Detection and monitoring of cerebral hemodynamic disturbances with transcranial color-coded duplex sonography in patients after head injury

Reduced cerebral blood flow after severe head injury results in an increased risk of ischemic brain damage. Blood flow should therefore be monitored with a simple, reliable method. Transcranial color-coded Doppler sonography (TCCS) is an accepted tool for the diagnosis of cerebral vasospasm; however, its usefulness in evaluating patients with head injury has not been proven. Cerebral blood-flow velocity in the middle, anterior, and posterior cerebral arteries was measured with a 2.5 MHz probe (Aplio SSA 770A, Toshiba, Japan) in 36 subjects with moderate or severe head injury. Serial measurements of resistance index (RI), peak-systolic, end-diastolic, and mean velocity in the middle cerebral arteries were performed 2–24 h after head trauma and in the subsequent days during hospitalization. Immediately after head trauma, increased RI values, and unusually decreased blood-flow velocity (mainly in MCA) were observed. Microcirculation disturbances were suspected because the end-diastolic velocity had substantially diminished. Changes in blood-flow parameters correlated with the clinical state, and in most cases, a poor prognosis. In some patients, blood-flow velocity increased above the normal reference limit and this implied poor prognosis. Transcranial color-coded Doppler sonography is a reliable, repeatable, and accessible tool that provides information about cerebral blood-flow disturbances and may hold diagnostic and prognostic importance.     

Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy

During 1982-86, 43/137 patients with cardiomyopathy, Classes II, III and IV, had ejection fractions (EF) below 40%, and a mean EF of 25.1 +/- 10.3%. During treatment of these 43 patients with coenzyme Q10 (CoQ10), EF increased to 41.6 +/- 14.3% (p less than 0.001) over a mean period of 3 months (range, 2-4 months). At four subsequent periods up to 36 months. EF ranged from 43.1 +/- 13.3 to 49.7 +/- 6.4% (each period, p less than 0.001). The mean CoQ10 control blood level was 0.85 +/- 0.26 micrograms/ml which increased on treatment to 1.7 to 2.3 micrograms/ml for five periods up to 36 months (each period, p less than 0.001). The survival rates for all 137 patients treated with CoQ10 and for the 43 patients with EF below 40% were both about 75%/46 months. These two survival rates were comparable between 24 and 46 months, which is of extraordinary significance and importance when compared to survival of about 25%/36 months for 182 patients with EF below 46% on conventional therapy without CoQ10. The improved cardiac function and pronounced increase of survival show that therapy with CoQ10 is remarkably beneficial due to correction of CoQ10 deficiency in mechanisms of bioenergetics.     

HIV transmission and retention in care among HIV‐exposed children enrolled in Malawi's prevention of mother‐to‐child transmission programme

Introduction : In Malawi, HIV‐infected pregnant and breastfeeding women are offered lifelong antiretroviral therapy (ART) regardless of CD4 count or clinical stage (Option B+). Their HIV‐exposed children are enrolled in the national prevention of mother‐to‐child transmission (PMTCT) programme, but many are lost to follow‐up. We estimated the cumulative incidence of vertical HIV transmission, taking loss to follow‐up into account. Methods : We abstracted data from HIV‐exposed children enrolled into care between September 2011 and June 2014 from patient records at 21 health facilities in central and southern Malawi. We used competing risk models to estimate the probability of loss to follow‐up, death, ART initiation and discharge, and used pooled logistic regression and inverse probability of censoring weighting to estimate the vertical HIV transmission risk. Results : A total of 11,285 children were included; 9285 (82%) were born to women who initiated ART during pregnancy. At age 30 months, an estimated 57.9% (95% CI 56.6–59.2) of children were lost to follow‐up, 0.8% (0.6–1.0) had died, 2.6% (2.3–3.0) initiated ART, 36.5% (35.2–37.9) were discharged HIV‐negative and 2.2% (1.5–2.8) continued follow‐up. We estimated that 5.3% (95% CI 4.7–5.9) of the children who enrolled were HIV‐infected by the age of 30 months, but only about half of these children (2.6%; 95% CI 2.3–2.9) were diagnosed. Conclusions : Confirmed mother‐to‐child transmission rates were low, but due to poor retention only about half of HIV‐infected children were diagnosed. Tracing of children lost to follow‐up and HIV testing in outpatient clinics should be scaled up to ensure that all HIV‐positive children have access to early ART.     

