Development of Hydrosalpinx After Prior Vaginal Hysterectomy and Bilateral Salpingectomy.

Hydrosalpinx is defined as the obstruction and fluid distension of the fallopian tube. It is most often seen in the setting of pelvic inflammatory disease, but preserved fallopian tubes or tubal segments after hysterectomy can also develop hydrosalpinx. This case report highlights an instance of painful hydrosalpinx after vaginal hysterectomy and advocates for the complete removal of fallopian tubes as the standard of care at the time of hysterectomy of any route. In this case, a 40-year-old female, G4P3104, with a history of vaginal hysterectomy and prophylactic bilateral salpingectomy for abnormal uterine bleeding and symptomatic uterine leiomyoma two years prior, presented with one month of left lower quadrant pain. She was found to have an anechoic, tubular structure adjacent to the left ovary on transvaginal ultrasound. At the time of diagnostic laparoscopy, a 10x4 centimeter (cm) dilated hydrosalpinx was found and removed. Pathology confirmed the hydrosalpinx, and the patient's pain resolved after the surgery. Given our findings of painful hydrosalpinx following incomplete bilateral salpingectomy at the time of vaginal hysterectomy, attempts at the removal of the entire fallopian tube including the fimbriae are strongly recommended to prevent the morbidity of repeated surgery.

New viral-genetic mapping uncovers an enrichment of corticotropin-releasing hormone-expressing neuronal inputs to the nucleus accumbens from stress-related brain regions.

Corticotropin-releasing hormone (CRH) is an essential, evolutionarily-conserved stress neuropeptide. In addition to hypothalamus, CRH is expressed in brain regions including amygdala and hippocampus where it plays crucial roles in modulating the function of circuits underlying emotion and cognition. CRH+ fibers are found in nucleus accumbens (NAc), where CRH modulates reward/motivation behaviors. CRH actions in NAc may vary by the individual's stress history, suggesting roles for CRH in neuroplasticity and adaptation of the reward circuitry. However, the origin and extent of CRH+ inputs to NAc are incompletely understood. We employed viral genetic approaches to map both global and CRH+ projection sources to NAc in mice. We injected into NAc variants of a new designer adeno-associated virus that permits robust retrograde access to NAc-afferent projection neurons. Cre-dependent viruses injected into CRH-Cre mice enabled selective mapping of CRH+ afferents. We employed anterograde AAV1-directed axonal tracing to verify NAc CRH+ fiber projections and established the identity of genetic reporter-labeled cells via validated antisera against native CRH. We quantified the relative contribution of CRH+ neurons to total NAc-directed projections. Combined retrograde and anterograde tracing identified the paraventricular nucleus of the thalamus, bed nucleus of stria terminalis, basolateral amygdala, and medial prefrontal cortex as principal sources of CRH+ projections to NAc. CRH+ NAc afferents were selectively enriched in NAc-projecting brain regions involved in diverse aspects of the sensing, processing and memory of emotionally salient events. These findings suggest multiple, complex potential roles for the molecularly-defined, CRH-dependent circuit in modulation of reward and motivation behaviors.