Sphenoidal electrode insertion using topical anesthesia.

C W Bazil; T S Walczak

doi:10.1111/j.1528-1157.1996.tb00520.x

Home/Archive/PubMed

PubMed · 8603614

Sphenoidal electrode insertion using topical anesthesia.

C W Bazil·T S Walczak

View original source ↗Export metadata ↓

Abstract

Sphenoidal electrodes are frequently used in epilepsy centers, but ins ertion can be painful. We used a topical anesthetic cream on patients (2.5% lodocaine, 2.5% prilocaine) before inserting electrodes and had patients rate their discomfort on an analogue pain scale. As a comparison, the same patients rated the pain caused by inserting a heparin lock. There was no significant difference between the pain of sphenoidal electrode insertion with use of topical anesthesia and that of heparin lock insertion. We suggest that when a topical anesthetic is used, the discomfort of inserting sphenoidal electrodes is minimal and comparable to that of inserting a heparin lock.

Explore related subjects

Administration, Cutaneous Adult Aged Anesthetics Catheterization, Peripheral Catheters, Indwelling Electrodes, Implanted Female Heparin Humans Lidocaine Male Middle Aged Pain Measurement Prilocaine Sphenoid Bone Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

C W Bazil, T S Walczak. 1996. Sphenoidal electrode insertion using topical anesthesia.. https://doi.org/10.1111/j.1528-1157.1996.tb00520.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1997

Responses of HDL subclasses, Lp(A-I) and Lp(A-I:A-II) levels and lipolytic enzyme activities to continuous oral estrogen-progestin and transdermal estrogen with cyclic progestin regimens in postmenopausal women.

Seventy postmenopausal women took part in the study. Subjects received either continuous oral 17 beta-estradiol 2 mg/day combined with norethisterone acetate 1 mg/day (E2/NETA, Kliogest) or transdermal treatment consisting of 28 day cycles with patches delivering 17 beta-estradiol 50 micrograms/day (Estraderm) combined with cyclic medroxyprogesterone acetate 10 mg/day (E2/MPA, Provera), on days 17-28. At baseline the serum lipid and lipoprotein concentrations, composition and concentrations of high density lipoprotein (HDL) subclasses, lipoprotein (Lp)(AI) and Lp(A-I:A-II) levels were comparable in the two groups. In the E2/NETA group, after 12 months hormone replacement therapy (HRT), the HDL2 cholesterol concentration decreased by 17% (P < 0.01) and the HDL3 cholesterol remained unchanged. The concentrations of HDL2b, HDL2a and HDL3a were reduced by 30, 26 and 15%, respectively, P < 0.001, and the cholesterol:triglyceride ratio decreased significantly in all HDL subclasses. Apolipoprotein (apo) A-I concentration decreased by 5% (P < 0.05), but apo A-II, Lp(A-I) and Lp(A-I:A-II) concentrations remained unchanged. In the E2/MPA group the HDL2 and HDL3 cholesterol levels were both reduced by 6% (P < 0.05) and the HDL3a, HDL3b and HDL3c concentrations decreased by 14, 12 and 17% during the E2/MPA phase compared with baseline (P < 0.01). No major changes in the composition of HDL subclasses occurred in the E2 MPA group during treatment. The apo A-I and Lp(A-I) levels were not changed, but apo A-II and Lp(A-I:A-II) concentrations decreased by 8 and 5%, P < 0.001 and P < 0.05, respectively. At 12 months the postheparin plasma hepatic lipase (HL) activity decreased only in the E2/NETA group (by 12%, P < 0.05). The cholesteryl ester transfer protein (CETP) activity was not affected by either HRT regimen. The results of our study show that the 2 HRT regimens have multiple effects on HDL particles and HRT induced changes in HDL are not associated with changes in activities of lipolytic enzymes or CETP.

Administration, Cutaneous↗

PubMed1997

Effects of hormone-replacement therapy on fibrinolysis in postmenopausal women.

