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OBJECTIVE To better understand the genital changes that occur during the female sexual response, using a gross anatomical and histological study of the vascular tissue of the vulva, supplemented with magnetic resonance imaging (MRI). MATERIALS AND METHODS Seven cadaveric vulvectomy specimens were used; they were serially sectioned in coronal, sagittal, and axial planes, and stained with haematoxylin and eosin. Selected blocks were stained with elastic Masson's trichrome. Axial MR images were taken of two healthy women with intact sexual functioning using a gadolinium‐based blood‐pool contrast agent. A 1.5 T system was used for all MRI studies, with images taken at baseline and during sexual arousal while viewing an erotic videotape. RESULTS There are five vascular compartments of the female external genitalia, found in the clitoris, clitoral bulbs, labia minora, urethra, and vestibule/vagina. Of these five compartments, two distinct types of vascular tissue were identified, i.e. erectile and non‐erectile/specialized genital. The erectile tissue compartments had the greatest change in blood volume during sexual arousal, as assessed by MRI. CONCLUSIONS The vulva contains a substantial amount of vascular tissue. These specialized tissues show a variable, but unified response to sexual arousal.

We evaluated 2,083 cases within the Wisconsin Stillbirth Service Program (WiSSP) that had autopsy reports or ultrasound data relevant to the heart. Of these, 167/1,782 (9.4%) stillbirths after 20 weeks and 11/301 (3.7%) miscarriages <20 weeks had congenital heart disease (CHD). Cases were classified by type of heart defect and whether it related to cause of death. Among cardiac anomalies that contributed significantly to fetal death, 125/151 (83%) were associated with underlying conditions or syndromes, nearly half of which were chromosomal. The most common forms of CHD in stillborns were severe cyanotic lesions (3%), then ventricular (2.6%) and atrial (1.9%) septal defects. Compared to livebirths, this represents a shift toward more severe cardiac lesions, although all comparable categories, including non-lethal conditions such as atrial septal defect, are more common in stillbirths. Clinical cardiomyopathy was identified as cause of death in 1.2% of stillborns. Cardiomegaly, occurring in 26.7% of all cases and 76.7% of infants born to diabetic mothers, may represent undiagnosed cardiomyopathy and/or may decrease fetal tolerance of hypoxia. In contrast, 78.5% of Turner syndrome infants, all <32 weeks, had small hearts. More attention to cardiac findings can lead to increased understanding of stillbirth causes. Based on our findings, we recommend chromosome studies on all stillbirths and close attention to the heart during second trimester ultrasounds, with chromosome studies offered if CHD is found. Consideration of heart size can result in prenatal identification of infants at risk for stillbirth, particularly large hearts in fetuses of diabetic mothers in the third trimester, which may identify fetal cardiomyopathy before it becomes life-threatening.

Stillbirth accounts for about 26,000 deaths annually in the US. In most previous studies, discrete causes are identified in less than half of all stillbirths. In order to identify causes and non-causal but potentially contributing abnormalities, we analyzed 416 of the most recent (2004-2010) Wisconsin Stillbirth Service Program (WiSSP) cases from a multifocal approach. In 70% of cases a cause sufficient to independently explain the demise was identified including 40% placental, 21.5% fetal, and 12.7% maternal. Results for stillbirths and second trimester miscarriages did not differ significantly. In 95% of cases at least one cause or non-causal abnormality was recognizable, and in two-thirds of cases, more than one cause or non-causal abnormality was identified. In cases with maternal cause, the placenta was virtually always abnormal. Both placentas (59%) and fetuses (38%) were frequently smaller than expected for gestational age. Previous miscarriage and/or stillbirth were risk factors for second and third trimester losses, with 35% of previous pregnancies ending in fetal demise. Recommendations include complete evaluation of all second and third trimester losses with special attention to placental pathology and thorough investigation for multiple causes or abnormalities whether or not a primary cause is initially recognized. Improved understanding of the causes of late miscarriage and stillbirth may contribute to recognition and management of pregnancies at risk and eventually to prevention of stillbirth.

Introduction The female genital sensory pathways that initiate sexual arousal reflexes begin with cutaneous corpuscular receptors in the glabrous genital skin, including those of the glans clitoris. Aim The aim of this study is to characterize the corpuscular receptors of the glans clitoris. In addition, we compared basic features with the receptors of the glans penis. Main Outcome Measure Number of stained receptors. Methods Five cadaveric vulvectomy specimens and four cadaveric penile specimens were used. They were serially sectioned and stained with hematoxylin and eosin. Selected blocks were stained with Masson's trichrome, and immunohistochemical staining was done with neuronal markers S-100 and neurofilament. Results Using the three stains, we identified an abundance of corpuscular receptors within the glans clitoris, as compared with the surrounding prepuce. These receptors were of varied arrangements, situated in the subepithelial tissues of the glans clitoris. They were indistinguishable from the receptors of the glans penis. The number of receptors per 100× high-powered field ranged from 1 to 14, whereas the receptor density in the glans penis ranged from 1 to 3. A second type of receptor, the Pacinian corpuscle, was identified within the suspensory ligament along the trunks of the dorsal nerve but not within the glans itself. Conclusions The glans clitoris is densely innervated with cutaneous corpuscular receptors, and these receptors are morphologically similar to the corpuscular receptors of the glans penis. The glans clitoris has greater variability in receptor density compared with the glans penis.