMS, motor threshold (MT), and responses to brain-stem stimulation. These effects were compared to those after PPS. To evaluate the QPS safety, we also studied the spread of excitation and after discharge using surface electromyograms (EMGs) of hand and arm muscles. RESULTS: Sizes of MEPs from the hand muscle were enhanced for longer than 75min after QPS; they reverted to the baseline at 90min. Responses to brain-stem stimulation from the hand muscle and cortical MEPs from the forearm muscle were unchanged after QPS over the hand motor area. MT was unaffected by QPS. No spreads of excitation were detected after QPS. The appearance rate of after discharges during QPS was not different from that during sham stimulation. CONCLUSIONS: Results show that QPS can safely induce long-lasting, topographically specific enhancement of motor cortical excitability. SIGNIFICANCE: QPS is more effective than PPS for inducing motor cortical plasticity.     

Pulmonary hemodynamics and home oxygen therapy in patients with chronic respiratory failure]

The authors examined pulmonary hemodynamics with respect to underlying diseases, severity and type of chronic respiratory failure, and the incidence and effect of home oxygen therapy (HOT) in 155 patients with chronic lung diseases (old pulmonary tuberculosis (OTB) 45, chronic pulmonary emphysema (CPE) 54, chronic bronchitis (CBR) 42 and fibrosing lung disease (FLD) 14). They underwent right heart catheterization during a stable period, while breathing room air. The arterial PO2 ranged from 64.3 +/- 9.7 Torr (CBR) to 69.9 +/- 10.0 Torr (CPE), and the mean pulmonary arterial pressure ranged from 17.3 +/- 4.6 mmHg (CPE) to 20.6 +/- 5.4 mmHg (OTB). The incidence of pulmonary hypertension (PH, PA mean greater than or equal to 20 mmHg) was 53.3% in OTB, 40% in CBR, 35.7% in FLD, 23.8% in CPE, 69% in respiratory failure, 40% in quasi-respiratory failure, and 2.1% in non-respiratory failure. The percentage of patients who received HOT was 84.5% in respiratory failure and 54.1% in quasi-respiratory failure. Comparing Type I with Type II chronic respiratory failure, the incidence of PH was lower in the former than the latter (38.3% vs 80.6%), whereas HOT was applied to an equal percentage of patients (67.4%) in both groups. The effect of HOT was evaluated in 11 patients with chronic respiratory failure. The mean pulmonary arterial pressure was 22.7 +/- 4.7 mmHg before HOT, and decreased to 20.7 +/- 5.6 mmHg after 24.5 +/- 10.1 months of HOT. Although this difference was not significant statistically, this result suggests the desirable effect of HOT on pulmonary hemodynamics.