Accuracy of transcranial colour-coded sonography in the diagnosis of anterior cerebral artery vasospasm

Background and purposeTranscranial colour-coded sonography (TCCS) has been proven to be a method of high performance in the diagnosis of spasm of the middle cerebral artery (MCA). Relevant data concerning the anterior cerebral artery (ACA) varies amongst studies. The aim of this study was to assess the performance of TCCS in the diagnosis of spasm affecting the ACA.Material and methodsNinety-two patients (39 women and 53 men, age 51 ± 12.1 years) were examined using TCCS before cerebral angiography. Of 184 examined ACAs, only 133 arteries could be visualized due to insufficiency of the temporal acoustic window. Therefore, only 15 out of 25 arteries in which vasospasm was diagnosed with angiography (by two neuroradiologists not informed about the sonographic findings) could be included in the analysis. Receiver operating characteristic (ROC) curves were constructed for specific blood flow velocities: peak systolic (PSV), mean (M) and end-diastolic (EDV). The area under the ROC curve was used to measure the overall diagnostic performance of TCCS.ResultsThe area under the ROC curve for PSV was 0.83, which indicates good performance. The PSV threshold of 98 cm/s corresponded to maximum accuracy and was associated with 71% sensitivity vs. 88% specificity. Average systolic blood flow velocity in the vessels with vasospasm was 129 cm/s, whereas in unaffected vessels it was 76 cm/s.ConclusionsThe accuracy of TCCS in the diagnosis of ACA spasm is relatively high – the value of the area under the ROC amounts to 0.83. PSV performs best and the threshold of 98 cm/s is associated with an optimal trade-off between sensitivity and specificity.     

Atraumatic suction tip for microneurosurgery--clinical experience.

Our two-year experience with a new atraumatic tip for the neurosurgical suction tube is described. During microneurosurgical procedures the tip reduces injury to fragile vital brain structures and protects them from being aspirated into the suction tube. The perforated membrane of the appended suction tip does not impede evacuation of blood in any situation and can be easily cleaned off without demounting. The device can be immediately attached to the tube and disconnected. The neurosurgeon need not concentrate on its use, in contrast to those systems with active suction pressure control. The atraumatic suction tip is available in several sizes to fit different callibers of suction tubes.     

Effects of calcium channel modulators on the proliferation of mouse spleen lymphocytes in vitro.

The effects of nimodipine (voltage-dependent calcium channel blocker), CGP 28392 and BAY K 8644 (novel dihydropyridine derivatives that are considered as calcium entry stimulators) on the spontaneous proliferation of mouse spleen lymphocytes were studied in vitro. [3H]-thymidine incorporation into DNA of lymphocytes was used as an sensitive index of the cell proliferation. It has been found that nimodipine (10(-4) M-10(-6) M) significantly inhibited the [3H]-thymidine uptake in a dose dependent fashion with ED50 value of 2.4 x 10(-5) M. Unexpectedly, CGP 28392 (10(-4) M-10(-7) M) acts as a calcium entry blocker and produces a strong inhibitory effect on lymphocyte proliferation (ED50-2 x 10(-5) M). BAY K 8644 at a high concentration (10(-4) M) also has an inhibitory effect but at a lower concentration (10(-6) M-10(-10) M) significantly increased [3H]-thymidine uptake and abolished the inhibitory effect of nimodipine. This effect of nimodipine was also reversed by 5 x 10(-3) M calcium chloride. These findings indicate that calcium channel modulators can regulate the proliferation of mouse spleen lymphocytes in vitro.     

