Stroke in Pregnancy and Post-partum – Latest Developments in Conduct and Management

Stroke in pregnancy and post-partum is a rare occurrence, yet with increasing incidence in the last decades. With a crude incidence rate of up to 30 per 100,000 pregnancies, high morbidity and mortality, research is needed to standardize prevention, diagnosis, treatment, and management of these cases. We present stroke particularities during pregnancy and puerperium and the current information from published articles regarding the latest developments in medical conduct. The mechanisms of stroke in pregnancy differ from those in the general population and are mostly in relation to the physiological changes during pregnancy. Stroke during pregnancy and post-partum is a rare but debilitating occurrence; with limited evidence and no clear guidelines, the treatment should be always individualized, and the risk-benefit ratio should always be considered

The Antenatal Detection of Fetal Limb Anomalies

The etiology of fetal limb abnormalities is very complex, involving different risk factors: chromosomal abnormalities, gene disorders, intrauterine factors, maternal diseases, or exposure to different risk factors. The prevalence of fetal limb anomalies is reported to be approximately 6 in 10,000 live births, and the impairments of the upper limbs seem to present a higher incidence in comparison to the inferior limbs, more often are affected unilaterally and on the right side in comparison to the left side, some being isolate or may associate other anomalies, as a part of an underlying syndrome. According to the current guidelines, the assessment of the fetal limbs should be performed in the late first and early second trimester. Three-dimensional ultrasound provides a better understanding of the fetal anomaly for the parents and helps a better counseling, and it is used to confirm the anomalies detected by the conventional ultrasound. In cases of treatable anomalies, a multidisciplinary approach involving an obstetrician, geneticist, neonatologist, pediatrician, and pediatric orthopedic surgeon is essential to improve the postnatal outcome. Ultrasound examination and genetic counseling for the parents has an important benefit since some conditions present a genetic inheritance, and the recurrence rate in further pregnancies is very high

Role-play regulates positive emotions and prosocial attitudes

Role play is one of the core creative processes in theatrical performance. Play leads to positive emotions in both children and adults. Role-play, a distinctive type of play is used in several types of therapeutic interventions to increase social competence as well as for other benefits. The highly individualized use of role-play in psychotherapy, drama therapy and psychodrama is effective but not generalizable. In the present study we developed a standardized controlled procedure to promote role-play in 38 participants, and we monitored its impact on affect, anxiety, prosocial attitudes, and salivary oxytocin dynamics. Compared to the control condition where participants participated as selves, role-play significantly increased perceived levels of positive affect and prosocial attitudes and decreased self-reported levels of anxiety. Basal salivary oxytocin levels predicted gains in positive affect following the role-play procedure. Our study points to standardized role-play as a mean to reduce anxiety, and to increase sociability and positive affect. Possible mechanisms of how role-play induces the observed changes in affect and attitudes are discussed

Pathophysiology of Placenta in Antiphospholipid Syndrome

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by clinical manifestations caused by arterial or venous thrombosis and pregnancy conditions such as recurrent miscarriage, fetal death, or premature birth in the presence of antiphospholipid antibodies. The obstetrical manifestations are strongly related to the placental alterations. The aim of this review is to summarize the latest data on pathophysiology of obstetrical APS, emphasizing the disturbance of the placentation process. Due to a lack of extravillous trophoblasts to properly reconstruct the spiral arteries, APS causes hypoxic or ischemic injury or high-speed blood flow that damages the placenta. This results in decreased or interrupted maternal blood flow to the placenta and a lack of nutrients for the fetus. Antiphospholipid antibodies can lower the proliferation and infiltration of the extravillous trophoblasts. The placental mal-perfusion causes the release of antiangiogenic substances such as soluble fms-like tyrosine kinase-1 and soluble endoglin. Placental growth factor and vascular endothelial growth factor (VEGF) may be sequestered by sFlt1 and blocked from binding to trophoblast and endothelial cell VEGF receptors, inhibiting their proangiogenic effects. Preeclampsia is the clinical result from a lack of angiogenic factors needed for endothelial vascular homeostasis due to an excess of sFlt1 in the maternal circulation

