Placental thickness in 2D prenatal ultrasonographic examination.

Introduction: The placental thickness (PTh) is an ultrasonographic measurement commonly used to assess the placenta. The study aimed to determine selected factors influencing PTh in 2D prenatal ultrasonographic examination. It might have a special value in difficult cases for interpretation when PTh is above or below the reference values. Material and methods: In this retrospective study, we analysed the results of foetal ECHO examination of 2833 foetuses performed between June 2016 and December 2019 in our single unit. 596 healthy foetuses older than 12 weeks of gestation from singleton pregnancies were enrolled in the study. The following parameters were used in the further analysis: placental implantation site, gestational age according to the last menstrual period (LMP) and foetal biometry (FB); maternal weight, height, and body mass index (BMI) at the time of examination; and PTh. Results: PTh was affected by its location: posterior 33 mm vs. anterior 30 mm (p < 0.001). Moreover, its thickness significantly correlated with gestational age according to FB (r = 0.386, p < 0.001), LMP (r = 0.369, p < 0.001), maternal weight (r = 0.192, p < 0.001), height (r = 0.125, p = 0.002), and BMI (r = 0.147, p < 0.001), but not with maternal age (r = 0.050, p = 0.219). A linear regression model based on these data explained the 16.38% variability of the tested subjects (p < 0.001). Conclusions: Our observations suggest that maternal weight correlated more strongly with PTh than maternal BMI. For PTh evaluation, it is important to pay attention to the placental implantation site - the posterior placenta was thicker than the anterior placenta. Moreover, PTh variability remains largely unknown; therefore, further research in this field is needed.

The Superior Cerebellar Artery: Variability and Clinical Significance.

The superior cerebellar artery (SCA) arises from the distal part of the basilar artery and passes by the oculomotor, trochlear, and trigeminal nerves. SCA is known to play a crucial role in the development of trigeminal neuralgia. However, due to its anatomical variability, it may also trigger other neurovascular compression (NVC), including hemifacial spasm, oculomotor nerve palsy, and ocular neuromyotonia. Additionally, it may be associated with ischemic syndromes and aneurysm development, highlighting its clinical significance. The most common anatomical variations of the SCA include duplication, a single vessel origin from the posterior cerebral artery (PCA), and a common trunk with PCA. Rarely observed variants include bifurcation and origin from the internal carotid artery. Certain anatomical variants such as early bifurcation and caudal course of duplicated SCA trunk may increase the risk of NVC. In this narrative review, we aimed to examine the impact of the anatomical variations of SCA on the NVCs based on papers published in Pubmed, Scopus, and Web of Science databases with a snowballing approach. Our review emphasizes the importance of a thorough understanding of the anatomical variability of SCA to optimize the management of patients with NVCs associated with this artery.

The Underlying Pathogenesis of Neurovascular Compression Syndromes: A Systematic Review.

Neurovascular compression syndromes (NVC) are challenging disorders resulting from the compression of cranial nerves at the root entry/exit zone. Clinically, we can distinguish the following NVC conditions: trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia. Also, rare cases of geniculate neuralgia and superior laryngeal neuralgia are reported. Other syndromes, e.g., disabling positional vertigo, arterial hypertension in the course of NVC at the CN IX-X REZ and torticollis, have insufficient clinical evidence for microvascular decompression. The exact pathomechanism leading to characteristic NVC-related symptoms remains unclear. Proposed etiologies have limited explanatory scope. Therefore, we have examined the underlying pathomechanisms stated in the medical literature. To achieve our goal, we systematically reviewed original English language papers available in Pubmed and Web of Science databases before 2 October 2021. We obtained 1694 papers after eliminating duplicates. Only 357 original papers potentially pertaining to the pathogenesis of NVC were enrolled in full-text assessment for eligibility. Of these, 63 were included in the final analysis. The systematic review suggests that the anatomical and/or hemodynamical changes described are insufficient to account for NVC-related symptoms by themselves. They must coexist with additional changes such as factors associated with the affected nerve (e.g., demyelination, REZ modeling, vasculature pathology), nucleus hyperexcitability, white and/or gray matter changes in the brain, or disturbances in ion channels. Moreover, the effects of inflammatory background, altered proteome, and biochemical parameters on symptomatic NVC cannot be ignored. Further studies are needed to gain better insight into NVC pathophysiology.