Imaging of Large Airway Disorders.

Large airway disorders encompass a large variety of diseases and pathology, with broad categories including anatomic variants, congenital abnormalities, acquired abnormalities, inflammatory/infiltrative causes, infection, and tumors. The most common diseases in each category are discussed with a focus on the salient imaging findings. Pitfalls to beware of are discussed through the article, and concludes with a general method to approaching large airways pathology that should provide the reader with a basic framework and understanding of this complex topic.

Beyond schwannomas and neurofibromas: a radiological and histopathological review of lesser-known benign lesions that arise in association with peripheral nerves.

Peripheral nerve sheath tumors comprise a significant percentage of both benign and malignant soft tissue tumors. The vast majority of these lesions are schwannomas and neurofibromas, which most radiologists are familiar with including the well-described multimodality imaging features. However, numerous additional often under-recognized benign entities associated with nerves exist. These rarer entities are becoming increasingly encountered with the proliferation of cross-sectional imaging, particularly magnetic resonance imaging (MRI). It is important for the radiologist to have a basic understanding of these entities as many have near-pathognomonic MR imaging features as well as specific clinical presentations that when interpreted in concert, often allows for a limited differential or single best diagnosis. The ability to provide a prospective, pre-intervention diagnosis based solely on imaging and clinical presentation is crucial as several of these entities are "do not touch" lesions, for which even a biopsy may have deleterious consequences. To our knowledge, the majority of these benign entities associated with nerves have only been described in scattered case reports or small case series. Therefore, the aim of this article is to provide a radiopathologic comprehensive review of these benign entities that arise in association with nerves with a focus on characteristic MRI features, unique histopathologic findings, and entity specific clinical exam findings/presentation.

Diazepam Inhibits Post-Traumatic Neurogenesis and Blocks Aberrant Dendritic Development.

Traumatic brain injury (TBI) triggers a robust increase in neurogenesis within the dentate gyrus of the hippocampus, but these new neurons undergo aberrant maturation and dendritic outgrowth. Because gamma-aminobutyric acid (GABA)A receptors (GABAARs) modulate dendritic outgrowth during constitutive neurogenesis and GABAAR-modulating sedatives are often administered to human patients after TBI, we investigated whether the benzodiazepine, diazepam (DZP), alters post-injury hippocampal neurogenesis. We used a controlled cortical impact (CCI) model of TBI in adult mice, and administered DZP or vehicle continuously for 1 week after injury via osmotic pump. Although DZP did not affect the neurogenesis rate in control mice, it almost completely prevented the TBI-induced increase in hippocampal neurogenesis as well as the aberrant dendritic growth of neurons born after TBI. DZP did not reduce cortical injury, reactive gliosis, or cell proliferation early after injury, but decreased c-Fos activation in the dentate gyrus at both early and late time-points after TBI, suggesting an association between neuronal activity and post-injury neurogenesis. Because DZP blocks post-injury neurogenesis, further studies are warranted to assess whether benzodiazepines alter cognitive recovery or the development of complications after TBI.

Conscious sedation versus rapid sequence intubation for the reduction of native traumatic hip dislocation.

BACKGROUND: Traumatic hip dislocations (THD) are a medical emergency. There is debate whether the painful reduction of a dislocated hip should be first attempted using primary conscious sedation (PCS) or primary general anesthesia (PGA) METHODS: All cases of native THD from 2006 to 2015 in the trauma registry of a level 1 trauma center were reviewed. The primary outcome was successful reduction of the THD. RESULTS: 67 patients had a native, meaning not a hip prosthesis, THD. 34 (50.7%) patients had successful PCS, 12 (17.9%) failed PCS and underwent reduction following PGA. 21 (31.3%) underwent PGA. Patients in the PGA group were more severely injured. Time to reduction greater than 6 h was associated with PCS failure (Odds ratio (95% confidence interval) 19.75 (2.06,189.10) p = 0.01). CONCLUSION: Clinicians treating patients with a THD can utilize either PCS or PGA with many patients safely reduced under PCS. However, patients whose hip have been dislocated for more than 6 h are at risk for failure with PCS, and are good candidates for PGA.

Neuroligin1 drives synaptic and behavioral maturation through intracellular interactions.

In vitro studies suggest that the intracellular C terminus of Neuroligin1 (NL1) could play a central role in the maturation of excitatory synapses. However, it is unknown how this activity affects synapses in vivo, and whether it may impact the development of complex behaviors. To determine how NL1 influences the state of glutamatergic synapses in vivo, we compared the synaptic and behavioral phenotypes of mice overexpressing a full-length version of NL1 (NL1FL) with mice overexpressing a version missing part of the intracellular domain (NL1ΔC). We show that overexpression of full-length NL1 yielded an increase in the proportion of synapses with mature characteristics and impaired learning and flexibility. In contrast, the overexpression of NL1ΔC increased the number of excitatory postsynaptic structures and led to enhanced flexibility in mnemonic and social behaviors. Transient overexpression of NL1FL revealed that elevated levels are not necessary to maintain synaptic and behavioral states altered earlier in development. In contrast, overexpression of NL1FL in the fully mature adult was able to impair normal learning behavior after 1 month of expression. These results provide the first evidence that NL1 significantly impacts key developmental processes that permanently shape circuit function and behavior, as well as the function of fully developed neural circuits. Overall, these manipulations of NL1 function illuminate the significance of NL1 intracellular signaling in vivo, and enhance our understanding of the factors that gate the maturation of glutamatergic synapses and complex behavior. This has significant implications for our ability to address disorders such as autism spectrum disorders.