Effect of amantadine on prolactin secretion, pituitary DNA synthesis and 3H-spiperone binding in male estrogen-treated rats

Amantadine, a well-known antiviral agent, causing an increase in dopamine synthesis, release and the inhibition of re-uptake of noradrenaline and dopamine in central and peripheral catecholaminergic neurons, is successfully used in the treatment of Parkinson's disease. In the present paper, we have studied the effect of various doses of amantadine on in vivo prolactin secretion and the incorporation of 3H-thymidine and 3H-spiperone binding by the anterior pituitary gland of long-term diethylstilboestrol-treated male Wistar rats. Four weeks after a subcutaneous implantation of Silastic tubes containing 10 mg of diethylstilboestrol, a dramatic rise in serum prolactin levels was observed, accompanied by an increased uptake of 3H-thymidine by DNA anterior pituitary cells. Amantadine, given in the subcutaneous doses of 50, 5 and 0.5 mg/kg of body weight attenuated the stimulatory effect of stilboestrol on serum prolactin concentration in a dose-dependent fashion. On the other hand, the incorporation of 3H-thymidine into DNA pituitary cells in all the groups of amantadine-treated rats was only slightly suppressed. In an additional experiment, Scatchard analyses were performed on the in vitro 3H-spiperone binding kinetics in a dispersed anterior pituitary cell culture prepared from the pituitaries of 6-week diethylstilboestrol-treated rats. It has been found that amantadine injected in the dose of 5 mg/kg of body weight for 14 days induced a twofold decrease in the density of dopamine D2 binding sites (36.6 +/- 9.4 vs. 70.3 +/- 3.4 fmol/10(6) cells; p less than 0.02), while the apparent affinity of the receptors was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of cholinergic agonists and antagonists on interleukin-2-induced corticotropin-releasing hormone release from the mediobasal hypothalamus

In previous research we found that interleukin-2 (IL-2)-induced corticotropin-releasing hormone (CRH) release in vitro is mediated by cholinergic activation of nitric oxidergic (NOergic) neurons. The NOergic neurons release nitric oxide that stimulates CRH release. To further characterize the mechanism of IL-2-induced CRH release, the possible role of nicotinic as well as muscarinic receptors in IL-2-stimulated CRH release was evaluated. Medial hypothalamic (MH) explants from adult male rats were preincubated in Krebs-Ringer (KRB) buffer for 45 min followed by incubation for an additional 30 min in fresh KRB or KRB containing various compounds. As previously reported, acetylcholine (ACH) stimulated CRH release in a dose-related fashion. IL-2 (10(-13) M) stimulation of CRH release was unaffected by the lower concentration of ACH (10(-9) M), but surprisingly was inhibited by a 100-fold higher concentration. Atropine (ATR) (10(-7) M) blocked CRH release induced by ACH (10(-7) M) and the release of CRH induced by IL-2. The cholinergic agonist carbachol (CAR) (10(-7) M) also released CRH and this action was blocked by ATR (10(-7) M). CRH release in the presence of CAR was lowered below basal when the concentration of ATR was increased to 10(-6) M. In contrast to ACH, CAR had an additive effect to release CRH when combined with IL-2 (10(-13) M). Nicotine (10(-7) M) also stimulated CRH release and this stimulation was completely blocked by 10(-6) M but not by 10(-7) M of the nicotinic receptor blocker, hexamethonium (HEX). The lower concentration of HEX blocked the stimulatory effect of ACH (10(-7) M) and IL-2 on CRH release. Combined blockade with ATR plus HEX completely blocked the action of ACH and even reduced the CRH concentration to below basal values. Furthermore, combined blockade completely blocked the release of CRH induced by IL-2. We conclude that nicotinic as well as muscarinic receptors play an important role in CRH release, and that they both act to mediate IL-2-stimulated CRH release.