BACKGROUND: Plasma levels of plasminogen-activator inhibitor type 1 (PAI-1), an essential inhibitor of fibrinolysis in humans, increase in women after menopause, and this may contribute to the risk of cardiovascular disease. We studied the effects of hormone-replacement therapy on PAI-1 levels. METHODS: In a randomized, crossover study, we investigated the effects of oral conjugated estrogen (0.625 mg per day) in 30 postmenopausal women and transdermal estradiol (0.1 mg per day) in 20 postmenopausal women, either alone or in combination with medroxyprogesterone acetate (2.5 mg daily) for one month, on plasma PAI-1 antigen levels. Degradation products of cross-linked fibrin (D-dimer) were measured in serum as an index of fibrinolysis. RESULTS: PAI-1 levels were inversely associated with D-dimer levels at base line (r= -0.540, P=0.002). Conjugated estrogen, both alone and in combination with medroxyprogesterone acetate, reduced mean (+/-SD) plasma levels of PAI-1 from 32+/-34 ng per milliliter to 14+/-10 ng per milliliter (P<0.001) and from 31+/-29 ng per milliliter to 15+/-11 ng per milliliter (P=0.003), respectively; there was a significant inverse correlation between pretreatment PAI-1 levels and the degree of reduction in these levels during therapy (r= -0.631, P<0.001 for conjugated estrogen; r = -0.507, P=0.004 for combined therapy). The degree of reduction in PAI-1 levels was associated with increases in D-dimer levels both when conjugated estrogen was given alone (r= -0.572, P=0.001) and when combined hormone therapy was given (r= -0.541, P=0.002). Transdermal estradiol caused no significant changes in PAI-1 levels from base-line values. CONCLUSIONS: Conjugated estrogen, alone or combined with progestin therapy, reduced PAI-1 levels by approximately 50 percent in postmenopausal women and was associated with enhanced systemic fibrinolysis. These findings may partly explain the protective effect of hormone-replacement therapy with respect to coronary artery disease.

Administration, Cutaneous↗

PubMed1997

Persistent inhibition of platelets during continuous nitroglycerin therapy despite hemodynamic tolerance.

BACKGROUND: Nitroglycerin has been shown to possess antiplatelet properties in both animals and humans. Tolerance to the hemodynamic effects of nitroglycerin develops with continuous therapy, but it is unclear whether there is tolerance to its antiplatelet effect. METHODS AND RESULTS: Tolerance to nitroglycerin was studied by exposing porcine aortic media to flowing arterial blood from control pigs (n = 9) or pigs treated with continuous nitroglycerin patches (Nitro-dur, 0.8 mg/h; n = 11) at a shear rate of 3397 s-1 for 3 minutes. Relative to baseline, mean arterial pressure fell by approximately 10% at 3 and 24 hours (P < .05) but returned to baseline at 48 hours of continuous nitroglycerin treatment, whereas no significant changes were observed in control animals. Autologous 51Cr-labeled platelet deposition (x 10(6)/cm2) on the aortic media at baseline and 3, 24, and 48 hours remained stable in control animals, with mean values of 94.8 +/- 5.9, 89.4 +/- 8.3, 89.3 +/- 8.8, and 84.3 +/- 5.7, respectively. However, in pigs treated continuously with nitroglycerin for 48 hours, platelet deposition was reduced significantly at 3 (65.9 +/- 4.8), 24 (63.8 +/- 6.4), and 48 hours (56.5 +/- 7.3) of nitroglycerin treatment compared with baseline (93.1 +/- 3.6). Platelet aggregation induced by thrombin also decreased at 3 (12.4 +/- 1.3), 24 (12.6 +/- 1.7), and 48 hours (10.8 +/- 1.6) of nitroglycerin treatment compared with baseline (16.3 +/- 1.4) but remained unchanged in the control group. Also, nitroglycerin treatment increased intraplatelet cGMP at 3, 24, and 48 hours compared with baseline. CONCLUSIONS: This study demonstrates the persistent inhibition of platelet function and platelet deposition on an injured arterial wall by continuous nitroglycerin therapy despite hemodynamic tolerance.

Administration, Cutaneous↗