Endocardial Tip Cells in the Human Embryo – Facts and Hypotheses

<div><p>Experimental studies regarding coronary embryogenesis suggest that the endocardium is a source of endothelial cells for the myocardial networks. As this was not previously documented in human embryos, we aimed to study whether or not endothelial tip cells could be correlated with endocardial-dependent mechanisms of sprouting angiogenesis. Six human embryos (43–56 days) were obtained and processed in accordance with ethical regulations; immunohistochemistry was performed for CD105 (endoglin), CD31, CD34, α-smooth muscle actin, desmin and vimentin antibodies. Primitive main vessels were found deriving from both the <i>sinus venosus</i> and aorta, and were sought to be the primordia of the venous and arterial ends of cardiac microcirculation. Subepicardial vessels were found branching into the outer ventricular myocardium, with a pattern of recruiting α-SMA+/desmin+ vascular smooth muscle cells and pericytes. Endothelial sprouts were guided by CD31+/CD34+/CD105+/vimentin+ endothelial tip cells. Within the inner myocardium, we found endothelial networks rooted from endocardium, guided by filopodia-projecting CD31+/CD34+/CD105+/ vimentin+ endocardial tip cells. The myocardial microcirculatory bed in the atria was mostly originated from endocardium, as well. Nevertheless, endocardial tip cells were also found in cardiac cushions, but they were not related to cushion endothelial networks. A general anatomical pattern of cardiac microvascular embryogenesis was thus hypothesized; the arterial and venous ends being linked, respectively, to the aorta and <i>sinus venosus</i>. Further elongation of the vessels may be related to the epicardium and subepicardial stroma and the intramyocardial network, depending on either endothelial and endocardial filopodia-guided tip cells in ventricles, or mostly on endocardium, in atria.</p></div

Human embryonic heart (48 days), hematoxylin-eosin staining.

<p>Hematoxylin-eosin stained heart in a 48 days embryo. The aortic sinus (1) and cushions (2) are indicated. Primitive coronary arteries emerge (arrows) the coronary sinus and dichotomize within the outer myocardium (OM, inset).</p

Human embryonic heart (56 days), CD 34, desmin and α-SMA immune labeling.

<p>Immune labeling for CD34 (A, detail in B), desmin (C) and α-SMA (D) of the future posterior interventricular groove in a 56 days human embryonic heart, oblique-sagittal cut. Endothelial sprouts guided by tip cells (arrow, A and B) invade the outer myocardium. The subepicardial vessels are embedded in a myoid stroma, α-SMA- and desmin-positive (arrowhead in C and D). Myoid cells (arrows in C and D) contact the endothelial sprouts within the outer myocardium.</p

Human embryonic heart (56 days), CD 34 immune labeling.

<p>Immune labeling with CD34 antibodies of a 56 days human embryonic heart, oblique-sagittal cut. General view (A) with detailed area in (B), indicated by the black connector. The CD34 positive endocardial cells cover the ventricular cavity (*). Endocardial tip cells (white arrows) are identified projecting filopodia within the myocardium. The endocardially-derived endothelial networks advance towards the epicardially-derived endothelial networks. ac: <i>apex cordis</i>; P:pericardium.</p

Human embryonic heart (43 days), CD 34, vimentin, CD105, desmin and CD31 immune labeling.

<p>Immune labeling with CD34 (A) and vimentin (B) antibodies of a 43 days human embryonic heart, oblique-sagittal cut at ventricle level. Corresponding epicardial vascular canals are indicated (white arrrows and white arrowheads). The walls of these canals seem to acquire a CD34-positive phenotype and are vimentin-positive. In (A) an active intramyocardial process of sprouting angiogenesis is detailed (inset), being guided by tip cells (double-headed arrows). CD105 immunolabeling of the ventricular wall (C) identifies filopodia-guided processes (arrows) of endocardial sprouting. Desmin-positive reactions were exclusively found (D) in the dorsal wall of the venous sinus (arrows) and in the atrioventricular ring (arrowheads) (VS: venous sinus; RA: right atrium; RV: right ventricle; avc: atrioventricular cushion). CD31-positive endocardial (arrows) and vascular (arrowhead) endothelia were identified. α-SMA intense labeling of the venous sinus (VS) myocardium (arrow) but not of subepicardium (arrowhead).</p

Human embryonic heart (56 days), CD105 (A, B) and vimentin (C, D) immune labeling.

<p>Intramyocardial endothelial networks result from processes of sprouting angiogenesis (arrows) of the underlying CD105-positive and vimentin-positive endocardium. The connector indicates corresponding areas of the left atrium (LA) wall.</p